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Child Psychologyand Psychiatry

Child Psychologyand PsychiatryFrameworks for Practice

Second Edition

Edited by

David Skuse, MD, FRCP, FRCPsych, FRCPCHHead of Behavioural and Brain Sciences Unit,University College London Institute of Child Health;Honorary Consultant, Great Ormond Street Hospital for Children,London, UK

Helen Bruce, FRCPsychConsultant Child and Adolescent Psychiatrist, East London NHS Foundation Trust;Honorary Senior Clinical Lecturer, Barts and the London School of Medicine and Dentistry,London, UK

Linda Dowdney, MA, M.Phil, PhDConsultant Child Clinical Psychologist;Honorary Senior Lecturer, University College London Institute of Child Health,London, UK

David Mrazek, MD, FRCPsychProfessor of Psychiatry,Mayo Clinic College of Medicine,Rochester, MN, USA

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Child psychology and psychiatry : frameworks for practice / David Skuse . . . [et al.].p. cm.

Includes index.ISBN 978-0-470-97382-0 (pbk.)1. Child psychology. 2. Child psychiatry. I. Skuse, D. (David)BF721.C5157 2011155.4–dc22

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Contents

Contents

List of Contributors vii

Preface xi

Section 1: DevelopingCompetencies1a: Contextual Influences upon Socialand Emotional Development

1. Family and Systemic Influences 3Barbara Maughan

2. Sibling Influences 8Judy Dunn

3. Culture and Child Development 13Ruma Bose and Sanjida Sattar

4. Neurobehavioural Developmentin Infancy 18Cindy H. Liu and Ed Tronick

5. Genetic and Biological Influences 23David Skuse

1b: General Patterns of Development6. Clinical Evaluation of Development

from Birth to Five Years 32Ajay Sharma and Tony O’Sullivan

7. Early Social and Emotional ExperienceMatters: The First Year of Life 41Howard Steele

8. Language Development 45Thomas Klee and Stephanie F. Stokes

9. Development of Social Cognition 51Virginia Slaughter

10. Social and Emotional Developmentin Middle Childhood 56Alan Carr

11. Social-Cognitive Development DuringAdolescence 62Sarah-Jayne Blakemore

Section 2: Promoting Well-Being12. Promoting Infant Mental Health 68

Christine Puckering

13. Promoting Children’s Well-Being 72Paul Stallard

14. Fostering Resilience in Adolescents 78Angela Veale

Section 3: Attachment andSeparation15. Attachment Theory: Research

and Clinical Implications 85Pasco Fearon

16. Children Bereaved by Parent orSibling Death 92Linda Dowdney

17. Adoption and Fostering 100Jill Hodges

Section 4: The Impact of Traumaand Maltreatment18. Stress and Reactions to Stress

in Children 107Guinevere Tufnell

19. Child Maltreatment 114Danya Glaser

20. The Neuroscience and Geneticsof Childhood Maltreatment 121Eamon McCrory, Stephane A. De Brito,and Essi Viding

v

Contents

Section 5: Atypical Development5a: Infancy and Early Childhood21. Feeding and Eating Disorders

in Infancy and Childhood 128Rachel Bryant-Waugh

22. Literacy Disorders 134Valerie Muter and Margaret J. Snowling

5b: Middle Childhood23. Autism Spectrum Disorders 141

Tony Charman

24. Somatization and SomatoformDisorders 147Elena Garralda

25. Attention-Deficit HyperactivityDisorder 153Anita Thapar and AntonioMunoz-Solomando

26. Challenges in Child and AdolescentObsessive-Compulsive Disorder 161Elaine Chung and Isobel Heyman

27. Anxiety Disorders in Childrenand Adolescents 169Aaron Vallance and Elena Garralda

28. Childhood Behavioural Disorders 175Graeme Lamb

29. Specific Language Impairment 180Gina Conti-Ramsden and Kevin Durkin

5c: Adolescence30. Depression and Suicidal Behaviour

in Children and Adolescents 187Julia Gledhill and Matthew Hodes

31. Eating Disorders in Adolescence 194Dasha Nicholls

32. Substance Misuse in Young People 201K.A.H. Mirza, Roshin M. Sudesh, andSudeshni Mirza

33. Early-Onset Bipolar Disorder 210Anthony James

34. Emerging Personality Disorder 217Eileen Vizard

Section 6: Assessment35. Diagnostic Classification: Current

Dilemmas and Possible Solutions 224Eric Taylor

36. Paediatric NeuropsychologicalAssessment I: An AssessmentFramework 229Judith Middleton

37. Paediatric NeuropsychologicalAssessment II: Domains forAssessment 234Jane Gilmour and Bettina Hohnen

38. Assessment of Child PsychiatricDisorders 245Helen Bruce and Navina Evans

39. Psychological Assessment 251Michael Berger

40. Family Therapy Assessment 255Alexandra Mary John

Section 7: Approachesto Intervention41. Discovering Psychiatric

Pharmacogenomics 261David A. Mrazek

42. Cognitive–Behavioural Therapy forChildren and Adolescents 265Cathy Creswell and Thomas G. O’Connor

43. Parenting Programmes for ConductProblems 271Stephen Scott and Sajid Humayun

44. Systemic and Family Approachesto Intervention 276Philip Messent

45. Psychotherapeutic Approaches:A Psychodynamic Perspective 281Eilis Kennedy

46. Paediatric Psychopharmacology:Special Considerations 286Paramala J. Santosh and Rakendu Suren

Index 295

vi

List of contributors

List of Contributors

Michael BergerDepartment of Psychology, Royal Holloway,University of London, Egham, TW20 0EX, UK

Sarah-Jayne BlakemoreInstitute of Cognitive Neuroscience, UniversityCollege London, 17 Queen Square, London,WC1N 3AR, UK

Ruma BoseAdolescent Mental Health Team, TowerHamlets, Children and Young People’s Centre,16–18 Greatorex Street, London, E1 5NF, UK

Helen BruceConsultant Child and Adolescent PsychiatristEast London NHS Foundation Trust; HonorarySenior Clinical Lecturer Barts and the LondonSchool of Medicine and Dentistry, London, UK

Rachel Bryant-WaughDepartment of Child and Adolescent MentalHealth, Great Ormond Street Hospital forChildren NHS Trust, Great Ormond Street,London, WC1N 3JH, UK

Alan CarrSchool of Psychology, Newman Building,University College Dublin, Belfield, Dublin 4,Ireland

Tony CharmanCentre for Research in Autism and Education(CRAE), Department of Psychology and HumanDevelopment, Institute of Education, 25 WoburnSquare, London, WC1H 0AA, UK

Elaine ChungChild and Adolescent Mental Health Service, TheRoyal Free Hospital, Pond Street, London, NW32QG, UK

Gina Conti-RamsdenSchool of Psychological Sciences, The Universityof Manchester, Ellen Wilkinson Building, OxfordRoad, Manchester, M13 9PL, UK

Cathy CreswellSchool of Psychology and Clinical LanguageSciences, University of Reading, Reading, RG66AL, UK

Stephane A. De BritoDevelopmental Risk & Resilience Unit,University College London, Clinical, Educational,and Health Psychology Research Department,Division of Psychology and Language Sciences,26 Bedford Way, London, WC1H 0AP, UK

Linda DowdneyInstitute of Child Health, University CollegeLondon, 30 Guilford Street, London, WC1N1EH, UK

Judy DunnKing’s College London, Institute of Psychiatry,London, SE5 8AF, UK

Kevin DurkinSchool of Psychological Sciences and Health,University of Strathclyde, Graham Hills Building,40 George Street, Glasgow, G1 1QE, UK

vii


Navina EvansCoborn Centre for Adolescent Mental Health,Newham Centre for Mental Health, Cherry TreeWay, Glen Road, London, E13 8SP, UK

Pasco FearonResearch Department of Clinical, Educationaland Health Psychology, University CollegeLondon, London, UK

Elena GarraldaAcademic Unit of Child and AdolescentPsychiatry, Imperial College London, St Mary’sCampus, Norfolk Place, London, W2 1PG, UK

Jane GilmourInstitute of Child Health, University CollegeLondon, 30 Guilford Street, London, WC1N1EH, UK

Danya GlaserDepartment of Child and Adolescent MentalHealth, Great Ormond Street Hospital forChildren NHS Trust, Great Ormond Street,London, WC1N 3JH, UK

Julia GledhillAcademic Unit of Child and AdolescentPsychiatry, Imperial College London, St Mary’sCampus, Norfolk Place, London W2 1PG, UK

Isobel HeymanNational and Specialist Child and AdolescentMental Health Services, South London andMaudsley NHS Foundation Trust, Denmark Hill,London SE5 8AZ UK; Children’s Department,Institute of Psychiatry, DeCrespigny Park,London SE5 8AF UK

Matthew HodesAcademic Unit of Child and AdolescentPsychiatry, Imperial College London, St Mary’sCampus, Norfolk Place, London, W2 1PG, UK

Jill HodgesDepartment of Child and Adolescent MentalHealth, Great Ormond Street Hospital forChildren NHS Trust, Great Ormond Street,London, WC1N 3JH, UK

Bettina HohnenGreat Ormond Street Hospital for Children NHSTrust, Great Ormond Street, London, WC1N3JH, UK

Sajid HumayunNational Academy for Parenting Research,Institute of Psychiatry, King’s College London, 16De Crespigny Park, London, SE5 8AF, UK

Anthony JamesUniversity of Oxford, Highfield Adolescent Unit,Warneford Hospital, Oxford, OX3 7JX, UK

Alexandra Mary JohnUniversity of Surrey and Sussex PartnershipFoundation NHS Trust, Department ofPsychology, University of Surrey, Guildford, GU27XH, UK

Eilis KennedyChild and Family Department, The Tavistock andPortman NHS Foundation Trust, TavistockCentre, 120 Belsize Lane, London, NW3 5BA,UK

Thomas KleeDepartment of Communication Disorders, NewZealand Institute of Language, Brain andBehaviour, University of Canterbury|Te WhareWananga o Waitaha, Christchurch 8140, NewZealand

Graeme LambNewham Child and Family Consultation Service,York House, 411 Barking Rd, London, E13 8AL,UK

Cindy H. LiuChildren’s Hospital, Boston, Harvard MedicalSchool, 1295 Boylston Street, Boston, MA 02115,USA

Eamon McCroryDevelopmental Risk and Resilience Unit,University College London, Clinical, Educational,and Health Psychology Research Department,Division of Psychology and Language Sciences, 26Bedford Way, London, WC1H 0AP, UK

viii


Barbara MaughanMRC Social, Genetic and DevelopmentalPsychiatry Centre, Institute of Psychiatry, King’sCollege London, De Crespigny Park, LondonSE5 8AF, UK

Philip MessentHead of Family Therapy, Tower HamletsCAMHS, 16–18 Greatorex Street, London, E15NF, UK

Judith MiddletonClinical Neuropsychologist, 15 Complins Close,Oxford, OX2 6PZ, UK

K.A.H. MirzaDepartment of Child and Adolescent Psychiatry,Institute of Psychiatry, King’s College London,De Crespigny Park, London, SE5 8AF, UK

Sudeshni MirzaDr. Somerwell Memorial CSI Medical CollegeHospital, Karakonam, Kerala, India

David A. MrazekDepartment of Psychiatry and Psychology, MayoClinic College of Medicine, 200 First Street SW,Rochester, MN 55905, USA

Antonio Munoz-SolomandoTonteg Child and Family Centre, TontegHospital, Church Road, Pontypridd, CF38 1HE,UK

Valerie MuterGreat Ormond Street Hospital for Children NHSTrust, Great Ormond Street, London, WC1N3JH, UK

Dasha NichollsDepartment of Child and Adolescent MentalHealth, Great Ormond Street Hospital forChildren NHS Trust, Great Ormond Street,London, WC1N 3JH, UK

Thomas G. O’ConnorDepartment of Psychiatry, University ofRochester Medical Center, 300 Crittenden Blvd,Rochester, NY 14642, USA

Tony O’SullivanKaleidoscope – Lewisham Centre for Childrenand Young People, 32 Rushey Green, Catford,London, SE6 4JF, UK

Christine PuckeringCaledonia House, Royal Hospital for SickChildren, Yorkhill, Glasgow, G3 8SJ, UK

Paramala J. SantoshCentre for Interventional PaediatricPsychopharmacology, Department of Child andAdolescent Mental Health, Great Ormond StreetHospital for Children NHS Trust, Great OrmondStreet, London, WC1N 3JH, UK

Sanjida SattarIslington Community CAMHS, 580 HollowayRoad, London N7 6LB, UK

Stephen ScottInstitute of Psychiatry, King’s College London,Department of Child and Adolescent Psychiatry,De Crespigny Park, London, SE5 8AF, UK

Ajay SharmaSunshine House, Southwark Centre for Childrenand Young People, 27 Peckham Road, London,SE5 8UH, UK

David SkuseInstitute of Child Health, University CollegeLondon, 30 Guilford Street, London, WC1N1EH, UK

Virginia SlaughterEarly Cognitive Development Centre, Universityof Queensland, Brisbane 4072, Australia

Margaret J. SnowlingDepartment of Psychology, University of York,York, YO10 5DD, UK

Paul StallardChild and Adolescent Mental Health Services,Oxford Health NHS Foundation Trust, Bristol,BS31 1HA, UK

ix


Howard SteeleDepartment of Psychology, New School for SocialResearch, Room 611, 80 Fifth Avenue, NewYork, NY 10011, USA

Stephanie F. StokesDepartment of Communication Disorders,University of Canterbury/Te Whare Wananga oWaitaha, Christchurch 8140, New Zealand

Roshin M. SudeshKing’s College Hospital,Guys Campus, St. Thomas StreetLondon SE1 7EH, UK

Rakendu SurenDepartment of Psychological Medicine, GreatOrmond Street Hospital for Children NHS Trust,Great Ormond Street, London, WC1N 3JH, UK

Eric TaylorInstitute of Psychiatry, King’s College London,De Crespigny Park, London, SE5 8AF, UK

Anita ThaparChild and Adolescent Psychiatry Section,Department of Psychological Medicine andNeurology, Cardiff University, School ofMedicine, Heath Park, Cardiff,CF14 4XN, UK

Ed TronickChildren’s Hospital, Boston, Harvard MedicalSchool, Boston, MA, USA; University ofMassachusetts, Department of Psychology, 100Morrisey Blvd, Boston, MA 02125, USA

Guinevere TufnellThe Traumatic Stress Clinic, Great OrmondStreet Hospital for Children NHS Trust, GreatOrmond Street, London WC1N 3JH, UK

Aaron Keith VallanceAcademic Unit of Child and AdolescentPsychiatry, Imperial College London, St Mary’sCampus, Norfolk Place, London, W2 1PG, UK

Angela VealeSchool of Applied Psychology, North Mall,University College Cork, Ireland

Essi VidingDevelopmental Risk and Resilience Unit,University College London, Clinical, Educational,and Health Psychology Research Department,Division of Psychology and Language Sciences, 26Bedford Way, London, WC1H 0AP, UK

Eileen VizardUniversity College London, 7–8 GreenlandPlace, London, NW1 0AP, UK

x

Preface

Preface

A key skill that professionals working with vul-nerable children need, is to understand how theydevelop competence. What role do neurobiologyand genetic variability play in development? Howdo relationships with parents and siblings affectsocial and emotional adjustment? How importantis the culture in which families live? We addressthese questions in the first part of the book.Here, leading researchers and clinicians discussthe physical, social, cognitive and emotionaldevelopment of the child within his or her familialand cultural context.

Practising clinicians wish to know how to pro-mote children’s well-being. In our second section,we address how this can be done throughout thestages of a child’s development, including ways offostering resilience in troubled adolescents. Thistheme is picked up in subsequent chapters, whereauthors discuss the clinical and research implica-tions of attachment theory and their influence onchildren’s adjustment to bereavement, adoptionand fostering. There are lessons to be learned too,from recent developments in neurobiology andgenetics, on individual differences to stress andmaltreatment.

Child development does not always follow asmooth or predictable trajectory. Common disor-ders tend to appear at key developmental stagesfrom infancy through to adolescence.

Feeding disorders usually have their onset ininfancy and early childhood. Early interventionis needed to avert persistence into later life; ourauthors discuss why and how clinicians shouldintervene. Literacy disorders are an issue for manychildren at school and can have far-reaching con-sequences for their educational progress. How toassess and manage this complex learning difficultyis illustrated by our authors. Throughout, the book

emphasizes early recognition and recommendsinterventions that favour optimal outcomes.

Middle childhood is a challenging time as rela-tionships with peers, school and the wider socialworld become ever more complex. Negotiatingone’s way successfully requires ever-increasingsocial awareness and empathy, and an understand-ing that other people’s perspective on things maybe quite different to your own. During this develop-mental period, clinicians see an increasingly widerange of difficulties and disorders emerging. Sothat we can provide appropriate and effectivetreatments, it is important to recognize the crit-ical symptoms early. The clinical goal is to buildup the resilience of the child and family so thatany disruption to the child’s psychological, socialand emotional development is minimized. In oursections about psychopathology, authors outlinethe key features of common disorders, alongsideguidance on how to intervene. Chapters summarizecurrent key practice points and anticipate futuredevelopments.

During adolescence, the child and family mustnegotiate issues of individuation, autonomy andparental authority. While family support remainscrucial to an adolescent’s development, theirworld outside the family exerts a major influenceon well-being. Despite the potential for the growthin emotional and social understanding, as well asin increasing independence, this is a time whenwe find significant internalizing and externalizingpsychopathology emerging. Common disordersinclude depression, self-harm, eating disordersand substance misuse, with some vulnerableyoung people affected by bipolar or schizophrenicpsychoses.

In the latter sections, contributors discuss thespecifics of assessment and intervention. What are

xi

Preface

the current dilemmas in diagnostic classification?Can the diagnostic systems reflected in ICD-11 andDSM-5 come close to resolving them? When wemake a clinical assessment, theoretical frameworksguide us, and these in turn draw on knowledgegleaned from research in neuropsychology, clinicalpsychology, psychiatry and an understanding offamily systems.

Finally, we consider approaches to intervention.When prescribing medication to rectify children’sbehaviour or emotional adjustment, we will infuture be drawing on new findings in pharmacoge-nomics. Discoveries about the way our genes shapeour biology will dramatically influence prescribingpractices. While we await such future develop-ments, contributors discuss current best practicein psychopharmacology, as well as reviewingother essential interventions such as parentingprogrammes, cognitive–behavioural therapy and

psychotherapy, alongside systemic and familytherapy approaches.

Based upon strong academic foundations, com-bined with state-of-the art clinical expertise, weprovide an essential text not only for traineeclinicians, but also for those wishing to updatetheir clinical practice. Conceived with busy pro-fessionals in mind, this introduction to clinicalchild psychology and psychiatry is concisely writ-ten, and its content is clearly presented so as tobe rapidly and easily absorbed. Key messages andfuture directions are highlighted. This book is anessential guide for those working or training in allclinical and community child settings.

David SkuseHelen Bruce

Linda DowdneyDavid A. Mrazek

xii

Section 1

Developing Competencies

Section 1a

Contextual Influencesupon Social and EmotionalDevelopment

Contextual influences upon social and emotional development

1Family and Systemic InfluencesBarbara MaughanMRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King’s CollegeLondon, London, UK

Numerous contexts interweave to support chil-dren’s emotional and behavioural development.In early childhood, family networks are central tothose contexts; as children develop, their socialworlds expand to take in childcare and schoolsettings, and relationships with friends and peers.Each of these systems, and the interactions withinand among them, influences children’s growingcompetencies. Each is also embedded within, andaffected by, broader social and cultural influences,and by variations in access to social and materialresources. Ecological theories of development [1]emphasize the interplay among these various levelsof influence, some proximal to, others more distantfrom, the child. Figure 1.1 shows a schematic ver-sion of a model of this kind, highlighting just someof the broad range of contextual factors knownto carry implications for children’s emotional andbehavioural development.

FAMILY RELATIONSHIPS AND PARENTING

Family relationships are complex: each dyadic rela-tionship is affected by other relationships in thefamily system, and children both influence and areinfluenced by those around them [2]. Even veryyoung infants affect the nature of interactions withcaregivers, and variations in children’s tempera-mental styles continue to evoke differing responsesfrom carers. In part, variations of this kind reflectchildren’s inherited characteristics; indeed, manyaspects of family relationships and functioningonce thought to be purely ‘environmental’ in ori-gin are now known to reflect elements of ‘nature’

Child Psychology and Psychiatry: Frameworks for practice, Second Edition. Edited by David Skuse, Helen Bruce,Linda Dowdney and David Mrazek. 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.

as well as ‘nurture’ [3]. Children play an activepart in shaping the environments they experience;their genetic make-up also affects individual dif-ferences in sensitivity to environmental influences,contributing to both resilience and vulnerability tostress [4].

Families are biologically and culturally evolvedto promote children’s development [5]. Some ofthe earliest steps in those processes – prenatal andpostnatal influences on neurobiological regulation,and early attachment relationships – are discussedin detail in other chapters. But family relation-ships and parenting show ongoing links with thedevelopment of children’s behavioural control,and with the regulation of their attentional, arousaland emotional systems throughout childhood. Inaddition, parents contribute to children’s cogni-tive development; socialize them into culturallyappropriate patterns of behaviour; promote theirunderstanding of moral values and the develop-ment of their talents; and select and secure theiraccess to key resources beyond the family system.

Successful parenting involves numerous skillsand capacities, varying with the age of the child,with culture, and with social context. Underlyingthis diversity, most models of parenting highlighttwo central dimensions, one related to parentalinvolvement and responsiveness (encompassingwarmth, availability, positive engagement and sup-port), the second centring on ‘demandingness’or behavioural control, and incorporating moni-toring, expectations and behaviour management.Combinations of these dimensions have been usedto characterize four general styles of parenting [6]:

3

Family and systemic influences

child

family

peers

school

neighbourhood

community

culture

socioeconomicstatus parentingparents material

circumstances

Figure 1.1 Ecological model of influences on development.

• Indulgent (responsive but not demanding):parents are non-traditional and lenient, allowconsiderable self-regulation, and avoid confron-tation.

• Authoritarian (demanding but not responsive):parents are obedience- and status-oriented, andexpect orders to be obeyed without explanation.

• Authoritative (both demanding and respon-sive): parents are assertive, but not intrusive orrestrictive. Disciplinary methods are supportiverather than punitive. Children are expectedto be assertive as well as socially responsible,self-regulated as well as cooperative.

• Uninvolved (both unresponsive and undemand-ing): most parenting of this type falls withinthe normal range, but in extreme cases itmight encompass both rejecting–neglecting andneglectful parenting.

Comparisons across these styles consistentlyhighlight authoritative parenting as most stronglyassociated with positive child outcomes in arange of domains: self-discipline, emotionalself-control, positive peer relationships and schoolperformance.

When children are under stress, family life canalso provide compensatory experiences. Cohesionand warmth within the family, the presence of agood relationship with one parent, close siblingrelationships, and effective parental monitoringare all known to represent protective influences of

this kind. Finally, when parenting is compromised,risks of emotional and behavioural difficultiesincrease. The implications of severe problems inparenting, involving abuse or neglect, are discussedelsewhere in this volume, as are family-based risksfor specific childhood disorders. At a more generallevel, risks of this kind appear to reflect problemsin four broad aspects of family relationships andparenting:

• Discordant/dysfunctional relationships betweenparents, or in the family system as a whole.

• Hostile or rejecting parent–child relationships,or those markedly lacking in warmth.

• Harsh or inconsistent discipline.• Ineffective monitoring and supervision.

Many family-based interventions and parentingprogrammes are designed to target difficulties ofthese kinds.

PARENT AND FAMILY CHARACTERISTICS

Some parent and family characteristics also showsystematic links with children’s risk of emotionaland behavioural problems. Parents’ own mentalhealth is among the most important of these. Inpart, these associations may reflect heritable influ-ences; in part, they seem likely to follow from theeffects of parents’ mental health problems on mar-ital relationships and parenting. Depressed moth-ers, for example, are known to be less sensitive

4


and responsive to their infants, and attend less,and respond more negatively, to older children[7]. Alcohol and drug abuse and major men-tal disorders in parents may impair parentingin more wide-ranging ways; when parents areantisocial, effects may also be mediated throughthe endorsement of antisocial attitudes and sociallearning.

Childhood conduct problems are more commonamong the children of very young mothers [8],often reflecting associated educational and socialdisadvantages and lack of social supports. Thespecific contributions of fathers’ parenting, fatherabsence and relationships with non-resident par-ents are attracting increasing attention in research[9]. Large family size may be associated withincreased risk for delinquency, but has few linkswith other aspects of children’s adjustment. Onlychildren are not typically at any increased psychi-atric risk, and share with other first-borns somesmall advantages in cognitive development. Birthorder also appears to have few implications forbehavioural adjustment, although youngest chil-dren show some increased rates of school refusal.

CHANGING FAMILY PATTERNS

Recent decades have seen major changes in pat-terns of family formation and stability in manyWestern societies [10]. Families are formed later,and are smaller, than in the past; fewer parentsmarry, and more divorce; and many more womennow return to work outside the home when theirchildren are young. As a result, more childrentoday experience out of home and other non-parental care in early childhood, and many alsoface transitions in their family lives: parental sep-aration and divorce are often followed by periodsin single-parent households, and subsequently bythe establishment of new step families.

Single parents and step familiesOn average, children in single-parent and stepfamilies show somewhat higher levels of emotionaland behavioural difficulties than those in stabletwo-parent homes [11,12]. In general, however,these effects are modest, and there is muchvariation within as well as between family types;importantly, associations between the qualityof mother–child relationships and children’sadjustment are similar across family settings.

Single-parent and reconstituted families also oftenface economic pressures, and may lack socialand family supports; mothers may also be undergreater stress. Once these variations are taken intoaccount, family type per se shows few consistentlinks with children’s adjustment.

Parental separation and divorceWhen parents separate, most children show someshort-term behavioural or emotional difficulties; ingeneral, these disturbances are not severe. Schoolprogress and motivation may also be affected,and longer-term influences have been detectedon young people’s own patterns of relationshipformation and stability later in life [13]. Researchsuggests that these responses are not simply ‘one-off’ effects of parental separation; many childrenexperience parental discord before their parentsseparate, and divorce itself is often followed by acascade of other changes. Problematic relation-ships between parents may continue, and par-ents themselves are likely to be distressed. Inaddition, many families face marked declines ineconomic circumstances, and for some childrenparental separation will be followed by housemoves, school changes, and other disruptions totheir social networks. Later outcomes for childrenmay be impacted by each and any element of thiscomplex network of change.

CHILDCARE AND SCHOOLING

By the late 1990s almost half of mothers in theUK returned to full or part-time work before theirinfants were 1 year old. As a result, grandpar-ents play an increasingly important part in manyyoung children’s lives [14], and there has beenmajor interest in the impact of non-maternal careon children’s development [9]. Research suggeststhat multiple features of early childcare need to betaken into account in assessing its effects. Higherquality childcare (including, e.g., variations in sen-sitive and responsive caregiving, and cognitive andlanguage stimulation) is associated with benefits incognitive and language domains, with better earlyacademic skills, and more prosocial behavioursand fewer adjustment difficulties. Especially in thefirst year of life, a higher quantity of childcare(in terms of hours per week in any kind of non-maternal care), is associated with some increasedrisks of behaviour problems and disobedience. As

5

Family and systemic influences

in family settings, individual children’s sensitivityto non-maternal care will vary; indeed, for someat-risk young children, out-of-home care has beenshown to have positive effects on behaviouraldevelopment.

School life offers further opportunities,demands and challenges. Starting and changingschools are significant events for all children.Although most adapt well, a significant minorityof young children show some difficulties whenthey start school, and many young adolescentsshow short-term declines in both their academicperformance and their self-esteem when theytransfer from primary to secondary school. Testsand examinations figure high on children’s lists offears, and major examinations are often associatedwith some increases in psychological distress.Bullying – a problem especially associated withthe school context – is attracting increasing atten-tion as a risk factor for children’s mental health[15]. Surveys suggest that quite large proportionsof children experience occasional bullying atschool, and that smaller groups are persistentlyvictimized. Although such children may haveshown anxious and insecure behaviours beforethey started school, there is now clear evidencethat bullying has independent effects on risks oflater adjustment problems.

Like families, schools vary in their social andorganizational ‘climates’ in ways that have modestbut independent effects on children’s academicprogress and behaviour [16]. In part, thesevariations reflect variations in the backgroundcharacteristics of the children each school admits;in part, they seem attributable to differences inorganizational characteristics and the tenor ofday-to-day school life. Schools with more positivechild outcomes have consistently been found tobe characterized by purposeful leadership, con-structive classroom management, an appropriateacademic emphasis, and consistent but not over-severe sanctions. For behavioural outcomes, thecomposition of pupil groupings may also be impor-tant. Young children are more likely to becomeaggressive if they are placed in classes with othervery aggressive children, and risks of delinquencymay be increased in secondary schools with largeproportions of low achievers. By the same token,school- and classroom-based interventions canprove highly effective in behaviour management,and for some severely disadvantaged children

schooling can be an important source of positiveexperiences and support. In addition, experi-mental studies of preschool programmes havedocumented important long-term gains in terms ofreduced risks of delinquency and unemploymentmany years after participants left school.

WIDER SOCIAL AND ENVIRONMENTALINFLUENCES

Poverty and social disadvantagePoverty and social disadvantage are consistentlyassociated with variations in children’s health,cognitive skills and academic achievements,and – though somewhat more modestly – withtheir social and emotional development [17].Disruptive behaviours in particular show linkswith persistent family poverty, with effects thatare more marked for boys than for girls, andare stronger in childhood than in adolescence.Research suggests that these associations reflectelements of both social selection and causal influ-ences. Especially in families of young children,effects are likely to be indirect, operating throughprocesses whereby poverty imposes stresses onparents, and these in turn impact on familyrelationships and parenting [18]. In more affluentsocieties, relative deprivation – the perception ofdisadvantage by comparison with others – mayalso contribute to parental stress.

Neighbourhood and community contextsRates of behavioural difficulties (and other mark-ers of child health status) also vary with neigh-bourhood context [19]; problem levels may beespecially high in chronically disadvantaged inner-city areas, and the task of parenting may bemore challenging when neighbourhood supportsare poor. Once again, many of these effects seemlikely to be indirect in early childhood, operatingvia increased stress on families. But in severelydisadvantaged settings even quite young childrenmay be directly exposed to community violence,and later in development neighbourhood influ-ences may be mediated through associations withdelinquent peers.

Multiple stressorsFor many children, exposure to these and otheradversities will covary: children in stressed families

6


may also live in poor neighbourhoods, attendpoorly resourced schools, and be exposed todeviant peers. Research suggests that risks atthe child, parenting, peer and sociocultural levelseach add uniquely to the prediction of emotionaland behaviour problems. The total number ofrisks explains further variance in outcomes, andevidence is beginning to accumulate that differingconfigurations of risk are associated with specificemotional and behavioural difficulties [20]. Expo-sure to poverty, for example, may differ in itsimpact depending on parental characteristics andthe quality of family relationships; comprehensiveassessments of family and systemic influencesrequire that each of these levels of influence, andthe interplay between them, be taken into account.

REFERENCES

[1] Bronfenbrenner U. (1979) The Ecology of HumanDevelopment: Experiments by Nature and Design.Cambridge, MA: Harvard University Press.

[2] Maccoby EE. (2007) Historical overview of social-ization research and theory. In: Grusec J and Hast-ings P (eds), Handbook of Socialization. New York:Guilford Press, pp. 13–41.

[3] Plomin R and Bergeman CS. (1991) The natureof nurture. Genetic influences on ‘environmen-tal’ measures. Behavioral and Brain Sciences 14,373–86.

[4] Belsky J, Bakermans-Kranenburg MJ, van IJzen-doorn MH. (2007) For better and for worse:Differential susceptibility to environmental influ-ences. Current Directions in Psychological Science16, 300–4.

[5] Masten AS and Shaffer A. (2006) How families mat-ter in child development: reflections from researchon risk and resilience. In: Clarke-Stewart A andDunn J (eds), Families Count. Cambridge: Cam-bridge University Press, pp 5–25.

[6] Maccoby EE and Martin JA. (1983) Socialization inthe context of the family: parent–child interaction.In: Mussen P and Hetherington EM (eds), Hand-book of Child Psychology, Vol. IV: Socialization,Personality, and Social Development, 4th edn. NewYork: Wiley, pp. 1–101.

[7] Beardslee WR. (1998) Children of affectively ill par-ents: A review of the past 10 years. Journal of the

American Academy of Child and Adolescent Psy-chiatry 37, 1134–41.

[8] Moffitt TE and the E-risk study team. (2002) Teen-aged mothers in contemporary Britain. Journal ofChild Psychology and Psychiatry 43, 727–42.

[9] British Academy. (2010) Social Science and FamilyPolicies. London: British Academy Policy Centre.

[10] Cabinet Office. (2008) Families in Britain: An Evi-dence Paper. London: Cabinet Office.

[11] Dunn J, Deater-Deckard K, Pickering K et al. (1998)Children’s adjustment and prosocial behaviour instep-, single-parent, and non-stepfamily settings:findings from a community study. Journal of ChildPsychology and Psychiatry 39, 1083–95.

[12] Chapple S. (2009) Child Well-being and Sole FamilyStructure in the OECD: An Analysis. OECD Social,Employment and Migration Working Papers No. 86.Paris: Organization for Economic Co-operation andDevelopment.

[13] Rodgers B and Pryor J. (1998) Divorce and Sep-aration: the Outcomes for Children. York: JosephRowntree Foundation.

[14] Dunn J, Fergusson E, Maughan B. (2006) Grandpar-ents, grandchildren, and family change in contempo-rary Britain. In: Clarke-Stewart A and Dunn J (eds),Families Count. Cambridge: Cambridge UniversityPress, pp. 299–318.

[15] Arseneault L, Bowes L, Shakoor S. (2010) Bullyingvictimization in youths and mental health problems:‘Much ado about nothing’? Psychological Medicine40, 717–29.

[16] Rutter M and Maughan B. (2002) School effective-ness findings 1979-2002. Journal of School Psychol-ogy 40, 451–75.

[17] Duncan GJ and Brooks-Gunn J (eds). (1997) Con-sequences of Growing Up Poor. New York: RussellSage.

[18] Conger RD, Conger KJ, Martin MJ. (2010) Socioe-conomic status, family processes, and individualdevelopment. Journal of Marriage and the Family72, 685–704.

[19] Sampson RJ. (2003) The neighborhood context ofwell-being. Perspectives in Biology and Medicine 46,853–64.

[20] Copeland W, Shanahan L, Costello EJ, Angold A.(2009) Configurations of common childhood psy-chosocial risk factors. Journal of Child Psychologyand Psychiatry 50, 451–9.

7

Sibling influences

2Sibling InfluencesJudy DunnKing’s College London, Institute of Psychiatry, London, UK

WHAT’S NEW

• Sibling relationships are characterized by strong emotions: positive, negative andambivalent. Coupled with the intimacy of their relationships (siblings know each other verywell from early infancy onwards) this emotional intensity means the potential fordevelopmental influence is large.

• Longitudinal research has documented connections between friendly early siblingrelationships and children’s later social understanding, prosocial behaviour and adaptivefunctioning. Evidence for continuities in quality of sibling relationships is accumulating.

• Conflict between siblings is now regarded as a normative feature of sibling relationships.The impact of parents on sibling conflict is currently under scrutiny, while sibling bullying athome has been shown to relate to the experience of being bullied at school. A warm siblingrelationship has a protective effect on children growing up in families with a high level ofmarital conflict, or faced with negative life events.

• Siblings growing up in the same family differ notably in adjustment, in personality andwell-being; this is a major challenge to understanding family influence. Processes implicatedinclude differential parental treatment, and other ‘non-shared’ experiences within andoutside the family.

• Children’s perspectives on their sibling relationships are increasingly recognized asimportant, and can be reliably studied.

• Interventions have focused on reducing sibling conflict; a new direction is to promote thepositive features of sibling relationships.

The great majority of us grow up with siblings,and the sibling relationship is the longest-lastingwe are likely to experience. How important aresiblings as an influence on the way we develop?Clinicians and family therapists have long arguedthat siblings play an important and influential partin children’s development, but until the last twodecades, systematic research on sibling influence


was relatively sparse. What has recent researchtold us about the factors that affect the ways inwhich siblings relate to one another? Is there con-tinuity over time in the friendliness or hostilitybetween siblings? What is the evidence for siblinginfluence on adjustment and well-being, on socialand emotional understanding, and on children’sother relationships?

8


INDIVIDUAL DIFFERENCES IN SIBLINGRELATIONSHIPS

From infancy to adolescence, relationshipsbetween siblings are emotionally powerful [1].Observational studies report that for some siblings,the majority of interactions between siblings areintensely negative, for others positive emotionsare frequently expressed, for others the emotionalquality is ambivalent. Continuities in the emo-tional quality of the relationship are evident frompreschool years through middle childhood [2].

Why do siblings differ in their relationships withone another? Research in the 1970s and 1980sfocused chiefly on birth order, gender and age gapas sources of individual differences. For young chil-dren the evidence on the importance of age gapand gender for sibling relations is inconsistent; inmiddle childhood gender differences become moreapparent, with boys reporting less warmth and inti-macy with their siblings. Links between children’stemperamental characteristics and their relation-ships with their siblings have been reported, butfindings are inconsistent across studies [3]. Recentresearch on siblings has now broadened to includethe quality of close relationships within and outsidethe family as sources of individual differences [4],and the evidence for sibling influence on children’ssociocognitive development.

SIBLING RELATIONSHIPS ANDPARENT—CHILD RELATIONSHIPS

Positive relationships with parents are linked tofriendly, caring relationships between siblings,while negative relationships between parentsand children are associated with sibling hostility.Children who have secure attachment relation-ships with their parents are reported to havepositive relations with their siblings [5]. Butcausal conclusions cannot be drawn from theseassociations: while such links are often interpretedas evidence for parental influence, it could well bethat children’s temperamental qualities contributeto difficulties in relationships with both siblingand parent. While a sunny, easy-going child’stemperament may contribute to positive rela-tionships with both parents and siblings, constantquarrelling between siblings may contribute todifficult parent–child relationships, and indeed todifficulties in the relations between parents.

In contrast to this evidence for hostility acrossfamily relationships, some studies report that sup-portive sibling relations can develop in families inwhich parent–child relations are distant or uninter-ested [6]. These ‘compensatory’ patterns of familyrelationships may be more common in familiesfacing stress and social adversity. Siblings can alsobe sources of support for children growing upin homes with marital conflict, and longitudinalresearch shows that children have fewer adjust-ment problems following negative life events ifthey have a good warm relationship with a sibling(Figure 2.1) [7].

A further point about the complex patternsof links between relationships within the familyconcerns the consistent evidence that in familiesin which there are differential relations betweenparents and their various children – where moreaffection and attention, or more negativity orharsh discipline is shown towards one sibling thanto another – there is more hostility and conflictbetween the siblings [8]. These links are par-ticularly clear in families that are under stress.Causal inferences cannot be made, however, if thestudies are cross-sectional. Recent evidence hasshown that children’s interpretation of differentialparental behaviour is important [9]. When chil-dren interpret their parents’ differential behaviouras evidence that they are less worthy of parentallove than their siblings, the sibling relationship isparticularly likely to be compromised [10]. Thesefindings remind us how important it is to recognizethe context of multiple family relationships withinwhich siblings grow up. From the second year on,children monitor the interactions between theirparents and siblings with vigilance [11].

The evidence that influential experiences withinthe family differ markedly between siblings hasshown us that it is sibling-specific experiencesthat need to be studied [4]. Innovative analytictechniques have been developed to assess and dis-tinguish between these ‘child-specific’ and ‘family-wide’ influences [12].

SIBLINGS AND THE DEVELOPMENTOF SOCIAL UNDERSTANDING

A striking feature of sibling relationships is theirintimacy. Siblings know each other very well.When young they spend more time interacting withtheir siblings than with their parents or friends, and

9

Sibling influences

Low life events0.40

0.45

0.50

0.55

Ch

ild B

ehav

ior

Ch

eck

Lis

t In

tern

aliz

ing

- se

con

d t

ime

po

int

of

stu

dy

0.60

0.65

0.70

High life eventsStressful life events

Low sibling affection High sibling affection

Figure 2.1 Internalizing symptomatology at second time point as a function of stressful life eventsand sibling affection at first time point. Reproduced from Gass et al. [7], with permission.

from very early in childhood know how to upset,tease and irritate their siblings as well as how tocomfort and amuse each other. Sibling researchhas given us an important new perspective on akey aspect of cognitive development – children’sdiscovery of the mind. The growth of children’sunderstanding of emotions, thoughts and beliefs,and the links between these inner states andpeople’s behaviour is a core feature of earlycognitive development, and one in which siblingrelations can play an important part. Children withsiblings begin to show powers of anticipatingothers’ intentions, sharing an imaginative world[1], and they engage in talk about why peoplebehave the way they do. Individual differencesin experiences of conversations with a siblingabout feelings and inner states, and cooperationin shared pretend play, are linked to differencesin children’s developing maturity in social under-standing. While the issue of direction of influenceremains a difficult one, the study of siblings hashighlighted the key social processes within thefamily (e.g. sharing cooperative pretend play, andmanaging conflict) for these core developmentsin social understanding. The key distinction is notbetween only children and those with siblings, butrather the individual differences in the quality ofthe relationship between the siblings. It is a warm,affectionate sibling relationship that is linked tothe growth of social understanding.

SIBLING INFLUENCES ON ADJUSTMENT

Evidence for links between children’s relation-ships with their siblings and their aggressiveoppositional behaviour, and also their internaliz-ing (worrying, anxious and depressive behaviour)has accumulated [1,13,14]. The influence is bothfrom older to younger siblings and vice versa. Lowlevels of prosocial behaviour (caring, empatheticand helpful, supportive behaviour) are associatedwith hostility between siblings and the develop-ment of conduct problems [14]. These patternsare independent of the contribution of poorparent–child relationships, and are evidence fordirect effects of sibling conflict and negativity onchildren. Indirect effects of siblings on adjustmenthave also been found, for instance in the impactof differential parent–child relations on children’sadjustment problems [15].

The evidence from research on the very begin-nings of the sibling relationship – the impact ofthe birth of a sibling on children’s well-being – isalso clear. Increases in problems of aggression,dependency, anxiety and withdrawal have beenreported for first-born children following the birthof a sibling [1].

SIBLINGS AND PEERS

Research that includes children’s perceptionsof their relationships with siblings, friends and

10


mothers, and links with their adjustment paintsa complex picture. This can be illustrated byStocker’s study of the self-reports of 7–8-year-oldson their relationships [16]. First, warmth inrelations with each partner was associated withfewer feelings of loneliness in peer contexts andbetter behavioural conduct. Warmth in siblingrelationships and in friendships was associatedwith a sense of self-worth, and in friendshipwas linked to less depressive mood. There wasevidence for some correlations across the differentrelationships, but these correlations were not high.Compensatory processes were found, for instance,in children’s sibling relationships and friendshipsin relation to behavioural adjustment. High levelsof warmth in friendships compensated for lowlevels of warmth in sibling relations (and viceversa) in relation to adjustment outcomes. Finally,children who perceived low levels of warmthin their relationships with both mother and sibhad significantly worse outcomes on loneliness,self-worth and behavioural conduct.

Bullying victimization by siblings at home hasbeen reported, and linked to bullying at schooland to adjustment problems [17]. In a study of12–15-year-olds in Israel, 16.2% were bullied athome by siblings, and more than half of these werealso involved in bullying incidents at school. Ethnic(Jewish vs Arab) and sex differences were smallcompared to the effects of the sibling relationshipon behaviour problems. The findings indicate thatintervention programmes targeted at children’sclose friendships and sibling relationships may beimportant in improving children’s well-being.

INTERVENTION PROGRAMMESAND SIBLING RELATIONSHIPS

The frequent conflicts between siblings, the evi-dence for sibling bullying and for links between sib-ling disputes and children’s aggressive behaviourhas led to an emphasis on reducing siblingconflict as the key mechanism for improving therelationship [18], for example by training parents[19]. The short-term effects of parental mediation(encouraging reasoning, discussion of emotions,and taking the perspective of the other child) werestudied with 5–8-year-olds in Canada. Childrenresponded appropriately to the mediation, and theprogramme empowered children to solve conflictissues. These programmes do lead to reduced

conflict, but fail to increase the positive aspects ofthe relationship. In contrast, Kramer has set out auseful review of the positive aspects of the relation-ship, and devised a programme for interventionwith siblings and parents, ‘Fun with Sisters andBrothers’, based on the competencies highlightedin the review [20]. These competencies include:

• play;• conversation;• mutual enjoyment;• valuing help and support;• appreciating sibs’ unique knowledge of each

other;• learning to respect sibs’ views and interests in

addition to one’s own;• managing emotions in challenging situations;• learning to check faulty hostile attributions;• refraining from wild behaviour or bossiness;• conflict management; and• for parents, discussing the impact of parental

differential treatment.

The contribution of the programme to siblings’relationships is awaited with great interest.

It should be noted that most studies of siblingshave been conducted with middle-class, urban,two-child, Caucasian families in North Americaor Britain; little is known about minority ethnicor linguistic groups. There are clear and importantopportunities for research, using longitudinal stud-ies, to fill some of the gaps in what we know aboutthis interesting, intense and life-long relationshipbetween siblings.

REFERENCES

[1] Dunn JF. (2006) Siblings. In: Grusec JE andHastings D (eds), Handbook of Socialisation: The-ory and Research. New York: Guilford Publications,pp. 309–27.

[2] Volling BL. (2003) Sibling relationships. In: Born-stein MH, Davidson L, Keyes CLM, Moore KA(eds), Wellbeing: Positive Development Across theLife Course. Mahwah, NJ: Erlbaum, pp. 205–20.

[3] Furman W and Lanthier RP. (1996) Personalityand sibling relationships. In: Brody GH (ed.), Sib-ling Relationships: Their Causes and Consequences.Norwood, NJ: Ablex, pp. 127–46.

[4] Plomin R. (2011) Commentary: Why are chil-dren in the same family so different? Non-sharedenvironmenty three decades later. InternationalJournal of Epidemiology (in press).

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Sibling influences

[5] Teti DM and Ablard KE. (1989) Security of attach-ment and infant-sibling relationships: A laboratorystudy. Child Development 60, 1519–28.

[6] Stocker CM. (1994) Children’s perceptions of rela-tionships with siblings, friends, and mothers: Com-pensatory processes and links with adjustment.Journal of Child Psychology and Psychiatry 35,1447–59.

[7] Gass K, Jenkins J, Dunn J. (2007) Are sibling rela-tionships protective? A longitudinal study. Journalof Child Psychology and Psychiatry 48, 167–75.

[8] Dunn J and Stocker CM. (1989) The significanceof differences in siblings’ experiences within thefamily. In: Kreppner K and Lerner R (eds), FamilySystems and Life-span Development. Hillsdale, NJ:Erlbaum, pp. 289–301.

[9] Kowal A and Kramer L. (1997) Children’s under-standing of parental differential treatment. ChildDevelopment 68, 113–26.

[10] Kowal A, Krull JL, Kramer L. (2006) Sharedunderstanding of parental differential treatment infamilies. Social Development 15, 276–95.

[11] Dunn J and Munn P. (1985) Becoming a fam-ily member: Family conflict and the developmentof social understanding in the secondyear. ChildDevelopment 56, 764–74.

[12] O’Connor TG, Dunn J, Jenkins J, Rasbash J. (2006)Predictors of between-family and within-family vari-ation in parent-child relationships. Journal of ChildPsychology and Psychiatry 47, 498–510.

[13] Pike A, Coldwell J, Dunn J. (2006) Family Rela-tionships in Middle Childhood. York: York Publish-ing/Joseph Rowntree Foundation.

[14] Garcia MM, Shaw DS, Winslow EB, Yaggi KE.(2000) Destructive sibling conflict and the develop-ment of conduct problems in young boys. Develop-mental Psychology 36, 44–53.

[15] Coldwell J, Pike A, Dunn J. (2008) Maternaldifferential treatment and child adjustment: Amulti-informant approach. Social Development 17,596–692.

[16] Stocker CM. (1994) Children’s perceptions of rela-tionships with siblings, friends and mothers: Com-pensatory processes and links with adjustment.Journal of Child Psychology and Psychiatry 35:1447–59.

[17] Wolke D and Samara MM. (2004) Bullied bysiblings: association with peer victimisation andbehaviour problems in Israeli lower secondaryschool children. Journal of Child Psychology andPsychiatry 45, 1015–29.

[18] Kramer L. (2004) Experimental interventions insibling relations. In: Conger RD, Lorenz FO, Wick-rama KAS (eds), Continuity and Change in FamilyRelations: Theory, Methods and Empirical Findings.Mahwah, NJ: Erlbaum, pp. 345–80.

[19] Smith J and Ross H. (2007) Training parents tomediate sibling disputes affects children’s negotia-tion and conflict understanding. Child Development78, 790–805.

[20] Kramer L. (2010) The essential ingredients of suc-cessful sibling relations: An emerging framework foradvancing theory and practice. Child DevelopmentPerspectives 4, 80–6.

12


3Culture and Child DevelopmentRuma Bose1 and Sanjida Sattar21Adolescent Mental Heath Team, Tower Hamlets, Children and Young People’s Centre, London, UK2Islington Community CAMHS, London, UK

INTRODUCTION

With increasing contact between cultural and eth-nic groups the concepts of childhood and thechild itself have become sites for intensive study.Anthropologists, historians and cultural child psy-chologists have attempted to study children’s livesand conceptions about childhood in different cul-tural contexts. Wide differences exist across cul-tures [1]. For professionals working in pluriculturalcontexts a pertinent question is: how are ethnicdifferences accounted for in prevailing concepts ofparenting and childhood behaviours, both ‘normal’and ‘variant’? These complexities are amplified bythe continually changing social and political con-texts in which children grow up, and highlightthe very social and historical framing of construc-tions of childhood. Ethnic variations in parentingmay express adaptations to different conditions forchild development necessitated by divergent eco-logical, social and cultural priorities, rather thaninherent, static ‘ethnic differences’.

DEVELOPMENTAL NICHE ANDECOCULTURAL PATHWAYS

The concept of a developmental niche wasintroduced as a framework for studying theproduction of health and development of the childvia the interaction between the physical and socialsettings of the child’s everyday life, culturallydetermined customs of childcare and parentaltheories about children [2]. The components of theniche form the larger strategy for childcare and the


daily routines for the child. The everyday routinesembody the core goals and fashion culturaldevelopmental pathways for children in specificecocultural contexts [3]. LeVine [4] demonstrateshow in parts of the world where child survivalis precarious, close physical proximity with thebaby is maintained by carrying, co-sleeping,breastfeeding, immediate response to crying, andsubstitute care by siblings when the mother isworking. The pursuit of learning is postponed untilsurvival is assured. The increased physical contactand stimulation promotes growth, and develop-ment of attentional processes and neuromuscularcompetence [5]. By contrast, in technologicallyadvanced North America, where child survival isof less concern, but preparation for competencyin future occupational roles graded by masteryof literacy-based skills is important, mothersemphasize the attainment of language skills andmastery of the object world through communica-tive interaction and naming of objects from anearly age, rather than close physical proximity.

The models are also useful in understandingchanges in parenting styles related to alterationsin the ecocultural context.

CHILDHOOD AND PARENTINGACROSS CULTURES

As most accounts of children’s development andneeds are framed within writings from NorthAmerica and Europe, the normative descriptionof childhood is often based on children growing upwithin the Northern cultures, and even within this

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Culture and child development

differences across class and socioeconomic strataare subsumed. Culture is often consigned to therole of an ‘add on’ variable to assumed normativestandards applied universally. However, recentcultural studies of children have questionedassumptions about ‘cultural universals’, and havehighlighted the centrality of culture in shapinghuman behaviours, crucially here of parents andchildren. How integral is culture to conceptsregarding childhood, child development andthe goals that frame parental strategies forbringing up children? Although children achievedevelopmental maturity along broadly similarspecies-specific lines, and the goal of parentingis similar across cultures, namely for children tobecome competent adults in one’s own cultural,moral and economic world, there are wide differ-ences in what constitute the desired competenciesand the means for achieving them. Shweder[6] makes the point that any aspect of humannature that we endeavour to understand musthave a central essence, but that essence consistsof a heterogeneous collection of structures andinclinations substantiated by the historical experi-ences of different cultural communities, resultingin ‘One mind, many mentalities: universalismwithout uniformity’. This is different from culturebeing perceived as variations from a normativestandard. For children, James [7] eloquentlyposed the question: ‘One childhood or many?’These issues are further explored via examplescommonly encountered in cross-cultural work.

INFANCY

Developmental stagesThe very notion of stages of childhood is cul-turally constructed. Developmental psychologistsmark the end of infancy with the beginning of‘toddlerhood’ normatively defined at age 2 yearsand marked by language and motor competency.However, this is not a biological fact, but a cul-tural convention based on the assumption that lifestages should be delineated by absolute points intime. It is different from norms in cultures wherethe crucial reference point is the acquisition ofmoral sense [8]. Puritans of New England beganstrict discipline at age 1 year, when they believedinfancy ended and the Devil begins to exert con-trol. The ethnographic record shows that in mostparts of the world active teaching begins at least

after 5 years, as it is believed that before thischildren are too immature or lacking in ‘sense’ tobe taught important lessons [1]. The Baganda ofUganda typically train their infants to sit indepen-dently as early as 4 months as sitting up and smilingis an asset amongst the Baganda, who value highlyface-to-face contact [8].

AttachmentCross-cultural research on attachment behaviourhas thrown up challenging questions regardinghow deviation from supposed universal normsis to be understood at a population level.The Bowlby–Ainsworth model of attachmentdescribes a universal model of attachmentbehaviour predicated on the primary carer’ssensitivity to the infant’s signals. Ainsworth’swork in different parts of the world testifies to theuniversality of attachment behaviour in infants,with group B attachment behaviour being modalin most cultures [9]. However, the model does notallow for variations other than as suboptimal orpathological. A review of the literature on attach-ment taking into account population variations,raises the question whether there is a multiplicityof optimum patterns for humans [10] reflectingdifferent meanings attributed to optimal patternsof attachment behaviour in different socioculturalgroups [9]. For example, a study of attachment[11] in Bielefeld (Germany), showed 49% ofthe infants to have anxious-avoidant attachmentbehaviour, which related to a highly valuedcultural emphasis on obedience and self-reliance,the training for which began in infancy. It was anaccepted practice to leave infants in bed alonefor short periods, and mothers compared theextent to which their babies could play aloneas indication of their developing self-reliance.Given the absence of evidence for a higherprevalence of personality disorder in Bielefeld, itcould be argued that the drive for self-sufficiencyengendered behaviours that counted as virtuousin some German communities, and delineatesa different pathway towards normal emotionaldevelopment. Historically, the prevention ofinfant dependency was also highly valued amongstBritish and American middle classes until the endof World War II.

The variety in infant care-taking patterns is high-lighted by hunter gathering Efe (Zaire), wheremultiple care-takers alongside the mother, provide

14


both lactating and non-lactating care, resulting inthe Efe infant being more diffusely attached tomany caregivers rather than intensely attached toone. Tronick et al. [12] propose that this modelof care-taking is moulded by specific ecologicaldemands and cultural values that emphasize groupidentification.

Co-sleepingCo-sleeping is widely practised in many parts ofthe world such as Africa, Asia and the indige-nous Americas, particularly where the economicunit of production was until recently the family.Babies and young children sleep with parents,grandparents or older siblings even where roomis available. Co-sleeping promotes togetherness incultures where the family is the economic unit andinterdependency highly valued. In advanced indus-trialized Northern economies where autonomy andindependence are emphasized, babies sleep apartfrom parents. Neither practice is morally superiorbut each is tied to the competency required for thespecific cultural context.

Parental involvement in play and learningParental facilitation of the child’s academicpreparedness through proto-conversations withbabies, active teaching through toys and makebelieve is considered critical by middle-class Euro-American parents as it promotes skills required forfuture school and occupational success. Althoughthe parent as teacher is often enshrined as an idealin manuals for parents, it is essentially a culturalmodel that promotes important developmentalskills required in complex urban societies. It isnot an ideal in agrarian pastoral societies whereprocesses are less demanding and where everyoneis a potential teacher or role model. Insteadqualities such as initiative, attention to details,sharing, obedience and respect for elders attractgreater value.

MIDDLE CHILDHOOD

With the introduction of compulsory educationin most parts of the world, middle childhood hasreceived relatively less attention in cultural work.However, a closer examination reveals startlingdifferences in how children’s lives are structured atthis stage. Ethnographic description of the Girima

(Kenya) encapsulates some differences from theNorth American normative expectations of chil-dren at this stage, but ones that are also seenin many other cultural groups in the developingworld [13]. Girima attach importance to provid-ing children with duties that teach responsibilityand mutuality necessary for future adult cooper-ative roles. Children aged 2–3 years take pridein running errands, and from 8 years a girl maybe expected to pound maize and a boy to herd.Work constitutes opportunities for acquiring skillsin future gender-specific roles, as well as opportu-nities to participate in cooperative activities withother children. These activities are often combinedwith attending school. Assistance within the homeis different from wage labour, which, however,remains a reality for children from socioeconom-ically very deprived families in many parts of theworld, and which keeps the world price of com-modities down [14].

ADOLESCENCE

Adolescence as a stage between childhood andadulthood where the participants behave and areregarded differently appears to exist worldwide.This stage may therefore not be a product of cul-ture, although many of its descriptions are [15]. Inmany cultures where socialization into adult occu-pational roles begins early, it is less, as describedin the West, a stage when identity questions aboutfuture roles begin, but rather a stage for prepa-ration for future reproductive roles, within whichindividuation is subsumed. The emphasis at thisstage on individuation and identity formation thatis adaptive for industrial and ever-changing capital-ist economies, is not shared across cultures wherethe social-relational self is emphasized.

ETHNICITY AND MENTAL HEALTH

This section addresses the relationship betweenethnicity and mental health problems. However,before a cultural explanation is offered to explaindifferences between ethnic groups, importantmethodological considerations need to be takeninto account, particularly whether ‘like is beingcompared with like’ in terms of sampling, socioe-conomic variables, ethnic groupings, populationversus clinic rates, cross-cultural validation

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Culture and child development

of instruments and diagnostic categories, andaccessibility of services.

Cross-cultural epidemiological studies are toovaried for firm conclusions to be drawn aboutworldwide rates and patterns. There is little evi-dence for culture-specific syndromes, but disso-ciative disorders such as trance and possession inadolescence related to rapid social change in partsof the world where possession beliefs exist, arereported [16].

The systematic review of the mental healthof children of the main ethnic groups in Britainby Goodman et al. [17] shows comparable, ifnot better mental health in minority children,given the socioeconomic deprivation of Pakistanis,Bangladeshis and Afro-Caribbeans in Britain, andit underscores the need to research the interplaybetween risk and protective factors for differentcommunities. A few child psychiatry disorders willbe used to explore the complexities involved.

A systematic review of attention deficit hyper-activity disorder [18] estimated the worldwidepooled prevalence at 5.29%, although notablyapproximately two-thirds of the 102 studies werefrom North America and Europe. The authorsemphasize caution in interpreting the resultsbecause of the variability in findings. Variationin prevalence ranged from 1% to 20%. Despiteattempts at standardization, significant differencesbetween raters from different countries remain.This has provoked a debate about culturalconstructions in diagnosis and treatment, andwhether the differences in ADHD rates alsoreflect different thresholds in tolerance fornon-conforming behaviours in children [19].

The evidence for the role of culture in theaetiology of eating disorders related to weight con-sciousness is evidenced by wide variation in ratesworldwide, and rising rates attributed to culturechange through urbanization and modernization.In The Netherlands, Van Son [20] found a five-fold increase of bulimia with urbanization between1985 and 1999.

A review of non-fatal self-harm in the UK[21] described higher rates amongst South Asianfemale adolescents. Notably, a high prevalenceis not reported from South Asia. Although theauthors refer to culture conflict, other explanationsneed to be considered. For example, Reese [22]found that migrant parents who perceive a higherrisk for young people in the new environment

exercise greater boundary control over adoles-cents than would be exercised in the countryof origin, resulting in greater inter-generationalconflict. Self-harming behaviour itself may be anappropriated cultural way of expressing distressby South Asian girls in the UK.

CONCLUSION

As culture and ethnicities are always evolving,a foreclosure of the debate is never possible. Amore productive alternative is the development ofa framework for understanding the centrality ofculture in child development based on the exten-sive cross-cultural literature available. However, asfamiliarity with one’s own cultural norms is oftenthe starting point for studying difference, ‘culturaldifference’ is often subsumed by the issue of ‘differ-ent moralities’. But for mental health professionsculture is a potent tool for promoting reflexivity,and widening our horizons by including knowledgeabout the everyday lives of children from parts ofthe world where the majority of children live.

REFERENCES

[1] Lancy DF. (2008) The Anthropology of Childhood:Cherubs, Chattels, Changelings. Cambridge Univer-sity Press.

[2] Harkness S and Super CM. (1994) The developmen-tal niche: A theoretical framework for analyzing thehousehold production of health. Social Science andMedicine 38, 217–26.

[3] Weisner TS. (2002) Ecocultural understanding ofchildren’s developmental pathways. Human Devel-opment 45, 275–81.

[4] LeVine RA, Dixon S, Levine S et al. (1996) ChildCare and Culture: Lessons from Africa. CambridgeUniversity Press.

[5] Harkness S and Super CM. (2002) Culture struc-tures the environment for development. HumanDevelopment 45, 270–4.

[6] Shweder RA, Goodnow J, Hatano G, Levine RA,Markus H, Miller P. (1998) The cultural psychologyof development: one mind, many mentalities. In:Damon D and Lerner RM (eds), Handbook of ChildPsychology. Vol. 1: Theoretical Models of HumanDevelopment. New York: Wiley, pp. 716–92.

[7] James A, Jenks C, Prout A. (1998) Theorizing Child-hood. Cambridge: Polity Press.

[8] Gottlieb, A. (2000) Where have all the babies gone?Toward an anthropology of infants (and their care-takers). Anthropological Quarterly 73(3), 121–32.

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[9] Harwood RL, Miller JG, Irizarry NL. (1995) Cultureand Attachment. New York: Guildford Press.

[10] LeVine RA and Norman K. (2008) Attachment inanthropological perspective. In: LeVine RA andNew RS (eds), Anthropology and Child Devel-opment: A Cross-Cultural Reader. Oxford: Wiley-Blackwell, pp. 127–42.

[11] Grossmann K and Grossmann KE. (1981) Par-ent infant attachment relationships in Bielefeld: aresearch note. In: Immelman G, Barlow G, Petro-vich L, Main M (eds), Behavioural Development:The Bielefeld Interdisciplinary Project. New York:Cambridge University Press, pp. 694–9.

[12] Tronick EZ, Morelli GA, Winn S. (2008) Multiplecaregiving in the Ituri Forest. In: LeVine RA andNew RS (eds), Anthropology and Child Develop-ment: A Cross-Cultural Reader. Wiley-Blackwell,pp. 73–83.

[13] Wenger M. (2008) Children’s work, play, and rela-tionships among the Girima of Kenya. In: LeVineRA and New RS (eds), Anthropology and ChildDevelopment: A Cross-Cultural Reader. Wiley-Blackwell, pp. 289–306.

[14] Nieuwenhuys O. (2005) The wealth of chil-dren: reconsidering the child labour debate. In:Qvortrup J (ed.), Studies in Modern Childhood:Society, Agency, Culture. Palgrave Macmillan,pp. 167–83.

[15] Schegel A. (1995) A cross-cultural approach to ado-lescence. Ethos 23, 15–32.

[16] Fabrega H, Miller BD. (1995) Towards a morecomprehensive medical anthropology; the case ofadolescent psychopathology. Medical AnthropologyQuarterly, New Series 9, 431–61.

[17] Goodman A, Patel P, Leon DA. (2008) Child mentalhealth differences amongst ethnic groups in Britain;a systematic review. BMC Public Health 8, 258.

[18] Polanczyk G, Silva de Lima M, Horta BL, Bieder-man J, Rohde LA. (2007) The worldwide prevalenceof ADHD: a systematic review and metaregres-sion analysis. American Journal of Psychiatry 164,942–8.

[19] Timimi S, Taylor E. (2004) In Debate: ADHD is bestunderstood as a cultural construct. British Journalof Psychiatry 184, 8–9.

[20] Van Son GE, Van Hoeken D, Bartelds AIM, VanFurth EF, Hoek HW. (2006) Urbanisation and eat-ing disorders. British Journal of Psychiatry 189,562–3.

[21] Bhui K, Mckenzie K, Rasul F. (2007) Rates, riskfactors and methods of self harm among ethnicminority groups in the UK, a systematic review.BMC Public Health 7, 336.

[22] Reese L. (2002) Parental strategies in contrastingcultural settings: families in Mexico and ‘El Norte’.Anthropology & Education Quarterly 33, 30–59.

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Neurobehavioural development in infancy

4Neurobehavioural Developmentin InfancyCindy H. Liu1 and Ed Tronick1,21Children’s Hospital, Boston, Harvard Medical School, Boston, MA, USA2University of Massachusetts, Department of Psychology, Boston, MA, USA

WHAT’S NEW

Neurobehavioural development is notsimply a biological process, but one that isshaped by the regulation that takes placethrough interactions between caregiverand infant. Notably these interactions arenot simply ‘biologically determined’, butvary by community and even by dyad.Understanding the infant neurobehavioralstate is a significant approach to assess-ing their capacities. It is also one wayto understand the effects of adversebiological and social factors on theirneurodevelopment.

Infant neurobehaviour and its developmentinclude behaviours generated by neurophysiolog-ical and psychological processes, which mediateinfants’ own internal processes and engagementwith the world. Ideally, neurobehaviour becomesadaptive within contexts that challenge infantson a daily basis. The purpose of this chapteris to introduce theory-driven and empiricallysupported influences on neurobehavioural devel-opment while emphasizing mechanisms currentlyknown to exemplify the interaction of neuro-biological and social domains of development.We begin with a rather narrow overview ofneurobehaviour, followed by the argument that


a broader biosocial view is needed to understandneurobehavioural development. Although it maybe surprising to some readers, we argue thatneurobehaviour is not self-contained, nor preset,nor a simple unfolding under the control of geneticmaturational processes. We see neurobehaviouras embedded in regulatory processes betweeninfants and caregivers that operate in a continuous,bidirectional and dynamic manner. Furthermore,these regulatory processes are affected by multiplefactors from health status to toxic exposures, notthe least of which is culture. We see these regu-latory processes sculpted by culture, in additionto biological and physiological processes. Thisbroader perspective implies that neurobehaviouraffects and is shaped by regulatory processesincluding the psychosocial and biological contextsthat make up human experience.

INFANT NEUROBEHAVIOURAL CAPACITIES

In the past, newborns were seen as reflexive.Infant neurobehaviour was modelled on spinalfrog behaviour, where responses to stimuli werethought to be fixed, under stimulus control, andautomatic; but the model was dramatically wrong[1]. The newborn’s brain and physiology producefour domains of complex neurobehaviour:

1. attention – visual and auditory abilities to pro-cess information such as tracking objects, dis-criminating faces;

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2. arousal – the expression and intensity of statesfrom sleep to alert to distress and their modula-tion using self-soothing of distress;

3. action – fine and gross motor skills for acting onthe world of things and people such as defensive‘reflexes’, reaching for an object;

4. affective social processes – communicative emo-tional displays, smiling [2].However, understanding infant neurobehaviour

requires a recognition that the quality of neurobe-haviour is mediated by state – the organization ofneurophysiological (heart rate, respiration, EEG)and behavioural systems (tone, movements) for aperiod of time. Six states have been identified andare now used to understand infant neurobehaviour:two sleep states (State 1, quiet sleep; and State 2,REM sleep), one semi-awake/transitional state(State 3), two awake or alert states (State 4, quietalert; and State 5, active alert) and a distressstate (State 6) [3,4]. Recognizing the mediatingrole of state overturned the spinal frog modelwhen infant reflexes (e.g. knee jerk, sucking) werefound to vary in intensity, robustness and qualitydepending on the infant’s state [5]; that is, theywere hardly single synapse spinal reflexes.

Beyond its effect on reflexes, each state impactsthe quality of infant neurobehaviour. States affectthe infants’ repertoire of complex motor and sen-sory/perceptual processes [3,6] and even determinevarious infant response modalities; for example,facial brightening and alerting to visual stimulionly occur during the awake states; startles occur inStates 1, 4, 5 and 6, but seldom in State 2 or 3; move-ments are smooth in State 4 but jerky and unco-ordinated in State 6, uncoordinated in State 3 andlargely absent in State 2 [7]. Furthermore, infantscollect information and modulate their behaviourdifferently in different states. Head turning tosound and cuddling occur primarily in States 4and 5, may occur in State 3 but not in States 2, andhabituation can occur in States 1, 2 and 4.

Infant neurobehaviour can be evaluated. TheNICU (Neonatal Intensive Care Unit) NetworkNeurobehavioral Scale (NNNS) is one suchneurobehavioural measure. As a standardizedassessment tool for infants [8,9], the NNNSassesses infants from the newborn period tolater in the postnatal period, as well as pre- andpost-term at-risk infants (e.g. drug-exposed, jaun-diced). Using different stimuli (bell, rattle, ball,human face and voice) and handling techniques

(cuddling, stimulation of neurological reflexes),the NNNS elicits a variety of attentional, motoricand regulatory responses and capacities to inhibitresponses to insignificant stimuli. Critically, theNNNS considers infant state for each neurobe-haviour and tracks the range of states and theirlability. The NNNS gives a holistic picture ofthe infant by assessing the interplay of statebehavioural and regulatory capacities.

The NNNS is sensitive to risk factors thataffect infant neurobehaviour [10,11], such asgestational age, birthweight, appropriateness ofgrowth, postnatal age at testing, quality of care andstress reduction of different delivery procedures,in utero exposure to drugs (cocaine, heroin,methadone, nicotine), and also maternal stressand depression [12]. Impressively, NNNS profilesof infants’ neurobehavioural organization (‘wellorganized’ to ‘poorly organized’) have predictedlong-term outcomes related to school readinessand IQ at 4.5 years of age [11], which speaks tothe significance of infants’ self-organized neuro-behavioural capacities for their long-termpsychosocial development.

MUTUAL REGULATION MODEL

Although we see infants as competent beings withan impressive ability to self-regulate and to actupon the world, we must recognize that theircapacities are limited and immature. The qualityof neurobehaviour dissipates unless infants receiveexternal support to scaffold their organization. Forinstance, infants are able to control heat loss by tak-ing a fetal position or increasing their activity, butmay require caregiver ventral contact to achievethermal homeostasis. Similarly, infants are capableof processing stimuli in an alert state, but that stateis energetically costly and often short lived. Theyare better able to sustain neurobehavioural alertstates with postural support and soothing fromtheir caregivers [13]. Altogether, infants activelyregulate their neurobehavioural systems to main-tain homeostasis and neurobehavioural coherence,especially when supported by a caregiver. Suchexternal supports are often overlooked, but arecritical to the quality of expression and develop-ment of infant neurobehaviour.

We propose the use of the Mutual RegulationModel (MRM) to describe external supports thatlead to organized infant neurobehaviour. It has

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been established that infants and adults jointlyregulate their behaviour, affect and communica-tion during social interactions, and share goalsto attain well-organized physiological, behaviouraland interpersonal states [14,15]. The MRM pro-poses that these processes are jointly regulated byinfants using internal self-organized capacities incoordination with regulatory input from caregivers[16,17]. The success or failure of mutual regulationto maintain infants’ neurobehavioural coherenceand engagement with others thus depends on bothinfant and caregiver capacities: the integrity ofthe infant’s physiological and central nervous sys-tems, the infant’s abilities to express the statusof these systems to the caregiver, and the care-giver’s abilities to read and act upon the infant’smessages. These processes are dynamic such thateach continuously influences and modifies theother; they are mutually regulated.

CULTURE

Once infant neurobehaviour is considered deeplyinterdependent with the actions of another person,a broader view of neurobehavioural organizationis required. It needs to be considered as a sociallyregulated process, not simply a biological process.As a social process, the brain and physiologicalprocesses controlling neurobehaviour are imbuedwith culture [18]. This perspective is demandedbecause culture determines caregivers’ implicit andexplicit view of infant capacities and their atten-tion and actions with their infant. This is seen inthe way that the caregiver responds to the infant’sneeds moment-to-moment. Thus caregiving prac-tices within cultures influence the developmentof infants’ central nervous systems and infants’responses to the particular constraints set by thecultural environment.

Yet, the role of culture on neurobehaviouraldevelopment has traditionally been overshadowedby biological factors, maturation and the effects ofbiological perturbations (e.g. illness, malnutrition)in part because they often demonstrate causaland immediate effects on physiological andbehavioural changes; the presupposition is thatthese factors are the primary determinants ofneurobehavioural development. The MRM, onthe other hand, posits that prenatal and post-natal experiences actually sculpt functional andstructural characteristics in neurodevelopment,

making culture much more proximal to neu-robehavioural development. Although studyingcultural effects is difficult compared to factorsthat can be manipulated (e.g. NICU care) orthat already vary within a community (e.g.exposure to toxicants), characterizations of infantdevelopment from various cultural groups supportthe interdependence of biology and culture, asdoes research on gene–environment interactionand epigenetic processes [13,19].

For instance, unique care-taking practicesamong the Peruvian Quechua influence thebiological and behavioural processes underlyinginfant neurobehavioural development. PeruvianQuechua dwelling at high altitude (4250 m) usea culturally created care-taking technology, theManta pouch, to ‘house’ their infants – a layeredset of cloths and blankets that tightly wrap aroundand fully enclose the infant. It protects infants fromthe extremes of the environment (i.e. freezingtemperatures, reduced oxygen, lack of humidity)[20]. Within the Manta pouch, the temperatureis stabilized and high, the air is humidified, andinfant movement is limited. Paradoxically, the O2

levels are lower and CO2 levels are higher in thepouch compared to hypoxic conditions at highaltitude. While these hypoxic conditions would beconsidered dangerous in other environments, theincrease of CO2 may actually be a microstressorthat induces adaptive functional and structuralchanges. In combination with other features of thepouch microclimate, high CO2 levels increase theduration of infant sleep, which conserves energy;this in turn leads to faster physical growth andresistance to temperature loss. Raised CO2 levelsare partly responsible for inducing the left shift ofthe Quechua’s CO2 sensor, a unique physiologicalcharacteristic that allows them to tolerate highlevels of CO2 that would debilitate people lackingthis adaptation. The left shift is a developmentalphenomenon directly related to the length oftime an individual lives at high altitude prior topuberty.

Although adaptive, the Manta pouch maybe costly to other aspects of neurobehaviouraldevelopment. Quechua infants are immobile andcompletely covered around the face while beingcarried on their mothers’ backs during infancy.Stimulation and social interaction are limited; thelimitations in socialization and stimulation mayreduce exploration and language development

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and other features of brain development. Infact, the infants have been found to lag devel-opmentally. Thus fundamental physiologicalprocesses – tolerance for CO2 – and fundamentalneurobehavioural processes – amount of sleep,motor development, and perhaps the developmentof emotions such as curiosity – are affected byQuechua care-taking practices. Nonetheless, theprotective shielding may be important for workingat high altitude and one can speculate that theManta’s experience of isolation perhaps preparesthe 6-year-old Quechua child to endure the socialisolation and vigilance needed for herding theirfamily’s animals alone for days at a time.

Such an example may seem extreme to Westernsocieties, but is not farfetched in light of challengesthat practitioners face when working with familiesthat hold different cultural expectations for infantdevelopment and preferences for caregiving. Cur-rently, Western practitioners urge caregivers toplace their infants on their back for sleep. Afternoticing motor delays (e.g. turning, crawling) asa result of this change in sleep position, manypractitioners consider it essential for caregivers topractice ‘Tummy Time’ with their infant – 30 min-utes of daily exercise where the infant strengthensneck muscles in preparation for sitting up andcrawling [21]. Furthermore, caregivers are givenrecommendations in the way to socially engagetheir infant during this time [22]. Perhaps thisrecommendation emerged from the recognitionthat an infant with poor head control is less ableto attend to the environment and to engage inaffectively charged face-to-face exchanges withcaregivers, a norm in the United States. By mod-ifying infant neurobehaviour, motor and socialdevelopment is now viewed again as ‘normal’.

However, ‘Tummy Time’ may not be readilyadopted by caregivers from certain cultures; forinstance, Asians have always placed their infantson their back to sleep and never considered infantmotor milestones delayed. In sub-Saharan Africa,infants are not played with in the same way asinfants in the West and recommendations to do sowould not be accepted. In fact, motor developmentis accelerated compared to the motor develop-ment of infants in the West from being carriedfrom birth [23]. The neurobehavioural develop-ment of infants who experience ‘Tummy Time’may differ from those who do not, yet each may bethe preferred development within their respective

culture. As decisions made by caregivers who donot readily adopt Western recommendations maybe considered problematic by Westerners from abiopsychological perspective, practitioners oughtto evaluate how these caregiver decisions fit withthe developmental goals of their own culture. Cul-tural comparisons indicate that there are no fixedand universal norms.

CONCLUSION

The consideration of only biological factors in neu-robehavioural development is an insufficient viewof neurobehavioural development. A broaderview of neurobehavioural development is neces-sary to capture the complexity of the processesthat unfold over time. Infant state acknowledgesthe overall organization of infants’ physiologicaland behavioural systems as it receives externalinputs from others. Through the MRM perspec-tive, caregiver and infant jointly make efforts tomaintain infant neurobehavioural coherence andorganization. Moment-to-moment organization ofneurobehaviour is partly governed by social input.Over the long run, the interplay of self-organizedneurobehavioural processes, caregiver practices,and resulting interpersonal states – however theymay differ across cultures – organizes infants ina coherent and culturally appropriate manner.And most telling, infants who are unable toengage socially in an appropriate way within theirculture will not develop normally. Fortunately,good parenting naturally flows when caregiversfunction well in their environments, which inturn helps infants to develop into culturallyappropriate beings.

REFERENCES

[1] Sherrington CS. (1906) The Integrative Action ofthe Nervous System. New Haven: Yale UniversityPress.

[2] Lester BM and Tronick EZ. (1994) The effects ofprenatal cocaine exposure and child outcome. InfantMental Health Journal 15, 107–20.

[3] Prechtl HFR, Beintema D. (1964) The Neurolog-ical Examination of the Newborn Infant. London:Lavenham Press.

[4] Wolff PH. (1959) Observations on newborn infants.Psychosomatic Medicine 21, 110–18.

[5] Prechtl HFR. (1981) The study of neural devel-opment as a perspective of clinical problems. In:

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Connolly KJ and Prechtl HR (eds), Maturation andDevelopment: Biological and Psychological Perspec-tives. Philadelphia: JP Lippincott; pp. 198–215.

[6] Brazelton T. (1973) Neonatal Behavioral Assess-ment Scale. London: Spastic International MedicalPublications.

[7] Prechtl HFR. (1972) Patterns of reflex behaviorrelated to sleep in the human infant. In: ClementeCD, Purpura DP, Mayer FE (eds), Sleep and theMaturing Nervous System. New York: AcademicPress, pp. 287–301.

[8] Lester BM, Tronick EZ. (2004) The NeonatalIntensive Care Unit Network Neurobehavior Scale(NNNS). Pediatrics 113, 631–99.

[9] Tronick EZ, Olson K, Rosenberg R, Bohne L,Lu JL, Lester BM. (2004) Normative neurobehav-ioral performance of healthy infants. Pediatrics 112,676–9.

[10] Lester BM. (1998) The Maternal Lifestyles Study.In: Harvey JA and Kosofsky BE (eds), Cocaine:Effects on the Developing Brain. New York: NewYork Academy of Sciences, pp. 296–305.

[11] Liu J, Bann C, Lester BM. (2010) Neonatal neurobe-havior predicts medical and behavioral outcome.Pediatrics 125, e90–8.

[12] Fink N, Tronick EZ, Olson K, Lester BM. Clini-cally healthy infants’ neurobehavioral performance:Norms and percentiles from the Neonatal Inten-sive Care Unit Network Neurobehavioral Scale(NNNS). Pediatrics. Under review.

[13] Tronick E. (2007) The Neurobehavioral and Social-Emotional Development of Infants and Children.New York: WW Norton & Co.

[14] Blumberg NL. (1980) Effects of neonatal risk,maternal attitude, and cognitive style on early

postpartum adjustment. Journal of Abnormal Psy-chology 89, 139–50.

[15] Tronick EZ, Beeghly M. (2011) Infants’ meaning-making and the development of mental healthproblems. American Psychologist 66, 107–11.

[16] Dicorcia JA, Tronick EZ. Quotidian resilience:exploring mechanisms that drive resilience from aperspective of everyday stress and coping (in press).

[17] Beeghly M, Tronick EZ. (1994) Effects of prenatalexposure to cocaine in early infancy: Toxic effectson the process of mutual regulation. Infant MentalHealth Journal 15, 158–75.

[18] Tronick EZ, Morelli G. (1991) Foreword: The roleof culture in brain organization, child development,and parenting. In: Nugent JK, Lester BM, Brazel-ton TB (eds), The Cultural Context of Infancy:Multicultural and Interdisciplinary Approaches toParent-Infant Relations, 2nd edn. Ablex Publishing.

[19] Miller G. (2010) The seductive allure of behavioralepigenetics. Science 329, 24–7.

[20] Tronick EZ, Thomas RB, Daltabuit M. (1994) TheQuechua manta pouch: A caretaking practice forbuffering the Peruvian infant against the multiplestressors of high altitude. Child Development 65,1005–13.

[21] Persing J, James H, Swanson J. (2003) Preventionand management of positional skull deformities ininfants. Pediatrics 112, 199–202.

[22] Ma D. (2009) Babies should sleep on backs, play onstomachs. American Academy of Pediatrics News30, 30.

[23] Super CM. (1976) Environmental effects on motordevelopment: The case of African infant precocity.Developmental Medicine & Child Neurology 18,561–7.

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5Genetic and Biological InfluencesDavid SkuseInstitute of Child Health, University College London, London, UK

INTRODUCTION

The Human Genome Project was completed in2003 [1], and the first draft sequence of DNA ina human cell was then available for everyone toscrutinize. What have we learned since, and havethose insights benefited patients with psychiatricdisorders?

Until relatively recently, what little was knownabout genes that contribute to neurodevelopmen-tal conditions came from the study of single genemutations, in which the normal activity of an indi-vidual gene is disrupted. Disorders attributableto errors in a single gene are exceptionally rare(typically with an incidence of no more than1 per 10 000). Remarkable advances are beingmade in our understanding of the pathogenesis of‘single gene’ conditions such as Fragile X or Rettsyndrome, and new opportunities for treatmentare being discovered that could potentially havewider applications [2,3].

Unlike single gene disorders, most psychiatricconditions are highly complex in terms of theirunderlying genetic predisposition. Whilst twinand adoption studies indicate an important rolefor heredity, risk is attributable to the sumof individual differences in hundreds or eventhousands of genes [4]. In order to take advantageof our developing knowledge of DNA sequences,we need to bridge the gap between those indi-vidual differences and their manifestations asphenotypes. In other words, we need to translateknowledge at the level of molecules into anunderstanding of cognition and behaviour [5].


Interactions between the entire genome andnon-genomic factors that ultimately result inhealth and disease, are core components of thenew era of ‘genomic medicine’ [6].

HOW MANY GENES ARE THERE?

Humans have around 19 000 protein-coding genes[6], far fewer than the approximately 120 000 pre-dicted 10 years ago. We possess about the samenumber of genes as a mouse, and rather fewer thanrice plants.

The information content of human DNA is builtfrom long chains of nucleotides. Nucleotides con-sist of the bases adenine, guanine, thymine andcytosine, combined with a sugar molecule (deoxyri-bose in DNA) attached to a phosphate group.These bases are usually depicted by the letters A,G, T and C. The nucleotides in a DNA strand arearranged in pairs, and our genome is made up ofaround 3 billion nucleotide pairs, per haploid set ofchromosomes. We normally have 23 pairs of chro-mosomes, and each member of the pair is identicalin females. In males, one of the sex chromosomesis a Y rather than an X, but the total is just thesame (46, the full diploid set). To fit such an enor-mous amount of information into a cell nucleus,the DNA double helix is incredibly tightly coiled.Recent research is focusing on how that coilingoccurs, by what rules, and how does the machinerythat wants to read the DNA sequence, to makeproteins and regulate cellular activity, get accessto it? Box 5.1 provides a glossary of basic terms.

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Genetic and biological influences

Reading the complete sequence of our DNA forthe first time was a mammoth achievement. Let usimagine each nucleotide has the dimensions of anAmerican 1-cent piece, equivalent to a 1 new pennypiece in the UK; both have a diameter of about2 cm. This is of course blowing up the size of eachnucleotide enormously from their actual dimen-sions. If laid down side-by-side, 3 billion pennieswould stretch about 35 000 miles, which is morethan the circumference of the Earth at the equator(25 000 miles).

SOURCES OF GENOMIC VARIATION

Nucleotides are read in triplets by the cell’s geneticmachinery, by convention from left to right in anyillustration (e.g. AAA, CCC, TTA, ATG). Eachtriplet codes for an amino acid or a signal of somesort (e.g. start, stop), or it may have no meaningthat we currently recognize.

Until relatively recently, we thought that themain reason individuals (of the same gender)differed from one another was due to small dif-ferences in the typical nucleotide sequence oftheir DNA. These changes are known as single-nucleotide polymorphisms (or SNPs for short). Onaverage, our DNA sequence of nucleotides is verysimilar from one person to another, with only about0.4% of our genome differing due to these SNPs.Nucleotide substitutions occur on average once inevery 800 base (nucleotide) pairs. If the change inour nucleotide sequence (e.g. . . .TCTGATTG. . .

becoming . . .ACTGATTG. . .) occurs in a geneticcoding or a regulatory region there may be animpact on gene expression or in the shape of theprotein ultimately formed from the gene in ques-tion. Alternatively, the substitution may be ‘silent’in its consequences.

We call such differences in gene sequence poly-morphisms, if they are fairly common. Polymor-phisms occur by definition in more than 1% of thepopulation. The prevalence of polymorphisms isstrongly influenced by the genetic background ofthe population being studied. This means that theirdistribution could be very different, for example,in Americans of African and of European origins.

There are other sources of genetic variation too.These include insertions and deletions of relativelysmall numbers of nucleotides (so-called indels) aswell as grosser structural rearrangements withinor between chromosomes (the latter can often be

detected by microscopy). Where these indels arerelatively large (larger than 1000 base pairs) andcause an increase or decrease in the number ofcopies of a single gene or a series of genes, theseare known as copy-number variations (CNVs).Either increasing or decreasing the number ofcopies of particular genes may alter susceptibil-ity to a variety of disorders. For example, severallarge-scale studies of autism and schizophrenia[7,8] have shown that particular CNVs are muchmore common in both conditions than in con-trol populations. Copy-number variations werenot recognized as important contributors to riskuntil very recently [9]. They are more likely tobe pathogenic if they comprise deletions ratherthan insertions of DNA sequences, and may beinherited or occur de novo. Their discovery hasboth challenged existing approaches in psychiatricgenetics and opened a new frontier for research, asthese CNVs could account for as large a proportionof genetic risk as SNP variation. Determining theimplications of a copy number variation for genefunction is problematic, because by definition theytend to disrupt large sequences of DNA. The factthat similarly positioned CNVs are found in severalmajor psychiatric conditions seems to indicate thegenes have not read the textbooks that so carefullydefine diagnostic classification [4].

MECHANISMS OF GENOMIC REGULATION

Advances in technology are giving us new insightsinto the consequences of individual differencesin DNA sequences. There is a lot of DNA inevery human cell, but rather fewer genes thanwe expected. Most of the DNA is identical in allhumans, but as we have seen, the variability thatdoes exist can have significant consequences for theprediction, prevention, diagnosis and treatment ofdisease.

Surprisingly, perhaps, we are faced with a num-ber of unexpected and rapidly increasing problemsconcerning exactly how we define genes, and howthey are regulated. We used to think that a genewas a segment of DNA, in the cell nucleus, thatcoded for a protein, and that the production ofthat protein was mediated by the action of RNAthat read the genetic material and transported thecode to protein-building machinery on the ribo-some, elsewhere in the cell. In recent years wehave found that there are many more classes of

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RNA than we ever suspected, and that there is atremendously complex regulatory machinery.

Genomic regulation is now known to comprisemultiple interactions between proteins and RNAmolecules, some of which can lead to modifica-tions of RNA itself [10]. Over the next few years,it seems likely there will be an enormous increasein our understanding of the role of small RNAmolecules, which are critically involved in thisprocess. Incidentally, they are being discoveredat a considerable pace (e.g. 21 microRNA geneshad been identified on the X-chromosome by July2009, but the equivalent figure was 128 just one yearlater). Unless we understand how individual differ-ences in gene regulation predispose to disorders,we are unlikely to be able to use the informationgained from the study of the basic DNA sequencein a human genome to develop models of disease.Risk of psychiatric disorder is not instantiated in afew triplets of DNA nucleotides.

Gene regulation is far more complicated at everylevel than we ever imagined. Understanding howsusceptibility to psychiatric disorder, measured atthe level of a small change in a DNA sequence,leads to phenotypic differences at the level ofobserved behaviour and mental activity will becaptured by integrating information from a host ofdifferent levels of analysis; from cellular activityto synaptic control, from the efficiency of neuraltransmission to cognitive processing.

MEASURING GENETIC SUSCEPTIBILITYTO PSYCHIATRIC DISORDERS

Gene—environment interactionsIt is self-evident that our genes do not whollydetermine our development. Even identical twins,who share 100% of their genetic make-up, are notexactly the same in their personality or propen-sity to develop psychiatric disorders. But how doour family circumstances, the unpredictable eventsthat happen in our lives, and our genetic-make-upinteract? Can we meaningfully predict that somepeople with a particular genetic predisposition,at the level of a single gene polymorphism, willbe vulnerable – but only if exposed to risky envi-ronments? For instance, is it true that childrenwith a particular genetic variant of the monoamineoxidase A (MAOA) gene are much more likelyto develop antisocial behaviour in adulthood ifsubject to maltreatment in childhood than if they

did not possess the variant [11]? Should we warnyoung people who have a polymorphism of thecatechol O-methyltransferase (COMT) gene thatthey should not smoke cannabis because of a dis-proportionate increased risk of psychosis [12]?

Do genetic and environmental risk factors com-bine in ways that lead to a relatively greater proba-bility of outcome than simply the arithmetic sum ofthe individual risks? The controversial argumentfrom the studies quoted above is that the simplesum of the risks (gene + environmental exposure)on outcome is much less than the observed risk. Inother words, some interaction must have occurred,between the genetic and the environmental vari-able that had increased the probability of a delete-rious outcome disproportionately, and may implythat these factors had interacted in some way at abiological level.

Interactions between variables are commonlymodelled to predict outcomes in epidemiologicalstudies, but many scientists regard gene × envi-ronment interactions as tenuous things, which arenot necessarily biologically real. Such interactionscould instead represent statistical artefacts, and wemay not be correct in assuming we can infer bio-logical interactions from statistical analyses of thistype [13]. While evidence of non-independence ata physiological level informs how genetic and otherrisk factors should be modelled in epidemiologicalstudies, the opposite is not true. In other words,we should not infer a biological mechanism fromepidemiological evidence of a ‘genotype × expe-rience’ interaction. Non-linear summation of risksmay prompt further investigation as to whether abiological interaction exists, but the observation ofan interaction is not conclusive that there is sucha mechanism operating. This somewhat scepticalview is reinforced by the observation that manyapparently exciting and novel results in psychiatricgenetics fail to be replicated, for a variety of rea-sons including over-optimistic data analysis andpublication bias [14]. This issue of non-replicationis discussed in the next section.

Genome-wide association studiesIn recent years, psychiatrists have been keen touse our newly found knowledge of the sequenceof the human genome, and of the genes containedwithin it (about 1% of the total) to evaluate asso-ciations between genetic variation (usually at thelevel of SNPs) and risk of disease. In principle,

25


this is simple, and the number of genetic variantsthat are associated with complex disorders such asattention deficit hyperactivity disorder (ADHD),schizophrenia or bipolar disorder is growing monthby month. The basic idea is to test whether a partic-ular genotype is more commonly associated withthe disorder than we would expect by chance, giventhe prevalence of the polymorphism in the generalpopulation. There are many pitfalls in the inter-pretation of such findings, not least the risk of falsepositive results that do not replicate [14]. Now,independent replication is mandated for studiesthat aim to be published in leading journals.

It is unusual for the polymorphisms of statis-tical significance to be found in coding regions,presumably because their impact is on regulatoryprocesses. However, in many cases we simply donot know for sure how identified polymorphismstranslate from gene expression to protein synthe-sis and beyond. Is this a clue that we need torevise our interpretation of the data? Another sur-prise from the results of psychiatric genome-wideassociation studies is that each polymorphism ofstatistical significance accounts for just a tiny pro-portion of variance in risk. Even in aggregate, thetotal number of replicated ‘risk-associated’ poly-morphisms accounts for far less of the variance(in, say, the chance of developing schizophrenia)than we anticipated from our knowledge of her-itability. The mystery of the ‘missing variance’ isnot peculiar to psychiatric disorders [15]. It hasbeen the subject of substantial recent debate [16].Clearly, even though we are now able to read theentire DNA sequence, our knowledge about thevariety of differences in the genetic code, and theirinteraction with other factors, remains inadequateat present to explain the observations made at thephenotypic level.

Epigenetic variationOur chance of developing a psychiatric disordermay also be influenced by changes in the complexregulatory structure that enables genes to be readefficiently, as a consequence of exposure to cer-tain environmental circumstances. Changes in themyriad mechanisms by which genetic activity isregulated but which do not alter the fundamentalDNA sequence, are termed ‘epigenetic’.

Epigenetic influences on gene expression arealmost certainly not heritable. Once acquired, epi-genetic marks can nevertheless allegedly change

gene expression for life. There are several mech-anisms by which this could happen. The mostintensively studied of these entails the attachmentof methyl groups to specific nucleotides in a regu-latory region of the gene, thereby silencing it.

Research in ‘behavioural epigenetics’ has grownover the past 10 years, centred on McGill Univer-sity in Montreal, Canada [17]. The excitement ofthe field is that it offers an explanation for whyearly adverse experiences might lead to lifelongchanges in behaviour. The usual experimental ani-mal is the rat, but some evidence is emergingthat epigenetic changes, arising from events inearly childhood, could influence human behaviourtoo [18]. The results of behavioural epigeneticexperiments, which characteristically examine theconsequence of individual differences in maternalcare, are controversial [19].

On the other hand, there is so much interestin the possibility that epigenetic influences couldhave a role in a wide range of disease suscep-tibility, from type 2 diabetes to cancer, that aNational Institutes of Health sponsored RoadmapEpigenomics Project was launched late in 2010(http://www.roadmapepigenomics.org/).

THE FUTURE OF PSYCHIATRIC GENETICS:OUR PERSONAL GENOME

A wide range of molecular genetic diagnostic tech-niques are coming on stream, and these are likelyto have increasing importance for the manage-ment of individual patients. They are typicallybased on computer chips, known as microarrays,and such chips can in principle carry a wide rangeof information. They can currently be used for thestudy of up to a million polymorphic SNPs at atime (although no doubt this figure will rapidlyincrease up toward the figure of 24 million bp,which is the amount by which individuals differon average). They can also capture copy numbervariations, and epigenetic changes. Chip technol-ogy is becoming much cheaper as the economiesof scale allow greater production at reducing cost.One application of gene chip technology, which isimportant for psychiatrists, is discussed by DavidMrazek (see Chapter 41, Discovering PsychiatricPharmacogenomics). He describes how we can tai-lor treatments to individuals, using the techniquesof pharmacogenomics.

26


Although we may soon be able to obtain, atmoderate cost, a copy of our personal genome, theinterpretation of the data in that genome is going tobe far from simple. When we have ‘$1000 genomes’(predicted to be before the end of 2012), how willthese benefit patients with psychiatric disorders?First, there will undoubtedly be implications forthe revision of conventional phenotypic distinc-tions within and between disorders. We alreadyknow that there is shared genetic risk betweendisorders that were thought to be quite distinct,such as autism and schizophrenia, and that it istheoretically possible to build modelling networksthat predict the underlying genetic covariance [20].Second, we will be able increasingly to understandthe origins of mental disorders in terms of dysregu-lated neural systems. To this end we are beginningto see the development of gene expression atlasesfor the brain [21]. So far, these techniques have lim-ited applicability to humans, but there is growingevidence that in mice we can use such information

to build models linking neural circuitry, regionalgene expression, and phenotypic variables such asmemory [22].

CONCLUSIONS

We are increasingly able to measure human geneticvariation reliably. The cost of providing each oneof us with a map of our personal genome is drop-ping rapidly. When that information is available,it will mark the end of an era where the focushas been on genetic sequencing, and the beginningof a new age in which the functional activity ofthat genome is front of stage. Inevitably, the worldof ‘-omics’, exemplified by genomics, transcrip-tomics, proteomics, epigenomics and so on, willcome to impinge on every aspect of medical sci-ence. Ultimately, it will influence the assessmentand treatment of all conditions discussed in thisvolume: forewarned is forearmed.

Box 5.1 Glossary of basic terms. Reproduced with permission from NEJM

Allele: One of two or more versions of a genetic sequence at a particular location in the genome.Base pair (bp): Two nitrogenous bases paired together in double-stranded DNA by weak bonds;specific pairing of these bases (adenine with thymine and guanine with cytosine) facilitatesaccurate DNA replication; when quantified (e.g. 8 bp), bp refers to the physical length of asequence of nucleotides.

Complex condition: A condition caused by the interaction of multiple genes andenvironmental factors. Examples of complex conditions, which are also called multifactorialdiseases, are cancer and heart disease.

Copy-number variation: Variation from one person to the next in the number of copies of aparticular gene or DNA sequence. The full extent to which copy-number variationcontributes to human disease is not yet known.

Deletion mutation: A mutation that involves the loss of genetic material. It can be small,involving a single missing DNA base pair, or large, involving a piece of a chromosome.

Diploid number: Refers to the number of chromosomes in a human somatic cell. Such a cellnormally contains 46 chromosomes, comprising two complete haploid sets (see ‘Haploidnumber’), which together make up the 23 homologous chromosome pairs.

DNA: Deoxyribonucleic acid; the molecules inside cells that carry genetic information and passit from one generation to the next.

Epigenetic change: A change in the regulation of the expression of gene activity withoutalteration of genetic structure.

Gene: The fundamental physical and functional unit of heredity. A gene is an orderedsequence of nucleotides located in a particular position on a particular chromosome thatencodes a specific functional product (i.e. a protein or an RNA molecule).

27


Gene chip: A solid substrate, usually silicon, onto which a microscopic matrix of nucleotides isattached. Gene chips, which can take a wide variety of forms, are frequently used tomeasure variations in the amount or sequence of nucleic acids in a sample.

Genome: The entire set of genetic instructions found in a cell. In humans, the genome consistsof 23 pairs of chromosomes, found in the nucleus, as well as a small chromosome found inthe cells’ mitochondria.

Genome-wide association study: An approach used in genetics research to look forassociations between many (typically hundreds of thousands) specific genetic variations(most commonly single-nucleotide polymorphisms) and particular diseases.

Genome-wide scan: An assay that measures hundreds of thousands to millions of points ofgenetic variation across a person’s genome simultaneously, either for research or for clinicalapplication.

Genotype: A person’s complete collection of genes. The term can also refer to the two allelesinherited for a particular gene.

Haploid number: The number of chromosomes in a gamete; that is, in an ovum or a sperm (inthe human this is 23). A somatic cell (anywhere else in the body apart from the germ cells)has twice that many chromosomes (46 — see ‘Diploid number’).

Human Genome Project: An international project completed in 2003 that mapped andsequenced the entire human genome.

Insertion mutation: A type of mutation involving the addition of genetic material. An insertionmutation can be small, involving a single extra DNA base pair, or large, involving a piece of achromosome.

Methylation: The attachment of methyl groups to DNA at cytosine bases. Methylation iscorrelated with reduced transcription of the gene and is thought to be the principalmechanism in X-chromosome inactivation and imprinting.

Microarray: A technology used to study many genes at once. Thousands of gene sequences areplaced in known locations on a glass slide. A sample containing DNA or RNA is deposited onthe slide, now referred to as a gene chip. The binding of complementary base pairs from thesample and the gene sequences on the chip can be measured with the use of fluorescence todetect the presence and determine the amount of specific sequences in the sample.

Mutation: A change in a DNA sequence. Germ-line mutations occur in the eggs and sperm andcan be passed on to offspring, whereas somatic mutations occur in body cells and are notpassed on.

Nucleotide: The basic building block of nucleic acids. RNA and DNA are polymers made of longchains of nucleotides. A nucleotide consists of a sugar molecule (either ribose in RNA ordeoxyribose in DNA) attached to a phosphate group and a nitrogen-containing base. Thebases used in DNA are adenine (A), cytosine (C), guanine (G), and thymine (T). In RNA, thebase uracil (U) takes the place of thymine.

Pharmacogenomics: A branch of pharmacology concerned with using DNA sequence variationto inform drug development and testing. An important application of pharmacogenomics isthe correlation of individual genetic variations with drug responses.

Phenotype: The observable traits of an individual person, such as height, eye colour and bloodtype. Some traits are largely determined by genotype, whereas others are largelydetermined by environmental factors.

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Rearrangement: A structural alteration in a chromosome, usually involving breakage andreattachment of a segment of chromosomal material, resulting in an abnormalconfiguration; examples include inversion and translocation.

Ribosome: A cellular particle made of RNA and protein that serves as the site for proteinsynthesis in the cell. The ribosome reads the sequence of the mRNA and, using the geneticcode, translates the sequence of RNA bases into a sequence of amino acids.

RNA: Ribonucleic acid; a chemical similar to DNA. The several classes of RNA molecules playimportant roles in protein synthesis and other cell activities.

Single-nucleotide polymorphism (SNP): A single-nucleotide variation in a genetic sequence; acommon form of variation in the human genome.

Small (or short) inferring RNA (siRNA): Any short, double-stranded regulatory RNA moleculethat binds to and induces the degradation of target RNA molecules.

Systems biology: Research that takes a holistic rather than reductionist approach tounderstanding organism functions.

Translation: During protein synthesis, the process through which the sequence of bases in amolecule of messenger RNA is read in order to create a sequence of amino acids.

Adapted from Feero WG, Guttmacher AE, Collins FS. Genomic medicine — an updated primer. New EnglandJournal of Medicine 2010;362:2001—11.

REFERENCES

[1] Collins FS, Morgan M, Patrinos A. (2003) TheHuman Genome Project: lessons from large-scalebiology. Science 300, 286–90.

[2] Guy J, Gan J, Selfridge J, Cobb S, Bird A. (2007)Reversal of neurological defects in a mouse modelof Rett syndrome. Science 315, 1143–7.

[3] Wang LW, Berry-Kravis E, Hagerman RJ. (2010)Fragile X: leading the way for targeted treatmentsin autism. Neurotherapeutics 7, 264–74.

[4] Craddock N and Owen MJ. (2010) The Krae-pelinian dichotomy – going, going . . . but still notgone. British Journal of Psychiatry 196, 92–5.

[5] Meyer-Lindenberg A. (2010) Intermediate or brain-less phenotypes for psychiatric research? Psycho-logical Medicine 40, 1057–62.

[6] Feero WG, Guttmacher AE, Collins FS. (2010)Genomic medicine – an updated primer. NewEngland Journal of Medicine 362, 2001–11.Available online at: http://www.nejm.org/doi/full/10.1056/NEJMra0907175 (accessed February 2011).

[7] McCarthy SE, Makarov V, Kirov G et al. (2009)Microduplications of 16p11.2 are associated withschizophrenia. Nature Genetics 41, 1223–7.

[8] Sebat J, Lakshmi B, Malhotra D et al. (2007) Strongassociation of de novo copy number mutations withautism. Science 316, 445–9.

[9] Bassett AS, Scherer SW, Brzustowicz LM. (2010)Copy number variations in schizophrenia: critical

review and new perspectives on concepts of geneticsand disease. American Journal of Psychiatry 167,899–914.

[10] Davidson EH and Levine MS. (2008) Properties ofdevelopmental gene regulatory networks. Proceed-ings of the National Academy of Sciences of the USA105, 20063–6.

[11] Caspi A, McClay J, Moffitt T et al. (2002) Roleof genotype in the cycle of violence in maltreatedchildren. Science 297, 851–4.

[12] Caspi A, Moffitt TE, McClay J et al. (2005) Moder-ation of the effect of adolescent-onset cannabis useon adult psychosis by a functional polymorphismin the catechol-O-methyltransferase gene: longitu-dinal evidence of a gene × environment interaction.Biological Psychiatry 57, 1117–27.

[13] Kendler KS and Gardner CO. (2010) Interpreta-tion of interactions: guide for the perplexed. BritishJournal of Psychiatry 197, 170–1.

[14] Munafo MR and Flint J. (2010) How reliable arescientific studies? British Journal of Psychiatry 197,257–8.

[15] Yang J, Benyamin B, McEvoy BP et al. (2010)Common SNPs explain a large proportion of theheritability for human height. Nature Genetics 42,565–9.

[16] Eichler EE, Flint J, Gibson G et al. (2010) Missingheritability and strategies for finding the underlyingcauses of complex disease. Nature Reviews Genetics11, 446–50.

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[17] McGowan PO, Sasaki A, D’Alessio AC et al. (2009)Epigenetic regulation of the glucocorticoid receptorin human brain associates with childhood abuse.Nature Neuroscience 12, 342–8.

[18] McGowan PO, Sasaki A, Huang TCT et al. (2008)Promoter-wide hypermethylation of the ribosomalRNA gene promoter in the suicide brain. PLoS One3: e2085.

[19] Buchen L. (2010) Neuroscience: in their nurture.Nature 467, 146–8.

[20] Feldman I, Rzhetsky A, Vitkup D. (2008) Networkproperties of genes harboring inherited diseasemutations. Proceedings of the National Academyof Sciences of the USA 105, 4323–8.

[21] Jones AR, Overly CC, Sunkin SM. (2009) The AllenBrain Atlas: 5 years and beyond. Nature ReviewsNeuroscience 10, 821–8.

[22] Geschwind DH and Konopka G. (2009) Neuro-science in the era of functional genomics and systemsbiology. Nature 461, 908–15.

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Section 1b

General Patternsof Development

Clinical evaluation of development from birth to five years

6Clinical Evaluation of Development fromBirth to Five YearsAjay Sharma1 and Tony O’Sullivan2

1Sunshine House, Southwark Centre for Children and Young People, London, UK2Kaleidoscope - Lewisham Centre for Children & Young People, London, UK

INTRODUCTION

Clinical evaluation of children with behaviouralconcerns requires considering their physical,emotional, behavioural and social development,alongside relevant environmental influences.Differential diagnosis includes the possibilityof organic and developmental disorders withbehavioural phenotypes, where developmentalmarkers aid identification. A working knowledgeof typical developmental milestones and ‘red flagalerts’ to possible developmental delay is essential.Required competencies include eliciting parentalconcerns, taking a relevant developmental history,observing and assessing child development,undertaking relevant physical examinations, andplanning investigations and access to local serviceswhere further assessment or intervention isrequired.

CHILD DEVELOPMENT

Child development is a dynamic process shapedby a complex interplay between genetic, biologicaland environmental factors that operate from thetime of conception through to the child’s birthand subsequent development [1]. While thereis enormous variation in both the pattern andrate of normal development, the sequences ofdevelopment are similar in most children. Thus,developmental milestones can act as convenientmarkers for the rate of development.


INDICATORS OF ABNORMALDEVELOPMENT

Warning signs of possible developmental problemsinclude:

• A rate of development outside the normal rangein one or more developmental domains (e.g.echolalia – repetitive imitation of speech – stillpresent by 3 years).

• Absolute failure to develop skills (e.g. absence ofmultisyllabic and tuneful babble by 10 months).

• Disordered developmental sequence (e.g.advanced reading coexisting with delayedlanguage).

• Motor asymmetry in hand use or walking.• Developmental regression, i.e. a loss or plateau-

ing of skills.

THE DEVELOPMENTAL EXAMINATION

A developmental examination includes history-taking and observing the child’s developmental,interactional and play skills during the assessmentprocess.

History-takingPrenatal, perinatal and postnatal histories arerequired, in addition to the family’s history andthat relating to the family and social environment.Questioning parents or caregivers about broadareas of function elicits concerns and guides

32

General patterns of development

clinicians on where to focus a more detailedhistory-taking and examination. The pervasive-ness of concerns about the child can be confirmedfrom information obtained from others such asteachers or health-care staff.

Parents can provide a reliable history whenasked open-ended questions and when requestedto give examples of behaviour. They are very goodat remembering whether or not they had concernsand what these were. Focusing enquiry aroundtransition points, such as starting at a nurseryor other significant events, will facilitate parentalmemory of developmental achievements. Parentalobservations of behaviour (e.g. ‘he will fetch hisshoes only if they are visible’) are generally moreaccurate than parental interpretations of behaviour(e.g. ‘he understands everything I say’). Parentalviews of the causation of any developmental prob-lems need to be elicited allowing parents to bereassured as to any unwarranted concerns thatthey are responsible in some way – for instance,that maternal depression may have resulted inautism. Parental misconceptions as to other typesof causation can also be corrected.

It is valuable to establish from independentenquiry, the reason for any obstetric interven-tion (e.g. fetal distress), the baby’s condition atbirth, and any history of neonatal fits. Gestationalage should be ascertained for children under 24months old and consequent adjustments madewhen assessing age-appropriate behaviours. Thechild’s current health and any history of seriousillness may be relevant and should be ascertained.

Observation and interactive assessmentSetting the context: Providing a suitable selectionof age-appropriate toys will allow assessment ofrelevant domains – for example, the child’s abili-ties to copy behaviour (use of rattle); understandcause and effect relationships (using a pop-up toy),define objects by use (hair brush); symbolic under-standing (use of doll, tea set); fine eye–motorcoordination (use of bricks, cubes), language andplay (toys and pictures).

Observing the child: Observations of children’sfree play and semistructured assessment provide ameaningful and valid ascertainment of children’sabilities. A cardinal rule of developmental assess-ment is to look not only at what the child does,but also at how s/he does it. Thus, the quality of

responses as well as the level of attainments shouldbe monitored.

A range of standardized materials are availableto gather detailed normative information for diag-nostic or monitoring purposes. Observations needto include the child’s attention, emotional stateand their initiations and responses. Any change infunction and behaviour with increasing task com-plexity, coping with transition from non-verbalto language-based activity and changes in perfor-mance as assessment time lengthens should benoted. Adult help should be kept to a level thatallows assessment of the child’s own ability toorganize their environment and generate ideas.

DEVELOPMENTAL DOMAINS

Children whose sequence of development showsmoderate or severe developmental delay, plateau-ing or regression, require further assessment,including an examination of their vision andhearing. ‘Red flag alerts’ can be found in Tables6.1 to 6.5.

Gross motorDelay in gross motor milestones (Table 6.1) mayindicate neurological abnormalities. Althoughthere is a weak correlation between gross motorand general developmental delay, it usuallyimpacts the learning and performance of skills. Aphysical examination should be combined withassessing the child’s sequence of development,style of learning, avoidance behaviours, sensorysensitivities or impairments, as well as a qualitativedescription of their motor competencies.

Table 6.1 Gross motor milestones.

Developmental Mean age Limit age —milestone (months) ‘red flag’

(months)

Hands open most ofthe time (not listed)

3 4

Good head controlwhen sitting

4 6

No head lag whenpulled to sit

Sits independently 7—8 10

Walks alone 11—13 18

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Visual behaviour, eye—hand coordinationand problem-solvingProgressive coordination of maturing vision withhead, body and fine motor movements can beobserved as the child manipulates a variety oftest/play materials. Observation can help tease outthe relative contributions of motor and cognitiveabilities, emotional factors and experience. Chil-dren’s achievements here represent the precursorto later non-verbal problem-solving abilities, cor-relate well with overall intellectual ability and mayprovide early markers for learning, psychologicaland psychiatric disorders. Early visual behaviourand eye–hand coordination milestones are pre-sented in Tables 6.2 and 6.3.

Object concepts and relationshipsTable 6.4 presents this developmental sequence,which reflects a growing understanding of thenature and visuospatial relatedness of objects,combined with a refined grasp and release ability.

Imitating and copying cube modelsThis sequence, assessed via children’s desire andability to copy models, combines the processesof encoding, decoding and execution using hor-izontal, vertical and three-dimensional alignments(Table 6.5).

DrawingThe developmental milestones in drawing abilitycan be found in Table 6.6. These are evidencethat children move through various stages – fromsimply making marks on paper to the ability to copya diamond shape by the age of 66–72 months. Chil-dren gradually refine their grasp – 50% of childrenby the age of 3 years and 80% by 4 years have agood tripod grasp of a pencil.

Table 6.2 Early visual behaviour milestones.

Visual behaviour Limit age ‘Red flag’milestone (months) (months)

Visually alert, orientto face

1 Any delay

Visually follows face 2 Any delay

Coordinates eyemovements with headturning

3 Any delay

Table 6.3 Eye — hand coordination milestonesfrom 3 months.

Developmental Mean agemilestone (months)

Holds objects briefly when placed inhands without visual regard

3

Visually examines own hand 4

Reaches out with a two-handed scoop 5

Reaches out and grasps objects ontable surface with a raking grasp

6

Transfers from hand to hand 6

Explores with index finger 6

Picks up a pellet/raisin betweenthumb and finger

9

Picks up a string between thumb andfinger

10

Can release in a container 10

Has mature grasp 12

Has precise release — without pressingon surface

13

Builds towers of 2 cubes 13

Builds towers to 3 cubes 16

Turns pages of book one page at atime

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Language and communicationThere is a considerable variation between childrenin milestone attainments as outlined in Table 6.7.Identification of language impairments requirescombining parental information with observationand assessment. The quality of parental informa-tion is improved if parents keep lists of spokenwords or phrases. It is worth noting that as childrendevelop good understanding of daily family rou-tines, their language comprehension can often beoverestimated by both parents and professionals.

Play and social behaviourA number of developmental sequences cometogether in children’s play (Figure 6.1). Theseinclude social initiations and responses, verbaland non-verbal communicative skills; imaginationand the generation and sustaining of ideas whilstremaining alert to the social environment [2].

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Table 6.4 Object concepts and relationshipsmilestones.


Permanence of object: looks forhidden object

8

‘Cast’: drops repeatedly-enjoyssound and attention

8

Cause and effect: presses orpushes to activate a toy

9

Means-end relationship: pullstoy placed out of reach with astring

9

Relating two objects together 10

Relating objects: enjoys puttingthings in and out of container

10

Simple posting games: roundshapes

12

Matches simple shapes 16—18

Matches three shapes with good‘scanning’

24

Table 6.5 Cube model copying milestones.


Builds tower of 6 cubes 22

Horizontal alignment ofbricks

24

3-cube bridge 33

4-cube train with achimney

39

3 steps with 6 cubes 48—54 months

4 steps with 10 cubes 60 months

Some red flag alerts for language,communication and social developmentFurther assessment would be required when thefollowing ‘red flags’ for language, communicationand social development are observed:

• no multisyllable babble, pointing or othergesture by 12 months;

• no joint attention by 18 months;

• absence of simple pretence play by 24 months;• no single words by 18 months;• lack of social interest in other children from 18

months;• no word combinations (non-echoed) by 30

months;• cannot follow two-step command (e.g. ‘give ball

to daddy’) by 30 months;• speech largely unintelligible by 4 years;• no conversational interchange by 4 years;• echolalia still present at 3 years.

Development of attentionAttention difficulties may contribute to poordevelopmental performances and interaction dif-ficulties, or indicate global developmental delay.Difficulties of behaviour, language, learningand coordination often coexist with deficits ofattention. A variety of medical conditions inpreschoolers, including epilepsy, hypothyroidism,low birthweight, hearing loss and prenatalexposure to teratogens (e.g. fetal alcoholsyndrome) may underlie attention deficits.

Attention skills develop sequentially, such thatchildren move from a relatively brief exploration

Table 6.6 Drawing milestones.


Shape copying

Makes a mark on paper 15

Scribble 18

Copies lines 24

Copies a circle 36 (90% by 42months)

Copies a cross 42 (90% by 48months)

Copies a square 48

Copies a triangle 60

Copies a diamond 66—72

Drawing a person

Figure with head, otherparts, no body

36 (80% by 45months)

Figure with head, body, limbs 54

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Table 6.7 Language and communication milestones.

Developmental milestone Mean age (months) Range (months)

Comprehension/receptive language

Understands ‘no’/‘bye’ 7 6—9Recognizes own name 8 6—10Understands familiar names 12 10—15Definition by use: using objects by 15Giving objects on request by 15Points to body parts on self/carer 15 12—18Points to body parts on doll 18 15—21Identifying objects on naming by 24Follows a 2-step command 24 18—27Functional understanding 30 21—33Understands prepositions (in/on) 24 18—33Understands prepositions (under) 30 24—39Understands action words (e.g. eating, sleeping) by 36Understands simple negatives 36 30—42Understands comparatives 42 36—48Follows 2 instructions (4 ideas) 42 36—48Understands complex negatives 48 42—60Follows 3 instructions (6 ideas) 54 48—66

Expressive language and non-verbal communication

Jargon 12 10—15Syllabic and tuneful babble 8 6—9Pointing to demand 9Pointing to share interest 10 9—14One word 12 10—182—6 words 15 12—217—20 words 21 18—2450+ words 24 18—272 words joining 24 18—30200+ words 30 24—363—4 words joining 30 25—36Speech usually understandable 30 30—42Question words 36 30—42Pronouns 42 36—48Uses conjunctions (and, but) 48 36—54Sentences of 5+ words 48 36—54Complex explanations and sequences 54 48—66

of toys at the age of 5 months to the flexible,focused and sustained attention of the 3–4-year-old. By 5 years of age children can integrateinformation from different sources and makeand carry out plans with sustained and flexibleattention [3].

Cognitive developmentHere, toys and developmental task materials areused to assess the child’s acquisition of objectpermanence, their understanding of cause andeffect, conceptual and complex thinking, andvocabulary and social understanding. Often

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Object orientedexploratory play (maturing

eye-hand coordinationand object concepts)

9 months

Social smile(90% by 6 weeks)

4–5 weeks

Social play sequence

Cognitive play sequence

Functional use of realobjects on self and other

(e.g. spoon, brush)

18 months

Social anticipationLap games (peek-a-boo,

pat a cake)

6–12 months

Plays with toys in asymbolic manner (e.g. toy

tea set, doll and teddy)

24–30 months

Joint attentionPoints to show

10–15 months

Pretend or imaginativeplay becoming

increasingly varied andcomplex

3–4 years

Social imitative role playwith other children

3–3.5 years

Figure 6.1 Developmental sequences involved in play and social skills.

Table 6.8 Investigation planning for developmental disorders.

Context Recommendedinvestigations

Comments

First-line tests

Children with severedevelopmentaldelay or moderatedelay that is globalor is associated withother significantfindings in historyand examination

Creatine kinase in boys

Thyroid function testsirrespective of neonatalscreening

Array CGH (if available)

Chromosomes forkaryotype and Fragile X ifarray CGH not available

MRI scan or CT scan inmore severe mentalretardation

Toxoplasma, rubella assayand CMV urine culture inchildren under 2 years

Some consensus guidelines also recommendserum lead, urate, U&E, ferritin andbiotinidase

Microarray-based comparative genomichybridization (aCGH) is advancedtechnology that allows detection of evensubmicroscopic alterations in chromosomebalance. These very small changes are oftencalled microdeletions andmicroduplications. This now incorporatesmany individual tests, e.g. specific FISHtests and Fragile X. aCGH is receivingincreasing support as a routine investigationfor generalized learning difficulties/mentalretardation (MR). Studies report suchchromosome subtelomere rearrangementsoccurring with a frequency of 7—10% inchildren with mild-to-moderate MR;approximately 50% of cases are familial.Positive results are eight times more likelythan Fragile X in some learning difficultypopulations.

Plasma calcium and alkaline phosphatasemay help with diagnosis and management

(continued overleaf )

37


Table 6.8 (continued)

Context Recommendedinvestigations

Comments

of DiGeorge syndrome, Williams syndrome,and pseudohypoparathyroidism, and wheremotor delay is due to vitamin D deficiency

Second-line tests

The above first-line investigations PLUS:

Associated abnormalhead size (micro- ormacrocephaly),seizures, focalneurologicalfeatures includingsevere oromotorimpairment andspeech abnormality

MRI

Where aCGH not availablekaryotype and specificmolecular genetic tests,e.g. looking for 22qdeletion in oromotor andspeech dysfunction

In some cases MRI studies can show acharacteristic signature for metabolic,neurocutaneous and degenerative disordersand can even give enough information todirect subsequent genetic testing

Specific history orexamination findingssuggestive ofneurometabolicdisorders

Metabolic investigations:serum amino acids,ammonia, VLCFA,carnitine, homocysteine,disialotransferrin

Urine: organic acids,orotate, GAGs,oligosaccharides

Key pointers for metabolic disorders in theclinical history include consanguinity,failure to thrive and episodicneurodevelopmental decompensations(often during minor illnesses). Examinationfindings may include coarse facial featuresor hepatosplenomegaly

Specific history orexamination findingssuggestive ofepilepsy or specificbehaviouralphenotypes, e.g.Angelman syndrome

EEG In Angelman syndrome, characteristic EEGchanges may precede seizures. Diagnosis isconfirmed by deletion or uniparental disomyon chromosome 15

Specific EEG changes also may help in rarepresentations such as regression in languageand differentiation of seizure-like episodessuch as in Rett syndrome

Regression with orwithout associatedfeatures

Referral to a paediatricneurologist/consultation for planningfurther appropriateinvestigations

In many countries human immunodeficiencyvirus (HIV) infections are becoming animportant cause of regression withneurological and neuropsychiatricmanifestations usually presenting in the first3 years of life

CMV, cytomegalovirus; EEG, electroencephalogram; FISH, fluorescence in situ hybridization; GAG, glycosamino-glycan; MRI, magnetic resonance imaging; U&E, urea and electrolytes; VLCFA, very long-chain fatty acids.

38


children presenting with significant developmentaldelay, global or domain-specific, have long-termcognitive and functional impairments.

CLINICAL DECISION-MAKING ANDSEVERITY OF DEVELOPMENTAL DELAY

Developmental delay in any given domain that isequivalent to 50% or less of the expected mile-stones at a given chronological age is always signif-icant and requires further investigations. Childrenwith less marked (‘moderate’) delay may or maynot have a developmental disorder. The delay ismore likely to be significant if global (i.e. acrossseveral domains including language and cognition)or where associated with other significant findingsor risk factors in the history and examination.If there are any abnormal physical findings suchas microcephaly or macrocephaly on neurologicalexamination, then further investigation would bewarranted without further delay. The context of afull social, family and medical history and physi-cal examination will help decide whether to watchand wait, promptly investigate, or refer on to otherspecialists for further assessment and intervention.

PHYSICAL EXAMINATION

The physical examination is generally left to theend of the assessment as any upset to the childwould interfere with a subsequent developmentalexamination. The following key guidelines shouldbe observed:

• Motor function: Determine whether there isa motor disorder or if any delay is part of aglobal learning difficulty. Observe movementpatterns and posture during the developmentalexamination, interaction and play. Formalexamination of tone, reflexes and power islargely confirmatory.

• Symmetry: Any significant asymmetry of motorskill, tone, reflexes or limb size may indicatehemispheric dysfunction or other pathology.

• Growth: Measure head circumference, heightand weight and plot on a centile growth chart.Compare the consistency of the parameters andassess the growth rate. Both macrocephaly andmicrocephaly may be associated with neurode-velopmental disorders. Macrocephaly is moreusually familial and it is advisable to measurethe parents’ head circumference.

• Sight: Where examination of the optic discs andfundi is necessary (e.g. for septo-optic dysplasiaor raised intracranial pressure) refer to anophthalmologist or paediatrician. All childrenwith significant developmental disordersshould be referred to ophthalmology for thisexamination.

• Hearing: Refer to audiology where there isany delay in language development or signifi-cant learning or other developmental disorders.Some sensorineural losses may be progressive;some children will have persistent middle earproblems.

• Dysmorphism and malformations: Dysmorphicfeatures and congenital malformations may sug-gest a particular syndrome or aetiology (e.g. fetalalcohol syndrome).

• Skin: Look for pigmented and hypopigmentedspots. With significant developmental delay, andespecially with epilepsy, a Wood’s ultravioletlight examination is required (for ash-leaf skinpatches in tuberous sclerosis).

PLANNING MEDICAL INVESTIGATIONS

Part of the responsibility of diagnosing a childwith developmental disorder is to consider anypotential contributing medical causes and whetherany associated or exacerbating condition, such ashypothyroidism in Down syndrome or hearing losscoexisting with autism, is present. Decisions con-cerning further investigations need to be based onthe likelihood of a condition being present, theconsequences of a missed diagnosis, the benefits ofearly diagnosis (e.g. genetic advice) and the conse-quences for parental planning and coping. Thereshould be a low threshold for getting hearing orvision checks undertaken.

Investigations will depend on the type of devel-opmental disorder and associated findings fromthe history and examination. The diagnostic yieldis highest for global developmental delay withassociated history or physical abnormalities onexamination, and lowest for isolated developmen-tal problems.

The advent of genetic screening tests withincreasing breadth – microarray-based compar-ative genomic hybridization (array CGH, oraCGH) – has led to a significant increase inpositive yield alongside a large number of ‘falsepositives’ in the form of benign rearrangements

39


of DNA picked up by aCGH. Table 6.8 offers anoutline of the current evidence-based guidance forinvestigations.

DEVELOPMENTAL DIAGNOSISAND MANAGEMENT

Evaluation of a child’s developmental abilitiesrequires paying attention to factors that mayimpinge upon a child’s performance, such as anx-iety or impulsivity, potentially indicating a needfor repeat assessment. Functional difficulties indaily living and the impact of social and biologicalrisk factors are also relevant. Therapy or otherintervention may be required even in the absenceof developmental delay. Good inter-agency liaisoncan provide additional information on the child’sbehaviour in different settings and is essentialwhere children have complex needs. This mayreveal concerns regarding a child’s protectionor care. Early discussions with experienced col-leagues and an inter-agency approach are essentialfor identification or prevention of potential risk tothe child.

Finally, a clear management plan is required,incorporating referrals and further investigations,

a date for review and identification of a lead/keyworker for the family.

REFERENCES

[1] Shonokoff JP, Phillips DA (eds). (2000) FromNeurons to Neighbourhoods: The Science of EarlyChildhood Development. Washington, DC: NationalAcademy Press.

[2] Baron-Cohen S, Wheelwright S, Cox A et al. (2000)Early identification of autism by the Checklist forAutism in Toddlers (CHAT). Journal of the RoyalSociety of Medicine 93, 521–5.

[3] Ruff HA, Rothbart MK. (1996) Attention inEarly Development: Themes and Variations. Oxford,Oxford University Press.

FURTHER READING

Bee H. (2007) The Developing Child. Boston: Pearson.Buckley B. (2003) Children’s Communication Skills:

From Birth to Five Years. London: Routledge.Egan DF. (1990) Developmental Examination of

Preschool Children. Oxford: Mac Keith Press.Hopkins B (ed.) (2005) The Cambridge Encyclopedia of

Child Development. Cambridge University Press.Sharma A, Cockerill H. (2007) From Birth to Five

Years – Mary D Sheridan (revised and updated). Lon-don: Routledge.

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7Early Social and Emotional ExperienceMatters: The First Year of LifeHoward SteeleDepartment of Psychology, New School for Social Research, New York, NY, USA

What do infants feel? When, why and with whatconsequences? This chapter is informed by afunctionalist theory of emotion that assumes thatemotions evolved as adaptive, survival-promotingprocesses with intrapersonal and interpersonalregulatory functions [1–3]. For example, Bowlby[4] proposed that fear of the dark, and fear of beingalone, are adaptive because there is an obviouslink between these events and potential danger.Emotions, in this view, are organizers of personaland interpersonal life, enhancing or restrictingdevelopment and mental health. The range ofemotions a young child feels, and gives expressionto, stem from the meaning social interactionsimpart, and in turn influence the expectations andappraisals one has vis-a-vis the self and others. Inother words, the experience of an emotion may bethe result of – or the cause of – social interactions.For example, stranger anxiety (which typicallyappears at 8–9 months of age) may lead an infantto cling to the mother and only feel settled whenshe holds the baby close saying ‘I am here foryou’. Through repetition, this kind of interactionwill lead the infant to have a sense of trust inthe mother, and a hopeful attitude in the face ofdistress. On the other hand, a different lesson maybe learned when infant stranger anxiety is met withan insistence by the caregiver that she must leave,and the baby must manage on his or her own withthe stranger. This interaction, if repeated, mayaccentuate the child’s anxiety and contribute to asense of mistrust in the mother (and others). Otherforces that influence infant social and emotional


development include the child’s biological make-up, in part determined by prenatal experiences asmuch current research highlights [5], the maritalrelationship, the wider family network, socialeconomic factors, neighbourhood and broadercultural forces [6,7]. Yet the architect of thismultilayered view of contextual influences in childdevelopment, Uri Bronfenbrenner, maintainedthat the family, and in particular the main caregiver(typically the mother) is the filter through whichall other influences have their immediate effect.

Early social interactions between caregivers andinfants matter greatly because patterns of inter-action become established and consolidated overthe first year of life into relationship or attachmentpatterns [8,9] that (i) tend to persist and (ii) havea potentially long-lasting influence on personalityand mental health [10] (see also Chapter 15). Sixcore infant emotional responses are highlightedin this chapter, each calling for sensitive responsesfrom caregivers. Two appear in the neonatal periodor soon after – (i) crying and (ii) smiling – and fourothers appear in consolidated and consistent waysonly in the second half of the first year – (iii) sad-ness, (iv) surprise, (v) anger and (vi) fear. Normalage-related shifts in these emotions are high-lighted, notwithstanding individual differenceslinked to deficits in neurobiological make-up, orsocial experience. A core take-home message ishow all children, whatever their make-up, willthrive to the best of their ability if their socialand emotional needs are noticed and respondedto in a way that does not overwhelm, or lead to a

41

Early social and emotional experience matters: the first year of life

feeling of neglect. Familiarity with the normativesequence of emotional development in the firstyear of life, outlined in this chapter, may aid theprofessional and parent alike in knowing how andwhen to respond to infants’ emotional signalling.

CRYING

Newborn babies cry for typically about 30–60 min-utes in a 24-hour period. This is about 10–20% oftheir waking time because newborns (fortunately)sleep for approximately 16 hours, or two-thirdsof the day. As with all behaviours, there is a widerange of normal variation, but the 10% of infantswho cry for more than 3 hours per day are dis-tressed as much as half of their waking time. Thisnot only causes great concern to caregivers but isalso linked to postnatal depression, marital stressand shaken baby syndrome. Fussiness appears topeak at 6 weeks universally [11], but fortunatelyvery cranky newborns typically become muchmore settled by 3 months of age. And babies whosecries are responded to promptly and efficiently inthe first three months, in the context of high maritalsatisfaction, cry significantly less at 9 months [12].

Infant cries have been reliably identified byscientists, mothers and others as fitting one ofthree types, indicating (i) hunger; (ii) fatigue or(iii) pain, the latter being a short, sharp, elongatedpiercing sound followed by apnoea. The hungercry is one that builds steadily, while the fatiguecry is more of a whimper. Clearly, being in closeproximity to an infant helps a caregiver to identifycorrectly the source of the distress, and respondingpromptly with sensitivity is the appropriate action.

SMILING OR JOY

The natural course of the smiling response is aninstructional illustration of how emotional capac-ities steadily and gradually appear only partly inresponse to the quality of care received. In otherwords, there are well-documented timetables bywhich certain positive and negative emotions showthemselves on infants’ faces and in their behaviour.At the same time, the infant’s capacity for showingand sharing a wide range of emotions is relatedto the face the baby sees on the mother or fatheror other who assumes the responsibility of provid-ing care. Attentive care, including simple verbal

descriptions of emotion, in response to infants’emotional expression, is likely to promote chil-dren’s accuracy in labelling and understandingemotional expressions, and sequences [13,14].

Newborns do not smile, or only appear to smileas when the corners of their mouths upturn slightlyin a Mona Lisa way. Such positive expressions arefleeting and appear to indicate sensory comfort, forexample following a feed, or the passing of wind,or otherwise becoming used to the good feelingsof having some control over being a body in thisworld. This fleeting positive expression becomesmore consistent and definite over the first 6–8weeks. By 8–10 weeks, there is progression towhat is a somewhat more elaborate closed or openmouth smile linked to familiarity with what theinfant is looking at, either animate (e.g. mother’sface) or inanimate (e.g. a mobile over the baby’scrib). For caregivers this is a noticeable advance,and infants of 2 months are frequently said to besmiling. This unfolds into a full social chuckle in the12–16-week period, completing the initial emer-gence and organization of the smiling responsesuch that frequent social smiling and laughterare commonly seen only at 4 months. Positivejoyful expressions take on an increasingly differen-tiated range, dependent on the interaction partner.The developmental course of the smiling responseappears to be the result of ‘hard-wired’ neurobio-logical programming insofar as smiles develop inbabies who are born blind. Yet, the smile of theperson who has never had sight lacks much of thenuance and complexity seen in sighted people, whohave had the benefit (and risk) of the full range ofvisually perceived social interaction [15].

SURPRISE, ANGER AND SADNESS

Surprise, anger and sadness represent a chain ofemotions that result from a functioning memoryand set of expectations regarding a hoped forexperience or interaction. Surprise, indicated bya vertical oval open mouth and raised eyebrows,is the natural result when things don’t appear asthey should, or things don’t go our way. Andwhen restoration of the hoped for event or inter-action does not follow, surprise can quickly turnto protest or anger, with a characteristic furrowedbrow and gritting of teeth [16]. And, finally, shouldthis not lead to a successful restoration of thehoped for outcome, resignation and sadness, even

42


depression, may follow [4]. The point here is thata rather sophisticated cognitive appraisal processunderpins these emotional expressions, and it isonly in the latter half of the first year that we seedefinite expressions of these facial expressions ofemotion. The caregiver who reads well these emo-tions on the face of his/her baby will know howvaluable it is to speak aloud about the good reasonsfor feeling these emotions, and the diverse ways ofaddressing them. Here the point is that researchunderlines how vital it is to speak to infants, espe-cially from 4 months onwards, in a simple clearway, describing what the infant is doing, appearsto want, and what one (or others) did or are doingin response. This is the ideal parental response toshared or joint attention [1,13]. In this way, infantswill learn the rewards of feeling a range of positiveand negative emotions, blended emotions, sequen-tial and mixed emotions, coming to see the naturalfunction and value of emotional experience.

FEAR

Interestingly, the appearance of an organizedexpression of fear is directly linked to the onsetof locomotion around 8–10 months, and thecognitive-motoric achievement of object perma-nence [17]. With organized knowledge that avalued object can be out of sight, but remains inmind, and can be recovered, infants show strangeranxiety [4], or 8-month anxiety [18]. Fearfulprotest may bring the caregiver back. Clinically,it is a source of concern when a 1-year-old infantseparates too easily from a caregiver withoutprotest. Once able to move on their own, infantscan easily find themselves in danger, lookingover a precipice. Fear is an adaptive response,and one that typically leads to social referencing(looking at the trusted caregiver for cues as tohow to behave). The powerful social influence ofthe trusted caregiver has been demonstrated inclassic experiments involving a visual cliff wherea crawling infant is placed atop a flat surface thatlooks (to the infant) as if proceeding would entailfalling. It is actually a transparent surface thatcan support the infant. On their own, infants aretypically fearful of the apparently imminent fall,and will not proceed. Yet, when their mothersignals to them in a positive way, assuring themit is safe, infants advance, conquering their fear[19]. This effect of trust in the caregiver has

been noted repeatedly, particularly when a secureinfant–caregiver attachment typifies the pattern ofrelating. Where fear appears on an infant’s face oris indicated by his or her behaviour (e.g. freezing)in the presence of the caregiver, evidence suggeststhat there is a troubling disorganizing element tothe child’s relationship with the caregiver, onewith long-term adverse mental health correlates(see Chapter 15).

The identifiable facial expressions of theseemotions – joy, sadness, surprise, anger andfear – were noted by Darwin [2] and then shownto be recognizable around the globe by Ekmanand his colleagues [16]. At the same time, theclarity and organization with which infants showthese emotions, and later demonstrate verballabels for them, has been linked to sensitive andresponsive care over the first year of life [12,13].Deficits in labelling emotion faces have beennoted during middle childhood for those whoseearly experience was deficient [20].

CONCLUSION

There is a paradox about early social andemotional development regarding two mattersof perhaps equal importance to note: (i) Infantsare far more perceptive and competent than wasappreciated 50 years ago, calling for respect andsensitivity on the part of caregivers from earliestinfancy, if not the moment of conception, forwards,and (ii) yet there is little evidence to support thenotion, very popular in 1970, that ‘bonding’ occursshortly after birth. The latter notion led to much(over) concern that no mother (or father) shouldmiss out on the ‘vital’ opportunity to bond withone’s infant in the seconds, minutes and hoursafter birth – an anxiety-provoking and unhelpfulmessage. Social experience, and attunementbetween caregivers and infants is vital, but mis-takes on the part of caregivers, hopefully not majorones, are inevitable. It is both consistency of care,and reparation following a ruptured, incompleteor confusing interaction [3], that typifies normalsocial development and optimal mental health out-comes. Professionals and parents alike can benefitfrom this knowledge that occasional conflict is tobe viewed as inevitable and repair/resolution – tobe initiated by the caregiver – is seen as essential.A caregiver who invests in reliably repairingruptures in early infancy, following caregiver

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Early social and emotional experience matters: the first year of life

misunderstanding, interference or neglect, islikely to realize the rewards of having a sociallycompetent child in the future, someone capableof establishing and maintaining meaningful andhealthy social relationships.

REFERENCES

[1] Bretherton I, Fritz J, Zahn-Waxler C, Ridgeway D.(1986) Learning to talk about emotions: A function-alist perspective. Child Development 57, 529–48.

[2] Darwin C. (1872) The Expression of Emotion inMan and Animals. London: Harper Collins.

[3] Tronick E. (1989) Emotion and emotional com-munication in infants. American Psychologist 44,112–19.

[4] Bowlby J. (1973) Attachment and Loss: Vol. 2, Sep-aration, Anxiety and Anger. London: The HogarthPress.

[5] O’Connor TG, Heron J, Glover V. (2002) Ante-natal anxiety predicts child behavioral/emotionalproblems independently of postnatal depression.Journal of the American Academy of Child & Ado-lescent Psychiatry 42, 1470–7.

[6] Bronfenbrenner U. (1978) The Ecology of HumanDevelopment: Experiments by Nature and Design.Boston: Harvard University Press.

[7] Mayes LC, Gilliam WS, Sosinsky LS. (2006) Theinfant and toddler. In: Andres M and VolkmarFR (eds), Lewis’s Child and Adolescent Psychiatry:A Comprehensive Textbook, 4th edn. Philadelphia:Walters Kluwer, pp 252–60.

[8] Ainsworth MS, Blehar MC, Waters E, Wall S. (1978)Patterns of Attachment: A Psychological Study of theStrange Situation. Oxford: Lawrence Erlbaum.

[9] Bowlby J. (1960) Grief and mourning in early child-hood. Psychoanalytic Study of the Child 15, 9–2.

[10] Sroufe LA. (2005) Attachment and development:A prospective, longitudinal study from birth toadulthood. Attachment and Human Development7, 349–67.

[11] Barr RG, Konner M, Bakeman R, Adamson L.(2008) Crying in !Kung san infants: A test ofthe cultural specificity hypothesis. DevelopmentalMedicine and Child Neurology 33, 601–10.

[12] Belsky J, Fish M, Isabella R. (1991) Continuityand discontinuity in infant negative and posi-tive emotionality: Family antecedents and attach-ment consequences. Developmental Psychology 27,421–31.

[13] Steele H, Steele M, Croft C, Fonagy P. (1999) Infant-mother attachment at one-year predicts children’sunderstanding of mixed emotions at six years. SocialDevelopment 8, 161–78.

[14] Steele H and Steele M. (2008) Early attachmentpredicts emotion recognition at 6 and 11 years.Attachment and Human Development 10, 379–93.

[15] Fraiberg S. (1968) Parallel and divergent patterns inblind and sighted infants. The Psychoanalytic Studyof the Child 23, 264–300.

[16] Ekman P. (2003) Emotions Revealed. New York:Henry Holt & Co.

[17] Piaget J. (1954) The Construction of Reality in theChild. London: Routledge and Kegan Paul.

[18] Spitz R. (1950) Anxiety in infancy: A study of itsmanifestations in the first year of life. The Interna-tional Journal of Psychoanalysis 31, 138–43.

[19] Sorce JF, Emde RN, Campos J, Klinnert MD. (1985)Maternal emotional signaling: Its effect on the visualcliff behavior of 1-year olds. Developmental Psy-chology 21, 195–200.

[20] Pollak SD, Cicchetti D, Hornung K, Reed A.(2000) Recognizing emotion in faces: Developmen-tal effects of child abuse and neglect. DevelopmentalPsychology 36, 679–88.

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8Language DevelopmentThomas Klee and Stephanie F. StokesDepartment of Communication Disorders and New Zealand Institute of Language, Brain & Behaviour,University of Canterbury, New Zealand

WHAT’S NEW

• Researchers are beginning to explore psycholinguistic processing measures, such asnon-word repetition, as clinical markers of language impairment in very young children.Poor performance on these psycholinguistic tasks (measures of verbal short-term memory) isindicative of late language onset (‘late talking’). However, the direction of the relationshipbetween memory and language development remains contentious and further work on theearliest phases of language learning will shed light on this issue.

• Usage-based models of language development lead to a more integrated view of whatdevelops when, and holistic assessments of language growth.

• Multidisciplinary work in developmental science (e.g. neural imaging, statistical modelling,behavioural and molecular genetics, computational modelling) will shed new light on themechanisms and phases of language development.

The ability to communicate using language is oneof the most basic human traits. Doing so involveslearning to understand and produce an abstractand complex linguistic code that provides the foun-dation for social interaction, personal relation-ships, reading and writing, problem-solving, formallearning and personal well-being. By the time chil-dren enter school at the age of 4 or 5, most haveachieved near adult-like mastery of the sounds andgrammar of their native language(s) and are able tocommunicate with others effectively. This chapterpresents some of the main developmental mile-stones in the language development of preschoolchildren developing in a typical manner, and someof the factors likely to be involved. First, we beginwith an overview of the territory.


PROCESSES AND COMPONENTSOF LANGUAGE DEVELOPMENT

The top part of Figure 8.1, adapted from a causalmodel of developmental disorders [1], illustratesthe relationship between language developmentand some of the factors known to affect it. This sim-plified model illustrates the interaction betweenthe child’s genetic endowment and his or her envi-ronment, as would be the case in any area of devel-opment. In the case of language development, thehuman genotype enabled a species-specific endow-ment for linguistic processing [2], the precise extentof which is still not entirely known. The model alsospecifies a key role played by the environment,both in the form of human (social) interaction

45

Language development

Genotype

Cognitive development

Neurobiology

Environmental stimulation:Social interaction, language

input, etc.


Motor development Psychosocial development

Cognitive mechanisms:Memory, psycholinguistic

processing, etc.

Language form:Grammar (syntax, morphology ),Phonology (phonemes, prosody)

Language content:Semantics (vocabulary, etc.)

Language use:Pragmatics

Language modality:Spoken language, sign language,

written language

Comprehension (receptive language)Production (expressive language)

Figure 8.1 Processes, components and modalities of language development.

and language input. The junction of these can beseen in adults’ use of a speech register known aschild-directed speech – developmentally sensitivespeech and language adjustments made by parentsand others when talking to children. Both geneticand environmental factors affect the developingbrain and its neurobiological mechanisms. Thesein turn underpin cognitive mechanisms, such aspsycholinguistic processing [3,4] and verbal mem-ory [5], which affect how language develops in thechild. The child’s language ability is also affectedby developments in the cognitive, psychosocial andmotor domains.

The bottom part of the figure depicts variouscomponents and modalities involved in under-standing and producing language. Language com-prehension (sometimes referred to as receptivelanguage in clinical contexts) refers to the pro-cess of decoding speech – the chain of events inwhich sound waves produced by the vocal tractof a human speaker are received, processed andgiven meaning by a human listener. Languageproduction (sometimes referred to as expressivelanguage) refers to the process of encoding – the

chain of events by which a message generated bythe brain is neurologically relayed to muscles thatmove the structures of the vocal tract.

In the figure, language is divided into threecomponents: content, form and use [6]. Languagecontent, or semantics, refers to how meaning isconveyed by linguistic elements such as words,idioms and sentences. Language form encom-passes grammar and phonology. One aspect ofgrammar involves the rules governing how wordsare combined to form phrases and sentences (syn-tax). For example, the grammar of English requiresthat the subject precedes the verb (e.g. ‘I shouldgo.’) in declarative sentences while in questions,the verb precedes the subject (e.g. ‘Should I go?’).Another aspect of grammar relates to the struc-ture of words (morphology). For example, inEnglish the past tense form of regular verbs iscreated by adding the ‘-ed’ inflection to the verbstem (e.g. ‘climbed’). Language form also involvesthe language’s sound system (phonology): bothits contrastive sound segments (e.g. phonemessuch as /p/, /t/ and /k/) and prosodic featuressuch as stress and intonation. Language use refers

46


to the interpersonal, communicative functions oflanguage during social interaction (pragmatics),such as a speaker’s communicative intentions. Themodel also illustrates various modalities throughwhich language can be communicated, such as itsspoken, signed or written forms.

This model is implicitly reflected in current theo-ries of language development, such as usage-basedaccounts [7,8], in which general learning processesand cognitive mechanisms underpinning languagedevelopment are mediated by environmentalfactors. Cognitive mechanisms include such thingsas pattern recognition and intention reading.Pattern recognition occurs when a child associatesnew information with something already known,recognizing similarities, such as when the child,knowing that the utterance ‘eat apple’ describesthat event, says ‘eat bread’ to describe a similarevent. Intention reading includes joint attention,such as when the adult and child share a focus onobjects, events or interactions, or using pointingand gesturing to indicate objects and events. Thereis little differentiation between the lexicon andsyntax in early language development; rather, thechild is learning to express relations in the world,such as ‘doggie eat’ to describe a dog eating,rather than grammatical relations such as subject+ verb. Language development is defined asform-function mappings or construction building.

MILESTONES OF SPEECHAND LANGUAGE DEVELOPMENT

It is beyond the scope of this chapter to presentdetailed charts outlining children’s speech andlanguage development. These can be found onthe websites listed at the end of this chapter.

While the sequence of developmental speechand language milestones is broadly similar acrosschildren, there is wide variability in terms of whenthese are reached due to individual differences [9].Milestones indicate the average age of childrenwhen they attain particular features of expres-sive language such as speech sounds, vocabularyand syntactic constructions, as well as featuresof receptive language. Both genetic and envi-ronmental factors (e.g. the quality or quantity oflanguage input [10]; the presence of developmentaldelays or disorders), contribute to variations in theattainment of particular milestones. Differencesbetween reported developmental sequences can

also be due to differences in definitions or researchmethods employed by researchers. For example,proposed sequences of speech sound developmentmay be affected by whether children’s speech isrecorded during spontaneous conversations withadults or during picture-naming tasks when wordsare elicited singly. It can also be influenced by themethods of data analysis – for example, whetherchildren’s speech forms are analysed on their own(phonetic inventory) or in relation to adult forms(phonemic inventory). Further, the national vari-ety (e.g. American, British, Australian or NewZealand English) or dialect (e.g. African AmericanEnglish) of the spoken language will also exert aneffect on the acquisition sequence. In what follows,we summarize general patterns of development intypically developing children.

DEVELOPMENTAL PHASES

After 6–7 months of gestation, the fetus respondsto sound, including the human voice, and at birthinfants prefer to listen to sounds heard before birth,such as the mother’s heartbeat and her voice. In thefirst 6 months of life the infant is highly responsiveto adult interaction, intently watching human facesand turning in the direction of sounds. Turn-takingemerges and infants imitate adult tongue protru-sion or raspberry blowing and laugh in response tothe human voice. By 2 months of age infants candiscriminate between phonemes [11] and producea wide range of speech-like sounds, including thosenot present in their own language[s].

Between 6 and 12 months the infant’s motorand cognitive development advances at a rapidpace. Sitting and crawling afford the opportunityto explore the environment, increasing opportu-nities for object manipulation and learning aboutobject function, shape and taste. The infant alsobegins to appreciate the role of others as agentsof change, as seen by the use of simple commu-nicative gestures, some of which are accompaniedby vocalizations, to indicate and request objects(e.g. pointing) and action (e.g. raising arms tobe lifted). At 6–7 months babbling emerges (e.g.‘ba ba ba’) and becomes more diversified overthe next few months. At around 9 months conven-tional social gestures emerge (e.g. waving goodbye,shaking head to indicate rejection). At around11 months infants begin to lose the ability todiscriminate among all phonemes, but begin to

47


discriminate better the speech sounds of their ownlanguage environment, fine-tuning their percep-tion to be language-specific [11]. At 10 monthsthe average receptive vocabulary size is about 50words [12].

By 12–18 months the infant begins to under-stand the intentions of others, engages in jointattention (sharing attention and focus with anadult) and attends to books for brief periods.Walking now contributes to a greater awarenessof self in space. This facilitates the developmentof comprehension of locative words, such as ‘in’and ‘on’, and simple questions like ‘what’s that?’and ‘where’s your teddy?’ Parents often reportthat their child understands most of what is said tothem, an impression fostered by the child’s use ofcomprehension strategies, which capitalize on con-text in the absence of understanding exactly what issaid [13]. Basic representational play emerges dur-ing this phase (e.g. ‘drinking’ from a toy cup), alongwith some single words. By now most children canidentify some body parts (‘where’s your nose?’)and pictures of family members. By 12 months,children’s average receptive vocabulary size is 85words, increasing to 250 words by 18 months; andby 20 months, some 75% of children are reportedby their parents to be combining words [12].

By 24 months representational play includesgreater symbolism (e.g. using a block for a car).The toddler shows an understanding of ‘what’ or‘where’ questions (e.g. ‘what x doing?’, ‘wherex going?’) and some children begin to use thepronouns ‘me’ and ‘you’ and grammatical markerssuch as the ‘-ing’ verb inflection, plurals (‘cats’)and past tense ‘-ed’. While the average Americantoddler has an expressive vocabulary size ofaround 300 words by 24 months of age, largeindividual differences exist (7 to 668 words) [12].Similar findings have been reported in 12 otherlanguages [14]. It is difficult to estimate the size ofchildren’s vocabulary beyond the age of 2 years.Psycholinguistic processing mechanisms can bemeasured at 2 years, with most children being ableto imitate one-, two- and three-syllable nonsensewords (e.g. ‘doe-per-lut’) [15].

By 3 years of age the child engages in coop-erative play. Phonological awareness and otheraspects of metalinguistic ability emerge, as seen inword play (e.g. ‘moo’, ‘goo’, ‘boo’). Print awarenessemerges and the child can point to familiar words in

books. The child understands the locative ‘under’and begins developing an awareness of causality,accompanied by an increase in asking ‘why’ ques-tions and producing complex sentences (e.g. ‘he’scrying ‘coz he fell down’), but sometimes with wordorder errors.

By 4 years, there is greater print awarenessand metalinguistic awareness, demonstrated by anappreciation of nursery rhymes. The child beginsto ask ‘who’ and ‘where’ questions. Play becomesrule-based (e.g. role taking) and the child uses lan-guage to organize and talk about their world (e.g.‘you be the mummy’). Sentences contain embed-ded clauses and are almost adult-like (e.g. ‘don’ttouch that ‘coz you’ll break it and I haven’t finishedyet’). The child can now describe basic events, suchas their birthday party.

By 5 years the child understands purpose,function and consequence questions (e.g. ‘howcan we open that jar?’, ‘what will happen if heloses his keys?’). With knowledge of how objectsare oriented in space comes an understanding ofmore locatives (‘in front of’, ‘behind’, ‘next to’,‘through’). The child can hold a conversation and,with an increase in schema (pattern) knowledge,can describe more abstract events, such as whathappens at birthday parties in general or how tomake a sandwich.

ATYPICAL LANGUAGE DEVELOPMENT

While language development is very robustfor most, some children experience delays orproblems in acquiring the sounds, meaningsand grammatical structures of their languagewhile others experience difficulty using languagesocially. Such delays may or may not be transientand are often the first signs of a problem relatedto hearing, cognition or other developmentaldomains. They may also be indicative of a primarylanguage disorder (see Chapter 29) or a socialcommunication disorder (see Chapter 23).

Pertinent to this chapter is a group of childrenwith late onset of language, often referred to as latetalkers. These are 2-year-olds with small expres-sive vocabularies or no word combinations. Tworecent large-scale epidemiological studies haveidentified several factors associated with late onsetof language. In one study [16], male gender, familyhistory of late talking, two or more children in

48


the family and early neurobiological growth wereidentified; in another study [17], a family historyof speech or language difficulties, non-English-speaking background and low maternal educationwere identified. While the majority of late talkerswill eventually catch up with their age peers, some30–40% may not. Several smaller scale studieshave indicated that poor receptive vocabularyand limited use of gestures may be indicative ofmore persistent problems but further researchis needed. The American Speech-Language-Hearing Association suggests that childrenshould be referred to a speech and languagetherapist whenever a parent expresses concern(see http://www.asha.org/public/speech/disorders/LateBlooming.htm).

FUTURE DIRECTIONS

Our understanding of language developmentwill be greatly enhanced by advances in, andapplication of, new technologies and methodsto explore neurophysiology, neuroplasticity,human growth models and the synergistic roles ofgenetic and environmental influences on learning.New techniques in neural imaging, statisticalmodelling, behavioural and molecular genetics,and computational modelling are being applied todevelopmental questions. Further innovations andcollaborations across physics, pharmacology, biol-ogy, psychology, neurology, computer science andengineering will generate new ways of thinkingabout development, leading to new discoveries.

REFERENCES

[1] Bishop DVM and Snowling MJ. (2004) Devel-opmental dyslexia and specific language impair-ment: same or different? Psychological Bulletin 130,858–86.

[2] Bates E. (1999) Language and the infant brain.Journal of Communication Disorders 32, 195–205.

[3] Gaskell MG and Altmann G (eds). (2007) TheOxford Handbook of Psycholinguistics. Oxford:Oxford University Press.

[4] Levelt WJM. (1993) Speaking: from Intention toArticulation. Cambridge, MA: MIT Press.

[5] Gathercole SE. (2006) Nonword repetition andword learning: the nature of the relationship.Applied Psycholinguistics 27, 513–43.

[6] Lahey M. (1988) Language Disorders and LanguageDevelopment. New York: Macmillan.

[7] Tomasello M. (2003) Constructing a Language: AUsage-based Theory of Language Acquisition. Cam-bridge, MA: Harvard University Press.

[8] Goldberg A. (2006) Constructions at Work: theNature of Generalization in Language. Oxford:Oxford University Press.

[9] Bates E, Dale PS, Thal D. (1995) Individual differ-ences and their implications for theories of languagedevelopment. In: Fletcher P and MacWhinney B(eds), The Handbook of Child Language. Oxford:Blackwell, pp. 96–151.

[10] Hart B, Risley TR. (1995) Meaningful Differencesin the Everyday Experience of Young AmericanChildren., Baltimore: Brookes.

[11] Kuhl PK, Conboy BT, Coffey-Corina S et al. (2008)Phonetic learning as a pathway to language: newdata and native language magnet theory expanded(NLM-e). Philosophical Transactions of the RoyalSociety B 363, 979–1000.

[12] Fenson L, Marchman VA, Thal DJ et al.(2007) MacArthur-Bates Communicative Develop-ment Inventories: User’s Guide and Technical Man-ual, 2nd edn. Baltimore: Brookes.

[13] Chapman R. (1978) Comprehension strategiesin children. In: Kavanagh JE and Strange W(eds), Implications of Basic Speech and LanguageResearch for the School and Clinic. Cambridge, MA:MIT Press, pp. 308–32.

[14] Bleses D, Vach W, Slott M et al. (2008) Early vocab-ulary development in Danish and other languages: aCDI-based comparison. Journal of Child Language35, 619–50.

[15] Stokes SF, Klee T. (2009) The diagnostic accuracyof a new test of early nonword repetition for dif-ferentiating late talking and typically developingchildren. Journal of Speech, Language, and HearingResearch 52, 872–82.

[16] Zubrick SR, Taylor CL, Rice ML et al. (2007) Latelanguage emergence at 24 months: an epidemiolog-ical study of prevalence, predictors, and covariates.Journal of Speech, Language, and Hearing Research50, 1562–92.

[17] Reilly S, Wake M, Bavin EL et al. (2007) Predictinglanguage at 2 years of age: a prospective communitystudy. Pediatrics 120, e1141–9.

INTERNET RESOURCES

Child Development Institute – Language Develop-ment in Children: http://www.childdevelopmentinfo.com/development/language_development.shtml

49


National Institute on Deafness and other Communica-tion Disorders – Speech and Language: http://www.nidcd.nih.gov/health/voice/speechandlanguage.asp#milestones

American Speech-Language-Hearing Association –Typical Speech and Language Development: http://www.asha.org/public/speech/development/

American Academy of Pediatrics Healthy Children:Ages & Stages: http://www.healthychildren.org/English/ages-stages/Pages/default.aspx

50


9Development of Social CognitionVirginia SlaughterEarly Cognitive Development Centre, University of Queensland, Brisbane, Australia

WHAT’S NEW

• Infants as young as 12—18 months havesome capacity for mentalizing. Recentexperimental studies in which infantsspontaneously help, communicate orimitate an adult have revealed thatinfants can take into account whatother people feel, want and know.

• Individual children differ in the rate atwhich they acquire a theory of mind.Correlational studies indicate thatthose children who are more skilful atmentalizing are also somewhat moresophisticated and effective in theirsocial lives.

• Environmental factors contribute toindividual differences in social-cognitive skill and the most significantcorrelate is exposure to mentalisticconversation with parents, siblings andfriends.

Social cognition in humans is uniquely complex.Unlike other mammals, which respond primarilyto each other’s outward behavioural signals, welook deeper, into each other’s minds, in orderto understand one another. For instance, if wewitness a stranger breaking into loud song on acrowded street, we might notice that outwardly,she is smiling and acting exuberantly, but ourprimary reaction would be to interpret her unusual


actions by considering what’s going on inside hermind. She may want to communicate a message.Perhaps she thinks this is a good way to get arecording contract. Maybe she just feels great.This process of reasoning about what other peoplefeel, want and know, is referred to as mentalizing,mindreading, or using our theory of mind. It is afundamental skill that helps us to understand andget along with the other people in our social world.

SOCIAL COGNITION IN INFANCY

Until recently, most psychologists thought thatthe capacity for mentalizing only emerged in thepreschool period, because that is when typicallydeveloping children begin to pass tests assessingtheir ability accurately to report what is likely tobe in someone else’s mind in differing circum-stances. Whether or not infants and toddlers alsohave a theory of mind has been debated for years.Recent experimental procedures, cleverly mod-elled on everyday situations, now confirm thatsome basic mentalizing is evident in infants’ non-verbal communication, helping and imitation.

For instance, in one experimental procedure,12- to 18-month-old infants watched an adult writeon a piece of paper with a marker. Then themarker dropped off the table, unseen by the adult,who began to search around for it. Already onthe floor were some other items, but the infantsconsistently pointed at or retrieved the marker,rather than the distractor items [1,2]. This showedthat 1-year-olds could work out the specific itemthat the adult wanted. In another experiment, 18-month-old infants were invited to interact with two

51

Development of social cognition

adults, who were playing with two different toys.After a while, the toys were put on a shelf andone of the adults left the room. The remainingadult then brought out a new toy, played with itand then put it on the shelf as well. When the firstadult returned and pointed toward the three toyson the shelf saying ‘Oh look! Give it to me please!’the infants immediately retrieved the new toy – theone that this particular adult had not yet playedwith. This indicates that the infants interpreted theadult’s pointing in terms of what the adult thoughtwas new and interesting [3].

Sometimes we witness someone trying and fail-ing to accomplish a simple act. For instance,someone may try to turn on a light switch buther fingers slip off. In this case we automaticallymentalize, and see past the external behaviour tothe underlying intention: She meant to turn on theswitch. Another recent experiment showed thatinfants as young as 12 months mentalize in thesame way [4]. When infants watched an adult trybut fail to turn on a switch, they recognized theadults’ intention and when given the opportunity,they fully turned on the switch. But if the infantswatched an adult handle the switch without tryingto turn it on, they did not turn it on themselvesthus showing that in the first situation, they weregenuinely mentalizing, rather than simply doingwhat might have seemed obvious.

Besides reading the intentions behind eachother’s actions, we also tend to anticipate eachother’s intentions and the behaviour they produce.For instance, if you know your friend likes sugarin his coffee, then as he pours himself a cupyou are likely to shift your eyes to the sugarbowl, anticipating his mental state as well as hisnext move. Recent eye-tracking research showsthat 25-month-olds anticipate in this way and,furthermore, they can anticipate another person’snext move even if that person is actually mistaken.In the eye-tracking study, toddlers watched a videoin which an actor repeatedly reached to get his toyout of a box. When the actor wasn’t looking, thetoy was moved to a different box. Upon the actor’sreturn, the toddlers anticipated his next move andlooked to the first box, where the actor still thoughthis toy was located, rather than to where it reallywas [5]. This experiment shows unmistakablementalizing because the toddlers focused on theinner experience of the actor, rather than on the

actual location of the toy. Another study usingprecisely the same set-up showed that 6- to 8-year-old children with an autism spectrum disorderfailed to do the same thing; they did not look to thebox where the actor thought the toy was [6]. Thisshows that automatic, non-verbal mindreading isdisrupted in children with autism, in addition to themore explicit social-cognitive and communicativeproblems characteristic of the disorder.

SOCIAL COGNITION IN YOUNG CHILDREN

The research described above shows that in typi-cal development, accurate mentalizing is present,in some instances within the second year of life.A direction for future research is to evaluatewhether and how these early non-verbal theoryof mind skills are linked to the more sophisticatedsocial cognition that develops later in childhood.Although more research is needed, the results ofone such study suggest a positive association [7]between infants’ imitation of unfulfilled intentions(as in the switch task described above) and theirperformance on measures of social cognition at 3years of age.

Soon after children begin to use language, theyalso begin to talk about what they and others feel,want and think. This facile ability to communi-cate about what is in our own and others’ mindshas allowed researchers to expand the range ofverbal tests used to assess young children’s social-cognitive reasoning. The standard procedure isfor children to listen to a description of a socialscenario, sometimes accompanied by cartoons oracted out with puppets. Once the scenario is inplace, they are then asked questions about whatthe protagonists feel, want or know, or what theywill do next. While there are potentially as manydifferent versions of these tests as there are uniquesocial scenarios, a subset of them has recently beenmade into a highly reliable developmental scale,illustrated in Table 9.1. The theory of mind scalereveals that 3- to 6-year-old children graduallymaster different elements of social cognition ina predictable sequence [8,9]. Children with clini-cal diagnoses that are characterized by delays ordeficits in social cognition, such as deafness orautism, pass the tasks in essentially the same orderbut at a later age. The one exception to scale con-formity is that children with autism pass the hidden

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Table 9.1 Six tests that make up the theory of mind scale. Research shows that the majority ofchildren acquire these concepts in order from ‘Diverse desires’ to ‘Sarcasm’.

Test Social-cognitive concept assessed Approximate proportionof 3- to 6-year-oldchildren who pass

Diverse desires Different people may like and wantdifferent things

95%

Diverse beliefs Different people can hold different beliefsabout the same thing

88%

Knowledge access People who see something also know aboutit; if they don’t see then they don’t know

79%

False belief People do things based on what they think,even if they are mistaken

49%

Hidden emotion People can deliberately conceal emotionsby facial expression management

27%

Sarcasm In order to be humorous, people sometimessay the opposite to what they really mean

20%

emotion task before they pass false belief [8,9].This subtle difference reinforces the conclusion,following from years of research, that the mental-istic concept of false belief is particularly difficultto grasp for people with autism.

INDIVIDUAL DIFFERENCES IN SOCIALCOGNITION: IMPLICATIONS FORCHILDREN’S SOCIAL LIVES

Alongside the consistent developmental sequencefor theory of mind concepts outlined in Table 9.1,there are measurable individual differencesamongst children in their rates of social-cognitivedevelopment. These individual differences havebeen linked to some specific consequences forchildren’s everyday social life. Although theeffects are typically small to medium-sized,meaning that other factors play a role, childrenwho perform well on theory of mind tests also tendto have relatively sophisticated social skills as wellas effective social relationships in their daily lives.

For instance, studies have shown that mentaliz-ing is related to social competence in 4- to 8-year-old children. That is, those children who are goodat working out what others feel, want and think,are nominated by their peers as being most likeable

and rated by their teachers as being most sociallymature [10]. It is important to note that these find-ings are correlational, so we do not know if skilfulmentalizing causes children to be socially adept andpopular, or if those qualities put them in the bestposition to develop their social-cognitive skills.

Other studies indicate that 3- to 8-year-old chil-dren who perform well on theory of mind testsare also especially good at keeping secrets, at dis-tinguishing right from wrong in complicated socialsituations, and at deceiving and lying convincingly[11]. This last point highlights that mentalizingenables children to take part successfully in a widerange of social interactions, including potentiallynegative ones. Thus acquiring a theory of minddoes not necessarily make for a well-adjusted child;indeed, more than one study has revealed that play-ground bullies, who are often somewhat popularas well as being feared for their manipulative andaggressive interpersonal tactics, possess good oreven superior mentalizing skills [12]. Acquiring atheory of mind enables children to understandtheir social world, but it appears that individ-ual children’s temperament and life experiences,among other things, determine how they use thatunderstanding. Predicting how individual childrenwill use their theory of mind – either prosocially

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Development of social cognition

or antisocially – is another important direction forfurther research [13].

INDIVIDUAL DIFFERENCES IN SOCIALCOGNITION: WHERE DO THEY COMEFROM?

Although it is in our nature to look past externalbehaviour and into each other’s minds, the fewgenetic studies on social-cognitive developmentcarried out to date suggest that nurture is moreimportant in determining individual differencesamong children. For instance, a major behaviourgenetic study comparing 1116 monozygotic anddizygotic 5-year-old twin pairs revealed that themajority of individual variation in the children’smentalizing (based on the kinds of tests listed inTable 9.1) was attributable to environment ratherthan to genes [14]. This finding contrasted withan earlier, smaller-scale study of 3-year-old twins,which revealed significant genetic influences onmentalizing [15]. More research is necessary toreconcile these findings; however, one possibilityis that genes play a role in early social-cognitivedevelopment, but by the age of 5, children’s theoryof mind is shaped primarily by their personalexperiences.

One environmental variable that is crucial fortheory of mind development is access to languageand conversation about people’s feelings, desiresand thoughts. Mentalizing is consistently corre-lated with language ability, and there is also aspecific link between children’s ability to suc-cessfully complete tasks like those described inTable 9.1 and their comprehension and produc-tion of mentalistic vocabulary. The importance oflanguage to mentalizing is perhaps most evidentin the deaf; those deaf children who do not haveaccess to fluent signing partners for daily conver-sation show social-cognitive delays similar to thoseobserved in children with autism. By contrast, deafchildren who have regular access to signed conver-sation are comparable to typical hearing childrenin their social-cognitive development [16].

The role of language in social-cognitive devel-opment is further demonstrated by the fact thatchildren’s theory of mind is consistently associatedwith their participation in meaningful conversa-tions about emotions, desires and thoughts withparents, siblings and friends [17]. The influenceof parents’ mentalistic conversation is especially

well documented; in a nutshell, the more parentsdiscuss and explain what they and others feel,want and think, the better their children under-stand those concepts. This principle has beendocumented in many conversational contextsfrom everyday disciplinary encounters (‘It wasreally unkind of you to take her dolly; just imaginehow it made her feel’) to mutual reminiscences(‘Remember when the bird stole the baby’s fruitbun right out of her hand? She was so surprisedand angry!’) to book-reading (‘Look at that boy’sface in the picture; why does he feel so sad?’). It isimportant to note that the link between children’stheory of mind and parents’ mentalistic conver-sation extends to children with autism [18] anddeafness [19]. While not yet translated into formalinterventions, training studies have shown thatexposure to mentalistic conversation boosts social-cognitive skill in typically developing children[20]. Therefore, parents should be encouraged totake the time to discuss feelings and thoughts withtheir young children; not only will it make forengaging conversation, but it is likely to benefittheir children’s social-cognitive development.

REFERENCES

[1] Warneken F. (2007) and Tomasello M. Helpingand cooperation at 14 months of age. Infancy 11,271–94.

[2] Liszkowski U, Carpenter M, Striano T, TomaselloM. (2006) Twelve- and 18-month-olds point to pro-vide information for others. Journal of Cognitionand Development 7, 173–87.

[3] Moll H. (2007) and Tomasello M. How 14- and18-month-olds know what others have experienced.Developmental Psychology 43, 309–17.

[4] Nielsen M. (2009) 12-month-olds produce others’intended but unfulfilled acts. Infancy 14, 377–89.

[5] Southgate V, Senju A, Csibra G. (2007) Actionanticipation through attribution of false belief intwo-year-olds. Psychological Science 18, 587–92.

[6] Senju A, Southgate V, Miura Y et al. (2010) Absenceof spontaneous action anticipation by false beliefattribution in children with autism spectrum disor-der. Development and Psychopathology 22, 353–60.

[7] Colonnesi C, Rieffe C, Koops W et al. (2008) Pre-cursors of a theory of mind: A longitudinal study.British Journal of Developmental Psychology 26,561–77.

[8] Peterson C, Wellman H, Liu D. (2005) Steps in the-ory of mind development for children with deafness,autism or typical development. Child Development76, 502–17.

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[9] Peterson C, Wellman H, Slaughter V. The mindbehind the message: Advancing theory of mindscales for typically developing children, and thosewith deafness, autism, or Asperger Syndrome. ChildDevelopment (in press).

[10] Peterson C, Slaughter V, Paynter J. (2007) Socialmaturity and theory of mind in typically developingchildren and those on the autism spectrum. Jour-nal of Child Psychology and Psychiatry and AlliedDisciplines 48, 1243–50.

[11] Talwar V and Lee K. (2008) Social and cogni-tive correlates of children’s lying behavior. ChildDevelopment 79, 866–81.

[12] Gasser L and Keller M. (2009) Are the competentthe morally good? Perspective taking and moralmotivation of children involved in bullying. SocialDevelopment 18, 798–816.

[13] Ronald A, Happe F, Hughes C, Plomin R. (2005)Nice and nasty theory of mind in preschool chil-dren: Nature and nurture. Social Development 14,664–84.

[14] Hughes C, Jaffee S, Happe F et al. (2005) Originsof individual differences in theory of mind: Fromnature to nurture? Child Development 76, 356–70.

[15] Hughes C and Cutting A. (1999) Nature, nurtureand individual differences in early understanding ofmind. Psychological Science 10, 429–32.

[16] Siegal M and Peterson C. (2008) Language andtheory of mind in atypically developing children:Evidence from deafness, blindness and autism. In:Sharp C, Fonagy P, Goodyear I (eds), Social Cog-nition and Developmental Psychopathology. NewYork: Oxford University Press, pp. 81–112.

[17] Dunn J and Brophy M. (2005) Communication, rela-tionships, and individual differences in children’sunderstanding of the mind. In: Astington JW andBaird JA (eds), Why Language Matters for Theoryof Mind. New York: Oxford University Press, pp.50–69.

[18] Slaughter V, Peterson C, Mackintosh E. (2007)Mind what mother says: Narrative input and theoryof mind in typical children and those on the autismspectrum. Child Development 78, 839–58.

[19] Moeller M and Schjick B. (2006) Relations betweenmaternal input and ToM understanding in deaf chil-dren. Child Development 77, 751–66.

[20] Tenenbaum HR, Alfieri L, Brooks PJ, Dunne G.(2008) The effects of explanatory conversations onchildren’s emotion understanding. British Journalof Developmental Psychology 26, 249–63.

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Social and emotional development in middle childhood

10Social and Emotional Developmentin Middle ChildhoodAlan CarrSchool of Psychology, Newman Building, University College Dublin, Belfield, Dublin, Ireland

WHAT’S NEW

• There is significant continuity in SED from middle childhood toadolescence — psychopathological disorders reflecting problematic SED persist; children whoare well adjusted in middle childhood tend to become well adjusted adolescents.

• Recent reviews of early intervention programmes for children at risk of SED problems reportsignificant positive effects in relation to: participants’ educational success; socialparticipation; cognitive, social and emotional development; family well-being, and lessinvolvement in the criminal justice system.

• The most effective early intervention programmes for children at risk of SED problems arethose that are of long duration and intensive, involving more than 500 sessions.

• Supportive family environments foster social and emotional development and bufferchildren from the negative long-term effects of bullying.

Social and emotional development (SED)involves the acquisition of skills for expressingemotions, regulating emotions, and managingsocial relationships within the family, schooland peer group [1,2]. Some of the milestonesassociated with these aspects of developmentare given in Table 10.1. Middle childhood, theperiod between 6 and 12 years, occupies apivotal position between the preschool years andadolescence with respect to SED. During thepreschool years rudimentary skills are acquired,while in adolescence, sophisticated skills arerefined. However, it is during middle childhood


that particularly important developments occurwithin the emotional and social domains.

THE PRESCHOOL YEARS

During the first year of life there is a gradualincrease in non-verbal emotional expression inresponse to all classes of stimuli including thoseunder the infant’s control and those under the con-trol of others. At birth infants can express interestas indicated by sustained attention, and disgust inresponse to foul tastes and odours. Smiling, reflect-ing a sense of pleasure, in response to the human

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Table 10.1 Social and emotional development.

Age Expression of emotions Regulation of emotions Managing emotionsin relationships

Infancy

0—1 year

Increased non-verbalemotional expression inresponse to stimuliunder own control andcontrol of others

Self-soothing

Regulation of attention toallow coordinated action

Reliance on ‘scaffolding’from caregivers during stress

Increased discrimination ofemotions expressed byothers

Turn taking (peek a boo)

Social referencing

Toddlerhood

1—2 years

Increased verbalexpression of emotionalstates

Increased expression ofemotions involvingself-consciousness andself-evaluation such asshame, pride or coyness

Increased awareness of ownemotional responses

Irritability when parentsplace limits on expression ofneed for autonomy

Anticipation of feelingstowards others

Rudimentary empathy

Altruistic behaviour

Preschool

2—5 years

Increased pretending toexpress emotions in playand teasing

Language (self-talk andcommunication with others)used for regulating emotions

Increased insight intoothers emotions

Awareness that falseexpression of emotions canmislead others about one’semotional state

Middlechildhood

6—12 years

Increased use ofemotional expression toregulate relationships

Distinction madebetween genuineemotional expressionwith close friends andmanaged display withothers

Increased autonomy fromcaregivers in regulatingemotions

Increased efficiency inidentifying and using multiplestrategies for autonomouslyregulating emotions andmanaging stress

Regulation of self-consciousemotions, e.g.embarrassment

Distancing strategies used tomanage emotions if child haslittle control over situation

Increased understanding ofemotional scripts and socialroles in these scripts

Increased use of social skillsto deal with emotions ofself and others

Awareness of feelingmultiple emotions aboutthe same person

Use of information aboutemotions of self and othersin multiple contexts as aidsto making and maintainingfriendships

Adolescence

13+ years

Self-presentationstrategies are used forimpression management

Increased awareness ofemotional cycles (feelingguilty about feeling angry)

Increased use of complexstrategies to autonomouslyregulate emotions

Self-regulation strategies areincreasingly informed bymoral principles

Awareness of importance ofmutual and reciprocalemotional self-disclosure inmaking and maintainingfriendships

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voice appears at 4 weeks. Sadness and anger inresponse to removing a teething toy are first evi-dent at 4 months. Facial expressions reflecting fearfollowing separation become apparent at 9 months.Infants also show an increasingly sophisticatedcapacity to discriminate positive and negative emo-tions expressed by others over the course of theirfirst year of life. During the first year of life infantsdevelop rudimentary self-soothing skills for regu-lating their emotions such as rocking and feeding.They also develop skills for regulating their atten-tion to allow themselves and their care-takers tocoordinate their actions to soothe them in dis-tressing situations. They rely on their care-takersto provide emotional support to help them man-age stress. The capacity for turn taking in gamessuch as peek-a-boo develops once children havethe appropriate cognitive skills for understandingobject constancy. Social referencing also occurstowards the end of the first year when childrenlearn the appropriate emotions to express in par-ticular situations by attending to the emotionalexpressions of their care-takers.

During their second year infants show increasedverbal expression of emotional states, andincreased expression of emotions involving self-consciousness and self-evaluation such as shame,pride or coyness. This occurs because theircognitive skills allow them to begin to think aboutthemselves from the perspective of others. Duringthe second year of life toddlers show increasedawareness of their own emotional responses.They show irritability – often referred to as the‘terrible twos’ – when parents place limits onthe expression of their needs for autonomy andexploration. In relationships they can increasinglyanticipate feelings they will have towards others inparticular situations. They also show rudimentaryempathy and altruistic behaviour.

Between the ages of 2 and 5 years childrenincreasingly pretend to express emotions inplay and when teasing or being teased by otherchildren. They use language in the form of bothinternal speech and conversations with othersto modulate their affective experience. Thereis increased insight into the emotions beingexperienced by others and an increased awarenessthat we can mislead others about what we arefeeling by falsely expressing emotions. More

sophisticated empathic and altruistic behaviouralso begins to develop within the family and peergroup during the preschool years.

MIDDLE CHILDHOOD

During middle childhood (6–12 years), withthe transition to primary school and increasedparticipation in peer group activities, children’sSED undergoes a profound change. Rather thanregularly looking to parents or caregivers to helpthem manage their feelings and relationships,school-aged children prefer to autonomouslyregulate their emotional states and depend moreon their own resources in dealing with their peers.As they develop through the middle childhoodyears they show increased efficiency in identifyingand using multiple strategies for autonomouslyregulating their emotions and managing stress.During this process they learn to regulate self-conscious emotions such as embarrassment andto use distancing and distraction strategies tomanage intense feelings when they have littlecontrol over emotionally challenging situations.There is increased use of emotional expressionto regulate closeness and distance within peerrelationships. Within this context, children makeclear distinctions between genuine emotionalexpression with close friends and managedemotional displays with others.

During middle childhood children develop anunderstanding of consensually agreed emotionalscripts and their roles in such scripts. There isalso an increased use of social skills to deal withtheir own emotions and those of others. Childrenbecome aware that they can feel multiple conflict-ing emotions about the same person; for example,that they can be angry with someone they like.They use information and memories about theirown emotions and those of others in multiplecontexts as aids to making and maintaining friend-ships. As adolescence approaches they developan increasingly sophisticated understanding of theplace of emotional scripts and social roles in mak-ing and maintaining friendships.

Cooperative play premised on an empathicunderstanding of other children’s viewpointsbecomes fully established in middle childhood.Competitive rivalry (often involving physical or

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verbal aggression or joking) is an important partof peer interactions, particularly among boys. Thisallows youngsters to establish their position ofdominance within the peer group hierarchy. Peerfriendships in middle childhood are importantbecause they constitute a source of social supportand a context within which to learn about the man-agement of networks of relationships. Childrenwho are unable to make and maintain friendships,particularly during middle childhood, are at riskfor the development of psychological difficulties.

ADOLESCENCE

During adolescence from 13 to 20 years thereis an increased awareness of complex emotionalcycles, for example feeling guilty about feelingangry or feeling ashamed for feeling frightened.In adolescence, youngsters increasingly use com-plex strategies, such as reframing, to autonomouslyregulate emotions. These self-regulation strate-gies are increasingly informed by moral principles.However, alongside this concern with morality,self-presentation strategies are increasingly usedfor impression management. Adolescents gradu-ally become aware of the importance of mutualand reciprocal emotional self-disclosure in makingand maintaining friendships.

FACTORS CONTRIBUTING TO SOCIALEMOTIONAL DEVELOPMENT

Available research indicates that SED in middlechildhood is influenced by complex interactionsamong multiple personal and contextual factors.Personal factors include genetic endowment [3],temperament [4], cognitive abilities [5], self-esteem[6], social cognition [7] and moral development[8]. Contextual factors include attachment [9], par-enting style [10], parental adjustment [11], familyfunctioning [12], school environment [13], peergroup relationships [14], and the wider social andcultural environment [15]. From a clinical per-spective, in any given case, we may expect moresuccessful SED where there are more positive thannegative personal and contextual factors. In con-trast, where there are more negative than positivepersonal and contextual factors, problems withSED may occur.

Positive SEDWith regard to personal factors, young people aremore likely to develop the skills for emotionalexpression and regulation and for making andmaintaining relationships if they have favourablegenetic endowments, easy temperaments, ade-quate cognitive abilities to understand theirfeelings and the emotional demands of theirimportant relationships, adequate self-esteem, thecapacity to understand social situations accuratelyand a well-developed conscience. With regardto contextual factors, positive SED is morelikely where children have developed secureattachments; where their parents have adoptedan authoritative parenting style characterized bywarmth and a moderate level of control; wheretheir parents have no major adjustment problems;and where the family, school, peer group andwider social environments have been supportive.For example, in a UK study Bowes et al. [16] foundthat children from supportive families showedresilience when bullied in primary school.

Problematic SEDProblematic SED may occur where there aredifficulties with genetic endowment, temperament,cognitive abilities, self-esteem, social cognitionand moral development. Problematic SED isassociated with unfavourable genetic endowmentsindexed by family histories of psychopathology. Achildhood history of difficult temperament is alsoassociated with problematic emotional develop-ment. With regard to cognitive abilities, childrenwith intellectual disabilities tend to acquire skillsfor expressing and regulating emotions and man-aging relationships at a slower rate than childrenwithout such disabilities. Disproportionately morechildren with intellectual disabilities, than with-out, show challenging behaviour associated withemotional regulation problems. Children with lowself-esteem, who evaluate themselves negatively,have difficulty regulating negative mood statesand managing relationships. Children who haveproblematic social cognition, notably those whohave developed a hostile attributional bias wherethey inaccurately attribute negative intentions toothers, have difficulties regulating anger and main-taining positive peer group relationships. Childrenwho have not internalized social rules and norms

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and developed a conscience, particularly thosewith callous unemotional traits, have difficultiesempathizing with others and making and main-taining social relationships. The foregoing aresome of the ways in which personal vulnerabilitiescan compromise SED in middle childhood.

Social and emotional development during thisperiod may also be compromised by environmentaladversity characterized by difficulties with attach-ment, parenting style, parental adjustment, familyfunctioning, the school environment, peer grouprelationships, and the wider social and culturalenvironment. Problematic SED is more commonwhere children have developed insecure attach-ments to their parents or caregivers. Non-optimalfamily environments can also impair SED. Suchfamily environments may be characterized by par-enting problems, child abuse or neglect; parentalmental health problems or criminality; and familyconflict or domestic violence. Where there is a poormatch between children’s educational needs andeducational placement, this can have an adverseeffect on their SED. For example, problems withSED may be exacerbated where a child with aspecific learning disability, intellectual disabilityor psychological disorder is placed in a main-stream class without adequate special educationalresources. Schools with inadequate policies andprocedures for managing bullying and victimiza-tion of pupils by peers or teachers can also have anegative effect on SED. Problematic SED may beexacerbated where children are rejected by theirpeers or where they spend a significant amountof time with antisocial peers. Within the widersocial and cultural environment a range of fac-tors can have a detrimental impact on SED. Theseinclude a high level of extrafamilial stress and alow level of extrafamilial perceived social support,and also exposure to media (TV, films, computergames) that model and reinforce the inappropri-ate expression of aggression, anxiety, depression,elation and other emotions.

CONSEQUENCES OF SED PROBLEMSIN MIDDLE CHILDHOOD

Emotional dysregulation is a risk factor forpsychopathology [17], and many types ofpsychopathology and behaviour problems areassociated with problematic SED. Anxiety and

mood disorders, and internalizing behaviour prob-lems are associated with difficulties regulating fearand sadness. Disruptive behaviour disorders andexternalizing behaviour problems are associatedwith difficulties regulating anger and aggression.Attention deficit hyperactivity disorder (ADHD)is associated with problematic impulse control.All of these types of disorders and behaviourproblems are associated with problems makingand maintaining relationships, as are otherconditions such as autism spectrum disorders andpsychoses. There is significant continuity in socialemotional development from middle childhoodto adolescence. Those who are well adjusted inmiddle childhood tend to become well adjustedadolescents [2], while problems tend to persist intothe teenage years in children who showed socialand emotional difficulties in primary school [18].

ADDRESSING SED PROBLEMS

Prevention and treatment programmes havebeen developed to address SED problems.Successful prevention programmes begin duringthe preschool years. They involve screening at-riskchildren on the basis of their status of personaland contextual risk factors, and offering complexinterventions such as family support, parent train-ing and child stimulation that target multiple riskfactors [19]. With regard to treating children withSED problems, it is best to base interventions inany particular case on a formulation of factors rel-evant to that specific case and the current evidencebase for effective interventions for such difficulties,because problems with SED are typically causedand maintained by the complex interaction ofmultiple personal and contextual factors [20].

REFERENCES

[1] Denham S, Wyatt T, Bassett H et al. (2009) Assess-ing social-emotional development in children froma longitudinal perspective. Journal of Epidemiologyand Community Health 63, 137–52.

[2] Saarni C, Campos J, Cameras L et al. (2008) Emo-tional development: Action communication under-standing. In: Eisenberg N (ed.), Handbook of ChildPsychology, Vol. 3: Social, Emotional and Personal-ity Development. New York: Wiley, pp. 226–300.

[3] Rutter M. (2006) Genes and Behaviour: Nature-nurture Interplay Explained. Oxford: Blackwell.

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[4] De Pauw S, Mervielde I. (2010) Temperament,personality and developmental psychopathology: Areview based on the conceptual dimensions under-lying childhood traits. Child Psychiatry and HumanDevelopment 41, 313–29.

[5] Hodapp R, Dykens M. (2009) Intellectual disabil-ities and child psychiatry: Looking to the future.Journal of Child Psychology and Psychiatry 50,99–107.

[6] Harter S. (2006) The self. In: Eisenberg N (ed.),Handbook of Child Psychology, Vol. 3: Social, Emo-tional and Personality Development. New York:Wiley, pp. 505–70.

[7] Sharp C, Fonagy P, Goodyer I. (2008) Social Cogni-tion and Developmental Psychopathology. Oxford:Oxford University Press.

[8] Kochanska G and Aksan N. (2006) Children’s con-science and self-regulation. Journal of Personality74, 1587–617.

[9] Kerns K. (2008) Attachment in middle childhood.In: Cassidy J and Shaver P (eds), Handbook ofAttachment, 2nd edn. New York: Guilford, pp.366–82.

[10] Parke R, Buriel R. (2008) Socialization in the family:Ethnic and ecological perspectives. In: EisenbergN (ed.), Handbook of Child Psychology, Vol. 3:Social, Emotional and Personality Development.New York: Wiley, pp. 429–504.

[11] Stein A, Ramchandani P, Murray L. (2008) Impactof parental psychiatric disorder and physical illness.In: Rutter M, Bishop D, Pine D et al. (eds), Rutter’sChild and Adolescent Psychiatry, 5th edn. Oxford:Wiley-Blackwell, pp. 407–20.

[12] Masten A, Shaffer A, Clarke-Stewart A et al.(2006) How families matter in child development:Reflections from research on risk and resilience.In: Clarke-Stewart A and Dunn J (eds), FamiliesCount: Effects on Child and Adolescent Develop-ment. The Jacobs Foundation Series on Adolescence.New York: Cambridge University Press, pp. 5–25.

[13] Sellstrom E and Bremberg S. (2006) Is there a‘school effect’ on pupil outcomes? A review of

multilevel studies. Journal of Epidemiology andCommunity Health 60, 149–55.

[14] Rubin K, Bukowski W, Parker J. (2006) Peerinteractions, relationships and groups. In: Eisen-berg N (ed.), Handbook of Child Psychology, Vol.3: Social, Emotional and Personality Development.New York: Wiley, pp. 571–645.

[15] Jenkins J. (2008) Psychosocial adversity andresilience. In: Rutter M, Bishop D, Pine D et al.(eds), Rutter’s Child and Adolescent Psychiatry, 5thedn. Oxford: Wiley-Blackwell, pp. 377–91.

[16] Bowes L, Maughan B, Caspi A. (2010) et al. Familiespromote emotional and behavioural resilience tobullying: Evidence of an environmental effect. Jour-nal of Child Psychology and Psychiatry 51, 809–17.

[17] Keenan K. (2006) Emotion dysregulation as a riskfactor for child psychopathology. Clinical Psychol-ogy: Science and Practice 7, 418–34.

[18] Sterba S, Copeland W, Egger H et al. (2010) Longi-tudinal dimensionality of adolescent psychopathol-ogy: testing the differentiation hypothesis. Journalof Child Psychology and Psychiatry 51, 871–84.

[19] Manning M, Homel R, Smith C. (2010) A meta-analysis of the effects of early developmentalprevention programs in at-risk populations on non-health outcomes in adolescence. Children and YouthServices Review 32, 506–19.

[20] Carr A. (2009) What Works with Children Ado-lescents and Adults. A Review of Research onthe Effectiveness of Psychotherapy. London: Rout-ledge.

FURTHER READING

Carr A. (2006) Handbook of Child and Adolescent Clin-ical Psychology, 2nd edn. London: Routledge.

Damon W and Lerner R. (2008) Child and Adoles-cent Development: An Advanced Course. Chichester:Wiley.

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Social-cognitive development during adolescence

11Social-Cognitive DevelopmentDuring AdolescenceSarah-Jayne BlakemoreInstitute of Cognitive Neuroscience, University College London, London, UK

HUMANS ARE EXQUISITELY SOCIAL

Humans are an exquisitely social species. We areconstantly reading each other’s actions, gesturesand faces in terms of underlying mental states andemotions, in an attempt to figure out what otherpeople are thinking and feeling, and what theyare about to do next. This is known as theoryof mind, or mentalizing. Developmental psychol-ogy research on theory of mind has demonstratedthat the ability to understand others’ mental statesdevelops over the first four or five years of life.While certain aspects of theory of mind are presentin infancy [1], it is not until around the age of 4years that children begin explicitly to understandthat someone else can hold a belief that differsfrom one’s own, and which can be false [2]. Anunderstanding of others’ mental states plays a crit-ical role in social interaction because it enablesus to work out what other people want and whatthey are about to do next, and to modify our ownbehaviour accordingly.

THE SOCIAL BRAIN

Over the past 15 years, a large number of indepen-dent studies have shown remarkable consistencyin identifying the brain regions that are involved intheory of mind, or mentalizing. These studies haveemployed a wide range of stimuli including sto-ries, sentences, words, cartoons and animations,each designed to elicit the attribution of mental


states (see Ref. [3] for review). In each case, thementalizing task resulted in the activation of anetwork of regions including the posterior supe-rior temporal sulcus (pSTS), the temporo-parietaljunction (TPJ), the temporal poles and the dorsalmedial prefrontal cortex (mPFC; see Ref. [4]). Theagreement between neuroimaging studies in thisarea is remarkable and the consistent localizationof activity within a network of regions includingthe pSTS/TPJ and mPFC, as well as the temporalpoles, suggests that these regions are key to theprocess of mentalizing.

Brain lesion studies have consistently demon-strated that the superior temporal lobes [5] andPFC [6] are involved in mentalizing, as damageto these brain areas impairs mentalizing abili-ties. Interestingly, one study reported a patientwith large PFC damage whose mentalizing abili-ties were intact [7], suggesting that this region isnot necessary for mentalizing. However, there areother explanations for this surprising and intrigu-ing finding. It is possible that, due to plasticity, thispatient used a different neural strategy in mentaliz-ing tasks. Alternatively, it is possible that damageto this area at different ages has different con-sequences for mentalizing abilities. The patientdescribed by Bird and colleagues had sustainedher PFC lesion at a later age (62 years) than mostpreviously reported patients who show impair-ments of mentalizing tasks. Perhaps mPFC lesionslater in life spare mentalizing abilities, whereasdamage that occurs earlier in life is detrimental.

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It is possible that mPFC is necessary for theacquisition of mentalizing but not essential forlater implementation of mentalizing. Intriguingly,this is in line with recent data from developmentalfMRI studies of mentalizing, which suggest thatthe mPFC contributes differentially to mentalizingat different ages.

DEVELOPMENT OF MENTALIZING DURINGADOLESCENCE

There is a rich literature on the development ofsocial cognition in infancy and childhood, pointingto step-wise changes in social cognitive abilitiesduring the first five years of life. However, therehas been surprisingly little empirical research onsocial cognitive development beyond childhood.Only recently have studies focused on develop-ment of the social brain beyond early childhood,and these support evidence from social psychologythat adolescence represents a period of significantsocial development. Most researchers in the fielduse the onset of puberty as the starting point foradolescence. The end of adolescence is harder todefine and there are significant cultural variations.However, the end of the teenage years representsa working consensus in Western countries. Ado-lescence is characterized by psychological changesin terms of identity, self-consciousness and rela-tionships with others. Compared with children,adolescents are more sociable, form more com-plex and hierarchical peer relationships, and aremore sensitive to acceptance and rejection by peers[8]. Although the underlying factors of these socialchanges are most likely to be multifaceted, onepossible cause is development of the social brain.

Recently, a number of fMRI studies have inves-tigated the development during adolescence of thefunctional brain correlates of mentalizing. Thesestudies have used a wide variety of mentaliz-ing tasks involving the spontaneous attributionof mental states to animated shapes, reflectingon one’s intentions to carry out certain actions,thinking about the preferences and dispositions ofoneself or a fictitious story character, and judgingthe sincerity or sarcasm of another person’s com-municative intentions. Despite the variety of men-talizing tasks used, these studies of mental stateattribution have consistently shown that mPFCactivity during mentalizing tasks decreases betweenadolescence and adulthood (Figure 11.1). Each of

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Figure 11.1 A section of the dorsal medial pre-frontal cortex (mPFC) that is activated in studiesof mentalizing: Montreal Neurological Institute(MNI) ‘y’ coordinates range from 30 to 60, and‘z’ coordinates range from 0 to 40. Dots indicatevoxels of decreased activity during six mentaliz-ing tasks between late childhood and adulthood;numbers refer to Brodmann areas (see Blake-more [10] for references). The mentalizing tasksranged from understanding irony, which requiresseparating the literal from the intended mean-ing of a comment, thinking about one’s ownintentions, thinking about whether charactertraits describe oneself or another familiar other,watching animations in which characters appearto have intentions and emotions, and thinkingabout social emotions such as guilt and embar-rassment [9]. Adapted from Blakemore [10], withpermission.

these studies compared brain activity in youngadolescents and adults while they were performinga task that involved thinking about mental states(see Figure 11.1 for details of studies). In eachof these studies, mPFC activity was greater in theadolescent group than in the adult group duringthe mentalizing task compared to the control task.In addition, there is evidence for differential func-tional connectivity between mPFC and other partsof the mentalizing network across age [9].

To summarize, a number of developmentalneuroimaging studies of social cognition have beencarried out by different labs around the world, andthere is striking consistency with respect to thedirection of change in mPFC activity. It is not yetunderstood why mPFC activity decreases betweenadolescence and adulthood during mentalizingtasks, but two non-mutually exclusive explanations

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have been put forward (see Ref. [10] for details).One possibility is that the cognitive strategy formentalizing changes between adolescence andadulthood. A second possibility is that the func-tional change with age is due to neuroanatomicalchanges that occur during this period. Decreasesin activity are frequently interpreted as beingdue to developmental reductions in grey mattervolume, presumably related to synaptic pruning.However, there is currently no direct way to testthe relationship between number of synapses,synaptic activity and neural activity as measured

by fMRI in humans (see Ref. [10] for discussion).If the neural substrates for social cognition changeduring adolescence, what are the consequencesfor social cognitive behaviour?

ONLINE MENTALIZING USAGE IS STILLDEVELOPING IN MID-ADOLESCENCE

Most developmental studies of social cognitionfocus on early childhood, possibly because chil-dren perform adequately in even quite complexmentalizing tasks at around age 4 years. This

(a) Instructions example 1

YOUR VIEW

Move thesmall ball left

Distractor Irrelevant object

Target

Move thesmall ball left

DIRECTOR'S VIEW

(b) Instructions example 2

(d) Control trial(c) Experimental trial

Figure 11.2 (a,b) Images used to explain the Director condition: participants were shown an exampleof their view (a) and the corresponding director’s view (b) for a typical stimulus with four objects inoccluded slots that the director cannot see (e.g. the apple). (c,d) Examples of an experimental (c)and a control trial (d) in the Director condition. The participant hears the verbal instruction: ‘Movethe small ball left’ from the director. In the experimental trial (c), if the participant ignored thedirector’s perspective, she would choose to move the distractor ball (golfball), which is the smallestball in the shelves but which cannot be seen by the director, instead of the larger ball (tennis ball)shared by both the participant’s and the instructor’s perspective (target). In the control trial (d),an irrelevant object (plane) replaces the distractor item. Adapted from Dumontheil et al. [12], withpermission.

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can be attributed to a lack of suitable paradigms:generally, in order to create a mentalizing task thatdoes not elicit ceiling performance in children aged5 and older, the linguistic and executive demandsof the task must be increased. This renders anyage-associated improvement in performance dif-ficult to attribute solely to improved mentalizingability. However, the protracted structural andfunctional development in adolescence and earlyadulthood of the brain regions involved in theoryof mind might be expected to affect mental stateunderstanding. In addition, evidence from socialpsychology studies shows substantial changes insocial competence and social behaviour duringadolescence, and this is hypothesized to rely on amore sophisticated manner of thinking about andrelating to other people including understandingtheir mental states.

Recently, we adapted a task that requires theonline use of theory of mind information whenmaking decisions in a communication game, andthat produces large numbers of errors even inadults [11]. In our computerized version of thetask, participants view a set of shelves contain-ing objects, which they are instructed to move bya ‘director’, who can see some but not all of theobjects [12] (Figure 11.2). Correct interpretation ofcritical instructions requires participants to use thedirector’s perspective and only move objects thatthe director can see (the director condition). Wetested participants aged between 7 and 27 yearsand found that, while performance in the directorand a control condition followed the same tra-jectory (improved accuracy) from mid-childhooduntil mid-adolescence, the mid-adolescent groupmade more errors than the adults in the directorcondition only. These results suggest that the abil-ity to take another person’s perspective to directappropriate behaviour is still undergoing develop-ment at this relatively late stage.

Many questions remain to be investigated inthis new and rapidly expanding field. The study ofneural development during adolescence is likely tohave important implications for society in relationto education and the legal treatment of teenagers,as well as a variety of mental illnesses that oftenhave their onset in adolescence.

Box 11.1 Key points

• The social brain is involved inunderstanding others’ minds.

• The social brain develops structurallyand functionally in adolescence.

• Activity in medial prefrontal cortexdecreases between adolescence andadulthood during social cognition tasks.

• Performance on an online theory ofmind usage task improves duringadolescence.

ACKNOWLEDGEMENTS

The author is supported by a Royal Society Univer-sity Research Fellowship. The author is grateful toNarges Bazargani for her help with this manuscript.

REFERENCES

[1] Baillargeon R, Rose M, Scott RM, Hea Z. (2010)False-belief understanding in infants. Trends in Cog-nitive Science 14, 110–18.

[2] Barresi J and Moore C. (1996) Intentional relationsand social understanding. Behavioral and Brain Sci-ences 19, 107–54.

[3] Amodio DM and Frith CD. (2006) Meeting ofminds: the medial frontal cortex and social cog-nition. Nature Reviews Neuroscience 7, 268–77

[4] Burnett S, Blakemore SJ. (2009) Functional con-nectivity during a social emotion task in adolescentsand in adults. European Journal of Neuroscience 29,1294–301.

[5] Samson D, Apperly IA, Chiavarino C, HumphreysGW. (2004) Left temporoparietal junction is neces-sary for representing someone else’s belief. NatureNeuroscience 7, 499–500.

[6] Stuss DT, Gallup GG Jr, Alexander MP. (2001)The frontal lobes are necessary for ‘theory of mind’.Brain 124, 279–86.

[7] Bird CM, Castelli F, Malik O, Frith U, Husain M.(2004) The impact of extensive medial frontal lobedamage on ‘Theory of Mind’ and cognition. Brain127, 914–28.

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[8] Steinberg L and Morris AS. (2001) Adolescentdevelopment. Annual Review in Psychology 52,83–110.

[9] Burnett S, Bird G, Moll J, Frith C, BlakemoreS-J. (2009) Development during adolescence of theneural processing of social emotion. Journal of Cog-nitive Neuroscience 21, 1736–50.

[10] Blakemore SJ. (2008) The social brain in adoles-cence. Nature Reviews Neuroscience 9, 267–77.

[11] Keysar B, Lin S, Barr DJ. (2003) Limits on theoryof mind use in adults. Cognition 89, 25–41.

[12] Dumontheil I, Apperly IA, Blakemore S-J. (2010)Online usage of theory of mind continues todevelop in late adolescence. Developmental Science13, 331–8.

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Section 2

Promoting Well-Being

Promoting infant mental health

12Promoting Infant Mental HealthChristine PuckeringCaledonia House, Royal Hospital for Sick Children, Glasgow, UK

WHAT IS GOOD INFANT MENTAL HEALTH?

Infant mental health is more than an absence ofmental illness, a concept that is difficult in any caseto apply to infants. Rather, mental health is a holis-tic view of the capacities of an infant that includegrowth, learning and relationships. For an infant itis difficult to imagine an environment in which justone of these might be promoted without also serv-ing the others. A definition that encompasses thisperspective is provided by Zero to Three (a multi-disciplinary organization that aims to describe anddefine infant and toddler development):

the young child’s capacity to experience, regulateand express emotions, form relationships andexplore the environment and learn. All of thesecapacities will be best accomplished withinthe context of the caregiving environmentthat includes family, community and culturalexpectations for young children. Developingthese capacities is synonymous with healthysocial and emotional development [1].

The infant, though physically dependent on itscaregivers, has a biological imperative and capac-ity to react to and interact with other humans [2].It is now clear that this process shapes not only thelearning and emotional capacity of the infant butthe very architecture of the brain, with long-termsequelae for infant emotional, social and cognitivegrowth. Comprehensive guidance on the embed-ding of infant development in its wider familial,social and cultural context, as well as variousavenues to interventions, has been provided [3,4].


WHY IS INFANCY SO IMPORTANT?

It has perhaps seemed paradoxical that the periodof ‘normal infantile amnesia’ for events before theage of about three years could have such a pivotalrole in later development. The assumption wasthat as the child could not remember this period,what happened during that time could not be ofany significance. Yet, the evidence suggests thatwhat goes on during this time frame has a powerfulpredictive value in relation to neuroanatomical andbiological processes, as well as social and emotionalcompetence. For instance, Chapter 20 outlines howcaregiver abuse and neglect can affect infant braindevelopment.

There is evidence, too, that early exposure topoor parenting leads to abnormal diurnal cortisolpatterns, with the normal morning peak and bed-time trough being flattened in children who areexposed to maltreatment. This blunted pattern ofcortisol production is seen later in both psychopa-thy and substance abusers, and may be associatedwith callous unemotional behavioural traits – apossible mechanism being that under-reactivityof the hypothalamic–pituitary axis (HPA) leadsto underarousal at the distress of others. Anattachment-based intervention [5] had the effectof normalizing HPA diurnal patterns in childrenunder 2 years, but was less effective with olderchildren suggesting a sensitive period.

The social and emotional development of chil-dren may be less obvious than their motor devel-opment or their communication skills. Yet, thefoundations of social and emotional competenceare also laid down in the early months and years

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Promoting well-being

and have been shown to be the precursors oflater social and emotional behaviour, as well asthe capacity to sustain attention and learn. Therehave previously been challenges to critical or sen-sitive periods in human development because theresilience and flexibility of human learning arguedagainst the sort of tight developmental time framessuggested by animal studies. Early evidence onchildren raised in institutions however suggestedthat there were at least some broad limits to toler-ance in social and emotional development.

Early research showed that 2-year-old chil-dren, adopted from children’s homes wherecaregiver–child relationships were discour-aged due to frequent staff changes and highchild:caregiver ratios, were at higher risk oflater emotional-behaviour problems even afteradoption into good homes [6]. More recently,the English and Romanian adoption studies haveshown that children who had spent more thantheir first 6 months in a depriving institution hadsubstantial IQ deficits that were not amelioratedby later good experiences in an adoptive familyThe children from Romanian institutions weredeprived in almost all aspects of their lives, and theduration and extent of deprivation was evident instunted brain growth, even in the absence of poornutrition. The authors propose that psychosocialdeprivation plays a major role in functional andstructural neuroanatomy [7].

So powerful now is the evidence for theimpact of the caregiving environment upon infantdevelopment, that it has been suggested that sincethe origins of childhood disruptive behaviourdisorders lie in epigenetic processes, interventionas ‘near to conception as possible’ is the key toeffective prevention [8]. The emotional well-beingand good social skills that lead to satisfying andsustained peer and family relationships duringchildhood and adolescence, also lead longer termto patterns of interaction that will later supportgood relationships with partners, holding down ajob and being a parent.

WHAT LEADS TO GOOD INFANTMENTAL HEALTH?

Of course the most fundamental conception ofthe promotion of infant mental health comes fromtheories of attachment, as it is within a secure care-giving relationship that infants and then children

learn both that they are valued and how to valueothers. (see Chapters 7 and 15) It is in this secureatmosphere that children can learn and developto their optimum. Babies cannot modulate theirarousal, and depend on an adult to soothe theirdistress or discomfort when they are overaroused,and to provide stimulation when they are drowsyor underaroused. It is only when the baby is ina state of active attention that it is possible forsocial interaction and learning to take place. Thebeginnings of social understanding grow fromwhether the child is appropriately soothed andstimulated by a carer as required. The child whomeets such carefully modulated interaction willlearn that other people are trustworthy and avail-able to help. Babies whose needs for emotionalmodulation are not met will fail to understandtheir own feelings, fail to read the feelings ofothers and fail to regulate their behaviour. Whenarousal is not held in the midrange, that is, it isneither over- nor under-stimulated, learning andthinking are also impaired.

ASSESSING INFANT MENTAL HEALTH

One immediate difficulty emerges in describingor measuring infant mental heath, namely, thelack of clear and predictive measures. The conceptof developmental psychopathology has providedsome helpful leads to intermediate markers, suchas language development, peer relationships andsocial cognition as well as maternal sensitivity,that are powerful predictors of later good func-tioning [9]. Even where the marker is somethingas robust as infant cognitive development, this isdifficult to discriminate within the normal range atsuch an early stage. Due to difficulties of accuratemeasurement during this period of development,very early cognitive measures do not always reli-ably predict later cognitive functioning. Less well-defined measures, such as well-being, will dependon the identification of intermediate markers, suchas aspects of infant–caregiver interaction.

The gold standard of measurement ofinfant–caregiver interaction, The Strange Situa-tion [10], is, however, not applicable before about12 months of age, hence often a proxy or predictorof good attachment, such as measurements ofcaregiver sensitivity, are substituted. However,screening of development is also a commonly usedmethod of assessment, as it is difficult to imagine

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Promoting infant mental health

an environment that promotes good developmentin infancy but would fail to be nurturing in thesocial and emotional sphere.

Widely used measures of infant mental healthinclude questionnaires for parents, observationalmethods and rating scales [11]. A recent valida-tion of the Neonatal Perception Inventory has ashown a remarkable continuity of attachment pro-cesses, with children of mothers who did not ratetheir babies as ‘better than the average baby’ on anumber of attributes, showing insecure attachmentstyles as adults some 30–40 years later [12]. Whilecognitive development or parent-completed ques-tionnaires of temperament or behaviour may notbe perfect indices of infant mental health, for prag-matic reasons they are used in various US stateswhere access to treatment resources may dependon meeting readily accessible criteria [13].

WHAT SUPPORTS GOOD INFANTMENTAL HEALTH?

Universal interventionsIn most cases, living in a normal family will providethe baby with exactly the responsive care that isneeded to support attachment. The presence of asmall number of caring adults who will attend andrespond to infant signals reinforces the emotionaldevelopment of the baby. Some recommendationssuch as immediate skin-to-skin contact after deliv-ery may have some utility where the relationshipis in peril, but these have few clearly demonstratedeffects in well-functioning families, although skin-to-skin contact may promote breastfeeding [14].One intervention that has been shown to be ofvalue is the use of the Brazelton BehaviouralAssessment Scale, which was initially designed asa measure of neurological intactness. Since it wasused in maternity wards, with mothers present, itbecame clear that gaining an understanding of theresponses of their own baby gave parents a headstart in early relationships via understanding whattheir baby was like and how they could best sootheand support him or her. This was further enhancedby the use of diaries, which prompted parents toobserve their babies closely and led to the devel-opment of the Touch Points programme [15].

There are a number of universal or population-based interventions that might be described aspublic health interventions and that can haveconsiderable impact. The use of baby slings and

backward-facing buggies which give the infantclose proximity and the chance to interact withthe carer, are simple low-cost interventions thatrequire little or no professional input. Otherrelatively simple interventions have been shownto have a significant impact on parent–childattachment. Baby massage has been suggested tohave some effect on mother–infant interaction,sleep relaxation and stress hormones, though nodirect effect on infant attachment [16].

Families with indicated additional needsA sound meta-analysis of controlled interventiontrials [17] has identified common aspects of effec-tive interventions that increase parental sensitivityor attachment for families where additionalsupport is needed. The common features arethat programmes focus specifically on attachmentrather than less specific support. It is evident thatfewer than five sessions may not be sufficient toproduce change, while participating in more than16 sessions has diminishing value. The ideal time tointervene appears to be between 6 and 12 monthsof age, a finding that is coherent with finding of thesensitivity of the infant to severe deprivation orabuse at that age. The review cites no direct impacton sensitivity for antenatal intervention, thoughengaging very needy mothers-to-be antenatallyand for a further 2 years has a substantial payoff,perhaps through the development of a workingtherapeutic alliance [18]. While most researchwas conducted with mothers, similar findingswere shown where intervention was with fathers,though including fathers and mothers togetherdiminished the effect size for mothers. Videofeedback proved to be a powerful tool andincreased effect sizes for intervention.

A number of programmes meet these criteria,notably Video Interaction Guidance, Circle ofSecurity Attachment, and Biobehavioral Catch-Up. Mellow Babies, Watch, Wait and Wonderand Parent-infant Psychotherapy also showed thepotential to improve attachment relationships,cognitive development and emotion regulationin infants [16,19,20]. Inevitably, these intensiveprogrammes require trained practitioners, withtraining being both expensive and time consuming.

Fortunately there is no need for specialistpsychological services for most families. Anormally loving family with a few caring adultsinvolved in the regular care of a baby will almost

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always provide the interaction that a baby needs.The resilience of the human infant allows atolerance of a range of parenting. Where parentalfactors such as postnatal depression, or factorsin the baby such as prematurity, or social factorssuch as poverty or teenage pregnancy, reducethe availability of attuned responsiveness, thenspecialist intervention is needed. However, wenow have very good indicators of how best tointervene and the evidence to promote the earliestpossible intervention.

REFERENCES

[1] Zero to Three website. http://www.zerotothree.org/child-development/early-childhood-mental-health/

[2] Trevarthen C. (2001) Intrinsic motives for com-panionship in understanding: Their origin, devel-opment, and significance for infant mental health.Infant Mental Health Journal 22, 95–131.

[3] Zeanah C. (2009) Handbook of Infant MentalHealth, 3rd edn. New York: Guilford Press.

[4] Shonkoff J and Phillips D (eds) (2000) for NationalResearch Council and Institute of Medicine.From Neurons to Neighborhoods; the Science ofEarly Childhood Development. Washington, DC:Board on Children, Youth and Families, NationalAcademy Press.

[5] Dozier M, Peloso E, Lewis E, Laurenceau J, LevineS. (2008) Effects of an attachment based interven-tion on the cortisol production of infants and tod-dlers in foster care. Developmental Psychopathology20, 845–59.

[6] Hodges J and Tizard B. (1989) Social and familyrelationships of ex-institutional adolescents. Journalof Child Psychology and Psychiatry 30, 77–97

[7] Rutter M and Sonuga-Barke EJ. (2010) Conclu-sions: overview of findings from the era study,inferences, and research implications. Monographsof the Society for Research in Child Development 7,212–29.

[8] Tremblay RE. (2010) Developmental origins ofdisruptive behaviour problems, the ‘‘original sin’’hypothesis, epigenetics and their consequences forprevention. Journal of Child Psychology and Psy-chiatry 51, 341–367.

[9] Miniscalco C, Nygren G, Hagberg B, Kadesjo B,Gillberg C. (2006) Neuropsychiatric and

neurodevelopmental outcome of children at age6 and 7 years who screened positive for languageproblems at 30 months. Developmental Medicineand Child Neurology 48, 361–6.

[10] Ainsworth MDM, Blehar MC, Waters E, Wall S.(1978) Patterns of Attachment. Hillsdale: Erlbaum.

[11] Puckering C and the Short Life Working Group onInfant Mental Health. (2007) Infant Mental Health:A Guide for Practitioners. HeadsUpScotland,(available at: http://www.headsupscotland.co.uk/documents/Infant%20Mental%20Health%20-%20Good%20Practice%20Guide%20-%20Final%20Edit.pdf).

[12] Broussard ER, Cassidy J. (2010) Maternal percep-tion of newborns predicts attachment organizationin middle adulthood. Attachment and Human Devel-opment 12, 159–72.

[13] Rosenthal J and Kaye N. (2005) State Approaches toPromoting Young Children’s Healthy Mental Devel-opment. National Academy for State Health Policy.

[14] Moore ER, Anderson GC, Bergman N. (2007)Early skin-to-skin contact for mothers and theirhealthy newborn infants. Cochrane Database of Sys-tematic Reviews issue 3; Art. No.: CD003519; doi:10.1002/14651858.CD003519.pub2.

[15] Brazelton TB. (1992) TouchPoints, the EssentialReference to Your Child’s Emotional and BehavioralDevelopment. Reading, MA: Addison-Wesley.

[16] Underdown A, Barlow J, Chung V, Stewart-Brown S. (2006) Massage intervention for pro-moting mental and physical health in infantsunder six months. Cochrane Database of System-atic Reviews Issue 4; Art. No.: CD005038; doi:10.1002/14651858.CD005038.pub2.

[17] Bakermans-Kranenburg MJ, van IJzendoorn MH,Juffer F. (2003) Less is more, meta-analyses ofsensitivity and attachment interventions in earlychildhood. Psychological Bulletin 129, 195–215.

[18] Olds DL. (2006) The nurse–family partnership,An evidence-based preventive intervention. InfantMental Health Journal 27, 5–25.

[19] Puckering C, McIntosh E, Hickey A, Longford J.(2010) Mellow Babies, A group intervention forinfants and mothers experiencing postnatal depres-sion. Counselling Psychology Review 25, 28–40.

[20] Zeanah P, Stafford B, Zeanah CH. (2005) ClinicalInterventions to Enhance Infant Mental Health, aSelective Review. National Center for Infant andEarly Childhood Health Policy at UCLA.

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Promoting children’s well-being

13Promoting Children’s Well-BeingPaul StallardChild and Adolescent Mental Health Services, Oxford Health NHS Foundation Trust, Bristol, UK

WHAT’S NEW

• School-based prevention programmes provide an opportunity to widely promote andmaintain the psychological well-being of children.

• The effects of these programmes are, however, variable with those focusing upon anxietyshowing more promise than those focusing upon depression.

• Targeted programmes produce greater immediate treatment effects although the potentialbenefits of universal prevention programmes in maintaining healthy status and reducing theprevalence of new disorders have seldom been assessed.

• Variability within studies indicates the need for methodologically robust research to identifyimportant mediators and moderators.

• An analysis of costs/benefits and delivery models is required to determine whetherschool-based prevention programmes should be widely available and are sustainable inschools.

Community surveys highlight that psychologicalproblems in children and young people are com-mon and can significantly impair everyday func-tioning [1,2]. If left untreated, problems persist andincrease the likelihood of psychological problemsin adulthood [3,4]. Improving the mental healthof children is an important public health objectiveand although effective treatments are available themajority of children, particularly those with emo-tional disorders, remain unidentified and untreated[5]. Focusing upon the treatment of established dis-orders will therefore have a limited impact uponthe psychological health of children.

An alternative approach is that of prevention,which aims to reduce the prevalence of psycho-logical problems and disorders while optimizing


psychological well-being. This can be achieved bythe widespread provision of programmes designedto reduce or mitigate the effects of known mentalhealth risk factors while enhancing protective fac-tors at the individual, family and community level.Prevention programmes, therefore, help childrento become more resilient and better able to copewith stress and adversity thereby maintaining theirhealthy status.

PREVENTION

Prevention programmes are typically conceptual-ized as universal, selective or indicated, with eachhaving a different focus and aim [6] (Table 13.1).Universal programmes are provided to all

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Table 13.1 Universal, selective and indicated prevention.

Prevention Provision Advantages Disadvantages

Universal prevention,e.g. anxiety preventionprogrammes for9/10-year-old children

Universal — providedto all regardless ofrisk status

Far-reaching coverage

Opportunity forprimary prevention,i.e. reduce prevalenceof new disorders

Screening not required

Avoids need forlabelling, which couldbe stigmatizing

Low cost/high volume

Limited resources used toprovide interventions tomany who are, and willremain, ‘healthy’

Intervention effects aretypically small

Face validity, relevanceand engagement can bedifficulties

Selective prevention,e.g. anxiety preventionprogrammes forchildren where parentsare separating

Targeted — uponthose at increasedrisk of developingproblems throughexposure to knownrisk factors

Resources focused upon‘at-risk’ groups

Opportunity forprimary prevention

Potentially stigmatizing

Difficulties in accuratelyidentifying ‘at-risk’ groupswithin the community

Indicated prevention,e.g. children withsignificant anxietysymptoms but notmeeting full diagnosticcriteria

Targeted — uponthose displayingmild/moderateproblems

Efficient use of limitedresources

Provide earlyinterventions for thosewith emergentproblems

Demonstrate largertreatment effects

May require screening,which can be costly andpractically complicated

Potentially stigmatizingand unacceptable to someof the identified group

members of the target population irrespectiveof risk status, such as children of a certain age.Selective programmes target children at increasedrisk of developing problems through exposure toknown risk factors – for instance, children of par-ents with a mental illness. Universal and selectiveprogrammes are primarily concerned with promot-ing well-being and in reducing the occurrence ofnew problems. Indicated programmes are earlyinterventions provided on a targeted basis to thosealready displaying mild or moderate problems toprevent them from worsening – for example, chil-dren with symptoms of anxiety or depression.

Each approach has strengths and limitations.Universal programmes offer the greatest potentialto optimize the well-being of the wider population.They provide opportunities for prevention (e.g.

maximizing potential), protection (e.g. developingcompetencies) and intervention (e.g. minimizingimpairment). Far-reaching and accessible, theyminimize any potential negative stigma arisingfrom more targeted approaches. However, theirgeneral focus may not be of sufficient depth ordosage to benefit those with more established dis-orders. Similarly, from an economic perspective,many of those who receive universal interven-tions are already healthy and do not, and will not,require any intervention to maintain this status ormaximize their potential.

Selective and indicated approaches are moretargeted, focusing limited resources upon thosewith potentially greater needs. The effects areoften large since initial levels of symptoms andthe subsequent change are greater. However,

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they require accurate identification of the targetgroup – a particular difficulty where children haveemotional problems or disorders.

School-based preventionIn terms of delivering prevention programmesschools provide convenient and familiar locationsthat are attended by the majority of young people.The integration of emotional health programmeswithin the school setting and curriculum offers thepotential to discuss openly mental health issuesand to promote psychological concepts and ideasas ‘skills for life’. This open and more visibleapproach serves to normalize common psycho-logical problems such as anxiety and depression,and can help to develop a supportive peer groupculture where worries and problems can be moreopenly acknowledged and discussed.

In terms of effectiveness, systematic reviewsof school-based emotional health prevention pro-grammes have found evidence to suggest thatuniversal and targeted/indicated approaches canhave positive effects upon emotional well-beingalthough the results are variable [7,8]. This chapterfocuses on interventions aimed at two of themost common emotional disorders, namely anxietyand depression. Issues and challenges involved indelivering effective prevention programmes arepresented and discussed.

DEPRESSION PREVENTION PROGRAMMES

A Cochrane review of depression prevention pro-grammes identified 18 psychological interventionsof which 10 were universal and eight were targeted[9]. The methodological quality of the studies waspoor resulting in half being excluded from theanalyses. Interventions were found to be effectivein comparison to no intervention, with significantreductions in immediate post-intervention depres-sion scores. The authors suggest further investi-gations are warranted alongside methodologicallyrobust investigations. A more recent review iden-tified 42 trials assessing 28 different programmes[10]. Of these trials, 26 were universal, 10 indicatedand six were selective. The majority (76%) of pro-grammes were based upon cognitive behaviouraltherapy (CBT) and involved eight or more sessions(88%). Two-thirds were led by graduate students,mental health practitioners or teachers. Indicated

programmes were most effective in reducing symp-toms of depression, with prevention programmesled by teachers tending to be the least effective.The authors noted variability in the effectivenessof programmes based upon the same theoreticalmodel suggesting that factors other than the pro-gramme content or mode of delivery (universalvs targeted) per se may be important mediatorsof outcome.

The effectiveness of universal prevention pro-grammes was investigated in a review of 12 studies[11]. The results were variable. Five showed signif-icant immediate post-intervention improvementson at least one measure of depression, but noneshowed any significant effects at follow-up (i.e. 12months or longer). The authors concluded thatthe widespread use of universal depression pro-grammes in schools would be premature. Theyadvocate that further research should be under-taken. The authors highlighted a number of issues,many of which were addressed in a recent ran-domized trial involving 5634 adolescents in whicha CBT-based intervention, ‘beyondblue’, was com-pared with no intervention [12]. ‘Beyondblue’was delivered by trained teachers and providedinterventions at individual, school and commu-nity levels. Individually adolescents learned skillsto improve problem-solving, social skills, resilientthinking and coping strategies. Within the schoolthe intervention aimed to build a supportive envi-ronment by improving social interactions and facil-itating access to support and professional services.Finally, community forums were provided in orderto facilitate a greater understanding of emotionalproblems and how to seek help. This multi-levelintervention, delivered over 3 years, failed to findany significant differences in depressive symptomswhen compared with the ‘no intervention’ group.This study provides a timely reminder of thedifficulties of implementing psychological inter-ventions in everyday settings.

Finally, Horowitz and Garber (2006) suggestthat evaluation of depression prevention researchhas focused upon demonstrating evidence oftreatment effects (i.e. reducing levels of depressivesymptoms) rather than on preventive effects, suchas a reduction in the emergence of new cases. Theirmeta-analysis of 30 studies found that selective andindicated programmes were more effective thanuniversal programmes. Only four studies providedany evidence suggesting a preventive effect [13].

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ANXIETY PREVENTION PROGRAMMES

The results of school-based anxiety preventionprogrammes are more consistent and encouraging.A recent review [14] identified 27 trials assess-ing 20 different programmes; 16 universal, eightindicated and three selective trials were evaluated.The majority (78%) were based upon CBT inter-ventions that were mainly led by mental healthpractitioners (44%) or teachers (26%). Only fourstudies included children under the age of 9 years.Seventy-eight percent of interventions reportedsignificant post-intervention reductions in symp-toms of anxiety, with universal and targeted pro-grammes being judged equally effective. Therewas considerable variability in effectiveness withinindividual programmes. Unlike depression preven-tion interventions, teacher-led anxiety preventioninterventions were equally as effective as those ledby mental health professionals. The authors sug-gest encouraging the widespread implementationof school-based anxiety prevention programmes,alongside rigorous evaluation of their longer-termoutcomes.

‘FRIENDS for life’ is one of the better evaluatedanxiety prevention programmes. The 10-sessionprogramme is based upon CBT and has versionsfor children (aged 7–11), youths (12–16) and morerecently for young children aged 4–6 years (FunFRIENDS). The programme is very engaging andinvolves a mix of large and small group work, roleplays, games, activities and quizzes, and teacheschildren skills in three main areas. Cognitively,children are helped to become aware of theiranxiety-increasing cognitions and to replace themwith more helpful and balanced cognitions. Emo-tionally, they are helped to understand the anxietyresponse and their unique physiological reactionto stressful situations. This helps children to detectearly signs of anxiety so that they can intervene tomanage and reduce these unpleasant feelings. Thefinal component addresses the behavioural domainand teaches children problem-solving skills andthe use of graded exposure to systematically faceand overcome their worries. FRIENDS can be ledby trained teachers or mental health practitionerssuch as school nurses or psychology graduates.

In addition to the child sessions, parents areinvited to two to four psycho-educational ses-sions. These help parents to understand anxietyand to develop strategies to cope with their own

anxiety. They are also taught problem-solving andthe principles of contingency management andreinforcement in which the child’s courageous andcoping behaviour is rewarded rather than theiranxious talk and problem avoidance.

Randomized controlled trials have demon-strated significant post-‘FRIENDS’ reductionsin anxiety, which have been maintained up to3 years after the intervention [15,16]. Similarly,the issue of effectiveness when delivered withineveryday settings has been assessed in a series ofsmall studies, with gains being present for up to 12months [17,18].

FUTURE DEVELOPMENTS ANDCHALLENGES

Whilst school-based prevention programmes offerthe potential to improve the psychological well-being of children, further research is requiredbefore their widespread implementation can beadvocated. Firstly, from a methodological view-point, sample sizes are often small, medium-termfollow-ups are lacking, and few have includedcomparisons with other active interventions. Moststudies have focused upon adolescents and fewhave been designed for, or included, childrenunder the age of 9 years. In terms of programmecontent, those based upon CBT, particularly foranxiety, show most promise although there areconsiderable differences between programmes inlength, core components and delivery. Variationsin effectiveness within similar programmes suggestthe importance of mediating factors relating toprogramme leaders (e.g. professional experience,training, rapport and confidence), students (e.g.age, gender, engagement) and schools (e.g. classsize, emotional health awareness and availablesupport).

Secondly, it is unclear whether preventive inter-ventions that are universal are more effective thantargeted interventions. Universal programmeshave the potential to maximize psychologicalwell-being. Typically such programmes aim toreduce symptoms, in addition to maintainingpsychological health. However, the focus ofevaluation has been on whether they reducesymptomatology, rather than on detailing whetherthey maintain emotional well-being and protectchildren from subsequent emotional healthproblems. The longer term primary preventive

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benefits of universal approaches need to beassessed alongside an economic evaluation todetermine the costs/benefits of such approaches.

Thirdly, integrating emotional health preven-tion programmes within schools poses many practi-cal issues that will impact upon their sustainability.In terms of effectiveness, most studies are effi-cacy trials, and the applicability and benefits ofthese programmes when delivered under less con-trolled everyday conditions are unclear. Flexibleprogrammes that can be delivered within the teach-ing timetable and within the length of the schoolsemester are required. In terms of programmeleaders, trained school staff appear to be effec-tive in delivering anxiety prevention programmesbut less so for depression programmes. Whetherdepression programmes require a higher level ofexpertise and understanding, or whether studentsare less willing to acknowledge or engage withteachers about more personal issues relating tolow mood requires further investigation. Attentionneeds to be paid to the skills and training of theprogramme leaders and the ongoing supervisionthat will be required to maximize effectiveness andmaintain intervention fidelity.

Finally, whilst there are a number of anxietyand depression prevention programmes available,very few have been subject to robust multipleevaluations by different research groups. Defin-ing the characteristics of effective and sustainableprevention programmes is important. Undoubt-edly these will include a number of factors suchas multi-level, developmentally sensitive, engaginginterventions that rest upon evidence-based con-ceptual frameworks. These need to be deliveredflexibly by appropriately trained and supervisedleaders and be consistent with the ideologies andpriorities of the schools involved [19].

REFERENCES

[1] Costello EJ, Mustillo S, Erkanli A et al. (2003)Prevalence and development of psychiatric disor-ders in childhood and adolescence. Archives ofGeneral Psychiatry 60, 837–44.

[2] Ford T, Goodman R, Meltzer H. (2003) The Britishchild and adolescent mental health survey 1999:the prevalence of DSM-IV disorders. Journal ofthe American Academy of Child and AdolescentPsychiatry 42, 1203–11.

[3] Kim-Cohen J, Caspi A, Moffit TE et al. (2003)Prior juvenile diagnoses in adults with mental dis-order: developmental follow-back of a prospective-longitudinal cohort. Archives of General Psychiatry60, 709–17.

[4] Woodward LJ and Fergusson DM. (2001) Lifecourse outcomes of young people with anxiety dis-orders in adolescence. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 40,1086–93.

[5] Ford T, Hamilton H, Meltzer H, Goodman R. (2008)Predictors of service use for mental health problemsamong British schoolchildren. Child and AdolescentMental Health 13, 32–40.

[6] Mrazek PJ and Haggerty RJ. (1994) ReducingRisks for Mental Disorders: Frontiers for PreventiveIntervention Research. Washington, DC: NationalAcademy Press.

[7] Adi Y, Killoran A, Janmohamed K et al. (2007)Systematic Review of the Effectiveness of Interven-tions to Promote Mental Wellbeing in Children inPrimary Education. Report 1: universal approaches(non-violence related outcomes). London: NationalInstitute for Health and Clinical Excellence.

[8] Shucksmith J, Summerbell C, Jones S et al. (2007)Mental Wellbeing of Children in Primary Education(Targeted/Indicated Activities). London: NationalInstitute for Health and Clinical Excellence.

[9] Merry S, McDowell HM, Hetrick S, Bir Jet al. (2004) Psychological and/or educational inter-ventions for the prevention of depression in childrenand adolescents. Cochrane Database of System-atic Reviews Issue 2; Art. No.: CD003380; doi:10.1002/14651858.CD003380.pub2.

[10] Calear AL and Christensen H. (2010) System-atic review of school-based prevention and earlyintervention programs for depression. Journal ofAdolescence 33, 429–38.

[11] Spence SH and Shortt AL. (2007) Research review:can we justify the widespread dissemination of uni-versal, school based interventions for the preventionof depression amongst children and adolescents?Journal of Child Psychology and Psychiatry 48,526–42.

[12] Sawyer MG, Pfeiffer S, Spence SH et al. (2010)School-based prevention of depression: a ran-domised controlled study of the beyondblue schoolsresearch initiative. Journal of Child Psychology andPsychiatry 51, 199–209.

[13] Horowitz JL and Garber J. (2006) The preventionof depressive symptoms in children and adolescents:a meta-analytic review. Journal of Consulting andClinical Psychology 74, 401–15.

[14] Neil AL and Christensen H. (2009) Efficacy andeffectiveness of school based prevention and early

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intervention programmes for anxiety. Clinical Psy-chology Review 29, 208–15.

[15] Lowry-Webster H, Barrett P, Lock S. (2003) A uni-versal prevention trial of anxiety symptomatologyduring childhood: Results at one-year follow-up.Behaviour Change 20, 25–43.

[16] Barrett PM, Farrell L, Ollendick TH et al. (2006)Long-term outcomes of an Australian universalprevention trial of anxiety and depression symp-toms in children and youth: an evaluation of theFRIENDS programme. Journal of Clinical Childand Adolescent Psychology 35, 403–11.

[17] Stallard P, Simpson N, Anderson S et al.(2008) The FRIENDS emotional health prevention

programme: 12 month follow-up of a universal UKschool based trial. European Journal of Child andAdolescent Psychiatry 17, 283–9.

[18] Stallard P, Simpson N, Anderson S et al. (2007)The FRIENDS emotional health programme: initialfindings from a school based project. Child andAdolescent Mental Health 12, 32–7.

[19] Giesen F, Searle A, Sawyer M. (2007) Identify-ing and implementing prevention programmes forchildhood mental health problems. Journal of Pae-diatrics and Child Health 43, 785–9.

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Fostering resilience in adolescents

14Fostering Resilience in AdolescentsAngela VealeSchool of Applied Psychology, University College Cork, Ireland

WHAT’S NEW

• There has been a shift from looking at variables correlated with resilient outcomes andprocesses such as attachment and support networks to understanding individuals dealingwith adversity within resilient systems.

• There is an increasing understanding of the importance and role of cultural processes.

• Future directions will integrate multidisciplinary knowledge gained from genetics,neuropsychology and cultural psychology about resilience in the developing individual.

• New forms of intervention are moving from promoting resilient individuals to mobilizingbasic protective systems at the individual, family, community and organizational level.

• ‘Prevention science’ seeks to prevent or limit damage at all levels of resilience-supportingsystems.

INTRODUCTION

There is increasing social concern about ‘outof control’ adolescents who exhibit challengingbehaviour. Many who come to the attentionof the mental health system have experiencedmultiple adversities in their lives, such as poverty,chaotic parenting, residential care, foster care orschool expulsion. They live in systems that lacksupportive capacity and are resource impover-ished. Significantly, these adolescents are alsodifficult to engage in therapeutic interventions,particularly because of a fear of stigmatization.There is a developmental challenge inherent inthis situation – the health-seeking part of thepsyche is outward looking, and strives towards


self-efficacy and autonomy; yet the prospect ofengaging in therapy may reinforce unconsciousfears of being ‘mad’ or a ‘psycho’.

A traditional clinical approach to this groupof young people would be that of healing psy-chopathology. Fostering resilience offers an alter-native lens and involves a fundamental shift from adeficits perspective, focused on individualized neg-ative functioning and vulnerability, to a dynamicsystems, strengths-based, participative orientation.This chapter outlines new theoretical resilienceframeworks and links them to a psychothera-peutically informed participatory action researchproject with ‘hard to reach’ adolescents in anexploration of how resilience can be fostered inpractice and community settings.

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WHAT DO WE MEAN BY RESILIENCE?

Resilience can be defined as ‘patterns of positiveadaptation during or following significant adversityor risk’ (Masten et al. [1], p. 118). The definitionrequires two judgements – first, that the exposureto risk or adversity was serious enough to posea serious threat to healthy development; second,that the individual subsequently meets age-relateddevelopmental tasks. Within this framework, therehas been a focus characterizing resilient outcomesas individual variables (e.g. effective problem-solving skills, emotional self-regulation, positiveparenting) or processes (e.g. attachment patterns,family and community interactions). One of themost significant shifts in resilience science overthe past decade has been a new emphasis onresilient systems. Here, resilience is seen to bemediated by risks, protective factors and resourcesat multiple levels ranging from the molecularneurobiological to the social, cultural and polit-ical [2]. An illustration is provided by analy-ses of resilience to trauma and stress. One ofthe most consistent research findings has beenthat close emotional relationships and support-ive informal and formal social networks fosterresilience [1,3,4]. Neurobiological research indi-cates that emotional support of this kind canreduce uncertainty and stress by impacting uponthe hypothalamic–pituitary–adrenal (HPA axis)and the sympathetic nervous system, which regu-late cortisol levels. This in turn enhances copingvia an impact on brain regulatory systems thatcontrol arousal and thus behavioural and cognitiveresponses to stress [5] (see Chapter 20). Mastenand colleagues suggest that systems operate atmultiple levels and include powerful motivationalsystems such as the mastery system as well asrelational systems at the level of family, commu-nity and society, and that the greatest threat tochildren’s resilience may be adversities that dam-age or undermine these basic human protectivesystems [1].

Agency in resilienceOf course, cultures influence definitions ofresilience, and this is explored in Ungar’s multi-country resilience project [6,7]. In many cultures,psychological explanatory models of distress areuncommon, and causality is more likely to beattributed to external social or structural factors.

For Ungar, therefore, resilience involves boththe capacity of individuals to navigate theirway to obtaining health-sustaining resources(including opportunities to experience feelings ofwell-being) and the capacity of the individual’sfamily, community and culture to provide theneeded resources and experiences in a way that isculturally meaningful [6].

Mobilizing social networks to foster copingand resilienceA further useful analysis of how social relation-ships foster resilience is provided in the SocialConvey model [8]. Social convoys are the multiplerelationships in the lives of children and youngpeople that facilitate the exchange of affectivesupport, self-affirmation and direct aid. Impor-tantly, the model extends the concept of attach-ment relationships to other close relationships andacknowledges that relationships between adultsand children are characterized by mutuality of sup-port and social exchange. That is, in adult–childrelationships, children and youth have the capac-ity both to give and to receive nurturance andsupport, and furthermore this is a powerful moti-vational force in relationship formation and main-tenance. The model is strengths-based as it positsan engaged young person who is active in recipro-cal support relationships. This may be particularlyrelevant for adolescents engaged in the devel-opmental task of negotiating a balance betweenautonomy and relatedness in relationships [9].

IMPLICATIONS FOR POLICY AND PRACTICE

The models outlined above indicate the impor-tance of supporting the agentive, help-seeking,mastery-oriented capacities of young people asthey negotiate the support needed from thosearound them. Several challenges face practitionersif these models are to be successfully applied.Practitioners need to foster adolescents’ capac-ities for: mobilizing adaptive support systems;negotiating access to resources for healthy growthand development; and participating in socialconvoys characterized by reciprocal supportiverelationships. They need also to foster resiliencein situations when adolescent support systemsmay be damaged, unsupportive or unavailable,as is often the case with the families of ‘hardto reach’ adolescents. Finally, they need to shift

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Box 14.1 Promoting resilience — a participatory action research (PAR) project.

PAR projectphases

Description Fostering resilience

Phase 1:Definingparticipation;question-posing;data gathering;analyses

Twelve weeks of creative artsworkshops facilitates:

• Exploration of participants’experiences with police, youthjustice and social integration

• Identification of priority issues

• Opportunities to socialize

• Exploration of important themes

• Meeting key policy-makers todiscuss priority issues

• Choice of social action project

Sharing of daily hassles anddifficulties, and co-constructed artresults in:

• Enhanced emotional regulation

• Communication skills

• Information-processing

• Behaviour respectful of groupmembers and facilitators

Phase 2:Planning a socialaction

• Control of budget line

• Plan and implement social actionproject

• Choose method of action anddissemination (produce a DVD)

• Develop trust in their ownershipof key project decisions

• Enhanced motivation

• Enhanced reflective capacity

• Responsible participation

Phase 3:Implementingsocial action

Skills development culminating ingirls’ DVD production ‘Girls OutLoud’, including:

• Undertaking socialaction — visiting other relevantprojects to learn aboutconsultation with ‘key’ players,e.g. politicians and communityleaders

• Make videos of project visits

• Interview other young people insocial projects

• Use interviewing skills in visit topolitical representatives inParliament Buildings, NorthernIreland Assembly

• Identification of further researchquestions and themes

• Design and art skills — videoingand photography; drawing;storylines; animated puppetshows; video editing

The production of the storylinesand DVD mobilized:

• Individual and collective mastery

• Confidence and self-esteem

• Persistence in the face of doubtand difficulty

• More powerful voice (makingoneself heard)

• Effective communication

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PAR projectphases

Description Fostering resilience

Phase 4:Analysis,reflection anddissemination ofproject findings

Present DVD and discuss issuesabout the justice and care systemswith:

• Ombudsman for Children

• Garda Juvenile Diversion service

• local police

• local school

• local communities

Subsequently local youthorganization starts participationinitiative, consulting with parents.Our project participants:

• train staff

• develop consultation work withparents

Changes in:

• Perspective-taking andinter-subjectivity

• Ability to adopt the perspectiveof the ‘other’ in theircommunications

away from an emphasis on internal psychologicalprocesses and clinician/patient-defined interven-tions, and become one part of the adolescent’s totalresilience system. In practice, this means initiatingprocesses that facilitate young people in definingtheir own needs, priorities and best interests and inmobilizing their social networks and communitiesto support them as they address those needs.

MOBILIZING RESILIENCE: ANILLUSTRATIVE EXAMPLE

Here I outline a participatory action research(PAR) social integration project with nine girls(aged 12–18 years), half of whom had receivedformal cautions from the police, and who hadalso been referred to an intensive support ser-vice for young people in crisis. A number werein foster or residential care, and some had actu-ally been ejected from the latter. The remainingparticipants were community peers without formalcontact with the police and who were not in crisis.Facilitator participants included a psychotherapist,a creative artist, and two peer researchers from the

same community. The author, a psychologist, wasprincipal investigator.

Summary of the projectThe intervention project unfolded in three phasesover 24 weeks (Box 14.1). It took the formof weekly creative arts workshops in whichexperiences of police, youth justice and socialintegration were explored. We anticipated that thegirls would undertake a leading role in planningand decision-making: they would choose the artmedium to work in; they would choose, design andimplement a social action project that reflectedtheir primary issues of concern; they wouldcontrol an allocated budget for their project.Throughout, the girls interacted with the outsideworld in ways determined by them – for instance,through visits to other social projects and meetingpoliticians, community leaders and other keyactors to question them about matters of concern.Their final social project – a DVD outlining theirissues with the justice and care systems, andsocial integration – was presented to Ireland’sOmbudsman for Children, senior members of the

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Garda Juvenile Diversion service, local police,schools and community organizations.

Implementing the projectSome of the developmental stages of this projectare outlined below.

• Getting the girls to engage with the project wasa key challenge – their experiences of feelingpowerless and unheard within the social careand justice systems were evident in an earlycomment by one young participant:

If you feel you’re not being heard, there’s nopoint, you feel there is no point in yourselfmaking progress

Such experiences fed into a manifest reluctanceto join in early workshop sessions. It was clearthat the girls felt they had nothing to contributeand found it hard to imagine a project directedby them without adults structuring and control-ling it. We tried engaging them in various ways.For instance, we included a drumming sessionto provide structure and focus while participantslearned about the project and each other. It wasdifficult to get them to drum making audiblesounds. It often seemed as if the young peoplewould disengage with the project and that itwould be impossible for the group to find direc-tion. This was evidenced in late arrivals, muchleaving and returning to the room and a lot ofmobile phone texting.

• The need to step back and leave the controland ownership of the project in the girls’ handsquickly became apparent, and gradually theybecame more engaged. For instance, they swiftlyassumed control of choosing and ordering theend of session food; they developed their ownrules for group meetings, including that mem-bers needed to arrive ahead of time so theycould chat together before the group meetingstarted; they chose the sessional art medium theywould use. First, however, they ‘interviewed’the group’s creative artist, seeking informationabout his work, examining examples of it, andasking questions. The group agreed that he was‘sound’ and they could work with him.

• Emerging group level properties graduallybecome evident as the girls chose art activities,

exchanged helpful ideas and began to workalongside each other.

• Individual and collective mastery developed. Ini-tially, participants were reluctant to use the artsmaterials – one was so inhibited at the start thatthe creative artist held her hand to scaffoldher early drawing attempts. A ‘transformational’came when the creative artist used the clay char-acters that participants had made in a previoussession to make an animated computer film.This created great enthusiasm and excitement.From then on, participants’ assurance in theircontribution to the group grew.

• A sense of ownership of the group had developedby session 6: members arrived on time, theyreminded each other to turn off mobile phonesand they more obviously helped each other, par-ticularly if someone had missed a session. Therewas a sense of focus and flow. The group assumedsignificant responsibility for managing their ses-sion. One asked ‘how many weeks have weleft?’ indicating how they valued the space. Onerequested that no new people should be allowedto join as ‘this is the group now’. Over the next 6weeks, their creative work and discussion abouttheir lives opened up. They developed a puppetshow and took charge of developing storylines.They began photographing their work.

• Participants underwent remarkable changes asthey gained in confidence, self-esteem and opti-mism. Emotional control and regulation becameapparent – in particular, inhibition of disruptivebehaviour. They showed the capacity to planand think ahead. Relationships between groupmembers and with the facilitators came to becharacterized by reciprocity and commitment tothe achieving group aims.

• Mobilizing supportive resilience systems flowedfrom the girls’ progress and development. Asthey moved from being angry and antagonis-tic towards authority figures, such as the ‘pigs’(police), they were able to engage construc-tively in discussions with them. Their new foundability to tolerate multiple perspectives (theirsand those of the police) and increased maturitymeant that when they showed their DVD tolocal police, their schools and local communityprojects, they were mobilizing supportive rela-tionships that would enhance resilience withintheir immediate microsystems.

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CONCLUSIONSpecific examples of the girls’ enhanced resilientcapacities are outlined in Box 14.1. In summary,our experience gained through this project hasshown us that fostering resilience with ‘hard toreach’ adolescents means giving them a good orpositive experience of power, control, ownershipof decision-making and resource management in away that stimulates their feelings of mastery (theirmastery system). They gain a sense that they areable to impact on their world in ways that arechosen by them and meaningful to them, and thatthey can actively mobilize others to support them(Box 14.2). These processes, so important in devel-oping resilience when in difficult circumstances,may inadvertently be undermined by many of ourmore traditional clinical practices. As researchersand practitioners, our moment of enlightenmentin this project came when the young people toldthe Irish Ombudsman for Children ‘This was ourproject’ and their sense of ownership was publiclycelebrated and claimed.

Box 14.2 Implications for clinicalpractice

Fostering resilient systems adds multiplelayers of complexity to clinical practice.It also positions the clinician and men-tal health organization as one element ofthe adolescent’s resilience system. Withinthat, what is the role of clinicians in fos-tering resilience in the system?

REFERENCES

[1] Masten AS, Cutuli JJ, Herbers JE et al. (2009)Resilience in development. In: Snyder CR and LopezSJ (eds), Oxford Handbook of Positive Psychol-ogy, 2nd edn. Oxford: Oxford University Press, pp.117–31.

[2] Masten AS and Obradovic J. (2008) Disaster prepa-ration and recovery: Lessons from research onresilience in human development. Ecology andSociety 13, 9–; available online at: http://www.ecologyandsociety.org/vol13/iss1/art9/.

[3] Luthar SS and Brown PJ. (2007) Maximizingresilience through diverse levels of inquiry: Prevailingparadigms, possibilities, and priorities for the future.Development and Psychopathology 19, 931–55.

[4] Dolan P. (2008) Prospective possibilities for buildingresilience in children, their families and communities.Child Care in Practice 14, 83–91.

[5] Ozbay F, Fitterling H, Charney D et al. (2008) Socialsupport and resilience to stress across the life span: aneurobiologic framework. Current Psychiatry Report10, 304–10.

[6] Ungar M. (2008) Resilience across cultures. BritishJournal of Social Work 38, 218–35.

[7] Ungar M. (2010) Cultural dimensions of resilienceamong adults. In: Reich JW, Hall JS, Zautra AJ(eds), Handbook of Adult Resilience. New York:Guilford Press, pp. 404–23.

[8] Levitt MJ. (2005) Social relations in childhood andadolescence: The convoy model perspective. HumanDevelopment 48, 28–47.

[9] Mahler MS. (1977) Separation-Individuation:Selected Papers of Margaret S. Mahler. New York:Aronson.

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Section 3

Attachment andSeparation

Attachment and separation

15Attachment Theory: Researchand Clinical ImplicationsPasco FearonResearch Department of Clinical, Educational and Health Psychology, University College London,London, UK

WHAT IS ATTACHMENT?

Broadly speaking, attachment refers to the ten-dency, particularly but not exclusively, of infantsand young children to rely on a parent figure forcomfort and support when frightened, stressed orill. It is thought to be a form of biobehaviouraladaptation, shaped by the forces of natural selec-tion to maximize survival and eventual repro-duction, and the key features of attachment aresimilar across many mammalian species, particu-larly the higher primates. The field of attachmentowes much to John Bowlby [1], who articulatedan evolutionary account of attachment, and MaryAinsworth [2], who pioneered its study in natural-istic contexts.

It is important to distinguish between attach-ment behaviour and an attachment bond. It isgenerally recognized that one cannot classify abehaviour as an attachment behaviour from itsoutward appearance alone. Instead, attachmentbehaviours are defined as such by recognizing theirfunction. They are thus any organized, systematicbehaviour that is triggered by the appearance ofa potential threat or stressor and that predictablyserves to achieve proximity to a selected caregiver[3]. This means that all manner of behaviours canserve the general purpose of achieving comfortand security for children, and some may be quiteidiosyncratic to a particular child.

Attachment behaviours generally are dividedinto three classes: (i) signalling or distal


communication (e.g. calling, crying); (ii) proximityseeking (e.g. crawling, walking, reaching) and (iii)contact maintenance (e.g. clinging). Monitoringthe whereabouts and availability of an attachmentfigure may also be described as attachmentbehaviour. Attachment is characterized byheterotypic continuity, meaning that while it evi-dences continuity over time in its basic functionalorganization, the specific child behaviours usedto achieve comfort or security change radicallyin complexity and sophistication as childrenmature [4].

Thus, attachment behaviour performs a kind ofhomeostatic function (Figure 15.1), and to oper-ate efficiently it needs to be guided by informationabout the environment, for example the nature andlocation of the threat, the caregiver’s whereabouts,and contextual information as to the potentialefficiency of various forms of action, etc. Devel-oping this idea, Bowlby proposed that duringrepeated experiences within an attachment rela-tionship, children develop internal working modelsof attachment that guide their thinking, feeling andbehaviour in attachment situations, and this shapesthe way they approach close relationships – andsee themselves within them – in the future.

An attachment bond [5] refers to the longer-term, stable tendency to seek out a selected parentfigure in times of stress. The processes that lead tothe establishment of a long-term attachment bondare quite different to those that trigger attachmentbehaviour. Crucially, certain forms of disturbance

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Attachment theory: research and clinical implications

Perceived threat Attachment system

Contact (physical or psychological)

Proximity seeking

Explorationreduces

reduces

Figure 15.1 Schematic diagram of the homeostatic function of attachment.

in attachment probably result from disruptions inthe formation of attachment bonds (e.g. disinhib-ited attachment disorder), while others result fromexperiences or influences that alter how attach-ment behaviour is organized and triggered (e.g.disorganized attachment).

ATTACHMENT VARIATIONS AND THEIRMEASUREMENT

Normative attachment patternsMary Ainsworth’s Strange Situation Procedure isthe most commonly used tool for studying attach-ment behaviour [2]. Involving an encounter with astranger and 2–3-minute separations from a par-ent in an unfamiliar setting, it is used with infantsaged approximately 11–18 months. The reliableand valid Ainsworth coding system quantifies fourdimensions of attachment behaviour, each ratedon a seven-point scale. It also enables raters tomake categorical judgements about the style orclassification of attachment behaviour displayedby individual children (Table 15.1). These divideinto two broad classifications – ‘secure’ (Type B)and three types of ‘insecure’ attachment: Type A(Avoidant), Type C (Resistant) and Type D (Dis-organized). These classifications have become amajor focus of research, with findings indicatingthat the majority of infants in low-risk circum-stances (approximately 65%) are described as‘secure’; approximately 15% as Avoidant; 10%as Resistant and 15% as Disorganized. It is this

latter category that has attracted the most atten-tion clinically, as it appears most closely related tomore severe forms of adverse parental care, and toraised risk of psychopathology [6]. The prevalenceof the different insecure subtypes varies consider-ably across cultures [7]. A host of similar measureshave been developed for assessing attachment inolder children [8].

CAUSES OF VARIATION IN ATTACHMENT

Ainsworth originally proposed that the extentto which the parent was sensitive and responsiveto the child’s attachment signals was the criticaldeterminant of attachment security (see Table 15.2for exemplars of sensitivity) [2]. Since then, thishypothesis has been supported by an impressivedatabase of longitudinal studies [9]. Furthermore,randomized controlled trials of clinical interven-tions designed to improve sensitive parenting havebeen shown to increase the likelihood of secureattachment, suggesting the association is a causalone [10]. However, many authors have noted thatthe effect sizes in correlational studies or clinicaltrials are not large and that other factors – eitherdifferent aspects of parenting or different typesof causal influence altogether – probably playa role. While sensitive care may be thought ofas the most important proximal determinant ofattachment security, a host of more distal orcontextual factors also appear to be consistentlyassociated with security and insecurity, includingparental depression, social support, marital quality

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Table 15.1 Attachment behaviour rating scales and classifications for the Strange SituationProcedure [2].

Interactive behaviour scales

Proximity seeking The intensity and persistence to make contact on reunion withthe caregiver. An infant scoring high on this scale makes apurposeful approach to the caregiver and takes initiative tomake contact

Contact maintenance The persistence in maintaining contact with the caregiver once itis achieved. A high score on this scale is given when an infantdisplays resistance to being put down (e.g. clinging), persistentefforts to remain close to the caregiver, or any sign the infant isnot ready to terminate contact (e.g. a sinking embrace tomother)

Resistance The intensity and duration of angry behaviour and resistance ofcontact directed towards the caregiver. Examples includepushing away, batting away, arching back, squirming to get down

Avoidance The intensity, duration and promptness of attempts to avoidcontact/interaction with the caregiver. Examples of avoidanceare averting gaze, moving away and ignoring the caregiver

Disorganized/ disoriented Anomalous behaviour, e.g.: sequential or simultaneous displaysof contradictory behaviour; undirected, misdirected orincomplete behaviours; stereotypies, freezing, disorientation;fearful responses in presence of the caregiver

Infant attachment classification profiles

Secure Secure infants use the caregiver as a secure base for explorationand as a source of comfort when needed. The infant is visiblyaware of the caregiver’s absence at separation. At reunion, theinfant greets the caregiver with an approach, smile, gesture orvocalization and seeks contact with the caregiver if distressed.Contact is comforting and infant is able to return to play

Insecure-Avoidant An avoidant infant appears to be more interested in theenvironment than the caregiver throughout the procedure.During separation from the caregiver the infant is typically notupset. Upon reunion, the infant will ignore or actively avoidcontact

Insecure-Ambivalent An ambivalent infant prefers to maintain contact with thecaregiver than to explore the environment, or exploration islimited. During separation the infant will be distressed. Atreunion the infant displays angry behaviours towards thecaregiver and/or is inconsolable. Contact with the mother is noteffective in regulating the infant’s state or supporting a return toplay

Insecure-Disorganized The infant’s behaviour lacks an organized, coherent strategy inrelation to the caregiver. See above for behavioural descriptions

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Table 15.2 Scales of parenting sensitivity and frightened/frightening behaviour.

Maternal sensitivity scales [2]

Sensitivity vs insensitivity The degree to which the infant cues are perceived, responded topromptly and appropriately. A sensitive parent is able to empathizewith the infant’s experience, promoting accurate interpretation ofthe infant’s cues, resulting in appropriate and flexible responding

Cooperation vs interference The degree to which participation in the infant’s ongoingexperience is gentle, co-determined and supportive, rather thanharsh, overwhelming, directive or controlling

Availability vs neglecting The degree to which the parent is physically and psychologicallyavailable to his/her infant. An available parent is perceptually alertand responsive to the infant even in the face of distraction orhis/her own thoughts and feelings

Acceptance vs rejection The degree to which the parent is able to integrate the joys andstresses of being a parent, as expressed in her/his behaviour towardthe child. An accepting parent will not direct, nor attribute negativefeelings towards their child or become irritable, enabling her/himto maintain a positive and accepting stance towards the infant

Anomalous parenting behaviours [14,15]

Frightened or frighteningparental behaviours

Behaviours towards the infant that are: threatening, dissociative(e.g. ‘spacing out’), frightened, timid/deferential,spousal/romantic or disorganized

Disrupted affectivecommunication

Behaviours that when displayed, particularly during times of stress,can result in unmodulated fear/arousal in the infant (e.g.contradictory signalling to the infant about the caregiver’savailability, failure to respond to infant cues; displays that thecaregiver is frightened by the infant; hostile/intrusive behaviours;dissociative and withdrawing behaviour)

and poverty [11]. Importantly, evidence indicatesthat genetic factors play a quite limited role inthe development of attachment in infants andpreschoolers (see, e.g., Ref. [12]).

Disorganized attachment has a quite differentset of determinants than the other insecurecategories. Critically, maltreatment has beenconsistently linked with Disorganized attachment[13]. Furthermore, in populations where ratesof maltreatment are likely to be low, observedsensitivity (or insensitivity) appears not to bea critical factor [13]. Instead, a quite differentset of parenting features has been implicated,representing behaviour that has been describedas frightened/frightening or extremely insensitive

[14] (Table 15.2). Aside from the great clinicalsignificance of these findings, they also providesupport for an intriguing theory about the causesof disorganized attachment behaviour originallyproposed by Main and Hesse [15]. They arguedthat the incoherent behaviour seen in disorgani-zation occurs when the parent is the source ofboth comfort and threat. This is thought to createan irreconcilable approach–avoidance conflict,which causes disruptions in attachment behaviour(see Table 15.1), as two incompatible tendenciescompete for control of behaviour. The data onfrightening parenting and maltreatment bear thisidea out well, although the precise mechanismsjust described have never been directly verified.

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Attachment disordersDisorders of attachment have been found whenchildren have experienced either the completeabsence of a consistent carer, severe maltreatmentor major disruption in the continuity of care – asin children raised in institutional or foster care.A significant number of children raised in suchcircumstances show quite pervasive patterns ofdisturbed social relatedness, collectively referredto as reactive attachment disorders (RAD).The current diagnostic systems – the Diagnosticand Statistical Manual of Mental Disorders IV,Fourth Edition – Text Revision (DSM-IV-TR)and the ICD-10 International Classification ofMental and Behavioural Disorders in Childrenand Adolescents (ICD-10) – define two types ofRAD. The first, known as the inhibited/withdrawntype, is marked by extreme withdrawal, a lack ofa clearly preferred attachment figure, a pervasivetendency not to seek comfort from others whendistressed, and a lack of social responsiveness orreciprocity. The second, known as the disinhibitedtype, by contrast is marked by indiscriminateattachment behaviour and friendliness and a lackof wariness of strangers (e.g. wandering off withstrangers). There are a number of tools for assess-ing attachment disorders and related behaviours,including standardized questionnaires, interviewsand observation schemes [16].

It is critical to note that RADs are quite dis-tinct from the normative patterns of attachmentdescribed in the previous section, both in terms ofthe behaviours that define them and the circum-stances that appear to give rise to them. Existingevidence suggests that normative attachment pat-terns represent variations in the organization ofattachment related to the style or quality of parent-ing among children who have formed one or moreselective attachment bonds. In contrast, disinhib-ited attachment disorder most likely represents thefailure of the establishment of a selective attach-ment bond in the first place [6]. The picture is alittle less clear for the inhibited-type attachmentdisorder, but it may occur when a child is ableto form some selective attachment bonds that aresubsequently severely disrupted.

CONSEQUENCES OF VARIATIONS INATTACHMENT

Early attachment relationships are thought to exerta significant and important influence on current

and later relationships, well-being and psycholog-ical health. Longitudinal research suggests thatsecurely attached children may have developmen-tal advantages over their insecure counterpartsin areas such as emotional regulation and under-standing, social cognition, social competence andemotional/behavioural problems. While not allfindings have been consistently replicated, recentmeta-analyses have found robust associations withpeer relationships and externalizing problems[17,18]. With respect to the latter, the evidenceindicates that Disorganized children are the mostat-risk amongst the insecure subtypes [6,17].

The jury is still out on whether the effects ofearly attachment on later development representthe direct influence of early experience, or whethercontinuities over time in other intermediary pro-cesses (within the individual and in their envi-ronment) are responsible. Considerable evidencesuggests that some of the effects of insecurity fallinto this latter category. For example, continuityin the quality of care is associated with longi-tudinal links between attachment and outcome[19]. On the other hand, some findings do suggestthat early experience can have specific and lastingeffects, particularly severe early deprivation andits effect on disinhibited attachment disorder andaccompanying symptoms [6].

INTERVENTIONS

Two broad types of attachment interventions areapparent in the literature. The most widely usedare those in the realm of prevention. Here, theaim is to improve rates of secure attachment witha view to promoting resilience and reducing therisk for later emotional or behavioural problems.The second type of intervention focuses on chil-dren where attachment problems are primary, orof great clinical relevance – for instance, childrenwho have experienced maltreatment and may be infoster care, or late-placed national or internationaladoptees.

Preventive interventionsAn example of a highly successful preventive inter-vention is that conducted by van den Boom [20], inwhich 100 highly irritable neonates were allocatedat random to a treatment or control group. Homevisits to mothers and infants in the treatment groupfocused on maternal interaction skills, encouraging

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mothers to respond appropriately to their infant’scues, encouraging soothing in response to infantdistress, and increasing playful interactions. Largepositive effects on maternal sensitivity, and oninfant attachment security, were found and thesewere maintained at a 3.5-year follow-up. A meta-analysis of interventions aiming to increase mater-nal sensitivity and promote secure attachment inlow-risk community samples or at-risk clinical sam-ples (e.g. maternal postnatal depression) has beenundertaken [10]. The authors found that the mosteffective interventions were those that were:

• less than 16 sessions in length;• were behaviourally oriented and focused on

sensitivity (rather than support, or parental rep-resentations);

• targeted clinical populations;• began after age 6 months.

Critically, intervention effects on attachmentwere strongest when the intervention successfullyimproved sensitivity, and when the treatedpopulation had a large percentage of insecureinfants, suggesting, perhaps not surprisingly, thatappropriate targeting is important in achievingsuccessful outcomes. Sensitivity-based interven-tions have also been shown to be effective inreducing rates of Disorganization [21]. While themajority of interventions concern infants andtoddlers, some very promising treatments areavailable for preschoolers and older children(e.g. the Circle of Security programme; seeRef. [22]).

Interventions with fostered and adoptedchildrenA number of effective treatment packages havebeen devised that are specially tailored for fostercare and adoption (see also Chapter 17). Forinstance, the Attachment and BiobehaviouralCatch-Up programme is a 10-session multi-component intervention addressing mutualprocesses between parent and child that mayinterfere, directly or indirectly, with the child’sself-regulatory capacities and attachment. Theseinclude: parental interaction skills; parental attri-butions; and how the parental childhood historymay contribute to current parenting attitudesand behaviour. This approach has been foundto improve attachment behaviour and normalize

stress patterns as indicated by the hormonecortisol [23].

CONCLUSIONS

The study of attachment has highlighted the poten-tial importance of understanding the early rela-tional roots of both adjustment and maladjustment.The field has also focused attention on how oneobserves and measures attachment and the some-times subtle interactional processes that take placewithin parent–child relationships. Critically, thishas led to the development of a range of quite effec-tive treatment techniques designed to enhance thesecurity of attachment relationships in early life.The long-term effectiveness of such treatments forreducing risk for psychopathology and promotingresilience remains to be fully established, and is animportant area for future clinical research.

REFERENCES

[1] Bowlby J. (1969) Attachment and Loss, Vol. 1:Attachment. London: Hogarth Press/Institute ofPsycho-Analysis.

[2] Ainsworth MDS, Blehar MC, Waters E et al. (1978)Patterns of Attachment: A Psychological Study of theStrange Situation. Hillsdale, NJ: Lawrence Erlbaum.

[3] Cassidy J. (2008) The nature of the child’s ties. In:Cassidy J and Shaver PR (eds), The Handbook ofAttachment: Theory, Research and Clinical Applica-tions, 2nd edn. New York: Guilford Press, pp. 3–22.

[4] Marvin RS, Britner PA. (2008) Normative devel-opment: the ontogeny of attachment. In: CassidyJ and Shaver PR (eds), The Handbook of Attach-ment: Theory, Research and Clinical Applications,2nd edn. New York: Guilford Press, pp. 269–94.

[5] Ainsworth MDS. (1991) Attachments and otheraffectional bonds across the life cycle. In: Parkes CMand Stevenson Hinde J (eds), Attachment Acrossthe Life Cycle. London: Tavistock/Routledge,pp. 33–51.

[6] Rutter M, Kreppner J, Sonuga-Barke E. (2009)Emanuel Miller Lecture: Attachment insecurity,disinhibited attachment, and attachment disorders:where do research findings leave the concepts? Jour-nal of Child Psychology and Psychiatry 50, 529–43.

[7] Van Ijzendoorn MH, Kroonenberg PM. (1988)Cross-cultural patterns of attachment: A meta-analysis of the strange situation. Child Development59, 147–56.

[8] Solomon J, George C. (2008) The measurementof attachment security and related constructs in

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infancy and early childhood. In: Cassidy J andShaver PR (eds), The Handbook of Attachment:Theory, Research and Clinical Applications, 2ndedn. New York: Guilford Press, pp. 383–416.

[9] De Wolff M and van Ijzendoorn MH. (1997) Sensi-tivity and attachment: A meta-analysis on parentalantecedents of infant attachment. Child Develop-ment 68, 571–91.

[10] Bakermans-Kranenburg MJ, van Ijzendoorn MH,Juffer F. (2003) Less is more: meta-analyses ofsensitivity and attachment interventions in earlychildhood. Psychological Bulletin 129, 195–215.

[11] Belsky J and Fearon RP. (2008) Precursors ofattachment security. In: Cassidy J and ShaverPR (eds), The Handbook of Attachment: Theory,Research and Clinical Applications, 2nd edn. NewYork: Guilford Press, pp. 295–316.

[12] Bokhorst CL, Bakermans-Kranenburg MJ, FearonRM et al. (2003) The importance of shared envi-ronment in mother-infant attachment security: abehavioral genetic study. Child Development 74,1769–82.

[13] van-Ijzendoorn MH, Schuengel C, Bakermans-Kranenburg MJ. (1999) Disorganized attachmentin early childhood: Meta-analysis of precursors,concomitants and sequelae. Development andPsychopathology 11, 225–49.

[14] Lyons-Ruth K, Bronfman E, Parsons E. (1999)Atypical attachment in infancy and early childhoodamong children at developmental risk. IV. Maternalfrightened, frightening, or atypical behavior and dis-organized infant attachment patterns. Monographsof the Society for Research in Child Development 64,67–96; discussion 213–20.

[15] Main M and Hesse E. (1990) Parents’ unresolvedtraumatic experiences are related to infant disorga-nized attachment status: Is frightened and/or fright-ening parental behavior the linking mechanism?In: Greenberg MT and Cicchetti D (eds), Attach-ment in the Preschool Years: Theory, Research,

and Intervention. The John D and Catherine TMacArthur Foundation series on Mental Health andDevelopment. Chicago, IL: University of ChicagoPress, pp. 161–82.

[16] O’ Connor T and Byrne G. (2007) Attachmentmeasures for research and practice. Child and Ado-lescent Mental Health 12, 187–92.

[17] Fearon RP, Bakermans-Kranenburg MJ, vanIjzendoorn MH et al. (2010) The significance ofinsecure attachment and disorganization in thedevelopment of children’s externalizing behavior: ameta-analytic study. Child Development 81, 435–56.

[18] Schneider BH, Atkinson L, Tardif C. (2001) Child-parent attachment and children’s peer relations: aquantitative review. Developmental Psychology 37,86–100.

[19] Belsky J and Fearon RM. (2002) Early attachmentsecurity, subsequent maternal sensitivity, and laterchild development: does continuity in developmentdepend upon continuity of caregiving? Attachmentand Human Development 4, 361–87.

[20] van den Boom DC. (1995) Do first-year interven-tion effects endure? Follow-up during toddlerhoodof a sample of Dutch irritable infants. Child Devel-opment 66, 1798–816.

[21] Bakermans-Kranenburg MJ, van IJzendoorn MH,Juffer F. (2005) Disorganized attachment and pre-ventive interventions: a review and meta-analysis.Infant Mental Health Journal 26, 191–216.

[22] Hoffman KT, Marvin RS, Cooper G et al. (2006)Changing toddlers’ and preschoolers’ attachmentclassifications: the Circle of Security intervention.Journal of Consulting & Clinical Psychology 74,1017–26.

[23] Fisher PA, Gunnar MR, Dozier M et al. (2006)Effects of therapeutic interventions for foster chil-dren on behavioral problems, caregiver attachment,and stress regulatory neural systems. Annals of theNew York Academy of Sciences 1094, 215–25.

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Children bereaved by parent or sibling death

16Children Bereaved by Parentor Sibling DeathLinda DowdneyInstitute of Child Health, University College London, London, UK

Bereaved children grieve in similar ways tobereaved adults, reporting shock and disbelief,followed by sadness, anger, a longing for thedead person to return, and difficulties withconcentration, sleeping and eating [1].

CHILDREN’S UNDERSTANDING OF DEATH

There is a developmental progression in chil-dren’s understanding that death is permanent,irreversible and implies the complete cessationof bodily function. Preschoolers believe, and actas if, a dead person can return. Until the age of 7years, children believe their thoughts and feelingscan cause or reverse death. Around the age of 11years, when the concept of death is fully under-stood, children cease worrying about the deceasedbeing cold or lonely, although they imagine anafterlife where the dead remain sensate and enjoyfavourite activities. This can comfort some chil-dren who believe their dead parent ‘watches over’or cares for them. Adolescents can be troubled bythe unfairness of death and existential questionsas to the meaning of life [2]. A full understandingof the concept of death is acquired faster in cogni-tively and verbally able children or those who haveknown a person die previously.

HOW CHILDREN EXPRESS GRIEF

The ability of children to distract themselves fromgrief through normative activities such as play orsocial activities can lead their carers to wonder


whether they truly grieve. This uncertainly iscompounded by young children’s inability toverbalize their feelings. Children’s curiosity aboutthe death will take new forms as they mature.

Early childhoodYoung children will search actively for thedeceased. Their play and fantasies reflect theirparticular concerns and preoccupations. Theirsense of loss, their carer’s grief, and changed dailyroutines can provoke bewilderment, developmen-tal regression and unprovoked expressions ofanger or aggression.

Middle childhoodAppropriate sadness exists alongside a rapidresumption of normative activities. Sleepingdifficulties appear and are influenced by the child’sage: 5–7-year-olds find it hard to settle to sleep;older children report nightmares, though somederive comfort from dreaming of the deceased[1]. Children of all ages settle more easily whenan attachment figure is nearby. From the age of8 years, physical manifestations of distress suchas headaches appear, as do temper outbursts,argumentativeness and concentration difficulties.Children’s natural curiosity about the death cansometimes reflect underlying anxieties abouttheir ‘responsibility’ for what happened. Parentaldistress in response to their questioning cansilence children, allowing misperceptions aboutthe death to persist. Separation anxiety takes

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the form of worries about the vulnerability ofloved ones.

AdolescenceGrief takes various forms, including withdraw-ing from family activities and/or seeking peersupport. Adolescents may challenge their ownmortality with risk-taking behaviour such as alco-hol or drug use. Their cognitive ability to reviewtheir prior relationship with the deceased maybring comfort or, for those troubled by guilt orregrets, increased distress. They may acquire newfamily roles and responsibilities and encounterexpectations of overmature behaviour. A sense ofresponsibility, alongside a desire to protect griev-ing adults, may result in disguised grief and mixedmessages to others.

RESILIENCE AND POSITIVE OUTCOMES INBEREAVED CHILDREN

The majority of children are resilient and fol-low a normal developmental trajectory subsequentto bereavement. Indeed, although parental deathchanges a child’s life path irrevocably, some chil-dren and adolescents report positive responsesfollowing bereavement, including increasing inde-pendence, better school performance, heightenedempathy to another’s distress, and a growth inspirituality [3].

Research exploring positive bereavement out-comes indicates that resilient children show greatercoping efficacy and fewer negative appraisals thanaffected children [4]. However, as ‘resilient’ chil-dren are chosen on the basis of being below agiven threshold of clinical disturbance, differencesin their cognitive styles may reflect differences inthe mental health status of ‘resilient’ and ‘affected’children.

PSYCHOPATHOLOGY IN BEREAVEDCHILDREN

Reported differences in rates of psychopathologyin bereaved children stem from differences in studyinclusion/exclusion criteria, recruitment practicesand measures used. The best controlled studiesindicate that only one in five will show disturbanceof clinical severity [5].

Commonly agreed bereavement symptomsinclude dysphoria (a state of unease), headaches,stomach aches and separation anxieties. Distur-bance is generally non-specific with a markedheightening in the frequency and persistence ofgrief symptoms that in other bereaved childrennormally attenuate within 4 months of the death[3,5]. An expressed wish to be dead generallyreflects the child’s desire to be reunited withthe deceased, although such statements requirecareful exploration particularly where familysuicide has occurred.

Children bereaved by family murder or sui-cide can evidence post-traumatic stress disorder(PTSD) and internalizing disorders [6]. Rates andtypes of psychopathology are similar to those inother bereaved children [7], with a raised risk ofdepressive disorder up to 2 years after the event[8]. An increased risk of suicidal behaviour [9,10]and higher levels of persistent anger, guilt, shameand social isolation are also reported [7].

Complicated traumatic grief (CTG) is character-ized by persistent intrusive and avoidant traumasymptoms that arise when the deceased died insubjectively traumatic circumstances. It can leadto avoidance of any positive or negative reminderof the deceased and social withdrawal at school[11]. The causes are unclear. One suggested con-tributory factor is that children’s sense of pre-dictability and stability can be undermined if theirprimary caregiver appears overwhelmed by thedeath [12]. Attempts to differentiate between dis-orders such as CTG and PTSD continue [13].Short-term trauma-based cognitive behaviouralinterventions (CBT) with parents and childrenoffer a promising approach to resolving CTG [11].

Recent research examines the hypothesisthat the stress of traumatic parental deathcan lead to long-term dysregulation of thehypothalamic–pituitary–adrenal (HPA) axis inbereaved children [14]. The differences foundbetween bereaved and control children in levelsof cortical suppression, thought to reflect ‘adrenalexhaustion’ in bereaved children, were attributedto adaptation to chronic stress, leaving unclearhow acute traumatic bereavement is associatedwith chronic HPA-axis dysregulation.

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WHAT INFLUENCES CHILD OUTCOME?

Difficulties in obtaining representative samples ofbereaved children make it difficult to examinesystematically factors that moderate or mediatetheir outcome.

Child morbidity is influenced by the age andgender of the child. Younger children evidencebehavioural or anxiety problems, while adoles-cents exhibit dysphoria or depression similar tothat found in bereaved adults. Generally, boysexhibit higher rates of overall difficulties and act-ing out/aggressive behaviours than girls, who aremore likely to show sleep disturbance, bedwettingand depressive symptoms.

Familial factors contribute to both child mor-bidity and resilience. Parents who report havingmental health difficulties post-bereavement aremore likely to have children with higher ratesof child disorder [5]. The converse appears true for‘resilient’ children, whose parents have lower levelsof disorder than do those of affected children [4].Child resilience is promoted by parental warmth,authoritative parenting and consistent discipline[4,15]. More recently, self-reports of interpersonalloss and conflict, and greater fears of abandon-ment have been linked to internalizing symptomsin bereaved girls [16].

Pre-bereavement factors predisposing to post-bereavement child disturbance include mentalhealth difficulties, marital conflict or separation,though this information rests on the retrospectiverecall of distressed parents. Genetic factorsmay influence child outcome in families wheremembers have pre-existing psychiatric disorders.

INTERVENTIONS WITH BEREAVEDCHILDREN

Theoretical and cultural influencesThere are two main theoretical bases for inter-ventions with bereaved children. The first sug-gests that children need to complete a sequenceof bereavement-related tasks in order satisfac-torily to resolve their grief and avoid maladap-tive outcomes. These tasks include acceptanceof the permanence of loss, constructing a posi-tive internal image of the deceased, and findingnew and supportive relationships [17]. In CTG,trauma is conceptualized as interfering with griefresolution, necessitating the relief of traumatic

symptomatology so that grieving tasks can beaccomplished [11].

In the second approach, children’s outcomes areseen to be the product of multiple, cumulative riskand protective factors operating in the post-deathenvironment. Interventions within this frameworkaim to foster resilience, for example by moderatingchildren’s coping styles and supporting positiveparenting [18].

Cultures provide frameworks that guide beliefsabout death, define ‘positive’ and ‘negative’ out-comes, and govern the expression of grief. Forinstance, in some cultures expressions of sorrowbring social opprobrium. Therapists need to gainan understanding of children’s familial, culturaland ethnic backgrounds, and be aware of howtheir practice is influenced by Western conceptu-alizations of grief and mourning.

What do bereaved children need?Bereaved children benefit from receiving accurateinformation about the death and related events.Reassurance that they could not have changed orinfluenced either, and that death mostly affectsthe elderly, is helpful. Explanations need to beage appropriate, clear and truthful, avoidingeuphemisms such as ‘gone to sleep’, which youngchildren will interpret literally. Little guidanceis offered where familial suicide or murderoccurs. Open sharing of information may beaffected by protectiveness towards children, orby adult survivors’ guilt and shame [10]. Adultsmay struggle with conveying understanding andempathy for the deceased without suggesting tovulnerable children that violence or suicide areacceptable coping strategies [7].

Children benefit from the re-establishment ofconsistent daily routines, the emotional availabilityof major caregivers and having their develop-mental competencies appreciated and fostered.Engagement in the wider social world, via activitiesand friendships, should be maintained.

Children are also helped by involvement in fam-ily expressions of grief, such as choosing flowersfor the deceased or speaking at the funeral service.They report that physical comforting and sharingtheir thoughts and feelings within the family arehelpful. Recognizing, normalizing and discussingtheir grief and concerns provides all children witha sense that death can be managed and need notoverwhelm them.

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What is helpful for parents?Distressed parents can, understandably, be uncer-tain about what to tell bereaved children and when.Often all that parents require is an opportunityto discuss their concerns and potential responseswith an understanding and supportive adult, whocan offer advice on management. Unexpecteddeaths require quick decisions from unpreparedparents, who can be reassured that decisions theylater regret can be addressed subsequently. Forexample, children who did not attend the funeralservice can have it described to them, and they canvisit the burial site. Explanations that children’sgrief can take different forms and will attenuateover time can reassure parents about the normalityof their children’s responses. Family reminiscingabout the deceased is of particular help to chil-dren who appear not to be grieving [1]. Givingchildren mementos of their dead parent or siblingprovides them with comfort and helps them tomaintain a positive relationship with the deceased.Normal limit setting increases children’s sense ofsecurity. Schools can promote bereaved children’sresilience by providing understanding and supportand by incorporating preparation for trauma andloss into educational thinking and practice.

Services for bereaved childrenThere has been a notable expansion in community-based services for bereaved children. Yet, quanti-tative evaluations of controlled bereavement inter-ventions have highlighted few positive treatmenteffects [19,20]. Treatment effects may be limitedby the fact that it is not necessarily the level ofchild distress that determines who receives ser-vices [5], and that outcomes judged in terms ofchanges in psychopathology may be ill-matchedto therapeutic inputs [19]. Interventions are nei-ther neutral nor always helpful and infrequentlymeasure potentially negative outcomes, such as anincrease in child distress.

The role of professionalsThe majority of bereaved children need neitherprofessional intervention nor therapy. Referralis appropriate where there is prolonged distressor disorder (Table 16.1). It is essential to gaina detailed understanding of the circumstances of

the death, what information and explanations thechild has been given and how their knowledge wasacquired. Relevant cultural or religious variablesneed to be understood.

It is therapeutically useful to see children andparents separately and together. Individual meet-ings with children can highlight hidden worries,cognitive distortions, self-blame or symptoms oftrauma. Individual meetings with parents can high-light concerns about what information to sharewith children. Seeing family members togethercan highlight which family processes to strengthenor modify. Widening family support networksis useful – for instance, via school consultationsor reassuring parents that other trusted familymembers or friends can also help in managingchildren’s grief.

Cognitive behavioural therapy (CBT) withchildren and their parents can effect significantimprovements in PTSD and internalizing disordersand complicated grief [12].

CONCLUSIONS

Bereaved children’s expression of grief is influ-enced by their developmental level and their ageand gender. The episodic quality of their grief canbe confusing to adults. Separation from attachmentfigures can induce anxiety across all age groups.Grief-related distress does not indicate pathology.Clinical disturbance affects approximately one infive children. Positive and authoritative parentingfacilitates childhood resilience. Parents appreci-ate information that normalizes children’s griefand traumatic symptoms, and provides guidanceon management. Bereaved children value oppor-tunities to share their thoughts and feelings. Themajority of families do not require psychologicalservices, although families bereaved by murder orsuicide would benefit from extra support. Consul-tation with other agencies in routine contact withchildren, such as schools, can enhance families’supportive community networks.

Referral for professional help is appropriatewhen grief and trauma symptoms disrupt normalfunctioning and persist over time. It is essential toconsider the impact of religious and cultural beliefsupon presentation and the implications of these forappropriate therapeutic goals and practice.

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Table 16.1 Bereaved children: assessing the need for support and intervention.

Time Context Post-death

Implications for Management Monitor Advise/consult Considerwith professional referral if:

Pre-death Children:

Developmental level If learningdisabilities

Liaise with school

Understanding of death

Temperament

Relationship with deceased If problematic

Prior history of loss/divorce/separations/death Yes

Prior disturbance/disorder Yes

Family:

Patterns of communication

Organization

Role differentiation

Quality of family relationships If poor/priordisturbance

Prior parental mental healthdifficulties Yes

Culture/religion/community:

Beliefs

— meaning of life/death/afterlife

— relationships with the dead— roles of adults/children/

family

Behaviour

— culturally appropriate rites/rituals

— culturally appropriateexpressions of grief

Practicalobstacles/communitysupport

Consider supportfrom/liaison withcultural community

Death occurs Nature/circumstances of death:

Traumatic, murder, suicide Yes

Presence of child

Information provided

Adults available to child

Degree of preparation/support available

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Immediateaftermath Children:

Impact upon routines/practical care

Suitability of substitute care Yes If unsuitableover longer term

Involvement in rites/rituals If requested

Expression of grief tolerated

Opportunities to gain understanding

Family:

Explanations given to child Psycho-education ongrief if requested

Availability of practical/emotionalsupport for all family members

Support for expression of grief anddistress

Extent to which able to appreciatechildren’s needs

Extended family:involvement with child

conflict around death/aftermath Yes

Short term (upto 4 months) Children:

Degree routines/activitiesre-established

Absence fromschool

If prolonged —family/school liaison

Persistent

Ability to use support withinfamily/from peers

Type of grief symptoms If signs of trauma Psycho-education —monitor

Severe/persisting

Opportunities to express grief

Level of distress/avoidance If marked Psycho-education —monitor

Opportunities to consolidate,increase understanding

Lack of stability/further losses Yes Family/schoolliaison — monitor

Family:

high level of distress/mental health difficulties

Assess help needed/wanted

Interferingwithfunctioning

Lack of support for adults Consider ways ofincreasing — monitor


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Longer term Children:

Persistence of marked distress/emergence of disturbance

Psycho-education/increase support

Interferingwithfunctioning

Trauma symptoms Yes

Difficulties with peers School liaison Persistent

Family:

Adult mental health difficulties Assess help needed/wanted

Persistent

Marked relationship difficulties Assess help needed/wanted

Persistent

REFERENCES

[1] Worden JW. (1996) Children and Grief: When aParent Dies. New York: Guilford Press.

[2] Balk DE. (1996) Models for understanding adoles-cent coping with bereavement. Death Studies 20,367–87.

[3] Dowdney L. (2000) Annotation: childhood bereave-ment following parental death. Journal of ChildPsychology and Psychiatry 7, 819–30.

[4] Lin KK, Sandler IN, Ayers TS et al. (2004)Resilience in parentally bereaved children andadolescents seeking preventive services. Journalof Clinical Child and Adolescent Psychology 33,673–83.

[5] Dowdney L, Wilson R, Maughan B et al. (1999)Bereaved children: psychological disturbance andservice provision. British Medical Journal 319,354–7.

[6] Freeman LN, Shaffer D, Smith H. (1996) Neglectedvictims of homicide: the needs of young siblings ofmurder victims. American Journal of Orthopsychi-atry 66, 337–45.

[7] Cerel J, Jordan JR, Duberstein PR. (2008) Theimpact of suicide on the family. Crisis 29, 38–44.

[8] Brent DA, Melhem N, Donohoe MB, Walker M.(2009) The Incidence and course of depression inbereaved youth 21 months after the loss of a par-ent to suicide, accident, or sudden natural death.American Journal of Psychiatry 166, 786–94.

[9] Kuramoto SJ, Brent DA, Wilcox HC. (2009) Theimpact of parental suicide on child and adolescentoffspring. Suicide and Life-Threatening Behaviour39, 137–51.

[10] Hung NC, Rabin LA. (2009) Comprehending child-hood bereavement by parental suicide: a criticalreview of research on outcomes, grief processes,and interventions. Death Studies 33, 781–814.

[11] Cohen JA, Mannarino AP, Staron VR. (2006) Apilot study of modified cognitive-behavioral therapyfor child traumatic grief (CBT-CTG). Journal ofthe American Academy of Child and AdolescentPsychiatry 45, 1465–73.

[12] Brown EJ, Amaya-Jackson L, Cohen J et al. (2008)Childhood traumatic grief: a multi-site empiricalexamination of the construct and its correlates.Death Studies 32, 899–923.

[13] Melhem NM, Moritz MSW, Walker MA et al. (2007)Phenomenology and correlates of complicated griefin children and adolescents. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 46,493–9.

[14] Pfeffer CR, Altemus M, Heo M et al. (2007) Salivarycortisol and psychopathology in children bereavedby the September 11, 2001, terror attacks. BiologicalPsychiatry 61, 957–65.

[15] Kwok OM, Haine RA, Sandler IN et al. (2005)Positive parenting as a mediator of the relationsbetween parental psychological distress and mentalhealth problems of parentally bereaved children.Journal of Clinical Child and Adolescent Psychology34, 260–71.

[16] Little M, Sandler IN, Wolchik S et al. (2009)Comparing cognitive, relational and stress mech-anisms underlying gender differences in recoveryfrom bereavement-related internalizing problems.

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Journal of Clinical Child and Adolescent Psychology38, 486–500.

[17] Baker JE, Sedney MA, Gross E. (1992) Psycholog-ical tasks for bereaved children. American Journalof Orthopsychiatry 62, 105–16.

[18] Sandler IN, Ma Y, Tein JY, et al. (2010) Long-term effects of the Family Bereavement Programon multiple indictors of grief in parentally bereavedchildren and adolescents. Journal of Consulting andClinical Psychology 78, 131–43.

[19] Curtis K and Newman T. (2001) Do community-based support services benefit bereaved children?A review of empirical evidence. Child Care, Healthand Development 27, 487–95.

[20] Currier JM and Holland JM. (2007) The effec-tiveness of bereavement interventions with chil-dren: a meta-analytic review of controlled outcomeresearch. Journal of Clinical Child and AdolescentPsychology 36, 253–9.

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Adoption and fostering

17Adoption and FosteringJill HodgesDepartment of Child and Adolescent Mental Health, Great Ormond Street Hospital for Children NHSTrust, London, UK

There are now very few non-relative adoptionsof UK infants, and international adoptions havedeclined in the UK as elsewhere since 2004 [1].Most UK adoptions are of older ‘looked after’children, who have usually been fostered prior toadoption.

CHILDREN ADOPTED IN INFANCY

These adoptees show somewhat higher levelsof difficulty than non-adopted children, mainlydisruptive problems [2,3], with difficulties mostmarked in later childhood and early ado-lescence [4]. Although the great majority ofinfant-adopted children are within the normalrange of adjustment, clinical referrals of infant-adopted children are substantially higher thanfor non-adoptees, apparently reflecting a smallhigh-risk subgroup [5,6].

Genetic risks probably account for some ofthis over-representation in clinical populations.However, a well-functioning adoptive family envi-ronment acts as a developmental protective factorfor children whose biological parents had a herita-ble mental illness, abused alcohol or had a criminalrecord [7].

Early short-term interventions can increaseparental sensitivity and infant attachment security,and reduce rates of attachment disorganization,in infant adoptions [8,9]. After infancy, clinicallyimportant issues concern children’s developmen-tally changing understanding of adoption [10],and curiosity about their origins. Children need torevisit these questions as they mature cognitively


and emotionally. Where adoptive parents areuneasy with the subject, children may avoidraising it; so parents may believe, sometimes withrelief, that the child is ‘not interested’ or ‘alreadyknows everything’. Voiced or not, children’squestions focus around two areas. One is thebirth parents – who were they? what were theylike? Adopters need good information here, toshare over time, and need to help the child to feelthat their adopters value aspects of them derivedfrom birth parents as well as from their adoptiveupbringing. Where information is lacking, as inmany international adoptions, children still needmental representations of their birth parents;parents can help them appreciate that their owncharacteristics may offer clues. The second focusof children’s questions is why they were given up.Commonly, young children have an underlyingfeeling that something was wrong with them thatled the birth parents to reject them. With agechildren become more able to understand thecomplex reasons why birth parents may have beenunable to care for them.

We now turn to foster children, and then to thesmall subgroup who move on to adoption.

FOSTER CHILDREN

The great majority of looked-after children (LAC)in the UK are fostered. Foster carers often possesslittle information about the child’s history withwhich to make sense of their behaviour. Even instable, long-term foster families, children may lacka sense of permanency or belonging. LAC show

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markedly lower educational performance thanother children, with the gap widening at each stage.Children entering care are already a severelysocially disadvantaged group, but foster caredoes not remedy this disadvantage [11]. Earliermaltreatment profoundly affects educationalattainment among foster children, even in stableplacements [12]. Adopters can often advocatestrongly for their children’s needs, in contrast tomany foster carers, who lack the adopters’ legalstatus as parents, their lifetime commitment tothe child, and often their educational and socialbackground.

Looked-after children show much higher ratesof psychiatric difficulty than children remaining intheir families. Ford et al. [13] found that 46.4%of LAC had at least one ICD-10 (ICD-10 Inter-national Classification of Mental and BehaviouralDisorders in Children and Adolescents) psychiatricdiagnosis, compared to 14.6% of deprived and8.5% of non-deprived children living in privatehouseholds. Children in residential care were mostdisturbed, but 38.6% of foster children showedpsychiatric difficulties. Comorbidity was high, anissue discussed below in relation to psychiatricclassification. Few children entered care becauseof any parental illness, so psychiatric disorder inthe birth parents cannot account for the enormousdiscrepancy between LAC and others. Althoughexperiences in care may themselves be associatedwith difficulties (e.g. prevalence of disorder washigher where there were many recent placementchanges) the children’s psychiatric difficulties arelikely to derive mainly from abusive or neglectfulparenting. In addition, neurological changes havebeen described in children subjected to prenataland neonatal stress, likely to be more common insocially disadvantaged families; and neurobiolog-ical changes are also known to result from earlymaltreatment [14,15].

Besides higher rates of difficulty on measuresdesigned for community and ordinary clinicpopulations, maltreated children also showcomplex and clinically significant problems thatare not well captured by these measures [16]. Arecently developed measure designed to examinesuch difficulties is the Assessment Checklist forChildren (ACC). The ACC scales illustrate thekinds of problem very commonly encountered inclinical work with maltreated children, includingvery disturbed relationship styles, self-injurious

behaviours, disturbances around eating, responsesto trauma, and inappropriate sexual behavior [17].

Current DSM-IV-TR (Diagnostic and StatisticalManual of Mental Disorders, Fourth Edition – TextRevision) psychiatric diagnostic classification doesnot adequately capture the difficulties shown bythe population of maltreated children. Childrenmay receive multiple diagnoses, not linked by ref-erence to the child’s developmental history andmaltreatment experiences; or show subthresholddifficulties in numerous areas, causing real impair-ment not reflected in their diagnosis.

Maltreatment is unlike other forms of traumain several ways. It usually occurs early in devel-opment; is chronic rather than a discrete event;and takes place within the child’s attachment rela-tionship, so that parental figures who would beexpected to provide protection are themselvessources of fear (producing attachment disorga-nization). It is often cumulative, involving severaldifferent types of trauma, and this is associatedwith symptom complexity [18]. Certain forms ofmaltreatment may not meet the trauma criterionof involving threat of death or injury, althoughthey may still produce symptoms of post-traumaticstress disorder (PTSD).

It has been argued that the resulting psycho-logical damage to children is better captured bya diagnostic category such as childhood complextrauma or developmental trauma disorder [19],reflecting the derailment of normal developmentalprocesses across multiple domains and the orga-nization of behaviour to prevent recurrence oftrauma effects. Instead of a child receiving severalapparently unrelated diagnoses – e.g. attentiondeficit hyperactivity disorder (ADHD), conductdisorder, reactive attachment disorder and sepa-ration anxiety – such a diagnostic category wouldrecognize a pattern of coexisting and somewhatinterrelated difficulties across several domains inmaltreated children. These include attachment,emotional dysregulation, behavioural and impulsecontrol, attention and cognition, dissociation andsomatic dysregulation.

Children adopted from careWhile most LAC are aged 10 years or older, themajority of children adopted are under 5 years ofage. It should be noted that Ford et al. [13] foundthat risk of psychiatric difficulties was just as highin this younger age group as in older children.

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Two obvious areas of difficulty in later-adoptedand foster children are the impact of maltreatment,and difficulties in attachment and relationships (seeChapters 15, 18 and 19).

Regarding maltreatment, the ACC, men-tioned above, assesses several areas of likelydifficulty. Clinicians should be alert to possiblepost-traumatic symptoms, and depression, oftencomorbid with PTSD. Traumatic memories mayonly resurface after the child feels safe in fostercare, or after the permanency of adoption.Triggers may include later losses or severe stressesas well as reminders like anniversaries or places.Children may have only fragmentary memories,and may feel ‘crazy’ or overwhelmed by emotions,flashbacks or dreams, and reassurance is essential.The original traumatic events have often not beenknown to services or foster/adoptive parents,making it more difficult for adults to help the childmake sense of traumatic memories or feelings.

Regarding attachments, maltreated children areobviously at high risk of an ‘insecure’ attachmentorganization; but additionally, because the attach-ment figure whom they need as a source of securityis simultaneously a source of fear, they are atgreatly increased risk of attachment disorganiza-tion [20]. Insecure-disorganized attachment, muchmore than insecure attachment alone, is related tolater behavioural and emotional difficulties, includ-ing aggressive and oppositional behaviour, laterdissociative symptoms, and poorer self-confidenceand social competence [21].

Once these children enter adoptive or fosterfamilies, they must form new attachments withstrangers, much later than normal and on the basisof existing internal working models of attachment,which can profoundly affect their expectations ofnew parental relationships. Attachment difficultiesoften relate to other areas of behaviour and canperpetuate existing models. For example, childrenmay avoid showing a need for comfort or affec-tion, so as not to reveal (or feel) dependence orvulnerability. This may have been the best avail-able strategy for the child who could not expectcomfort, but may conceal from new adoptive par-ents the chance to respond in a way that couldbegin to alter the child’s expectation.

Children showing difficulties in their relation-ships with caregivers (usually alongside otherbehavioural and emotional difficulties), are oftendescribed as showing an attachment disorder.

‘Attachment disorders’, as defined by ICD-10and DSM-IV, cover two types of difficulty, theprecondition of both being very adverse earlycaregiving. Not all maltreated children show suchdisorders, and some children show features ofboth. These types are:

• Directing sociable and attachment behaviourstowards people without showing the usualselectivity (‘disinhibited’). Such indiscriminatebehaviour appears fairly resistant to change,even though the child may also begin to showclear attachment behaviour towards a preferredadult once long enough in placement.

• Inhibition of sociability and of seeking andaccepting comfort (‘inhibited’); this usuallychanges once the child has a responsivecaregiver.

Alongside these defined classifications therehas also been an explosion in the use of theterm ‘attachment disorder’, claimed to underlie avast range of difficulties. Many popular websitesput forward a version that ‘is not discerniblyrelated to attachment theory, is based on nosound empirical evidence and has given rise tointerventions whose effectiveness is not provenand may be harmful’ [21]. ‘Attachment disorder’as a diagnosis for older maltreated children shouldnot be overextended to their difficulties in otherareas of functioning, which need examination andtreatment in their own right.

TREATMENT CONSIDERATIONS

Where children have suffered maltreatment anddisruption before adoption placement, they canprofoundly affect previously well-functioningadoptive families, and clinicians should be waryof pathologizing these families as the apparentsource of difficulties. However, models that locateall the difficulty in the child’s behaviour and abusehistory, seeing adoptive parents as ‘co-therapists’,risk denying the importance of the child–parentinteraction; abused children can ‘push the buttons’of particular vulnerabilities in adoptive parents, inways that are not necessarily predictable either byprofessionals or parents.

An important part of clinical work is a historyof the placement, including the adoptive parents’expectations, what information about the childthey were actually given, what potential difficulties

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they were led to expect, whether they can identifylikeable qualities in the child, and what supportthey have, including extended family.

Adoptive parents need full background infor-mation about the child’s history. If this is lackingit should be obtained as soon as possible; the clin-ician can use this with the parents to help themattune and make sense of their child’s responses,and alter negative interaction patterns. The childneeds help to construct a coherent story of theirlife if one is lacking. This is often done in the formof a ‘Life Story Book’, which should incorporatethe child’s own memories and feelings alongsidea chronological account. Parents should be fullyinvolved in this, rather than it being seen as directindividual work with the child; this helps childand parents to share the child’s history, helps inunderstanding the child better, and helps adopterstowards the role that parents ordinarily fulfil inrelation to their birth children, of a ‘memory bank’that the child can draw on when needed.

As regards attachment, the move to newadoptive parents is itself the most radical form oftreatment possible. A study assessing the child’sattachment representations showed increasingsecurity over the first 2 years of placement,although insecure and disorganized represen-tations also persisted [22]. Reports of adoptiveparents and retrospective reports of adoptedadults indicate positive results for the majority oflate-adopted children in terms of attachments andrelationships, and show that even where adoles-cence is very troubled, improved family relation-ships may follow. Support for parents is essential;sensitive caregiver interaction with the child, andthe capacity to respond in security-promoting wayseven to negative and provocative behaviour bythe child, can be difficult for parents to maintain.

As the developmental trauma of maltreat-ment has usually occurred in the context ofthe child’s attachment relationship, treatmentapproaches often incorporate work on both,although techniques such as trauma-focusedcognitive–behavioural therapy (CBT), or Eyemovement desensitization and reprocessing(EMDR) may be useful where there are partic-ular traumatic incidents and PTSD symptoms.The ‘Attachment, Self-Regulation and Compe-tency’ (ARC) framework for treating complextrauma [23] focuses on increasing positive attach-ment, helping the caregiver to manage the child’s

affect, attune to the child, respond consistentlyand develop safe, predictable routines. On thisbasis, the ARC framework outlines interventionsdesigned to develop other competencies damagedby the history of maltreatment, such as theidentification and regulation of emotion, includingpsycho-education about the trauma response;cognitive competencies, including executivefunction skills; and social skills.

Numerous therapeutic approaches to attach-ment difficulties have been described, butsystematic evaluation is lacking. Examples ofinterventions are given in Box 17.1.

There is no evidence for benefit from ‘holding’,‘rebirthing’ and similar ‘attachment therapy’techniques that employ physical restraint or

Box 17.1 Examples of interventionsfor attachment difficulties

• Direct work to support parents, e.g. inhelping them to reframe behaviour viaknowledge of the effects of maltreat-ment, and hence to manage itdifferently. A ‘story stem’ narrativeassessment of the child can give apicture of the child’s expectations andperceptions of attachmentrelationships, which can help parentsattune better to a child.

• Standard parenting programmes, e.g.Webster—Stratton, adapted to includeadoption-specific areas.

• Active learning in the child—parentinteraction, with the therapistsupporting the parent’s responses, anddirecting and facilitating the child [24].

• ‘Theraplay’ [25] involving activeengagement of the child in physical playwith the therapist, seen as modelled onthe healthy parent—infant relationship,with the parent involved first asobserver and later as co-therapist.

• Individual psychoanalytic psychotherapyfor the child, with concurrent workwith the parents, can help to alterunderlying negative expectations ofattachments and relationships [26].

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domination, coercion, regression, and so on. Theseare not based on attachment theory, though usu-ally claiming to be so; they risk retraumatizing achild already traumatized by an adult in a parentalor ‘caring’ role; they have been responsible fora number of child deaths and are strongly con-traindicated [27].

Parental satisfaction with adoption is gener-ally high, despite difficulties. Adoption breakdownrates vary greatly between agencies, attesting to theimportance of preparation and post-adoption sup-port for the family. Parents often feel that Childand Adolescent Mental Health Services do notadequately understand these children’s difficulties;as described above, problems are inadequatelycaptured by the usual diagnostic classifications,and treatment provision may be fragmented iforganized by diagnosis. Support is essential, but itsavailability varies enormously. Local authoritiesnow have a duty to provide assessment and sup-port services (often outsourced to other agencies),but variation is likely to continue in the level ofservices provided.

REFERENCES

[1] Selman, P. (2010) Intercountry adoption in Europe1998–2008: Patterns, trends and issues. Adoptionand Fostering 34, 4–19.

[2] Fergusson DM, Lynskey M, Horwood LJ. (1995)The adolescent outcomes of adoption: a 16-yearlongitudinal study. Journal of Child Psychology andPsychiatry 36, 597–615.

[3] Juffer F and van Ijzendoorn MH. (2005) Behaviorproblems and mental health referrals of interna-tional adoptees: a meta-analysis. Journal of theAmerican Medical Association 293, 2501–15.

[4] Bohman M and Sigvardsson S. (1990) Outcomein adoption: Lessons from longitudinal studies. In:Brodzinsky D and Schechter MD (eds), The Psy-chology of Adoption. New York: Oxford UniversityPress, pp. 93–106.

[5] Keyes MA, Sharma A, Elkins IJ, Iacomo WG,McGue M. (2008) The mental health of US ado-lescents adopted in infancy. Archives of Paediatricand Adolescent Medicine 162, 419–25.

[6] Brand AE and Brinich PM. (1999) Behavior prob-lems and mental health contacts in adopted, foster,and nonadopted children. Journal of Child Psychol-ogy and Psychiatry 40, 1221–9.

[7] Howe D. (1998) Patterns of Adoption: Nature,Nurture, and Psychosocial Development. Oxford:Blackwell Science.

[8] Bakermans-Kranenburg, MJ, van IJzendoorn MHand Juffer F. (2003) Less is more: meta-analysesof sensitivity and attachment interventions in earlychildhood. Psychological Bulletin 129, 195–215.

[9] Juffer F, Bakermans-Kranenburg MJ, van IJzen-doorn MH. (2005) The importance of parentingin the development of disorganized attachment:Evidence from a preventive intervention study inadoptive families. Journal of Child Psychology andPsychiatry 46, 263–74.

[10] Brodzinzki DM, Singer LM, Braff AM. (1984)Children’s understanding of adoption. Child Devel-opment 55, 869–78.

[11] Viner RM and Taylor B. (2005) Adult health andsocial outcomes of children who have been in publiccare: population-based study. Pediatrics 115, 894–9.

[12] Heath AF, Colton MJ, Aldgate J. (1994) Failureto escape: a longitudinal study of foster children’seducational attainment. British Journal of SocialWork 24, 241–60.

[13] Ford T, Vostanis P, Meltzer H, Goodman H. (2007)Psychiatric disorder among British children lookedafter by local authorities: comparison with chil-dren living in private households. British Journal ofPsychiatry 190, 319–25.

[14] Glaser D. (2000) Child abuse and neglect and thebrain – a review. Journal of Child Psychology andPsychiatry 41, 97–116.

[15] McCrory E, De Brito SA, Viding E. (2010) Researchreview: the neurobiology and genetics of maltreat-ment and adversity. Journal of Child Psychologyand Psychiatry 51, 1079–95.

[16] DeJong M. (2010) Some reflections on the use ofdiagnosis in the looked after or ‘‘in care’’ childpopulation. Clinical Child Psychology and Psychia-try 15, 1–11.

[17] Tarren-Sweeney M. (2007) The Assessment Check-list for Children – ACC: A behavioural rating scalefor children in foster, kinship or residential care.Children and Youth Services Review 29, 672–91.

[18] Cloitre M, Stolbach BC, Herman JL et al. (2009) Adevelopmental approach to complex PTSD: child-hood and adult cumulative trauma as predictors ofsymptom complexity. Journal of Traumatic Stress22, 399–408.

[19] van der Kolk BA. (2005) Developmental TraumaDisorder: toward a rational diagnosis for childrenwith complex trauma histories. Psychiatric Annals35, 401–8.

[20] Van IJzendoorn MH, Schuengel C, Bakermans-Kranenberg MJ. (1999) Disorganized attachmentin early childhood: Meta-analysis of precursors,concomitants, and sequelae. Development and Psy-chopathology 11, 225–50.

[21] Prior V and Glaser D. (2006) Understanding Attach-ment and Attachment Disorders; Theory, Evidence

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and Practice. London and Philadelphia: JessicaKingsley, .

[22] Hodges J, Steele M, Hillman S, Henderson K,Kaniuk J. (2005) Change and continuity in mentalrepresentations of attachment after adoption. In:Brodzinsky DM and Palacios J (eds), PsychologicalIssues in Adoption. Research and Practice. Westport,CT: Praeger, pp. 93–116.

[23] Blaustein ME and Kinniburgh KM. (2010) Treat-ing Traumatic Stress in Children and Adolescents:How to Foster Resilience Through Attachment, Self-regulation and Competency. New York and London:The Guilford Press.

[24] Hughes DA. (1997) Facilitating DevelopmentalAttachment; The Road to Emotional Recoveryand Behavioural Change in Foster and Adopted

Children. Maryland and Oxford: Rowman and Lit-tlefield Publishers Inc..

[25] Booth PB and Jernberg AM. (2010) Theraplay;Helping Parents and Children Build Better Relation-ships through Attachment-Based Play, 3rd edn. SanFrancisco: Jossey-Bass, John Wiley and Sons.

[26] Lush D, Boston M, Grainger E. (1991) Evaluation ofpsychoanalytic psychotherapy with children: thera-pists’ assessments and predictions. PsychoanalyticPsychotherapy 5, 191–234.

[27] Chaffin M, Hanson R, Saunders B et al. (2006)Report of the APSAC Task Force on Attach-ment Therapy, Reactive Attachment Disorder,and Attachment Problems. Child Maltreatment 11,76–89.

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Section 4

The Impact of Traumaand Maltreatment

The impact of trauma and maltreatment

18Stress and Reactions to Stress in ChildrenGuinevere TufnellThe Traumatic Stress Clinic, Great Ormond Street Hospital for Children NHS Trust, London, UK

WHAT’S NEW

• Stress in pregnant mothers can betransmitted to the foetus and causeenduring effects on offspring [14].

• Diagnostic criteria are being revised toallow more rational diagnosis ofcomplex trauma in children [11,17].

• Building resilience is recognized as akey factor in treatment ofstress-related disorder [27].

• Trauma-focused psychological therapyhas been shown to be more effectivethan medication in the treatment ofPTSD [24].

WHAT IS STRESS?

Stress may be defined as a real or interpreted threatto the physiological or psychological integrity ofan individual that results in physiological and/orbehavioural responses [1]. It is increasingly recog-nized that stress cannot be fully defined in objectiveterms. The way in which an event is perceived asstressful or threatening has a major effect on theway an individual will respond and is influenced by:

• the child’s developmental stage;• the circumstances surrounding and following

the incident;• the support subsequently available.


THE PSYCHOPHYSIOLOGICAL RESPONSETO STRESS

The ability to perceive danger and to protectourselves effectively from it is crucial for ourday-to-day survival. Danger is a powerful stressorand produces an automatic psychophysiolog-ical response enabling us to ‘freeze, fight orflee’ [2]. When danger is perceived, there isan immediate arousal response via the limbicsystem (Figure 18.1), with activation of thehypothalamo–pituitary–adrenal (HPA) axis andinhibition of non-essential physical and psycho-logical functions. The body is prepared for action.Sensations become more acute, attention becomeshighly focused towards the potential danger andreaction time speeds up. Pain sensation may bediminished, as a consequence of the release ofendorphins in the brain, even after severe injury.The release of noradrenaline and cortisol intothe bloodstream helps to ensure that the bodyremains able to cope with stress for a considerableperiod of time. Memory processing and othercognitive functions are also affected [3,4]. Inextremis, a freeze response can occur, when pulseand respiration slow and may even stop [5]. Ofcourse, not all stressful events will be experiencedas dangerous and the associated stress response islikely to be modulated accordingly.

Later reactions after a stressful eventWhen safety and security are felt to be restored,recovery can be rapid; but where the situationinvolves dealing with ongoing stress, differenttypes of response will occur. For example, loss of a

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Stress and reactions to stress in children

Threat/Stress

Hypothalamus[CRH, AVP]

Stimulate

Inhibit

Modulates,Inhibits HPAaxis

Long-termmediation

Adrenal cortex[cortisol]

Stimulate

Anterior pituitary[ACTH]

- Cardiovascular adaptation- Increased arousal, vigilance- Decreased vegetative function (catabolism)- Immune suppression- Growth suppression

Figure 18.1 The hypothalamic—pituitary axis (HPA) and the threat response. ACTH, adrenocorti-cotropic hormone; AVP, arginine vasopressin; CRH, corticotropin-releasing hormone.

loved one by death or separation may be followedby a bereavement response in which initialnumbness gives way to grief and mourning. Whenloss is unexpected and traumatic, however, theinitial shock may be followed by intrusive thoughtsand images that make it difficult to come to termswith the loss in the normal way. This may give riseto complicated and prolonged grief reactions.

Some stressful events bring with them enor-mous changes for the individuals affected. Naturaldisasters or war, for example, disrupt the wayof life of whole communities for long periods.But even changes on a smaller scale can resultin catastrophic disruption of the individual’sassumptions about the world, including theframework for self-identity, understanding events,planning and taking action. Repairing the damageand developing new ways of functioning may takeconsiderable time [6].

Longer-term effectsMuch of what is known about stress and reac-tions to it comes from research in the USA withVietnam veterans. This has shown that the effectsof extreme, protracted and repeated stress can

be enduring. Mental health problems range fromrelatively mild and self-limiting to severe andlong-lasting. Although they are necessary for sur-vival, it seems that frequent neurobiological stressresponses increase the risk of physical and men-tal health problems, particularly when experiencedduring periods of rapid brain development [7,8].

DEVELOPMENTAL ISSUES

Our bodies and brains automatically respond todangerous situations without understanding orconscious awareness. For example, in a newbornany sudden change of sensation is sufficient to pro-voke a startle response. As young children growolder, what they learn about danger and safetylays the foundations for how they will understandand cope with stress in later life. The relationshipbetween the child and its primary caregiver pro-vides a particularly crucial learning environment. Ifthis environment does not provide protection butinstead exposes the child to repeated danger (e.g.domestic violence or abuse), there are likely to belong-term effects both on the child’s assumptionsabout the world and on their mental health [8,9].

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EPIDEMIOLOGY AND HISTORY

The effect of stressful experience will depend on anindividual’s ability to cope and the support that isavailable, as well as on the event itself [10]. Thereappears to be a range of possible stress-relateddisorders, ranging from mild to severe (Box 18.1).

At present, stressful experience is only formallyrequired in diagnostic criteria for adjustment dis-orders and post-traumatic stress disorder (PTSD).The conceptualization and understanding of stressresponse syndromes has changed enormously overthe last century and remains a major focus forresearch. For example, it was only in the 1980sthat criteria for PTSD were published in DSM-III(Diagnostic and Statistical Manual of Mental Dis-orders, 3rd edn.), with the ICD-10 (ICD-10 Inter-national Classification of Mental and BehaviouralDisorders in Children and Adolescents) definitionfollowing in 1992. Further revisions are expectedwith the publication of DSM-5 in 2013 [11,12].

The experience of stress is part of normal life,and traumatic stress is far from rare, especiallyin populations afflicted by violence or natural dis-aster. The prevalence of mental health disordersresulting from traumatic stress can only be guessedat, but are clearly considerable. For example, epi-demiological studies of PTSD alone estimate apoint prevalence of 1%, and 4–12% for a life-time diagnosis [13]. Rates in clinical populations,however, are likely to be much higher.

Box 18.1 The response to stress

Stressful experiences can lead to:

• Normal stress responses

• Adjustment disorders

• Psychiatric disorders, including:

− mood disorders (anxiety states,PTSD, depression)

− dissociative states

− psychosomatic complaints

− eating disorders

− attachment disorders

− personality disorders in adulthood

− substance abuse.

STRESS REACTIONS IN CHILDREN

A child’s immediate reaction to extreme stress isusually one of distress and tearfulness. Once theevent is over, it takes time for the child to adjust toand recover from what has happened. The natureand severity of the reaction will depend on char-acteristics of the event, factors affecting the child’sresilience, and the recovery environment [14,15].The type of stressful experience, the suddennessof the event, the amount of preparation that hasbeen possible, the sensory exposure entailed andthe degree of secondary trauma will all affect theimpact of the event on the child. The appraisal ofthe stressful event – what it means for the childand how this is processed cognitively – is one ofthe most important factors in determining how anindividual responds and copes.

Stressful experience that overwhelms the child’scoping abilities can be traumatizing even whennot actually life-threatening. Young children whoexperience overwhelming sensory exposure duringthe event may be unable to process this cognitively,which makes them particularly vulnerable to flash-backs and intrusive re-experiencing of the event(Box 18.2).

Box 18.2 Factors affecting risk andresilience

• Type and duration of traumaticexperience

• Perceived severity of stress/traumaexposure

• The child’s age and maturity

• Exposure to stress at a young age

• The child’s gender

• Personality characteristics

• Previous exposure to stressfulexperience

• Time elapsed since exposure (symptomsoften reduce over time)

• Pre-trauma psychopathology

• Coping abilities/resources

• Parental mental health problems

• Social/cultural resources and support

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If the consequences of the event are manageableand disruption is minimal, the child’s distress andupset may resolve within a few days or weeks.The ability of parents (who may themselves bedistressed and traumatized) to provide adequatecare, and the presence of a stable caring systemaround the child, is crucial in promoting recovery.When these are absent, significant mental healthproblems can develop. And of course, if traumaticexperience is repeated there is a risk that chronicand complex responses will develop [16].

PSYCHOPATHOLOGY

Following a traumatically stressful experience,repetitive and intrusive memories of the eventare common. A chance noise or other stimulusmay trigger a flashback. Disturbing images mayalso occur at quiet moments such as bedtime,making it difficult for the child to settle to sleep.In very young children, sleep disturbances such asnight terrors and night waking are common. Olderchildren often report that their sleep is disturbedby bad dreams and nightmares. Children whoare too young to be able to understand what hashappened to them or to express their thoughts andfeelings in words are likely to re-enact a traumaticevent in their play or drawings. They often developsymptoms of hyperarousal, such as overactivity,irritability, difficulty concentrating and hyper-vigilance. Signs of generalized anxiety are alsocommon, including clinginess and fears of the dark.Language, toilet-training and other developmentalskills may regress or even be lost altogether. Thechild may become withdrawn or unresponsive andtry to avoid situations, objects or even words thatremind them of the traumatic experience.

When children are exposed to chronic andrepeated stress such as abuse or domestic violence,many domains of development may be affected[17]. Such children present a diagnostic challengeto the clinician, not uncommonly presenting withcomplex disorders of arousal, mood and conduct.When trauma is not identified, such children maybe misdiagnosed as suffering from attention deficithyperactivity disorder (ADHD), conduct disorderor psychosis.

As children get older, their reactions toextreme stress become more like those of adults.

Adolescents may meet DSM or ICD criteria forPTSD and other disorders. Those exposed toprolonged or repeated stress may also presentwith dissociative symptoms, angry outbursts,self-injury and substance abuse [16]. Memory andconcentration difficulties are common and canaffect school work and grades. Moodiness, anxiety,depression and irritability can put pressure onpeer and family relationships.

ASSESSMENT

When asked to assess a child following a majorstressful event, it may be helpful, before arrang-ing to meet the child, to have a planning meetingwith the parents/carers. Interviewing parents andchild together about the child’s current circum-stances and functioning is often a good place tostart the assessment. Parents can provide usefulbackground information such as family history, andthe child’s developmental history. It is often help-ful to see parents separately to obtain informationabout the parental developmental history (includ-ing trauma and attachments), marital relationship,and life experience of separations, abuse, illnessand other stressors or life events. The parentalaccount of any traumatic events should includetheir own and the child’s reactions to the trauma,and how these have been managed.

Interviewing the child individually is especiallyimportant following traumatic experience. Parentsoften lack crucial detailed information about theirchild’s experience and may therefore be unable toprovide all the information needed. Children oftencommunicate more freely about their experienceswhen not afraid of causing distress to carers. It isusually necessary to ask the child direct questionsabout their experience of traumatic events andtheir symptoms. Asking the child about what hashelped them to cope is also important. A semi-structured interview can be helpful [18] (Box 18.3).

Young children respond best to an approachusing play and drawing to help them to expressthemselves. At the end of any interview abouttrauma, the interviewer needs to help the child‘wind down’, to review and summarize the ses-sion, and to discuss anything that was particularlydisturbing or helpful. Providing information abouttraumatic experience and its consequences helps to

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Box 18.3 Trauma interview for children and adolescents

1. Ask the child:

• ‘Have you ever been in [e.g.] a car accident . . . or a house fire [other stressfulexperience] . . . or thought you might get hurt or die?’

• ‘Have you ever seen someone else get hurt badly?’‘Did someone important to you ever die, such as someone in your family or a good friend?’

2. Having identified traumatic event/s, ask the child to tell his/her own story about it/them.Use free recall as much as possible.

• Assist recall with questions about context of the traumatic event (e.g. when/where/who.

• Ask about the child’s physical/psychological responses at the time.

3. Track the course of symptoms from immediately after trauma to the present.

• Ask about meaning/attributions: the child’s feelings (e.g. of guilt and being different,damaged or isolated); reactions of others.

• Ask about what has helped them to cope.

4. Ask the child to describe his/her thoughts/plans about the future.

5. Wind down (see text).

normalize the child’s reactions; acknowledging thechild’s courage in having shared their experiencecan boost self-esteem.

DIFFERENTIAL DIAGNOSIS

Stressful experience can provoke a range of pos-sible responses, both normal stress responses anda variety of post-traumatic stress disorders [19].A single, brief, unexpected stressor (e.g. an acci-dent) is likely to produce a very different responsefrom traumatic experiences that are repeated, pro-longed and expected (e.g. sexual abuse). Depend-ing on the circumstances, a child may develop thesymptoms of a disorder (e.g. PTSD) but fall shortof meeting the full criteria. The most commondisorders are listed in Box 18.1. Comorbidity iscommon following severe trauma [12].

Careful history-taking and clinical examinationare crucial for accurate diagnosis. Traumatizedchildren are often withdrawn, avoidant or disso-ciative. This affects their ability to communicate,so that definitive diagnosis is likely to take time.Standard questionnaires can be helpful adjunctsto the detailed clinical interview [20] and provideuseful baselines for treatment.

EFFECTIVE MANAGEMENTAND TREATMENT

Management will depend on the specific circum-stances and needs of the individual child andfamily. A broad, multisystemic approach may beneeded in order to identify and address all ofthe child’s needs, especially following chronic orcomplex trauma [16]. Situational factors such asfamily adjustment problems, school difficulties orcomplex legal processes could cause significantongoing stress and require practical help or advice.Clearly, given the range of possible stress-relateddisorders, a number of treatment approaches maybe needed. What follows is just a brief outline ofwhat may help a child to recover from severe stress.

Immediate measuresFor any child who has been exposed to life-threatening danger, the most immediate require-ment is restoration of safety and security. Muchdistress in the immediate aftermath can be allevi-ated by providing basic information and practicalhelp. Later, screening to identify those at risk ofdeveloping mental health problems can also bevaluable [13].

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Psychological First Aid is an early interven-tion that aims to promote healthy recovery fromtraumatic stress by ensuring that support can beaccessed, thus optimizing the ability to cope andenhancing resilience. An approach known as Psy-chological Debriefing remains controversial owingto conflicting reports about its efficacy [21].

Cognitive-behavioural treatment (CBT)This well-validated approach essentially relies onhelping the child to recall the distressing experi-ence (imaginal exposure) in such a way as to reducedistress (desensitization) and enable symptoms tobe mastered (cognitive restructuring) [13]. Veryyoung children, however, are unlikely to be ableto make use of formal CBT, but can benefit fromsimilar therapeutic approaches using play, drawingand narrative techniques.

Eye movement desensitization andreprocessing (EMDR)This is a relatively new technique that has shownpromising results so far in research with trau-matized adults [22–24]. As yet, there are fewcontrolled trials with children [13]. Symptomimprovement is rapid and well maintained, evenin very young children. EMDR uses many of thesame elements as CBT but relies less on homeworkand verbal competency. It is particularly helpfulwith avoidant, or very young children.

MedicationMedication is increasingly used as an adjunct tomultidimensional psychological therapy packages

Box 18.4 Practice points

• Traumatic experiences are common andcan have long-lasting psychologicaleffects [13]

• Children are especially vulnerable tothe effects of extreme stress [8,9]

• Parental accounts are unreliable — it istherefore important to interview thechild

• Specific treatments work best as part ofa multi-modal intervention [13]

for post-traumatic disorders [25]. However, fewstudies have looked specifically at children [13].Antidepressants, especially selective serotoninreuptake inhibitors (SSRIs), are effective, at leastin the short term, in treating symptoms of hyper-arousal, such as irritability and sleep disturbance,as well as those of depression. Night terrors, startleresponses, avoidance reactions and overactivitymay respond to propranolol (a β-blocker) orclonidine (an α2-noradrenergic agonist) [26].

REFERENCES

[1] McEwen B. (2000) Stress, definition and conceptsof. In: Fink G (ed.), The Encyclopedia of Stress. SanDiego: Academic Press, pp. 508–9.

[2] Ledoux J. (1996) The Emotional Brain. New York:Simon & Schuster.

[3] Steckler T. (2005) The neuropsychology of stress.In: Steckler T, Kalin NH, Ruel JMHM (eds), Hand-book of Stress and the Brain. Amsterdam: Elsevier,pp. 25–42.

[4] Lupien SJ, Maheu S, Weekes N. (2005) Glucocor-ticoids: effects on human cognition. In: StecklerT, Kalin NH, Ruel JMHM (eds), Handbook ofStress and the Brain. Amsterdam: Elsevier, pp.387–402.

[5] Porges SW. (2003) The Polyvagal Theory: phyloge-netic contributions to social behavior. Physiologyand Behaviour 79, 503–13.

[6] Morgan L, Scourfield J, Williams D et al. (2003) TheAberfan disaster: 33-year follow-up of survivors.British Journal of Psychiatry 182, 532–6.

[7] Felitti VJ, Anda RF, Nordenberg D et al. (1998)Relationship of childhood abuse and household dys-function to many of the leading causes of death inadults. The Adverse Childhood Experiences (ACE)Study. American Journal of Preventive Medicine 14,245–58.

[8] Glaser D. (2000) Child abuse and neglect and thebrain – a review. Journal of Child Psychology andPsychiatry 41, 97–116.

[9] Bradley SJ. (2000) Stress, trauma and abuse.In: Affect Regulation and the Developmentof Psychopathology. Guilford Press, pp. 81–96(chapter 5).

[10] Lauterbach D, Koch EI, Porter K. (2007) Therelationship between childhood support and lateremergence of PTSD. Journal of Trauma Stress 20,857–67.

[11] Pynoos RS, Steinberg AM, Layne CM et al. (2009)DSM-V PTSD diagnostic criteria for children andadolescents: A developmental perspective and rec-ommendations. Journal of Traumatic Stress, 22,391–398.

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[12] Cloitre M, Stolbach BC, Herman JL et al. (2009) Adevelopmental approach to complex PTSD: Child-hood and adult cumulative trauma as predictors ofsymptom complexity. Journal of Traumatic Stress22, 399–408.

[13] NICE. (2005) Post-Traumatic Stress Disorder: theManagement of PTSD in Adults and Children inPrimary and Secondary Care. London: NationalInstitute for Clinical Excellence.

[14] Yehuda R, Mulherin Engel S, Brand SR et al.(2005) Transgenerational effects of posttraumaticstress disorder in babies of mothers exposed tothe World Trade Center attacks during pregnancy.Journal of Clinical Endocrinology and Metabolism90, 4115–18.

[15] Bonanno GA, Galea S, Bucciarelli A, Vlahov D.(2007) What predicts psychological resilience afterdisaster? The role of demographics, resources, andlife stress. Journal of Consulting and Clinical Psy-chology 75, 671–82.

[16] Cook A, Spinazzola J, Ford J et al. (2005) Com-plex trauma in children and adolescents. PsychiatricAnnals 35, 390–8.

[17] van der Kolk BA. (2005) Developmental TraumaDisorder: Toward a rational diagnosis for childrenwith complex trauma histories. Psychiatric Annals35, 401–8.

[18] Pynoos R and Eth S. (1987) Witness to violence:The child interview. In: Chess Stella TAE et al.(eds), Annual Progress in Child Psychiatry and ChildDevelopment. Philadelphia, PA: Brunner/Mazel,Inc., pp. 299–326.

[19] Yule W, Perrin S, Smith P. (1999) Post traumaticstress disorders in children and adolescents. In: YuleW (ed.), Post Traumatic Stress Disorders: Conceptsand Therapy. London: Wiley, pp. 25–50.

[20] Perrin S, Smith P, Yule W. (2000) The assessmentand treatment of Post-traumatic Stress Disorder inchildren and adolescents. Journal of Child Psychol-ogy and Psychiatry 41, 277–89.

[21] Bisson JI, McFarlane AC, Rose S. (2000) Psycho-logical debriefing. In: Foa EB, Keane TM, FriedmanMJ (eds), Effective Treatments for PTSD: PracticeGuidelines from the International Society for Trau-matic Stress Studies. New York: Guilford Press, pp.39–59.

[22] Shapiro F. (2001) Eye Movement Desensitizationand Reprocessing: Basic Principles, Protocols, andProcedures, 2nd edn. New York: Guilford Press.

[23] Spector J and Read J. (1999) The current status ofEye Movement Desensitisation and Reprocessing(EMDR). Clinical Psychology and Psychotherapy6, 165–74.

[24] van der Kolk BA, Spinazzola J, Blaustein ME etal. (2007) A randomized clinical trial of eye move-ment desensitization and reprocessing (EMDR),fluoxetine, and pill placebo in the treatment ofposttraumatic stress disorder: treatment effects andlong-term maintenance. Journal of Clinical Psychi-atry 68, 37–46.

[25] Stein DJ, Ipser JC, Seedat S. (2006) Pharmacother-apy for posttraumatic stress disorder. CochraneDatabase of Systematic Reviews, Issue 1; Art. No.:CD002795; doi: 10.1002/14651858.CD002795.pub2.

[26] Donelly CL. (2003) Post-traumatic stress disorder.In: Martin A, Scahill L, Charney DS, Leckman JF(eds), Pediatric Psychopharmacology. New York:Oxford University Press, pp. 580–91.

[27] Bonanno GA. (2004) Loss, trauma, and humanresilience: have we underestimated the humancapacity to thrive after extremely aversive events?American Psychologist 59, 20–8.

FURTHER READING

Black D, Newman M, Harris Hendricks J, Mezey G(eds). (1997) Psychological Trauma: a DevelopmentalApproach. London: Gaskell.

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Child maltreatment

19Child MaltreatmentDanya GlaserDepartment of Child and Adolescent Mental Health, Great Ormond Street Hospital for Children NHSTrust, London, UK

INTRODUCTION

Child abuse and neglect is a relatively commonexperience in childhood. At the very least itis unpleasant, and at worst fatal. Non-fatalchild abuse and neglect causes a variety ofharmful effects that are mostly psychological andbehavioural, though some are physical. Intentionto harm children is not required for the definitionof child abuse and neglect. Different forms ofmaltreatment are recognized (Table 19.1) and theyoften co-occur. Retrospective studies of adultssuggest that different forms of abuse and neglectlead to different sequelae [1] but because of theco-occurrence of different forms of abuse, it isdifficult definitively to apportion the nature of theharm to the different forms. Nevertheless, somemore robust associations are now recognized, asoutlined below in the section ‘Harm to the child’.

TYPES OF MALTREATMENT

Table 19.1 shows the four types of maltreatment.Most cases of maltreatment occur within thefamily [2], with children being harmed either bytheir parents or primary carers, and occasionallyby siblings. The exception to this is sexualabuse, which is equally commonly perpetratedby someone who is known to the child or youngperson, but is not a parent or sibling. Childmaltreatment is recognized across all cultures [2].Some cultural practices, such as female genitalmutilation, constitute maltreatment.

While physical and sexual abuse may consistof single or repeated events in the child’s life,


emotional abuse and physical neglect are moreappropriately considered as pervasive aspects ofthe primary carer–child relationship. Table 19.2lists contrasting features and relationships of thedifferent forms of child maltreatment.

EPIDEMIOLOGY

In England in 2009, 34 100 children were subject toa Local Authority child protection plan, resultingfrom a decision based on a multidisciplinary con-sensus that the child continues to be at risk of harm,rather than on the substantiation of maltreatment.These numbers are, therefore, an underestimateof the actual prevalence of child maltreatment.Table 19.1 shows the distribution of forms ofmaltreatment within all child protection plans in2009 in England. However, epidemiological find-ings depend on the source of the data. Self-reportsby community samples of both children and, ret-rospectively, adults indicate that official statisticsfrom child protection agencies present a substan-tial, up to tenfold, underestimate of the occurrenceof the various forms of abuse [3].

SOCIAL AND FAMILY FACTORS

Physical child abuse and neglect are more clearlyassociated with social disadvantage in the fami-lies of the children [4]. People who abuse chil-dren, including parents, are troubled individuals,a proportion of whom have experienced abuse orneglect in their own childhood. Adolescent boyswho sexually abuse children are more likely to

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Table 19.1 Forms of maltreatment, distribution within protection plans and cumulative rates basedon self-reports, for England in 2009.

Type of Variants within Percent of Percent of youngmaltreatment type of child protection adult respondents

maltreatment plans (2009) reporting childhoodmaltreatment [3]

NeglectLack of provision

46 6—12

Lack of supervision

Physical abuse(non-accidental injury)

Causing death, injury or visible markssuch as bruises

13 5—35

Fabricated or induced illness by:

• misreporting of child’s symptoms

• interfering with investigations,specimens and treatment

• direct interference with, or harmingthe child so as to produce symptomsand signs

Sexual abusePenetrative genital or oral contact

6 25 girls, 8.7 boys

Non-penetrative genital or genital-oralcontact

5—10 girls, 1—5 boys

Non-contact sexual exposure andexploitation

13 girls, 3.7 boys

Emotional abuseEmotional unavailability

27 4—9

Hostility and rejection

Developmentally inappropriateinteractions

Exposure to domestic violence

Using the child for the fulfilment of theadult’s needs

Failing to promote the child’ssocialization

More than one type 8

Table 19.2 Differences between various forms of child abuse and neglect.

Sexual abuse Physical abuse Emotional abuse andneglect

Maltreating act orinteraction

Hidden Hidden or observed Observable

Identity of the maltreatingperson

Usually in question Sometimes known Known

Abuser and primary carer Usually differentpersons

Same or different persons Same person

Immediate protectionindicated

Yes Usually, especially withyoung children

Rarely

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have suffered or witnessed physical violence andto have experienced emotional abuse or disrup-tion to their care [5]. Emotional abuse, physicalabuse and neglect are often found in familieswhere one or both parents are suffering from men-tal illness, have a personality disorder or abusedrugs/alcohol. Violence between parents is alsoa risk factor [6]. However, no single adult psy-chopathology is consistently associated with childmaltreatment. Sexual abusers are mostly male.

Children of all ages may experience abuse andneglect. Physical neglect and emotional abuseoften start early in the child’s life, and continueas enduring patterns of care and interaction dur-ing childhood and adolescence. Physical abuse ininfancy may result from the parent’s inability tocope with the demands of the baby; this some-times causes serious injury and even death. Laterin childhood, physical abuse is more associatedwith inappropriate and harsh punishment. Sexualabuse occurs more commonly in adolescence and

in girls, although young boys and girls are alsosexually abused.

Fabricated or induced illness (previously knownas Munchausen syndrome by proxy, or factitiousdisorder by proxy) is nearly always perpetrated bymothers, and the child may also have a genuineillness.

Abuse and neglect may be self-limiting orsingle events but often continue over manyyears either as a pattern of interaction within aparticular parent–child relationship, as a patternof child-rearing or, in child sexual abuse, as anaddiction-like propensity that the same abuserextends towards more than one child.

THE HARM TO THE CHILD

Harm may be caused by a number of mechanisms(Table 19.3). Effects depend on the child’s geneticvulnerability [9], age and gender; the natureand duration of the maltreatment; the child’s

Table 19.3 Mechanism of harm associated with maltreatment.

Mechanism Examples

Specific direct effects Physical abuse causing injury or death

Emotional neglect leading to emotional withdrawal orindiscriminate affection-seeking

Effects on the developing brain [7]

Sexual abuse causing sexually transmitted diseases orunwanted pregnancy

Indirect effects Effects on later health including obesity, ischaemicheart disease, cancer [8]

Fabricated or induced illness leading to experienceunnecessary investigations and treatments

Effects of the meaning of maltreatment Sexual abuse leading to a sense of shame, depression,deliberate self-harm

Hostility and rejection leading to low self-esteem

Effects of associated emotional abuse Most physical abuse and neglect are accompanied byemotional abuse

Effects of associated carer—childrelationship

Sexual abuse may be associated with blame andnon-belief of the child by the child’s caregivers

Effects of associated social adversity Poverty, social isolation, migration, natural disasters

Effects of intervention Effects of removal of the child to inadequatealternative care

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relationship to the maltreating person; and thepresence of other, protective relationships and asupportive social context.

Mental healthThe greatest morbidity associated with childmaltreatment is psychological, emotional andbehavioural [10]. Many maltreated childrendevelop disorganized patterns of attachment [11],which are associated with maladaptive interper-sonal relationships. Physical abuse is associatedwith aggressive behaviour [12] and low self-esteem. Emotional neglect leads to educationalunderachievement and difficulties in peer rela-tionships as well as to oppositional behaviour.Sexual abuse is particularly associated withlater depression, substance abuse and self-harm,post-traumatic phenomena and inappropriatesexual behaviour, with the latter being particularlytroublesome in young children [13].

Educational progress and employmentChildren and adolescents who have been mal-treated, especially by neglect or physical andemotional abuse, underachieve educationally toa significant extent with later poor prospects foroptimal employment, even when socioeconomiceffects are controlled for [14].

Antisocial behaviourAntisocial behaviour has been shown to be sig-nificantly associated with prior child maltreat-ment [15].

RECOGNIZING MALTREATMENT

As illustrated in Table 19.2, some forms of mal-treatment are readily visible such as neglect and

emotional abuse. However, the hallmark of sexualabuse is its secrecy; physical abuse is sometimesobserved as it occurs, but is usually recognized bythe marks it leaves (Table 19.4).

Parents and abusers do not as a rule reporttheir maltreating actions. When a child presentswith difficulties suggestive of abuse or neglect, theprocess of identification and investigation is usuallymarked by:

• absence of an acceptable explanation;• some degree of denial of the possibility of abuse;• a lack of, or only partial assumption of, respon-

sibility for the child’s difficulties by the carer orabuser.

Such responses by the parents or alleged abusersconstitute the basic context for the investigation,recognition and management of child abuse andneglect. Many professionals find it difficult to con-template or accept the possibility that a parent(who may also be a patient) has harmed theirown child [16]. Almost invariably, therefore, thereis some degree of dispute or doubt during theprocess of recognizing child maltreatment. Thisis important not so much for the apportioning ofblame, but rather for the subsequent processesof both protecting the child and bringing aboutchange in the relationship between the child andtheir abuser, if they are to remain living togetheror in contact. The fact that child maltreatment mayalso lead to criminal prosecution further compli-cates matters.

The onus of proof that abuse has occurredoften falls on paediatricians, child psychiatristsand psychologists and social workers, sometimesclouding the issue of the child’s well-being infavour of parental interests. This is compoundedby a societal approach that often favours a narrowchild protection approach, which seeks evidence

Table 19.4 How child maltreatment comes to light.

Neglect Physical abuse Emotional abuse Sexual abuse

Ill-treatment of the childobserved

√May or may not

√

Harmful effects to thechild observed

√ √May or may not May or may not

Ill-treatment reported bythe child

May or may not√

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Child maltreatment

of maltreatment, over a family welfare approach.The latter, however, runs the risk of leaving chil-dren unprotected. With respect to the recognitionof child maltreatment:

• In physical abuse (including faltering growth andfabricated or induced illness) the identificationis usually made by paediatricians, radiologists orsometimes retrospectively by pathologists.

• Physical neglect is recognized by the absenceof social norms of basic child care andprovision.

• Recognition of sexual abuse relies most stronglyon the child’s verbal descriptions; 80% or moreof cases have no conclusive physical signs ofabuse. It is therefore the child’s words andcredibility that are closely tested and chal-lenged. Professionals may receive unexpecteddisclosures of abuse, usually from children. Theappropriate response is to listen but not probe,not to promise confidentiality, but to explainthat this information will need to be passed onto social services and to explore misgivings thatthe child may have about this. It is vital that awritten record is made of all such conversations.

• The ill-treatment and harmful interactions inemotional abuse are observable, but it is theextent of their harmfulness that is disputed.Emotional abuse cannot be reliably recognized

by the effects on the child, since these are notspecific to this form of maltreatment.

Regarding the suspicion of child maltreatment,the National Institute for Health and ClinicalExcellence (NICE) divides alerting features intotwo categories: Consider and Suspect, and offersgood practice guidelines appropriate to each ofthese categories to both clinicians and other pro-fessionals working with children [17].

INTERVENTION

Table 19.5 outlines four tiers of concern withrespect to child, family and environmental factors.In order to intervene appropriately, it is helpful toseparate the information arousing concern aboutthe child and family into these tiers.

Aims of interventionThe aims of intervention are, if necessary, imme-diate treatment and immediate protection. Theyusually also include healing the effects of the mal-treatment and protection from future harm.

Immediate treatmentA minority of children who have been maltreatedwill require immediate medical or psychiatric treat-ment, including children who have been seriously

Table 19.5 Tiers of concern.

Tier 0

Family and environmental factors:

Including poverty, social isolation, displacement

Tier 1

Parental risk factors:

Including mental ill-health, substance abuse, history of significant own maltreatment,domestic violence [18]

Tier 2

Parent—child interactions:

Forms of maltreatment — emotional abuse, neglect, physical abuse, sexual abuse

Tier 3

Child’s functioning:

Aspects that are attributable to maltreatment

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injured or infected with a sexually transmitted dis-ease, or who are acutely traumatized by the abuse.

Child protectionAs shown in Table 19.2, some forms of maltreat-ment require immediate protection of the child.The determination of this need is a multiagencyendeavour, led by children’s social care services.The approach with neglect and emotional abuseis usually to work towards child protection, ratherthan to gain immediate protection. Protection canbe achieved by one of the following:

• A change in the maltreating parent or their cir-cumstances through therapeutic or other work,during which the child will continue to be at risk.

• Supervision of all contact between the child andthe abuser, in practice only sustainable for briefperiods.

• Separation of the child from the maltreatingperson, which is therefore the only way ofensuring the immediate safety of the child.However, if the abuser is also the child’s primarycaregiver, there is a significant cost to achievingimmediate protection. Even when the person(s)caring for the child are not the maltreating ones,it is nevertheless necessary to assess their capac-ity to protect the child from maltreatment byothers. The most important determining factorhere is the nature of the relationship betweenthe non-abusing caregiver(s) and the abuser.The closer this is the more precarious will thechild’s position be. ‘Closeness’ here includeslove, but may also mean fear or dependency.

Ensuring protection may, therefore, requirestatutory measures either by a children’s socialcare protection plan, or through family (civil)court proceedings. The criminal law has little ifany part to play in child protection.

Treatment for the effects of maltreatmentand prevention of further maltreatmentA comprehensive treatment plan includes:

• Help for the symptomatic child, following pro-tection or accompanying work with the mal-treating caregiver to prevent continuation of themaltreatment.

• Work with the maltreating parent(s).• Support for the non-abusing caregiver(s).

• Work with the whole family, including siblingswho may not be (or appear not to be) immedi-ately involved.

• Attention to social/environmental disadvantage.

Evidence for the effectiveness of interventionsis variable [19].

As described above, there is no unitary post-abuse syndrome, even following specific formsof abuse such as sexual abuse. Evidence-basedtherapeutic approaches for the various childand adolescent mental health difficulties areindicated. In particular, children who are expe-riencing post-traumatic stress disorder (PTSD)and inappropriate sexualized behaviour benefitfrom trauma-focused cognitive behavioural ther-apy [20]. The developmental and emotional deficitsfollowing neglect need to be addressed, as far asis possible. This may be achievable by supportingthe child’s parents, providing they are willing toaccept help, and may include the treatment ofthe adults’ mental ill health and substance abuse.Experience shows that such help often needs to bemaintained for long periods, and that change is notsustained following a short, albeit intensive, courseof intervention. Many children also require educa-tional remediation for the associated educationalunderachievement. Special attention is neededfor the depression, substance abuse and self-harmthat may develop in adolescence following theexperience of childhood or adolescent abuseor neglect.

As well as emotional and behavioural difficul-ties, many maltreated children also undergo socialdisruption as a consequence of the necessary pro-tection process. These children are preoccupiedwith separations and impermanence, and shouldbe involved in age-appropriate decision-making.They require active support through this process.

The child’s parents may initially oppose profes-sional intervention. Acknowledging responsibilityfor the maltreatment, and sometimes for theirinability to protect the child, is a difficult andpainful process for the parents. They require sup-port and specific therapy geared towards change.

CONCLUSION

Child maltreatment carries a heavy burden ofharm to the child, which may continue into adult-hood and is a public health issue. Early recognition

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and intervention are necessary for preventionor the worst harm. However, recognition andeffective management involve a complex processthat requires alertness to its possibility and acoordinated, multidisciplinary and multiagencyapproach. While the family is of central impor-tance to the child’s well-being, the child’s owninterests are paramount and sometimes these maynot be achievable within the original family.

REFERENCES

[1] Mullen P, Martin J, Anderson S et al. (1996) Thelong-term impact of the physical, emotional, andsexual abuse of children: a community study. ChildAbuse and Neglect 20, 7–21.

[2] Pinheiro PS. (2006) World Report on Vio-lence Against Children. United Nations Secretary-General’s study on violence against children. NewYork: United Nations.

[3] Gilbert R, Spatz Widom C, Browne K et al. (2009)Burden and consequences of child maltreatment inhigh-income countries. Lancet 373, 68–81.

[4] Sidebotham P, Heron J, Golding J. (2002) Childmaltreatment in the ‘‘Children of the Nineties:’’deprivation, class, and social networks in a UKsample. Child Abuse and Neglect 26, 1243–59.

[5] Skuse D, Bentovim A, Hodges J et al. (1998) Riskfactors for the development of sexually abusivebehaviour in sexually victimised adolescent males:Cross-sectional study. British Medical Journal 317,175–9.

[6] Dixon L, Browne K, Hamilton-Giachritsis C. (2005)Risk factors of parents abused as children: A medi-tational analysis of the intergenerational continuityof child maltreatment. Journal of Child Psychologyand Psychiatry 46, 47–57.

[7] Glaser D. (2000) The effects of child abuse andneglect on the brain: A review. Journal of ChildPsychology and Psychiatry 41, 97–116.

[8] Felitti VJ, Anda RF, Nordenberg D et al. (1998)Relationship of childhood abuse and household dys-function to many of the leading causes of death inadults. The Adverse Childhood Experiences (ACE)Study. American Journal of Preventive Medicine 14,245–58.


[10] Herrenkohl TI, Herrenkohl RC. (2007) Examiningthe overlap and prediction of multiple forms of child

maltreatment, stressors, and socioeconomic status:a longitudinal analysis of youth outcomes. Journalof Family Violence 22, 553–62.

[11] Carlson V, Cicchetti D, Barnett, D et al. (1989) Find-ing order in disorganization: Lessons from researchon maltreated infants’ attachments to their care-givers. In: Cicchetti D and Carlson V (eds), ChildMaltreatment: Theory and Research on the Causesand Consequences of Child Abuse and Neglect. Cam-bridge: Cambridge University Press, pp. 494–528.

[12] Lansford JE, Dodge KA, Pettit GS et al. (2002) A12-year prospective study of the long-term effects ofearly child physical maltreatment on psychological,behavioral, and academic problems in adolescence.Archives of Pediatric and Adolescent Medicine 156,824–30.

[13] Glaser D. (2008) Child sexual abuse. In: Rut-ter M, Bishop D, Pine D et al. (eds), Rutter’sChild and Adolescent Psychiatry. Oxford: Wiley-Blackwell Publishing, pp. 440–58.

[14] Perez CM, Widom CS. (1994) Childhood victim-ization and long-term intellectual and academicoutcomes. Child Abuse and Neglect 18, 617–33.

[15] Egeland B, Yates T, Appleyard K et al. (2002)The long-term consequences of maltreatment inthe early years: a developmental pathway modelto antisocial behavior. Children’s Services: SocialPolicy, Research, and Practice 5, 249–60.

[16] Gilbert R, Kemp A, Thoburn J et al. (2009) Recog-nising and responding to child maltreatment. Lancet373, 167–80.

[17] National Institute for Clinical Excellence (NICE).(2009) When to Suspect Child Maltreatment: ClinicalGuidelines. RCOG Press, available at: http://www.preventviolence.info/showResourcespdf.aspx?id=7c126565-10a7-43fb-9ac4-4c46d22fff8b.

[18] Cleaver H, Unell I, Aldgate J. (1999) Children’sNeeds – Parenting Capacity: The Impact of ParentalMental Illness, Problem Alcohol and Drug Use, andDomestic Violence on Children’s Development. Lon-don: The Stationery Office.

[19] MacMillan H, Wathen CN, J Barlow et al. (2009)What works? Interventions to prevent child mal-treatment and associated impairment. Lancet 373,250–66.

[20] Cohen J, Mannarino A, Knudsen K. (2005) Treatingsexually abused children: 1 year follow-up of a ran-domized controlled trial. Child Abuse and Neglect29, 135–45.

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20The Neuroscience and Genetics ofChildhood MaltreatmentEamon McCrory, Stephane A. De Brito, and Essi VidingDevelopmental Risk and Resilience Unit, Division of Psychology and Language Sciences, UniversityCollege London, London, UK

THE IMPACT OF MALTREATMENTON BRAIN DEVELOPMENT

A growing body of research has investigated howstress, and specifically different forms of childhoodmaltreatment, can influence neural structure andfunction. These studies have employed both chil-dren who have experienced maltreatment or adultsreporting childhood histories of early adversity.The main brain imaging modalities are summa-rized in Figure 20.1. In this chapter we focus onstudies of children, first considering those thathave investigated differences in brain structure,followed by the smaller number of studies thathave investigated the potential impact of maltreat-ment on brain function.

STRUCTURAL DIFFERENCES

Subcortical structures: hippocampusand amygdalaAnimal research has shown that the hippocampusplays a central role in learning and various aspectsof memory and that these functions are impairedwhen animals are exposed to chronic stress. Stud-ies of adults with post-traumatic stress disorder(PTSD) who have histories of childhood maltreat-ment, an early form of stress, consistently reportthat these individuals have smaller hippocampalvolumes. It is surprising then that structural mag-netic resonance imaging (sMRI) studies of childrenand adolescents with maltreatment-related PTSD


consistently fail to detect decreased hippocampalvolume [1]. It is possible that the impact of stressis delayed and becomes manifest only later indevelopment.

The amygdala, another key subcortical struc-ture, plays a central role in evaluating potentiallythreatening information, fear conditioning,emotional processing and memory. Given thatexperiences of maltreatment typically occur infamily environments characterized by unpre-dictability and threat, it might be expected thatchildren growing up in such contexts wouldshow increased amygdala volume, comparableto that found in stress-exposed animals, whichshow increased dendritic arborization [2]. How-ever, a recent meta-analysis of children withmaltreatment-related PTSD did not find signif-icant differences in amygdala volume betweenmaltreated and non-maltreated children [3].By contrast, more recent studies have reportedan increase in amygdala volume in maltreatedchildren (see, e.g., Ref. [4]), suggesting thatperhaps such effects are subtle and difficult todetect reliably or are associated with heightenedforms of adversity experienced as a result ofinstitutionalization.

Cortical structures: prefrontalcortex and cerebellumThe prefrontal cortex (PFC) plays a major rolein the control of many aspects of behaviour,regulating cognitive and emotional processes

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The neuroscience and genetics of childhood maltreatment

DisadvantagesAdvantagesHow it worksImaging modality

• Difficult to conduct group comparisons• High cost• Only an indirect measure of the structural integrity of white matter

• Non-invasive• High spatial resolution

Provides information about thestructural integrity of axonalwhite matter by measuring themolecular diffusion of water inbrain tissue

DTI

• Poor temporal resolution• Analyses are complex and time consuming• Very susceptible to movement• Many contraindications• High cost• Indirect measure of brain functioning

• Non-invasive and no radiation• High spatial resolution

Detects the changes in bloodoxygenation and flow thatoccur in responses to neuralactivity

fMRI

• Poor spatial resolution• Limited to surface (cortical) activity

• Non-invasive• High temporal resolution• Low cost• Easy to use with children to study early brain functioning

Records the brain’s electricalactivity and yields detailedinformation about the temporalsequence (resolution inmilliseconds) of cognitiveoperations throughout the brain

ERP

Figure 20.1 An overview of the characteristics, advantages and disadvantages of the main brainimaging modalities used to investigate the impact of childhood maltreatment. ERP, event-relatedpotential; fMRI, functional magnetic resonance imaging; DTI, diffusion tensor imaging.

through extensive interconnections with othercortical and subcortical regions.

There are mixed findings from studiescomparing the PFC volume of children withmaltreatment-related PTSD and non-maltreatedchildren. Recent studies have reported smallerprefrontal volume associated with the experienceof maltreatment (e.g. Ref. [5]), and less prefrontalwhite matter, while other studies have reportedlarger grey matter volume of the middle-inferiorand ventral regions of the PFC in maltreatedgroups. There are several possible reasonsfor these inconsistent findings and it is likelythat methodological differences across studies,including the use of different imaging techniquesand age groups of children, might at least partlyaccount for these reported differences [6]. It isalso possible that there are regionally specificwindows of vulnerability in brain development;the frontal cortex undergoes significant structuralchange during adolescence. We know that sexualabuse, for example, during the adolescent periodis more associated with structural differences inthis brain region compared to other regions [7].Unfortunately, most brain imaging studies havenot systematically considered the age at which

different kinds of abuse have occurred; from aclinical perspective it would be helpful for furtherresearch to systematically investigate the relativevulnerability of different brain regions at differentages to different forms of early adversity.

By contrast, decreased volume of the cerebel-lum in children and adolescents with a historyof maltreatment has been a consistent findingin the literature [6], chiming with growingevidence that this structure plays a crucial rolein emotion processing and fear conditioningvia its connection with limbic structures andthe hypothalamic–pituitary axis (HPA). Thecerebellum has also been shown to be involvedin executive functioning, which is impaired inchildren with a history of maltreatment [8].

Corpus callosum and other whitematter tractsThe corpus callosum (CC) is the largest whitematter structure in the brain and controls inter-hemispheric communication of a host of processes,including, but not limited to, arousal, emotion andhigher cognitive abilities. With the exception ofone study, decreases in CC volume have consis-tently been reported in maltreated children and

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adolescents compared to non-maltreated peers [1].Recent studies that have employed diffusion tensorimaging (DTI) have found differences in mal-treated children in frontal and temporal whitematter regions, including the uncinate fasciculus,which connects the orbitofrontal cortex to the ante-rior temporal lobe, including the amygdala (e.g.Ref. [9]). The extent of the white matter differ-ences observed by Govindan and colleagues wasassociated with longer periods within an orphan-age and may underlie some of the socio-emotionaland cognitive impairments exhibited by maltreatedchildren.

FUNCTIONAL DIFFERENCES

In contrast to the number of studies examiningstructural brain differences, only a few have inves-tigated possible functional correlates associatedwith maltreatment using brain imaging techniquessuch as functional MRI (fMRI) or electrophysio-logical techniques.

fMRI studiesTo date, five fMRI studies have compared mal-treated children to non-maltreated children. Build-ing on the experimental evidence that maltreatedchildren show hypervigilance to threatening facialcues, two fMRI studies have examined the neuralcorrelates of face processing in this population.These studies have reported that maltreatedchildren are characterized by increased amygdalaresponse to threatening cues in comparison tonon-maltreated children [10] – findings consistentwith amygdala volume differences observed in thestructural MRI studies reviewed above. Two otherstudies assessed response inhibition and observedincreased activation in the anterior cingulatecortex (ACC) in maltreated youths as comparedto controls. These results suggest impairedcognitive control in maltreated youths, which, inturn, could confer risk for psychopathology [11],especially in the context of heightened subcorticalresponses such as that observed during affectiveprocessing. The fifth study used a verbal declar-ative memory task and compared youths withpost-traumatic stress symptoms (PTSS) secondaryto maltreatment with healthy controls [12]. Duringthe retrieval component of the task, the youthswith PTSS exhibited reduced right hippocampal

activity, which was associated with greater severityof avoidance and numbing symptoms.

Event-related potential (ERP) studiesMuch of the existing ERP research has comparedthe pattern of brain response of adversely treatedchildren and healthy children when processingfacial expressions, an ability that is usually mas-tered by the preschool years. When comparedwith non-institutionalized peers, institutionalizedchildren who have experienced severe social depri-vation showed a pattern of cortical hypoactivationwhen viewing emotional facial expressions, andfamiliar and unfamiliar faces [13]. In contrast, asecond set of important studies has provided con-vincing evidence that school-aged children whohad been exposed to physical abuse show increasesin brain activity specific to angry faces and requiremore attentional resources to disengage from suchstimuli (e.g. Ref. [14]). These ERP findings areconsistent with recent fMRI evidence and suggest

Box 20.1 Summary of structuraland functional brain differencesassociated with maltreatment

In summary, there is relatively consistentevidence for reduced white matter andreduced grey matter volume in thecerebellum of maltreated children, but nodifferences in relation to the hippocam-pus. The structural findings are moremixed for the PFC. Functional brain imag-ing research suggests that experience ofmaltreatment is associated with increasedamygdala and anterior cingulate cortexresponse in affective and cognitive controlparadigms, respectively. Event-relatedpotential (ERP) studies have found thatchildren who have experienced severesocial deprivation show a generalized pat-tern of cortical hypoactivation. Increasedbrain activity, specifically to angry faces inprefrontal regions, has also been observedin physically maltreated children, likelyto represent the neural correlates ofincreased attentional monitoring for socialthreat.

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that some maltreated children are allocating moreresources and remain hypervigilant to potentialsocial threat in their environment, likely to be atthe cost of other developmental processes.

THE ROLE OF GENETIC INFLUENCES

It is a common but often striking clinical experienceto find that two children who have experiencedvery similar patterns of early adversity have verydifferent outcomes. While this may be partly dueto specific environmental or psychological factorscharacterizing one child, but not the other, there isincreasing evidence that such differential outcomemay in part at least be due to genetic differences.

We now know that many of the psychiatric out-comes that are associated with maltreatment, suchas PTSD, depression and antisocial behaviour, arepartly heritable. However, it is incorrect to thinkthat there are particular genes for these disor-ders. Rather, we are learning that there are a widenumber of genetic variants that may subtly alterthe structure and functioning of neural circuitryand hormonal systems that are crucial in cali-brating our individual response to social affectivecues, and in regulating our stress response [15].In recent years, researchers have focused in par-ticular on the way in which such genetic variantsand adverse environments may interact. Such geneby environment (G × E) interaction research hasdemonstrated that for a range of genetic variants(known as polymorphisms) childhood maltreat-ment can increase the risk of later psychopathol-ogy for some children more than others. Forexample Caspi and colleagues [16] were the first toreport on an interaction of a measured genotype(MAOA, monoamine oxidase A) and environ-ment (maltreatment) for a psychiatric outcomeand demonstrated that individuals who are carri-ers for the low-activity allele (MAOA-l) were at anincreased risk for antisocial behaviour disordersfollowing maltreatment. Imaging genetic studieshave found that the risk genotype, MAOA-l, isrelated to hyper-responsivity of the brain’s threatdetection system and reduced activation in emo-tion regulation circuits. This work suggests a neuralmechanism by which the MAOA genotype engen-ders vulnerability to reactive aggression followingmaltreatment [17].

In other words, G × E research suggests thata child’s genotype may partly determine their

level of risk and resilience for adult psychiatricoutcomes, including depression and PTSDfollowing childhood maltreatment (e.g. Ref. [18]).It is important to bear in mind, however, that pos-itive environmental influences, such as social sup-port, can promote resilience, even in those childrencarrying ‘risk’ polymorphisms exposed to maltreat-ment [18]. This finding illustrates the importantpoint that when considering a G × E interaction,positive environmental influences (such as contactwith a supportive attachment figure), are asrelevant to consider as negative environmentalinfluences such as maltreatment. Future researchwill investigate the influence of clinical interven-tions as a positive environmental factor that mayserve to moderate environmental and genetic risk.

CLINICAL IMPLICATIONS

There is accumulating evidence pointing to avariety of neurobiological changes associated withchildhood maltreatment. Such changes can, on theone hand, be viewed as a cascade of deleteriouseffects that are harmful for the child; however, amore evolutionary and developmentally informedview would suggest that such changes are infact adaptive responses to an early environmentcharacterized by threat. If a child is to respondoptimally to the challenges posed by his/hersurroundings then early stress-induced changesin neurobiological systems can be seen as ‘pro-gramming’ or calibrating those systems to matchthe demands of a hostile environment. From aclinical perspective, such adaptation may heightenvulnerability to psychopathology, partly due to thechanges in how emotional and cognitive systemsmediate social interaction [19]. For example,early-established patterns of hypervigilance, whileadaptive in an unpredictable home environment,may be maladaptive in other settings, thus increas-ing vulnerability for behavioural, emotional andsocial difficulties.

While initial research has focused on these neu-robiological adaptations following maltreatment,there is increasing interest in exploring the conceptof resilience and those factors that may promote orenhance neurobiological mechanisms importantfor emotional regulation and coping. Specifically,there is emerging evidence from genetic and neu-robiological research supporting the importanceof a reliable adult caregiver, and the role they

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can play in helping to scaffold the child’s abilityto regulate stress [18,20]. Such work will begin toshed light on how professionals can intervene moreeffectively to promote better systemic structuresaround children that improve resilience and mod-erate the impact of maltreatment. We are likelyto see an increasingly fruitful dialogue betweendevelopmental research, focused on a child’s psy-chological representations of their social world,and neurobiological research, focused on putativeneural mechanisms underlying adaptive responsesto stress and effective emotional regulation.

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[2] Lupien SJ, McEwen BS, Gunnar MR, Heim C.(2009) Effects of stress throughout the lifespan onthe brain, behaviour and cognition. Nature ReviewsNeuroscience 10, 434–45.

[3] Woon FL, Hedges DW. (2008) Hippocampaland amygdala volumes in children and adultswith childhood maltreatment-related posttraumaticstress disorder: A meta-analysis. Hippocampus 18,729–36.

[4] Tottenham N, Hare TA, Quinn BT et al. (2010)Prolonged institutional rearing is associated withatypically large amygdala volume and difficultiesin emotion regulation. Developmental Science 13,46–61.

[5] Carrion VG, Weems CF, Richert K, Hoffman BC,Reiss AL. (2010) Decreased prefrontal cortical vol-ume associated with increased bedtime cortisol intraumatized youth. Biological Psychiatry 68, 491–3.

[6] McCrory E, De Brito SA, Viding E. (2010) Researchreview: The neurobiology and genetics of maltreat-ment and adversity. Journal of Child Psychologyand Psychiatry and Allied Disciplines 51, 1079–95.

[7] Andersen SL, Tomada A, Vincow ES et al. (2008)Preliminary evidence for sensitive periods in theeffect of childhood sexual abuse on regional braindevelopment. Journal of Neuropsychiatry and Clin-ical Neurosciences 20, 292–301.

[8] Beers SR, De Bellis MD. (2002) Neuropsycholog-ical function in children with maltreatment-related

posttraumatic stress disorder. American Journal ofPsychiatry 159, 483–6.

[9] Govindan RM, Behen ME, Helder E, Makki MI,Chugani HT. (2010) Altered water diffusivity incortical association tracts in children with earlydeprivation identified with tract-based spatial statis-tics (TBSS). Cerebral Cortex 20, 561–9.

[10] Tottenham N, Hare T, Millner A et al. Elevatedamygdala response to faces following early depri-vation. Developmental Science (in press); DOI:10.1111/j.1467-7687.2010.00971.x.

[11] Mueller SC, Maheu FS, Dozier M et al. (2010)Early-life stress is associated with impairment incognitive control in adolescence: an fMRI study.Neuropsychologia 48, 3037–44.

[12] Carrion VG, Haas BW, Garrett A, Song S, ReissAL. (2010) Reduced hippocampal activity in youthwith posttraumatic stress symptoms: an fMRI study.Journal of Pediatric Psychology 35, 559–69.

[13] Parker SW, Nelson CA, Zeanah CH et al. (2005) Anevent-related potential study of the impact of insti-tutional rearing on face recognition. Developmentand Psychopathology 17, 621–39.

[14] Pollak SD, Tolley-Schell SA. (2003) Selective atten-tion to facial emotion in physically abused children.Journal of Abnormal Psychology 112, 323–38.

[15] Viding E, Williamson DE, Hariri AR. (2006)Developmental imaging genetics: Challenges andpromises for translational research. Developmentand Psychopathology 18, 877–92.


[17] Viding E and Frith U. (2006) Genes for suscepti-bility to violence lurk in the brain. Proceedings ofthe National Academy of Sciences of the USA 103,6085–6.

[18] Kaufman J, Yang BZ, Douglas-Palumberi Het al. (2006) Brain-derived neurotrophic factor-5-HTTLPR gene interactions and environmentalmodifiers of depression in children. Biological Psy-chiatry 59, 673–80.

[19] Pollak SD. (2008) Mechanisms linking early expe-rience and the emergence of emotions: Illustrationsfrom the study of maltreated children. CurrentDirections in Psychological Science 17, 370–5.

[20] Dozier M, Peloso E, Lewis E, Laurenceau JP,Levine S. (2008) Effects of an attachment-basedintervention on the cortisol production of infantsand toddlers in foster care. Development and Psy-chopathology 20, 845–59.

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Section 5

Atypical Development

Section 5a

Infancy and Early Childhood

Feeding and eating disorders in infancy and childhood

21Feeding and Eating Disorders in Infancyand ChildhoodRachel Bryant-WaughGreat Ormond Street Hospital for Children NHS Trust, London, UK

INTRODUCTION

Feeding behaviour develops and is best understoodwithin a bio-psycho-social context. Normal feedingrequires the successful integration of healthy,developing physical and psychological function, aswell as a facilitative interpersonal context. Normalchildhood eating is not well defined, and thereare limited data to help determine the edges ofdisorder, or ‘caseness’. Additionally, some parentsor caregivers might experience their child’s eatingbehaviours as problematic, yet on clinical assess-ment the child might be deemed to be presentingwith feeding or eating behaviours well withinthe normal range. In such instances, interactionsaround feeding can become dysfunctional, requir-ing clinical intervention. It has been suggestedthat early feeding and eating disturbances mighthelpfully be approached and understood moreexplicitly within an interpersonal context ratherthan being located solely in the child [1]. Thedistinction between transient feeding problemsand those likely to become more chronic andsevere is often difficult to make; there is almost noresearch evidence underpinning the identificationof presenting features, or combinations of features,associated with a poorer prognosis or response totreatment.

PRESENTATION

In clinical practice children present with a range offeeding and eating difficulties (see Box 21.1), manyof which are of uncertain nosological status [2].


Delayed or absent feeding skills can result fromdifferent factors. Some children with developmen-tal disorders or specific medical conditions mightbe unable to drink or eat due to delay or dysfunc-tion in their ability to latch, suck, chew or swallow.Others might present with delay in feeding skillsdue to having experienced enteral feeding. Notuncommonly children remain dependent on tubefeeding longer than is medically necessary dueto missed learning opportunities or lack of atimely structured programme of tube weaning.Children who remain tube dependent beyond theage of 5 years experience particular difficultieswith tube weaning [3]. A few children presentwith delayed feeding skills because they have notbeen offered opportunities to progress with feedingdevelopment.

A number of children present with difficulty inmanaging or tolerating ingested fluids or foods, asevidenced by gagging, retching, choking or vom-iting. Some children brought to clinical attentionfor a feeding disorder have a previously undiag-nosed underlying intolerance or other gut problem,resulting in diarrhoea, constipation or abdominaldiscomfort. Reluctance to feed can significantlyresolve with appropriate medical management ofphysical symptoms where indicated. Where nophysical causes can be identified, psychologicalor behavioural treatment approaches are moreappropriate.

Lack of appetite or disinterest in food can alsobe associated with a number of different factorsencompassing other mental and behavioural

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Infancy and early childhood

Box 21.1 Common childhood feedingand eating disorder presentations

• Delayed or absent feeding skills

• Difficulty managing or toleratingingested fluids or foods

• Lack of appetite or interest in food

• Avoidance or refusal to eat based onsensory aspects of food

• Fear-based avoidance or refusal to eatbased on aversive consequences

• Utilizing specific behaviours related tofeeding/eating to comfort, self-sootheor self-stimulate.

disorders such as pervasive developmental disor-der, hyperkinetic disorder or attachment disorder,as well as chronic medical conditions and use ofcertain medications. In infants, lack of appetiteor interest in food might be associated withregulatory difficulties, such as excessive crying orsleeping. Infants experiencing parental neglect,stress or trauma may fail to develop healthyhunger-satiety responses, presenting with feedingproblems and associated growth delay. However,some children present with a clear lack of interestin food and eating but are otherwise developingand functioning normally. Such children fail orrefuse to eat sufficient amounts, tend not to com-municate hunger, and can present with falteringgrowth and in some cases extreme underweight.This presentation is seen throughout childhood,and in older children is often associated withsadness, worry and other emotional difficulties.

Avoidance or refusal to eat based on sen-sory aspects of food is a relatively commonpresentation, and is referred to by a number ofdifferent terms in the literature, such as sensoryfood aversion, or selective eating. Children withthis type of presentation consistently refuse foodsbased on texture, taste, appearance, smell ortemperature. In general such children have arelatively restricted range of preferred foods,which they will eat without difficulty. Often weightand growth are normal, but the accepted dietcan be deficient in essential vitamins or mineralsand/or be excessively high in fats, salt or sugar.

This type of presentation is relatively common inchildren with autism spectrum disorders, but alsooccurs in children without such a diagnosis. Attimes of pressure or stress, the accepted range maybe reduced to a smaller number of ‘safe’ foods.

Children who have had traumatic or unpleas-ant experiences involving the gastrointestinal tract(e.g. frequent vomiting, nasogastric tube feeding,suctioning) may present with an extreme unwill-ingness or reluctance to eat. On observation suchchildren may display typical fear-based avoidancebehaviours, or safety behaviours such as very slowchewing or reluctance to accept anything otherthan smooth textures. Food refusal or avoidance isrelated to past experience, and associated expec-tation or concern about aversive consequences ofeating. In some cases these presentations can beconceptualized as a specific phobia, and can behelpfully formulated and treated as such.

Finally, a number of children present withbehaviours related to feeding or eating where theprimary function seems to be to derive some levelof comfort, self-soothing or self-stimulation. Suchbehaviours include the eating of non-nutritivesubstances, as in pica (see ‘Diagnosis’ below).This is often found in association with mentalretardation, but not exclusively so, as it is also seenin children of normal cognitive ability. Repeatedregurgitation and re-chewing, and re-swallowingof food, as in rumination disorder (see ‘Diagnosis’below) appears to serve a similar function.

DIAGNOSIS

Children with feeding difficulties tend to presentin a range of different clinical settings and are seenby clinicians from a range of specialties, whichhas contributed to a wide array of descriptive anddiagnostic terms being used often for very similarpresentations. ‘Feeding Disorder’ is the diagnosticterm used in ICD-10 (International Classificationof Mental and Behavioural Disorders in Childrenand Adolescents: F98.2 Feeding disorder of infancyand childhood) [4] and DSM-IV-TR (Diagnosticand Statistical Manual of Mental Disorders, FourthEdition – Text Revision: 307.59 Feeding Disorderof infancy or early childhood) [5]. Both sets of cri-teria require failure to eat adequately associatedwith weight loss or failure to gain weight over aperiod of at least 1 month prior to presentation.Both state that the failure to eat adequately is

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not directly due to another medical condition oranother mental disorder, and both require onsetof the disturbance before the age of 6 years. Inpractice, many children presenting with significantfeeding problems do not present with low weight,and they therefore fail to meet diagnostic crite-ria. The mismatch between what is seen in clinicalpractice and current diagnostic criteria is illus-trated by a study demonstrating that only around12% of children presenting to one feeding disor-ders clinic met DSM-IV-TR criteria for FeedingDisorder [6].

Other disorders currently included under thegeneral heading of feeding disorders include Picaand Rumination Disorder. Pica is included in ICD-10 in the mental and behavioural disorders section;it is also included in DSM-IV-TR. RuminationDisorder is included in DSM-IV-TR, but doesnot appear as a separate diagnosis in the mentaland behavioural disorders section of ICD-10. Thediagnostic criteria for ICD-10 Feeding Disorderinclude mention of rumination, and the sectionFeeding Problems of Newborn (P92) includesRegurgitation and Rumination in Newborns,although not identified as a behavioural or mentaldisorder. Both pica and rumination presentationsare seen in young children, but are also seen inolder individuals. Current proposals for DSM 5include revising the placement of these twodisorders so that they are no longer identifiedas disorders of infancy or early childhoodalone [7].

Some clinicians working with young childrenwith feeding disorders prefer to use the Zero toThree system (DC:0–3R) [8]. This is a diagnosticclassification system specifically for mental healthand developmental disorders of infancy andearly childhood. It includes a section on FeedingBehaviour Disorder and provides descriptivecriteria for six subcategories (Feeding Disorder ofState Regulation; Feeding Disorder of Caregiver-Infant Reciprocity; Infantile Anorexia; SensoryFood Aversions; Feeding Disorder Associatedwith Concurrent Medical Conditions; FeedingDisorder Associated with Insults to the Gastroin-testinal Tract). Finally, a number of children withfeeding disorders present to paediatric services,in particular paediatric gastroenterology clinics.Rome III is an internationally established systemfor the diagnosis and classification of functionalgastrointestinal disorders (FGIDs) [9], which

overlaps with behavioural and mental disorderclassifications. Relevant to this chapter is theoverlap between Infant Rumination Syndrome(in Rome III as a FGID), Regurgitation andRumination in Newborns (ICD-10) and Rumina-tion Disorder as a mental/behavioural disorder inDSM-IV-TR.

ASSESSMENT

Due to the complex nature of feeding, clinicalassessment must include information across a num-ber of areas. Box 21.2 summarizes core recom-mended components of assessment for a childhoodfeeding or eating disorder.

There are few standardized, well-validatedassessment measures relating to early feedingand eating difficulties. There are no widely useddiagnostic interviews, and the majority of instru-ments are parent-completed questionnaires suchas the Behavioral Pediatrics Feeding AssessmentScale [10]. Observation of a feeding situation isextremely useful.

EVALUATION OF RISK ANDPRIORITIZATION OF AREASFOR INTERVENTION

Box 21.3 includes the main domains of develop-ment and function usefully considered by cliniciansin relation to determining clinical risk and prioriti-zation of areas for intervention.

Determining the nutritional adequacy of achild’s diet includes an estimation of the overallenergy intake as well as a nutritional breakdown.Specific nutritional deficits, for example as in irondeficiency anaemia, should be treated. It is impor-tant to note that children’s energy needs varyconsiderably between individuals. The main issuefor the clinician is to determine whether the child isat short- and/or longer-term physical risk if currentintake continues, and if so to put in place stepsto improve nutritional adequacy. This might bethrough supplementation, behavioural or psycho-logical interventions, or a combination of these.

Childhood feeding and eating difficulties canhave varying effects on weight, growth and physicaldevelopment/function; if growth is clearly drop-ping down centiles, intervention is indicated. Otheraspects of development are also important to con-sider; for example, is a dependence on soft or

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Box 21.2 Core components of clinical assessment interview

• Current feeding — oral, tube-fed, self feeding, etc.

• Energy and nutritional breakdown of current intake

• Weight, height, BMI (body mass index) centile

• Developmental history — including early feeding and any history of forced feeding

• Medical history — including oro-motor/swallow problems, history of reflux, vomiting, tubefeeding, allergies/intolerances

• General behaviour — at home and at nursery/school, including child’s attitude to messyplay, signs of oral aversion (e.g. refusal to brush teeth)

• Caregiver concept of problem (e.g. medical/psychological), expectations and previouslytried strategies

• Relevant family medical history — atopy, intolerances, feeding problems in siblings

• Structure of family mealtime and family attitudes to mealtimes

• Caregiver mental health and food/eating/weight history

• Family life events and caregiver support network

• Observation of mealtime situation to assess feeding interaction between child and caregiver

• School/nursery/relevant other views about child and ability to offer support around feeding.

pureed foods holding the child back in terms ofdeveloping appropriate biting and chewing skills?

Some children with eating difficulties mightnot present with nutritionally inadequate diets orweight or growth impairment, for example wherethere is a continued dependence on toddler orbaby foods in a school-aged child. In such casesthe eating problem can have a significant negativeimpact on social and emotional development andfunction. The child might refuse to mix with peersat mealtimes and miss out on important social andeducational occasions, such as visiting friends orgoing on school outings. Such events are importantin relation to developing independence, autonomyand social competence. Some children present withincreasing anxiety or distress in relation to theireating problems, experiencing embarrassment, lowmood or frustration. Irrespective of the presenceor absence of physical sequelae of the eating dif-ficulty, such features form an important focus forclinical attention.

It is well recognized that parenting a child withfeeding or eating difficulties can be stressful anddistressing. In some families, interactions between

Box 21.3 Main domains for consider-ation at presentation

Recommended areas for consideration atassessment in relation to risk and prioriti-zation of intervention:

• Nutritional adequacy of intake (overallenergy intake and nutritionalbreakdown).

• Impact of feeding/eating disturbanceon weight, growth and physicaldevelopment/function.

• Impact of feeding/eating disturbanceon social and emotional development/function.

• Impact of feeding/eating disturbanceon interaction with caregiver andfamily function.

child and caregiver can become fraught anddifficult, and parents may feel anxious, frustratedor inadequate. Family social behaviour around

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food and eating can be affected, and disagreementsbetween caregivers about management of eatingbehaviour can contribute to family tension andconflict. This can carry with it a risk of the childbeing hit, risk of precipitating or exacerbatingparental mental health problems, increased riskof relationship difficulties between parents andother close family members, and the emergence ofbehaviour problems in siblings.

TREATMENT

There is a very poorly developed evidence base forfeeding disorder treatment interventions. A reviewof the literature on treatment of childhood feed-ing disorders characterized by significant refusalor selectivity highlights that the majority of pub-lications over the past few decades have beenbased on single case research [11]. There are nowell-designed, well-controlled treatment studies oflarge cohorts of well-defined cases. In general thereis a lack of standardized, replicable interventions.Behavioural interventions are common, but otherareas are important in intervention, as summarizedin Box 21.4 [12]. In general, comprehensive, multi-faceted approaches are required, which are usuallydelivered in a multidisciplinary team context [13].

CONCLUDING COMMENTS

It is often difficult for clinicians to clearly separateout somatic and psychological aspects of pre-sentations, and a significant number of childrenpresenting with clinically significant difficultiesfail to meet diagnostic criteria. The prevailingsituation regarding classification and terminology

Box 21.4 Core components oftreatment

• Improve nutritional status

• Facilitate development ofappetite/skills acquisition opportunities

• Behavioural/psychological interventions

• Educate and support caregivers

• Liaison with wider system, to includeschool, other care providers

represents a significant problem for the fieldand has contributed to a relatively poor state ofknowledge with regard to treatment interventions,course, prognosis and outcome. This represents amajor challenge and a priority for further work.In addition robust, well-validated assessmenttools are lacking, making it difficult to obtainreliable incidence and prevalence rates. There arefew long-term follow-up studies of early feedingproblems from which to gauge longer term risks,and very limited longitudinal data of specific typesof feeding difficulty leading to relatively poorknowledge about course and prognosis. We doknow, however, that behavioural interventions areoften associated with significant improvementsin feeding behaviour [11], and with proposalsfor DSM 5 and ICD-11 on the horizon, newopportunities for research in relation to treatmentand outcome may be stimulated.

REFERENCES

[1] Davies WH, Berlin KS, Sato AF et al. (2006)Reconceptualising feeding and feeding disordersin interpersonal context: The case for a relationaldisorder. Journal of Family Psychology 20, 409–17.

[2] Nicholls D and Bryant-Waugh R. (2009) Eatingdisorders of infancy and childhood: definition, symp-tomatology, epidemiology and comorbidity. Childand Adolescent Psychiatric Clinics of North America18, 17–30.

[3] Wright CM, Smith KH, Morison J. (2010) With-drawing feeds from children on long term enteralfeeding: factors associated with success or fail-ure. Archives of Disease in Childhood doi:10.1136/adc.2009.179861.

[4] World Health Organization. (1992) The ICD-10Classification of Mental and Behavioural Disorders.Clinical Descriptions and Diagnostic Guidelines.Geneva: World Health Organization.

[5] American Psychiatric Association. (2000) Diagnos-tic and Statistical Manual of Mental Disorders, 4thedn. Text Revision. Arlington, VA: American Psy-chiatric Association.

[6] Williams K, Riegel K, Kerwin M. (2009) Feedingdisorder of infancy or early childhood: How often isit seen in feeding programs? Journal of Child HealthCare 38, 123–36.

[7] Bryant-Waugh R, Markham L, Kreipe RE, WalshBT. (2010) Feeding and eating disorders in child-hood. International Journal of Eating Disorders 43,98–111.

[8] ZERO TO THREE. (2005) Diagnostic Classifica-tion of Mental Health and Developmental Disorders

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of Infancy and Early Childhood: Revised edition(DC:0–3R). Washington, DC: ZERO TO THREEPress.

[9] Drossman DA, Corazziari E, Delvaux M et al. (2006)Rome III: The Functional Gastrointestinal Disor-ders, 3rd edn. McLean, VA: Degnon Associates.

[10] Crist W and Napier-Phillips A. (2001) Mealtimebehaviors of young children: a comparison of nor-mative and clinical data. Journal of Developmentaland Behavioral Pediatrics 22, 279–86.

[11] Sharp WG, Jaquess DL, Morton JF, Herzinger CV.(2010) Pediatric feeding disorders: a quantitativesynthesis of treatment outcomes. Clinical Child and

Family Psychology Review doi: 10.1007/s10567-010-0079.7.

[12] Bryant-Waugh R and Piepenstock E. (2008) Child-hood disorders: Feeding and related disorders ofinfancy or early childhood. In: Tasman A, Kay J,Lieberman JA, First MB, Maj M (eds), Psychiatry,3rd edn. New York: Wiley, pp. 830–46.

[13] Wolke D, Skuse D, Reilly S. (2006) The manage-ment of infant feeding problems. In: Cooper PJand Stein A (eds), Childhood Feeding Problemsand Adolescent Eating Disorders. Hove: Routledge,pp. 41–91.

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Literacy disorders

22Literacy DisordersValerie Muter1 and Margaret J. Snowling21Great Ormond Street Hospital for Children NHS Trust, London, UK2Department of Psychology, University of York, York, UK

WHAT’S NEW

• Literacy disorders are now recognized as dimensional, with no clear cut-off between typicaland impaired reading; ‘diagnosis’ is defined according to context, e.g. the school system.

• Disorders of reading accuracy stemming from phonological (speech sound processing)difficulties are partially independent from disorders of reading comprehension, which areassociated with broader oral language impairments.

• Literacy disorders tend to co-occur alongside other learning difficulties (e.g. maths disordersand attention disorders).

• Different forms of literacy disorder require different interventions; there is now an evidencebase of effective interventions to promote phonological skills and for treatments that fosterlanguage (especially vocabulary) development.

• Protective factors play an important part in improving the outcome for children with literacydisorders. These include early identification and high-quality intervention, the child’s abilityto maintain attention and motivation, conditions that foster high levels of print exposure,encouragement to engage in activities in which the child might excel, and family support.

• Children who have severe and complex literacy problems (treatment non-responders) willneed intensive and high-quality learning support that is sustained into the teenage years andbeyond.

DEFINITION, INCIDENCE,PERSISTENCE AND CO-OCCURRENCE

Disorders of literacy are arguably the most studiedand best understood of all the cognitive disordersof childhood. In this chapter we shall focus onboth disorders of reading accuracy (dyslexia) andreading comprehension difficulties. Dyslexia is acommon disorder affecting around 3–6% of chil-dren, with an over-representation of boys [1]. A


simple definition of dyslexia is a learning disorderthat primarily affects reading and spelling devel-opment. A more precise definition used by theInternational Dyslexia Association views dyslexiaas ‘a specific learning difficulty of neurobiologi-cal origin [. . .] characterised by difficulties withaccurate and/or fluent word recognition and poorspelling. These difficulties typically result from adeficit of the phonological component of language.’The notion that in dyslexia ‘reading achievement is

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substantially below expectation given the person’schronological age, measured intelligence and age-appropriate education’ has now fallen from favourand this discrepancy definition may not be used inDSM-5 (Diagnostic and Statistical Manual of Men-tal Disorders, Fifth Edition – in preparation). It isnow recognized that dyslexia occurs across a widerange of abilities; dyslexia is not an ‘all-or-none’category but rather a dimensional disorder witha number of behavioural outcomes. The child’seducational history is also of critical importance indetermining the clinical picture and it should beborne in mind that inadequate teaching may bea sufficient explanation for some children’s poorreading skills.

Dyslexia is a life-long disorder, and manyaffected individuals experience problems of read-ing fluency and spelling that persist into adulthooddespite intervention. Dyslexia commonly co-occurs alongside other learning difficulties, such asspecific language impairment (SLI), mathematicalproblems, attention deficit hyperactivity disorder(ADHD) or motor difficulties [2].

The goal of reading is not only to access theprinted word, but also to extract meaning fromit. It is estimated that 7–10% of middle school-age children can read words accurately but fail tounderstand what they read [3]. These poor compre-henders are often ‘hidden’ within their classroomsbecause their fluent reading masks underlyingdifficulties.

ACQUIRING LITERACY SKILLS

In order to understand why children fail to learnto read accurately and with understanding, it isimportant to have a clear picture of typical readingdevelopment. The Simple View of Reading pro-poses that variations in reading development canbe understood in terms of two relatively separateunderlying skills: word recognition and languagecomprehension.

Two critical foundation skills for acquiring wordrecognition skill during the first 2 years at schoolare phoneme awareness (the ability to analysespeech sounds within words) and letter-soundknowledge. Together these skills in pre-schoolyears account for almost 90% of the variancein reading skill at age 6 years. Performance onspeeded naming tasks (naming pictures, colours,letters or digits as rapidly as possible) is also

predictive of individual differences in reading,especially of reading fluency.

While learning to recognize printed wordsdepends largely on creating ‘mappings’ betweenorthography and phonology, the developmentof reading comprehension depends on broaderoral language skills, such as knowledge of word-meanings, the ability to understand sentences,to make inferences where appropriate and toremember what was read in order to create anintegrated and cohesive sense of the text [4].

It has been argued that the ease of acquir-ing fluent and accurate reading depends on thewriting system in which the child is learning [5].English orthography contains inconsistent letter-sound mappings and permits irregular forms; it istherefore classified as ‘opaque’. In contrast, lan-guages such as Italian, Greek and German havea ‘transparent’ writing system in which sound-to-letter correspondences are regular and consistent.Empirical studies suggest that it is harder to learnto read in English than in transparent orthogra-phies but findings are difficult to interpret becauseof variations in cultural practices surrounding read-ing instruction in different languages. The childwith dyslexia learning in a transparent (as opposedto opaque) orthography would be expected tohave fewer difficulties in learning about spelling-to-sound consistencies, but may nonetheless havepersisting difficulties with reading fluency.

THE NATURE OF IMPAIRMENT INCHILDREN WITH LITERACY DISORDERS

Children with dyslexia fail to learn to read becauseof an underlying weakness in their phonologi-cal system. This weakness is indicated by poorperformance on a wide range of phonologicaltasks, such as verbal short-term memory tests,deleting specified phonemes from words, speeded(rapid) naming and repeating nonwords. Diffi-culties in processing, memorizing and analysingspeech segments in words invariably results inproblems of learning to decode in children withdyslexia. The most direct means of investigatingthis decoding deficit is to ask children to readnonwords like ‘kig’ and ‘ploob’. Children withdyslexia have great difficulty reading nonwords,even when compared with younger children. Chil-dren with dyslexia learning to read in transparentorthographies tend to have fewer difficulties in

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Literacy disorders

word decoding, but are still likely to have problemswith reading fluency and spelling [6].

In contrast to children with dyslexia, poor com-prehenders perform well on tests of phonologicalskills. They do, however, experience problemswith a wide range of language-related tasks thatassess oral language (vocabulary, grammar andoral expression), higher level language skills(including narrative and use of figurative lan-guage), metacognitive processes (integration andinference making, knowledge of story conventionsand structures) and executive processes (verbalworking memory, suppression and inhibition).Nation et al. [7] carried out a longitudinal studyof poor reading comprehenders from the ages of 5to 8 years; the children assessed as having readingcomprehension difficulties at age 8 showed orallanguage problems that were present at schoolentry 3 years earlier. Such findings suggest thatlanguage problems are causally related to laterreading comprehension difficulties.

Like most developmental disorders, dyslexiaand reading comprehension difficulties occuralong a continuum of severity. In dyslexia, theseverity of the child’s phonological deficit willinfluence the extent of their reading and spellingdifficulties, and very likely also their response toremedial intervention. However, other cognitivefactors also play a role. Children with dyslexia whohave comorbid language impairment will presentwith problems in reading comprehension as wellas word recognition. Pennington and Bishop [8]have suggested it is important to consider thenumber and type of ‘risk’ factors present in achild with a reading problem (these could begenetic or environmental). In considering thecomorbidity of dyslexia, language impairmentand speech sound disorders, they conclude thatthere are some risk factors that are general to allthree disorders, especially difficulties in acquiringphoneme awareness (see Table 22.1). However,there are also risk factors that are specific toparticular disorders; a deficit in rapid naming isspecific to children with dyslexia, but is not evidentin most children with language impairment.

PATTERNS OF IMPAIRMENT FROMPRESCHOOL TO ADOLESCENCE

It has been known for many years that dyslexiaruns in families, and recent studies suggest there

Table 22.1 Risk factors for dyslexia in thepreschool and early school years.

Stage of Risk factorsdevelopment for dyslexia

Birth Affected family member

Preschool Late talker

Speech difficulties

Slow to learn colours and letters

School entry Poor knowledge of letters

Poor rhyming or phoneme skills

Expressive language difficulties

is a 40% risk of dyslexia developing in first-degreerelatives [9]. While dyslexia is most usually diag-nosed in middle childhood it is clear from prospec-tive longitudinal studies that its effects are evidentas early as 3 years of age and persist throughadolescence into adulthood.

Although there are different pathways to liter-acy development, studies of children at familial riskof dyslexia typically show that children who go onto develop reading problems experience delayedlanguage development in the preschool years [10].These subtle language problems may persist intothe school years when they are associated withphonological impairments at the time of readinginstruction. In one such study, language-delayedpreschoolers experienced persisting literacy dif-ficulties into early adolescence, when they alsotended to present with low self-esteem in relationto their academic skills, avoidance of reading, andattentional and emotional difficulties [2]. Impor-tantly, children from ‘at-risk’ families who werereading within the normal range at the age of 8years, went on to experience difficulties in spellingand reading fluency at the age of 12, thus showinga ‘broader phenotype’ of dyslexia. These findingsindicate that dyslexia is a dimensional disorderand that the family risk of dyslexia is continu-ous. Children from ‘at-risk’ families who were notreading impaired in the early years tended to haverelatively good oral language skills. It seems thattheir good semantic knowledge enabled them todevelop compensatory strategies; for instance, theywere able to draw on context cues available in textto aid and support reading processes.

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ASSESSING LITERACY DISORDERS

Most children with literacy disorders are referredfor assessment in the middle school years.However, there is increasing recognition of theimportance of early identification before the childhas fallen too far behind educationally and beginsto experience declining levels of motivation andconfidence. Since early screening batteries tendto have low reliability, a recently commissionedreview for the UK government [11] recommendedthe identification of ‘at-risk’ children via closemonitoring of their response to reading instructionduring the first 2 years at school. Children who failto progress sufficiently in response to mainstream,differentiated and additional literacy support

require further assessment for likely dyslexia orreading comprehension disorder (Figure 22.1).

A brief diagnostic assessment of dyslexia shouldinclude tests of single word reading and spelling,a test of phonological awareness, a test of short-term verbal memory and an (optional) test ofarithmetic. In addition, using a short-form IQ testmakes it possible to determine whether the childhas a general learning difficulty or a more specificdevelopmental disorder [12].

In order to determine whether a child may havea complex learning difficulty, a more comprehen-sive evaluation is needed. Such an assessmentneeds to recognize both the multiple componentsof literacy assessment and the dimensional natureof disorders; not all components of literacy skill

Check level of letter knowledge, phonological andlanguage skills

Small group intervention (phonological awareness,decoding and oral language)

Assess childs response to intervention

Specialist teacher assessment & identification oftargets for teaching

One-to-one intervention (using phonics methods orlanguage intervention as appropriate)

Monitor response to intervention

Management Plan/Further referral

Quality mainstream teaching

Diagnostic assessment by specialist teacheror psychologist

Progressgood

Progressgood

Progressgood

Return

to

Mainstream

Figure 22.1 Steps in the early identification and assessment of literacy disorders: a staged process.

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Literacy disorders

Table 22.2 Components of a comprehensive diagnostic assessment for readingdisorders.

Construct Test

Reading Single word readingNonword reading (decoding)Reading fluency (single words and continuous text)Prose reading accuracyReading comprehension (literal and inferential)

Spelling Single word spellingSpelling in free writing

Writing Written narrative (structure and organization)Writing speedQuality analysis of handwriting

Mathematics Mental arithmeticMathematical reasoningWritten arithmetic

Phonological skills Phonological awarenessRapid naming

Verbal working memory Verbal short-term memory spanNonword repetition

Language skills Sentence repetitionGrammar and morphology

will be equally impaired in a given child (seeTable 22.2). For the child with suspected dyslexia,the nature of the child’s underlying difficultycan be assessed using measures of phonologicalawareness, short-term verbal memory, rapidnaming and decoding (nonword reading). For thechild with reading comprehension difficulties, itis important to evaluate their oral language skillsand text comprehension strategies. Finally, in viewof the common co-occurrence of developmentaldisorders, the assessment needs to determinewhich particular additional difficulties the childmight have that will impact on their behaviourand school adjustment. Given time constraints,useful information can be sought from parentsand teachers using standardized questionnairesthat assess, for instance, attention or languagedifficulties.

TEACHING CHILDREN WITH LITERACYDISORDERS

There is a growing evidence base of effectiveinterventions for literacy disorders. Interventionprogrammes with proven efficacy for children withdyslexia emphasize the integration of text level

reading with training in phonological awarenessand decoding skill [13]. Children with readingcomprehension difficulties need a broad and richlanguage curriculum, with a strong emphasison developing vocabulary knowledge and textcomprehension skills. A recent interventionstudy [14] demonstrated that children’s com-prehension skills can be significantly improvedwith a programme that specifically targeted orallanguage skills (vocabulary enrichment, listeningcomprehension, use of figurative language andspoken narrative) and text comprehension strate-gies (including metacognitive strategies such asre-reading and mental imagery, reading compre-hension strategies, and making inferences fromtext). Preschool programmes aimed at strength-ening the foundations of literacy (specifically orallanguage skills and phoneme awareness) can alsohave positive effects [15].

While teaching programmes are rightlyexpected to attempt to remediate the child’sunderlying deficit, there is nonetheless a place forencouraging children to draw on their cognitivestrengths so that they can develop compensatorystrategies. The verbally able child with dyslexiaencountering an unfamiliar word may be taught

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a strategy of combining a partial decodingstrategy with their vocabulary knowledge and thesentential framework within which the word isembedded. This enables them to make the ‘bestpossible estimate’ as to its actual pronunciation.

As children get older, their needs extend beyonddirect teaching of reading and spelling to includeinstruction in the use of information technology(computers, spell-checks and voice-activated soft-ware) and techniques for improving organizationalskills alongside curriculum differentiation (whichmay include exemption from studying a foreignlanguage) and assessment arrangements (typicallyextra time in examinations but also possibly beingsupplied with a ‘reader’ or scribe).

Understandably, the teaching of children withdyslexia has focused largely on remediating theirreading and spelling problems. However, co-occurring difficulties need to be addressed in theirown right. Management programmes should notbe limited to literacy instruction, but should alsoconsider the individual child’s need for speech andlanguage therapy, occupational/physiotherapy,medication or behavioural programmes forattention deficits and additional maths support.

REFERENCES

[1] Snowling MJ. (2009) Changing concepts of dyslexia:nature, treatment and co-morbidity. Journal ofChild Psychology & Psychiatry epub: http://www.wiley.com/bw/vi.asp?ref=0021-9630&site=0021#0436.

[2] Snowling MJ, Muter V, Carroll JM. (2007) Childrenat family risk of dyslexia: a follow-up in adoles-cence. Journal of Child Psychology and Psychiatry48, 609–18.

[3] Clarke PJ, Snowling MJ, Truelove E et al. (2010)Ameliorating children’s reading comprehension dif-ficulties: A randomised controlled trial. Psycholog-ical Science 21, 1106–16.

[4] Cain K. (2010) Reading Development and Difficul-ties. Oxford: Wiley-Blackwell.

[5] Ziegler JC and Goswami UC. (2005) Reading acqui-sition, developmental dyslexia and skilled reading

across languages: a psycholinguistic grain size the-ory. Psychological Bulletin 131, 3–29.

[6] Hulme C and Snowling MJ. (2009) DevelopmentalDisorders of Language, Learning and Cognition.Oxford: Wiley-Blackwell.

[7] Nation K, Cooksey J, Taylor J et al. (2010) A lon-gitudinal investigation of the early language andreading skills in children with reading comprehen-sion impairment. Journal of Child Psychology andPsychiatry 51, 1031–9.

[8] Pennington BF and Bishop D. (2009) Relationsamong speech, language, and reading disorders.Annual Review of Psychology 60, 283–306.

[9] Paracchini S, Scerri T, Monaco AP. (2007) Thegenetic lexicon of dyslexia. Annual Review ofGenomics and Human Genetics 8, 57–79.

[10] Lyytinen H, Erskine JM, Tolvanen A et al. (2006)Trajectories of reading development; a follow-upfrom birth to school age of children with and with-out risk for dyslexia. Merrill-Palmer Quarterly 52,514–46.

[11] Rose J. (2009) Identifying and teaching childrenand young people with dyslexia and literacy dif-ficulties. Department for Education. Availableat http://www.teachernet.gov.uk/wholeschool/sen/(accessed 29 August 2010).

[12] Snowling MJ and Maughan B. (2006) Reading andother learning disabilities. In: Gillberg C, Harring-ton R, Steinhausen H-C (eds), Clinician’s Deskbookof Child and Adolescent Psychiatry. Cambridge:Cambridge University Press, pp. 417–46.

[13] Hatcher PJ, Hulme C, Miles JNV et al. (2006)Efficacy of small group reading intervention forbeginning readers with reading-delay: a random-ized controlled trial. Journal of Child Psychologyand Psychiatry 47, 820–7.

[14] Clarke PJ, Snowling MJ, Truelove E et al. (2010)Ameliorating children’s reading comprehension dif-ficulties: A randomized controlled trial. Psycholog-ical Science 21, 1106–16.

[15] Bowyer-Crane C, Snowling MJ, Duff F et al. (2008)Improving early language and literacy skills: Differ-ential effects of an oral language versus a phonologywith reading intervention. Journal of Child Psychol-ogy and Psychiatry 49, 422–32.

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Section 5b

Middle Childhood

Middle childhood

23Autism Spectrum DisordersTony CharmanCentre for Research in Autism and Education (CRAE), Department of Psychology and HumanDevelopment, Institute of Education, London, UK

INTRODUCTION

Autism spectrum disorders (ASDs) is the termused to describe the range of conditions that sharea common core with childhood autism, the proto-typic disorder in the spectrum of autistic disorders.All ASDs share the following characteristics:

• Qualitative impairments in social interaction,shown by: the use of non-verbal behaviourssuch as eye gaze and body posture to regulatesocial interaction; a failure to develop peerrelationships; a lack of spontaneous showingand sharing of interests; and a lack of socialemotional reciprocity.

• Qualitative impairments in social communica-tion, shown by: delayed language developmentwithout non-verbal compensation; problemsstarting/sustaining conversations; repetitive andstereotyped language; and a lack of imaginativeand imitative play.

• Restricted repertoire of interests, behaviours andactivities, shown by: abnormal over-focus onparticular topics; adhering to non-functionalroutines/rituals; repetitive, stereotyped motormannerisms; and preoccupation with objectparts rather than whole.

Sensory abnormalities, including either hypo-sensitivity or hypersensitivity, and unusual inter-ests in some sensations (e.g. the feel of clothes orthe smell of hair) are common. A lack of imagi-native play indicates an underlying difficulty withthe generation of ideas that is highly relevant inthe development of understanding, and thinkingabout, other people and other situations.


Individuals with impairments that do not meetfull criteria for the diagnosis of autism, such asAsperger syndrome, atypical autism or perva-sive developmental disorder – not otherwise speci-fied, are currently classified in DSM-IV-TR (Diag-nostic and Statistical Manual of Mental Disor-ders, Fourth Edition – Text Revision) and ICD-10 (ICD-10 International Classification of Men-tal and Behavioural Disorders in Children andAdolescents) as having ‘pervasive developmentaldisorders’ – though the term ‘autism spectrum dis-orders’ is widely used in its place. This groupincludes a mix of presentations including greaterseverity in one area than in others, mild impair-ments in several areas or late onset. The lack ofvalidity for the distinctions between autism-relatedconditions has led to the proposal that in the forth-coming DSM-5, separate diagnostic categories willbe replaced by severity dimensions within oneautism spectrum disorder (see Chapter 35).

PREVALENCE

Childhood autism was once considered a rare neu-rodevelopmental condition, but recent researchsuggests prevalence rates of 20–40 per 10,000 [1].Prevalence for the broader autism spectrum maybe as high as 100 per 10,000, or 1% [2]. Factorsinfluencing increased recognition of the disor-der include: changing diagnostic criteria; morethorough epidemiological studies; recognition thatASD can occur alongside average IQ, and the iden-tification of ASD in those with comorbid disordersor conditions. The prevalence of autism is four

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times higher in boys than girls, and this increaseswith IQ; in Asperger syndrome the ratio is 10:1in referred samples. The reasons for this genderdifference have not been determined.

ASSOCIATED DISORDERS

Medical conditions of possible aetiological signif-icance have been reported in 10–30% of cases.Figures are lower in population-based samplesthan in clinically accrued samples, and lower inhigh-functioning cases than in developmentallydelayed cases. The risk of ASD is increased intuberous sclerosis and in some genetic anomaliessuch as fragile-X syndrome and Turner syndrome.Tuberous sclerosis may provide an important clueto brain pathology, since lesions in the tempo-ral lobe have been shown to be a risk factor forcomorbid ASD. There is a high rate of epilepsy andseizure disorders. Some children develop seizuresin infancy, while in others the onset of epilepsy isin adolescence. By adulthood, one-third of indi-viduals with ASD have developed epilepsy.

AETIOLOGY

Autism is a strongly heritable disorder. Thisgenetic predisposition is polygenic in character,with multiple genes responsible, many of likelysmall effect. None has yet been identified, althoughconsiderable international collaborative effortshave indicated that susceptibility genes may belocated on chromosomes 2, 7, 16 and 17. It isentirely plausible that the autism phenotype mightresult from a number of genetic components andmechanisms, and recent evidence has emergedthat spontaneous mutations called ‘copy numbervariations’ (CNVs) may account for a proportionof cases [3]. The recurrence risk for subsequentlyborn siblings is approximately 5–10%. However,it is now known that milder impairments insocial communication skills or language affect upto 10–20% of first-degree relatives, especiallythose who are male. Familial susceptibility tothe ‘broader phenotype’ has implications forgenetic counselling. Non-genetic causation insome cases has not been ruled out, but suchinstances are probably a small minority. Althougha history of prenatal and perinatal obstetriccomplications is not uncommon, these are likelyto be secondary phenomena, consequent on analready abnormal fetus.

In 15–30% of children with ASD there is aperiod of stasis of development and even a frankloss of skills, most commonly speech (usuallybefore the 10-word stage) [4]. This regression,which is usually noted at 14–20 months, is oftenaccompanied by social withdrawal of the child into‘a world of his own’, with less following of others’gaze and a lack of response to speech. Repetitiveplay behaviours are sometimes noted at this time.There is no explanation why this pattern is presentin some children and not others, and the relianceon parental report of behaviour limits knowledgeof how widespread such a developmental courseis. Later-onset regression following a period ofnormal development up to 3 years of age orbeyond is rare and is referred to as childhooddisintegrative disorder.

DIAGNOSIS

Progress has been made in the earlier identifica-tion of ASD such that many children, especiallythose with a more classic presentation of autismin combination with language delay, are identi-fied in the preschool period [5]. Our improvedunderstanding of the emergence of autism in thepreschool years stems from recent improvementsin screening and study design; prospective studiesof genetically at-risk siblings of diagnosed children;and the retrospective analysis of home movies [6].The utility of early diagnosis stems from evidencethat behavioural and social communication inter-ventions can improve outcomes and help parentsto understand and better manage their child’sbehaviour [7].

However, it is still rare for ASDs to be diag-nosed before 2 years of age, even though it mainlyonsets in infancy and is the result of genetic andother organic factors affecting brain developmentvery early in life. In part this is because abnormal-ities in behaviours during infancy may be subtle(see Table 23.1). Poor coordination of attention,poor social orienting and play, and a lack of emo-tional reciprocity may not be noticed before thesecond year of life. In the high-functioning group(e.g. Asperger syndrome), where language mile-stones are not delayed and cognitive skills are inthe average or superior range, the diagnosis isoften not made until school age, or even later.When the affected child is the first, or only child,parents will be less certain about abnormalities of

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Table 23.1 Summary of parental concerns thatare possible indicators of autism spectrumdisorder (ASD) and require further monitoring.

Communication concernsDoes not respond to nameCannot tell me what he wantsLanguage is delayedDoesn’t follow directionsAppears deaf at timesSeems to hear sometimes but not othersDoesn’t point or wave bye-byeUsed to say a few words but now he doesn’tSocialization concernsDoesn’t smile sociallySeems to prefer to play aloneGets things for himselfIs very independentDoes things ‘early’Has poor eye contactIs in a world of his ownIgnores usIs not interested in other childrenBehavioural concernsTantrumsIs hyperactive/uncooperative or oppositionalDoesn’t know how to play with toysGets stuck on things over and overToe walksHas unusual attachments to toys (e.g. is alwaysholding a certain object)Lines things upIs over-sensitive to certain sounds or texturesHas odd movement patternsAbsolute indications for immediate furtherevaluationNo babbling by 12 monthsNo gesturing (pointing, waving bye-bye, etc.) by12 monthsNo single words by 16 monthsNo two-word spontaneous (and not just echolalic)phrases by 24 monthsANY loss of ANY language or social skills at ANYage

Adapted with permission from Charman T and Baird G.Practitioner Review: Diagnosis of autism spectrum dis-order in 2- and 3-year-old children. Journal of ChildPsychology and Psychiatry 2002;43:289—305.

development during infancy or the early preschoolyears. Recognition of ASD is an important aspectof differential diagnosis in preschool children pre-senting with developmental problems.

The particular pattern of symptoms thatpresents in a 2- or 3-year-old with ASD maydiffer from that seen at the more prototypic ageof 4 or 5 years [8]. In particular, overt repetitiveand stereotyped behaviours may be less notable,although when these are seen alongside socialand communicative impairments they are highlyindicative of ASD.


The differential diagnosis of autism includeshearing problems, global developmental delay andlanguage delay or disorder, especially receptivelanguage delay. In very young or profoundlydelayed children, differentiating autism plusdevelopmental delay from developmental delayalone may be difficult. However, social interest,use of pointing and other non-verbal gestures,imitation and pretend play skills would usuallybe commensurate with overall developmentallevel in a child with general developmental delay.In contrast, these are areas that are specificallydelayed in children with ASD. Behaviouralproblems that may present a differential diagnosisof ASD, and are possible comorbidities, include:

• attention deficit hyperactivity disorder(ADHD);

• deficits in attention, motor skills and perception(DAMP);

• oppositional behaviour, including resistance tochange;

• acutely anxious behaviour;• particular fears in certain situations.

Eating and sleeping problems, although com-mon in young children, are seen to a more extremeextent in children with an ASD. Dyspraxic orclumsy children may demonstrate features thatoverlap with an ASD presentation, and more than50% of children with ASD will have a problemwith coordination.

Approximately 50% of individuals with anASD have IQs in the intellectual disability range(<70); this percentage has recently been reviseddownwards from 75% with the increasing recogni-tion of ASD in children with average intelligence.

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Typically, non-verbal abilities are considerablybetter than verbal skills, although this pattern isless clear in high-functioning individuals.

ASSESSMENT AND INVESTIGATIONS

A multidisciplinary approach to assessmentis required. The composition of teams varies,but commonly includes a paediatrician, a childpsychiatrist, a speech and language therapist, aclinical psychologist and an occupational therapistor physiotherapist.

The information necessary for diagnosisincludes a detailed developmental history, par-ents’ descriptions of the everyday behaviour ofthe child, and direct assessment of the child’ssocial interaction style and communicative andintellectual function [9,10].

• Observation of the child’s social and communi-cation abilities should take place in structured(e.g. IQ and language assessments) and unstruc-tured (e.g. interactive play assessments) settings.In the unstructured setting it is important to varythe degree of social ‘press’ in order to elicit spon-taneous social overtures, requests and commentsand the child’s response to and understandingof adult approaches. Another important ele-ment, where possible, is the opportunity toobserve the child with peers of the same ageat nursery/school. This is important because ofthe difficulty of separating response to famil-iar and undemanding social routines from themore demanding responses to unfamiliar socialpresses. The latter require social reciprocityand understanding of the pragmatics of socialexchanges, and it is in these situations thatthe social and communicative impairments thatcharacterize children with ASD will be elicited.

• Interviews – the use of structured interviewassessments, such as the Autism DiagnosticInterview – Revised (ADI-R), and structuredinteraction schedules, such as the AutismDiagnostic Observation Schedule – Generic(ADOS-G), help systematize the range anddepth of information collected. However,these are time consuming and are not alwaysfeasible within the organizational constraintsof the clinic, especially when the consultationis led by very specific parental concerns. IQ,language and communication skills and adaptivebehaviour should be measured.

• Physical investigations may be indicated in somecases, particularly when there is evidence ofseizures, if a child has a fluctuating clinicalcourse, or additional features such as motorimpairments, e.g. ataxia or loss of skills [9].Relevant investigations include EEG, screen-ing for fragile-X and chromosomal anomalies,use of a Wood’s light to look for white skinpatches suggestive of tuberous sclerosis, and ahearing test.

MANAGEMENT AND INTERVENTION

Educational provision should maximize the child’ssocial and communicative abilities, as well as theirintellectual functioning and academic attainments.There is increasing evidence that appropriatelytargeted intervention improves outcome in somechildren with ASD. There is some evidence of thebenefits of intensive early behavioural interven-tion, particularly when combined with approachesthat also target the core deficits in social relatingand communication [11]. In addition, there is pos-itive evidence, including from randomized clinicaltrials, for intervention approaches that emphasizethe development of non-verbal social commu-nicative skills in preschool children, including viaparent training approaches [12].

Whatever the underlying approach, provisionof a structured (and predictable) environmentand emphasis on communication skills areimportant aspects of the preschool and schoolcurriculum for children with ASD. In some,behavioural interventions are needed in orderto reduce repetitive, stereotyped, self-injuriousand challenging behaviours. Many parents needsupport, and in both the UK and USA there areweb-based national autism societies providingexcellent sources of information and services (see‘Sources of support’ below). For families with themost challenging children, respite care may benecessary.

MedicationCurrent pharmacological treatments do not treatthe core features of ASD. Neuroleptics such astrifluoperazine and haloperidol have been usedto manage stereotyped (including self-injurious)behaviours and hyperactivity but can produce dys-tonic reactions and drowsiness. Such behaviouralproblems are usually found in individuals with

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Box 23.1 Practice points

• Autism spectrum disorders (ASDs) constitute a diagnostic spectrum of variable severity alongat least three dimensions: deficits in social communication, poor language and non-verbalcommunicative abilities, and circumscribed interests and rigid, repetitive and stereotypedbehaviours.

• Diagnosis should rely on information from several sources: a parental report of thedevelopmental history, together with observations of the child undertaking structured socialtasks, and in the company of peers. The particular pattern of symptoms that presents inpreschoolers may differ from that seen at the more prototypic age of 4—5 years; inparticular, overt repetitive and stereotyped behaviours may be less notable.

• The specific genetic and neurobiological basis of autism has not yet been identified and,although it is a highly heritable condition, non-heritable genetic and non-genetic factorsmay play a role in aetiology.

• Pharmacological treatments are used for epilepsy and for the management of severebehaviour disorders, including self-injury and stereotypies, but their role is relatively aminor one. Appropriate educational placement, behavioural management, socialcommunication interventions and support for parents are the primary management tools.The course and prognosis of autism are variable, and hard to predict until the child is ofschool age. High IQ and good language ability are the best prognostic signs.

severe developmental delay. Some recent reportssuggest that irritability, anxiety, aggression andrepetitive behaviours may be ameliorated by theserotonin 2A-dopamine D2 antagonist risperi-done, and that parent training in behaviouralmanagement provides additional benefits overmedication alone [13]. Other studies suggestthat autistic symptomatology could be improvedby the selective serotonin reuptake inhibitor(SSRI) fluoxetine, but the evidence is weak.Adolescents and adults with Asperger syndromewho have mood disorders may respond well toSSRIs. Clomipramine, a tricyclic antidepressantand 5-HT-uptake inhibitor, has been used totreat obsessional and compulsive behaviours withmoderate success.

COURSE AND PROGNOSIS

The course and outcome of ASD are largely depen-dent on language and IQ, and vary considerably.There is often improvement after the preschoolyears, especially in the acquisition of languageskills. However, for the majority of individuals,significant social impairment is life-long. An IQabove 70 and onset of functional language by 5

years of age are good prognostic signs. Aspergersyndrome is associated with a better prognosisbecause of relatively good IQ and language skills,but only some children with this disorder will beable to make close social relationships outside theirfamily.

REFERENCES

[1] Fombonne E. (2009) Epidemiology of pervasivedevelopmental disorders. Pediatric Research 65,591–8.

[2] Baird G, Simonoff E, Pickles A et al. (2006) Preva-lence of disorders of the autism spectrum in apopulation cohort of children in South Thames: theSpecial Needs and Autism Project (SNAP). Lancet368, 210–15.

[3] Freitag CM, Staal W, Klauck SM et al. (2010)Genetics of autistic disorders: review and clinicalimplications. European Child and Adolescent Psy-chiatry 19, 169–78.

[4] Lord C, Shulman C, DiLavore P. (2004) Regressionand word loss in autistic spectrum disorders. Journalof Child Psychology and Psychiatry 45, 936–55.

[5] Charman T and Baird G. (2002) Practitioner review:diagnosis of autism spectrum disorder in 2- and 3-year-old children. Journal of Child Psychology andPsychiatry 43, 289–305.

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[6] Yirmiya N and Charman T. (2010) The prodromeof autism: early behavioral and biological signs,regression, peri- and post-natal development andgenetics. Journal of Child Psychology and Psychia-try 51, 432–58.

[7] Rogers SJ and Vismara LA. (2008) Evidence basedcomprehensive treatments for early autism. Journalof Clinical Child and Adolescent Psychology 37,8–38.

[8] Charman T, Taylor E, Drew A et al. (2005) Outcomeat 7 years of children diagnosed with autism age 2:predictive validity of assessments conducted at 2and 3 years of age and pattern of symptom changeover time. Journal of Child Psychology and Psychi-atry 46, 500–13.

[9] Baird G, Cass H, Slonims V. (2003) Diagnosis ofautism. British Medical Journal 327, 488–93.

[10] Johnson CP and Myers SM. (2007) Identificationand evaluation of children with autism spectrumdisorders. Pediatrics 120, 1183–215.

[11] Dawson G, Rogers SJ, Munson J et al. (2010)Randomized, controlled trial of an interventionfor toddlers with autism. The Early Start DenverModel. Pediatrics 125, e17–23.

[12] Green J, Charman T, McConachie H et al.(2010) Parent-mediated communication-focusedtreatment for preschool children with autism (MRCPACT); a randomised controlled trial. Lancet 375,2152–60.

[13] Aman MG, McDougle CJ, Scahill L et al. (2009)Medication and parent training in children withpervasive developmental disorders and seriousbehaviour problems: results from a randomized clin-ical trial. Journal of the American Academy of Childand Adolescent Psychiatry 48, 1143–54.

FURTHER READING

Levy SE, Mandell DS, Schultz RT. (2009) Autism. Lancet374, 1627–38.

SOURCES OF SUPPORT

UK – National Autistic Society (http://www.nas.org.uk/).USA – Autism Speaks ( http://www.autismspeaks.org/).

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24Somatization and Somatoform DisordersElena GarraldaAcademic Unit of Child and Adolescent Psychiatry, Imperial College London, London, UK

WHAT’S NEW

• Demonstration of high levels of anxietydisorder comorbidity [2]

• Description of intergenerationaltransmission and parental influences[4,5,10,11]

• Replication of the effectiveness ofcognitive-behavioural familytherapy [12].

INTRODUCTION

Somatic symptoms are common in children andadolescents. In some surveys, young people reporta mean of two somatic symptoms (on a 27-itemsomatization questionnaire) present ‘a lot’ in the2 weeks prior to assessment; girls aged 12 yearsand older have higher scores than similar-agedboys. The most common symptoms are headache,low energy, sore muscles, nausea and upsetstomach, back pains and stomach pains. In thegeneral population, 2–10% of children haveaches and pains, which are mostly unexplained,and 5–10% of children and adolescents reportdistressing somatic symptoms or are regarded bytheir parents as ‘sickly’.

Parental reactionIn judging the significance of these symptoms,parents need to decide whether the child is ill,is ‘exaggerating’ or is upset. Parents are usually


aware that worries about school, friendships orfamily discord may contribute to the symptom, orthat symptoms may be used to avoid something thechild finds difficult. Common and effective parentalreactions are to ‘play down’ the importance of thesymptom, so that the child learns to cope, or tocomfort the child and try to find the cause forthe distress. There are times, however, when thesymptoms become marked and persistent.

Somatization‘Somatization’ describes psychological difficultyor distress that is manifested through somaticsymptoms, a tendency to experience and commu-nicate somatic distress and symptoms unaccountedfor by pathological findings, to attribute themto physical illness and to seek medical help.It is a crucial feature of a number of ICD-10(ICD-10 International Classification of Mental andBehavioural Disorders in Children and Adoles-cents) and DSM-IV-TR (Diagnostic and StatisticalManual of Mental Disorders, Fourth Edition – TextRevision) somatoform and allied disorders, ofwhich the following are most commonly seen inchildren and adolescents:

• persistent somatoform pain disorder;• dissociative/conversion disorder;• chronic fatigue syndrome (‘neurasthenia’ in

ICD-10).

CLINICAL CHARACTERISTICS

Most research on severe, recurrent unexplainedpain that leads to medical help-seeking has

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been done on children presenting with stomachaches and headaches, but multiple complaintsare common in these children. In a classic study,Apley found that around 10% of schoolchildrenhad at least three bouts of abdominal pain severeenough to affect activities over a period of 3months; comparable rates have been found inpreschool children [1]. Associated physical symp-toms include pallor, vomiting, fever, headacheand subsequent sleepiness and lethargy. Childrenmay look quite unwell, which reinforces parentalworries about physical illness.

Headaches commonly present as migraineand tension headaches, although in practice thedifferentiation between the two types is often notclear-cut and both may coexist.

• In migraine the headache is periodic, severe andunilateral, accompanied by a visual aura, nausea,vomiting and a family history of migraine.

• Tension headaches are described as non-paroxysmal, frequent, bilateral, like ‘a band’or ‘heavy weight’ or ‘fullness’, with associateddizziness.

Abdominal pains and headaches form part ofICD-10’s persistent somatoform pain disorder,when the pain is persistent, severe and distressingand occurs in association with emotional conflictor psychosocial problems that are sufficient tobe considered to have an aetiological influence.In dissociative (conversion) disorders there is apartial or complete loss of bodily sensations ormovements. Symptoms may be brought on by aparticularly traumatic event and they tend to remitafter a few weeks or months. Pseudoseizures arealso seen in children.

In chronic fatigue syndrome (CFS), the maincomplaint is increased fatigue after mental effort.It is associated with a decrease in occupationalperformance or coping efficiency in daily tasksand involves:

• difficulty in concentrating;• dizziness;• physical fatigue with physical weakness and

exhaustion after only minimal effort;• muscular aches and pains;• tension headaches;• sleeping problems;

• worry about decreasing mental and physicalwell-being.

Functional impairment that is not explained byany associated physical or psychiatric pathologyis a key feature of somatoform disorders seen inspecialist clinics.

ASSOCIATED FEATURES

Precipitating factorsSomatoform disorders may be precipitated byphysical problems and medical treatments; forexample, severe abdominal pains may start afteran acute gastrointestinal infection. An injuryfollowed by treatment with immobilization mayprecede loss of sensation or motility in a limb. Aflu-type or infectious illness may bring on chronicfatigue syndrome. Stressful events are known tocontribute to the development or continuationof problems such as recurrent abdominal pains.Their effect may be mediated by problems insocial competence (i.e. child, parent and teacherperceptions of the child’s social skills or peeracceptance) in the child and high levels of stressor of physical symptoms in families.

ComorbidityBetween one-third and one-half of children withsomatization-related disorders have psychiatriccomorbidity [2]; but in severely affected childrenwith chronic fatigue syndrome and in more recentstudies of children with recurrent abdominalpain attending paediatric clinics this rises tothree-quarters [3]. Emotional spectrum disorders(usually anxiety or depressive disorders) are themost common association. Psychiatric disordersmay precede the development of the handicappingfunctional symptoms, or they develop during itscourse.

Personality featuresThese may be relevant precursors. Clinicianshave consistently described affected childrenas conscientious – even obsessional – sensitive,insecure and anxious, and this may be linked toenhanced stress sensitivity in these children.

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Box 24.1 Engaging the family in assessment and treatment

• Fully discuss the physical concerns preoccupying the family and the physical tests carriedout.

• Address the physiological mechanisms contributing to symptoms when understood (e.g.muscle pains as a consequence of immobilization and abnormal gait; excessive rest mayalter sleep).

• Attributing symptoms to being ‘all in the mind’ is particularly unhelpful. Avoid questioningthe child’s truthfulness regarding the symptom.

• Families and children are more likely to accept stress and psychological factors contributingto the maintenance of the condition than to its cause.

• Move from the physical to the psychological at a pace the family can cope with.

• Developing strategies to help the child and family cope with the symptoms and reduce theassociated functional impairment is the essence of treatment.

• Emphasize that response to treatment may be slow and intermittent but that most childrencan recover.

Family factorsFamily factors are thought to contribute, anda combination of psychological distress andhealth problems in the family may be specificto childhood somatization. While a geneticcontribution is likely – possibly reflecting abiological vulnerability to experiencing differenttypes of symptoms – family ill-health couldserve as a model for the child’s symptoms, thussensitizing the child and family and focusingtheir attention on physical symptoms. Parentalemotional over-involvement and reinforcement ofthe symptoms have been noted [4,5], for examplethrough positive consequences for symptoms, suchas allowing the child to stay home from school andgiving the child gifts when he or she is sick.

In a few cases, associated problems in the fam-ily include profound disorganization, sexual abuseand ‘fabricated’ illness (e.g. factitious disorder,or Munchhausen by proxy), leading to the childpresenting repeatedly for medical assessment andcare [6].

Educational concernsEducational concerns are often noted. The phys-ical problems may start shortly after transfer to

secondary school; children may be overconcernedabout academic achievement or there may be ahistory of sensitivity or other problems in socialrelationships, sometimes including bullying.

DIAGNOSTIC ASSESSMENT

Children with mild disorders will be seen by theirgeneral practitioner. Paediatricians and otherspecialists often see more severe cases. Fewerchildren attend child and adolescent psychiatricclinics, where assessment needs to include adetailed psychiatric history, mental state of thechild and assessment of family function. Psychom-etry is useful when a mismatch between the child’sachievements, capability and expectations is sus-pected. A detailed history of school attendance isessential.

Even after specialist referral, many familiesremain anxious about the possibility of anas-yet undisclosed underlying physical disorderaccounting for the child’s symptoms, and theneed for this to be uncovered and treated.The main principles in the assessment of theseconcerns and in planning treatment are outlinedin Box 24.1.

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Physical symptoms are commonly found in chil-dren and adolescents with psychiatric disorders.The following should be considered in differentialpsychiatric diagnosis:

• school phobia and refusal, where key featuresare marked fear and avoidance of school;

• anorexia nervosa, with deliberate weight lossand an intrusive dread of fatness;

• depressive disorder, with consistent and persis-tent lowering of mood;

• anxiety disorders, with prominent, prolongedand persistent feelings of anxiety, worry andrestlessness.

Factors that raise suspicion that psychologicalfactors are playing a part in somatic presentationsinclude:

• when stress and physical symptoms occur closetogether;

• a symptom whose severity is out of keeping withthe established pathophysiology;

• concurrent psychiatric disorder;• the presence of the characteristic child, family

and illness factors described above.

REFERRAL TO CHILD AND ADOLESCENTMENTAL HEALTH CLINICS

A psychiatric referral is especially appropriate:

• for diagnostic purposes, when there is uncer-tainty about the relevance of psychologicalfactors;

• when there is associated psychiatric disorder;• when major family problems affect the resolu-

tion of the symptoms;• when the child fails to respond to standard pae-

diatric treatment.

PLANNING TREATMENT

Treatment should aim to develop a partnershipwith the child and family and to adopt a coor-dinated approach with schoolteachers and othertherapists involved. A treatment programme islikely to involve the features outlined in Box 24.2.Weekly therapy sessions at earlier stages may helpto identify and review goals.

SchoolLooking at ways to reduce stresses in discussionwith parents and teachers is important. In very

Box 24.2 Features of a treatment programme

• Ascertaining precise daily variations in severity of symptom and associated impairment(diaries can help with this).

• Special techniques to deal with individual symptoms (e.g. distraction techniques, restperiods, relaxation for headaches, analgesics as appropriate, physical exercises for musculardysfunction).

• Attention to dietary habits and sleep, which may have become altered.

• Acknowledging and addressing as appropriate concerns of the child and family that arehabilitation programme might make the symptoms worse.

• Modest initial goals to increase normalization of daily activities.

• Gradually increasing daily activities (including school work and attendance), change beingset at achievable, consistent, agreed levels.

• Exploring the child’s expectations of ultimate goals (e.g. for usual well-being or fatiguelevels) as these may be unrealistically high.

• Treatment of associated emotional disorders.

• Management of underlying anxieties.

• Family work.

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incapacitated children a period out of school, doinghomework only or working with a home tutor, maybe indicated. Rehabilitation into school will usu-ally involve gradual and partial reintroduction anda school for ‘delicate’ children may be required.Some children benefit from admission to a paedi-atric unit with psychiatric input, or to a psychiatricunit with educational provision.

Family workThis is essential in all cases. The aim is threefold:

• facilitate the parents’ engagement in treatment,discussing their ongoing concerns about illness;

• plan a treatment programme and help developdistracting and other coping mechanisms;

• intervene as appropriate for any associated fam-ily dysfunction, parental psychopathology orother source of family stress that may impederecovery. Family stresses that were not appar-ent at initial stages of treatment may becomeapparent in the course of it.

Drug treatmentsAntidepressants can be helpful if there areassociated depressive features or because of theirsedative effects. Tricyclic antidepressants orfluoxetine, a selective serotonin reuptake inhibitor(SSRI) can be used. Citalopram has provedpromising in an open trial. However, the use ofSSRIs in children and adolescents is subject torestrictions.

EFFECTIVENESS OF TREATMENT

There have been few satisfactory controlled studiesof treatments for childhood somatoform disor-ders, but clinical reports by hospital paediatriciansand child psychiatrists have outlined beneficialeffects. Helping parents to understand the linksbetween psychological and physical pain is in itselfappreciated by many parents and help make thechild’s pain less intense and more manageable. Thebest available evidence of efficacy for unexplainedabdominal pain comes from cognitive-behaviouralfamily interventions. Sanders and colleagues [7]in a randomized controlled trial of 7–14-year-olds found that children who had the psycho-logical intervention had a higher rate of com-plete elimination of pain, lower levels of relapse

at 6-month and 12-month follow-up, and lowerlevels of interference with their activities frompain than children receiving standard paediatriccare.

Tension headaches in children and adolescentscan be substantially improved by relaxationtraining. In some studies of adolescents this issuperior to attention placebo control and equallyeffective when administered at the clinic and as ahome-based self-administered treatment.

Psychiatric admission is indicated if the childis very incapacitated, if there is associated psy-chopathology and progress is not made with out-patient treatment. Admission may not be acceptedby families until psychiatrists have done some facil-itating work together with paediatricians.

Legal considerationsIn exceptional cases a somatoform disorder willbe an expression of severe family disruption andchild abuse (including factitious illness). The neces-sary statutory mechanisms need to be explored tosafeguard the child’s safety and to allow treatmentto proceed. Close cooperation between differ-ent professionals involved will be important toavoid different points of view about the condi-tion contributing to protracted investigation andits continuation. If parents are unable or unwill-ing to engage in any type of treatment for thechild, consideration should be given to whetherthe child’s development and safety are being putat risk and care would be better provided awayfrom the family (i.e. by taking the child into care).This is rarely a clear-cut issue and a second opinionfrom clinicians with special expertise in the area isusually required.

OUTCOME

Clinical reports indicate that the majority ofmarkedly affected children with somatoformdisorders who are seen in specialist clinics recoverin the short term. Some symptoms persist to alesser degree in a considerable proportion (aboutone-third in some studies) and may continueinto adulthood (half the subjects in a long-termfollow-up study of abdominal pains). Long-termfollow-up indicates that these children also havean increased risk for psychiatric disorders inadulthood [8].

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PREVENTION

Efforts at prevention might profitably addresschildren of parents with somatoform disorders,young preschool children with functional symp-toms [9], and older children with a history ofpersistent school non-attendance. Once childrenare receiving treatment, addressing the man-agement of personality features that are likelyto render them vulnerable to stress reactionsand somatization (e.g. sensitivity to criticism,conscientiousness, proneness to anxiety, as well asexcessive academic and behavioural expectations)may help to prevent relapse.

CURRENT CHALLENGES AND FUTUREDIRECTIONS

The psychiatric management of children withsomatization and somatoform disorders can behampered by reluctance by families to entertain apsychosocial contribution to children’s symptoms.Hence good liaison between paediatric andpsychiatric services is of the essence, and this willbe facilitated by further development of paediatricliaison psychiatric teams. Future research intophysical and psychological vulnerabilities and intoefficacious treatment strategies is called for.

REFERENCES

[1] Apley J. (1975) The Child with Abdominal Pains,2nd edn. Oxford: Blackwell Scientific.

[2] Campo JV, Bridge J, Ehmann M et al. (2004) Recur-rent abdominal pain, anxiety and depression inprimary care. Pediatrics 113, 817–24.

[3] Rangel L, Garralda ME, Hall A, Woodham S. (2003)Psychiatric adjustment in chronic fatigue syndromeof childhood and in juvenile idiopathic arthritis.Psychological Medicine 33, 289–97.

[4] Rangel L, Garralda ME, Jeffs J, Rose G. (2005)Family health and characteristics in chronic fatiguesyndrome, juvenile rheumatoid arthritis and emo-tional disorders of childhood. Journal of the Amer-ican Academy of Child and Adolescent Psychiatry44, 150–8.

[5] Walker LS, Williams SE, Smith CA, Garber J, VanSlyke DA, Lipai TA. (2006) Parent attention versusdistraction: impact on symptom complaints by chil-dren with and without chronic functional abdominalpain. Pain 122, 43–52.

[6] Bass C, Adshead G. (2007) Fabrication and induc-tion of illness in children: the psychopathology

of abuse. Advances on Psychiatric Treatment 13:169–77.

[7] Sanders MR, Shepherd RW, Cleghorn G, Wood-ford H. (1994) Treatment of recurrent abdominalpain in children: a controlled comparison of cogni-tive behavioural family intervention and standardpediatric care. Journal of Consulting and ClinicalPsychology 62, 306–14.

[8] Campo JV, di Lorenzo C, Chiapetta L et al. (2001)Adult outcomes of pediatric recurrent abdominalpain: do they just grow out of it? Pediatrics 108: e1.

[9] Domenech-Llaberia E, Jane C, Canals J, Ballespi S,Esparo G, Garralda ME. (2004) Parental reports ofsomatic symptoms in preschool children: prevalenceand associations in a Spanish sample. Journal ofthe American Academy of Child and AdolescentPsychiatry 43, 598–604.

[10] Campo JV, Bridge J, Lucas A et al. (2007) Physicaland emotional health of mothers of youth withfunctional abdominal pain. Archives of Pediatricsand Adolescent Medicine 161, 131–7.

[11] Ramchandani PG, Stein A, Hotopf M, Wiles NJ,ALSPAC Study Team. (2006) Early parental andchild predictors of recurrent abdominal pain atschool age: results of a large population based study.Journal of the American Academy of Child andAdolescent Psychiatry 45, 729–36.

[12] Robins PM, Smith SM, Glutting JJ, Bishop CT.(2005) A randomized controlled trial of a cognitive-behavioral family intervention for pediatric recur-rent abdominal pain. Journal of Pediatric Psychol-ogy 30, 397–408.

FURTHER READING

Eminson DM, Postlethwaite RJ. (1992) Factitious illness:recognition and management. Archives of Disease inChildhood 67, 1510–16.

Helpful outline of the complexities that need to beexplored in factitious illness.

Garralda ME. (2010) Unexplained physical complaints.Child and Adolescent Psychiatric Clinics of NorthAmerica 19, 199–209.

Recent review.Garralda ME, Chalder T. (2005) Practitioner Review:

chronic fatigue syndrome in childhood. Journal ofChild Psychology and Psychiatry 46, 1143–51.

Review of current knowledge and management.Husain K, Browne T, Chalder T. (2007) A review of

psychological models and interventions for medicallyunexplained somatic symptoms in children. Child andAdolescent Mental Health 12, 2–7.

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25Attention-Deficit Hyperactivity DisorderAnita Thapar1 and Antonio Munoz-Solomando21Child & Adolescent Psychiatry Section, Department of Psychological Medicine and Neurology, CardiffUniversity School of Medicine, Cardiff, UK2Tonteg Child and Family Centre, Tonteg Hospital, Pontypridd, UK

DEFINITION

Attention-deficit hyperactivity disorder (ADHD)is a childhood-onset, impairing, neurodevelopmen-tal disorder [1]. ADHD is a diagnostic categoryin the Diagnostic and Statistical Manual of MentalDisorders, 4th edition (DSM-IV). Hyperkineticdisorder is the diagnostic term used in the Inter-national Classification of Diseases, 10th revision(ICD-10), and specific criteria are listed in Box25.1. ICD-10 also includes the category of hyperki-netic conduct disorder. Children with both ADHDand conduct disorder deserve distinction in thatthey have more severe symptoms of ADHD anda poorer clinical outcome than those with ADHDalone. DSM-IV differs from ICD-10 in severalways; notably it divides ADHD symptoms into tworather than three groups (hyperactive/impulsiveand inattention). A diagnosis of ADHD, combinedtype, requires symptoms in both groups. DSM-IValso allows for diagnosing ADHD, inattentivetype and hyperactive-impulsive type.

Comorbidity is common and includes:

• oppositional defiant disorder and conduct dis-order;

• developmental problems including reading dis-ability (dyslexia), developmental coordinationdisorder, speech and language problems;

• tic disorders, including Tourette syndrome;• anxiety and depression;• learning/intellectual disability;• pervasive developmental disorders.


Current diagnostic criteria state that ADHDshould be diagnosed in the absence of anxietydisorders, mood (affective) disorders, pervasivedevelopmental disorders and schizophrenia. Theco-occurrence of ADHD with these disorders is,however, being recognized and these exclusioncriteria may change in ICD-11 and DSM-V, asmay the age of onset criterion.

EPIDEMIOLOGY

In the most recent UK epidemiological study [2],prevalence rates were 1.4% for DSM-IV ADHDcombined type and 1% for ICD-10 hyperkineticdisorder. Some studies have found higher rates ofup to about 5–6%. Although the rates of ADHDrecognition, clinician-provided diagnosis and treat-ment have markedly increased since the 1980s inthe UK, USA and Europe, there is no evidencethat the prevalence of the disorder or symptomsis rising over time [3]. This suggests that increasedrates of treatment are in part due to greater clini-cian and public awareness of ADHD. Likewise, ithas sometimes been assumed that the prevalenceof ADHD varies widely in different countries andis especially high in the USA. However, a meta-analysis of worldwide studies found no significantdifferences between European and US prevalenceestimates in ADHD. The results also suggestedthat reported differences in prevalence appear tobe influenced by methodological variation, notablywhether or not there is associated impairment,

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Attention-deficit hyperactivity disorder

Box 25.1 Symptoms of hyperkinetic disorder in ICD-10

Hyperactivity

• Often fidgets with hands or squirms in seat

• Difficulty remaining seated when required

• Runs about or climbs on things excessively in situations when it is inappropriate

• Exhibits a persistent pattern of motor activity (always on the go)

• Often noisy in playing or difficulty engaging quietly in leisure activities

Inattention

• Fails to sustain attention in tasks or play activities

• Often fails to follow through on instructions from others

• Often avoids tasks that require sustained mental effort

• Often easily distracted

• Often loses things that are necessary for tasks or activities

• Appears not to listen to what is being said to him/her

• Fails to pay attention to details, or makes careless mistakes

• Often forgetful in daily activities

• Often has difficulty organizing tasks and activities

Impulsivity

• Difficulty waiting turn in games or group situations

• Often blurts out answers before questions have been completed

• Often interrupts or intrudes on others

• Often talks excessively

Other

• Onset before the age of 7 years

• Impairment/interference

• Pervasiveness of symptoms

the source of information, and higher rates usingDSM-IV compared with ICD-10 [4]. Like all neu-rodevelopmental disorders, boys are more com-monly affected than girls. The male:female sexratio is higher in clinics (7–8:1) than in the com-munity (3–4:1), suggesting that ADHD in femalesis under-recognized.

AETIOLOGY

Attention-deficit hyperactivity disorder is a com-plex disorder influenced by the interplay of mul-tiple risk factors. No single risk factor is sufficientto result in disorder. Although there is a strong

genetic contribution [5], non-inherited factors arealso important. A number of environmental riskfactors have been found to be associated withADHD [1,6], but they have not yet been shown tobe definitely causal. Risk factors include:

• Genetic factors: ADHD is highly heritable, likeautism (heritability around 80%).

• Specific gene variants: The most consistent evi-dence is that dopamine D4 and D5 receptorgene variants are associated. Effect sizes aresmall. There is replicated evidence for associ-ation between a catechol-O-methyltransferase(COMT) gene variant and conduct disordersymptoms in ADHD.

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• Genetic syndromes: syndromes such as frag-ile X, velocardiofacial syndrome, and tuberoussclerosis may lead to features of ADHD but arerare. Rare subtle chromosomal deletions andduplications (copy number variants), includingones associated with autism and schizophrenia,may also contribute but again do not explain thepathogenesis of disorder on their own. Routinescreening of genetic syndromes in non-learning-disabled children is unwarranted.

• Maternal smoking and stress in pregnancy: Theseare associated, but recent evidence suggests thatthey might not be causal [7,8].

• Alcohol use in pregnancy: Exposure to highdoses of alcohol results in fetal alcohol syn-drome. Evidence that mild alcohol use is impor-tant is sparse [7].

• Low birthweight/prematurity are associated [7].• Extreme early adversity [9] can lead to features

similar to ADHD. It is not known whethermilder adversities are important.

• Environmental toxins: Lead toxicity and earlyexposure to pesticides have been consideredto be associated with ADHD, besides possiblydietary factors in some children.

• Family adversity, notably a negative mother–child relationship, appears to be a consequenceof ADHD and seems to improve when ADHDsymptoms are treated.

COGNITIVE AND NEUROBIOLOGICALCORRELATES

Routine cognitive testing is not necessary ordiagnostically useful. Children with ADHD canunderperform on IQ tests. They also show deficitson measures of executive function, responseinhibition, prefrontal cortical function, delayaversion, and timing deficits. Structural andfunctional imaging studies [10] show reducedcerebral, cerebellar and caudate volume, anddelayed cortical maturation especially in theprefrontal regions; functional magnetic resonanceimaging studies implicate corticostriatal circuitinvolvement. Animal, genetic and pharmaco-logical studies have implicated involvement ofdopaminergic pathways.

DIAGNOSTIC ASSESSMENT

Diagnosis is based on the presence of reportedsymptoms. The diagnostic process includes a

Box 25.2 Key areas of assessment

• Presence of ADHD symptoms asspecified in ICD-10 or DSM-IV

• Information from parents and child

• Neurodevelopmental assessment

• Establish degree of impairment andpervasiveness of symptoms

• Information from school or otherinformants

• Assess for comorbidity and considerdifferential diagnoses

• Cognitive assessment of the child iflearning difficulties suspected

• Physical examination including height,weight and cardiovascular systemchecks

• Use of rating instruments such as theConners Rating Scale

ADHD, attention-deficit hyperactivity disorder;DSM-IV, Diagnostic and Statistical Manual ofMental Disorders, 4th edition; ICD-10, Interna-tional Classification of Diseases, 10th revision.

detailed history from the family, observation of thechild, and reports from school or other observers(Box 25.2).

Information from parentsThis includes a developmental and psychiatric his-tory, exploring symptoms and behaviour in detail.Asking for examples of the behaviour often illus-trates the severity of problems and the level ofimpairment. The clinician should ask the parentsto explain what they think could be causing theproblems and their attitude to treatment. Finally,completion of rating scales such as the ConnersParental Rating Scale [11] provides baseline infor-mation on symptoms and can also be used tomonitor treatment response.

Child information and observationThese are important to assess ADHD symptomsand comorbidity, and to consider differential

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diagnoses, such as anxiety and mood disorders.The clinician needs to consider the developmentalage of the child. Observation while performingtasks that require a certain level of self-control andsustained attention can be helpful but the diagnosisshould not be based purely on observed behavioursin clinic. When possible, a school visit can provideinvaluable information to support the diagnosis.Teenagers can often describe their symptoms,for instance subjective feelings of restlessness,and provide information on their level of socialfunctioning. However, self-reports of ADHDare not a substitute for reports from informants,have poorer predictive validity than parentalreports, and should not be used alone to make thediagnosis [12].

Report from school or other informantsAfter gathering consent, a report from the schoolor other informants is crucial. A school report froma teacher who knows the child well provides infor-mation on how the child’s symptoms and behaviourmanifest in a more structured environment, andon academic performance and social relationships.The use of instruments such as the Child ADHDTeacher Telephone Interview (CHATTI) [13] orteacher rating scales (e.g. the Conners TeacherRating Scale) [14] can be valuable. In young adultswho have left school, informant reports still remainan important part of the diagnostic process. A cog-nitive assessment of the child may be necessaryto identify learning disability, but is not routinelyrequired. Some children require assessment by anoccupational therapist or physiotherapist if motorcoordination problems are noted.

Physical examinationThis can be important in ruling out physicalcauses of the symptoms (e.g. hearing and visionproblems). Physical examination needs to includechecks on weight, height and the cardiovascularsystem, especially if medication is later prescribedas part of the treatment plan and the child has alearning disability.

TREATMENT

Current guidance supports the use of multimodalpackages of care for the treatment of ADHD;Box 25.3 shows the types of treatment used. Mostfamilies benefit from written information about

Box 25.3 Management of ADHD

Pharmacological interventions

First line:• Methylphenidate∗

• Dexamfetamine∗

• Atomoxetine∗

Second line:• Clonidine

• Modafinil

• Bupropion

• TCAs (tricyclic antidepressants)

Psychosocial interventions

• Behaviour therapy including parenttraining programmes*

• Cognitive—behavioural therapy

• Social skills training

• Family support to reduce stress

School interventions

• Classroom interventions

• Management of general and specificlearning difficulties

Related areas

• Elimination and supplementation diets

∗Supported by evidence base.

the features and treatment of ADHD, and theaddresses of reliable internet websites and volun-tary organizations.

Pharmacological interventionIn preschool-aged children medication is rarelyused. Instead, behaviourally oriented parent train-ing programmes are the first treatment option.In cases where ADHD symptoms are severe andthere is a marked degree of impairment, anda parenting programme has already been used,medication should be considered. In school-agedchildren and young adults suffering with ADHD,stimulant medication such as methylphenidate andthe non-stimulant atomoxetine have been shownto reduce hyperactivity and improve concentra-tion; these drugs are endorsed by the National

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Institute for Health and Clinical Excellence [15].Although there are short-term therapeutic effectsof ADHD medication, there is uncertainty aboutlong-term benefits [16]. Once medication hasbeen started, the child’s physical health, includ-ing weight and height, and ADHD symptomsneed to be monitored regularly and the dosagetitrated accordingly (Figure 25.1). The potentialadvantages of using medication are an initialrapid reduction in core symptoms; this could helpchildren and parents better utilize non-medicationstrategies, and reduce immediate stress at homeand school, which could avoid an escalation ofproblems leading to school exclusion and familybreakdown in the short term. Disadvantagesmight include an over-reliance on medicationalone, side effects, or repeat prescribing overyears without consideration of whether there arecontinued benefits and whether there is the needfor additional new non-medication interventions.

StimulantsMethylphenidate and dexamfteamine are centralnervous system stimulants. The mode of action of

methylphenidate is not entirely clear, although itappears to result in an increased dopamine concen-tration in the synaptic cleft by partially blocking thedopamine transporter (DAT). Methylphenidate israpidly absorbed, reaching maximum plasma levels1–4 hours after oral administration (see Figure 25.1for the treatment regimen). Sustained-release for-mulations with a therapeutic effect of 8–12 hoursare also available, making single daily dose admin-istration possible. The main advantage is that thechild does not have to take medication at school,reducing problems with storage of tablets and asso-ciated stigma for these children. Dexamfetaminealso enhances dopaminergic neurotransmission inthe central nervous system. The elimination half-life of dexamfetamine allows once- or twice-dailyoral administration. The recommended startingdose for treatment of ADHD depends on the ageof the child (see Figure 25.1).

Frequent short-term side effects of stimulantdrugs include:

• decreased appetite• sleep disturbance, such as insomnia

Confirmed ADHD Diagnosis

Stimulants Non-stimulant

MethylphenidateStart at 5 mg twiceor three times a day

Start at 2.5 mg daily(3 to 5-year-olds)

or5–10 mg/day(> 6 year old)

Start at0.5 mg/kg/day

(Minimum 7 days)

Monitor regularlyMax. 60 mg/day

Monitor regularlyMax. 20 mg/day

Monitor regularlyMaintenance dose1.2 –1.8 mg/kg/day

Titrate the dose byincreasing

5–10 mg/weekaccording to

response

Titrate the dose byincreasing

2.5 mg/weekaccording to

response

Titrate the dose andevaluate after4–6 weeks

According toresponse

Consider long-actingpreparations

Dexamfetamine Atomoxetine

Figure 25.1 Using medication to treat attention-deficit hyperactivity disorder (ADHD).

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• headaches• stomach aches• drowsiness• irritability• tearfulness• increased blood pressure and pulse.

The effect of methylphenidate on growth inthe long term is not clear [17]. The use of drugholidays not only provides the opportunity toassess improvement of ADHD symptoms, but alsogives children the opportunity to catch up withtheir growth by improving their appetite. Finally,the use of stimulant drugs in children with ticsand seizures can be considered, but with caution.Stimulants have also been shown to be usefulfor treating ADHD in children with pervasivedevelopmental disorders and intellectual disabil-ity [18], although there is increased sensitivity toside effects in these groups.

Non-stimulantsAtomoxetine is a non-stimulant drug also usedin the treatment of ADHD in children aged 6years and over. The therapeutic effect of atomox-etine is currently considered to be related to theincrease of noradrenaline in the cortex throughinhibition of presynaptic reuptake. Atomoxetinecan be administered as a once-daily dose, althoughsome children benefit from divided daily doses(see Figure 25.1). Common undesired effects ofatomoxetine include:

• abdominal pain• nausea and vomiting• decreased appetite with associated weight loss• dizziness• slight increases in heart rate and blood pressure.

Suicidal thoughts have also been reported tobe more frequent among children and adolescentstreated with atomoxetine. Finally, although rare,atomoxetine can cause liver damage. Therefore, aswith stimulants, regular monitoring of side effectsand symptoms is necessary.

Other medicationsThere is limited evidence supporting the use ofother drugs. However, drugs such as clonidine,bupropion, and modafinil have been shown toproduce some improvement in ADHD symptoms.Some uncontrolled studies have also suggested the

use of tricyclic antidepressants such as imipramineand desipramine. These drugs should be usedonly as a second-line treatment and when otherinterventions have not been successful.

Psychosocial interventionsIt is recommended that non-pharmacologicalinterventions are also provided to children andadolescents suffering with ADHD. Cliniciansmust emphasize to parents the need to implementthese interventions despite the use of pharma-cological treatment. The largest trial to date, theMultimodal Treatment Study of ADHD [19],showed short-term benefits of medication, thatadding behavioural treatment reduced the dosageof medication required, but that behavioural treat-ment alone was not helpful. Children with ADHDmay benefit from scheduled activities and regulartimetables. Reducing family stress by increasingsupport, either formally through social services orvia voluntary organizations, can be helpful.

Parent training programmes/behaviour therapyare aimed at modifying symptoms and shouldbe considered first for preschool children withADHD [20]. Parenting packages, such as theWebster–Stratton programme, are behaviourallyoriented, usually delivered in groups, and empha-size the use of play, praise, incentives, limitsand discipline to improve the child’s symptomsand behaviours. Parent training programmes arewidely used in CAMHS at present.

Cognitive–behavioural therapy for older chil-dren and adolescents can help them to developa better understanding of their feelings, thoughtsand actions, and, theoretically, could improvecore ADHD symptoms. Recent work suggestspotential benefits for adults who are alreadybeing treated with medication [21]. However, todate there is little evidence to support its use inadolescents with ADHD.

Social skills training can be useful to help thechild develop socially acceptable behaviours andimprove peer relationships. Social skills train-ing includes the use of anger management andproblem-solving strategies. At present there is noevidence to suggest that this type of treatment iseffective in ADHD.

School interventionsThe management of ADHD in school-agedchildren needs to consider the school setting.

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Therefore, training of teachers about the conditionand increased support in the classroom is impor-tant. Behavioural interventions include classplacement, and the promotion of structure androutines in the classroom, and during breaktimesand play activities. Setting small, achievable goalscan have a positive effect on self-esteem. Finally,educational psychologists can provide advice onthe management of specific educational difficultiesand appropriate school placement for childrenwith more complex difficulties.

Other interventionsThere has been interest in whether the eliminationof certain artificial colourings and preservativesfrom the individual child’s diet can improve thesymptoms of ADHD. There is some evidence thatthis can help a few selected individuals. Some chil-dren could also benefit from the use of omega-3and omega-6 polyunsaturated fatty acids to sup-plement their diet. However, the evidence base forthese interventions is limited at present.

CLINICAL COURSE

Symptoms of ADHD decline with age, but longi-tudinal studies show that ADHD and associatedproblems tend to persist into adolescence and adultlife [22]. Problems include:

• continuing to meet full diagnostic criteria orshowing some symptoms with associated impair-ment;

• adult ADHD;• conduct disorder, antisocial behaviour, crimi-

nality;• drug and alcohol misuse;• educational and employment failure;• relationship difficulties, driving offences.

Consideration must also be given to the possibleeffects of ADHD on safe driving in adolescents andyoung adults.

REFERENCES

[1] Taylor E, Sonuga-Barke E. (2008) Disorders ofattention and activity. In: Rutter M, Bishop D, PineD et al. (eds), Rutter’s Textbook of Child Psychiatry,5th edn. Oxford: Blackwell.

[2] Ford T, Goodman R, Meltzer H. (2003) The BritishChild and Adolescent Mental Health Survey 1999:

the prevalence of DSM-IV disorders. Journal ofthe American Academy of Child and AdolescentPsychiatry 42, 1203–11.

[3] Collishaw S, Maughan B, Goodman R, Pickles A.(2004) Time trends in adolescent mental health.Journal of Child Psychology and Psychiatry 45,1350–62.

[4] Polanczyk G, de Lima MS, Horta BL, BiedermanJ, Rohde LA. (2007) The worldwide prevalenceof ADHD: a systematic review and metaregres-sion analysis. American Journal of Psychiatry 164,942–8.

[5] Thapar A, Langley K, Owen MJ, O’DonovanMC. (2007) Advances in genetic findings on atten-tion deficit hyperactivity disorder. PsychologicalMedicine 37, 1681–92.

[6] Taylor E. (2009) Developing ADHD. Journal ofChild Psychology and Psychiatry 50, 126–32.

[7] Linnet KM, Dalsgaard S, Obel C et al. (2003)Maternal lifestyle factors in pregnancy risk of atten-tion deficit hyperactivity disorder and associatedbehaviors: review of the current evidence. AmericanJournal of Psychiatry 160, 1028–40.

[8] Thapar A, Rutter M. (2009) Do prenatal risk factorscause psychiatric disorder? Be wary of causal claims.Britsh Journal of Psychiatry 195, 100–1.

[9] Stevens SE, Sonuga-Barke EJ, Kreppner JM etal. (2008) Inattention/overactivity following earlysevere institutional deprivation: presentation andassociations in early adolescence. Journal of Abnor-mal Child Psychology 36, 385–98.

[10] Kelly AM, Margulies DS, Castellanos FX. (2007)Recent advances in structural and functional brainimaging studies of attention-deficit/hyperactivitydisorder. Current Psychiatry Reports 9, 401–7.

[11] Conners CK, Sitarenios G, Parker JD, Epstein JN.(1998) The revised Conners’ Parent Rating Scale(CPRS-R): factor structure, reliability, and criterionvalidity. Journal of Abnormal Child Psychology 26,257–68.

[12] Barkley RA, Fischer M, Smallish L et al. (2002) Thepersistence of attention-deficit/hyperactivity disor-der into young adulthood as a function of reportingsource and definition of disorder. Journal of Abnor-mal Psychology 111, 279–89.

[13] Holmes J, Lawson D, Langley K et al. (2004)The Child Attention-Deficit Hyperactivity DisorderTeacher Telephone Interview (CHATTI): reliabil-ity and validity. British Journal of Psychiatry 184,74–8.

[14] Conners CK, Sitarenios G, Parker JD, EpsteinJN. (1998) Revision and restandardization of theConners Teacher Rating Scale (CTRS-R): factorstructure, reliability, and criterion validity. Journalof Abnormal Child Psychology 26, 279–91.

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[15] National Collaborating Centre for Mental Health.(2009) Attention Deficit Hyperactivity Disorder:Diagnosis and Management of ADHD in Children,Young People and Adults. London: The BritishPsychological Society and The Royal College ofPsychiatrists.

[16] Jensen PS, Arnold LE, Swanson JM et al. (2007)3-year follow-up of the NIMH M TA study. Journalof the American Academy of Child and AdolescentPsychiatry 46, 989–1002.

[17] Poulton A. (2006) Growth and sexual maturation inchildren and adolescents with attention deficithyperactivity disorder. Current Opinion in Pedi-atrics 18, 427–34.

[18] Pearson DA, Santos CW, Roache JD et al.(2003) Treatment effects of methylphenidate onbehavioural adjustment in children with mentalretardation and ADHD. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 42,209–16.

[19] MTA Cooperative Group. (1999) A 14-month ran-domized clinical trial of treatment strategies forattention-deficit/hyperactivity disorder. MultimodalTreatment Study of Children with ADHD. Archivesof General Psychiatry 56, 1073–86.

[20] Munoz-Solomando A, Kendall T, Whittington CJ.(2008) Cognitive behavioural therapy for childrenand adolescents. Current Opinion in Psychiatry 21,332–7.

[21] Safren SA, Sprich S, Mimiaga MJ et al. (2010)Cognitive behavioral therapy vs relaxation with edu-cational support for medication-treated adults withADHD and persistent symptoms: a randomizedcontrolled trial. Journal of the American MedicalAssociation 304, 875–80.

[22] Langley K, Fowler T, Ford T et al. (2010) Adolescentclinical outcomes for young people with attention-deficit hyperactivity disorder. British Journal ofPsychiatry 196, 235–40.

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26Challenges in Child and AdolescentObsessive-Compulsive DisorderElaine Chung1 and Isobel Heyman2

1Child and Adolescent Mental Health Service, The Royal Free Hospital, London, UK2National and Specialist Service for paediatric obsessive compulsive disorder, South London andMaudsley NHS Foundation Trust, UK; Institute of Psychiatry, King’s College London, London, UK

THE ‘HIDDEN PROBLEM’

Young people with obsessive-compulsive disorder(OCD) and their families report that one of themost challenging aspects of dealing with OCD isrecognition of the problem. This includes realizingthat the symptoms, as they emerge, are part ofOCD (Box 26.1).

Box 26.1 Symptoms of obsessive-compulsive disorder

Obsessions

• Intrusive, repetitive, distressingthoughts or images

• Most common themes: contamination,harm coming to others, sexual,aggressive, religious

Compulsions

• Repetitive, stereotyped, unnecessarybehaviours

• Most common rituals: washing,checking, repeating, reassuranceseeking, ordering


Obsessive-compulsive disorder generallyresponds to treatment, and the emotional, socialand educational disabilities that children mayacquire secondary to chronic OCD are likely tobe minimized by prompt intervention [1]. Earlierdetection and treatment will be promoted bygreater public awareness, and there is evidencethat early diagnosis and intervention improveslong-term outcomes [2]. Fifty percent of adultswith OCD remember that their disorder startedin childhood, but many failed to get help at thisstage, with average delays in diagnosis of 12years in adults and over 3 years in children [3].Though paediatric OCD was once consideredrare, epidemiological studies have revealed aprevalence of about 1% for OCD [4].

A possible reason for delays in recognizingOCD is the nature of the illness itself. Individualswith OCD usually have good insight, realizingtheir thoughts and behaviours are unnecessary.They often feel embarrassed by the symptoms andhide them for as long as possible, or may fear theywill be asked to stop ritualizing and worry thiswould be anxiety provoking. Even in a brief pri-mary care consultation, some screening questionssuch as those in the 7-item Short OCD Screener(SOCS) can be used (available online: http://ocdyouth.iop.kcl.ac.uk/downloads/socs.pdf) [5].

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Challenges in child and adolescent obsessive-compulsive disorder

WHEN DO ORDINARY CHILDHOOD RITUALSBECOME OCD?

Rituals are a part of normal childhood develop-ment (e.g. carrying out a bedtime ritual) and shouldnot be confused with OCD [6]. Rituals are com-mon in young children (usually from the age of 2 to7 years), and parents may fail to notice their child’srituals are becoming more prolonged or distress-ing. A child’s obsessions or rituals may be OCD if:

• the rituals or thoughts upset the child;• they take up a lot of time (more than one hour

per day);• they interfere with the child’s everyday life.

To make a diagnosis of OCD, not only do com-pulsions and/or obsessions need to be present, butalso they must cause functional impairment.

AETIOLOGY

The cause of OCD is not known, but there isincreasing research evidence for a biological basisto this disorder [7], although it is highly responsiveto psychological intervention.

Family and twin studies support a strong geneticrole in the aetiology of OCD, with heritabilityin children ranging from 45 to 65% [8]; however,the heterogeneity of the disorder complicates thesearch for specific genes. A promising approachfor genetic, imaging and treatment studies isthe consideration of OCD dimensions as quan-titative phenotypes. OCD is a heterogeneouscondition, and factor- and cluster-analyticalstudies in adults and children have identifiedfour relatively independent symptom dimensionsof contamination/cleaning, obsessions/checking,symmetry/ordering and hoarding [6,9].

Brain imaging studies demonstrate differingblood flow patterns in OCD patients comparedwith controls, and support a frontal-striatal-thalamic model of OCD [10]. Treatment witheither medication or CBT is associated with areversal of functional neuroimaging findings. Theneurochemical basis of these differences is notknown, but the effectiveness of SSRIs suggeststhat serotonin is an important neurotransmitter.Glutamate has also been implicated, and trials ofglutamate-modulating agents, such as riluzole, intreatment are underway [4,11].

A further finding implicating the basal gan-glia in OCD, is that a subgroup of children

with OCD may have the disorder triggered byinfections. Streptococcal infections trigger animmune response, which in some individualsgenerates antibodies that cross-react with antigensin the basal ganglia. This subgroup has beengiven the acronym PANDAS (paediatric autoim-mune neuropsychiatric disorder associated withStreptococcus) [12,13].

ASSESSMENT OF THE YOUNG PERSONWITH POSSIBLE OCD

Differential diagnosis and identifying OCDDiagnosing OCD may involve asking the childdirect questions about obsessions and compul-sions, as these may not be revealed spontaneously.Clinicians need to consider alternative diagnoses,such as depression, other anxiety disorders,developmental disorders that include repetitivebehaviours (e.g. autism spectrum disorders) andtic disorders. Psychological instruments may beused to assist with diagnosis and rating of severity.The best validated is the Children’s Yale-BrownObsessive Compulsive Scale (CY-BOCS) [14].

Phenomenology of obsessionsand compulsionsChildren with OCD usually have both obsessionsand compulsions, and an obvious link betweenthem can often be detected, for example con-tamination fears and excessive washing. However,in some the connection may be less obvious, forexample fear of a parent’s misfortune if the childdoes not touch something a certain number oftimes. Obsessions may not be present; a child maydescribe that things are just ‘not right’ if theydo not do their ritual. The distressing nature ofobsessions can make it difficult for younger chil-dren to recognize them as their own thoughts. Itis not unusual for younger children to call theirobsessions ‘voices’, and careful examination ofthe psychopathology is needed to avoid confus-ing these experiences with psychotic phenomena.Children may have less insight into the irrationalnature of obsessions and compulsions, and ICD-10(ICD-10 International Classification of Mental andBehavioural Disorders in Children and Adoles-cents) and DSM-IV-TR (Diagnostic and StatisticalManual of Mental Disorders, Fourth Edition – TextRevision) allow diagnosis of OCD with reducedinsight in young people.

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Obsessions may cause moredistress than compulsionsParticularly in teenagers, predominantly obses-sional problems can be difficult to diagnose. Thecommonest obsessive themes – sexual, aggressiveand religious – are often particularly embarrass-ing to disclose. It is helpful to enquire aboutthese directly, and explain that everyone has intru-sive thoughts. It is important to explain that anobsessive thought should not be confused with animpulse to act, and in no way reflects the natureor behavioural leanings of the person experiencingit. This is especially important when someone hassocially concerning obsessions, such as having sexwith children. If these recurrent thoughts are notrecognized as an obsession (which does not implyan actual wish to act on this intrusive thought), aninappropriately high level of risk may be inferred,when there is none.

Secondary risks, the unintended consequencesof acting on compulsions or avoidance, shouldbe considered. For example, a person with con-tamination fears about food may restrict theirdietary intake. Also, without effective treatment,harm may occur in individuals whose OCD issevere during critical phases of development; forexample, withdrawal from school due may meanthey also miss out on important educational andsocial developmental experiences [15].

ComorbiditiesConsistent with adult studies, approximately 80%of young people with OCD have at least onecomorbid psychiatric disorder [16]. The common-est comorbidities in children are attention deficithyperactivity disorder (ADHD; 34–51%), depres-sion (33–39%), tics (26%), specific developmentaldisabilities (24%), oppositional defiant disorder(ODD; 17–51%) and anxiety disorders (16%)[4]. Careful assessment is required both to dis-tinguish symptoms of OCD from other disordersand because some comorbidities may influenceresponse rates to particular treatments [17–20].

TREATMENT

Helping parents and young people becomeinformed about OCD is crucial, and there areseveral good publications available (see ‘Furtherreading’ below). The UK National Charity, OCD

Action, provides information and links to supportgroups. For many families, knowing they are notalone is the first step towards recovery.

There are two interventions of proven efficacy:cognitive–behavioural therapy (CBT) with expo-sure and response-prevention (ERP), and specificmedication, which can be used independently orin combination. One randomized controlled trial(RCT) has directly compared the efficacy of CBTand SSRIs (sertraline), and showed no significantdifference between them, whilst combination ther-apy was more effective [16]. A meta-analysis ofRCTs found that whilst both CBT and medicationare effective treatments for paediatric OCD, CBTis associated with greater effect sizes than pharma-cotherapy. Pooled effect sizes were 1.45 and 0.48respectively [21]. There is no evidence that psy-choanalytic psychotherapy is of benefit for OCD.

In the UK, the National Institute for Healthand Clinical Excellence (NICE) recommendsa ‘stepped care’ model, with increasing inten-sity of treatment according to clinical severity(Figure 26.1) [22]. The assessment of the severityand impact of OCD can be aided by the use ofthe CY-BOCS [14]. CBT incorporating ERP isrecommended as first-line treatment in childrenand adolescents, with the subsequent additionof an SSRI, then consideration of clomipramineand augmentation strategies with atypical antipsy-chotic medications as necessary. Admission tohospital is rarely indicated, but may be needed ifthere is risk to safety or physical health.

Young people becoming experts:causes of OCDIt is helpful for patients and families to have appro-priate information about our current knowledge ofthe aetiology of OCD. Understanding that OCD isa neurobiological disorder helps young people andfamilies realize it is not their fault. It is also help-ful to stress that treatments really work, and thatmany successful people have coped with OCD.

Cognitive—behavioural therapy (CBT)Studies in adults and young people have shownCBT to be an effective treatment for OCD, with40% to 88% of young people achieving remission.Studies have shown that CBT for paediatric OCDcan also be effectively delivered in groups or bytelephone [20,21,23].

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Who isresponsible

for care?What is the focus? Type of

care

Step 6CAMHS Tier 4

OCD with risk tolife, severe neglect,or severe distressor disability

Reassess,discuss optionsand carecoordination.As per Step 4and consideraugmentationstrategies,admission orspecial livingarrangements

Step 5CAMHS Tiers 3 & 4

OCD withsignificantcomorbidity, ormore severelyimpairedfunctioning and/ortreatmentresistance, partialresponse or relapse

Reassess, discussoptions.As per Step 3 andconsider referral tospecialist servicesoutside CAMHS ifappropriate


OCD withcomorbidity or

poor response toinitial treatment

Assess, review, discussoptions.

CBT (including ERP),then consider combined

treatments of CBT(including ERP) with

SSRI, alternative SSRI orclomipramine


Management andinitial treatment

Guided self-help, CBT(including ERP), involve

family/carers and considerinvolving school

Step 2CAMHS Tier 1

Recognition andassessment

Detect, educate, discuss treatmentoptions, signpost voluntary supportagencies, provide support to young

people, families/carers/schools.Refer if necessary

Step 1Individuals, public organisations, NHS

Awareness andrecognition

Provide, seek and share informationabout OCD and its impact onindividuals and families/carers

Figure 26.1 NICE (National Institute for Health and Clinical Excellence) stepped-care model forobsessive-compulsive disorder (OCD) in children and adolescents [22]. CAMHS, child and adolescentmental health services; CBT, cognitive—behavioural therapy; ERP, exposure and response-prevention;SSRI, selective serotonin reuptake inhibitor. Adapted from NICE Guideline 31, The Stepped-Care Model2005.

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Obsessions

Compulsions

AnxietyTemporary relief

Figure 26.2 The ‘vicious cycle of obsessive-compulsive disorder (OCD)’. Obsessions generate anxiety,whilst compulsive rituals are performed to reduce the anxiety, but in fact this produces only temporaryrelief and reinforces the cycle. Exposure and response-prevention (ERP) acts by exposing a youngperson to the feared situation whilst resisting compulsions, in a graded manner, to break this cycle.

Anxiety: A key aspect of overcoming OCD andengaging in psychological treatment is understand-ing the role of anxiety in OCD. Education aboutanxiety forms a starting point for any successfulcognitive–behavioural programme (Figure 26.2).

OCD as an ‘intruder’: Child-oriented manualsfor treating OCD commonly use an externaliz-ing approach [24]. The child is helped to see OCDas an ‘intruder’ who is spoiling their life by seekingto control their thoughts and actions. Treatmentis aimed at giving the child and family effectivemeans of controlling the intruder – saying ‘No’ toOCD. This ‘externalizing’ approach to the disor-der, giving it a name, and learning how to ‘fight’it, is a useful technique in child and adolescenttreatment. The Secret Problem is a helpful chil-dren’s cartoon book about OCD that exemplifiesthis approach [25].

Exposure and response-prevention: CBT proto-cols are generally based on ERP: ‘exposure’ (facingup to the feared stimulus) and ‘response-prevention’ (resisting the urge to carry out aritual in these circumstances) [24]. In adultand child studies, ERP appears to be a criticaltherapeutic component. Cognitive protocols,which tackle underlying beliefs about connectionsbetween thoughts and behaviours, are also beingevaluated [26].

It helps to explain to children that the first stepof CBT involves a detailed assessment of the prob-lem, often starting with keeping a symptom diary.Resisting compulsions makes OCD sufferers very

anxious, and it is important for them to learn howto confront this anxiety. Step-by-step exposureto the anxiety-provoking situation, while resistingthe urge to respond with compulsive behaviour,shows the patient that their anxiety level steadilydecreases under these conditions, and they realizethat compulsive behaviour is not the only way torelieve their anxiety. The young person designsthe treatment programme with the therapist, sothat little by little they can overcome their fears.‘Accommodation’, or the participation by familymembers in OCD rituals, is common, elicited bytheir child’s distress and unwittingly reinforcingthe OCD, and is reported in up to 75% of par-ents [27]. Families need to learn about OCD, andhow to help their child fight back [27,28]. CBT isnot usually a long treatment; most children whorespond to this approach do so in 8–12 sessions.

MedicationThere is extensive clinical trial literature in adultsand young people with OCD demonstrating effi-cacy for the serotonin reuptake inhibitor (SRI)group of antidepressants. Clomipramine, an SRI,remains a useful drug for some, although its side-effect profile (sedation, dry mouth, cardiac sideeffects) make it generally less acceptable thanselective serotonin reuptake inhibitors (SSRIs),which are now the first-line medication. All SSRIsappear to be equally effective, although they havedifferent pharmacokinetics and side effects [29].There has been concern about the use of SSRIsin depressed youths, with meta-analyses suggestinglow levels of efficacy and an increase in behavioural

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activation including suicidal behaviours, althoughrecent evidence is more positive. In contrast, SSRIsappear effective in paediatric OCD, with ‘numbersneeded to treat’ (NNT) ranging from 2 to 10, andthere is no significant evidence of increased sui-cidality [30,31]. However, given recent concernsthere should be close monitoring for side effects.

Only sertraline and fluvoxamine are currentlylicensed for use in children in the UK, but otherSSRIs could be used ‘off-label’ by a specialist inexceptional circumstances. For example, in comor-bid depression, SSRIs should be used with caution,and the only one not currently contraindicated indepressed youth is fluoxetine.

About 70% of individuals with OCD respondfavourably to medication, and if a first SSRI is inef-fective or not tolerated, it is worth trying a second.Both clomipramine and SSRIs have a delayedonset of action, with full therapeutic effects notbeing apparent for 8–12 weeks. It is thereforeworth waiting for a response at a moderate thera-peutic dose, rather than moving rapidly to highdoses, which will increase the chances of sideeffects. The optimal dose is variable, and should bedetermined by titrating from a low starting dose.The effective doses needed for adult OCD seemto be higher than for depression, and this may alsobe the case in younger people.

PROGNOSIS AND ONGOING CARE

Early detection and treatment is likely to mini-mize secondary disabilities and continuation intoadulthood, but as yet, few assertively treatedearly-onset cohorts have been followed up longterm. Long-term follow-up studies thus far havefound a persistence rate of 40%, and further stud-ies into predictors of outcome and augmentationstrategies are needed [32,33]. If a young personhas responded to medication, treatment shouldcontinue for at least 6 months after remission[22]. CBT should give individuals strategies fordealing with transient symptom recurrence, andtheoretically obviate the need in some peoplefor long-term medication. Many people withearly-onset OCD respond to treatment andlead fully functioning lives. It is important thatthroughout their lifespan, people with OCDshould have access to support as needed, andNICE recommends that if relapse occurs, they

should be seen as soon as possible, rather thanplaced on routine waiting lists.

Box 26.2 Key learning points

• Obsessive compulsive disorder (OCD) isa neurobiological disordercharacterized by obsessional thoughtsand compulsive behaviours leading tofunctional impairment.

• It is common in young people; however,delays in diagnosis can occur.

• Without treatment, OCD can becomesevere and chronic; however, effectiveevidence-based treatments exist:cognitive—behavioural therapy (CBT)with exposure and response-prevention(ERP) alone, or in combination therapywith selective serotonin reuptakeinhibitors (SSRIs).

REFERENCES

[1] Rapoport JL and Inoff-Germain G. (2000) Treat-ment of obsessive-compulsive disorder in childrenand adolescents. Journal of Child Psychology andPsychiatry 41, 419–31.

[2] Leonard HL, Swedo SE, Lenane MC et al. (1993)A 2- to 7-year follow-up study of 54 obsessive-compulsive children and adolescents. Archives ofGeneral Psychiatry 50, 429–39.

[3] Chowdhury U, Frampton I, Heyman I. (2004) Clin-ical characteristics of young people referred to anobsessive compulsive disorder clinic in the UnitedKingdom. Clinical Child Psychology and Psychiatry9, 395–401.

[4] Kalra SK and Swedo SD. (2009) Children withobsessive-compulsive disorder: are they just ‘‘lit-tle adults’’? Journal of Clinical Investigation 119,737–46.

[5] Uher R, Heyman I, Mortimore C et al. (2007)Screening young people for obsessive-compulsivedisorder. British Journal of Psychiatry 191, 353–4.

[6] Leckman JF, Bloch MH, King RA. (2009) Symptomdimensions and subtypes of obsessive-compulsivedisorder: a developmental perspective. Dialogues inClinical Neuroscience 11, 21–33.

[7] Mataix-Cols D, van den Heuvel OA, vanGrootheest DS et al. (2008) Obsessive-compulsive

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disorder. In: Squire LR (ed.), Encyclopedia of Neu-roscience. Oxford: Academic Press, pp. 1–8.

[8] Van Grootheest DS, Cath DC, Beekan AT et al.(2005) Twin studies on obsessive-compulsive disor-der: a review. Twin Research and Human Genetics8, 450–8.

[9] Mataix-Cols D, Nakatani E, Micali M et al. (2008)Structure of obsessive-compulsive symptoms inpediatric OCD. Journal of the American Academyof Child and Adolescent Psychiatry 47, 773–8.

[10] MacMaster FP, O’Neill J, Rosenberg DR. (2008)Brain imaging in pediatric obsessive-compulsive dis-order. Journal of the American Academy of Childand Adolescent Psychiatry 47, 1262–72.

[11] MacMaster FP and Rosenberg DR. (2010) Glu-tamate and the treatment of obsessive-compulsivedisorder. Psychopharmacology Review 45, 33–9.

[12] Swedo SE, Leonard HL, Rapoport JL. (2004) Thepediatric autoimmune neuropsychiatric disordersassociated with streptococcal infection (PANDAS)subgroup: separating fact from fiction. Pediatrics113, 907–11.

[13] Snider LA and Swedo SE. (2004) PANDAS: cur-rent status and directions for research. MolecularPsychiatry 9, 900–7.

[14] Scahill L, Riddle MA, McSwiggin-Hardin M et al.(1997) Children’s Yale-Brown Obsessive Compul-sive Scale: reliability and validity. Journal of theAmerican Academy of Child and Adolescent Psy-chiatry 36, 844–52.

[15] Veale D, Freeston M, Krebs G et al. (2009)Risk assessment and management in obsessive-compulsive disorder. Advances in Psychiatric Treat-ment 15, 332–43.

[16] Pediatric OCD Treatment Study (POTS) Team.(2004) Cognitive-behavior therapy, sertraline, andtheir combination for children and adolescents withobsessive-compulsive disorder: the Pediatric OCDTreatment Study (POTS) randomized controlledtrial. Journal of the American Medical Association292, 1969–76.

[17] Storch EA, Merlo LJ, Larson MJ et al. (2008) Impactof comorbidity on cognitive-behavioural therapyresponse in pediatric obsessive-compulsive disor-der. Journal of the American Academy of Child andAdolescent Psychiatry 47, 583–92.

[18] Bloch MH, Craiglow BG, Landeros-WeisenbergerA et al. (2009) Predictors of early adult outcomesin pediatric-onset obsessive-compulsive disorder.Pediatrics 124, 1085–93.

[19] March JS, Franklin ME, Leonard H et al. (2007)Tics moderate treatment outcome with sertralinebut not cognitive-behavior therapy in pediatricobsessive-compulsive disorder. Biological Psychi-atry 61, 344–7.

[20] Krebs G and Heyman I. (2010) Treatment-resistantobsessive-compulsive disorder in young people:assessment and treatment strategies. Child and Ado-lescent Mental Health 15, 2–11.

[21] Watson HJ and Rees CS. (2008) Meta-analysis ofrandomized, controlled treatment trials of pediatricobsessive-compulsive disorder. Journal of ChildPsychology and Psychiatry 49, 489–98.

[22] National Institute for Health and Clinical Excel-lence. (2005) Obsessive-Compulsive Disorder: CoreInterventions in the Treatment of Obsessive-Compulsive Disorder and Body Dysmorphic Dis-order. Clinical Guideline 31. London: The BritishPsychological Society and The Royal Collegeof Psychiatrists, available at: http://www.nice.org.uk/nicemedia/pdf/cg031fullguideline.pdf.

[23] Turner CM. (2006) Cognitive-behavioural therapyfor obsessive-compulsive disorder in children andadolescents: current status and future directions.Clinical Psychology Review 26, 912–38.

[24] March J and Mulle K. (1998) OCD in Childrenand Adolescents: A Cognitive-Behavioural Treat-ment Manual. New York: Guilford Press.

[25] Wever C. (1994) The Secret Problem. Concord West,NSW: ShrinkRap Press.

[26] Salkovskis PM, Bolton D, Williams TI et al. (2008)Improving the efficiency of cognitive behaviouraltreatment in childhood obsessive-compulsive dis-order (OCD). Paper presented at the 36thAnnual Conference of the British Association forBehavioural and Cognitive Therapies.

[27] Peris TS, Bergman L, Langely A et al. (2008) Cor-relates of accommodation of pediatric obsessive-compulsive disorder: parent, child and family char-acteristics. Journal of the American Academy ofChild and Adolescent Psychiatry 47, 1173–81.

[28] Freeman JB, Garcia AM, Coyne L et al. (2008) Earlychildhood OCD: preliminary findings from a family-based cognitive-behavioural approach. Journal ofthe American Academy of Child and AdolescentPsychiatry 47, 593–602.

[29] Geller DA, Biederman J, Stewart SE et al. (2003)Which SSRI? A meta-analysis of pharmacotherapytrials in pediatric obsessive-compulsive disorder.American Journal of Psychiatry 160, 1919–28.

[30] March JS, Klee BJ, Kremer CM. (2006) Treatmentbenefit and the risk of suicidality in multicenter, ran-domized, controlled trials of sertraline in childrenand adolescents. Journal of Child and AdolescentPsychopharmacology 16, 91–102.

[31] Bridge JA, Iyengar S, Salary CB et al. (2007) Clinicalresponse and risk for reported suicidal ideation andsuicide attempts in pediatric antidepressant treat-ment: a meta-analysis of randomized controlledtrials. Journal of the American Medical Association297, 1683–96.

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[32] Stewart SE, Geller DA, Jenike M et al. (2004) Long-term outcome of pediatric obsessive compulsivedisorder: a meta analysis and quantitative reviewof the literature. Acta Psychiatrica Scandinavica 11,4–13.

[33] Micali N, Heyman I, Perez M et al. (2010) Long termoutcomes of obsessive-compulsive disorder: follow-up of 143 children and adolescents. British Journalof Psychiatry 197, 128–34.

FURTHER READING

Goodman WK, Rudorfer, MV, Maser JC (eds). (1999)Obsessive Compulsive Disorder: Contemporary Issuesin Treatment. Lawrence Erlbaum Associates.

A comprehensive account of recent research and itsimpact on treatment strategies and choices.

Derisley J, Heyman I, Robinson S et al. (2008) BreakingFree from OCD. A CBT Guide for Young Peopleand Their Families. London and Philadelphia: JessicaKingsley Publishers.

March JS and Benton CM. (2007) Talking Back toOCD: the Program that Helps Kids and Teens Say‘‘No Way’’ – and Parents to Say ‘‘Way to Go.’’ NewYork: Guilford Press.

Both of these are CBT self-help books that young peoplecould work through alone, or ideally with a parent ortherapist.

Wagner A. (2002) Up and Down the Worry Hill: a Chil-dren’s Book About Obsessive-Compulsive Disorderand its Treatment. New York: Lighthouse Press.

An illustrated book designed to help parents and profes-sionals explain OCD to younger children through thestory of ‘Casey’, a young boy with OCD.

Waltz M. (2000) Obsessive Compulsive Disorder: Helpfor Children and Adolescents. Patient Center Guides.

Written by a woman with OCD who has two children withOCD, this book provides information about OCD, itsdiagnosis and treatment and advice for working withschools.

Wells J. (2006) Touch and Go Joe. An Adolescent’s Expe-rience of OCD. London: Jessica Kingsley Publishers.

A revealing insight into the life of a teenager with OCD.

USEFUL WEBSITES

OCD youth: www.ocdyouth.infoOCD Action: www.ocdaction.org.ukInternational OCD Foundation: www.ocfoundation.org

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27Anxiety Disorders in Childrenand AdolescentsAaron Vallance and Elena GarraldaAcademic Unit of Child & Adolescent Psychiatry, Imperial College London, London, UK

Anxiety is an unpleasant feeling of tensionor apprehension accompanied by physiologicalchanges and worries or fears. It can becomemaladaptive if excessive or developmentally inap-propriate; if it also causes significant functionalimpairment, it can be considered to be an anxietydisorder.

It is important to bear in mind developmentaldifferences in the presentation of normal anxietyand anxiety disorders (Table 27.1). Cognitive skillendows adolescents with the capacity to imagineand ruminate on increasingly complex and abstractthreats. What is seen as normal for a young childmay be considered a disorder in an older child.

DIAGNOSTIC FEATURES

Children with anxiety disorders show a range ofsymptoms, from mild distress to incapacitating anx-iety. ICD-10 (ICD-10 International Classificationof Mental and Behavioural Disorders in Childrenand Adolescents) requires the presence of a num-ber of physiological changes occurring either in aspecific feared situation or for a specific duration.Making an early diagnosis is important: many anx-iety disorders remain untreated in the community,causing distress and impeding academic and socialfunctioning. Failure to diagnose may interfere withthe child’s acquisition of social skills and result insocial dysfunction.

Separation anxiety disorder is an excessiveand/or developmentally inappropriate anxiety


about separation from attachment figures orexcessive worrying about the figure’s welfare.Impairment might include school refusal. ICD-10criteria include an onset before 6 years old and aduration of at least 4 weeks.

Generalized or over-anxious anxiety disorderis characterized by excessive worry and anxiety,which is generalized and persistent, and notrestricted to any particular situation or object.This ‘free-floating’ anxiety is hard to control andis frequently accompanied by a more restricted setof somatic complaints than those found in adults,including restlessness, fatigue, muscle tensionand sleep disturbance. These children may showconcerns about their competence, excessive self-consciousness, and a strong need for reassurance.

Social phobia involves the marked, persistentfear of embarrassment in social situations involv-ing exposure to unfamiliar people or to scrutiny;

Table 27.1 Fear, and its typicaldevelopmental stages.

Age Fears

9 months to3 years

Separation, strangers

3—6 years Animals, darkness, ‘monsters’

6—12 years Performance anxiety

12—18 years Social anxiety

Adulthood Illness, death

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these situations are then usually avoided, therebyreinforcing the anxiety associated with them andleading to social isolation. When confronted witha phobic situation (e.g. public speaking or goingto a party) the adolescent will experience anxietysymptoms, and at least one of: blushing, shaking,or fear of vomiting, micturition or defecation.

Panic disorder involves recurrent and unex-pected attacks of severe anxiety that are notrestricted to any particular situation (Box 27.1).The young person may show persistent apprehen-sion about future attacks (anticipatory anxiety) orits feared implications (e.g. losing control, havinga heart attack).

Box 27.1 Characteristic symptoms ofpanic disorder

A discrete period of intense fear or dis-comfort that develops acutely and is asso-ciated with multiple physical symptoms,including:

• palpitations

• sweating

• trembling

• shortness of breath

• chest pain

• nausea.

Specific or simple phobias are characterizedby excessive fears of discernible, circumscribedobjects or situations that provoke an imme-diate anxiety response. In children this may

be manifested as crying, tantrums, freezing orclinging. Adolescents may recognize that thefear is excessive. Particularly significant formedical practice are phobias of injections andmedical procedures.

EPIDEMIOLOGY

Anxiety disorders are one of the most prevalentcategories of psychopathology in children and ado-lescents (Table 27.2). At least one-third of childrenwith anxiety disorders meet the criteria for twoor more anxiety disorders. General comorbiditywith other psychiatric disorders – including oppo-sitional defiant, depressive, hyperkinetic disorders,and substance abuse – is 40%. Muris et al. [1]found that 84% of their sample of children andadolescents with pervasive developmental disor-ders had anxiety disorder.

AETIOLOGY

TemperamentLongitudinal studies suggest that anxiety dis-orders tend not to arise de novo but build onpre-existing temperamental traits. Examplesinclude: behavioural inhibition (showing fearand withdrawal in unfamiliar situations and highsympathetic reactivity), passivity, shyness and ananxious-resistant attachment style.

GeneticsFamily and twin studies show that genetic factorsplay a significant role. These disorders tend to runin families but with little specificity, except forpanic disorder.

Table 27.2 Epidemiological characteristics of anxiety disorders in children and adolescents.

Disorder Prevalence Age of onset Sex ratio

Separation anxiety disorder 2—4% Pre-puberty; peaks at 7years

Approx. equal

Generalized anxiety disorder 3% Increased incidence inadolescence

Approx. equal

Panic disorder 5% Late teens Approx. equal

Social anxiety disorder 1—7% 11—15 years Commoner in girls

Specific phobia 2—4% > 5 years Equal

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Table 27.3 Information processing biases: threat attention and threat appraisal.

Process What is it? Bias in anxiety disorder Relative specificity toanxiety disordersubcategories

Threat attention Attention is rapidlydirected towardsenvironmental threats

Tendency to allocateattention automaticallytowards threats

Low

As threat intensityincreases, a tendency toavoid the threatdevelops

Threat appraisal Events are interpreted asmeaningful andthreatening to theindividual

Children with anxietydisorders exhibit areduced threshold forclassifying stimuli asdangerous

High

E.g. adolescents withsocial phobia exhibit athreat appraisal biasspecifically for socialstimuli

Neurobiology/neuropsychologyPine has constructed a neuropsychologicalmodel of childhood anxiety [2]. Neuroimagingstudies, mostly in adults, have demonstratedamygdala–prefrontal circuitry abnormalities,areas well known for their role in memory,learning and emotional regulation. Such bio-logical changes are associated with informationprocessing biases, namely threat attention, threatappraisal and fear conditioning (Table 27.3).

Parent—child interactionsRetrospective and observational studies havefound that parents of anxious children have anexcess of controlling and/or rejecting styles ofchild-rearing, high ‘expressed emotion’ with emo-tional over-involvement towards their children. Itis unclear, however, whether the parenting stylecontributes to the child’s anxiety, or vice versa.It is possible that parental behaviour of this typeimpedes the development of autonomy, so that thechild feels less safe and more anxious. Parents withanxiety problems who feel threatened themselvesmay promote the perception of threat in thesechildren and impede the development of copingskills; children may therefore develop anxietyproblems via modelling.

Catastrophic life eventsThese are related to post-traumatic stress disorder.Other anxiety disorders may be related to adverselife events, particularly those characterized bythreat or loss, such as a death or break-up in thefamily.

Social adversityParents’ emotional availability and ability to helpcontain their children’s anxieties and fears maybe affected if they are having to deal with mul-tiple social problems. Children living in familieswhere the parents are facing chronic stressors suchas overcrowding, poverty and marital discord aremore likely to experience insecurity and feel anx-ious and fearful.

ASSESSMENT

A diagnostic assessment involves addressingthe possible aetiological factors and seekinginformation from several perspectives (as reportsof anxiety symptoms may differ with differentinformants). One should bear in mind devel-opmental differences in the presentation ofanxiety disorders, as compared with transient,developmentally appropriate fears; assessmentalso needs to consider undiagnosed learning

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disability. Differential and comorbid diagnosesinclude: autistic spectrum disorder, oppositionaldefiant disorder, attention deficit hyperactivitydisorder (ADHD), depression, alcohol abuse andpost-traumatic stress disorder.

Medical assessment should include a thoroughmedical history and physical examination, exclud-ing disorders (e.g. hyperthyroidism, arrhythmias,epilepsy, caffeinism) and drugs (e.g. steroids,sympathomimetics) that can mimic or provokeanxiety states.

PROGNOSIS

The prognosis of anxiety disorders depends on:comorbidity, age of onset, increased severity atbaseline, and type of disorder.

The highest one-year remission rates occur inseparation anxiety disorder (almost all children),the lowest in panic disorder (less than 75%) and inmore severely affected children. Many childrendevelop new psychiatric disorders at follow-up(often new anxiety disorders) and in adulthood.Data from a community epidemiological studyshowed that different types of anxiety disorderin childhood predicted anxiety and other psychi-atric disorders in adolescence; the only exceptionwas generalized anxiety disorder, which predictedonly conduct disorder [3].

Although most adolescent anxiety disordersdo not persist into adulthood, most adulthooddisorders are preceded by an anxiety disorderin adolescence. Moreover, anxiety disordersof childhood lead to a 2–5-fold increase inanxiety disorders, depression, suicide attemptsand psychiatric admissions in later life. They areassociated with increased rates of alcohol andsubstance abuse and smoking, possibly as a meansof self-medicating. In adults, anxiety disordersare linked to an increased risk of academicfailure, low-paid employment, dependence onstate benefits, and reduced quality of life.

TREATMENT

Even though anxiety disorders are common inchildhood, affected children often do not receivetreatment. Treatment may involve a combinationof approaches, the type of which should depend onthe ever-evolving evidence base, as well as on theindividual case. For example, patients with specific

phobias are more likely to be offered behaviouraltreatment, whilst comorbid family dysfunctionmay require family therapy. The preference of thechild and/or family and the resources availablemay also influence the choice of treatment.Although the UK’s National Institute for Healthand Clinical Excellence (NICE) developednational guidelines on anxiety disorders in 2004and 2007, these pertain only to adults.

The main principles of treatment should includestress reduction, education about the nature of anx-iety, improving coping mechanisms, and engage-ment of the family to help support changes. Parentsmay need to resolve their own problems related toseparation and anxiety to avoid exacerbating thechild’s symptoms.

Behavioural therapy andcognitive—behavioural therapyBehavioural therapy models derive from (classi-cal and operant) conditioning, social learning, andinformation processing theories. Behaviour ther-apy can target the child’s behaviour in the contextof home and school. Specific techniques include:

• systematic desensitization and exposure for spe-cific phobias, including school phobia;

• relaxation training;• modelling of appropriate behaviour;• role playing;• rewards for desirable behaviour.

Cognitive–behavioural therapy (CBT) com-bines a behavioural approach (e.g. exposure) withcognitive techniques (e.g. positive self-statements)aimed at altering cognitions and behaviour. Thechild is asked to reframe his or her thoughts in amore positive way, which in turn alters behaviour.Children aged 10 years and above can benefit fromcognitive techniques. Various books, such as theThink Good, Feel Good series, provide accessiblecognitive–behavioural material for the clinicianand patient alike [4]. A recent meta-analysisdemonstrated CBT’s efficacy in childhood anxietydisorders and found little difference in effect sizebetween short (<10 sessions) or long, group orindividual CBT; this might have implications forcost-effectiveness [5].

Other individual psychotherapiesPsychodynamic psychotherapy focuses on underly-ing fears and anxieties. Although a strong evidence

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base is lacking, a prospective outcome study anda retrospective case review documented good out-come in a number of children, especially those whounderwent more sessions, were younger, and hadphobic symptoms.

Family therapyIf the child’s symptoms are seen as a sign of familydysfunction, family therapy may work with thefamily to help change dysfunctional patterns ofinteraction and thus reduce the child’s anxietysymptoms.

PharmacotherapyMedication can be used, although rarely in iso-lation. It is more commonly an adjunct to acomprehensive package of care, including psycho-logical techniques for symptom management, asthis may help prevent relapse after medication hasbeen discontinued. Medication should be consid-ered in older children and adolescents with moresevere symptoms, bearing in mind side-effect pro-files and comorbidity.

Antidepressants: These are the most commonlyprescribed medication, although there is a smallerevidence base in children than in adults. Tricyclicantidepressants have previously been prescribed,but selective serotonin reuptake inhibitors (SSRIs)are now favoured due to better side-effect profilesand because they are relatively safe in overdose.Fluoxetine and fluvoxamine have been shown tobe effective in the treatment of children and ado-lescents with social phobia, generalized anxietydisorder and separation anxiety disorder [6].

Two studies showed that sertraline was effec-tive and generally well tolerated in patients withgeneralized anxiety disorder [7,8]. Walkup et al.also included patients with separation anxiety andsocial phobia and demonstrated the added effi-cacy of combining pharmacotherapy with CBT;however, the combined therapy group was notdouble-blinded [8].

In studies of depressed children and adolescents,SSRIs have been associated with suicidal ideationand non-fatal acts, and the Medicines and Health-care products Regulatory Agency (MHRA) (andNICE in the UK) have recommended that onlyfluoxetine has a favourable risk–benefit profilefor depression. The risk of such side effects in

non-depressed patients is uncertain, although it isimportant to be mindful of the frequent comor-bidity of anxiety with depression. In the UK, noantidepressants are licensed for the treatment ofchildren with anxiety disorders, but fluvoxamineand sertraline are licensed for use in children withobsessive-compulsive disorder. The evidence baseand guidelines on the use of antidepressants inchildren are ever-evolving, and the reader is urgedto consult the latest reports.

Other medication: Benzodiazepines are generallynot recommended in children: double-blind con-trolled trials have failed to demonstrate efficacy,and behavioural disinhibition is a risk. There arefew data on beta-blockers. Case reports and opentrials have shown a reduction in anxiety symptomsafter buspirone treatment, although it can be asso-ciated with disinhibitory reactions and aggression.

PREVENTION

Given the high prevalence rates and negative con-sequences of anxiety disorders, as well as theclinical and public concerns over the use of medica-tion, cost-effective prevention measures would bea welcome strategy. Prevention interventions arewell placed to target multiple risk factors simul-taneously; this is important given the complexinterplay between risk factors and the multiplepathways of development for psychological disor-ders. Farrell and Barrett have reviewed currentpractice in prevention research in anxiety anddepressive disorders, and described an evidence-based cognitive behavioural programme run inAustralian schools [9].

CONCLUSION

Anxiety disorders in children and adolescents arerelatively common, but can be disabling and per-sist into later life. They may first present to thepaediatrician or general practitioner. It is there-fore important for all professionals who deal withchildren and adolescents to be aware of possi-ble manifestations of anxiety in this age group.Early differentiation between anxiety symptomsand anxiety disorder facilitates appropriate mentalhealth referrals for further assessment and treat-ment, enabling the child or adolescent to return tonormal functioning.

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ACKNOWLEDGEMENT

The authors would like to thank Grace Fong forher help with this chapter.

REFERENCES

[1] Muris P, Steerneman P, Merckelbach H, HolorinetI, Meesters C. (1998) Comorbid anxiety symptomsin children with pervasive developmental disorders.Journal of Anxiety Disorders 12, 387–93.

[2] Pine D. (2007) Research review: a neuroscienceframework for pediatric anxiety disorders. Journalof Child Psychology and Psychiatry 48, 631–48.

[3] Bittner A, Egger HL, Erkanli A, Costello EJ, FoleyDL, Angold A. (2007) What do childhood anxietydisorders predict? Journal of Child Psychology andPsychiatry 48, 1174–83.

[4] Stallard P. (2002) Think Good, Feel Good: a Cogni-tive Behaviour Therapy Workbook for Children andYoung People. Chichester: John Wiley.

[5] Ishikawa S, Okajima I, Matsuoka H, Sakano Y.(2007) Cognitive behavioural therapy for anxiety dis-orders in children and adolescents: a metaanalysis.Child and Adolescent Mental Health 12, 164–72.

[6] Research Unit on Pediatric PsychopharmacologyAnxiety Study Group. (2001) Fluvoxamine for thetreatment of anxiety disorders in children and ado-lescents. New England Journal of Medicine 344,1279–85.

[7] Rynn MA, Siqueland L, Rickels K. (2001) Placebo-controlled trial of sertraline in the treatment ofchildren with generalized anxiety disorder. AmericanJournal of Psychiatry 158, 2008–14.

[8] Walkup JT, Albano AM, Piacentini J et al. (2008)Cognitive behavioral therapy, sertraline, or a combi-nation in childhood anxiety. New England Journal ofMedicine 359, 2753–66.

[9] Farrell LJ, Barrett PM. (2007) Prevention of child-hood emotional disorders: reducing the burden ofsuffering associated with anxiety and depression.Child and Adolescent Mental Health 12, 58–65.

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28Childhood Behavioural DisordersGraeme LambNewham Child and Family Consultation Service, East London NHS Foundation Trust, London, UK

INTRODUCTION

Childhood behavioural disorders, includingoppositional defiant disorder (ODD) and conductdisorder (CD), continue to represent the mostcommonly presenting disorders at communitychild and adolescent mental health services [1,2].Concern regarding childhood deviance is not arecent development. Since the time of Plato, soci-eties have struggled with how to understand andmanage the behaviour of out-of-control children,with ongoing debate as to the responsibility andculpability of children for their actions [3]. How-ever, there is evidence that such disorders havebecome significantly more common over the last25 years [4], and this is reflected in the increasingmedia and public concern around such behaviours.

DEFINITION

Oppositional defiant disorder refers to a patternof negative, hostile and defiant behaviour that isclearly outside the normal range of behaviour fora child of the same age and sociocultural context.These behaviours include a variety of featuressuch as often losing one’s temper, arguing withadults, refusing to comply with adults’ requests,often being angry and spiteful, and deliberatelyannoying others. Such children do not presentwith more severe dissocial or aggressive acts [5].

In contrast, CD involves a repetitive andpersistent pattern of behaviour in which the basicrights of others or major age-appropriate societalnorms are violated. Such behaviour includesaggression to people and animals, destruction


of property, deceitfulness or theft, and seriousviolations of rules such as often staying outovernight or running away from home [5].

SUBTYPING

Childhood behavioural disorders are categorizedin different ways in the two major diagnostic sys-tems. In the Diagnostic and Statistical Manual ofMental Disorders, Fourth Edition – Text Revision(DSM-IV), they are divided into childhood onset(before age 10 years), adolescent onset (after age10 years) and ODD [5]. In the ICD-10 InternationalClassification of Mental and Behavioural Disor-ders in Children and Adolescents (ICD-10), similarbehavioural disorders are classified as socialized,unsocialized, confined to the family context, andODD, reflecting the social context in which thesebehaviours occur [6].

There has been considerable debate regardingwhether or not ODD and CD are distinctdisorders or simply represent a continuum ofincreasingly challenging behaviours. AlthoughDSM-IV excludes a diagnosis of ODD in thepresence of CD, there is considerable symptomoverlap between the two groups. Most researchsupports the distinction of oppositional behaviourand covert delinquent behaviour, but it is not yetclear whether aggression should be grouped witheither or represents a separate category of its own[7]. Whilst some children will grow out of ODD, inothers it can be a precursor of CD, which in turncan lead to the later development of antisocialpersonality disorder [7].

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One of the reasons for subtyping conductdisorders is to try to separate those young peoplewho are likely to grow out of their behaviourproblems from those who persist with suchbehaviours into adulthood. DSM-IV refers tothe number and intensity of symptoms as clinicalindicators of severity. Other relevant factorsinclude the presence of overt (confrontational,such as fighting) versus covert (hidden, such astheft) symptoms, comorbid mental health disor-ders, particularly ADHD, and early symptoms ofantisocial personality disorder [7].

The presence of callous-unemotional traits,characterized by a lack of empathy for others,lack of guilt and inability to express emotions toothers, does appear to signify a distinct subgroupof young people with a more extreme pattern ofaggressive behavioural problems [8].

EPIDEMIOLOGY

As with many epidemiological studies of childmental health disorders, prevalence rates for child-hood behavioural disorders are difficult to quantifydue to changing diagnostic criteria and method-ological variations in study design. In 1975 Rutteret al. compared the rates of child mental health dis-orders in different settings within the UK, showinga prevalence rate for CD of 4% for rural popula-tions, increasing to 9% in urban centres [9]. Manystudies have shown CD to be more common in boysthan in girls. In more recent UK-based communitysurveys, conduct disorders occur in 6.9% of pri-mary school-aged boys and 2.8% of girls, whilst insecondary school-aged children these prevalencesrise to 8.1% and 5.1% respectively [10].

There is also evidence of a clear increase inthe prevalence of CD with age, with boys show-ing a linear rise from an early age throughoutchildhood, whilst girls show a different pattern,with rates increasing in adolescence [11]. How-ever, different subsets of behaviours appear tohave differing epidemiological trends. Whilst seri-ous physical aggression and rule violations rise inadolescence, lesser forms of aggression, such asfighting with peers, decline with age [11].

Childhood behavioural disorders often appearto show some longevity of symptoms, with 40% of7–8-year-olds with CD becoming young offendersin later life, whilst over 90% of such offenders havea history of CD as children [12]. Those children

who develop CD at an earlier age will often havea worse prognosis than those who develop suchproblems in adolescence [13].

Epidemiological studies also show the relation-ship between childhood behavioural disorders andother mental health disorders including ADHD,depression and anxiety [13]. More than one-thirdof girls and almost one-half of boys with ODD orCD present with a comorbid non-antisocial disor-der [11]. The presence of ADHD is particularlyfound to influence the development, course andseverity of CD. Young people with CD and comor-bid ADHD have a much earlier age of onset of dis-ruptive behaviour than those with CD alone [14].

AETIOLOGY

The development of childhood behavioural disor-ders incorporates a broad and complex range ofbiological and psychosocial risk factors.

Biological factors, including genetics, havelong been implicated in the development ofchildhood behavioural disorders, although muchof the research has focused upon aggressive ratherthan other antisocial behaviours. Studies in thepast decade show that the genetic effects appearto vary according to subtype. Children withcallous-unemotional traits show much strongerheritability for antisocial behaviour than childrenwithout such traits (0.81 vs 0.30 respectively) [15].In addition, more aggressive children who offendearly have an increased heritability to do so [15].

Other biological risk factors include prenatalor perinatal exposure to toxins and early physicaldamage to the frontal lobe and other regions ofthe brain [16]. Research indicates a possible linkbetween serotonin levels in the brain and aggres-sive behaviours, although the exact nature of thislink has not been demonstrated [16].

Young people with aggressive behaviours havebeen shown to experience general autonomicunderarousal, as demonstrated by lower heartrates and skin conductance, indicating an associ-ated lack of inhibitory anxiety, which may protectagainst antisocial behaviours [16].

Innate temperament, which may be apparentin very early childhood, has been shown to be pre-dictive of future behavioural disorders. Childrenwith vulnerable temperamental characteristics aremore likely to be subject to poor parenting styles.Moreover, adoption studies suggest that these

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children’s behaviour may exacerbate a negativeparenting response, leading to an additive effect[17]. Whilst attachment and conduct disordersdisplay similar behavioural manifestations, sup-porting evidence for an aetiological connectionbetween the two is weak [16].

Although cognitive and reading impairmentsare often thought to be related to behaviouraldisorders in children, research evidence is inconsis-tent due to confounding variables such as ADHD,poor school attainment and gender. Other fac-tors including impulsivity and social withdrawalhave been shown to be associated with antiso-cial behaviours, as have social skills deficits suchas failing to notice relevant social cues, whilstmisattributing hostile intent to others [16].

Children from socially disadvantaged areashave higher levels of conduct disorders [18]. How-ever, much of this effect is thought to be mediatedby intrafamilial social processes associated withpoor parenting and parental psychopathology[16], including mental illness, and alcohol andsubstance misuse.

Certain parenting styles have been consistentlyshown to link to behavioural disorders in children,including lack of parental involvement, harsh andinconsistent discipline, and poor monitoring andconflict management. Children who have beenexposed to sexual or physical abuse have a sig-nificantly increased risk of developing CD [16].Peer relationships and community factors such asdrug availability and crime rate may also influ-ence the development of behavioural problems inchildren [16].

PREVENTION AND TREATMENT

There are many good reasons for trying to alle-viate childhood behavioural disorders. As well ascausing distress and damage to individual chil-dren and families, conduct disorders are known tohave a considerable cost to the wider society. Scottet al. have shown that by the age of 28 years, costsfor people with CD were 10 times higher than forthose with no problems. These costs include crime,extra educational provision, foster and residentialcare, and state benefits as well as smaller costs tothe health service [19].

As parenting practices have been identifiedas relevant aetiological factors in the develop-ment and maintenance of childhood behavioural

disorders, there has been considerable interest inthe use of parenting programmes as a form ofprevention and treatment.

In 2006, the National Institute for Health andClinical Excellence (NICE) and Social Care Insti-tute for Excellence (SCIE) jointly commissioneda review of parenting programmes in the manage-ment of children aged 12 years or younger [1]. Theyconcluded that group-based parenting/educationprogrammes are to be recommended in the man-agement of children with conduct disorders. Forthose parents with whom it is difficult to engageor for whom problems are more complex, similarindividual-based programmes can be used instead.

Parenting programmes aim to improve thechild’s behaviour by helping parents to changethe ways in which they approach parentingand to improve their relationship with theirchildren. Whilst most group-based programmesfocus upon the actions of parents without thedirect involvement of the child, some individualprogrammes include observation of parent–childinteractions, allowing these to be modified asnecessary. Most parenting programmes comprisebehavioural management techniques based uponsocial learning theory. These teach parents howto increase desired behaviours through posi-tive reinforcement, whilst decreasing unwantedbehaviours by reducing social reinforcement, suchas by ignoring behaviours or using Time Outtechniques. Programmes will also usually includeelements to help parents to understand their chil-dren’s feelings and behaviours and subsequentlyimprove understanding and communicationbetween parent and child [1].

Analysis of relevant research studies indicatesthat such interventions are clinically effective atimproving children’s behaviour, may lead to animprovement in maternal mental health, and arecost-effective ways of treating children with con-duct disorders [20].

There is now a wide variety of group-based par-enting programmes devised to prevent the devel-opment of childhood behavioural disorders aswell as to help treat those children who havealready developed such problems. Examples ofeffective programmes include the Triple P, PositiveParenting Programme and the Webster–StrattonIncredible Years Programme, with evidence thatthese effects continue over several years [18].Several long-term follow-up studies in the USA

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and Canada have shown a reduction in latercriminal activity in those children exposed to avariety of early interventions, with huge cost ben-efits to society [21].

In some circumstances parent training pro-grammes may not be feasible or as effectiveas hoped. Some families may be unwilling totake part in such programmes or there maybe additional risk factors in the child, such ascallous and unemotional traits, which may reducethe potential effectiveness of this approach. Inthese cases, NICE recommends that alternativeapproaches such as individual cognitive problem-solving skills training should be considered [22].Other theoretical models such as attachmenttheory, systems theory or cognitive attributiontheory may also be helpful [23].

As children with conduct disorders often presentwith other comorbid child mental health disorders,these disorders may require treatment in their ownright, which may in turn lead to a reduction inthe behaviour problems. Studies have suggestedthat the treatment of ADHD with stimulantsor atomoxetine may lead to an improvement incomorbid oppositional behaviour, whilst atypicalantipsychotics have been shown to be effective forthe treatment of acute and chronic aggression inyoung people with learning disabilities or pervasivedevelopmental disorders [24].

It is generally agreed within the scientificcommunity that short-term interventions such asmilitary-style boot camps, whilst often promotedwithin certain sections of the British media, arenot effective in the long term [24]. Frighteningchildren with the aim of reducing aggressivebehaviour but without offering them any otherbehavioural alternatives, has the opposite effect ofthat intended, perhaps as a result of an increasedfear-aggression reaction or due to modelling ofdeviance [24].

CONCLUSION

Childhood behavioural disorders have always beenand still remain a common problem and, given cur-rent epidemiological trends, are likely to continueto do so for the foreseeable future. These disorderslead to considerable damage, both in terms ofthe quality of life for young people, their familiesand their victims, and the wider economic cost tosociety as a whole. Simple behavioural disorders

can progress to much more serious personalitydisorders in adulthood. We know that there areeffective treatments for conduct disorders andthese are increasingly being made available acrossthe country via community parenting programmes.Our challenge remains to identify which factorswithin such programmes may be effective upondifferent symptom subtypes, to help identifythose children who are not responsive to theseapproaches and consider which alternative meth-ods may be best employed in these cases, and tospread effective treatments to those hard-to-reachfamilies who perhaps need these most.

REFERENCES

[1] National Institute for Health and ClinicalExcellence. (2006) Parent-Training/Education Pro-grammes in the Management of Children withConduct Disorders. NICE Technology AppraisalGuidance 102. London: NICE.

[2] Audit Commission. (1999) Children in Mind. Lon-don: Audit Commission.

[3] Costello J and Angold A. (2001) Bad behaviour: anhistorical perspective on disorders of conduct. In:Hill J and Maughan B (eds), Conduct Disorders ofChildhood and Adolescence. Cambridge UniversityPress, pp. 1–31.

[4] Collishaw S, Maughan B, Goodman R, Pickles A.(2004) Time trends in adolescent mental health.Journal of Child Psychology and Psychiatry 45,1350–62.

[5] American Psychiatric Association. (2000) Diagnos-tic and Statistical Manual of Mental Disorders, 4thedition, text revision (DSM-IV-TR). Washington,DC: APA.

[6] World Health Organization. (1992) The ICD-10Classification of Mental & Behavioural Disorders.Geneva, WHO.

[7] Loeber R, Burke J, Lahey B, Winters A, Zera M.(2000) Oppositional defiant disorder and conductdisorder: a review of the past 10 years, part I. Journalof the American Academy of Child and AdolescentPsychiatry 41, 1468–84.

[8] Frick P and White S. (2008) Research Review:The importance of callous-unemotional traits fordevelopmental models of aggressive and antisocialbehaviour. Journal of Child Psychology and Psychi-atry 49, 359–75.

[9] Rutter M, Cox A, Tupling C, Berger M, Yule W.(1975) Attainment and adjustment in two geograph-ical areas. I The prevalence of psychiatric disorder.British Journal of Psychiatry 126, 493–509.

[10] Green H, McGinnity A, Meltzer H, Ford T, Good-man R. (2005) Mental Health of Children and Young

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People in Great Britain, 2004. Basingstoke, Hamp-shire: Palgrave Macmillan.

[11] Maughan B, Rowe R, Messer J, Goodman R,Meltzer H. (2004) Conduct Disorder and Oppo-sitional Defiant Disorder in a national sample:developmental epidemiology. Journal of Child Psy-chology and Psychiatry 45, 609–21.

[12] Farringdon D. (1995) The development of offend-ing and antisocial behaviour from childhood: keyfinding from the Cambridge study in delinquentdevelopment. Journal of Child Psychology and Psy-chiatry 36, 929–64.

[13] Angold A and Costello J. (2001) The epidemi-ology of disorders of conduct: nosological issuesand comorbidity. In: Hill P and Maughan B (eds),Conduct Disorders of Childhood and Adolescence.Cambridge University Press, pp. 126–68.

[14] Moffitt T. (1990) Juvenile delinquency and attentiondeficit disorder: boys’ developmental trajectoriesfrom age 13 to age 15. Child Development 61,893–910.

[15] Viding E, Larsson H, Jones AP. (2008) Review.Quantitative genetic studies of antisocial behaviour.Philosophical Transactions of the Royal Society ofLondon B: Biological Sciences 363, 2519–27.

[16] Burke J, Loeber R, Birmaher B. (2002) Oppo-sitional defiant disorder and conduct disorder: areview of the past 10 Years, part II. Journal ofthe American Academy of Child and AdolescentPsychiatry 41, 1275–93.

[17] Cadoret RJ, Yates WR, Troughton E et al. (1995)Genetic-environmental interaction in the genesis

of aggressivity and conduct disorders. Archives ofGeneral Psychiatry 52, 916–24.

[18] Bywater T, Hutchings J, Daley D et al. (2009) Long-term effectiveness of a parenting intervention forchildren at risk of developing conduct disorder.British Journal of Psychiatry 195, 318–24.

[19] Scott S, Knapp M, Henderson J, Maughan B. (2001)Financial cost of social exclusion: follow-up study ofantisocial children into adulthood. British MedicalJournal 323, 191–4.

[20] Scott S, Spender Q, Doolan M, Jacobs B, AsplandA. (2001) Multicentre controlled trial of parentinggroups for childhood antisocial behaviour in clinicalpractice. British Medical Journal 323, 194–7.

[21] Sainsbury Centre for Mental Health. (2009) TheChance of a Lifetime. Preventing Early ConductProblems and Reducing Crime. London: SainsburyCentre for Mental Health.

[22] National Institute for Health and Clinical Excel-lence. (2009) Antisocial Personality Disorder: Treat-ment, Management, Prevention. NICE ClinicalGuideline 77. London: NICE.

[23] Scott S and Dadds MR. (2009) Practitioner Review:When parent training doesn’t work: theory-drivenclinical strategies. Journal of Child Psychology andPsychiatry 50, 1441–50.

[24] American Academy of Child and Adolescent Psy-chiatry. (2007) Practice parameter for the assess-ment and treatment of children and adolescents withoppositional defiant disorder. Journal of the Amer-ican Academy of Child and Adolescent Psychiatry46, 126–41.

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Specific language impairment

29Specific Language ImpairmentGina Conti-Ramsden1 and Kevin Durkin2

1School of Psychological Sciences, The University of Manchester, Manchester, UK2School of Psychological Sciences and Health, University of Strathclyde, Glasgow, UK

WHAT’S NEW

• Children with specific language impairment (SLI) are late talkers. Language loss in earlyinfancy is not a feature of SLI. Language loss appears to be strongly and specificallyassociated with autism spectrum disorders (ASD).

• Difficulties with the comprehension of language appear to be prognostic. Lower abilities tounderstand language are associated with poorer outcomes. Poor language comprehension isa marker of SLI.

• SLI is a relatively stable condition in middle childhood. Group data suggest that, on average,children with SLI do not catch up with their peers nor do they fall further behind. Theydevelop language at a strikingly similar rate to their typically developing peers, maintainingthe degree of attainment/impairment they experienced at around 7 years of age.

• Oral language abilities matter throughout development. There is a need for the assessmentof oral language beyond childhood in children with SLI. Also, language assessment is crucialin children and adolescents who present with difficulties in learning (mild-moderate learningdisabilities), literacy (including dyslexia), behavioural (conduct), emotional and socialfunctioning (including broader phenotype ASD).

WHAT IS SPECIFIC LANGUAGEIMPAIRMENT?

Specific language impairment (SLI) is usuallydefined as language difficulties in the contextof adequate non-verbal skills, normal hearing,absence of frank neurological damage or autism.There is variation in precisely how SLI isdiagnosed (see Box 29.1). Nonetheless, there isconsensus that SLI represents impairments inlanguage that are disproportionate to difficultiesin other non-linguistic domains.


Typically, SLI comes to the attention of clini-cians as a result of concern from significant othersabout the child’s progress with language learning.In practice children with this condition rarely havedifficulties only with language. Furthermore, thereis considerable variation not only in the severitybut also in the nature of the language difficultiesevident in SLI. These considerations raise chal-lenges for the diagnosis, explanation and treatmentof the disorder in particular, as SLI presents sub-stantial issues calling for the investment of clinical,

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Box 29.1 Definitions of specific language impairment (SLI)

SLI is generally defined in terms of a discrepancy between non-verbal cognitive functioningand language skills, as measured on standardized tests. Debate centres on the required size ofthat disparity, the level of language impairment required, and the measurement of verbal andnon-verbal abilities. For example:

• The International Classification of Diseases, 10th revision (ICD-10) requires languagedifficulties greater than 2 standard deviations (SD) below the mean, with verbal skills atleast 1 SD below measures of non-verbal cognitive functioning.

• The Diagnostic and Statistical Manual of Mental Disorders-IV-Text Revision (DSM-IV-TR),requires substantially worse performance on measures of verbal abilities compared tonon-verbal cognitive functioning. What constitutes ‘substantial’ is not defined operationally,though functional impairment is required — i.e. SLI interferes with academic oroccupational achievement, or with social interaction.

• The clinical research definition of SLI [19] works with threshold and discrepancy measuresthat enable consistent identification of SLI by speech and language therapists. It requires acombination of language difficulties, assessed on a composite standardized languagemeasure, that fall 1.25 SD below the mean (approximately, the 10th centile). Plus,adequate non-verbal cognitive functioning (i.e. a Performance IQ greater than 1 SD belowthe mean, equating to a standard score of 85 or higher).

educational and public health resources. SLI isa common disorder, estimated to affect approxi-mately 6% of the population, with boys being moreaffected than girls at a ratio of 2:1. Although SLIis the term most commonly used in research, it isworth noting that it is rarely used in clinical set-tings, where the condition is more likely to presentunder a variety of other names. These can include:‘language disorders’ subdivided into ‘expressive’and ‘mixed expressive-receptive’ types [Diagnosticand Statistical Manual of Mental Disorders, FourthEdition – Text Revision (DSM-IV-TR) and pro-posed DSM-5]; ‘speech, language and commu-nication needs’ (Royal College of Speech andLanguage Therapists); ‘developmental languagedelay’, ‘language impairment’, ‘primary languagedifficulties’ and other similar names (educationalpractice settings).

WHAT CAUSES SPECIFICLANGUAGE IMPAIRMENT?

It has become clear that SLI is not a single-causedisorder. A number of theories have been put for-ward, all of which have received some empiricalsupport. It seems likely that multiple risk factors

are implicated. These include genetic, neurobio-logical, cognitive and environmental influences.

Biological bases of SLI: geneticand neurobiological factorsThere is strong evidence that SLI runs in families.The majority of children with SLI have a posi-tive family history of language difficulties, with afirst-degree relative usually affected. The contribu-tion of genetic factors is most clearly indicated intwin studies, where identical twins have a muchhigher concordance for SLI than non-identicaltwins [1]. Patterns of inheritance appear to becomplex, involving interactions among multiplegenes [2]. Technological advances have made itpossible to examine brain development in chil-dren with SLI. However, few atypicalities havebeen identified. The most consistent neuroimag-ing findings suggest leftward asymmetry and areduction in cerebral volume. Electrophysiologicalevidence suggests abnormal auditory processing[3]. However, these abnormalities have also beenobserved in other developmental disorders. Thus,further research is needed to identify distinc-tive features of brain development in individualswith SLI.

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Cognitive bases of SLI: non-linguisticand linguistic factorsDifferent approaches emphasize different systemsas influential in the aetiology of SLI. One promi-nent approach highlights memory impairments inSLI.

• Phonological short-term memory deficits havebeen extensively documented, and there is evi-dence of heritability of this type of difficulty [4].Such an impairment has a key impact on thechild’s ability to retain verbal information longenough to develop accurate speech and languagerepresentations.

• More general impairments in working memoryhave been identified in SLI, and more recentlydifficulties with implicit, procedural memory [5].Such deficits affect children’s ability to extractthe regularities of the language they are learning,such as suffixation, as in the use of regular pasttense ‘ed’ in English.

Other views focus on limitations in other areas ofcognitive functioning such as perceptual and infor-mation processing capabilities, temporal auditoryprocessing capacity and executive functions. Fur-thermore, some accounts assume that languagestructures are autonomous of other cognitive sys-tems. These theories emphasize linguistic factorsand suggest SLI involves deficits or immaturityin systems responsible for the representation ofgrammar, of linguistic features, or of structuralrelationships.

Environmental influencesIn general, samples of children with SLI containdisproportionately high numbers of individualsfrom socioeconomically disadvantaged back-grounds. This could be interpreted as an outcomeof disadvantage or as a consequence of intrafamil-ial transmission, or as due to some more complexinteraction. Overall, present evidence supportsthe assumption of multicausality.

WHAT TYPES OF LANGUAGE DIFFICULTIESDO CHILDREN WITH SLI HAVE?

The heterogeneity of SLI is widely recognized.A number of different classification systems havebeen devised. The more enduring clinical types dif-ferentiate children with only ‘expressive’ language

problems versus children with both ‘expressive andreceptive’ difficulties.

• Expressive SLI (E-SLI): Children exhibit mainlylanguage production difficulties in the context ofadequate comprehension abilities. Subtle com-prehension deficits, however, can be detectedwhen using sufficiently sensitive instruments.

• Mixed expressive-receptive SLI (ER-SLI): Chil-dren have difficulties with both language com-prehension and language production. Difficultiesare usually evident at the word (vocabulary) andsentential levels, especially complex sentences.

These two types of SLI are recognized byDSM-IV-TR [6], ICD-10 (ICD-10 InternationalClassification of Mental and Behavioural Disor-ders in Children and Adolescents) [7], and theclinical research definition of SLI. However, it isnot clear if these profiles of impairment are quali-tatively different or represent different points on acontinuum of severity, with ER-SLI representingthe more severe cases. More recently, a third clin-ical type has received attention. This is childrenin whom the social use of language, that is, prag-matic abilities, is the most prominent difficulty.Vocabulary and grammar can be relatively strong,that is, sentences may appear well formed, butcomprehension of extended discourse is usuallypoor and social interactions can be odd (verboseor overformal with poor turntaking skills). Thesechildren are currently referred to as having prag-matic language impairment (PLI). There is debateregarding the overlap between PLI and autismspectrum disorders (ASD).

Major types of SLI in middle childhoodExpressive SLI is thought to be more commonin the preschool and early school-age years. Bymiddle childhood, the most common profile ofSLI is mixed expressive-receptive SLI. A smallproportion of children have PLI (see Figure 29.1for major types of SLI in middle childhood).

DISTINCTIVE FEATURESOF LANGUAGE IN SLI

The language difficulties of children with SLI canbe manifested in various areas of language func-tioning at varying levels. However, there are somenoteworthy areas of difficulty.

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ExpressiveSLI (aroundone-third)

PLI (around 20%)

Expressive-Receptive SLI(around half)

Figure 29.1 Distribution of major types of spe-cific language impairment (SLI) in middle child-hood. PLI, pragmatic language impairment.

The majority of children with SLI learningEnglish have difficulties with grammar, in par-ticular verb morphology. For example, they fail tomark tense accurately (they say ‘play’ for ‘played’,omitting ‘ed’) and do not always use auxiliaries (‘Istaying there’ for ‘I am staying there’). These dif-ficulties are evident even when children with SLIare compared to younger typical children learn-ing language. Grammar can be disproportionatelyaffected in SLI and has been suggested as a hall-mark of the disorder [8].

DEVELOPMENTAL PROGRESSIONOF LANGUAGE SKILLS IN SLI

Specific language impairment is characterizedby language difficulties from the outset of thelanguage-learning process. Instead of reachingdevelopmental language milestones on schedule(first words between 12 and 24 months, wordcombinations between 24 and 30 months of age),children with SLI are slow from the beginning.It is a hallmark of SLI that these children arelate talkers: they are late in acquiring their firstwords and in putting together their first wordcombinations. It is not the case that children withSLI start developing language normally and thenstop and become delayed or lose what they havelearned. Occurrence of ‘language loss’ in infancyis reported in some children with autism spectrum

disorders (ASD) but not in children with SLI. Thisfeature appears to distinguish between the twodisorders [9], and can be particularly useful forthe differential diagnosis between SLI and ASDin the preschool period. In childhood, difficultieswith the sound system of the language, that is,phonology, can co-occur with SLI. However, bymiddle childhood problems with sound productionare usually resolved or less evident (unless thereare oral-facial motor difficulties/apraxia), andmost children with SLI are intelligible.

It used to be thought that SLI was a short-term difficulty in language learning that, withsupport, could be resolved by the early schoolyears. Although this is true for a proportion ofchildren experiencing transient language delay(approximately 40%), developmental follow-upstudies have shown that children with SLI have per-sisting language difficulties well into adolescenceand even adulthood [10]. Research on the growthtrajectories of language-impaired individuals fromchildhood to adolescence is only just emerging. Theevidence suggests that children with SLI show simi-lar, parallel patterns of language growth in compar-ison with their typically developing peers. The levelof language that children with SLI reach at 7 yearsin relation to their peers is predictive of their levelof language attainment in middle childhood andadolescence. As a group, individuals with SLI donot ‘catch up’ with their peers nor do they fall fur-ther behind. Children with SLI develop languageat a strikingly similar rate to their typically devel-oping peers, maintaining the degree of attainment/impairment they experienced in childhood (Conti-Ramsden et al., unpublished).

ASSOCIATED DEVELOPMENTALPROBLEMS AND OUTCOMES

Language is fundamental to human behaviour.Hence, it is not surprising to find that individualswith language impairments tend to have associateddifficulties in other aspects of their lives. Forexample, recent research indicates developmen-tal interactions between oral language skills andareas of functioning such as literacy, memory skillsand more general non-verbal abilities through-out middle childhood, adolescence and beyond[11,12].

Still more broadly, there is evidence that youngpeople growing up with SLI experience greater

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difficulties in social interaction than do typicalchildren and adolescents [13]. These children aremore vulnerable to social exclusion, behaviouraland emotional difficulties, and to being bullied[14]. Their linguistic and literacy problems impacton their educational progress and attainment andon their uses of new technologies [15]. As ado-lescents, they have greater difficulties in dealingwith the myriad tasks of autonomous daily life[16,17]. A proportion of children with SLI developbroader phenotype autistic symptomatology inadolescence [18].

There is much debate with regard to the pro-cesses underpinning the above-mentioned devel-opmental observations: Do they reflect the impacton language development of still more funda-mental cognitive and perceptual capacities? Arethey manifestations of comorbid conditions thatemerge during the developmental process? Arethey developmental manifestations of bidirectionalinteractions between language impairment andother areas of functioning? The answers to thesequestions require further empirical research andclinical data. However, what is clear is: (i) thatoral language abilities matter throughout devel-opment; (ii) that children with SLI are likelyto demonstrate a range of associated difficul-ties; and (iii) that these children are at risk ofless successful developmental and educational out-comes.

IMPLICATIONS

There is a need for the assessment of orallanguage abilities in children with SLI in middlechildhood and beyond. Furthermore, becauseof the observed changing profiles of these indi-viduals, when children and adolescents presentwith difficulties in learning (mild-moderatelearning disabilities), literacy (including dyslexia),behaviour, or emotional and social functioning(including broader phenotype ASD) they shouldbe assessed for their oral language skills. This isimportant not only because they may be in needof support for their development but becausemany of the foundations of intervention in clinical,educational and mental health practice involvethe oral verbal medium. For example, languageis the mode of educational instruction and a keyelement in interactions between clinician andclient in cognitive–behaviour therapy.

All practitioners who work with young peoplewith developmental difficulties need to be sensi-tive to the possibility that these children may have,among other problems, language impairments.When we have a young person walking through ourdoor, we need to be more aware of the potentialneed to evaluate and, if required, obtain supportfor his or her oral language skills. Only in this waywill we be able to make it possible for individualswith SLI to have a good quality of life, find employ-ment, and establish long-term relationships.

ACKNOWLEDGEMENT

The first author (G.C-R.) gratefully acknowledgesthe support of a fellowship from the Economic andSocial Research Council (RES-063-27-0066).

REFERENCES

[1] Bishop DVM. (2002) The role of genes in the eti-ology of specific language impairment. Journal ofCommunication Disorders 35, 311–28.

[2] Bishop DVM. (2006) Developmental cognitivegenetics: how psychology can inform genetics andvice versa. Quarterly Journal of Experimental Psy-chology 59, 1153–68.

[3] Webster RI and Shevell MI. (2004) Neurobiologyof specific language impairment. Journal of ChildNeurology 19, 471–81.

[4] Falcaro M, Pickles A, Newbury DF et al. (2008)Genetic and phenotypic effects of phonologicalshort-term memory and grammatical morphologyin specific language impairment. Genes, Brain andBehavior 7, 393–402.

[5] Lum JAG, Gelgic C, Conti-Ramsden G. (2010) Pro-cedural and declarative memory in children with andwithout specific language impairment. InternationalJournal of Language and Communication Disorders45, 96–107.

[6] American Psychiatric Association. (2000) Diagnos-tic and Statistical Manual of Mental Disorders, 4thedn, Text Revision (DSM-IV-TR). Washington,DC: American Psychiatric Association.

[7] World Health Organization. (1992) The ICD-10Classification for Mental and Behavioural Disorders:Diagnostic Criteria for Research. Geneva: WorldHealth Organization.

[8] Rice ML. (2000) Grammatical symptoms of spe-cific language impairment. In: Bishop DVM andLeonard LB (eds), Speech and Language Impair-ments in Children: Causes, Characteristics, Interven-tion and Outcomes. Hove, UK: Psychology Press,pp. 17–34.

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[9] Pickles A, Simonoff E, Conti-Ramsden G et al.(2009) Loss of language in early development ofautism and specific language impairment. Journalof Child Psychology and Psychiatry 50, 843–52.

[10] Nippold MA, Mansfield TC, Billow JL et al. (2009)Syntactic development in adolescents with a historyof language impairments: A follow-up investigation.American Journal of Speech-Language Pathology18, 241–51.

[11] Conti-Ramsden G and Durkin K. (2007) Phono-logical short-term memory, language and literacy:developmental relationships in early adolescence inyoung people with SLI. Journal of Child Psychologyand Psychiatry 48, 147–56.

[12] St Clair MC, Durkin K, Conti-Ramsden G et al.(2010) Growth of reading skills in children with ahistory of specific language impairment: The role ofautistic symptomatology and language-related abil-ities. British Journal of Developmental Psychology28, 109–32.

[13] Durkin K and Conti-Ramsden G. (2007) Language,social behavior, and the quality of friendships inadolescents with and without a history of spe-cific language impairment. Child Development 78,1441–57.

[14] St Clair MC, Pickles A, Durkin K et al. (2011) A lon-gitudinal study of behavioral, emotional and social

difficulties in individuals with a history of specificlanguage impairment (SLI). Journal of Communi-cation Disorders 44, 186–199

[15] Durkin K, Conti-Ramsden G, Walker A, SimkinZ. (2009) Educational and interpersonal usesof home computers by adolescents with andwithout Specific Language Impairment (SLI).British Journal of Developmental Psychology 27,197–217.

[16] Conti-Ramsden G and Durkin K. (2008) Languageand independence in adolescents with and withouta history of specific language impairment (SLI).Journal of Speech, Language and Hearing Research51, 70–83.

[17] Durkin K and Conti-Ramsden G. (2010) Youngpeople with specific language impairment: A reviewof social and emotional functioning in adolescence.Child Language Teaching and Therapy 26, 105–21.

[18] Conti-Ramsden G, Simkin Z, Botting N. (2006) Theprevalence of autistic spectrum disorders in adoles-cents with a history of specific language impairment(SLI). Journal of Child Psychology and Psychiatry47, 621–8.

[19] Tomblin JB, Records NL, Zhang X. (1996) A systemfor the diagnosis of specific language impairment inkindergarten children. Journal of Speech, Languageand Hearing Research 39, 1284–94.

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Section 5c

Adolescence

Adolescence

30Depression and Suicidal Behaviour inChildren and AdolescentsJulia Gledhill and Matthew HodesAcademic Unit of Child and Adolescent Psychiatry, Imperial College London, London, UK

This chapter focuses on depressive disorder – asdefined by ICD-10 (ICD-10 International Clas-sification of Mental and Behavioural Disordersin Children and Adolescents) and DSM-IV-TR(Diagnostic and Statistical Manual of MentalDisorders, Fourth Edition – Text Revision) – andsuicidal behaviour. Whilst suicidal behaviour maybe indicative of a range of difficulties, it mayalso be a symptom of depressive disorder. Theepidemiology, aetiological factors, course, diag-nostic assessment and management for depressivedisorder and suicidal behaviour will be described.

DEPRESSIVE DISORDER

Whilst there was little recognition of depressivedisorders in children and adolescents before the1970s, the use of symptom-oriented psychiatricinterviews with children and adolescents led toan acknowledgement that depressive disordersresembling those seen in adults do occur in thisage group; the current diagnostic criteria are thesame as those used in adults – mood change (lowmood/irritability) or loss of enjoyment lastingat least 2 weeks, associated cognitive (e.g. guilt,pessimism about the future, suicidal ideation)and biological (e.g. change in appetite, sleepdisturbance, fatigue) symptoms, together withfunctional impairment (at home, school or withregard to peer relationships).


EpidemiologyThe prevalence of depressive disorder increasesfrom childhood to adolescence, with a reportedprevalence in community samples of adolescentsranging from 1% to 8% [1–3]. It is equallycommon in girls and boys during childhood,but during adolescence the female:male ratioincreases to about 2:1 [4]. It has been suggestedthat pubertal status rather than age is associatedwith the increase in depressive disorders amongadolescent girls [5]. Whilst the prevalence ofdepressive disorders in this age group has notchanged greatly over the last 30 years, recognitionand treatment have increased [6]. Psychiatriccomorbidity, especially with anxiety disorders,conduct disorder and substance misuse, arecommon [7].

Aetiological factorsThe aetiology of depressive disorder is multifacto-rial [8]; risk factors may be divided into those thatpredispose to (increase vulnerability to) and pre-cipitate (lead to its development at a specific pointin time) a depressive episode. These influencesact through biochemical and psychological pro-cesses. Once established, depressive episodes maybe prolonged by maintaining factors that treat-ment approaches aim to alleviate. These risks aredescribed more fully in Table 30.1.

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Table 30.1 Aetiological factors for depressive disorders.

Risk factor Evidence

Predisposing factors

Genetic factors Greater genetic influence for adolescent than for childhooddepression

Children of depressed parents at greater risk

Twin studies — heritability 15—80% for depressive symptoms

Indirect genetic influences, e.g. increased risk of experiencing morenegative life events

Family environment Low levels of parental warmth, high levels of hostility and conflictare associated with increased depressive symptoms

Parental mental health problems impact on parenting, making itmore difficult to meet the child’s emotional needs and provide aconfiding relationship

Temperament/personality Children who are slow to adapt to new experiences, sociallyreticent, easily upset

Elevated levels of anxiety, high self-criticism and negativeattributional style — tendency to blame self rather than others

Early/chronic adversity Poverty/social disadvantage

Physical,sexual or emotional abuse

Neurobiological factors Underactivity of cerebral amine systems

Abnormalities in cortisol secretion

Functional and anatomical brain differences in depressed andnon-depressed young people

Precipitating factors

Stressful life events Examples include losses (e.g. parental separation or bereavement),disappointments and failures (e.g. peer problems, bullying,academic difficulties, failing exams)

Maintaining factors

Persistent depressivesymptoms

Recognized as a risk factor for further depressive episodes

Psychosocial scars Individuals may experience residual effects from a depressiveepisode — ‘psychosocial scarring’, which increases the likelihood offurther episodes

Persistentbiological/cognitivevulnerabilities

As above

Persistent adversity Examples include family dysfunction, lack of a confidingrelationship with mother, poor peer relationships

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Diagnostic assessmentThis is facilitated by a mental state examination ofthe young person via an interview with him/heralone; adolescents themselves are the most accu-rate informants about internalizing symptoms,which parents may not be aware of. Depressivedisorder is often associated with psychiatriccomorbidity (40–70%) [4], particularly dysthymicdisorder, anxiety disorders, eating psychopathol-ogy, conduct disorders and substance abuse. It isimportant to recognize comorbidity as this hasimplications for management and outcome.

OutcomeThe outcome of depressive disorder (assessed byepisode duration or risk of recurrence) differsaccording to the population studied (mental healthservice referred or community); it is influencedby factors including age, symptom severity,past history of depressive episodes, comorbidpsychopathology and family factors, for example,conflict and parental psychopathology. Recoveryis the norm, with 88% recovering within 1 year incommunity samples [9], and 80–90% by 12–18months in clinic samples [10,11]. The medianduration of depressive episodes is 9 months inclinic-referred samples [12] and 8–12 weeks incommunity samples [13] – the former generallyhaving more severe episodes. Recurrence isfrequent: 12% relapse within 1 year in communitysamples [13], and 27% within 9 months forclinic samples [14]. Continuity into adulthoodis high, with an increased risk of self-harm,completed suicide and impaired psychosocialfunctioning [15].

ManagementThe aims of management are:1. to make an adequate assessment;2. to treat the depressive disorder, and reduce

associated psychosocial impairment;3. to manage associated comorbidity and risk

factors;4. to prevent relapse.

Initial assessment: This largely depends on thecontext in which the young person is seen and theexpected level of severity of the problems. Thus,in primary care settings where youngsters withmilder depression are seen, the brief assessment

will focus on mood, including self-harm risk,and current difficulties including social function.Those seen in specialist child and adolescentmental health services are likely to have moresevere depression with more comorbidity andcomplex family situations. In this context a moredetailed assessment will cover developmentalhistory and functioning at school, as well as familyrelationships and other problems.

Treatment: Treatment of brief or minor depres-sion will include exploration of difficulties, activityscheduling, and follow-up. Mild to moderatedepression, where social function might beimpaired, should be managed initially with psy-chological treatment [16]. Most frequently usedis cognitive–behavioural therapy (CBT), whichstarts with psycho-education and includes self-monitoring, for example, diary keeping, increasingcompetence in emotion recognition, challengingcognitive distortions, and activity scheduling. Analternative appropriate psychological therapyis interpersonal psychotherapy for adolescents(IPT-A), which addresses problem relationshipareas such as role conflict, transitions or losses.While both CBT and IPT-A have evidence foreffectiveness [16] there are currently few childmental health professionals in the UK trained inIPT-A, but CBT is becoming widely available.

More persistent moderate or severe depressionwill require antidepressant medication. Recentstudies, predominantly with adolescents, sug-gest that selective serotonin reuptake inhibitors(SSRIs), particularly fluoxetine, are helpful [17]. Inrecent years there has been a high level of concernregarding the possible increase of suicidal eventswith the use of SSRIs. Although the increasedrisk is slight, close monitoring is appropriate.Failure to respond to fluoxetine can be managedwith a change to another SSRI, or another classof antidepressant such as venlafaxine, with theaddition of CBT [18]. Poor progress or high riskof self-harm may require psychiatric admission.

Managing associated comorbidity and risk factors:The presence of comorbidities and associated riskfactors means that additional interventions may berequired. The associated anxiety or conduct prob-lems might require specific interventions. For someyoungsters if the associated disorders are effec-tively treated the depression might lift. Addressing

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problems in family relationships, in school or withpeers will require specific interventions.

Preventing relapse: If medication achieves remis-sion it should be continued for 6–9 months. Psy-chological treatment sessions may also be requiredafter the depression has improved. While thereis little evidence about the best way to preventrelapse it is likely that recognition of stressors,early identification of symptoms and early referralto specialist services is appropriate. Options willbe booster sessions of CBT or a short course ofantidepressants.

SUICIDAL BEHAVIOUR

EpidemiologySuicide is very uncommon in childhood and earlyadolescence but the rate increases markedly inmid-adolescence. World Health Organization(WHO) data from 2004 indicate that the UKsuicide rate for males aged 15–24 was 8 per100,000 as compared with 2.3 per 100,000 forfemales. Males tend to use more violent methods,and rates vary by country and ethnicity.

Deliberate self-harm (DSH) is common in ado-lescents; studies report a 12-month prevalence rateof 7–9% [19,20], and it is approximately threetimes more common in females. However, only aminority (12.6%) of DSH episodes lead to hospitalpresentation [20,21]. The most common methodsare self-poisoning and cutting. The term DSH isfrequently used as it does not imply a specific levelof suicidal intent.

Thoughts of suicide (in the absence of deliberateself-harm) are not uncommon (approximately 15%in the previous year), and are more frequent infemales [20].

Aetiological factorsThese may be divided into predisposing factors(e.g. within the young person, their family and thewider environment) and precipitating factors.

Predisposing factors:

• Individual: Psychiatric disorder, especiallymajor depressive disorder, but also anxiety,substance misuse and conduct disorder, are keyrisk factors for DSH [20]. In the context ofdepression, feelings of hopelessness, despair,

low self-esteem and a tendency to self-blame areparticularly relevant. Psychological factors suchas impulsivity and poor problem-solving skillsreduce the ability to discuss and contemplatedifficulties [22], and in this context DSH mayrepresent an impulsive response to problemsin an attempt to find an immediate relief fordistress or an escape from a troubling situation,rather than using problem-solving strategies oraccessing social support to work out a solution.Young people who are socially or emotionallyisolated, and particularly those who lack afamily confidant(e) with whom they can shareproblems, are at increased risk of self-harm [23].Young people who have experienced abuse,particularly physical and sexual abuse, are atgreater risk of DSH [20,21,24]. A history ofDSH is predictive of future episodes; up to 30%report a previous episode (which may not havecome to medical attention) [25].

• Family: Communication difficulties within thefamilies of young people who self-harm are typ-ical; adolescents who self-harm (compared tothose who do not) are less likely to feel able totalk to their parents. This is also a risk factorfor repeated compared to a single episode ofself-harm [26]. A family history of mental healthproblems, particularly parental DSH, is an addi-tional vulnerability factor. Parental divorce isalso more common in families of young peoplewho self-harm [20].

• Wider environment: School problems may bevery relevant in this age group and include aca-demic difficulties leading to underachievementand pressure to achieve, as well as bullying.Difficulties with regard to relationships withpeers, boy/girlfriends and teachers are alsoaetiologically important. Exposure to suicideor suicide attempts in family or friends alsoincreases risk [25].

Precipitating factors: Deliberate self-harm is fre-quently precipitated by stressful life problems;often these are interpersonal conflicts or difficul-ties with parents or siblings, such as arguments, orrejection by boy/girlfriends or peers, and schoolproblems such as academic difficulty and bullying.It is frequently an impulsive act, with many individ-uals thinking about it for just minutes before acting.Over 50% consult their GP in the month before

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deliberate self-harm but presentation is generallynot with psychological symptoms [27].

Risk associated with self-harmThe factors associated with high risk from self-harm are given in Box 30.1. The physical severityof the self-harm is not a good indicator of intent asyoung people are often unaware of the objectivedegree of lethality of specific substances and quan-tities; it is their belief about potential lethality thatis important.

Box 30.1 Factors associated withhigh suicidal intent

• Carried out in isolation

• Timed so that intervention is unlikely,e.g. after parents are at work

• Precautions taken to avoid discovery

• Preparations made in anticipation ofdeath, e.g. leaving directions as to howpossessions should be distributed

• Other people informed of individual’sintention beforehand

• Advance planning of attempt

• Suicide note

• Failure to alert others following theattempt

CourseAt least 10% of adolescents who self-harm doso again in the following year; this is especiallylikely in the first two or three months. Factors thatincrease the likelihood of repetition include previ-ous self-harm, personality disturbance, depression,substance misuse, extensive family psychopathol-ogy, poor social adjustment, social isolation anda poor school record [25]. Approximately 0.5%eventually kill themselves; risk factors include malegender, older age, high suicidal intent, mood disor-der, substance abuse, violent method of self-harmand previous psychiatric admission.

ManagementThe aims of management are:1. to make an adequate assessment;

2. to treat the depressive disorder, and reduceassociated psychosocial impairment;

3. to manage associated psychiatric disorder andrisk factors;

4. to prevent further episodes of DSH.

Type of assessment: This will depend on the con-text in which the young person is seen [28]. Thus, inprimary care settings the main goal is to ascertainrisk and consider whether self-harm has actuallytaken place, as this will often require referral tothe appropriate local hospital accident and emer-gency service. In the hospital setting paediatricmanagement is required for physical effects of self-harm, coordinated with child and adolescent men-tal health assessment, and social work input. Whenthe young person is referred to the out-of-hourshospital accident and emergency service, existingguidance is that admission is required overnightwith the assessment taking place the followingday [28]. The mental health assessment requiresthe identification of a psychiatric disorder andthe range of risk factors. The assessment shouldinclude interviewing the young person alone aswell as with his or her parent(s). The purpose ofthis assessment is: (i) to assess the current riskwith regard to suicidality and further deliberateself-harm; (ii) to understand the young person’sand the family’s difficulties and how these haveled to self-harm; (iii) to determine whether theyoung person is suffering with a psychiatric dis-order, for example depression (and the level ofhopelessness), or drug or alcohol misuse; and (iv)to assess the resources of the young person andthe family. It is important to establish whether theindex episode of deliberate self-harm was asso-ciated with a high degree of suicidal intent (seeBox 30.1); whilst a minority of patients may tryto conceal their true intent, assessment of intentis best facilitated by obtaining a detailed under-standing of the circumstances of the attempt andcomparing this information with factors known tobe associated with high intent. The outcome ofthis assessment will inform discharge and furthermanagement planning.

Treatment: This requires that the young personshould be kept safe, which means restricting accessto potentially harmful substances, such as drugs,used for self-harm, as well as alcohol. Appropri-ate care and emotional support are needed [29].

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This often requires family intervention, and twomain approaches have been described. Family-based problem-solving therapy aims to improvecommunication and reduce conflict in the fam-ily. This may be effective for adolescents whoare not depressed [30]. Family systems-orientedtherapy will address problems in family organiza-tion, communication and affect. A newer interven-tion is dialectical behaviour therapy, which aimsto improve self-acceptance, increase assertivenessand reduce interpersonal conflicts, and avoid situ-ations that trigger distress. Cognitive–behaviouraltherapy for DSH has also been described and hasa clear rationale [31]. Drug treatments have notbeen shown to be effective, although may have arole in the treatment of underlying psychiatric dis-order. Overall, the evidence base for treatmentsfollowing DSH is weak. Unfortunately less thanone-half of adolescents who self-harm, and theirparents, will remain in therapy after the initialassessment. However, the assessment will revealspecific psychiatric disorders, such as depression,in a significant proportion of cases and treatmentshould then be targeted at the underlying disorder.

Prevention: The main elements are identificationof those at highest risk by the prompt recognitionof depression or other problems associated withsuicidal behaviour; establishing crisis intervention;and reducing access to methods of self-harm, suchas decreasing the availability of poisonous domes-tic gas, and restricting the pack size of analgesicsin the UK [29].

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[8] Brent D and Weersing VR. (2008) Depressive dis-orders in childhood and adolescence. In: RutterM, Bishop D, Pine DS et al. (eds), Rutter’s Childand Adolescent Psychiatry, 5th edn. Oxford: Wiley-Blackwell, pp. 587–612.

[9] Dunn V and Goodyer IM. (2006) Longitudinalinvestigation into childhood and adolescence-onsetdepression: Psychiatric outcome in early adulthood.British Journal of Psychiatry 188, 216–22.

[10] Kovacs M, Feinberg TL, Crouse-Novak MA,Paulauskas SL, Finklestein R. (1984) Depressivedisorders in childhhod I. A longitudinal prospectivestudy of characteristics and recovery. Archives ofGeneral Psychiatry 41, 229–37.

[11] McCauley E, Myers K, Mitchell J, Calderon R,Schloredt K, Treder R. (1993) Depression in youngpeople: initial presentation and clinical course.Journal of the American Academy of Child andAdolescent Psychiatry 32, 714–22.

[12] Kovacs M, Obrosky S, Gatsonis C, Richards C.(1997) First-episode major depressive and dys-thymic disorder in childhood: Clinical and sociode-mographic factors in recovery. Journal of the Amer-ican Academy of Child and Adolescent Psychiatry36, 777–84.

[13] Lewinsohn PM, Clarke GN, Seeley J, Rhode P.(1994) Major depression in community adolescents:age at onset, episode duration and time to recur-rence. Journal of the American Academy of Childand Adolescent Psychiatry 33, 809–18.

[14] Goodyer IM, Herbert J, Secher SM, Pearson J.(1997) Short-term outcome of major depression: IComorbidity and severity at presentation as predic-tors of persistent disorder. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 36,179–87.

[15] Weissman MM, Wolk S, Goldstein RB et al. (1999)Depressed adolescents grown up. Journal of theAmerican Medical Association 281, 1707–13.

[16] Schloredt K, Gershenson R, Varley CK, WilkinsonP, Goodyer IM. (2007) Treatment of depressive dis-orders in children and adolescents. In: Tyrer P andSilk KR (eds), Handbook of Effective Treatments

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in Psychiatry. Cambridge: Cambridge UniversityPress, pp. 808–18.

[17] Bridge JA, Iyengar S, Salary CB et al. (2007) Clinicalresponse and risk for reported suicidal ideation andsuicide attempts in pediatric antidepressant treat-ment: A meta-analysis of randomized controlledtrials. Journal of the American Medical Association297, 1683–96.

[18] Brent DA, Emslie G, Clarke GN et al. (2008)Switching to another SSRI or to venlafaxine with orwithout cognitive behavioural therapy for adoles-cents with SSR-resistant depression. Journal of theAmerican Medical Association 299, 901–13.

[19] Grunbaum JA, Kann L, Kinchen SA et al. (2002)Youth risk behaviour surveillance – United States2001. Journal of School Health 72, 313–28.

[20] Hawton K, Rodham K, Evans E, Weatherall R.(2002) Deliberate self-harm in adolescents: selfreport survey in schools in England. British MedicalJournal 325, 1207–11.

[21] Whitlock J, Eckenrode J, Silverman D. (2006)Self-injurious behaviours in a college population.Pediatrics 117, 1939–46.

[22] Kingsbury S, Hawton K, Steinhardt K, James A.(1999) Do adolescents who take overdoses havespecific psychological characteristics? A compara-tive study with psychiatric and community controls.Journal of the American Academy of Child andAdolescent Psychiatry 38, 1125–31.

[23] Evans E, Hawton K, Rodham K, Deeks J. (2005)The prevalence of suicidal phenomona in adoles-cents: A systematic review of population-basedstudies. Suicide and Life-Threatening Behaviour 35,239–50.

[24] Dube SR, Anda RF, Felitti VJ, Chapman DP,Williamson DF, Giles WH. (2001) Childhood abuse,

household dysfunction and the risk of attemptedsuicide throughout the lifespan. Journal of the Amer-ican Medical Association 286, 3089–96.

[25] Hawton K and James A. (2005) Suicide and delib-erate self-harm in young people. British MedicalJournal 16, 891–4.

[26] Evans E, Hawton K, Rodham K. (2004) In whatways are adolescents who engage in self-harm orexperience thoughts of self-harm different in termsof help-seeking, communication and coping strate-gies? Journal of Adolescence 28, 573–87.

[27] Houston K, Haw C, Townsend C, Hawton K. (2003)General practitioner contacts with patients beforeand after deliberate self harm. British Journal ofGeneral Practice 53, 365–70.

[28] National Collaborating Centre for Mental Health.(2004) The Short-term Physical and PsychologicalManagement and Secondary Prevention of Self-Harm in Primary and Secondary Care. London:British Psychological Society and Royal College ofPsychiatrists.

[29] Shaffer D and Gutstein J. (2002) Suicide andattempted suicide. In: Rutter M and Taylor E (eds),Child and Adolescent Psychiatry, 4th edn. Oxford:Blackwell, pp. 648–69.

[30] Harrington R, Kerfoot M, Dyer E et al. (1998) Ran-domized trial of a home-based family interventionfor children who have deliberately poisoned them-selves. Journal of the American Academy of Childand Adolescent Psychiatry 37, 512–18.

[31] Harrington R and Saleem Y. (2003) Cognitivebehavioural therapy after deliberate self-harm inadolescence. In: King RA and Apter A (eds),Suicide in Children and Adolescents. Cambridge:Cambridge University Press, pp. 251–70.

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Eating disorders in adolescence

31Eating Disorders in AdolescenceDasha NichollsDepartment of Child & Adolescent Mental Health, Great Ormond Street Hospital for Children NHSTrust, London, UK

DIAGNOSIS AND CLASSIFICATION

The term ‘eating disorder’ is restricted to disor-ders of eating behaviour driven by overvaluedideas about weight and shape. Within this narrowdefinition, there are two well-described disorders,anorexia nervosa (AN) and bulimia nervosa (BN).AN is characterized by determined food avoid-ance in pursuit of thinness, resulting in clinicallysignificant weight loss, which may or may not beenhanced by so-called ‘compensatory behaviours’designed to counteract the fattening effect of food.The DSM-IV-TR (Diagnostic and Statistical Man-ual of Mental Disorders, Fourth Edition – TextRevision) [1] recognizes a restrictive (AN-R; foodrestriction and exercise only) and a binge-purging(AN-BP) subtype of AN. Two main features dis-tinguish AN from BN. The first is the centrality ofbinge eating to BN, characterized by loss of con-trol over eating. The second is that, although in BNthinness is pursued and desired, sufferers are bydefinition within the normal weight range. DSM-IV recognizes purging (BN-P) and non-purging(BN-NP) subtypes of BN.

Despite features in common, each disorder hasa distinct course, outcome and treatment response,with accumulating evidence for differential familial(including genetic), personality, and neurodevel-opmental risk. The current challenge, given theoverlap in clinical features, is accurately to predictthe course and prognosis for a given individual atthe time of presentation.

The other important diagnostic issue is thatthe majority (around 60%) of patients at all ages


presenting with a clinically significant eating disor-der do not meet full diagnostic criteria for eitherAN or BN, and would be diagnosed with EatingDisorders Not Otherwise Specified (EDNOS) inthe DSM-IV [1], or Atypical AN or BN in ICD-10(ICD-10 International Classification of Mental andBehavioural Disorders in Children and Adoles-cents) [2], or be unclassifiable. Common examplesof EDNOS include patients with AN-like illnesswho have lost considerable weight but are still inthe healthy weight range or have not lost menses;patients who binge and purge but at a lower fre-quency than the BN criteria specify; patients whopurge but do not binge (purging disorder), or bingebut do not purge [Binge Eating Disorder (BED)];or patients for whom disordered eating is one ofa number of risk behaviours or comorbidities [3].Of more uncertain nosological status are patientswho have determined food avoidance that doesnot appear to be driven by a drive for thinnessor fear of weight gain (non-fat phobic AN) [3].Such presentations are common in young patients,when it is sometimes known as Food AvoidanceEmotional Disorder [4], and in non-Western cul-tures and minority ethnic groups. It is likely thatBED will be included in the DSM revision, whileother presentations such as ‘purging disorder’ [5]and ‘non-fat phobic AN’ require further research.

Developmental issues with respect to diagnosisinclude the degree of reliance on self-reported cog-nitions, developmental differences in the impact onphysical health, and the way that parental reportingof behaviours and eating concerns is assimilatedinto the diagnostic process [6]. The diagnostic

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process should include a family interview, a medi-cal assessment, and an individual assessment withthe young person. Core eating disorder cogni-tions are best identified using a semi-structureddiagnostic interview such as the Eating DisordersExamination (EDE) [6,7]. Key diagnostic ques-tions include asking how much the young personwould like to weigh, how they feel about theirweight and shape, and whether they or anyoneelse is worried about their eating or exercising.

EPIDEMIOLOGY AND AETIOLOGY

Some form of eating disorder is experienced by3–12% of adolescents [8,9]; most would be diag-nosed with EDNOS. For many this will be atransient period of eating pathology, with recoveryrates at 1 year of around 91–96% [9]. In an adoles-cent population, the prevalence of full syndromeAN is around 0.3% (range 0–0.9%) in 11–15-year-olds [10], but because of its chronicity onceestablished, AN is often cited as the third com-monest chronic illness of adolescence. For BN theaverage prevalence is 1%, but of these only around5% will reach mental health services [10]. The hid-den nature of eating disorders means that whenpatients do present, often as a result of parentalconcern, the illness is often well established, andshould therefore be taken seriously from the firstconsultation [11].

Eating disorders are biopsychosocial disordersof complex aetiology; no single factor is sufficientto account for onset or maintenance of any givenpresentation. Table 31.1 outlines the best estab-lished risk factors, as well as common behavioural

indicators of a potential eating disorder, suggestingthat a full assessment is indicated. Familial factorsare important; female relatives of someone witha clinical eating disorder is more than four timesas likely to have BN and more than 11 times aslikely to have AN than someone with no familyhistory of eating disorders. This figure is probablyhigher for subclinical or partial syndromes. Fromtwin studies, AN has an estimated heritability of58–76% and BN of 31–83% [8]. There is emerg-ing evidence that specific cognitive profiles in termsof cognitive inflexibility, cognitive inhibition, visu-ospatial construction and memory, may be relevantto the aetiology of AN [9], and neuroimaging stud-ies show persistent processing deficits in limbicfunction [12]. There is also increasing recognitionof impaired ‘social cognition’ in a proportion ofyoung people with AN [13], which may have impli-cations for treatment style and treatment response.

A formulation of individual, systemic and cul-tural factors, divided into predisposing, precipitat-ing, perpetuating and protective factors, is helpfulin teasing out the elements important for any oneindividual patient, and can be a therapeutic tool toaid engagement. An example is given in Table 31.2.In eating disorders there is an interplay betweendietary restraint, weight and eating, with issuessuch as negative affect, low self-esteem, adversity,shame, feelings of personal ineffectiveness or pow-erlessness, and for young people specifically, issuesaround growing up, identity formation/finding avoice, learning about risk taking and risk avoid-ance, other people’s issues, and cultural pressures.The formulation gives a starting point for disen-tangling these themes.

Table 31.1 Risk factors for and behavioural indicators of eating disorders.

Risk factors for developing an eating Psychological or behavioural markersdisorder in adolescence of an eating disorder

Female sex Reluctant attender

Repeated dieting Seeks help for physical symptoms

Early puberty Resists weighing and examination

Temperament — perfectionist personality Covers or hides body with loose clothes

Teasing about weight and dieting Secretive/evasive

Low self-esteem Increased energy ± agitation

Losses and major life events Gets angry when confronted

Family history of eating disorder

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Table 31.2 Hypothetical example of a formulation for an adolescent who has developed an eatingdisorder.

Individual Systemic Cultural

Predisposing Perfectionist naturePicky eater from a youngage

Grandmother hospitalizedfor weight loss as ateenager

Precipitating Onset of mensesFalling out with bestfriend

Older sister dieting

Perpetuating Social avoidanceLow mood

Highly competitive groupof friends

Protective Enjoys school Intact, motivated andsupportive family

Supportive schoolMaintained some linkswith peer group

Table 31.3 Indicators of high risk.

Indicator Comment

Very low weight orrapid weight loss

Less than 70% of BMI for age and gender or loss of over 1 kg forconsecutive weeks in a low-weight child

Bradycardia Symptomatic or with asymptomatic awake and resting heart rate <45 bpm

Postural hypotension Symptomatic or asymptomatic with a postural drop in systolic bloodpressure of greater than 15mmHg (note some authorities recommendadmission if drop greater than 10mmHg)

Severe electrolyteimbalance

E.g. potassium <3mmol/L, hyponatraemia or hypernatraemiaHypoglycaemia

Severe-to-moderatedehydration

Difficult to assess clinically; will rely on history too

Other severe medicalcomplications

E.g. seizures or pancreatitis, hypothermia

Psychiatric reasons E.g. suicidality, self-harm (e.g. head banging) or aggression

Child protectionreasons

Violence from sufferer towards others, or towards the sufferer; risk ofsexual abuse; parent/carer treatment non-attendance

MANAGING EATING DISORDERS

Assessment and management of a young personwith an identified eating disorder must tackle med-ical, nutritional and psychological aspects of care,and be delivered by health-care staff who areknowledgeable about normal adolescent devel-opment. When management is shared betweenprimary and secondary care, or between paediatricand mental health services, clear agreement is

needed about who is responsible for monitoringpatients, and this should be communicated to thepatient and his or her family. Consideration shouldbe given to the impact of the problem on siblings,who should be involved in treatment when possi-ble. Admission to hospital is necessary if there isacute physical compromise, high psychiatric risk,or for a specific intensive treatment. Indicators ofhigh risk are given in Table 31.3.

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Box 31.1 Medical complications of eating disorders

Medical complications of calorie restriction

• Cardiovascular: ECG abnormalities — bradycardia; T-wave inversion; ST segment depression;prolonged Q-T interval; dysrhythmias (SVT, VT); pericardial infusions

• Gastrointestinal system: delayed gastric emptying; slowed GI motility; constipation;bloating; fullness; hypercholesterolaemia; abnormal liver function (carotenaemia)

• Renal: increased blood urea (from dehydration and reduced GFR) with increased risk of renalstones; polyuria (from abnormal ADH secretion); depletion of Na and K stores; peripheraloedema with refeeding due to increased renal sensitivity to aldosterone

• Haematology: leucopenia; anaemia; iron deficiency; thrombocytopenia

• Endocrine: sick thyroid syndrome (low T3); amenorrhoea; growth failure; osteopenia

• Neurological: cortical atrophy; seizures

• Death

Medical complications of purging

• Fluid and electrolyte imbalance: low K; low Na; low Cl

• Chronic vomiting: oesophagitis; dental erosions; oesphageal tears; rarely rupture andpneumonia

• Use of ipecac/laxatives: myocardial damage; renal stones; low Ca; low Mg; low KCO3

• Amenorrhoea

AssessmentThe purpose of assessment is to clarify the diagno-sis, undertake a risk assessment, assess the impactof the problem on the young person’s develop-ment and general functioning and the functioningof the family, consider treatment expectations andmotivation, and observe family relationships andcommunication, to reach an understanding (for-mulation) of the problem with the young personand their family. Assessment also serves to engagethe young person and their family, whose moti-vations for seeking help may be very different.Many young people are brought to treatment, andthe egosyntonic nature of eating disorders is suchthat consent (or assent) to treatment cannot beassumed, but needs to be balanced against actingin the best interests of the child, and the responsi-bilities, rights and duties of parents to provide, ina manner consistent with the evolving capacitiesof the child, appropriate direction and guidance.If necessary, formal legal frameworks surround-ing child welfare or mental health may need tobe invoked, but a collaborative and motivational

stance is likely to minimize the need for this exceptin rare situations.

Medical aspectsMedical complications of eating disorders can bea result of calorie restriction leading to weightloss, poor nutrition or purging behaviours [14].Box 31.1 summarizes the complications of eatingdisorders, some of which are short term and somelong term. Figure 31.1 shows why body massindex is inappropriate in children and adolescents.In adolescents, degree of underweight is bestexpressed as percent BMI/median BMI for ageand gender (also known as weight for height).Using this terminology, less than 85% BMI wouldbe considered underweight, and less than 70%BMI would indicate severe malnutrition. Weightalone is not adequate to assess medical risk, how-ever. Table 31.3 outlines the risk parameters thatrequire assessment, and when to be concerned.Acute malnutrition is a medical emergency.

In adolescents, assessment of pubertal devel-opment is important for determining risk forcomplications such as growth retardation and

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32

30

Males Females

28

26

24

22

20

18

16

14

12

10

2

9

25

50

75

91

9830

25

2

9

25

50

75

91

9830

25

0 2 4 6 8 10 12 14 16 18

Age (years) Age (years)

20 0 2 4 6 8 10 12 14 16 18 20

Bod

y m

ass

inde

x (k

g/m

2 )

Figure 31.1 Body Mass Index (BMI: weight in kg/square of height in m) varies with age and gender,so centile charts are needed to assess degree of underweight. The red line crosses through BMIof 17.5, defined as underweight in an adult, but which is in the normal range for an adolescentunder 16.

osteopenia, and also gives an indication of whetherresumption of menses is likely to be the indicatorthat a ‘healthy weight’ has been achieved; apatient in early puberty would not be expected tomenstruate. Serial pelvic ultrasound can be usedto monitor pelvic organ maturation and predictonset of menses [15]. Because puberty in boysruns about 2 years later than in girls, boys aremore vulnerable to the impact of low weight ongrowth and development.

Bones are at risk in eating disorders as a resultof endocrine as well as nutritional inadequacy,and adolescence is the time of greatest boneacquisition. The most effective treatment for andprevention of osteopenia is weight restorationand resumption of endocrine function. Thereis no evidence for the role of calcium or othervitamin supplements, although some guidelinesrecommend them.

Management of nutritional disturbances in ado-lescents with eating disorders should take into

account the pubertal development and activitylevel. This is likely to mean that they will needa higher calorie intake for adequate weight gainthan the intake required by adult patients witheating disorders.

Psychiatric aspects of managementEating disorders generate a lot of anxiety, oftenappropriately, and parents and young peopleappreciate their concerns being taken seriously,and knowing that the professionals are confidentand knowledgeable about the problems. Manyseriously ill patients can be managed as outpatientsprovided an adequately skilled multidisciplinaryteam is involved and risks can be managed. Involv-ing families in treatment and involving youngpeople in decision-making increases cooperation,motivation and outcome.

Family interventions that directly addressthe eating disorder should be offered to ado-lescents with AN [16], usually in the form of

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family-based treatment [17], in a conjoint orseparated family therapy format [18]. Individualtherapy becomes the mainstay of treatment forAN when the young person is ready develop-mentally to take responsibility for managing theireating disorder, or when the eating disorder hasbecome chronic [19]. This may be in the form ofcognitive–behaviour therapy, cognitive analytictherapy or other form of psychotherapy. Treat-ment should address the eating disorder, includingweight and nutritional aspects. Potentially usefulpsychotropic medications in AN include selectiveserotonin reuptake inhibitors (SSRIs) for comor-bid obsessive-compulsive disorder or depressionthat has not improved with weight restoration,or atypical antipsychotics such as olanzapine orrisperidone [20].

Adolescents with BN can be treated withcognitive–behaviour therapy (CBT) specific tothe disorder, with the family included as appro-priate [21], or with family-based treatment [22,23].CBT can be delivered in a CD-ROM format withtherapist support [24]. SSRIs are also potentiallyhelpful as an adjunct to psychological treatmentfor BN.

Inpatient treatment has long been used as atherapeutic option when risks are high or whenoutpatient treatment response has been poor.Recent studies have questioned the efficacy ofinpatient treatment in addressing AN in partic-ular, and even suggested in some cases it maybe counterproductive [25]. This has led to effortsto seek alternative treatments for the sickestpatients, including increased use of paediatricwards for medical stabilization prior to outpatienttreatment, a practice common in the USA [21] andAustralia, or intensive family-based outpatienttreatments such as multifamily therapy [22].

KEY MESSAGES AND FUTURE DIRECTIONS

Eating disorders are serious mental illnesses [23]with a high morbidity and mortality, but the prog-nosis is good if appropriate treatment is startedearly [26], the majority of sufferers recoveringwithin 5 years [27]. Families should be involved intreatment as the main source of support for the suf-ferer [28]. The trend is away from hospital-basedtreatment for adolescents, towards treatment thatallow relationships with peers and family to be

maintained, and for functional aspects of the suf-ferer’s life, such as involvement in education, to bemaintained.

REFERENCES

[1] American Psychiatric Association. (1994) Diagnos-tic and Statistical Manual of Mental Disorders, 4thedn. Washington DC: American Psychiatric Asso-ciation.

[2] World Health Organization. (1991) ICD-10 Clas-sification of Mental and Behavioural Disorders.London: Churchill Livingstone.

[3] Becker AE, Thomas JJ, Pike KM. (2009) Shouldnon-fat-phobic anorexia nervosa be included inDSM-V? International Journal of Eating Disorders42, 620–35.

[4] Nicholls D and Bryant-Waugh R. (2009) Eatingdisorders of infancy and childhood: definition, symp-tomatology, epidemiology, and comorbidity. Childand Adolescent Psychiatric Clinics of North America18, 17–30.

[5] Keel PK. (2007) Purging disorder: subthresholdvariant or full-threshold eating disorder? Inter-national Journal of Eating Disorders 40(Suppl.),S89–S94.

[6] Bryant-Waugh R, Cooper P, Taylor C, Lask B.(1996) The use of the Eating Disorder Examinationwith children: A pilot study. International Journalof Eating Disorders 19, 391–7.

[7] Fairburn CG and Cooper Z. (1993) The EatingDisorders Examination (12th Edition). In: FairburnCG and Wilson GT (eds), Binge Eating: Nature,Assessment and Treatment. New York: GuilfordPress, pp. 317–32.

[8] Klump KL and Gobrogge KL. (2005) A reviewand primer of molecular genetic studies of anorexianervosa. International Journal of Eating Disorders37(Suppl.), S43–S48.

[9] Tchanturia K, Campbell IC, Morris R, TreasureJ. (2005) Neuropsychological studies in anorexianervosa. International Journal of Eating Disorders37(Suppl.), S72–S76.

[10] Hoek HW and van Hoeken D. (2003) Review of theprevalence and incidence of eating disorders. Inter-national Journal of Eating Disorders 34, 383–96.

[11] Lask B, Bryant-Waugh R, Wright F, Campbell M,Willoughby K, Waller G. (2005) Family physicianconsultation patterns indicate high risk for early-onset anorexia nervosa. International Journal ofEating Disorders 38, 269–72.

[12] Lask B, Gordon I, Christie D, Frampton I, Chowd-hury U, Watkins B. (2005) Functional neuroimagingin early-onset anorexia nervosa. International Jour-nal of Eating Disorders 37(Suppl.), S49–S51.

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[13] Wentz E, Lacey JH, Waller G, Rastam M, TurkJ, Gillberg C. (2005) Childhood onset neuropsychi-atric disorders in adult eating disorder patients. Apilot study. European Child and Adolescent Psychi-atry 14, 431–7.

[14] Nicholls D, Hudson L, Mahomed F. (2010) Man-aging anorexia nervosa. Archives of Disease inChildhood Oct, epub ahead of print.

[15] Allan R, Sharma R, Sangani B et al. (2010) Pre-dicting the weight gain required for recovery fromanorexia nervosa with pelvic ultrasonography: anevidence-based approach. European Eating Disor-ders Review 18, 43–8.

[16] National Collaborating Centre for Mental Health.(2004) Core Interventions in the Treatment and Man-agement of Anorexia Nervosa, Bulimia Nervosaand Related Eating Disorders. Report No. ISBN1 85433 398 4. The British Psychological Society andGaskell.

[17] Lock J, le Grange D, Agras S, Dare C. (2000) Treat-ment Manual for Anorexia Nervosa. New York:Guilford Press.

[18] Eisler I, Dare C, Hodes M, Russell G, Dodge E,le Grange D. (2000) Family therapy for adolescentanorexia nervosa: the results of a controlled com-parison of two family interventions. Journal of ChildPsychology and Psychiatry 41, 727–36.

[19] Gowers SG and Green L. (2009) Eating Disor-ders: Cognitive Behaviour Therapy with Childrenand Young People. Hove, UK: Routledge.

[20] Couturier J and Lock J. (2007) A review of medica-tion use for children and adolescents with eatingdisorders. Journal of the Canadian Academy ofChild and Adolescent Psychiatry 16, 173–6.

[21] Lock J. (1999) How clinical pathways can be useful:An example of a clinical pathway for the treatmentof anorexia nervosa. Clinical Child Psychology andPsychiatry 4, 331–40.

[22] Scholz M and Asen E. (2001) Multiple family ther-apy with eating disordered adolescents: conceptsand preliminary results. European Eating DisordersReview 9, 33–42.

[23] Klump KL, Bulik CM, Kaye WH, Treasure J,Tyson E. (2009) Academy for Eating Disordersposition paper: eating disorders are serious mentalillnesses. International Journal of Eating Disorders42, 97–103.

[24] Schmidt U, Andiappan M, Grover M et al. (2008)Randomised controlled trial of CD-ROM-basedcognitive-behavioural self-care for bulimia nervosa.British Journal of Psychiatry 193, 493–500.

[25] Gowers SG, Clark A, Roberts C et al. (2007) Clinicaleffectiveness of treatments for anorexia nervosain adolescents: randomised controlled trial. BritishJournal of Psychiatry 191, 427–35.

[26] Steinhausen HC. (2009) Outcome of eating disor-ders. Child and Adolescent Psychiatric Clinics ofNorth America 18, 225–42.

[27] Keel PK and Brown TA. (2010) Update on courseand outcome in eating disorders. International Jour-nal of Eating Disorders 43, 195–204.

[28] le Grange D, Lock J, Loeb K, Nicholls D. (2010)Academy for Eating Disorders position paper: therole of the family in eating disorders. InternationalJournal of Eating Disorders 43, 1–5.

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32Substance Misuse in Young PeopleK.A.H. Mirza1, Roshin M. Sudesh2, and Sudeshni Mirza31Department of Child and Adolescent Psychiatry, Institute of Psychiatry at the Maudsley, King’s College,London, UK2King’s College Hospital, London, UK3Dr. Somerwell Memorial CSI Medical College Hospital, Kerala, India

INTRODUCTION

Substance misuse is a major public health problem,with substantial levels of morbidity and mortal-ity. Most children in their middle childhood areexposed to various substances including alcoholand tobacco, and a substantial minority, as highas 10%, continue to use drugs into adolescenceand adulthood [1,2]. Many youngsters who mis-use drugs have multiple antecedent and coexistingmental health problems, unrecognized learningdifficulties, family difficulties, involvement withthe justice system and deeply entrenched socialproblems. Substance misuse takes a high toll interms of health-care costs, violent crimes, acci-dents, suicides, social and interpersonal difficulties,and educational impairment [3].

EPIDEMIOLOGY

Estimates from the 2009/10 British Crime Surveysuggest that 40% of those aged 16–24 have usedone or more illicit drugs at some point in theirlife, with up to 12% having used illicit drugs inthe last month [4]. Tobacco, alcohol and cannabisare the most commonly abused substances, withcocaine and heroin accounting for less than 10%[4,5]. Volatile substance use peaks in early ado-lescence: about 4–7% of 11–15-year-olds sniffedvolatile substances in the last year, and roughly 1%inhale solvents regularly, with the prevalence beingsubstantially higher for youngsters from deprivedbackgrounds [3] (Table 32.1).


Most of the campaigns against substance misuseare directed at illegal drugs such as cannabis,heroin, cocaine and ecstasy. However, many morepeople die or develop problems, either directly orindirectly, as a result of using tobacco and alco-hol than all illegal drugs combined, and some ofthe leading experts in the field of addictions haveproposed alternatives to the contentious Britishsystem of classification of drugs [6].

DEFINING SUBSTANCE MISUSE IN THEYOUNG: A DEVELOPMENTAL PERSPECTIVE

The effects of a drug are not just dependent onthe drug itself. The mindset of the individual whotakes it and the setting in which it is used arecrucial variables. Young people report that theytake drugs for a variety of reasons: for pleasure;to conform to attitudes and values of their peergroup; to block out traumatic and painful memo-ries; and to relieve sadness and worries associatedwith their everyday lives. For some young people,the use of drugs and alcohol may become a prob-lem in itself, and a very small minority developsubstance dependence. Early onset of substanceuse and a rapid progression through the stages ofsubstance use are among the risk factors for thedevelopment of substance misuse [3]. Longitudinalstudies have shown that the highest peak of drugand alcohol use is between the ages of 14 and 18years, and that most youngsters reduce or stop useby the age of 24 years [7]. The Christchurch Health

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Substance misuse in young people

Table 32.1 Use of drugs and alcohol in young people in the UK, 2007/2010.

Substance Use last year: Use last month: Lifetime use/use Regular use in16—24-year-olds 16—24-year-olds last year: 11—15-year-olds and

11—15-year-olds 15—16-year-olds

Tobacco NA NA 29% (lifetime) 6% (more than onecigarette per day in11—15-year-olds): 7%in boys and 4% in girls

Alcohol NA NA 51% (lifetime) 52% of boys and 55% ofgirls aged 15—16engaged in episodicheavy drinking in thelast month

Cannabis 16.1% 16% 8.9% (last year) 9% of 15—16-year-oldsused in the lastmonth [6]

2% of 15—16-year-oldsreported harmful useof cannabis

Cocaine (cocainepowder andcrack)

5.6% 2.6% 1.8% (last year) NA

Ecstasy 4.3% 1.9% 1.2% (last year) NA

Alkyl nitrites(‘poppers’)

3.2% 0.8% 1.8% (last year) NA

Amphetamines 2.4% 0.7% 0.8% (last year) NA

Opiates 0.3% 0.2% 0.7% (last year) NA

Hallucinogens 1.5% 0.4% 2.2% (last year) NA

Volatilesubstances (glue)

3% 0.1% 5.5% (last year) NA

Ketamine 1.7% 0.9% 0.6% (last year) NA

Sources: Reproduced with permission from Flatley et al. [4], Fuller, Sanchez [5], and Hibell et al. [6].

and Development study estimated that 10% ofcannabis users would become dependent, and atthe age of 18 years, about 6% were dependent ondrugs or alcohol [2].

Given the natural history of substance usein young people and the heterogeneity of thepatterns of use, most researchers and cliniciansstruggle to define what constitutes substancemisuse in young people.

DefinitionsInternational classificatory systems – the Inter-national Classification of Diseases, 10th revision(ICD-10) and the Diagnostic and StatisticalManual of Mental Disorders, 4th edition (DSM-IV) – suggest that adult categories like ‘harmfuluse’ and ‘dependence’ (ICD-10) and ‘substanceabuse’ and ‘dependence’ (DSM-IV) could bereliably used to diagnose substance misuse in

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young people. Unfortunately, both systems lacka developmental perspective in psychopathology,and the categories such as ‘harmful use’, ‘depen-dence’ and ‘substance abuse’ do not seem tocapture all stages of substance use in young people[8,9]. For example, tolerance and withdrawal,which typically develop in response to longperiods of chronic substance use, are rarely seenin young people.

Alternative classifications in young peopleClinicians and researchers have proposed alterna-tive criteria to classify substance misuse in youngpeople [8,9]. Based on the seminal work by JosephNovinsky and colleagues, Mirza and Mirza pro-posed a developmentally sensitive and dimensionalmodel to classify the stage of substance use inyoung people [10], starting with non-use at oneend, moving through an experimental stage, socialstage, at-risk (prodromal) stage, and stage of harm-ful use to substance dependence at the other end.The above model has the potential to ascertainstages of substance use across the dynamic contin-uum and choose the most appropriate interventionto suit the stage of substance misuse (Table 32.2).

AETIOLOGY: RISK AND PROTECTIVEFACTORS

Substance use does not occur in a vacuum. In vul-nerable individuals, substance misuse is producedby the interaction of a drug with genetic, envi-ronmental, behavioural, psychosocial and culturalfactors (Table 32.3; Boxes 32.1 and 32.2).

The complex mechanisms by which risk andprotective factors mediate and modulate develop-ment of substance misuse are beyond the scope ofthis chapter, and interested readers may refer toexcellent reviews or textbooks [11,12].

Antecedent and comorbid mental healthproblemsCommunity-based longitudinal studies show thatdepression may predict alcohol dependence andcannabis use [13]. In addition, conduct problemsin childhood predict substance abuse and depen-dence in early adulthood, after controlling for arange of social and other covariates [2]. Similarly,

untreated attention-deficit hyperactivity disorder(ADHD) has been shown to be a significant riskfactor for development of substance misuse inadolescence and adulthood [14]. The combinationof conduct disorder and hyperactivity carries aparticularly high risk. The risk of development ofsubstance misuse is high in children exposed toneglect and maltreatment [15,16].

Significant rates of comorbid psychiatric dis-orders were reported in the community and inclinical samples of young people with substancemisuse [17,18], the most common being conductdisorder, major depression, ADHD (with or with-out comorbid conduct disorder), anxiety disorders[post-traumatic stress disorder (PTSD) and pho-bias] and bulimia nervosa. Coexisting substancemisuse has implications for the onset, clinicalcourse, treatment compliance and prognosis foryoung people with psychiatric disorders [17,18].Comorbid substance misuse is the single mostimportant factor that increases the risk of sui-cide in young people with psychosis or majordepression [19].

CONSEQUENCES AND ASSOCIATEDFEATURES OF SUBSTANCE MISUSE

A hallmark of substance misuse in adolescents isimpairment in psychosocial and academic func-tioning. Impairment can include family conflictor dysfunction, interpersonal conflict, and aca-demic failure. Associated characteristics such asoffending behaviour, other high-risk behavioursand comorbid psychiatric disorders contribute fur-ther to risks and impairments. Injecting drug useis rare and only a small minority of young peo-ple develop physical dependence. Mortality is highdue to accidents, suicides and physical compli-cations of substance misuse. In the UK, volatilesubstance misuse accounts for 65 deaths per year,which is about 2% of all deaths below the age of18 years [5].

ASSESSMENT

Information should be obtained from a varietyof sources including the young person, par-ents/other caregivers, general practitioner, school,

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Table 32.2 A pragmatic classification of adolescent substance use and the range of interventions.Reproduced from Mirza and Mirza [11].

Stage Purported Setting Frequency Emotional Behaviour Impact on Suggestedmotive impact functioning interventions

[3]

Experimentalstage

Curiosity andrisk taking

Alone or withpeer group

Occasionalat best

Mind-alteringeffects ofdrugs are lessrelevant

No activedrug-seekingbehaviour

Relativelylittle, butrarely resultsin dangerousoutcome

Universalprevention(drugeducation) byTier 1services

Social stage Socialacceptance

Usuallyfacilitated bypeer group

Occasionalbutvariable,dependingon peergroup

Mind-alteringeffects ofdrugs areclearlyrecognizedandappreciated

No activedrug-seekingbehaviour

Usually anormativeexperience.May beassociatedwithsignificantdangers inrare instances

Universalprevention(drugeducation) byTier 1services

At risk orprodromalstage

Cope withnegativeemotions orenhancepleasure

Alone or withpeer group:mostly ontheir own

Frequentuse

Uses drugspurportedlyto alter moodor behaviour

Activedrug-seekingbehaviour

Impairment infunctioning insome areas,but able tohide them byand large

Targetedintervention/treatment byTier 2—3agencies

Stage ofharmful use(similar toICD-10)

Drug use isthe primarymeans ofrecreation,coping withstress or both

Alone or withan alteredpeer group

Regular use,despitenegativeconse-quences

Veryimportant

Activedrug-seekingbehaviour

Impairment inalmost allareas of lifeand ordistress innear and dear

Treatment byTier 3agencies

Stage ofdependence(similar toICD-10)

To deal withwithdrawalsymptoms,and stopcraving

Alone Compulsiveuse,toleranceand loss ofcontrol ofuse

Veryimportantespeciallydealing withdysphoria andotherwithdrawalsymptoms

Compulsivedrug-seekingbehaviour;may engagein acquisitivecrimes

Physical andpsychologicalcomplica-tions;impairment inall spheres oflife

Treatmentandhabilitationby Tier 3 andTier 4agencies

ICD-10, ICD-10 International Classification of Mental and Behavioural Disorders in Children and Adolescents.

social services, youth justice system or any othersocial agencies involved. Clinical and researchexperience shows that young people are gen-erally more reliable informants than might beassumed. The attitude of the clinician should beflexible, empathic and non-judgemental to engagethe young person in the assessment process and toobtain a valid estimate of substance use. Explorethe young person’s leisure activities and gentlyguide them to talk about the nature and extent

of substance use, its context, and its impact onvarious domains of their psychosocial function-ing. This will enable the clinician to determinewhether the current pattern of substance use con-stitutes normative stages of substance use, or meetsdiagnostic criteria for harmful use or dependence.Detailed exploration of comorbid psychiatric dis-orders and their relationship to substance misusewould help to formulate a differential diagnosisand treatment plan. Substance misuse is almost

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Table 32.3 Risk factors for the development of adolescent substance misuse.

Domain Risk factor

Neurobiological Genetic susceptibility to substance misusePsychophysiological vulnerability (EEG, ERPs)Neurochemical abnormalities (DA, 5-HT, opioids etc.)

Psychological Depressive disorderAnxiety disorderEarly/persistent conduct symptoms, ADHDPhysical and sexual abuseTraumatic/stressful life eventsEarly onset of drug useSensation-seeking traits in personality

Family Drug use by parents/other family membersFamily conflict and disruptionInconsistent or harsh disciplineLack of parental expectations about the child’s future

Peer group/school Peer rejection/alienation from peer groupAssociation with drug-using peer groupPoor commitment to schoolAcademic failure/underachievement

Social/cultural Easy availability of drugsSocial norms or laws favourable to drug useExtreme economic deprivationDisorganized, anomic neighbourhood

ADHD, attention deficit hyperactivity disorder; DA, dopamine; EEG, electroencephalogram; ERP,Event Related Potential; 5-HT, 5-hydroxtryptamine (serotonin).

Box 32.1 Protective factors

• Close, affectionate parent—childrelationship

• Parental monitoring of young person

• Authoritative parenting style

• High educationalaspiration/commitment

• Having a non-drug-using peer group

• Good social and interpersonal skills

• Sense of bonding to school or othersocial institutions (sports club, church,mosque)

• Acceptance of socially approved valuesand norms of behaviour

always not the only problem and a comprehensivedevelopmental, social and medical history shouldbe undertaken to determine the multiple com-plex needs across different domains. Particularattention should be paid to the young person’svulnerability, resilience, hopes and aspirations.Evaluating the adolescent’s readiness for treat-ment or stage of change may help determine theinitial treatment goals or level of care.

Mental state examination and physicalexaminationYoung people may present with features of intoxi-cation or withdrawal. Recent injecting sites, blood-shot eyes, nicotine stains on fingers, unsteady gaitand tremulousness give indications of the extentof substance use. Perceptual abnormalities maysuggest a primary psychotic illness or the use ofdrugs such as cannabis, alcohol, amphetamine orcocaine. Inhaling solvents from the bag may lead

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Box 32.2 High-risk groups (based onlongitudinal studies)

• Young offenders

• Children of drug-misusing parents

• Children excluded from school/truants

• Young people looked after by localauthority

• Young people leaving care

• Young homeless people

• Teenage mothers

• Young people attending mental healthservices

• Regular attendees ofaccident-and-emergency services

to a rash around the mouth and nose. Risk ofharm to self and others should be systematicallyassessed, especially in young people with a historyof offending behaviour and those with comorbidpsychopathology. Psychiatrists should not hesitateto use their hard-won medical skills, and a detailedphysical examination including basic neurologicalexamination should always be undertaken. Specificattention should be paid to signs of liver disease,tachycardia and high blood pressure, which mayindicate excessive substance use or withdrawalstates.

InvestigationsHaematological and biochemical investigationslike liver function tests are helpful to establishdrug- and alcohol-related harm. Testing bodilyfluids (urine, saliva, blood) for specific substancesshould be part of the initial evaluation, especiallyin inpatient settings and for court-mandatedassessments. Most substances – except benzodi-azepine, methadone and cannabis – are detectablein urine for a few days only. Considering the aboveand the potential for adulteration of samples, anegative urine result does not necessarily meanthat the young person is not using drugs. A hairtest is more reliable as it gives a longer historicalprofile of drug use (up to 1 month). However,some professionals argue that testing adds littleto the verbal reports of substance use in young

people, especially when clinicians have managedto nurture a trusting therapeutic relationshipwith them. There is little evidence at present torecommend repeated testing of bodily fluids tomonitor routine clinical treatment.

TREATMENT

The primary goal of treatment is to achieve andmaintain abstinence from substance use. Whileabstinence should remain the explicit, long-termgoal of treatment, harm reduction may be aninterim, implicit goal, in view of both the chronicityof substance misuse in some young people and theself-limited nature of substance misuse in others.Treatment modalities used are largely psychoso-cial. Medication is used as an adjunct only, thoughit may offer a window of opportunity for youngpeople to engage in psychosocial treatment [19,20].

Evidence base for treatmentReviews of the literature on adolescent treatmentoutcomes have concluded that treatment is betterthan no treatment [21]. Naturalistic follow-up ofyoung people in a number of treatment settingsin the USA showed decreased substance misuseand criminal involvement, as well as improvedpsychological adjustment and school performance,one year after treatment [21,22]. Family therapyapproaches such as multisystemic therapy [23] andmultidimensional family therapy [24] have thebest evidence base for efficacy across a number ofdomains [25], although individual approaches suchas cognitive–behavioural therapy (CBT) – bothalone and in combination with motivationalenhancement – have been shown to be efficacious[26,27]. There is an emerging evidence base forbrief motivational interviewing as well [28–30].

Most of the research on psychological treat-ment comes from the USA, and is not necessarilydirectly applicable to the UK context, both in termsof the resources required and cultural differences.However, there are significant overlaps betweendifferent forms of psychotherapies in both theoret-ical conceptualizations and therapeutic techniques,and building on existing skills of practitionersworking across voluntary and statutory agenciesin the UK could prove to be an effective andcost-effective way of delivering evidence-basedinterventions. Essential elements of a successfultreatment programme may include the following:

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• An empathic and non-judgemental therapist,who takes painstaking efforts to engage eventhe ‘hard-to-reach’ youngster in the treatmentprocess and rekindles the ability to hope anddream.

• A therapeutic process that involves structuredand personalized feedback on risk and harm toyoung people; emphasis on personal responsi-bility for change; and strategies to increase self-esteem, self-efficacy, practical problem-solvingskills and social skills.

• Involvement of family and other ‘systems ofcare’ – such as school, judicial system and socialservices – to address the multiple complex needsof young people.

• A lengthy period of retention in service to ensuregood aftercare.

Treatment should be tailored to meet the needsof the individual young person. Integrated men-tal health and substance misuse treatment shouldbe offered to young people with comorbid psy-chiatric disorders [29,31,32]. Inpatient treatment isrequired for a very small minority: those withsevere and chaotic substance misuse; repeatedfailed community detoxification; intravenous druguse with complications; and severe mental ill-ness and risk of self-harm. Variables consistentlyrelated to successful outcome are treatment com-pletion, low pre-treatment substance use, and peerand parent social support [21]. Other factors pre-dictive of outcome are involvement of family,use of practical problem-solving, and provision ofcomprehensive services such as housing, academicassistance and recreation [26].

Role of child and adolescent mental healthservices (CAMHS)Despite the significant expansion of specialist sub-stance misuse services over the past decade, manyyoungsters still do not receive adequate treatment,and there are ongoing debates regarding the roleof CAMHS in adolescent substance misuse Pro-fessionals working in CAMHS have an unrivalledopportunity to play a significant role in the earlyidentification and treatment of substance misuse,including children of substance-misusing parentsand other high-risk groups. Specific treatment of‘core’ mental health problems such as depression,eating disorders, ADHD and PTSD is a primary

role of the specialist CAMHS [33]. CAMHS pro-fessionals could help develop multi-agency treat-ment services and train other professionals inevidence-based interventions.

CONCLUSIONS

The notion of a drug-free society is almost cer-tainly a chimera. Young people have always usedsubstances to change the way they see the worldand how they feel, and there is every reason tothink they always will. However, early identifica-tion and comprehensive treatment could help toreduce distress and prevent further deterioration.Everything that is done to help troubled and trou-blesome children should be informed by a sense ofhistory, a reflective awareness of current value sys-tems, economic and social factors, and by a matureand balanced judgement of what is possible andwhat is not. Integrative, multi-agency treatmentsaddressing a range of ecologically valid aetiologi-cal factors have the potential to engender a cultureof therapeutic optimism.

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[2] Fergusson D, Horwood L, Ridder E. (2007) Con-duct and attentional problems in childhood andadolescence and later substance misuse and depen-dence. Results of a 25-year longitudinal study. Drugand Alcohol Dependence 88, 14–26.

[3] Gilvarry E. (2000) Substance abuse in young peo-ple, Journal of Child Psychology and Psychiatry 41,55–80.

[4] Flatley J, Kershaw C, Smith K, Chaplin R, Moon D.(2010) Crime in England and Wales 2009/10: Find-ings from 2009/10 British Crime Survey. London:Home Office, British Crime Survey. Available at:http://rds.homeoffice.gov.uk/rds/pdfs10/hosb1210.pdf

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[6] Hibell B, Guttormsson U, Ahlstrom S et al.(2009) The 2007 ESPAD Report: SubstanceUse Among Students in 35 European Countries.Stockholm: Swedish Council for Information on

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[9] Halikas A, Lyttle M, Morse C. (1990) Proposedcriteria for the diagnosis of alcohol abuse in adoles-cence. Comprehensive Psychiatry 25, 581–5.

[10] Nutt D, King LA, Saulsbury W, Blakemore C.(2007) Development of a rational scale to assessthe harm of drugs of potential misuse. Lancet 369,1047–53.

[11] Mirza KAH and Mirza S. (2008) Adolescent sub-stance misuse. In: Bruce H and Skuse D (eds),Psychiatry. London: Elsevier, for the Medicine Pub-lishing Group, pp. 357–62.

[12] Swadi H. (1999) Individual risk factors for adoles-cent substance use. Drug and Alcohol Dependence55, 209–24.

[13] Pardini D, White Raskin H, Stouthamer-Loeber M.(2007) Early adolescent psychopathology as a pre-dictor of alcohol use disorders by early adulthood.Drug and Alcohol Dependence 88, 38–49.

[14] Wilens TE, Faroane S, Biederman J, GunawardeneS. (2003) Does stimulant therapy of attention-deficit/hyperactivity disorder beget later substancemisuse? A meta analytic review of the literature,Pediatrics 111, 179–85.

[15] Kendler KS, Bulik CM, Silberg J, Hettema JM,Myers J, Prescott CA. (2000) Childhood sexualabuse and adult psychiatric and substance use dis-orders in women: an epidemiological and cotwincontrol analysis. Archives of General Psychiatry 57,953–9.

[16] De Bellis MD. (2005) The psychobiology of neglect:a review. Child Maltreatment 10, 150–72.

[17] Boys A, Farrell M, Taylor C et al. (2003) Psychi-atric morbidity and substance use in young peopleaged 13-15 years: results from the Child and Ado-lescent Survey of Mental Health. British Journal ofPsychiatry 182, 509–17.

[18] Roberts R, Roberts C, Yun X. (2007) Comorbid-ity of substance use and other psychiatric disordersamong adolescence. Evidence from an epidemio-logical survey. Drug and Alcohol Dependence 88,513–16.

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[20] Marshall E and Mirza KAH. (2007) Psychophar-macological treatment. In: Gilvarry E and McArdleP (eds), Clinics in Developmental Medicine, Alco-hol, Drugs and Young People. Clinical Approaches.London: Mac Keith Press, pp. 197–216.

[21] Williams R and Chang SY. (2000) A comprehensiveand comparative review of adolescent substanceabuse treatment outcome. Clinical PsychologicalScience Practice 7, 138–66.

[22] Hser Y, Grella CE, Hubbard RL. (2000) An evalu-ation of drug treatments for adolescents in four UScities. Archives of General Psychiatry 58, 689–95.

[23] Henggeler SW, Clingempeel WG, Brondino MJ,Pickrel SG. (2002) Four year follow up of mul-tisystemic therapy with substance abusing andsubstance-dependent juvenile offenders. Journal ofthe American Academy of Child and AdolescentPsychiatry 41, 868–74.

[24] Liddle HA, Dakof GA, Parker K, Diamond GS,Barret K, Tejada M. (2001) Multidimensional familytherapy for adolescent substance abuse: results of arandomised clinical trial. American Journal of Drugand Alcohol Abuse 27, 651–87.

[25] Stanton MD and Shadish WR. (1997) Outcome,attrition, and family-couple treatment for drugabuse: a meta-analysis and review of the con-trolled, comparative studies. Psychological Bulletin10, 35–44.

[26] Williams RJ and Chang SY. (2000) A comprehen-sive and comparative review of adolescent substanceabuse treatment outcome. Clinical Psychology Sci-ence Practice 7, 138–66.

[27] Waldron HB and Kaminer Y. (2004) On thelearning curve: the emerging evidence supportingcognitive-behavioural therapies for adolescent sub-stance abuse Addiction 99, 93–105.

[28] Hulse GK, Robertson SI, Tait RJ. (2001) Ado-lescent emergency department presentations withalcohol and other drug related problems in Perth,Western Australia. Addiction 96, 1059–67.

[29] McCambridge J and Strang J. (2004) The efficacy ofsingle-session motivational interviewing in reducingdrug consumption and perceptions of drug-relatedrisk and harm among young people: results froma multi-site cluster randomised trial. Addiction 99,39–52.

[30] O’Leary TA and Monti PM. (2004) Motivationalenhancement and other brief interventions for ado-lescent substance abuse: foundations, applicationsand evaluations. Addiction 99, 63–75.

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[31] Libby AM and Riggs PD. (2005) Integrated sub-stance use and mental health treatment for adoles-cents: aligning organizational and financial incen-tives. Journal of Child and Adolescent Psychophar-macology 5, 826–34.

[32] Mirza KAH and Buckstein O. (2010) Assessmentand treatment of young people with ADHD, dis-ruptive behaviour disorder and co morbid substanceuse disorder. In: Kaminer Y and Winters K (eds),

Clinical Manual of Adolescent Substance AbuseTreatment. Washington, DC: American PsychiatricPublishing, pp. 283–305.

[33] Mirza KAH, McArdle P, Gilvarry E, Crome I(eds). (2007) The Role of CAMHS and AddictionPsychiatry in Adolescent Substance Misuse. London:The National Treatment Agency. Available at:http://www.nta.nhs.uk/uploads/yp_camhs280508.pdf.

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Early-onset bipolar disorder

33Early-Onset Bipolar DisorderAnthony JamesUniversity of Oxford, Highfield Adolescent Unit, Warneford Hospital, Oxford, UK

INTRODUCTION

Early-onset bipolar disorder (EOBPD) (i.e. onsetbefore 18 years) is a serious psychiatric disorderassociated with social and academic difficultiesand suicidality. Recently there has been increasedrecognition of this disorder but no clear consensuson definition.

DIAGNOSTIC CRITERIA

The ICD-10 International Classification of Men-tal and Behavioural Disorders in Children andAdolescents (ICD-10) criteria [1] for bipolar dis-order require at least two episodes of significantlydisturbed mood and activity with, on occasion,either mood elevation (mania or hypomania) andincreased activity or depression with decreasedactivity and energy. The Diagnostic and StatisticalManual of Mental Disorders, Fourth Edition – TextRevision (DSM-IV-TR) criteria [2] for bipolar dis-order differ slightly, requiring a manic episode – anelevated, expansive or irritable mood lasting 1week or shorter if hospitalization is required.By convention there are two subtypes of bipo-lar disorder – bipolar I, where the patient has hadat least one manic or mixed episode; and bipolarII, where the patient has had one or more episodesof both major depression and hypomania, but nomanic or mixed episodes.

CLINICAL CHARACTERISTICS

There is debate, particularly in the USA, aboutthe clinical presentation of EOBPD, with some


authorities recognizing EOBPD as presentingwith:1. chronicity with long episodes;2. predominantly mixed episodes and/or rapid

cycling;3. prominent irritability; and4. high rate of comorbid attention deficit

hyperactivity disorder (ADHD) and anxietydisorders.There two main diagnostic issues, which are

at variance with the diagnostic practice for adultbipolar disorder (BPD) – firstly, whether ele-vated/expansive mood is required for a diagnosisof mania, or whether irritability alone is sufficient;and secondly, whether EOBPD is characterizedby a chronic, non-episodic course, rather thanan illness with manic episodes as required inDSM-IV-TR.

Early-onset bipolar disorder can be conceptual-ized as narrow, intermediate or broad phenotypes[3]. Those with the narrow phenotype, or BPDtype I or II as described in DSM-IV-TR [2], haverecurrent periods of major depression and maniaor hypomania. The category BPD not otherwisespecified (BPD NOS) is reserved for children whofail to meet the duration criteria of 4–7 daysrequired to fulfil the DSM-IV-TR criteria for hypo-mania or mania. Children presenting with severeirritability, affective storms, mood lability, severetemper outbursts, symptoms of depression, anxi-ety or ADHD-like symptoms – poor concentrationand impulsivity – with or without clear episodic-ity, are regarded as having the broad phenotype.Recent findings point to a continuum of symptomsand severity from BPD NOS, BPD II to BPD

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I with elevated mood being a common featurethroughout [4].

EPIDEMIOLOGY

The peak onset of bipolar disorder is in the 15–19-year-old group, with males and females equallyrepresented. Retrospective studies in adults withBPD report that over 50% of patients experiencethe onset of their BPD before 20 years of age, andbetween 10 and 20% report the onset before 10years of age [5]. The initial presentation may beone of depression; around 20–30% of depressedchildren, particularly those with psychosis, a familyhistory of BPD and/or pharmacologically inducedmania, eventually develop BPD [6].

A community school survey of older adolescents(14–18 years) showed the lifetime prevalence rateto be around 1% [7], although only 0.1% hadmania. Most of the identified cases had hypothymiaor cyclothymia. Manic symptoms are common inup to 13% of the school population of 14–16-year-olds; however, this figure is reduced to 0.6% ifseverity and impairment criteria apply [8]. In theGreat Smoky Mountains Study of children aged 9,11 and 13, no cases of BPD type I were found [9].Subsequent studies focused on those children withchronic irritability and hyperarousal, designatedas having ‘broad BPD phenotype’ or severe mooddysregulation (SMD). The lifetime prevalence ofSMD in children and adolescents aged 9–19 was3.3%, or 1.8% with severe impairment [10]. How-ever, although SMD appears to be part of theaffective spectrum with SMD at age 10, predictingdepressive disorder in early adulthood, it did notpredict BPD.

ASSESSMENT

Semistructured interviews, such as the Kid-die Schedule for Affective Disorders andSchizophrenia – Present and Lifetime (K-SADS-PL) [11], and for children the WashingtonUniversity in St Louis-Kiddie Schedule forAffective Disorders and Schizophrenia (WASH-U-KSADS) [12] reliably elicit operationallydefined symptoms and can be recommendedfor use in both research and clinical settings.The Young Mania Rating Scale (YMRS) [13]is commonly used in research to assess the

severity of manic symptoms, and assess treatmentresponse. However, the YMRS is not a diagnosticinstrument.


The symptom overlap between ADHD andEOBPD can create diagnostic problems, partic-ularly in the young, where there are high ratesof comorbidity – 60–90% according to some[14]. However, the symptoms of grandiosity,elated mood, flight of ideas and decreased needfor sleep reliably differentiate the two. Bipolardisorder can be associated with a sudden onset ofsevere behavioural disturbance. Such disturbancecontrasts with the usually longer-standing conductdisorder. A family history of affective disorderrather than conduct or personality disorder mayaid diagnosis. In children, mood instability, andirritability associated with pervasive develop-mental disorders need to be noted [15], whilein adolescence affective instability seen in casesof borderline personality disorder can causediagnostic confusion [16]. In the latter case theremay well be considerable overlap, with reportsof 15% of patients with bipolar disorder havingborderline personality disorder [17]. Psychosisin adolescence, particularly if florid with mood-incongruent hallucinations and thought disorder,has been misdiagnosed as schizophrenia [18].Factors in favour of a diagnosis of schizophreniainclude: premorbid personality abnormalities,schizotypal personality disorder, a family historyof schizophrenia, and an insidious onset ofpsychosis. Mania needs to be distinguished fromdrug-induced states secondary to drug misuse or,rarely, from medical treatments such as steroids.

LONGITUDINAL COURSE AND PROGNOSIS

An important step in judging the validity ofEOBPD is the stability of the diagnosis over theshort and long term. The EOBPD phenotype hasbeen reported to be reliable, with stability overfollow-up assessments at 6 months and 1, 2 and 4years. High rates of chronicity and relapse werefound during a 4-year follow-up period despitecommunity treatment [19].

Although symptoms of EOBPD appear sta-ble over time [20], EOBPD has not yet been

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shown to progress into the classic adult BPD. Theevidence is not sufficient to indicate that EOBPDis continuous with adult BPD. The COBY study(Course and Outcome of Bipolar Youth) [21] of413 youths (aged 7–17 years) with bipolar I dis-order (n = 244), bipolar II disorder (n = 28) andbipolar disorder not otherwise specified (n = 141)found that at 2.5 years after the index episode,81.5% of the participants had fully recovered.However, 1.5 years later 62.5% had a syndro-mal recurrence, particularly depression. Manicsymptomatology, especially syndromal, was lessfrequent. Twenty-five percent of youths with bipo-lar II converted to bipolar I, and 38% of those withbipolar disorder not otherwise specified convertedto bipolar I or II. Overall the outlook is concerningand emphasizes the seriousness of this diagnosis inthis age group.

SUICIDE

Bipolar disorder is a risk factor for suicide. Ado-lescents with bipolar disorder have higher rates ofcompleted suicide [22] and attempted suicide [23].Suicide attempts are associated with older age,depressive episodes, mixed states and psychoticfeatures [24]. Comorbid substance abuse, panicdisorder and past histories of suicide attemptsand physical or sexual abuse add to the riskprofile.

TREATMENT

The treatment of early-onset bipolar disorderrequires a multimodal approach. An assessmentof comorbid disorders such as substance abuseand conduct disorder needs to be undertaken,including an appraisal as to whether these aremood dependent. Comorbid disorders may needtreatment in their own right. The treatment planclearly needs to take account of the developmentallevel of the child and adolescent and the differingage presentations of bipolar disorder (Table 33.1).

The treatment of bipolar disorder can be dividedinto two stages: acute treatment of mania ordepression, and prophylaxis.

Acute phaseThere is an increasing trend to use atypical antipsy-chotics in children and adolescents, both in the

Table 33.1 Evidence for medication treatmentfor child and adolescent bipolar disorder.

Medication Evidence level

Lithium A&BValproate B&CCarbamazepine BOxcarbazepine —Topiramate —Clozapine CRisperidone A (FDA approval)Olanzapine A (FDA approval)Quetiapine A (FDA approval)Aripiprazole A (FDA approval)Lamotrigine CZiprasidone B&C

Level A data: child randomized controlled clinicaltrials.Level B data: adult randomized clinical trials.Level C data: open trials and retrospective analyses.Level D data: case reports and expert opinion torecommended current clinical practices.

acute manic phase and in the longer-term as moodstabilizers. With the recent US Food and DrugAdministration (FDA) indication of risperidone,aripiprazole, quetiapine and olanzapine for thetreatment of bipolar youth, the atypical antipsy-chotics are rapidly becoming a first-line treat-ment option. However, with the exception of arip-iprazole these agents are associated with adverseeffects such as increased appetite, weight gain,lipid abnormalities and a risk of type II diabetesmellitus.

Expert guidelines on the treatment of paedi-atric bipolar disorder [25] recommend the use ofmood stabilizers and or atypical antipsychotics(Figures 33.1 and 33.2). A combination of moodstabilizers and atypical antipsychotics is oftenadvocated if there is no response to single-medication treatments. However, some argueagainst this, as trials of sodium valproate [26]and oxycarbazepine [27] have been negative. Thechoice of medication depends on the phase of theillness, presence of psychosis, presence of rapidcycling, risk of side effects, and, crucially, patientand family acceptance. Atypical antipsychotics arerecommended for treating psychotic symptomsbut they also act as mood stabilizers. Premature

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Stage 2 Alternate mood stabiliser or atypical antipsychotic

Stage 3 Alternate mood stabiliser and atypical antipsychotic

Stage 4 Combination of two mood stabilisers & atypical antipsychotic

Stage 5 ECT (adolescents) Clozapineor

Stage 1 Monotherapy with mood stabilizer or atypicalantipsychotic∗

∗Mood stabilizers – lithium; sodium valproate; carbamazepine∗Atypical antipsychotics – olanzapine; quetiapine; risperidone; aripirazole

Figure 33.1 Bipolar disorder type I (BPD-I), manic, mixed, without psychosis. ECT, electroconvulsivetherapy.

discontinuation of antipsychotic medication leadsto a recurrence of psychotic symptoms in a largepercentage of cases [28].

Opinion is that medication tapering or discon-tinuation be considered if the patient has achievedremission for a minimum of 12–24 consecutivemonths. However, for many patients long-termor even life-long pharmacotherapy might beindicated.

Treatment of depression in bipolardisorderThe first-line treatment for milder depres-sion should be psychological (e.g. cognitive–behavioural therapy). In patients with bipolardisorder, selective serotonin reuptake inhibitors(SSRIs) are recommended antidepressants, butthese may need to be used alongside a moodstabilizer. The use of lamotrigine has been shownto be effective in children and adolescents [29].For severe depression with psychotic symptomsan antipsychotic, such as risperidone, with anantidepressant and a mood stabilizer would beappropriate. Electroconvulsive therapy (ECT)is recommended in severe psychotic depression,especially if there is a risk of suicide.

Psychological treatmentsFor bipolar disorder, adjunctive psychother-apy enhances the symptomatic and functionaloutcomes over a 2-year period, although thereis less evidence for early-onset cases [30]. Treat-ments that emphasize medication adherence andearly recognition of mood symptoms such aspsycho-education have stronger effects on mania,whereas treatments that emphasize cognitiveand interpersonal coping strategies, such as CBTand family therapy, have stronger effects ondepression.

Family-focused therapy for adolescents withEOBPD (13–17 years) (FFT-A) involving 21sessions over 9 months and follow-up at 2 years,showed that FFT-A was associated with a fasterrecovery from depression compared to briefpsycho-education [31]. High expressed emotion(EE) attitudes among parents are generallyassociated with an increased likelihood of relapsein EOBPD. This highlights the importance ofa family approach with FFT-A, which resultsin a greater reduction in depressive and manicsymptoms in high EE families [32]. There is apreliminary report of an open 1-year trial ofdialectic behavioural therapy with family and

213


Stage 2 Alternate mood stabiliser & atypical antipsychotic

Stage 3 Combination of two mood stabilisers & atypical antipsychotic

Stage 4 ECT (adolescents) Clozapineor

Stage 1 Monotherapy with mood stabilizerand atypical antipsychotic∗

∗Mood stabilizers – lithium; sodium valproate; carbamazepine∗Atypical antipsychotics – olanzapine; quetiapine; risperidone; aripirazole

Figure 33.2 Bipolar disorder type I (BPD-I), manic, mixed, with psychosis. ECT, electroconvulsivetherapy.

individual components for bipolar disorder [33],which may be a promising treatment.

Overall, there are clear limitations to presenttreatments, with one study finding that participa-tion in community treatment (including mood sta-bilizers) did not improve outcome at 2 years [20].

Refractory casesClozapine is recommended for refractory bipolardisorder but with caution due to the side effects.Require regular monitoring with blood tests isessential.

ECT is rarely used in adolescents, but caseseries and reports support its use in severe life-threatening psychotic depression or treatment-resistant mania. The response rate for psychoticdisorders is 50–60% [34]. ECT requires appro-priate consent, and given the mental state of thepatient this is very likely to be under appropriatelegislative powers.

SCHIZOAFFECTIVE DISORDER (SA)

The concept of schizoaffective disorder remainsproblematic. Indeed, there is little evidence fortemporal stability for the diagnosis of SA in this agegroup [35]; however, genetic studies [36] show thatbroadly defined schizoaffective disorder, bipolartype, is genetically homogeneous. Nevertheless,there are questions over the distinction betweenschizophrenia and bipolar disorder with psychosison the grounds of a largely shared genetic basis,with the exception of copy number variations [37].

ACKNOWLEDGEMENT

Acknowledgement goes to Anthony RichardJames for the helping to prepare the manuscript.

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[2] American Psychiatric Association. (2000) Diagnos-tic and Statistical Manual of Mental Disorders, 4thedn, Text Revision. Washington, DC: APA.

[3] Leibenluft E, Charney DS, Towbin KE, BhangooRK, Pine DS. (2003) Defining clinical phenotypesof juvenile mania. American Journals of Psychiatry160, 430–7.

[4] Axelson D, Birmaher B, Strober M et al. (2006)Phenomenology of children and adolescents withbipolar spectrum disorders. Archives of GeneralPsychiatry 63, 1139–48.

[5] Loranger AW and Levine PM. (1978) Age at onsetof bipolar affective illness. Archives of General Psy-chiatry 35, 1345–8.

[6] Strober M and Carlson G. (1982) Bipolar illness inadolescents with major depression: clinical, genetic,and psychopharmacologic predictors in a three-to four-year prospective follow-up investigation.Archives of General Psychiatry 39, 549–55.

[7] Lewinsohn P, Klein DN, Seeley JR. (1995) Bipolardisorders in a community sample of older ado-lescents: prevalence, phenomenology, comorbidity,and course. Journal of the American Academy ofChild and Adolescent Psychiatry 34, 454–63.

[8] Carlson GA and Kashani JH. (1988) Manic symp-toms in a non-referred adolescent population. Jour-nal of Affective Disorders 15, 219–26.

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[9] Costello EJ, Angold A, Burns BJ, Erkanli A, StanglD, Tweed DL. (1996) The Great Smoky Moun-tains Study of Youth. Functional impairment andserious emotional disturbance. Archives of GeneralPsychiatry 53, 1137–43.

[10] Brotman MA, Schmajuk M, Rich BA et al. (2006)Prevalence, clinical correlates, and longitudinalcourse of severe mood dysregulation in children.Biol Psychiatry, 60,991–7.

[11] Kaufman J, Birmaher B, Brent D et al. (1997) Sched-ule for Affective Disorders and Schizophrenia forSchool-Age Children-Present and Lifetime Version(K-SADS-PL): initial reliability and validity data.Journal of the American Academy of Child andAdolescent Psychiatry 36, 980–8.

[12] Geller B, Zimerman B, Williams M et al. (2001)Reliability of the Washington University in St.Louis Kiddie Schedule for Affective Disordersand Schizophrenia (WASH-U-KSADS) mania andrapid cycling sections. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 40,450–5.

[13] Youngstrom EA, Gracious BL, Danielson CK, Fin-dling RL, Calabrese J. (2003) Toward an integrationof parent and clinician report on the Young ManiaRating Scale. Journal of Affective Disorders 77;179–90.

[14] Biederman J, Faraone SV, Wozniak J, Mick E,Kwon A, Aleardi M. (2004) Further evidenceof unique developmental phenotypic correlates ofpediatric bipolar disorder: findings from a largesample of clinically referred preadolescent childrenassessed over the last 7 years. Journal of AffectiveDisorders 82(Suppl. 1): S45–58.

[15] Wozniak J and Biederman J. (1997) Mania in chil-dren with PDD. Journal of the American Academyof Child and Adolescent Psychiatry 36, 1646–7.

[16] McClellan J and Hamilton JD. (2006) An evidence-based approach to an adolescent with emotional andbehavioral dysregulation. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 45,489–93.

[17] Kutcher SP, Marton P, Korenblum M. (1990) Ado-lescent bipolar illness and personality disorder.Journal of the American Academy of Child andAdolescent Psychiatry 29, 355–8.

[18] Carlson GA. (1990) Child and adolescent mania –diagnostic considerations. Journal of Child Psychol-ogy and Psychiatry 31, 331–41.

[19] Geller B, Tillman R, Craney JL, Bolhofner K. (2004)Four-year prospective outcome and natural historyof mania in children with a prepubertal and earlyadolescent bipolar disorder phenotype. Archives ofGeneral Psychiatry 61, 459–67.

[20] Geller B, Craney JL, Bolhofner K, NickelsburgMJ, Williams M, Zimerman B. (2002) Two-year

prospective follow-up of children with a prepubertaland early adolescent bipolar disorder phenotype.American Journal of Psychiatry 159, 927–33.

[21] Birmaher B, Axelson D, Goldstein B et al. (2009)Four-year longitudinal course of children and ado-lescents with bipolar spectrum disorders: the Courseand Outcome of Bipolar Youth (COBY) study.American Journal of Psychiatry 166, 795–804.

[22] Brent DA, Perper JA, Moritz G, Baugher M,Schweers J, Roth C. (1994) Suicide in affectively illadolescents: a case-control study. Journal of Affec-tive Disorders 31, 193–202.

[23] Lewinsohn PM, Klein DN, Seeley JR. (2000) Bipo-lar disorder during adolescence and young adult-hood in a community sample. Bipolar Disorders2, 281–93.

[24] Goldstein TR. (2009) Suicidality in pediatric bipolardisorder. Child and Adolescent Psychiatric Clinicsof North America 18, 339–52, viii.

[25] Kowatch RA, Fristad M, Birmaher B, WagnerKD, Findling RL, Hellander M. (2005) Treatmentguidelines for children and adolescents with bipolardisorder. Journal of the American Academy of Childand Adolescent Psychiatry 44, 213–35.

[26] Wagner KD, Redden L, Kowatch RA et al. (2009) Adouble-blind, randomized, placebo-controlled trialof divalproex extended-release in the treatment ofbipolar disorder in children and adolescents. Journalof the American Academy of Child and AdolescentPsychiatry 48, 519–32.

[27] Wagner KD, Kowatch RA, Emslie GJ et al. (2006) Adouble-blind, randomized, placebo-controlled trialof oxcarbazepine in the treatment of bipolar disor-der in children and adolescents. American Journalof Psychiatry 163, 1179–86.

[28] Kafantaris V, Dicker R, Coletti DJ, Kane JM. (2001)Adjunctive antipsychotic treatment is necessary foradolescents with psychotic mania. Journal of Childand Adolescent Psychopharmacology 11, 409–13.

[29] Biederman J, Joshi G, Mick E et al. (2010)A prospective open-label trial of lamotriginemonotherapy in children and adolescents with bipo-lar disorder. CNS Neuroscience and Therapeutics16, 91–102.

[30] Miklowitz DJ. (2008) Adjunctive psychotherapy forbipolar disorder: state of the evidence. AmericanJournal of Psychiatry 165, 1408–19.

[31] Miklowitz DJ, Axelson DA, Birmaher B et al. (2008)Family-focused treatment for adolescents with bipo-lar disorder: results of a 2-year randomized trial.Archives of General Psychiatry 65, 1053–61.

[32] Miklowitz DJ, Axelson DA, George EL et al. (2009)Expressed emotion moderates the effects of family-focused treatment for bipolar adolescents. Journalof the American Academy of Child and AdolescentPsychiatry 48, 643–51.

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[33] Goldstein TR, Axelson DA, Birmaher B, Brent D.(2007) Dialectical behavior therapy for adolescentswith bipolar disorder: a 1-year open trial. Journalof the American Academy of Child and AdolescentPsychiatry 46, 820–30.

[34] Ghaziuddin N, Kutcher SP, Knapp P et al. (2004)Practice parameter for use of electroconvulsivetherapy with adolescents. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 43,1521–39.

[35] Hollis C. (2000) Adult outcomes of child- andadolescent-onset schizophrenia: diagnostic stability

and predictive validity. American Journal of Psychi-atry 157, 1652–9.

[36] Hamshere ML, Green EK, Jones IR et al. (2009)Genetic utility of broadly defined bipolar schizoaf-fective disorder as a diagnostic concept. BritishJournal of Psychiatry 195, 23–9.

[37] Craddock N and Owen MJ. (2010) The Krae-pelinian dichotomy – going, going . . . but still notgone. British Journal of Psychiatry 196, 92–5.

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34Emerging Personality DisorderEileen VizardUniversity College London, London, UK

DEFINITIONS

TemperamentTemperament includes individual differences inself-regulation, affect, attention and activity. Thesetraits have a biological, partly genetic basis whilstat the same time their development is affectedby maturation and life experience [1]. Tempera-mental features are noted more often in youngerchildren such as babies or toddlers, who may bedescribed as having a ‘sunny’, ‘placid’ or ‘restless’temperament.

PersonalityPersonality is a more complex, multidimensionalconstruct than temperament, and this may bepartly why it is more likely to be applied toolder children and adolescents. Obvious person-ality traits such as neuroticism and extraversioncan be readily noted as well as other processesassociated with different personality types, suchas coping styles, attachment styles, motives andgoals [2].

Current thinking favours consideration of tem-peramental style and personality traits together‘Because of the significant commonalities betweentemperament and personality traits’ (Ref. [3],p. 182).

PERSONALITY DEVELOPMENT

While the exact definitions of both temperamentand personality have evolved over time [3], itis currently recognized that both will developunder the influence of interactions and transactions


between constitutional, genetic and environmentalfactors [1].

Research demonstrates both continuity andchange in personality trait development. Thus,while childhood personality traits are moderatelystable by the age of 4 years, developmentalchanges continue into adult life – though onlymoderate change is to be expected after the age of50 years [4].

CHILDHOOD PERSONALITY TRAITS ANDADULT OUTCOMES

Most research has focused on pathological out-comes with the evidence linking certain childhoodpersonality traits and behaviours with specific adultoutcomes. For instance, children showing earlyneurocognitive problems (including early diffi-cult temperament) and a ‘life course persistent’trajectory of antisocial behaviour may developconduct disorder and antisocial personality disor-der in adult life [5,6]. A small number of high-riskchildren on this trajectory start offending earlier,commit more violent offences and have higherlevels of recidivism [7–9]. This group has a sub-stantial genetic risk of psychopathy and shows‘callous unemotional’ personality traits found inadult psychopaths [10,11].

Recent neuroscientific evidence has increasedunderstanding of some childhood personalitytraits. Brain studies suggest structural differencesin the brains of children with callous unemotionaltraits [12]. There are also suggested links betweenpsychophysiological features, such as skin con-ductance measures, in early childhood and later

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psychopathy, as measured by self-report, at 28years of age [13].

However, longitudinal research looking atoutcomes for normal developmental personalitytraits is still lacking although the ‘Big Five’ model(Table 34.1) may provide a framework againstwhich positive and negative trait outcomes couldbe measured [14].

PERSONALITY ASSESSMENTAND PERSONALITY DISORDERIN CLINICAL PRACTICE

Why assess childhood personality?Clinicians do not routinely assess infant tem-perament or childhood personality. There areconcerns about applying pejorative diagnosticlabels to young children, alongside a concernthat focusing on child temperament may exertpressure on clinicians to make diagnoses ofpersonality ‘disorder’ in later adolescence. Thereare also groundless fears that personality traits areunchangeable, whereas they evolve and developthrough transactions between individuals and theirenvironments [3].

Even where underlying personality/tempera-mental traits do contribute to presentingproblems, interventions are likely to focuson their behavioural expression. For instance,interventions for childhood oppositional defiant

behaviour may take the form of parenting pro-grammes rather than beginning with an assessmentof the child’s inherent temperament.

This lack of personality assessment is regret-table as it has been suggested that treatmenteffectiveness may well be maximized whereinterventions are tailored to the personality ofyoung participants [3].

Definitions of disorder: diagnostic issuesUse of diagnostic criteria from either the Diagnos-tic and Statistical Manual of Mental Disorders, 4thedition, Text Revision (DSM-IV-TR) or the Inter-national Classification of Diseases, 10th revision(ICD-10) allows the clinician to codify any pre-senting signs of personality dysfunction in childrenand adolescents Within DSM-IV-TR it is possiblefor a child or younger adolescent to be given adiagnosis of a personality disorder, although Anti-social Personality Disorder (ASPD) can only bediagnosed at age 18 years old [15].

In community-based clinical practice (Child andAdolescent Mental Health Services, or CAMHS),it may be unusual for a child or young person topresent with the full criteria for any one personalitydisorder. However, the presence of subthreshold (afew) traits of a personality disorder does not meanthat there is no cause for concern. Rather thissituation should alert the clinician to the need forfollow-up and to reassess the child or young personto provide or to modify treatment interventions.

Table 34.1 ‘Big 5’ and possible Positive and Negative Outcomes [14].

Trait Positive outcome Negative outcome

Extraversion Social competence Promotes goodhealth; better romance/ long-termrelationships

Antisocial behaviour; callousness

Neuroticism Conscience development; guiltwhen expected

Poor relationships; relationconflict; relation abuse; lesscompetent parenting; risk forunemployment

Conscientiousness School adjustment; educationaland occupational achievement; jobperformance

Obsessive

Agreeableness Social competence; positiveparenting; responsible parenting

Exposure to risks

Openness Exploring friendliness; academicachievement

Exposure to risks

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In contrast, more complex cases seen in special-ist services (Tier 4 NHS) may fully satisfy criteriafor various personality disorders. Co-morbidity fora range of other psychiatric and behavioural disor-ders is also the norm in samples of children (andalso adults) referred to specialist services such asadolescent psychiatric units and forensic services.

In cases where there is concern about a child’spersonality traits or an emerging personalitydisorder, an assessment should be done, coveringall aspects of the child’s development includ-ing temperament, personality and family life(17; Figure 34.1). A family assessment of childrenat risk of ASPD or psychopathy is particularlyimportant given the role of family risk factors,including parental mental illness and criminality,in their development [5,6,9,14].

Lessons from clinical practiceThe following childhood precursors of personalitydisorders can be considered in assessment:

Paranoid Personality Disorder: This is uncom-mon in adolescence. Those presenting with suspi-cious, distrustful or apparently paranoid featuresshould be assessed to exclude drug abuse, par-ticularly cocaine dependency, and communicationproblems such as a hearing impairment. Delin-quent adolescents who have criminal records mayalso present as suspicious, distrustful and anti-authoritarian on the basis of negative experienceswith care and courts systems.

Schizoid Personality Disorder: Some of the diag-nostic criteria for this disorder (such as choosingsolitary activities, few close friends, emotionalcoldness, etc.) overlap with and should be dis-tinguished from other childhood conditions suchas shyness, intellectual disability and autistic spec-trum disorders.

Schizotypal Personality Disorder: Children withschizotypal features usually present to serviceswith queries about autistic spectrum disorders orincipient schizophrenia. These should be excludedwith a full mental state assessment and develop-mental history. Some schizotypal features such asbizarre behaviour and facial expressions can beseen in children with serious learning disabilitieswho are on the autistic spectrum.

Schizotypal children may show quasi-psychoticfeatures such as ideas of reference, which just stopshort of delusions. They may also feel that theyhave magical powers over others; in children fromcertain ethnic minority families, these individual,distorted magical beliefs need to be distinguishedfrom widespread cultural beliefs such as voodoo,speaking in tongues, shamanism, etc. This maybe important in the management of cases withsuspicions of child abuse or where children areseen as witches, being possessed by the devil andneeding exorcism, etc.

Anti-Social Personality Disorder (ASPD): Inpractice, children with persistent, severe conductdisorder will have a wide range of other social,emotional, educational and intellectual difficul-ties all of which need a full multidisciplinaryassessment [16,17]. Co-morbidity for psychiatricdisorders is the norm for children with persistent,severe conduct disorder including pervasivedevelopmental disorders and other disabilities[18]. Children of parents with an ASPD orpsychopathy traits may be at greater genetic riskof developing a personality disorder.

An assessment of the risk of that child devel-oping an ASPD or psychopathy should be under-taken. These cases usually involve child protectionconcerns and complex developmental disorders soa holistic assessment covering all aspects of thechild’s needs, family functioning and parentingcapacity should be undertaken (see Figure 34.1).Parental ASPD or psychopathy may also havemajor implications for the parenting, placementand care of high-risk children [19].

Borderline Personality Disorder (BPD): Adoles-cents with BPD may be comorbid for other per-sonality disorders and psychiatric disorders – acommon feature amongst disturbed forensic pop-ulations [8]. The life course outcome for indi-viduals with BPD suggests that the dysfunctionalbehaviour will wane in their 30s and 40s. Mean-while, clinical experience shows that these individ-uals can create havoc amongst their own families,within agencies and in society. Hence, identifica-tion of adolescents at risk of acquiring BPD isimportant in preventing offending, incarcerationand subsequent poor parenting [19].

219


CHILDSafeguarding &

PromotingWelfare

Family & Environmental Factors

Parenting Capacity

•Pre-natal and birth history•Neuro-cognitive profile•Early difficult temperament•Developmental delays•Unresponsive to punishment•Poor social skills;callous-unemotional traits;lack of empathy•Severe behaviouralproblems –torturing animals,sadism, physicaland sexualassaults onothers•IQ < 70

Cross-generational family history/genetics of ASPD/psychopathy and developmental disorders;Cruelty/sexual abuse of animals; Child exposed to domestic violence; Schedule 1 offenders infamily; Inadequate sexual boundaries; Adult sadistic and sexually perverted behaviour

6+ changes to home placementParental mental health

Parental childhood abuseParental time in care

Child removed to LA careInsecure attachment

Inconsistent parenting

Pers

iste

nt in

crea

sing

inte

rper

sona

l vio

lenc

e

thro

ugh

child

hood

Chi

ld‘s

Dev

elop

men

t Nee

ds

Figure 34.1 NCATS Emerging Severe Personality Disorder (ESPD) assessment triangle [17].

Histrionic Personality Disorder: Histrionic Per-sonality Disorder does not present frequently toCAMH services until later in adolescence. Nev-ertheless, the shallow and transient nature ofemotional relationships achieved by individualswith Histrionic PD suggests that identification andtreatment of adolescents at risk of this disorderwould be beneficial for them and their families ofprocreation.

Narcissistic Personality Disorder: Few adoles-cents present to clinical services solely withmarked narcissistic traits. However, narcissisticattitudes may be seen in other PDs, such as theadolescent sex offender with an ASPD who alsohas a strong narcissistic sense of entitlement (toabuse whom he pleases) but who fails to fulfilcriteria for Narcissistic PD.

If narcissistic traits persist after adolescence intolater life, such individuals may have difficulties inadjusting to the inevitable limitations of the ageingprocess. In some adult individuals this may presentas a ‘Peter Pan’ or denying attitude towards grow-ing older with attempts to recapture a mythicalyouth through surgery, inappropriately youthfuldressing, etc.

Avoidant Personality Disorder: There are over-laps between Avoidant Personality Disorder andmany other disorders such as social phobia, Depen-dent Personality Disorder, and paranoid, schizoidand schizotypal disorders. Caution is needed inapplying this diagnosis to children and youngpeople, some of whom may have acculturationproblems following immigration or may simply beshy adolescents passing through a normal develop-mental phase.

Dependent Personality Disorder: Crucially, thedegree of dependency on others should be ageinappropriate and situation inappropriate. Forinstance, adolescents may expect their parentsto take all decisions about which friends theyshould have and how they should spend theirfree time. With younger children who may showapparent traits of Dependent Personality Disor-der, great caution should be taken in applyingthe diagnosis because dependent behaviour maybe developmentally appropriate in many youngerchildren.

Some victimized children may show signs of anattachment disorder, aspects of which may overlapwith Dependent Personality Disorder. Alterna-tively, the child’s cultural norms may be such that

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acquiescent or passive behaviour could be con-fused with dependency.

Obsessive-Compulsive Personality Disorder:Obsessive-Compulsive Personality Disorder(OCPD) should be distinguished from Obsessive-Compulsive Disorder (OCD). The presence oftrue obsessions and compulsions differentiatesOCD from OCPD, where gaining control oversituations is a key element.

In practice, many young children may passthrough an age appropriate phase where theyshow apparently obsessional characteristics suchas arranging their toys or possessions in a particu-lar order, lining up their food on the plate to eat in aset sequence, etc. These behaviours are usually ageappropriate and will pass in time. Adolescents withhobbies that, for instance, involve collecting andcategorizing items and acquiring extensive knowl-edge of a particular hobby topic, such as football,may present as obsessive or ‘nerdy’ but will usuallygrow out of this phase and move on to anotherinterest, likely to be less obsessively followed.

Personality Disorder Not Otherwise Specified(NOS): This diagnosis is useful for those who donot completely fulfil criteria for a particular PDbut show one or more traits of several PDs.

CONCLUSIONS

Natural pathways exist that take the infant througha series of physical, emotional, cognitive and socialdevelopmental stages towards childhood, adoles-cence and adult life [20]. Links appear to existbetween infant temperament, childhood personal-ity traits and adolescent personality styles.

Empirical research has not yet tracked theselinks across childhood and adolescence withdetailed reference to a wide range of personalitytraits and outcomes including diagnoses of adultpersonality disorders. An exception to this isthat adult outcomes for children with certainpersonality traits and behavioural profiles, suchas conduct disorder, are now reasonably wellmapped [5].

Personality disorders carry a burden of psy-chopathology, relationship and parenting prob-lems in adult life [19]. Hence, it seems advisablefor mental health assessments of children and ado-lescents routinely to include reference to normal

personality traits and to any signs of emergingpersonality disorders.

ACKNOWLEDGEMENTS

I would like to acknowledge the support of theNational Society for the Prevention of Cruelty toChildren (NSPCC) in funding my clinical servicefrom which my current clinical experience withchildren and adolescents is derived and also forNSPCC’s support of my academic work, includingthis chapter.

REFERENCES

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[2] McAdams DP and Pals JL. (2006) A new Big Five:fundamental principles for an integrative science ofpersonality. American Psychologist 61, 204–17.

[3] Caspi A and Shiner R. (2008) Temperament andpersonality. In: Rutter M, Bishop D, Pine D, ScottS, Stevenson J, Tharpar A (eds), Rutter’s Child andAdolescent Psychiatry, 5th edn. Wiley-BlackwellPublishing, pp. 182–98.

[4] Roberts BW and DelVecchio WF. (2000) Therank-order consistency of personality traits fromchildhood to old age: A quantitative review of lon-gitudinal studies. Psychological Bulletin 126, 25–30.

[5] Moffitt TE. (1993) Adolescence-limited and life-course-persistent antisocial behaviour: A devel-opmental taxonomy. Psychological Review 100,674–701.

[6] Rutter M, Giller H, Hagell A. (1998) AntisocialBehaviour by Young People. Cambridge: Cam-bridge University Press.

[7] Viding E. (2004) Annotation: Understanding thedevelopment of psychopathy. Journal of Child Psy-chology and Psychiatry 45, 247–60.

[8] Hodgins S. (2007) Persistent violent offending:what do we know? British Journal of Psychiatry190(Suppl. 49):s12–s14.

[9] Vizard E, Hickey N, McCrory E. (2007) Devel-opmental trajectories towards sexually abusivebehaviour and emerging severe personality dis-order in childhood: the results of a three yearUK study. British Journal of Psychiatry 190(Suppl.49):s27–s32.

[10] Viding E, Blair RJR, Moffitt TE, Plomin R. (2005)Evidence for substantial genetic risk for psychopa-thy in 7 year olds. Journal of Child Psychology andPsychiatry 46, 592–7.

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[11] Viding E, Frick PJ, Plomin R. (2007) Aetiology ofthe relationship between callous-unemotional traitsand conduct problems in childhood. British Journalof Psychiatry 190(Suppl. 49):s33–s38.

[12] De Brito SA, Mechelli A, Wilke M et al. (2009) Sizematters: increased grey matter in boys with conductproblems and callous-unemotional traits. Brain 132,843–52.

[13] Glenn AL, Raine A, Venables PH, Mednick SA.(2007) Early temperamental and psychophysiolog-ical precursors of adult psychopathic personality.Journal of Abnormal Psychology 116, 508–18.

[14] Salekin R. (2009) Developmental pathways towardschildhood psychopathy: The potential for effectiveearly intervention. In: Vizard E, Jones A, VidingE, Farmer E, McCrory E (eds), Early Interven-tion in Personality Disorder: MST and OtherTreatments for Socially Excluded High Risk/HighHarm Children and Families. Available at:http://www.personalitydisorder.org.uk/resources/emerging-pd/.

[15] American Psychiatric Association (APA). (2000)Diagnostic and Statistical Manual of Mental Disor-ders, Text Revision, 4th edn. Arlington, VA: APA.

[16] Utting D, Monteiro H, Ghate D. (2007) Interven-tions for children at risk of developing antisocialpersonality disorder. Report to the Department ofHealth and Prime Minister’s Strategy Unit. London:Policy Research Bureau.

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[18] Bladon E, Vizard E, French L, Tranah T. (2005)Young sexual abusers: a descriptive study of aUK sample of children showing sexually harmfulbehaviours. Journal of Forensic Psychiatry and Psy-chology 16(1):109–26.

[19] Adshead G. (2003) Dangerous and severe parentingdisorder? Personality disorder, parenting and newlegal proposals. Child Abuse Review 12, 227.

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Section 6

Assessment

Diagnostic classification: current dilemmas and possible solutions

35Diagnostic Classification: CurrentDilemmas and Possible SolutionsEric TaylorInstitute of Psychiatry, King’s College London, London, UK

WHAT’S NEW

• A draft for the DSM-5 classificationscheme has been prepared and postedon the internet.

• It provides more developmentalconsiderations, such as psychosis riskand adult ADHD.

• There are some new categories ofparticular relevance to child psychiatry,including temper dysregulation,non-suicidal self-injury and acallous-unemotional type of conductdisorder.

Developments in classification can sometimes havea major impact on the clinical world. The Diag-nostic and Statistical Manual of Mental Disorders,Third Edition (DSM-III) and International Clas-sification of Mental and Behavioural Disorders inChildren and Adolescents, Ninth Revision (ICD-9)were both great steps forward for the ability ofclinicians to communicate effectively with eachother and the world of research. Inter-rater relia-bility started to be good enough for effective audit,sharing of clinical lessons and establishing researchseries [1]. The revised third edition of DSM (DSM-III-R) and DSM-IV refined the process, added newcategories and responded to research findings [2].ICD-10 came into greater harmony with DSM and


developed algorithmic criteria for research pur-poses. They were not, however, conceptual leapsforward. Revisions into DSM-5 and ICD-11 arenow underway, so it is timely to consider what theyhave to achieve.

The next big conceptual advance in clas-sification is likely to be the establishment ofpathophysiologically grounded diagnoses. Weaspire to use advances in neuroscience to establishpsychiatric illnesses that can be assessed objec-tively and treated rationally. Some might arguethat the time for this has come. Should we use ourknowledge – for instance of dopamine changes inschizophrenia, or frontal and striatal underacti-vation in attention deficit hyperactivity disorder(ADHD) – to redefine conditions in a way thatwould allow diagnosis by neuroimaging? Theanswer must be ‘not yet’. Our neurobiologicalknowledge is based on group studies; withingroups there is considerable heterogeneity andbetween diagnostic groups there is considerableoverlap. The implications for individual diagnosiswill need better understanding before a radicalchange is feasible.

The groups working on DSM-5 include somewhose purpose is to consider whether a prelim-inary regrouping of disorders is feasible on thebasis of present neuroscience knowledge. Shouldwe, for instance, group ADHD with the disor-ders of addiction on the basis of neurochem-istry, rather than with disruptive behaviour dis-orders on the basis of longitudinal course, orwith neurodevelopmental disorders on the basis

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of neuropsychological findings? Even in this well-studied condition, controversy is strong. It seemsunlikely that a broad consensus can be achieved inthe near future.

If a new basis for classification has not yetarrived, is there still a need for revising the clas-sification schemes? Any revision brings penalties.Knowledge and practice based on existing entitiescan be outdated unnecessarily, and apparently triv-ial changes in wording can have marked effects onthe prevalence of conditions. I would argue thatthe current schemes, valuable though they havebeen, contain some flaws that limit their usefulnessand can be amended.

• We have increasingly learnt that many syn-dromes behave as continua in the population. Asa result, cut-offs are often arbitrary, reliabilityis low around the point of cut-off, and there isscope for a runaway expansion of diagnoses.

• The relationship between symptoms andimpairment of function is often remote [3]. Inthe absence of clear points that delimit thepathological from the normal, we often haveto require impairment as a necessary conditionfor diagnosis. There are disadvantages forprevention, and it is rather offensive if a personwho has compensated well should no longer beconsidered as having the condition.

• For many conditions the threshold for diagnosisis set by a fixed number of symptoms. Thishas proved useful, but takes too little accountof possible differences between the genders orbetween different levels of maturity [4].

• Many childhood conditions have proved to per-sist into adult life. The changing circumstancesand demands of adulthood mean that differentaspects of the condition should be given moreweight in the diagnostic criteria. Diagnosticcriteria may therefore have to change in theirnature and number in order to do justice todevelopmental changes.

• The features of an adult-type disorder in child-hood need recognizing – but they may be verysimilar to those of other conditions. For instance,the antecedents of schizophrenia may includeclumsiness, neuropsychological changes, socialincompetence and odd thinking. These features,however, may also be seen in other neurode-velopmental problems, including autism spec-trum. This could result in a mistaken diagnosis of

‘pre-schizophrenia’ or ‘psychosis risk’ for a childwith a different condition [5].

• Most children with one DSM diagnosis alsohave others. This mirrors reality: problems inyoung people’s mental life are often multiple.The resulting proliferation of diagnoses in theindividual case is conceptually untidy, does notallow for some problems being complicationsof an underlying disorder, and makes fordifficulties in patients’ understanding and inthe commissioning and planning of services.‘Comorbidity’ between disorders is a topic ofactive research but we do not yet have theclarity of understanding that would let us coperationally with these overlaps [6].

• The sheer number of categories available,the overlap between some of them, and thepossibility of impaired people meeting nodiagnosis, all limit practicality. They deter non-specialists from using the psychiatric scheme.ICD-10 has avoided some of this difficulty by asystem of descriptive and exclusion categoriesthat create an expectation of a single diagnosisfor most people. On the other hand, singlediagnoses can lead to an under-recognition ofnon-classical features of disorder. Obsessive-compulsive problems, for instance, may needrecognition even in a person in the autismspectrum.

The approaches to solving some of these dif-ficulties can be illustrated from specific disorders:the so-called paediatric bipolar disorder, thepresence of ADHD in adult life, the presenceof post-traumatic stress disorder in early life, the‘lumping’ or ‘splitting’ of conditions within theautism spectrum and the description of syndromesinvolving self-harm (Table 35.1).

PAEDIATRIC BIPOLAR DISORDER

The traditional definition of bipolar disorderincludes a requirement for distinct periodsof altered mood with the key qualities ofmania – euphoria, grandiosity and irritability. Inadult psychiatry, however, it has become plain thatmany severely affected people have a conditioninvolving very rapid and frequent cycles of mood.

Irritability is a very common problem of childmental health. It often challenges both parentsand schools and is a very frequent reason for

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Table 35.1 Some issues in currentclassification.

Problem Example DSM-5 proposal

Unvalidateddistinctions

Autism-relatedconditions

Severitydimensionswithin oneautismspectrum

Gender/ageadjustment

Adult ADHDChild PTSD

Newage-specificcriteria

Frequentcomorbidity

Irritability Cross-cuttingdimensions

Manycategories

Anxiety-baseddisorders

Superordinateclustering

Heterogeneitywithincategories

Self-harm New category ofnon-suicidalself-injury

NOScategories

Paediatricbipolardisorder

New conditionof temperdysregulation

ADHD, attention deficit hyperactivity disorder; DSM-5,Diagnostic and Statistical Manual of Mental Disor-ders, 5th edition (draft); PTSD, post-traumatic stressdisorder.

referral. The symptom of irritability, however, isa feature of several different disorders. In orderto do justice to the problems of children withintense and volatile moods, the proposal has beenmade that the diagnosis of bipolar disorder shouldbe expanded in children, to include non-episodicstates of angry outbursts, not necessarily accom-panied by euphoria [7]. The result, however, hasbeen a disquietingly large increase in the rates ofdiagnosis and in the prescription of neurolepticsand mood stabilizers. The issue has become highlycontroversial. DSM-IV allowed this expansion ofdiagnosis, partly because the wording of items wasnot adapted to children, and partly because thesubcategory of ‘not otherwise specified’ allowsbipolar disorder to be diagnosed even in theabsence of defining criteria.

The draft of DSM-5 therefore proposes a newdisorder: ‘temper dysregulation disorder with dys-phoria’. This is intended to provide a conceptualhome for severely affected children who combine

a persistent mood of misery or anger with verymarked irritable outbursts. There is some empiricalsupport for such a category, for instance in the ten-dency of the condition to persist in the same formover time, and neuroimaging distinctions betweenchildren with ‘severe mood dysregulation’ andthose with classic bipolar disorder. Nevertheless,such a category may prove to have disadvantages.It will usually coexist with other conditions (e.g.oppositional disorder, depression or dysthymia). Itdoes not yet meet all the stringent requirements fora new disorder. The name of ‘temper dysregula-tion’ could invite a pathologizing of normal childishtempers – even though the criteria of the new dis-order are written to describe only a high level ofseverity. Field trials will therefore be very useful toassess the robustness of the new diagnosis in prac-tice and its knock-on effect on other conditions.

There is a general issue of how to deal withcommon symptoms that cut across existing diag-nostic categories. My own view is that this is bestdealt with by the use of cross-cutting dimensionsthat allow the clinician to describe not only thepresence but also the severity of clinical problemssuch as irritability, anxiety and social impairment.It remains to be seen how far, and in what waythe revised DSM will cope with this. Such a revi-sion could be a significant advance in the conceptsavailable to clinicians.

ATTENTION DEFICIT HYPERACTIVITYDISORDER (ADHD) IN ADULTS

There have been advances in knowledge, bothfrom surveys in adult populations and from follow-up studies into adult life of people with ADHD.They have indicated that people can be impairedby symptoms of ADHD that fall short of the fullcriteria for the diagnosis. The DSM-5 work groupshave responded to this with a review of the studies,and a consequent relaxation of the number ofcriteria that have to be met by people over theage of 18. There are more examples provided ofinattentive, overactive and restless behaviours thatcan be shown by adults. The requirement for anonset of disorder before the age of 7 has alsobeen relaxed, and now expects only the presenceof symptoms (not necessarily impairment) beforethe age of 12 years. The practical effects are likelyto be a substantial increase in the recognition andtreatment of ADHD in adult life.

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Other ADHD issues are unresolved. Thequestion of different criteria for males and femaleshas not been satisfactorily answered. The differentsubtypes (inattentive, hyperactive-impulsive andcombined) have failed to generate significantdifferences between them in course and associ-ations; so there would be a case for abolishingthe distinctions. On the other hand, ‘inattentivesubtype’ is popular with clinicians. The apparentlack of validity may stem from the inclusionof cases who are only just subthreshold forhyperactivity-impulsivity. A more strictly definedinattentive subtype could be useful. Such childrenmay be sluggish in their cognitive tempo, and mayhave a course characterized more by educationaland occupational failure than by the conductproblems associated with hyperactivity. System-atic review, however, failed to find a clear basis fora cut-off, and the issue remains unresolved – as itwas in DSM-III, DSM-III-R and DSM-IV.

DISRUPTIVE DISORDERS

The current distinction between oppositional andconduct disorders seems likely to remain, becauseof the affective components in the definition ofoppositional disorder (e.g. anger and spitefulness).It remains to be seen whether this will still benecessary if the affective component proves to besatisfactorily described by ‘temper dysregulationdisorder with dysphoria’ (or whatever nameis eventually agreed for conditions of severeemotional dysregulation).

The callous and unemotional aspects of somechildren and adults with conduct disorder havebeen increasingly recognized in recent research. Asubcategory or specifier within conduct disorderwill therefore be included in the DSM-5, toprovide a standard way of diagnosis. The name,however, is controversial. On the one hand‘callous-unemotional’ sounds as if it could bestigmatizing language and hard to explain tofamilies. On the other hand, the ‘C-U’ phrase iswidely used and easy to understand.

SELF-INJURY

Harming oneself is not a disorder, but a featureof other conditions – including depression andborderline personality disorder (BPD). There is,

therefore, a problem for the diagnostician whenthe behaviour of self-harm is not accompaniedby a diagnosable condition. This can lead to theloose use of a diagnosis such as BPD; and it cansometimes lead to inappropriate practice. Manyforms of self-injury do not include suicidal ideationbut may lead to inappropriate hospital admission.A new category is therefore being proposed – non-suicidal self-injury – to provide a way of describingthe infliction of superficial skin injury without theintent to endanger life. It is a way of coping withthe heterogeneity of self-harming actions.

FURTHER PROGRESS

The development of the fifth edition of theDiagnostic and Statistical Manual of the AmericanPsychiatric Association has reached the stage ofdraft proposals. This chapter cannot, of course,describe all the changes. Interested readers canpursue them, and references, further on thewebsite (www.dsm5.org). The next stage will bethat of field trials focusing on the reliability andacceptability of new conditions and new criteria.There is still much to do, and there are likely to beplenty of further changes.

The 11th edition of the World Health Organiza-tion’s classification of disease is also in preparation,though not yet as advanced. It will be importantthat the detailed algorithms and multiple cate-gories of the DSM can be transformed into asimpler system for the use of non-psychiatrists. Inprimary care, for example, the need is for broadcategories that will generate appropriate actionand suitable referral when needed. We can there-fore expect to see some clustering of disorders intosuperordinate classes. This will need to be basedupon clinical value rather than brain physiology orgenetic aetiology.

REFERENCES

[1] Cantwell D and Baker L. (1988) Issues in the clas-sification of child and adolescent psychopathology.Journal of the American Academy of Child and Ado-lescent Psychiatry 27, 521–33.

[2] American Psychiatric Association. (2000) Diagnosticand Statistical Manual of Mental Disorders, 4th edn,Text Revision. Washington, DC: American Psychi-atric Association.

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[3] Angold A, Costello EJ, Farmer EM et al. (1999)Impaired but undiagnosed. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 38,129–37.

[4] Shaffer D, Campbell M, Cantwell D et al. (1989) Childand adolescent disorders in DSM-IV: Issues facingthe work group. Journal of the American Academy ofChild and Adolescent Psychiatry 28, 830–5.

[5] Taylor E and Rutter M. (2008) Classification. In:Rutter M, Bishop D, Pine D et al. (eds), Rutter’s

Child and Adolescent Psychiatry, 5th edn. Oxford:Wiley-Blackwell Publishing, pp. 18–31.

[6] Jensen PS, Martin D, Cantwell DP. (1997) Comor-bidity in ADHD: Implications for research, practiceand DSM-V. Journal of the American Academy ofChild and Adolescent Psychiatry 36, 1065–79.

[7] Dilsaver SC and Akiskal HS. (2004) Preschool-onsetmania: Incidence, phenomenology and family his-tory. Journal of Affective Disorders 82(Suppl. 1),S35–S43.

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36Paediatric NeuropsychologicalAssessment I: An Assessment FrameworkJudith MiddletonThe Child Brain Injury Trust, Oxford, UK

This chapter sets the framework for the companionchapter of Hohnen and Gilmour (see Chapter 37)by discussing theory and issues in neuropsycholog-ical assessment and intervention. A summary ofthe characteristics and parameters of recent andwidely used neuropsychological tests is presentedin Chapter 37.

THEORETICAL BACKGROUND

What is neuropsychological assessment?The purpose of a neuropsychological assessmentis to raise hypotheses, which may have a neuro-biological basis, to explain functional behaviourand relate this to any underlying neuropathologyin order to inform treatment, rehabilitation andeducation. What it is not, is a reductionist useof test results alone to diagnose neuropathology.Neuropsychological assessment is a complexprocess involving the application of carefullyselected tests in conjunction with comprehensiveclinical interviewing and specialized observation,encompassing the child’s functioning and theirfamilial and social context. A useful summary ofwhat is involved in terms of collecting information,decision-making in the assessment process andinterpretation can be found in Goldstein andMcNeil [1].

Assessment may be requested when there is: (i)known underlying neuropathology such as trauma,stroke, infections, neoplasms, disease, hypoxia oriatrogenic causes; (ii) mental health issues, forexample attention deficit hyperactivity disorder


(ADHD); (iii) congenital or syndromic causes;(iv) systemic and metabolic disorders impactingthe central nervous system; (v) unknown neu-ropathology in a child who is not functioning asexpected, particularly when there is unevennessin cognitive development; and (vi) for litigationpurposes, specifically following accidents, or acombination of these. A request for assessmentwith no explanation should occur rarely: if thisoccurs, it is critical to respond by asking about theconcerns driving the referral and the purpose ofthe assessment. There are times when it is decidedthat neuropsychological assessment is not relevantor appropriate. Such a decision can be taken at anytime during the process. When this occurs, it shouldbe stated clearly, with reasons for the decisiongiven to both referring clinicians and the family.

While psychosocial reasons may explainbehaviours in children referred to neuropsycho-logical services, clinicians working with childrenin mental health should always consider whetherbehaviour has a possible neuropathological cause.For example, an unreported brain injury acquireda few years ago may explain failure to listen,impulsiveness and forgetfulness, which mightotherwise be seen as oppositional behaviour.

The importance of a developmental modelA developmental model characterized by changeis needed when assessing children. Neuropsycho-logical functioning changes with age in adults,but change is relatively slow and assessmentsat ages 25 and 45 may show relatively small

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differences, except in the case of underlyingpathology. In contrast, change, often rapid, isexpected in children. Alteration in the trajectoryof previous normal development, or failure todevelop between two assessment points is thecritical issue. Even a relatively small loss of skillsshould be taken seriously in children even thoughthis can be a feature of typical development.

Neurological damage may lead to differentproblems depending on the age at injury, andthe age at which assessment is undertaken. Forinstance, damage to language areas at 3 or 4 yearsof age may lead to problems coping with complexgrammatical structures, but at puberty might resultin problems with abstract thought and reasoning.If injury occurs at a time of rapid change, thereis an increased likelihood that functional damagewill be greater than when development is slow.Knowledge of normal development is thereforean absolute prerequisite in assessment andformulation in child neuropsychology.

Theoretical models of childneuropsychological assessmentTwo of the more influential models of childneuropsychological assessment are a functional-organizational approach [2] emphasizingbrain–behaviour relationships and relationshipsbetween behaviours, and a systemic approach [3]emphasizing the interactive interplay between theneurobiological, psychological and environmentalaspects of development. The former model consid-ers three levels of information in assessment: thebehavioural symptoms, the associated cognitiveprofile and the neuropathology, and emphasizesthe importance of change. The latter modelemphasizes both the neurological and psycho-logical aspects in terms of developmental timing,the context and neuropsychological systems, andparticularly three different axes of brain structure:laterality (i.e. left/right), anterior/posterior andcortical/subcortical.

KNOWLEDGE BASE AND COMPETENCIES

Clinicians working in mental health will have com-petency at carrying out basic tests such as theWechsler Intelligence Scale for Children (WISC-IV) [4], but will need more specialist competenciesto administer and interpret neuropsychologicalassessments [5], as well as specialist knowledge

of neuropsychology. Table 36.1 summarizes bothcompetencies and breadth of knowledge required.

INFORMATION GATHERING

Psychologists carrying out a neuropsychologicalassessment will themselves need to gather a widerange of information and interview children andfamilies before commencing testing. Reviewing themedical notes goes beyond mental health recordsor family doctor notes, and should include hos-pital records, where accessible. If questionnairesand rating scales can be completed by familiesbefore the young person and family are seen,inconsistencies and concerns can then be inves-tigated in depth during the clinical interview. Timecan be saved, which is important in a service whereassessments are time-consuming. Throughout theinformation-gathering process hypotheses can beregularly created and revised, that is after review-ing medical/hospital notes, at the clinical interview,on the basis of test results and observations duringassessment, and so on, before a final (working)formulation is reached.

ASSESSMENT ISSUES

As well as the neuropathology, there are otherfactors that will influence neuropsychological func-tioning and hence the outcome of the assessment,which need to be considered.

Environmental influencesThe social, cultural and ethnic context of devel-opment of any child referred to psychologicalservices at any time is important. This is criticallyso when planning formal testing. Judging theappropriateness of undertaking a psychometricassessment will include whether English is asecond language, whether the child has hadexposure to different social mores, experiencesand educational systems, and general psychosocialinfluences on development.

Informal observationsGeneral observations of a child during interviewand while carrying out tests, the child’s strategy,engagement, application and effort can be usefulas a means of interpreting results and in finalformulation. The validity and reliability of such

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Table 36.1 Areas of specialist knowledge and competency required when undertakingneuropsychological assessment.

Area Breadth/examples

Specialist knowledge

Fundamentals of neurobiology anddevelopment

Neurobiological development; theoretical models ofbrain/behaviour development, linkages to experiences andatypical environments

Clinical developmental cognitiveneuroscience

Basic principles underlying common brain/behaviourtechniques, e.g. neuroimaging and electrophysiology

Development of sensory, motor andcognitive neural systems

Neuroanatomy; neural cognitive systems and cognitivetrajectories; neural plasticity and reorganization

Developmental disorders, theirprofiles and functional implications

Neuropsychological systems such as executive and memorysystems; and neuropsychological disorders such as epilepsy,hydrocephalus, consequences of abuse and neglect, etc.

Neurodevelopmental assessment inkey phases

Infancy, early childhood/preschool, childhood,adolescence

Rehabilitative practice ineducational and specialist settings

Professional issues for paediatricneuropsychologists

Maintenance of competence; working in legal contexts,etc.

Specific competencies

Test selection for specificneuropsychological problems

Taking account of age, function, test psychometricproperties

Test administration andbehavioural observations duringtesting

Test scoring

Test analysis and interpretation Taking account of behaviour during testing, and feedback,including writing both specialist reports and reportscomprehensible to carers

microanalysis may be questionable, so hypothesesderived from this informal information need to betreated cautiously and corroborated by interviewsand test results. Any observed behaviour may giverise to a number of hypotheses. For example, achild giving short, inadequate answers in the Ver-bal Comprehension subtest of the WISC IV couldhave: (i) a hearing problem; (ii) poor attention;(iii) poor language comprehension; (iv) failure tounderstand the meaning; (v) a memory problem;(vi) speech difficulties; (vii) word finding difficul-ties; (viii) problems with planning and initiating

a response; (ix) anxiety or depression; and (x)oppositional behaviour, or a combination of these.See Table 36.2 for a more detailed description ofobservations and presenting problems [6].

Setting and task characteristicsWhen considering children’s test results and theirbehaviour during assessment, it is important tobear in mind the importance of both the char-acteristics of the testing situation and the taskdemands [7]. This analysis may explain why somechildren do well in one-to-one testing, but poorly

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Table 36.2 Examples of observations during assessment, by domain.

Domain Example of observations

Attention Needing regular refocusing to taskRequesting questions/instruction be repeatedEarly failures but passing more difficult subtest itemsSlowing down and stopping halfway through subtest itemsPartial understanding of longer instructionsNeeds gesture or verbal prompts to scan visual informationFiddles and fidgets

Memory andlearning

Forgets questions/tasksFrequent requests for questions/instruction to be repeatedQualitative analysis of how stories/word list are recalled (e.g. correct sequence)Forgets where consulting room is after breakLooks for prompts/clues from clinician or parents

Language Needs simplification of questions/instructions (where possible)Socially quietFailure to initiate conversationGrammatical and articulation errorsWord finding difficultiesSimplified or inadequate verbal answersDifficulties making inference or in abstractionBetter at leading/controlling than following conversation

Visuoperceptualskills

Writing/drawing untidy, uneven, too large or too smallPoor visual scanning strategiesConsistently misses information in one part of visual fieldBetter with concrete than abstract visual informationSeems unable to ‘get the picture’

Executive skills Poor task planningNeeds prompting to initiate tasksStarts impulsively and tries to restartFailure to change strategy despite restartingPerseveration in response to tasksUnaware and/or unconcerned about failureSocially inappropriate/disinhibitedBizarre or unusual answers

in school or at home. The testing situation itselfis usually quiet and distraction free, unlike manyclassrooms, although like many classrooms it isstructured and relatively contained. Converselyhome may be quieter but freer and less structured.Consequently children, who need help and struc-ture to focus and sustain attention and are easilydistracted by what is going on around them, maydo better in testing than elsewhere. Others may

become anxious in a setting where they becomethe focus of attention themselves.

Individual tasks in tests may be structuredor unstructured, timed or untimed, and requirechildren to work quickly or at their own pace.Open-ended questions or forced choice answers,predictability and prompting are characteristicof some tasks and not others. All this affects anindividual child’s test performance.

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INFORMAL ASSESSMENT

It is important to note that while testing is com-monly necessary, neuropsychological assessmentcan be made without testing, where childrencannot or will not be formally tested. It isstill possible to gain critical neuropsychologicalinformation through talking systematically tothem about everyday activities, a process that isin any event helpful prior to testing. For instance,discussion with a 13-year-old, who refused to betested, about his model-building hobby revealed:(i) his approximate level of reading ability andunderstanding through his intelligent discussionof the content of an adult magazine on model-building; (ii) his executive skills when talkingabout how he initiated and planned buildinghis models, and organized the parts and toolshe needed before starting, and his intention tosave future birthday money to purchase furthermodel kits; (iii) his memory and attention throughhis speaking about visiting an exhibition aboutmodel-building, and his ability to focus andconcentrate for 2 to 3 hours while he worked;and (iv) his social awareness when asked aboutissues relating to a model-building club and themodel-building community; and the importanceof safety when using adhesives and Stanley knives.

CONCLUSIONS: CREATING THE BALANCE

Neuropsychological assessment of children isa specialist, complex process, and it is time-consuming. It can take at least a half-day orcommonly longer to get an appropriate history,select, administer and score several tests, completea clinically relevant report and provide feedbackto the child and family. Given the pressures onhealth-care budgets, the time and other resourcecosts of such a process are likely to be questioned.While recognizing the importance of such issues,

the primary task of the neuropsychologist remains.This is to ensure that the assessment is sufficientlycomprehensive and accurate, and that it respondsto the needs and concerns of the child, the family,and the requests of the referrers. This will enablethe assessor to take account of the strengths andneuropsychological difficulties of the child inplanning intervention, education and care.

REFERENCES

[1] Goldstein LH and McNeil JE. (2004) General intro-duction: What is the relevance of neuropsychologyfor clinical psychological practice. In: Goldstein LHand McNeil JE (eds), Clinical Neuropsychology: APractical Guide to Assessment and Management forClinicians. Chichester, UK: John Wiley & Sons, pp.3–20.

[2] Fletcher J and Taylor HG. (1984) Neuropsychologi-cal approaches to children: Towards a developmentalneuropsychology. Journal of Clinical Neuropsychol-ogy 6, 24–7.

[3] Holmes-Bernstein J. (1999) Developmental neu-ropsychological assessment. In: Yeates KO, RisMD, Taylor HG (eds), Paediatric Neuropsychology:Research, Theory and Practice. New York: GuildfordPress, pp. 405–38.

[4] Wechsler D. (2003) Wechsler Intelligence Scale forChildren, 4th edn. San Antonio, TX: The Psycholog-ical Corporation.

[5] Berger M. (2009) A Standards-Based Approach toTraining in Psychological Testing in Clinical Psy-chology: A Discussion Paper. Occasional paper No 7.Division of Clinical Psychology, British PsychologicalSociety.

[6] Middleton J. (2004) Clinical neuropsychologicalassessment of children. In: Goldstein LH and McNeilJE (eds), Clinical Neuropsychology: A PracticalGuide to Assessment and Management for Clinicians.Chichester, UK: John Wiley & Sons, pp. 275–300.

[7] Betts J, McKay J, Maruff P, Anderson V. (2006) Thedevelopment of sustained attention in children: Theeffect of age and task load. Child Neuropsychology12, 205–22.

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Paediatric neuropsychological assessment II: domains for assessment

37Paediatric NeuropsychologicalAssessment II: Domains for AssessmentJane Gilmour1 and Bettina Hohnen2

1Institute of Child Health, University College London, London, UK2Great Ormond Street Hospital for Children NHS Trust, London, UK

INTRODUCTION

We provide here an introduction to the char-acteristics and parameters of specialist childneuropsychological assessments for clinical orresearch purposes, as a companion chapter to thatof Judith Middleton (see Chapter 36). We discussmeasurement issues, the main neuropsychologicaldomains requiring specialized assessment, somerelevant standardized assessments appropriate tothese domains, alongside a consideration of theirpsychometric properties.

WHY UNDERTAKE A SPECIALIZEDNEUROPSYCHOLOGICAL ASSESSMENT?

For the purposes of this review, specializedtests are those that describe specific aspects ofbrain function, such as memory and language, asopposed to tests of general ability (IQ). Manyspecific areas of cognitive functioning contributeto IQ; therefore one would predict that anindividual with an IQ below 70, for example(where the mean is 100 and the standard deviationis 15), would score in the low-performance bandsof specialized tasks. On the other hand, someindividuals, including those with average orhigh-range IQ scores, have a markedly low testperformance in one or more areas of specific brainfunctioning relative to general ability. Such indi-viduals are described as having a specific learningdifficulty (SLD). Specialized neuropsychological


assessment is therefore likely to be important inidentifying the nature of an SLD for single clinicalcases or groups in research.

WHEN IS A SPECIALIZEDNEUROPSYCHOLOGICALASSESSMENT JUSTIFIED?

Gaining an objective measure of IQ and attain-ment is usually the first stage of a clinical orresearch investigation into cognitive functioning,and can be obtained by full administration of anage appropriate standardized IQ assessment, suchas the Wechsler Intelligence Scales for Children(WISC-IVUK) [1]. In many cases no further test-ing is warranted, for example when an IQ testindicates that a child has general learning difficul-ties. However, there are two common scenarioswhere additional specialized neuropsychologicalassessment is justified:

• Groups or individuals with a markedly unevenIQ profile may require an assessment ofspecific cognitive functioning. Differences ingeneral-ability domains that have statisticalsignificance (i.e. the probability that thedifference found between groups could haveoccurred by chance) are, by definition, relativelycommon, but discrepancies that have clinicalsignificance (which considers how often thisdifference would be found in the population) areusually notably larger and may warrant further

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investigation. For example, individuals with adisproportionately low perceptual reasoning(PR) factor score relative to other factor scores(verbal comprehension, working memory andprocessing speed) on the WISC-IVUK may havevisual difficulties, dyspraxia (clumsiness), visualmotor integration problems or – since a highPR score depends on a swift response – simplylow motivation. Tests of specialized neuro-psychological functioning can be used to excludecompeting explanatory hypotheses.

• A child who has an attainment level significantlybelow the predicted level given their measuredIQ may have an SLD such as primary lan-guage or literacy dysfunction. It is importantto note that low attainment relative to IQ iscommon in children of school age. Many factorscould explain this profile, including emotionaland behavioural difficulties or school-based vari-ables. In other words, an SLD is a possible causefor poor school performance relative to generalability, but it is not the only feasible explanation.

MEASUREMENT CONSIDERATIONS

A number of issues should be considered whenassessing paediatric and clinical populations.

Developmental considerationsBroadly speaking there are relatively few special-ized tests appropriate for preschool children. Inpart this is because very young children are a chal-lenge to test reliably and their neuropsychologicalfunction is more difficult to capture. There area few tests that are useful adjuncts to a generalIQ assessment, such as tests of phonological pro-cessing [2], working memory [3] and declarativememory [4]. When interpreting data at this youngage, bear in mind that some children may ‘catchup’ in their test performance over time becauseof neural plasticity or behavioural compensationstrategies. For research studies in particular it isoften interesting to take a developmental approachin the assessment of specific areas of functioning.

Be sure of why the child fails a task — what istheir route to failure?The non-specific abilities required to complete agiven task should be considered, as there are manyroutes to failure. Many clinical populations havecomplex neuropsychological cognitive profiles. For

example, reading problems are proportionatelymore common in children with attention deficithyperactivity disorder (ADHD) [5]. Many, butnot all, children with ADHD perform poorly onthe Continuous Performance Task (CPT) [6], atest of selective attention. McGee et al. reportthat children with reading disorder score signifi-cantly lower than non-reading-disordered groupson the CPT [7]. For such reading-disordered chil-dren it would be wrong to conclude that a lowscore on the CPT necessarily indicates difficultywith the target skill – that is, selective attention.Reading-disordered children have difficulty pro-cessing moving visual stimuli [8]. The CPT includessuch stimuli but the aim of the task is to capturethe ability to attend to pertinent information andscreen out irrelevant data, rather than to assessgeneric visual processing abilities. In other words,the CPT identifies children with target function dif-ficulties (selective attention) and those who haveproblems with the non-specific demands of the test(processing dynamic visual stimuli).

Where possible, clinical populations should beassessed using a number of tests, presented in avariety of modalities that purport to assess thesame target function so that specific deficits canbe identified.

PsychometricsReliability and validity: Some published tests havequestionable psychometric properties. In somecases, the reference populations are inadequateand it is important to look at the ‘N’s beforeinterpreting scores with confidence. Reliability andvalidity are also important considerations whenchoosing a test and deciding how much weight toplace on findings. There is no objective cut-off butthe general consensus is that, in relation to reliabil-ity, a correlation coefficient (r) of greater than 0.6on test-retest is the accepted minimum for a testto be judged reliable. The validity of a test is mea-sured in a number of ways, the most important ofthese being construct validity (the degree to whichthe test measures what it purports to measure).

Interpreting scores: Be careful when interpretingmany test items not to overinterpret one or twooutliers in the sample of tests as indicating realdeficits. There is a risk of making a type 1 error(reporting a difference when there is none).Composite scores are created from individual

235


subtest scores. These are more reliable thaninterpretations based on individual scores as thestandard error of measurement is reduced due tothe larger number of items making up the score [9].

DOMAINS OF SPECIALIST ASSESSMENT

Tables 37.1 to 37.6 review a selection of publishedtasks assessing specific aspects of brain function.They include target functions and some of thenon-specific skills required to complete the task.

General abilityAny specialized neuropsychological assessmentrelies on measured IQ to establish a general levelof cognitive functioning, as an indicator of generalability. A full IQ assessment is usually required,although for research purposes a short version ofa test can often be used from which to calculate apro rata full-scale IQ score. Crawford et al. haverecently published on the reliability of a short-formadministration procedure for the WISC-IV [10].

MemoryStandardized tests in this domain (Table 37.1)assess explicit memory or conscious recollection(for facts or events) as opposed to implicit (forskills or procedures) traces. There are separatedimensions of memory – working (short-term),stored (long-term), verbal, spatial (visual) andlearning capacity. Individuals may have impair-ment in one domain but not in another. Inaddition, it is important to test both delayed recalland recognition. Children who do poorly on atest of recall but accurately recognize previouslypresented items can often store information buthave problems accessing it.

LanguageTests of language assessment fall into two cate-gories: receptive and expressive. Visual languagechannels are independent from spoken languagechannels, and so assessments that focus on spokenlanguage (reviewed in Table 37.2) do not necessar-ily exclude written language problems. However,specific written language impairment and spo-ken language vulnerabilities often co-occur [11].Assessments of written language are likely tobe classed as assessments of attainment, such assubtests of the Wechsler Individual AttainmentTest [12].

AttentionAttention has two main components: sustained(effortful processing over a significant period oftime) and selective (vigilance for target stimuliwhile ignoring distracter stimuli). Many childrenwith ADHD do poorly on these tests but there isno diagnostic cognitive test for the condition. It isidentified on the basis of a pervasive behaviouralprofile rather than performance on a cognitive task.Until recently, many tests of attention for childrenwere rather theoretical, attempting to define acore cognitive deficit in children who have theADHD behavioural profile (the debate about theexistence and nature of such a core deficit contin-ues). The Test of Everyday Attention for Children(TEACh) [13] provides a battery of tests of atten-tion and inhibition presented in a variety of visualand auditory modalities (see Table 37.3).

Spatial abilitySpatial skills include the ability to mentallyrotate visual configurations in space and torecognize that same configuration, regardless ofits orientation. The Benton Face RecognitionTest [14] (see Table 37.4) is a good example ofa visual orientation task that uses meaningfulstimuli. The Mental Rotation subtest of the BritishAbility Scales [15] – note that this is not the mostrecent version – assesses orientation using abstractstimuli.

Spatial ability also includes the naming ofobjects – though it could be argued that namingmakes such high demands on visual memory thatit is better described as a visual memory skillrather than a spatial ability per se. The GestaltClosure subtest of the Kaufman AssessmentBattery for Children is a test of visual naming thatis appropriate for children [16].

Motor skillsMotor tests (Table 37.5) assess a number of sep-arate elements – strength, speed and dexterity.Many tests of motor dexterity include a visual com-ponent (e.g. the Rey–Osterrieth Complex Figure)[17,18]. The Visual Motor Integration Test is auseful tool to assess visual, motor and visuo-motorintegration skills [19].

Executive functionExecutive function (EF) includes initiation, plan-ning, inhibition, flexibility, self-regulation, concept

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Assessment

generation and working memory (Table 37.6). It isargued that grouping these together into a unitaryconcept is flawed as they are so diverse. There isalso controversy over the construct validity of thetasks that profess to assess EF. There is strongclinical and theoretical justification to developmore refined classifications of the functions asso-ciated with EF, particularly as investigations ofEF are often central to the assessment of manyclinical conditions. Deficits in EF are implicatedin many disorders (e.g. ADHD, autistic spectrumdisorders and schizophrenia) [20–22]. In additionto the psychometric assessments of EF outlinedin Table 37.6, the Behavioural Rating Index ofExecutive Function (BRIEF) [23,24], a parent,teacher and child rating questionnaire, providesinformation about behaviours that are associatedwith executive function difficulties (preschool andschool age versions).

Social cognitionSocial cognition (see Table 37.6) covers manyhigh-order brain functions, such as the expressionand understanding of emotion, facial expressionand subtleties of language embedded in socialinteraction. ‘Theory of mind’ describes the abilityto ‘mentalize’ and infer another person’s stateof mind. For the purposes of this review, theoryof mind is not considered an aspect of socialcognition, but is regarded as a theoretical concept.Describing theory of mind as a concept rather thana brain function is not an attempt to disregard thesignificant empirical data showing that childrenwith autistic spectrum disorders, particularlylow-functioning individuals, perform poorly ontheory-of-mind tasks.

The measurement of social cognition relies onconsensus opinion, in contrast to other brain func-tions, which can be quantified using objective rightor wrong answers. The complex nature of socialcognition may explain why there are few stan-dardized tests assessing this aspect of functioning,but the paucity of standardized measurement is achallenge to those working in the specialist assess-ment of cognitive functions. The NEPSY-II (2007)has two subtests that measure ‘Theory of Mind’(ability to understand mental functions such asbelief, intention, deception, emotion, imaginationand pretending as well as how emotion relates tosocial context) and ‘Affect Recognition’ (ability torecognize affect) [25].

CONCLUSIONS

This chapter outlines measurement and testingconsiderations in the field of paediatric neuropsy-chology. As a clinician or researcher one mustconsider how to interpret test results in the contextof neuropsychological theory, and one should alsoinclude considered dissemination of test results.Empirical data ideally indicate specific recommen-dations, which may simply raise awareness abouta child’s profile to the child themselves, family,school staff and other professionals so that theenvironment may adapt to accommodate a child’scognitive vulnerability. In some cases, test resultsmay indicate an intervention that could improvecognitive functioning in the child. These principlesof careful interpretation apply equally to clinicalcases and research populations. In some instances,results could inform theory – for example, groupdata could point towards a function (or particu-lar phenotype) and may be mapped genotypically,or results could be correlated with neuroimagingdata. Our task as professionals might be summa-rized as raising awareness about the utility anddelicacy of paediatric neuropsychology.

REFERENCES

[1] Wechsler D. (2004) Wechsler Intelligence Scales forChildren, 4th UK edn. London: The PsychologicalCorporation.

[2] Wagner R, Torgesen J, Rashotte C. (1999) Compre-hensive Test of Phonological Processing. PearsonEducation.

[3] Pickering SJ and Gathercole SE. (2001) The Work-ing Memory Test Battery for Children. London:Harcourt.

[4] Jordan CM, Johnson AL, Hughes SJ, Shapiro EG.(2006) The Color Object Association Test (COAT):the development of a measure of declarative mem-ory for 18-to-36 month-old toddlers. Child Neu-ropsychology 141, 21–41.

[5] Dykman RA, Ackerman PT. (1991) Attentiondeficit disorder and specific reading disability: sep-arate but often overlapping disorders. Journal ofLearning Disabilities 24, 96–103.

[6] Conners CK, (2000) Multi-Health Systems Staff.Conners’ Continuous Performance Test Version 3.0.Toronto: Multi-Health Systems.

[7] McGee RA, Clark SE, Symons DK. (2000) Doesthe Conners’ Continuous Performance Test aid inADHD diagnosis? Journal of Abnormal Child Psy-chology 28, 415–24.

237


Table 37.1 Memory assessment measures.

Assessment Target Reference Non-specific Age range Commentsfunction population abilities∗ (to nearest

(n) in each whole year)age band

AutomatedWorking MemoryAssessment [26]

Memory — short-termand working memoryVisual-spatial andverbal

59—67 4—22 Computeradministrationand scoring

Working MemoryTest Battery forChildren [3]

Memory — short-termand working memoryVisual-spatial andverbal

59—100 4.7—16

Children’sAuditory VerbalLearningTest — 2 [27]

Memory — verbal,immediate and delayedrecall and recognition

30—81 6—17

Wide RangeAssessment ofMemory andLearning [28]

Memory — verbal andvisual, delayed andimmediate, recall andrecognition

110—117 5—15

Rey—OsterriethComplex Figure[29,30]

Memory — visual,immediate, delayedand recognition

18—48 Planning, visuo-motor skills

6—15

Children’sMemoryScale [31]

Memory — visual,verbal, immediate,delayed recall,attention, recognition,learning

100 2—16 It is possible topredict aGeneral MemoryIndex Scorefrom WISC FS IQ

Digit Span(WISC-IVUK) [1]

Memory — auditoryworking

74 6—16

RivermeadBehaviouralMemory Test[32,33]

Memory — everydaytasks

100 5—14

The VisualMemoryBattery [34]

Memory — working andstored, recognition andlearning

40 Sustainedattention(Matching toSample subtest)

4—adult Computeradministrationand scoring.Motor speed iscontrolled

NEPSY — memorysubtests [25]

Memory — visual,verbal, immediate anddelayed

100 3—16 Appropriatesubtests: namesand faces;narrative;sentences; listlearning

Color ObjectAssessment Test(COAT) [4]

Declarative memory 94—139per 6-monthage band

18—36 months Only preschoolmemoryassessment

∗Intact senses and motivation are assumed in all cases.

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Table 37.2 Language assessment measures.



ClinicalEvaluation ofLanguageFundamentals —3 [35]

Language —spokenexpressive andreceptive

151—267 Auditoryattention

5—adult Test—retestreliability onsome subtests islow

ClinicalEvaluation ofLanguageFundamentals —preschool [36]

Language —spokenexpressive andreceptive

100 Auditoryattention

3—6 Test—retestreliability onsome subtests islow

Test for theReceptionof Grammar(TROG) [37]

Language —spoken receptivegrammar

120—217 4—adult TROG-E waspublished in 2005and is acomputerizedversion of sametest

British PictureVocabularyScale [38]

Language —spoken receptivenaming grammar

183—423 Visualdiscrimination

3—16 1997 stimuli areless ambiguousthan those inprevious editions

RenfrewLanguageScales [39]

Language —spokencomprehension,word finding,expression,narrative speech

58—101 3—8

Token Test [40] Language —spoken receptivecomprehension oflanguageconcepts

29—53 Short-term(working)auditorymemory

6—13

NEPSY —languagesubtests [25]

Language —expressive andreceptive,cognitiveprocesses relatedto language

100 3—16 Appropriatesubtests:phonologicalprocessing;speeded naming;repetition ofnon-words;comprehension ofinstructions


239


Table 37.3 Attention assessment measures.



ContinuousPerformanceTest [6]

Attention — visualsustainedattention andimpulsivity(behaviouralinhibition)

40 Age-appropriatereading

6—adult Gender-differentiatednorms

Test ofEverydayAttention [13]

Attention —auditory and visualsustained andselectiveattention,response inhibition

29—58 Basic numeracy isrequired for somesubtests

6—15

CambridgeNeuropsycho-logical TestAutomatedBattery [34]

Attention —sustained,selective anddivided

40 4—adult Computeradministrationand scoring.Motor speed iscontrolled

NEPSY —attentionsubtests [25]

Attention —auditory —selective andsustained(vigilance)

100 5—-16 Appropriatesubtest: AuditoryAttention andResponse Set


[8] Eden GF, VanMeter JW, Rumsey JM et al. (1996)Abnormal processing of visual motion in dyslexiarevealed by functional brain imaging. Nature 382,66–9.

[9] Lezak MD, Howieson DB, Loring DW, Hannay HJ,Fischer JS (2004) Neuropsychological Assessment.Oxford Unitversity Press.

[10] Crawford JR, Anderson V, Rankin PM, MacDonaldJ. (2010) An index-based short-form of the WISC-IV with accompanying analysis of the reliability andabnormality of difference. British Journal of ClinicalPsychology 49, 235–58.

[11] Snowling MJ, Adams JW, Bishop DV, StothardSE et al. (2001) Educational attainments of schoolleavers with a preschool history of speech-languageimpairments. International Journal of Language andCommunication Disorders 36, 173–83.

[12] Wechsler D. (2005) Wechsler Individual AttainmentTest. London: The Psychological Corporation.

[13] Manly T, Robertson IH, Anderson V. (1999) Testof Everyday Attention for Children (TEACh). BurySt Edmunds: Thames Valley Test Co..

[14] Benton AL. (1994) Neuropsychological assessment.Annual Review of Psychology 45, 1–23.

[15] Elliot C. (1983) British Ability Scales Manual II.Windsor, UK: NFER-Nelson.

[16] Kaufman AS and Kaufman NL. (1983) KaufmanAssessment Battery for Children. Circle Pines, MN:American Guidance Service.

[17] Rey A. (1941) L’examen psychologique dans un casd’encephalopathie traumatique. Archives of Psy-chology 28, 286–340.

[18] Osterrieth PA. (1944) Le test de copie d’une figurecomplexe: contribution a l’etude de la percep-tion memoire. Archives of Psychology 30, 286–356.

[19] Beery KE. (1997) The Visual Motor Integration Test:Administration, Scoring and Teaching Manual, 4thedn. Cleveland, OH: Modern Curriculum Press.

[20] Kempton S, Vance A, Maruff P et al. (1999) Exec-utive function and attention deficit hyperactivitydisorder: stimulant medication and better executivefunction performance in children. Psychology andMedicine 29, 527–38.

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Table 37.4 Spatial/visual assessment measures.



DevelopmentalTest of VisualMotor Integra-tion [19]

Visual discrim-ination, motorskill andvisuo-motorintegration

6—16 Impulsivity mayinterfere withperformance inthe motor skillsubtest

2—14 Some debateregarding thegraduation oftest itemdifficulty

Trail Making Aand B [41—43]

Visual searchand sequenc-ing/motoroutput

10—101 Knowledge ofnumber andalphabetsequence

6—15 Parts A and Bmeasuredifferentfunctions

MentalRotation —British AbilityScales [15]

Visual —rotation ofabstractfigures

90—189 Conceptualability to takeanother person’sperspective

8—14

GestaltClosure —KaufmanAssessmentBattery forChildren [16]

Visual —meaningfulstimuli naming

200—300 Knowledge ofindustrializedworld objects

2—13

FaceRecognitionTest [14]

Visual/spatialability — facerecognition

19—59 6—14

Judgement ofLine Orienta-tion [44]

Visual—spatialjudgement

23—50 7—14

Rey—OsterriethComplexFigure Test(copycondition)[17,18,29,30]

Visual/motorplanning

18—48 6—15

Right-left ori-entation [45]

Spatialdiscrimination

7—16 6—16†

NEPSY — visualspatialsubtests [25]

Motor andvisualperception;linediscrimination

100 3—16 Appropriatesubtests:Design copy;arrows; routefinding

∗Intact senses and motivation are assumed in all cases.†Some extrapolated norms.

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Table 37.5 Motor assessment measures.

Assessment Target Reference Age range Commentsfunction population (to nearest


Finger TappingTest [46]

Motor speed 20 6—14 Gender-differentiatednorms. Boys aresignificantly better atthis task

PurduePegboard Test[47,48]

Motor dexterity(fine)

23—40 5—15 Practice effects arenotable

Cambridge Neu-ropsychologicalTest AutomatedBattery [34]

Motor speed andreaction time

40 4—adult Computeradministration andscoring. Motor speed iscontrolled

Gripstrength [46]

Motor strength 20 6—14 (nonorms for9—11)

Sex and handpreferencedifferentiated norms

NEPSY —sensorimotorsubtests [25]

Motor dexterity andmotor speed;imitation ofsequences;graphomotor speedand accuracy

100 3—16 Appropriate subtests:fingertip tapping;imitating handpositions, manualmotor sequences,visuomotor precision

[21] Ozonoff S, Strayer DL, McMahon WM, FillouxF. (1994) Executive function abilities in autismand Tourette syndrome: an information processingapproach. Journal of Child Psychology Psychiatry35, 1015–32.

[22] Bryson G, Whelahan HA, Bell M. (2001) Mem-ory and executive function impairments in deficitsyndrome schizophrenia. Psychiatry Research 102,29–37.

[23] Gioia GA, Isquith PK, Guy SC, Kenworthy L.(1996) Behaviour Rating Inventory of ExecutiveFunction. Psychological Assessment Resources,Inc.

[24] Sherman EM and Brooks BL. (2010) BehaviourRating Inventory of Executive Function –Preschool Version (BRIEF-P): test review and clin-ical guidelines for use. Child Neuropsychology 16,503–19.

[25] Korkman M, Kirk U, Kemp S. (2007) NEPSY - II: ADevelopmental Neuropsychological Assessment II.San Antonio, TX: Psychological Corporation.

[26] Alloway TP. (2007) Automated Working MemoryAssessment (AWMA). Pearson Education.

[27] Talley JL. (1993) Children’s Auditory Verbal Learn-ing Test – 2. Professional Manual. Lutz, FL: Psycho-logical Assessment Resources.

[28] Sheslow D and Adams A. (1990) Wide RangeAssessment of Memory and Learning (WRAML).Wilmington, DE: Wide Range.

[29] Kolb B and Wishaw I. (1990) Fundamentals ofHuman Neuropsychology, 3rd edn. New York:Freeman.

[30] Meyers JE and Meyers KR. (1995) Rey ComplexFigure Test and Recognition Trial: ProfessionalManual. Odessa, FL: Psychological AssessmentResources Inc..

[31] Cohen M. (1997) The Children’s Memory Scale. SanAntonio, TX: The Psychological Corporation.

[32] Aldrich FK and Wilson B. (1991) RivermeadBehavioural Memory Test for Children: a prelimi-nary evaluation. British Journal of Clinical Psychol-ogy 30, 161–8.

[33] Wilson BA, Forester S, Bryant T et al. (1991) Per-formance of 11–14-year-olds on the RivermeadBehavioural Memory Test. Clinical PsychologyForum 30, 8–10.

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Assessment

Table 37.6 Executive function and social cognition assessment measures.



Delis—KaplanExecutive FunctionSystem(D-KEFS) [49]

Executive function Approx. 100 8—adult Some parallelversions of tasks.Good variety oftasks

BehaviouralAssessment ofDysexecutiveSyndrome(BADS) [50]

Executivefunction — predictseveryday function

22—32 7—15 Computeradministration andscoring. Motorspeed is controlled

CambridgeNeuropsychologicalTest AutomatedBattery [34]

Executivefunction — workingmemory andplanning

40 Sustainedattention(matching tosamplesubtest)

4—adult Computeradministration andscoring. Motorspeed is controlled

Trail Making A andB [41,42,43]

Executivefunction — motorplanning anddisinhibition

10—101 Number andalphabetsequenceability

6—15 (someextrapolatednorms)

Parts A and Bmeasureindependentfunctions

Rey—OsterriethComplex FigureTest (copycondition only)[17,18,29,30]

Executivefunction—visualplanning

18—48 Visuo-motorskills

6—15

Wisconsin CardSorting Test [51]

Executivefunction — cognitiveflexibility; conceptformation

27—55 Colour vision,basicnumeracy

6—adult There is a positiverelationshipbetween years ineducation andperformance

Stroop Word andColour Test [52,53]

Executivefunction — inhibitionof a prepotentresponse

14—29 Colour vision,literacy

Collatednorms for7—16

All three conditionsmust beadministered tocontrol for speed ofprocessing

Diagnostic Analysisof Non-verbalAccuracy 2 [54]

Social cognition —receptivenon-verbal ability;voice and facerecognition

25—305 Sustainedauditoryattention

3—adult(collatednorms)†

Body languagesubtest has beendropped for themost recent edition

NEPSY — attentionand executivefunctionsubtests [25]

Executivefunction — inhibitautomatic response,planning andorganization, shiftset

100 3—16 Appropriatesubtests: inhibition,clocks, animalsorting, designfluency, Statue

∗Intact senses and motivation are assumed in all cases.†Child faces only.

243


[34] The Cambridge Neuropsychological Test AutomatedBattery (CANTAB). Cambridge, UK: CeNeS Phar-maceuticals, 2001.

[35] Semel E, Wiig EH, Secord WA. (2006) ClinicalEvaluation of Language Fundamentals, 3rd UK edn.London: The Psychological Corporation.

[36] Wiig EH, Secord W, Semel E. (2006) The ClinicalEvaluation of Language Fundamentals – Pre-schoolVersion. San Antonio, TX: The Psychological Cor-poration.

[37] Bishop DVM. (2003) Test for the Reception ofGrammar. Manchester, UK: Chapel Press.

[38] Dunn L, Dunn D. (2009) The British Picture Vocab-ulary Scale, 3rd edn. Windsor, UK: NFER-Nelson.

[39] Renfrew C. (1995) The Renfrew Language Scales.Oxford: Winslow.

[40] De Renzi E and Faglioni P. (1978) Developmentof a shortened version of the token test. Cortex 14,41–9.

[41] Reitan RM. (1971) Trail making test results fornormal and brain-damaged children. Perceptual andMotor Skills 33, 575–81.

[42] Spreen O and Gaddes WH. (1969) Developmentalnorms for 15 neuropsychological tests age 6 to 15.Cortex 5, 170–91.

[43] Army Individual Test Battery. Trail Making B Man-ual of Directions and Scoring. Washington, DC: WarDepartment, Adjutant General’s Office, 1994.

[44] Lindgren SD and Benton AL. (1980) Developmen-tal patterns of visuospatial judgement. Journal ofPediatric Psychology 5, 217–25.

[45] Benton AL. (1959) Right-Left Discrimination andFinger Localization. New York: Hoeber.

[46] Finlayson MAJ and Reitan RM. (1976) Handednessin relation to measures of motor and tactile functionin normal children. Perceptual and Motor Skills 43,475–81.

[47] Tiffin J. (1968) Purdue Pegboard: Examiner Manual.Chicago, IL: Science Research Associates.

[48] Gardner RA and Broman M. (1979) The PurduePegboard: normative data on 1334 school children.Journal of Clinical and Child Psychology 8, 156–62.

[49] Delis DC, Kaplan E, Kramer JH. (2001) The Delis-Kaplan Executive Function System (D-KEFS). SanAntonio, TX: Psychological Corporation.

[50] Emslie H, Wilson F, Burden V, Nimmo-Smith I,Wilson B. (2003) Behavioural Assessment of Dysex-ecutive Syndrome. Thames Valley Test Company.

[51] Heaton RK, Chelune GJ, Talley JL, Kay GC,Curtiss G. (1993) Wisconsin Card Sorting TestManual – Revised and Expanded. Lutz, FL: Psy-chological Assessment Resources.

[52] Golden JC. (1992) Stroop Word and Colour Test:A Manual for Clinical and Experimental Uses.Chicago: Stoelting.

[53] Comalli PE, Wapner S, Werner H. (1962) Inter-ference effects of the Stroop Colour Word Testin childhood, adult and aging. Journal of GeneticPsychology 100, 63–5.

[54] Nowicki S, Duke MP. (1994) Individual differencesin the non-verbal communication of affect. Thediagnostic analysis of a non-verbal accuracy scale.Journal of Non-Verbal Behaviour 18, 9–35.

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Assessment

38Assessment of Child Psychiatric DisordersHelen Bruce1 and Navina Evans21Emanuel Miller Centre, London, UK2Coborn Centre for Adolescent Mental Health, Newham Centre for Mental Health, London, UK

INTRODUCTION: WHY DO A PSYCHIATRICASSESSMENT?

What is the rationale for choosing to undertakea psychiatric assessment? Various answers tothis question have been suggested. For instance,Harrington [1,2] argues that a psychiatric assess-ment focuses on four key questions:

• is a psychiatric disorder present?• what sort of disorder is it?• what other problems are present?• why does the patient have the presenting

problem(s)?

Hoyos [3] takes a more developmental perspec-tive and contrasts assessment in child psychiatrywith assessment of psychiatric disorders in adults,arguing that understanding child developmentis critical when assessing children as normativebehaviour changes with developmental age.Scott [4] argues that making a correct diagnosisrequires applying a body of knowledge basedon extensive research. The American Academyof Child and Adolescent Psychiatry (AACAP)Practice Parameters and Guidelines [5] say thatthe psychiatrist needs to prioritize symptoms anddiagnoses so that a reasonable treatment plan canaddress multiple problems.

As we illustrate below, all of these rationalesemphasize important aspects of the psychiatricdiagnostic process. In a busy, multidisciplinary,generic child mental health service, an additionalquestion might be posed concerning which chil-dren need to be assessed by a child psychiatrist.


Given the pragmatics of time and availability, whenis it important to apply the specific additionalskills utilized in psychiatric diagnoses? We wouldsuggest that psychiatric assessments be undertakenwhen the following questions are pertinent:1. Is there a coexisting significant medical problem

where medical skills can contribute to under-standing the illness process?

2. Is there a question of diagnosis – for example,whether the child’s symptoms meet the diag-nostic criteria for a bipolar disorder?

3. Is there a likelihood that medication will berequired as part of the management/treatmentplan?

4. Is an admission to hospital for further assess-ment or treatment required?

SETTING THE STAGE FOR ASSESSMENT

The general principles of assessment outlinedapply to children of any age. However, it is partic-ularly important to bear in mind that the range ofpsychiatric disorders seen may differ according tothe child’s age and developmental stage.

The assessment of a child and adolescent usuallywill take place over several meetings, using infor-mation from several different sources. An initialassessment interview is a key time to begin thetherapeutic process of engagement with a familyand it is important to try to get it right. It is alsoa key part of any assessment of factors that maypose a risk to the child’s safety or well-being.

Consideration should be given as to whom tosee. With a younger child, it is usually helpful to

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meet with the whole family at the start of theinterview, but at some stage in the assessment ofa younger child, the parent/s or guardian shouldbe seen without the child being present. Where itis age appropriate, a younger child must also begiven time to speak with the interviewers – eitherby focusing some of the family interview on them,or by meeting with the child alone. An adoles-cent will usually wish to be seen for some of theassessment without their parents. The assessmentinterview unfolds in a number of stages that areoutlined below.

INTERVIEWING FAMILIES

Family interviews should begin by making thefamily welcome and putting them at their ease.Then, exploration around key issues follows: whatdo the family see as the problem, and who hasthe problem? How are they trying to deal withit at present? What have they already tried andwhat help have they already received? How doesit affect their lives?

One strategy the assessor may use is to askthe family to work together in the session on anexercise, for example drawing up a family tree.This gives the assessor an insight into how familymembers relate to each other and also into the pre-senting problem. Are the parents sensitive to thechild’s communications? How do they respond?What is the parent’s own relationship like? Is onefamily member ignored?

It is also important to ask who else is importantto the child but is not present. This could be aseparated parent, or a grandparent, for example.How would the family describe this absent person,and what would they say if they were in the room?

INTERVIEWING CHILDREN ANDADOLESCENTS

With the younger child, it may not be possibleformally to examine the child’s mental state andthe clinician will need to rely on observation.This should include an observation of the child’sbehaviour, interactions with family, interactionswith clinicians, and play. Key aspects of the child’sfunctioning and behaviour to note are shown inTable 38.1.

It is important to take into account develop-mental issues and have a good understanding of

Table 38.1 Observing the child. Adapted fromBruce and Evans [6] and Bruce and Keene [7],with permission.

Aspect Observations

Behaviour Appearance and dress

Emotional responsiveness

Mannerisms andstereotypies

Activity level

Any risky behaviour

Talk Form:

• coherence and speed

• spontaneity

• spontaneity

• prosody

• articulation

Content:

• persistence

• interruption of attention

• child’s interests

Anxiety andmood

Fearful or anxious

Restless

Disturbed or aggressive

Withdrawn or shy

Sadness

Interactions Parent—child interaction

Interaction with otherfamily members

Interaction with clinician

Interaction with theenvironment — toys andplay

Intellectualfunctioning

A brief overview of thechild’s current level ofcognitive ability will beneeded

Does this differ greatly fromtheir chronological age?

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the particular young person’s stage of emotional,cognitive and psychological development, whichmay differ according to their physical maturity. Itis important that the child’s or adolescent’s individ-ual autonomy is given due respect. This issue cancause tension in the assessment phase, but shouldnot be ignored. Confidentiality is linked with thisissue. It will be important that children can speakin confidence about certain issues. However, thelimits to confidentiality with respect to concernsabout the safety/well-being of themselves and oth-ers need to be outlined to them. Thus, it may notalways be possible to guarantee full confidentiality,and the young person is entitled to a full expla-nation of how this right will, as far as possible,be respected. Many of those young people whosedifficulties persist into adulthood will have theirfirst encounter with mental health services dur-ing their childhood. The nature of this experiencewill affect their future compliance and engage-ment with mental health services, so it is especiallyimportant to consider the long-term implicationsof their interaction with professionals at this stage.

When seeing an adolescent it is helpful toestablish what they personally see as the problem.

They may not agree they have a problem at all.Even if they do not agree with the parent orreferrer, the examiner can still establish a rapport,and it is important to engage with the youngperson. As with younger children, the issue ofconfidentiality and its limits should be established.The process of assessment should be explainedclearly. A psychiatric mental state examinationshould be carried out (see Box 38.1). The interviewshould also include a sexual, forensic, and drugand alcohol history.

It is important to end the interview in a way thatleaves children and adolescents feeling that theirperspective matters. Other useful information canalso be gained at this stage. It is important to askthe young person if there is anything else theywould like to talk about or that they think theinterviewer should know that would be helpful forthe assessment. It is also important to ask if theywant to ask any questions about the assessment,possible interventions, or any other matters ofconcern or interest to them. With a younger child,a helpful technique is to ask the child: ‘if youhad three wishes what would you wish for?’ Theyoften respond giving useful information about their

Box 38.1 Mental State Examination (MSE)

An MSE should be conducted with every child and adolescent being assessed. It is informed bythe child’s history, the assessment of other relevant factors and the conditions under which theassessment is taking place. It will also be informed by the developmental stage of the child/adolescent.

The MSE is used as part of the wider formulation to plan the next steps in management.It is an active process conducted as often as needed throughout any intervention with thechild/adolescent.

The domains covered in a MSE include:

• Appearance, attitude and behaviour

• Mood and affect

• Speech

• Thought processes and content

• Perception

• Cognition

• Insight and judgement

• Risk

Clinicians will need to draw on their communicative skills with children and adolescents inorder to conduct a successful MSE.

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situation, fears and worries, using terms and acontext that is meaningful to them.

INTERVIEW WITH THE PARENT(S)OR CARER

It is important to obtain from the parent(s) a thor-ough description, both of the current problem andan account of the child’s developmental, medicaland school history. The key points are summarizedin Box 38.2 [6,7].

The parents can be interviewed together withthe young person or separately. Many young peo-ple want to know what is being said about themand should not be excluded. At times it may bemore appropriate for the parents to be seen sep-arately, as when the young person is extremelyagitated or unwell, or if the parents feel concernedabout talking in front of the young person. If thisis done, the young person should be informed thatthe discussion is taking place and it should be madeclear to all involved what level of information will

be shared between family members. It is importantto be aware of not being drawn in to colluding withany secrets between family members.

PHYSICAL EXAMINATIONAND INVESTIGATIONS

Most children who attend child mental health ser-vices are not routinely examined medically. It isimportant that consideration is given to a physicalexamination, if one has not already been done bythe GP or Community Paediatrician. Reasons forthis assessment include the possibility of an under-lying undetected physical condition that has causeda child’s difficulties, or the prescription of medi-cation that could have physical side effects, suchas risperidone or methylphenidate. Guidelines canbe found that are relevant to each medicationand indicate the essential elements of physicalexamination – for example, the European Clini-cal Guidelines for Hyperkinetic Disorder [8] – butmost National Health Service Trusts also have their

Box 38.2 Information to be obtained from the parent(s)

• Current problem as parent/s sees it and its effect on the family

• Behavioural problems (e.g. aggression, conduct problems, truancy, running away)

• Any risky behaviour

• Emotional symptoms (anxiety, fears, depression, suicidality)

• Attention and concentration

• Activity levels

• School history, performance and attendance

• Family life and relationships, including any family history of illness

• Peer and sibling relationships

• Any recent adversity (e.g. bereavement, trauma)

• Developmental history

• Physical health

• The child’s temperamental characteristics

• The child’s strengths

• What the parents see as the child’s difficulties

• What help/interventions have already been tried

• What has previously been successful.

Adapted from Bruce and Evans [6] and Bruce and Keene [7], with permission.

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own prescribing guidelines that state minimum lev-els of physical investigations required in their poli-cies. The AACAP Parameters [5] also recommendphysical examination or referral to a practitionerwho can undertake this. A baseline height andweight should always be recorded. Where there issuspicion of an underlying medical condition, a fullphysical examination is essential. A full neurolog-ical examination may also be required if there ishistory indicative of a neurological disorder such asdevelopmental delay, epileptic fits or loss of skills.Other indicators include a history or physiognomythat suggests the child could have a congenital syn-drome. Useful pointers to congenital syndromesinclude learning difficulty, dysmorphic features(including unusual facial features) and extremevalues for height, weight or head circumference [1].

Most children will not require further medicalinvestigations unless there is a clinical indicationor abnormalities have been found on the physicalexamination. However, it is important to carryout appropriate blood tests if medication is beingconsidered.

OTHER SOURCES OF INFORMATION

Other agencies, such as education or socialservices, which are involved with the familyor child, may have useful information to helpunderstand the child’s problems. Schools canprovide particularly valuable accounts of achild’s difficulties. It is usually best to obtainstructured reports, in the form of a set of specificenquiries. Potential informants include the child’sclass teacher and any schools special educationneeds advisors. Depending on the nature of thechild’s problem, the enquiry can be supported bystandardized questionnaires that are available forteachers such as the Conners’ Rating Scales forHyperactivity/Inattention. A school or nurseryobservation by the clinician (if resources allow)will also yield valuable information. It is importantto ensure that parental consent has been obtainedif the clinician wishes to seek information fromsuch other sources.

PUTTING IT ALL TOGETHER:CONSTRUCTING A FORMULATION

First of all, the clinician will need to considerwhether the child’s behaviour, emotional state

or presenting difficulty is abnormal in relation tohis or her age, gender, developmental stage andcultural background. The symptom needs to bepersistent, severe and frequent and of a sufficientextent in order to be considered abnormal.

It will also be important to know if the symptomis leading to functional impairment in the everydaylife of the child. Four main criteria can be used toassess impairment:1. interference with a child’s development;2. social restriction;3. suffering or distress to the child;4. effect on others.

Different aspects of the child’s problems can beconsidered using a multiaxial framework, as haspreviously been done in the ICD-10 InternationalClassification of Mental and Behavioural Disordersin Children and Adolescents (ICD-10). However,revisions to our current classification systems inboth the UK and USA are underway, and we referthe reader to Chapter 35.

An adequate formulation of the child’s difficul-ties will require the clinician to piece together thepresenting features of the problem, with any aetio-logical factors, and to comment on the differentialdiagnosis, management and prognosis. This evalu-ation will form the basis on which any interventionis planned.

Attention must be paid to risk assessment andassociated management, especially with adoles-cents. Risks can include risk to self, risk to oth-ers (within or outside of the family) or risk ofabuse/neglect. The psychiatrist plays a crucial rolein risk management, and should attempt to manageanxiety within the young person’s social network.

Formulation also requires the assessor to havea good understanding of strengths, resilience andprotective factors. These can be exploited in themanagement plan and enhance outcome.

ACKNOWLEDGEMENTS

We acknowledge with thanks Quay Books, MarkAllen Healthcare Ltd, for giving permission to useTable 38.1 and Box 38.2 as updated and adaptedversions from Bruce and Keene [7].

REFERENCES

[1] Harrington R. (2005) Assessment of psychiatric dis-orders in children. Psychiatry 4, 19–22.

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[2] Harrington R. (2004) Assessment of child and ado-lescent psychiatric disorders. Medicine 32, 11–13.

[3] Hoyos C. (2008) Assessment of child psychiatric dis-orders. Medicine 36, 475–7.

[4] Scott S. (2002) Classification of psychiatric disordersin childhood and adolescence: building castles in thesand? Advances in Psychiatric Treatment 8, 205–13

[5] American Academy of Child and AdolescentPsychiatry. (1997) Practice Parameters and Guide-lines. Journal of the American Academy of Child andAdolescent Psychiatry 36(10; Suppl.).

[6] Bruce H and Evans N. (2008) Assessment of childpsychiatric disorders. Psychiatry 7, 242–5.

[7] Bruce H and Keene B. (2010) Child mental health.In: Ali A, Hall I, Dicker A (eds), Essential Psychiatryin General Practice. Quay Books, pp. 127–37.

[8] Taylor E, Dopfner M, Sergeant J et al. (2004)European Clinical Guidelines for Hyperkinetic Dis-order. European Child and Adolescent Psychiatry13(Suppl. 1), 17–30.

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39Psychological AssessmentMichael BergerDepartment of Psychology, Royal Holloway, University of London, Egham, UK

Psychological problems in children and youngpeople commonly result from the interplay of acomplex of factors over time. The same problemshown by different individuals can arise for any of avariety of reasons, and the same instigator can leadto individuals showing different problems. Aggres-sion at home may occur because one individual issocially isolated, another is not coping with thelearning demands of school, or in a third, becauseof family tensions. One child bullied at school maybecome withdrawn and uncommunicative whereasanother may be aggressive at home and disruptivein school. Complexity is increased because the fac-tors that give rise to difficulties may not alwaysbe the same as those maintaining them. Rejectionby peers can lead to a loss of self-esteem, andeven if subsequently reaccepted, the individualmay remain hypersensitive to signs of rejection.

Assessment (or ‘evaluation’, ‘diagnosis’, or‘case conceptualization’) is the process wherebyclinicians gather and interpret information from avariety of sources to help understand and managesuch problems. The information is elicited andcollected using formal (structured) or informalobservations and interviews, and special tests.An ‘assessment’, ‘evaluation’ or similar refersto a set of statements conveying the clinician’sunderstanding of the nature of the problems andthe actions needed to manage them. This productof the assessment process, referred to here asa ‘formulation’, is essentially an explanation orhypothesis about the nature of the problems andwhat is required to manage or resolve them.

Assessment requires specialist knowledge andskills and is arguably the most critical part of


clinical practice: what the clinician learns throughtheir investigations profoundly influences whathappens by way of further action. Where the pri-mary focus is on psychological functioning, a majorfeature differentiating forms of clinical practice isthe clinician’s theoretical orientation or ‘model’.Models influence how the practitioner approachesassessment, how the problems are understood, thenature of the eventual formulations they offer, theinterventions undertaken and even the structureof services [1]. This chapter describes an approachto the psychological assessment of children, youngpeople (hereafter children), their families andothers involved in their care based on a modelderived from several sources.

MODELS

Models in health care commonly reflect the char-acteristics of medical diagnostic systems for iden-tifying disorders. In simplified form, these viewa psychiatric disorder as something in the personcaused by a (usually) diagnosable disease or injury,requiring individual treatment by professionals torestore a healthy state. The appropriateness ofsuch models for understanding psychological prob-lems is questioned, reflecting disagreements withboth the specifics of diagnostic systems – such ascategorical conceptualizations [2] – and the associ-ated approaches to psychological problems [1]. A‘social’ model, also simplified, views dysfunctionand disability as social constructs, not individ-ual attributes, requiring social change to removethe disabling consequences, ignoring the contribu-tion of biological and psychological factors. From

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a psychological perspective, a model incorporat-ing biological, psychological and social parametersand their impacts on functioning – a biopsychoso-cial model – has greater ‘real-world’ meaningful-ness [3].

A BIOPSYCHOSOCIAL MODEL

A biopsychosocial model recognizes the interplayof multiple factors in the origins, maintenance andimpacts of psychological problems on personalfunctioning. As an alternative starting point,it is complemented by adopting experimentalpsychology and psychopathology as the primaryknowledge bases. For child psychologists, sys-temic, developmental, individual difference andsociocultural considerations are also basic to theirapproach. This recognizes that biological systemsdevelop and function in ongoing transactionsbetween genetic endowment and experiences,within and across all levels of the developingorganism and environment, from cellular biochem-istry to the physical and psychosocial worlds. Theseinfluences operate from conception (and before),over the lifespan [4], and may need to occur

in certain developmental (sensitive) phases foremerging patterns to function effectively [5]. Post-natal development is recognized as non-linear,involving major qualitative and quantitativetransitions from birth onwards. Underlying devel-opment are differential changes in neural systemsfunctioning in typical environments. Some systemsonly become fully functional well into adolescenceor beyond [6]. Such requirements for an accept-able model are encompassed in Bronfenbrenner’sdevelopmental bioecological theory [7].

In a bioecological-inspired ‘model’ (seeFigure 39.1), the individual is at the centre ofinteracting nested systems extending from care athome to the broader sociocultural and physicalmilieu. These influence and can be influenced bythe developing individual, ‘the biopsychosocialperson’ at the centre of the microsystem (Ref. [7],p. xvi), and by each other. Bronfenbrenner’s [8]ideas have had a profound effect on thinkingin developmental psychology, manifest in variedapplications of bioecological theory. Figure 39.1 isan instance applied both to understanding clinicalproblems and to assessment. In this model, theindividual is at the centre of increasingly broader

Intra-individual

Development

Family

School & peer group

Intra-individual systems

SelfIQ Motor skills

Executive functions

TemperamentMemory

Language

Social functions

Wider community

State

Physical world

Figure 39.1 Schematic model of the main systems conceptualized as the major components of abiopsychosocial model.

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ecologies. The dashed circles symbolize ‘gated’bidirectional transactions among and across all themain systems. That is, systems are not necessarilyopen to all influences: for example, some indi-viduals are more resilient than others; auditorysignals inaudible to people influence animals.Within-system transactions occur and impacton other systems. When parents collaborate,rather than argue about the management of theirchild, this can help the child to feel more secureand confident at home, supporting the parents’engagement. It also leads to the child being morelikely to respond positively to their teachers andother adults outside the home.

The intra-individual elaboration on the rightof Figure 39.1 illustrates some of the main gen-eral within-individual functional areas. These canbe differentiated if necessary, for instance, intofiner-grain temperamental characteristics [9]. Themodel is superimposed on a developmental trajec-tory symbolizing changes over time. The shadingindicates that factors operating pre-conception(such as radiation exposure), can influence physi-cal status and functional development of childrenconceived many years later.

A model such as this has several advantagesfor thinking about clinical problems and assess-ment. It identifies potentially influential systemsinteracting and giving rise to complexity inclinical phenomenology. It provides a structurefor systematic assessment, reminding cliniciansof the factors within the individual and thebroader ecologies that need to be considered.Assessment also needs to take account of typicaldevelopmental changes, individual differences,and the ways in which characteristics are manifestin cultural and ethnic variants.

Assessment is commonly structured using amental or other aide memoir, identifying thedomains to investigate that are relevant to theidentified problems. Within each, certain featuresmay trigger more detailed probing, includingthe use of psychological tests. Other areas mightbe ignored. Investigations can entail familymeetings, home or school visits and the like,where information from these contexts might beuseful. Importantly, the assessment process shouldalso identify the strengths within the individualand the broader environments that protect andsupport daily functioning. Such information aidsunderstanding of the presenting difficulties and

points to potential resources for intervention.The proposed model thus emphasizes the need toadopt a multilevel perspective in assessment whileleaving the clinician free to decide when, whereand what to explore in more detail.

Nevertheless, all practitioners, irrespective ofapproach, must be familiar with and take accountof psychiatric and other relevant medical diagnosesand treatments, partly for ethical reasons, partlyfor risk management, and because the functionalimpacts found in individuals with such diagnosescommonly need to be managed. For example,an individual with attention deficit hyperactivitydisorder (ADHD) whose activity levels andconcentration have benefited from medicationmay still need psychological assessment and inter-ventions to manage the personal and other impactson family life, education and peer relationships, ofgrowing up with ADHD characteristics.

Ultimately, as with other models, it is theclinician who has to integrate the assessmentinformation into a coherent formulation withimplications for intervention. Formulations aretentative explanations of the clinical phenomena.They can change following feedback from clinicalencounters, from further investigations, and by theways in which the individual or family responds.Depending on the assessment, the formulation maylead to one or more individualized interventions,ranging from focal to broad-based, implementedwithin any or several of the environments wherethere are significant functional impacts. Thisapproach again stems from recognizing thatmultiple differing influences may be involvedin instigating and maintaining clinical problems.Whether or not evidence-based interventions areused will depend on the availability of suitable pro-cedures, taking account of developmental statusand the circumstances of the child or young person.

Although there are differing views about thecontribution of psychological tests, when properlyused, tests can provide essential information toaid clinical understanding and decision-making,and can be an important source of outcome-monitoring data.

PSYCHOLOGICAL TESTING

A psychological (psychometric) test is a system-atic or rule-governed procedure for samplingpsychological attributes and processes. These

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are not directly observable but are inferredfrom behaviour that occurs naturally or that isspecifically provoked by the test procedure. Forinstance, written responses to focused questionscan tap attitudes to the ‘self’; special puzzle tasksrequire the use of spatial abilities. One of thestrengths of psychological tests is that questionsand tasks are clearly described in a test manualwith everyone asked to do the same thing undersimilar conditions. Answers or performance on atask are converted to a numerical score, which iscompared with the scores of a reference group.This gives an indication of severity, for exampleof depressed mood, the level of an ability (e.g.above or below average spatial skills) or theextent of functional difficulties such as social skillsdifficulties.

Clinical tests take many forms, includingsome that can be administered and scored bya stand-alone computer or over the internet. Anumber produce computer-generated reports. Alltests used clinically should meet accepted qualitystandards [10], including applicability to the indi-vidual to be tested. While tests are relatively easyto administer and score, clinical testing requiresadvanced knowledge and skills: an understandingof measurement errors and their effects on scoreinterpretation; judgement of the reliability ofthe results from the individual administration;cross-checking (do the scores make sense?); andincorporating the test results in a meaningful formin the broader assessment. Criteria for ensuringthe competence of test users are available [11].

Tests encompass the full range of clinicaldiagnoses in children and young people [12]as well as abilities, attainments (achievement),temperament, social skills, self-image and otherpsychological phenomena [13]. Tests of attention,memory and other special procedures, used forinstance in neuropsychological assessment, areconsidered in Chapter 37.

CONCLUDING COMMENTS

This account does not cover the training andexperience necessary for the clinical psychologi-cal assessment of children and young people, northe prioritization of objectives and other aspectsof the assessment process, including linking it tointervention. Nor does it address applications instepped and managed care or in other servicesresponsive to the economic and other constraints of

health-care delivery. However, the model outlinedhere provides an adaptable and appropriate frame-work for thinking about the often complex psycho-logical problems, circumstances and resources ofchildren and young people, and for the clinicalassessment and management of such problems.

REFERENCES

[1] Kinderman P. (2005) A psychological model ofmental disorder. Harvard Review of Psychiatry 13,206–17.

[2] Widiger TA. (2004) Classification and diagnosis:Historical development and contemporary issues.In: Maddux J and Winstead B (eds), Psychopathol-ogy: Foundations for a Contemporary Understand-ing. Hillsdale, NJ: Lawrence Erlbaum, pp. 63–83.

[3] Schneiderman N and Siegel SD. (2007) Mental andphysical health influence each other. In: LillienfeldSO and O’Donohue WT (eds), The Great Ideas ofClinical Science. New York: Routledge, pp. 329–46.

[4] Gottlieb G. (2007) Probabilistic epigenesis. Devel-opmental Science 10, 1–11.

[5] Thomas MSC and Johnson MH. (2008) Newadvances in understanding sensitive periods in braindevelopment. Current Directions in PsychologicalScience 17, 1–5.

[6] Burnett S, Bird G, Moll J et al. (2008) Develop-ment during adolescence of the neural processingof emotion. Journal of Cognitive Neuroscience 219,1736–50.

[7] Lerner RM. (2004) Urie Bronfenbrenner: Careercontributions of the consummate developmen-tal scientist. In: Bronfenbrenner U (ed.), MakingHuman Beings Human: Bioecological Perspectiveson Human Development. Thousand Oaks, CA: SagePublications, pp. ix–xvi.

[8] Bronfenbrenner U. (ed.). (2004) Making HumanBeings Human: Bioecological Perspectives onHuman Development. Thousand Oaks, CA: SagePublications.

[9] Rothbart MK. (2007) Temperament, development,and personality. Current Directions in PsychologicalScience 16, 207–12.

[10] American Educational Research Association(AREA). (1999) Standards for Educational andPsychological Testing. Washington, DC: AREA.

[11] Berger M. (2009) A Standards-based Approachto Training in Psychological Testing: A discussionpaper. Leicester: Division of Clinical Psychology,British Psychological Society.

[12] Mash EJ and Barkley RA (eds). (2007) Assess-ment of Childhood Disorders, 4th edn. New York:Guilford Press.

[13] Murphy LL, Spies RA, Plake BS (eds). (2006) TestsIn Print VII. Lincoln, NE: University of NebraskaPress.

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40Family Therapy AssessmentAlexandra Mary JohnDepartment of Psychology, University of Surrey, Guildford, UK

In this chapter I provide a brief overview of familytherapy assessment, outlining how theoretical ori-entations can influence assessment, the main goalsfor the assessment process, and the strengths andlimitations of a family systems therapy approachto assessment.

WHAT IS FAMILY THERAPY?

Family therapy, also referred to as couple andfamily therapy, and family systems therapy, isan evidenced-based psychotherapy that seeksto address a variety of emotional, behaviouraland other biopsychosocial difficulties throughworking with family members who are in intimaterelationships. Such relationships could include,for instance, married couples, children with theirparents, grandparents with their adult childrenand grandchildren, and other kinship groups.Within modern family therapy, however, all familymembers do not need to be directly involvedin therapy, though their roles and perspectivescan be discussed and considered by the familymembers who are present

From the perspective of the family therapist, thefamily milieu will have a significant bearing eitheron the development of a person’s presenting emo-tional and behavioural difficulty and/or on its main-tenance. The individual’s ability to accommodateand adjust to life experiences such as a change infamily configuration or a physical health difficulty,as well as the meaning ascribed to those experi-ences, will be influenced by other family members.

Presenting difficulties are not, therefore, seento reside in individuals per se, but to result from


a complex interplay of family relationships andprocesses. For instance, a child’s school refusalcould be regarded as serving a ‘positive’ functionwithin the family if it facilitated communicationsbetween parents who were otherwise emotionallydistant from each other. Equally, the presentingdifficulty may have arisen as a result of a family’sinability to adapt and adjust to changing fam-ily circumstances – as, for instance, when a fatherwho previously worked away from home, nowworks locally and begins to play a greater role indisciplining the children within the family, a rolepreviously undertaken by the children’s mother.

Whatever the family conceives as the‘difficulty’ – that is, the reason they are seekingtherapy – the family therapist will seek to reduceany associated stigmatization and to work withthe family towards a situation where there is somerecognition that all family members have an impor-tant part to play in facilitating an understandingof the problem and in generating a solution.

Family therapy and family-based approacheshave been shown to be effective for a varietyof clinical problems, such as anxiety, depression,psychosomatic problems and eating disorders [1].More detail of family therapy interventions can befound in the Chapter 44.

TYPES OF FAMILY THERAPY AND THEFOCUS OF ASSESSMENT

Over the last 10 years there has been a growth offamily therapy models, with each having differenttheoretical underpinnings, and a variety of psy-chotherapeutic influences have become integrated

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alongside structural, strategic communication andnarrative family approaches. For instance, we haveseen a shift from didactic approaches where ther-apists were experts in charge of changing familyrelationships, to post-modern approaches such asNarrative Family Therapy, in which family mem-bers are considered experts on family functioningand where one goal of therapy is the recognitionand use of family strengths to facilitate change.

Inevitably, theoretical models will influenceto some extent where the focus of assessmentlies. For example, those working within a therapymodel that emphasizes the importance of cognitiveprocesses will encourage individuals to comparetheir thought processes with a rational evaluationof evidence, and also to hear how other membersof the family, who each undertake their ownevaluations, view the matter. Thus the assessmentprocess will focus on ascertaining family membercognitions and their evaluations of alternativeexplanations for events.

In contrast, where presenting difficulties pertainto family communication processes, emotional dif-ficulties or life transition challenges, postmodernapproaches will view the problem as arising out of‘oppressed’ stories that dominate an individual’slife and constrain the possibility of change.Assessment focuses on eliciting narratives fromfamily members that illustrate their perspectiveon the matter of concern, and also the ways inwhich individuals see themselves in relation toeach other and to the presenting difficulty. Oncethe dominant narrative has been identified (i.e.‘assessed’), then the way is open for a possiblereauthoring (or rewriting) of the family story.

While the referral problem will influence thetype of systemic approach that therapists adopt,their choice of approach will also be influencedby their personal values and the characteristicsof the services in which they work. For instance,some therapists working within a legal frameworkmay need to bear in mind that this can militateagainst adopting certain postmodern therapeuticpractices – such as deliberately adopting a ‘con-trary position’ – as legal frameworks have rigidrules acting as an external reality that needs to betaken into account.

Despite the various theoretical frameworkswithin which assessment takes place, all familysystem approaches share the recognition thatthe perceptions, emotions and behaviours of all

family members are relevant. Further, that thevarious assessment processes will in some wayseek to enable therapists and families to considerthe relevance and importance of each familymember’s contribution to the situation with a viewto identifying potential solutions to the family’sconcerns.

GENERAL PRINCIPLES OF FAMILYTHERAPY ASSESSMENT

Several principles guide the process of assessmentin modern systemic approaches. First, thatan explicit theoretical framework guides theassessment process so that it will link coher-ently into subsequent interventions, providing‘theory–practice’ links. Secondly, that the assess-ment process is designed to provide insights intoimportant aspects of family functioning. Thirdly,that assessment offers opportunities for gatheringbaseline measures of problematic aspects of familyfunctioning against which future outcomes can bemeasured [2].

GOALS OF FAMILY THERAPY ASSESSMENT

Family therapy assessment is guided by a funda-mental assumption that the observation of familystructure and processes as they unfold in the clin-ical interview will reveal something of the natureof the presenting problem, its genesis and main-tenance over time. Gaining an understanding ofthese relationships can enable family therapistsand the family to form intervention plans aimedat addressing the relevant family relationships,processes or narratives.

The question for the family therapist is how tostructure the assessment in such a way that impor-tant areas of family functioning are revealed. Var-ious assessment frameworks have been proposed[3–6]. There are differences of focus and emphasisbetween the various models and a variety of termsare used to capture different aspects of family func-tioning. Some major themes that emerge include:

• Gaining an understanding of the presentingproblem: Families most frequently present toclinical services with a ‘problem’, or ‘difficulty’,which is regarded as ‘belonging’ to one familymember. The family therapist will seek to gainan understanding of the complexities of the

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problem – for instance, its salience for all familymembers, its meaning to them, their responsesto it, and their views on aspects of the problemssuch as how and why it arose, and the effects itis having upon the family.

• Family structure, composition and organization:Here, the therapist will try to elicit factors suchas who is in the family, the roles and responsi-bilities adopted by various family members, andhow the family organizes and regulates itself. Forinstance, do the parents form a dyadic subsystemin which they are united in taking on the parent-ing role, or is one parent more closely alignedwith other family members? Over time, how dofamilies accommodate to internal and externalforces that impact upon them? For example, allfamilies will need to adapt to developmentalchild processes that lead the child from infancyto adulthood. In response to these forces forchange, does the family reorganize itself in away that is adaptive or in a way that provesmaladaptive? Is the family organization stableenough for the family to respond to crises with-out fragmentation?

• Family processes: The therapist will want to elicitthe nature of reciprocal interactions and trans-actions. That is, how family members respond toeach other and how interactions at one point intime have influenced, or potentially will influ-ence, subsequent interactions between them.Sequences of interactions will give rise to rela-tionship patterns that the therapist will be keento ascertain in so far as they are relevant tospecific outcomes of interest.

• Patterns of communication: Together, familymembers construct an understanding of givenhappenings. What are these co-constructedunderstandings, and how do they influencethe ways in which families communicatewith each other? What is the affective toneof interactions – how are families conveyingemotion and how are emotions influencing thecommunications between them?

• Biopsychological factors: These factors havebeen seen to be important in, for instance,medical family therapy models where the rela-tionship between medical health conditions andpsychosocial dimensions is explored – as, forexample, in diabetes, anorexia and asthma [7].More recently, attention has been drawnto emerging knowledge of brain chemistry,

neurology and genetic factors and how theseimpact upon behaviour and emotions [8]. Thiscould lead the therapist to seek to ascertain, forinstance, if a child’s difficulties within the schoolsystem are related to genetically influenceddevelopmental factors. One question for thefamily therapist when biopsychosocial factorsare of particular relevance is how do they influ-ence both individual and family functioning,that is, what is the dynamic interrelationshipbetween biological, psychological and family orsocial factors?

• Relationship levels: The focus here is on thesocial relations within the family – what are thesubsystems within the larger family system, andhow do these function in such a way as to accountfor variance between different families? Thesesubsystems may be formalized in some modelsof therapy into, for instance, tracking consis-tent patterns of behaviour that are displayedor elicited between and from various combi-nations of family members, ranging from theindividual level (‘actor’ effects), to the familyas a whole (the ‘group’ effect) [9]. To illustrate,when examining the expression of affect withinthe family, how warmth is consistently expressedby a given family member constitutes an ‘actor’effect, while the way in which one individualin the family elicits warmth from other fam-ily members would be regarded as a ‘partner’effect [10].

Within such frameworks, information will beelicited from family members through a seriesof discussions between therapist and family. It isnot easy, therefore, to make a sharp distinctionbetween assessment and intervention as these dis-cussions may, in themselves, begin to have animpact upon family communication, organizationand relationship patterns.

THE PROCESS OF FAMILY THERAPYASSESSMENT

The therapist initially meets the family andfocuses upon gaining the perspectives of all familymembers through using both direct and circularquestioning. Circular questions enable the thera-pist to take the feedback gained from one questionand use it to shape the next and so allow for a jointconstruction. The style of questioning aims to draw

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out similarities and differences in perspectives,and the strengths and limitations of familymembers; through this process the family can gaina new way of understanding and experiencingeach other.

Reflecting teams are usually a part of the infras-tructure of this type of therapy. They usuallyconsist of two or three clinicians who observethe therapeutic process, with the aim of offer-ing opinions on both the process and content ofthe therapy as it unfolds. They can contributeadditional thoughts – for instance, with regard toobserved or inferred family strengths and themeanings associated with behaviours within thefamily. Through this reflective process, more cre-ative and effective intervention strategies can begenerated. In addition, the reflecting team canensure that the therapist’s own responses to thefamily, as well as any prejudices, are managed anddo not interfere with the therapeutic endeavour.

When and how the reflecting team offers theirobservations is dependent on the school of familytherapy adopted. Some teams choose to sit behinda one-way mirror, whilst others sit in the roomwith the family. The team can choose to interruptthe assessment or intervention if they consideran area needs further exploration. Or they cantake a prearranged break with the therapist toconsider information gained so far. Feedback fromthe reflecting team can be fed back directly to thetherapist, with the therapist feeding back in turnto the family. Alternatively, the reflecting teamcan discuss the assessment with each other in frontof both the therapist and family, who can in thisway share in their observations. These proceduresprovide a collaborative way for families to generateempowering solutions to their difficulties.

RESEARCH ASSESSMENT TOOLS

There are a variety of more formal direct andindirect assessment tools that can provide a pictureof aspects of family functioning. These include, forinstance, the Family Environment Scale [11] andthe Circumplex model and Family Adaptabilityand Cohesion Evaluation Scale (FACES) [12]. Thestrengths and limitations of a wide variety of suchassessment tools with respect to their utility withina child welfare context, and the ease with whichthey link to therapeutic models of intervention,can be found in Johnson et al. [13].

CONCLUSIONS

Family systems therapy offers an approach toassessment that sets an individualized present-ing ‘difficulty’ or ‘problem’ firmly within its widersystemic context, offering opportunities for des-tigmatizing individuals, for enabling all familymembers to feel heard and understood, to gainnew insights and recognize new meanings. It offersthe potential for families to start the process ofconstructing new and more helpful realities. Somelimitations of the approach have been noted. Themajority of family therapy models use Westernwhite culture as their main frame of reference, andthe majority of therapists in the UK come fromthis background. While the appreciation of differ-ent cultures, religions and family forms has beenacknowledged in recent years, there is a limitedevidence base regarding the applicability of somesystemic models to particular minority groups (e.g.single parent, gay, lesbian or blended families). Anopen attitude regarding the legitimacy of a range ofvalues and attitudes across the diversity spectrumis essential if sensitive areas are to be explored ina helpful and constructive way.

REFERENCES

[1] Carr A. (2009) The effectiveness of family ther-apy and systemic interventions for child problems.Journal of Family Therapy 31, 3–45.

[2] Cook WL. (2005) The SRM approach to familyassessment. An introduction and case example.European Journal of Psychological Assessment 21,216–25.

[3] Stanton M. (2009) The systemic epistemology ofthe speciality of family psychology. In: Bray JH andStanton M (eds), The Wiley-Blackwell Handbook ofFamily Psychology. Wiley-Blackwell, pp. 5–20.

[4] Van Geert PLC and Lichtwarck-Aschoff A. (2005)A dynamic systems approach to family assessment.European Journal of Psychological Assessment 21,240–8.

[5] Pincus D. (2001) A framework and methodologyfor the study on nonlinear, self organising fam-ily dynamics. Nonlinear Dynamics, Psychology andLife Sciences 5, 139–73.

[6] Bray JH. (2009) Couple and family assessment. In:Bray JH and Stanton M (eds) The Wiley-BlackwellHandbook of Family Psychology. Wiley-Blackwell,pp. 151–164.

[7] Graca Pereira M and Smith TE. (2006) Evolutionof the biopsychosocial model in the practice of

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Family Therapy. International Journal of Clinicaland Health Psychology 6, 455–67.

[8] Sluzki CE. (2007) Interfaces: towards a new gen-eration of systemic models in family research andpractice. Family Process 46, 173–84.

[9] Cook WL. (2007) The Round–Robin Family assess-ment and Social Relations Model Analysis. In:Smith SR and Hander L (eds), The Clinical Assess-ment of Children. Lawrence Erlbaum Associates,pp. 99–114.

[10] Eichelsheim VI, Dekovic M, Buist KL et al. (2009)The Social Relations Model in family studies: asystematic review. Journal of Marriage and Family71, 1052–69.

[11] Moos R and Moos B. (1986) Family EnvironmentScale Manual, 2nd edn. Palo Alto, CA: ConsultingPsychologists Press; San Francisco: Jossey-Bass,

[12] Olson D H. (1989) Circumplex Model of familysystems: family assessment and intervention. In:Olson DH, Sprenkle DH, Russell CRS (eds), Cir-cumplex Model: Systemic Assessment and Treatmentof Families. New York: Haworth Press, pp. 7–49.

[13] Johnson MA, Stone S, Lou C, Ling J, MizrahiP, Austin MJ. (2006) Family Assessment in ChildWelfare Services: Instrument Comparisons. ReportPrepared by the Centre for Social Services Research(CSSR) at the University of Berkeley.

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Section 7

Approaches toIntervention

Approaches to intervention

41Discovering PsychiatricPharmacogenomicsDavid A. MrazekDepartment of Psychiatry and Psychology, Mayo Clinic College of Medicine, Rochester, MN, USA

THE TREATMENT OF CHILDRENWITH PSYCHOTROPIC MEDICATIONS

The development of psychopharmacologicalinterventions for the treatment of child psychiatricconditions dramatically changed the practice ofchild psychiatry over the course of the twentiethcentury. At the beginning of the century, therewas not yet a single medication identified thatcould help children to deal with the symptomsof child psychiatric illnesses. By 1937, it wasdiscovered that stimulants could help childrenwith hyperkinetic behaviour [1]. Gradually, overthe intervening years many other psychotropicmedications have been demonstrated to havepotential therapeutic benefits for children with awide range of psychiatric disorders and symptoms.

The history of the treatment of children withsevere obsessive-compulsive disorder (OCD)provides insight into the clinical appreciationof the power of new medications. Before thedevelopment of medications to treat the mostextreme forms of OCD, there were many childrenwho were treatment resistant to psychotherapyand behavioural therapy. These included quiteintelligent children who had been very intensivelytreated. Many of the families of these childrenhad nearly given up hope until reports of positiveclinical trials in adult patients were published.Clomipramine became available in Canada beforeit was approved for use in the USA. Duringthis time, US families would make regular tripsto Canada, until clomipramine was eventually


approved for use in the USA. The introductionof fluoxetine a few years later had another majorimpact on the treatment of OCD and againchildren treated with fluoxetine who had beenintractable to any form of psychotherapeutictreatment did respond to this new medication. Ofcourse, not all children responded to clomipramineor fluoxetine, but some children did show dramaticimprovements in response to treatment withthese medications. This variability in response tospecific medications remains one of the greatestchallenges in using psychotropic medications.The introduction of pharmacogenomic testinghas provided the first important tool that is nowavailable to improve our ability to identify a safeand effective medication for a specific patient.

NATIONAL DIFFERENCES IN THEPRESCRIPTION OF PSYCHOTROPICMEDICATIONS FOR CHILDREN

In both the USA and Britain, the benefit of the fullrange of psychotropic medications has been gradu-ally appreciated. However, it is widely recognizedthat the use of psychotropic medication in theUSA is far more extensive than in Britain. Whileit is important to understand better the multiplereasons that psychopharmacological treatment ismore widespread in the USA, one reason for thisdifference is that with more experience of pre-scribing psychotropic medication clinicians havepersonally observed the clinical benefit for somechildren. Given this observation, many clinicians

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have focused on this potential for positive outcomeeven in the light of relatively low certainty that anygiven child will benefit. Essentially, the potentialreward of a dramatic response has been judgeda sufficiently valuable benefit to justify treatmenteven knowing that as many as half of the treatedpatients will not have an effective response.

Currently, psychotropic medications play arole in the treatment of children with virtuallyevery psychiatric diagnosis. Yet, the evidencebase for the implementation of psychopharma-cological treatment remains relatively subjective.Furthermore, inconsistencies in the conduct andreporting of clinical trials have led to considerablecontroversy. At the heart of this dialogue is theclinical observation that many children responddramatically to psychotropic medications whileother children do not respond at all or, in fact, getworse. Despite years of investigation, it has onlybeen in the last decade that our understanding ofsome of the biological factors responsible for thesevariable responses has begun to come into focus.

There are two major issues that have slowedthe adoption of psychopharmacological treatmentin both the USA and Britain. The first is therecognition that there are a wide range of adversedrug effects that occur in patients treated with anyclass of psychotropic medications. The second isan almost universal appreciation that there is wideindividual variability in the response of childrento treatment with psychotropic medications. Afteryears of using empirical approaches to guidethe use of psychotropic medications for childpsychiatric illnesses, there is now an evidence-based methodology to aid clinicians both to selectmedications and to predict the appropriate dosagefor a specific patient.

WHAT IS PSYCHIATRICPHARMACOGENOMICS?

Psychiatric pharmacogenomics is a scientificapproach to using the measurement of geneticvariability to predict the medication response of aspecific child. Pharmacogenomics is not an easydiscipline to approach for psychiatrists who arenot familiar with molecular genetics, but it can bemastered by systematically working through thebasics of how changes in gene structure influencegene function [2].

Schoolchildren in the USA and Britain learnthat both the Rosetta stone and the genetic codeare important examples of famous breakthroughsin our understanding of the world. The Rosettastone represents an ability to use a familiarlanguage to translate a cryptic form of writing ofthe past. Breaking the genetic code allowed us totranslate the language of nucleotides in a way thatprovides an understanding of the nature of individ-ual genetic variability. What has been amazinglyslow to be realized is that variations in the geneticsequences of our patients give us the ability to pre-dict their responses to psychotropic medications.

As outlined in the previous section, we havesuccessfully developed medications to treatthe symptoms of child psychiatric disorders.In addition to the selective serotonin reuptakeinhibitors (SSRIs) that are used for mood disorderand OCD, we also have stimulants and atomox-etine for attention deficit disorder. The atypicalantipsychotics are used for schizophrenia andbipolar disorder, which is also treated with lithiumand other mood-regulating medications. Whileclinicians have learned that these medicationscan be extremely effective for some children, thesobering reality is that they can also make otherchildren much worse. Until very recently, therewas no other alternative but to proceed with a‘trial-and-error’ strategy to search for the rightmedication for a particular child.

An appreciation of how predictions of medi-cation response can be derived requires learningabout gene structure and function. The moststraightforward examples are genotyping drugmetabolizing genes, such as the cytochrome P4502D6 gene, that produce enzymes that metabolizepsychotropic medications (Table 41.1).

Table 41.1 The 2D6 relative role in themetabolism of common antidepressants.

Primarily Substantially Minimallymetabolized metabolized metabolizedby 2D6 by 2D6 by 2D6

Desipramine Amitriptyline CitalopramDoxepine Bupropion DesvenlafaxineFluoxetine Duloxetine EscitalopramNortriptyline Imipramine FluvoxamineParoxetine Mirtazapine SertralineVenlafaxine Trazodone

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THE CYTOCHROME P450 2D6 GENE

The cytochrome P 450 2D6 gene (CYP2D6) hasbeen studied for the last 30 years and is only oneof dozens of genes that can provide insight into theresponse of a patient to a medication [3]. However,the beginning of child psychiatric pharmacoge-nomics emerged from the study of variations indrug metabolism of 2D6 substrate medications.For child psychiatrists, the testing of CYP2D6allows them to determine with a high degree ofcertainty whether a particular child will be ableto tolerate a medication like paroxetine, fluoxe-tine, atomoxetine, risperidone or haloperidol as aconsequence of their ability to metabolize thesemedications.

The CYP2D6 gene is located on the smallestautosome, which is chromosome 22. Its chromo-somal address is 22q, which indicates that it ison the long arm of this short chromosome. It iscomposed of 1491 nucleotides and has nine exonsthat code for an enzyme with 497 amino acids. Itis one of the most highly variable genes that arecommonly genotyped. The more than 100 variantsare catalogued on the Karolinska Institute web-site (http://www.cypalleles.ki.se/). Essentially, it ispossible to identify children who are either slowmetabolizers or fast metabolizers.

Poor 2D6 substrate metabolizersChildren who lack even one ‘good’ copy of theCYP2D6 gene are classified as poor metaboliz-ers. These children cannot make enough 2D6enzyme to metabolize standard doses of fluoxe-tine or paroxetine. Approximately 10% of patientsof European ancestry are poor metabolizers andexperience moderate to severe side effects at stan-dard doses of these drugs. Both children and adultswho are poor metabolizers of 2D6 have had fataltoxic reactions to 2D6 substrate medications [4,5].

The case of a 9-year-old boy who was treatedwith up to 100 mg of fluoxetine for the treatment ofOCD with comorbid Tourette’s disorder has beendescribed [4]. The boy developed status epilep-ticus and then died of a cardiac arrest. It wassubsequently determined that he had two inac-tive copies of the CYP2D6 gene. At autopsy,it was determined that his serum fluoxetine andserum norfluoxetine levels were both in the toxicrange. This provided evidence that the elevatedserum fluoxetine level was not the result of an

acute overdose of fluoxetine. Pharmacogenomictesting would have revealed that this child was athigh risk for a fatal outcome if given high dosesof fluoxetine.

Ultra-rapid 2D6 substrate metabolizersChildren who have three or more active copies ofthe 2D6 gene or who have two or more copies of theupregulated alleles of CYP2D6 have been demon-strated to metabolize 2D6 substrates very quickly.These children are usually unable to achieve ther-apeutic serum levels of 2D6 substrate medicationsat traditional doses. The demonstration of thisvery rapid metabolism has been documented bypharmacokinetic studies that have revealed signif-icantly decreased drug exposure in patients withultra-rapid metabolism [6].

Child psychiatrists must also become aware ofthe implications of the CYP2D6 metabolic capacityof the mothers of breastfed infants, as the mentalstatus of these infants can be dramatically affectedif these mothers take prodrugs like codeine. Abreastfeeding mother who is an ultra-rapid meta-bolizer of 2D6 substrate medications will rapidlymetabolize codeine to morphine. Given that highserum levels of morphine in the mother will resultin high levels of morphine in her breast milk,her infant will become increasingly lethargic as aconsequence of nursing. A tragic case of an infantwho died as a consequence of morphine toxicitywas reported in the Lancet and has fortunatelyled to much greater awareness of the value ofpharmacogenomic testing in pregnant women [7].

BEYOND CYP2D6

Given that there are many gene variations thataffect both drug metabolism and response, psy-chiatric pharmacogenomic testing is increasinglyassessing variation in many relevant genes thatultimately influence how a particular patient willrespond to a specific medication. It is increasinglyapparent that clinicians will need to systematicallyreview the implications of these gene variations forthe medications that they prescribe [2].

Currently, it is possible to order the geno-typing of both drug-metabolizing enzyme genesand key target genes such as the serotonintransporter (SLC6A4) and the serotonin receptorgenes (HTR2A, HTR2C) to guide the selectionand dosing of psychotropic medications. Other

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informative genes include the catecholamine-O-methyltransferase gene (COMT) and thedopamine receptor genes (DRD2, DRD3, DRD4).

It is clearly most practical for clinicians to orderthese pharmacogenomic panels from laboratoriesthat provide comprehensive guidance on the impli-cations of these gene variations for specific psycho-tropic medications. Fortunately, there are nowmultiple reference laboratories that are providingpharmacogenomic testing and interpretations.

FUTURE EXPECTATIONS FORPHARMACOGENOMICS TESTING

Many child psychiatrists in the USA have begunto adopt clinical pharmacogenomic testing [8].However, pharmacogenomic testing is still largelyundiscovered in Britain. This is almost certainly thedirect result of the much wider use of psychotropicmedications in the USA. However, it is safe to pre-dict that within the next decade there will be rapidadoption of psychiatric pharmacogenomic testingon both sides of the Atlantic. The most importantreason is that gene sequencing will become avail-able as a standard component of a comprehensiveclinical diagnostic evaluation. Today, in order forchild psychiatrists to order a panel of informativepharmacogenomic genes, they must have a cogni-tive understanding of the rationale for the potentialbenefit of testing. Of course, there is also a consid-eration about whether the benefit is worth the costof the testing. When the cost of genotyping theentire genomic sequence of a patient falls belowUS$1000, sequencing will become a standard com-ponent of a comprehensive patient evaluation. Thecurrent director of the National Institute of Healthin the USA has predicted that patients will beroutinely sequenced when the cost of sequencingreaches $1000. Furthermore, he estimates that thisprice point will be reached by 2015 [9]. After 2015,it will still be necessary to develop software tointerpret the implications of the genetic variabil-ity of our patients, but there will be a stampede ofbioinformaticists who will be competing to developthe most effective methodologies to diagnose andtreat both the traditional physical illnesses as wellas what we currently refer to as mental illnesses.

It is likely that in the next five years the genotyp-ing of panels of pharmacogenomically informative

genes will become increasingly commonplace inthe USA. As the number of adverse effects ofpsychotropic medications decreases, the use ofthese medications will, in all likelihood, increaseeven in children with less severe psychiatric ill-nesses. Ultimately, the societal cost of mentalillness will drop as the chronic disabilities thatwe currently manage become more of a historicalmemory than our daily responsibility.

REFERENCES

[1] Bradley C. (1937) The behavior of children receivingbenzedrine. American Journal of Psychiatry 94,577–85.

[2] Mrazek DA. (2010) Psychiatric Pharmacogenomics.New York: Oxford University Press.

[3] Kirchheiner J, Nickchen K, Bauer M et al. (2004)Pharmacogenetics of antidepressants and antipsy-chotics: the contribution of allelic variations to thephenotype of drug response. Molecular Psychiatry9, 442–73.

[4] Sallee FR, DeVane CL, Ferrell RE. (2000)Fluoxetine-related death in a child with cytochromeP-450 2D6 genetic deficiency. Journal of Child andAdolescent Psychopharmacology 10, 27–34.

[5] Koski A, Ojanpera I, Sistonen J et al. (2007) Afatal doxepin poisoning associated with a defectiveCYP2D6 genotype. American Journal of ForensicMedicine and Pathology 28, 259–61.

[6] Dalen P, Dahl ML, Ruiz ML et al. (1998) 10-Hydroxylation of nortriptyline in white persons with0, 1, 2, 3, and 13 functional CYP2D6 genes. ClinicalPharmacology and Therapeutics 63, 444–52.

[7] Koren G, Cairns J, Chitayat D et al. (2006) Phar-macogenetics of morphine poisoning in a breastfedneonate of a codeine-prescribed mother. Lancet368, 704.

[8] Wall CA, Oldenkamp C, Swintak C. (2010) Safetyand efficacy pharmacogenomics in pediatric psy-chopharmacology. Primary Psychiatry 17, 53–8.

[9] Collins FS. (2010) The Language of Life: DNA andthe Revolution in Personalized Medicine. New York:Harper.

INTERNET RESOURCE

Karolinska Institute, Human Cytochrome P450 (CYP)Allele Nomenclature Committee: http://www.cypalleles.ki.se/.

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42Cognitive–Behavioural Therapyfor Children and AdolescentsCathy Creswell1 and Thomas G. O’Connor21School of Psychology and Clinical Language Sciences, University of Reading, Reading, UK2Department of Psychiatry, University of Rochester Medical Center, Rochester, NY, USA

Cognitive–behavioural therapy (CBT) is atreatment approach based on the general notionthat a psychological disorder is caused or main-tained by ‘dysfunctional’ thought patterns andlack of positively reinforced adaptive behaviouralcoping strategies. CBT is a class of treatment; allcognitive–behavioural treatments aim to identifyand reduce cognitive biases or distortions andbuild effective coping and problem-solving skills.After decades of extensive research on CBT inadult populations [1], CBT is now being appliedto child and adolescent populations with success.

BASIC PREMISES OF THE CBT APPROACHAND ITS ADMINISTRATION

According to the basic CBT model, disorder isconceptualized as resulting, in part, from theindividual’s cognitive distortions (such as falseattributions or expectations of the self or other)that undermine positive coping and problem-solving behaviour. There is now considerableevidence that cognitive distortions exist and mayplay a causal – or at least contributing – rolein many childhood disorders, with much ofthe work focusing on depressed, anxious andconduct-problem youth [2–5] (Box 42.1). Severalclinical and developmental models have informedand been informed by research into the processesby which distorted cognitions are developedand influence behavioural/emotional problems.One example, the social information processing


model [5], was developed in the context of conductdisorder but has proved useful for other childhooddisorders, including depression and anxiety. Themodel focuses on the following:

• the child’s attending to, encoding and interpret-ing social cues (e.g. why did that child step onmy foot?);

• developing goals for one’s own behaviour (e.g.what do I want to do now?);

• generating potential solutions and evaluatingtheir effects (e.g. what would happen if I hitback at him?).

Several CBT programmes have been devisedand shown to be clinically effective. Although thereis some tendency to tailor the CBT treatment fora particular disorder (see studies cited below), itis possible to make several basic statements abouthow CBT is administered. In general, CBT inter-ventions seek to break the cascade of maladaptivethoughts and feelings that lie between the cogni-tive distortion and the destructive behaviour. Thisoccurs in a logical, stepped manner usually lasting8–16 sessions, typically on a 1 session/week sched-ule (Box 42.2). A first step is to collate detailedinformation about the settings that lead the childto feel, for example, anxious and unable to copewith a particular situation. A second step is tohelp the child/adolescent to identify and differ-entiate thoughts, feelings and somatic reactionslinked with these situations Subsequently, there is afocus on self-talk, or helping the child to recognize

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Box 42.1 Examples of key cognitions associated with childhood

Characteristics of clinically anxious children [3]• Vigilant to threat

• Interpret ambiguity as more threatening

• Come to faster conclusions about threat

• Underestimate personal coping ability

• Anticipate distress (often exaggerated) in the face of threat

Characteristics of clinically aggressive children [4]• Attend to less social cues

• Direct attention towards hostile social cues

• Interpret stimuli in a hostile manner

• Generate fewer solutions to social problems

• Positively appraise aggressive responses

• Positively appraise own ability to perform aggressive response

Characteristics of clinically depressive children [5]• Selectively attend to negative features of events

• Report negative attributions (i.e. internal, stable explanations for positive events andexternal, unstable explanations for negative events)

Box 42.2 Core steps in cognitive—behavioural therapy (CBT) forchildhood anxiety

• Recognize feelings and physicalreactions

• Identify associated thoughts (e.g.interpretations, attributions andexpectations)

• Cognitive restructuring/coping self-talk

• Progressive muscle relaxation

• Imaginary/in vivo (graded) exposure

• Self-evaluation and reward

how certain kinds of self-talk can be destructive(‘I’ll look silly’) and promoting positive self-talk(‘I have done this OK before’). Using these skills,children are then supported to develop a hierarchyof anxiety-producing situations, which theygradually face, with a clear reward structure in

place. Relaxation is often included to improve thechild’s coping strategies and expand his/her copingrepertoire. Throughout treatment children arehelped to evaluate their newly developed copingskills in ‘real-life’ settings, and these are rewardedwhere appropriate. This can continue for severalsessions, as the child learns to test new strategiesand, through trial and error, to find strategies thatwork and to diagnose why other strategies donot. Homework throughout the treatment processfosters understanding of why feelings of anxiety ordepression develop and how they might be man-aged effectively. In addition, emphasis is placedon developing rapport with the child/adolescentthroughout the treatment. CBT programmesvalue rapport, but unlike some approaches, donot construct the treatment as working throughthe relationship with the therapist. Instead, theCBT therapist guides the child/adolescent toreshape attributions and expectations in orderto change behaviour. Treatments including afamily component are increasingly common, andtypically this means an ancillary focus on theparents’ behaviour, or a parent’s own anxiety

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and how that may influence the child via thechild–parent relationship. These approaches buildon and address the finding that parental anxietyhas been found to be a significant predictor oftreatment failure of individual treatment of thechild [6]; parents who model poor coping, parentin an overprotective manner and communicateexpectations to the child that she/he cannot copewith effectively may undermine the child’s individ-ual treatment [7]. Particularly valuable in this areaare studies now underway that seek to manipulatethe degree of family involvement in order tobetter understand treatment mechanisms. It is notyet clear what additional benefits are conferred bythese treatment models, but findings from thesestudies should be closely monitored because theymay have a substantial impact on how CBT-relatedtreatments for children may be optimized.

DEVELOPMENTAL CONSIDERATIONS

We now know that depressed, anxious or conduct-problem-related cognitions are evident at anearly age. In a study of 5-year-olds, Murray andcolleagues found that higher rates of negativecognitions, defined as ‘spontaneous’ expressionsof hopelessness or low self-worth during an exper-imentally manipulated card game with a friend,were observed in children whose mothers were, orhad been, depressed [8]. Significantly, differencesbetween the children of depressed and non-depressed mothers were apparent only when thechildren were losing. Evidence that cognitive dis-tortions do not operate in a trait-like manner, evenin 5-year-olds, is an important clinical and devel-opmental lesson. Other studies also suggest thatcognitive biases or distorted ‘filters’ exist in youngchildren and may be learned from parent-childinteractions. A study of 2–6 1

2 -year-olds foundthat insecurely attached children showed poorerunderstanding of negative emotions comparedwith securely attached children; in other words,they had more difficulty explaining or makingsense of negative emotions [9]. Findings from theseand many other studies are valuable not only forwhat they say about the phenomena, but also forthe practical lessons they yield for assessing youngchildren. Greater integration of these methods inclinical settings is feasible and a valuable next stepfor advancing clinical assessment and treatmentmonitoring (Box 42.3). Demonstrating that young

children with elevated behavioural/emotionalsymptoms exhibit cognitive distortions doesnot mean that these cognitive processes arecausally linked with disorder; neither does itnecessarily imply that altering these cognitionswill produce positive behavioural change. Indeed,it is somewhat surprising that little is known aboutthe developmental constraints around CBT-basedtreatments, and clinical research has not yetdemonstrated that a child’s developmental stagepredicts treatment outcome. This may be becausethe predictors so far considered (e.g. age) are weakindicators of the cognitive and social processesthat are required for successful CBT. However,the theory and implementation of CBT has notbeen especially developmentally informed. So,for example, the traditional CBT model is notexplicit about why the approach might workwith a 12-year-old but not with a 5-year-old. Ifthere is a general impression, it is that CBT isan effective treatment for depression and anxietyin children aged around 8 years, with both short-and long-term gains. In any event, it is clear thatCBT may be very effective. It is worth notingthat Kendall and Southam-Gerow found thatindividual CBT was highly effective in treatingchildren/adolescents with anxiety disorders, andthat approximately 90% were diagnosis-free morethan 3 years after treatment ended [10].

RECENT ADVANCES IN CBT PROGRAMMESFOR CHILDREN AND ADOLESCENTS

Recent clinical research findings on CBT inchildren and adolescents are noteworthy in severalrespects. One is the enlarged range of conditionsfor which CBT has produced large, reliable andclinically meaningful findings. So, for example,in addition to depression and anxiety [10,11],there are now studies showing positive effectsfor post-traumatic stress disorder [12,13] andobsessive-compulsive disorder [14]. However, itremains the case that most of the CBT studiesare efficacy studies, that is, the treatment hasbeen shown to work under relatively controlledconditions. As a result, concerns about the gener-alizability of the study effects have been expressed.These are real and important, but they should notbe seen as reasons for not undertaking standardtreatment protocols. In any event, what is needed

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Box 42.3 Sample responses to ambiguous scenarios

You have arranged to have a party at 4pm and by 4.30 no one has arrived

Cognitive bias — What do you think is most likely to have happened?

• Anxious: ‘Nobody wants to come to the party’

• Aggressive: ‘Nobody wants to come to the party’

• Non-clinical controls: ‘They might be late because there is bad traffic’

Behaviour — What will you do about it?

• Anxious: ‘Nothing. Feel upset’

• Aggressive: ‘Get cross and when I see them at school I will tell them I don’t want to befriends with them’

• Non-clinical controls: ‘Phone around and see where they are and when they will arrive’

You are playing inside and your dog starts barking and growling outside

Cognitive bias — What do you think is most likely to have happened?

• Anxious: ‘There is someone I don’t know trying to get into my house’

• Aggressive: ‘Someone is stealing my bike from outside’

• Non-clinical controls: ‘Another dog is walking past outside’

Behaviour — What will you do about it?

• Anxious: ‘Hide’

• Aggressive: ‘Find the thief and hit them’

• Non-clinical controls: ‘Look out of the window and tell my dog to be quiet’

Adapted from Barrett PM, Rapee PM, Dadds MR, Ryan SM. Family enhancement of cognitive style in anxiousand aggressive children. Journal of Abnormal Child Psychology 1996;24:187—203.

now are studies that carry out CBT-based interven-tions for child populations in conventional clinicalsettings using samples that are representative ofclinic settings. Work of that kind is underway. Ina recently completed study of 41 children withanxiety disorder treated within a primary caresetting, we found equivalent outcomes (61% freeof primary anxiety diagnosis post-treatment) tothose found in trials conducted in specialist childanxiety clinics [15]. These preliminary findings arepromising and encourage the application of theseprotocols in non-specialist settings.

Another recent advance in work on CBT inchildren and adolescents is that it is increasinglybeing set up against or in addition to medication.In fact, there are several large-scale trials com-paring CBT with drug and combined conditions.Probably the best known are the Treatment for

Adolescents with Depression Study (TADS [11])and the Child Anxiety Multisite (CAM [16]) study.In the TADS study, follow-up to 36 weeks showsthat treatment-group differences apparent in theearlier phases of treatment diminished over time,with the result that there was convergence amongthe CBT-only, medication-only (fluoxetine), andCBT plus medication conditions [11]. The rate ofadolescents with suicidal ideation (none commit-ted suicide in the trial) was considerably higherin the medication-only group (15%) than in thecombined (8%) or CBT only (6%) conditions; thatis naturally a major consideration when makingtreatment decisions. Perhaps even more impres-sive are data showing that CBT can be effectiveas a treatment strategy even where drug treat-ment was ineffective [17]. However, this studydid not include a CBT-only arm, and so it is not

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possible to know whether CBT alone would havebeen successful following drug treatment failure.The CAM study, in contrast, compared outcomesof children aged 7 to 14 years with a diagnosedanxiety disorder randomized to either 14 sessionsof CBT, sertraline, a combination of sertraline andCBT, or a placebo drug [16]. Based on a clini-cian’s global impressions of improvement, 81% ofchildren were reported as ‘much’ or ‘very much’improved following the combination treatment,60% for CBT, and 55% for sertraline, all of whichwere superior to outcomes from placebo (24%).Importantly there was not a greater frequency ofadverse events amongst the sertraline group; how-ever, there were significantly greater incidence ofsymptoms of insomnia, fatigue, sedation and rest-lessness amongst children who received sertralinein comparison to CBT.

These findings and those of other studieshave shown that assumptions about CBT beingappropriate only for more mild cases is no longersupported by the evidence. Indeed, although itsimpact is even greater when coupled with medica-tion, CBT is an important stand-alone treatmentand, in terms of its effectiveness and side-effectprofile, it can be considered as a first-choice treat-ment rather than an add-on to other approaches,such as medication. The question now for mentalhealth professionals is not whether CBT is areasonable treatment option, but rather how toincrease the availability of CBT to children andfamilies. Another recent advance in CBT workconcerns the mediators of treatment (why doestreatment work?) and the moderators of treatment(what predicts who will respond and who willnot?). Findings from this research are importantfor improving our understanding of the treatmentprocess and for better targeting those who are mostlikely to benefit from treatment. There are sug-gestions but, to date, not much consistency acrossstudies. This is likely to improve as research studiesmove on from asking if treatment works and takeon the next stage of research, namely questionsabout why and for whom treatment works.

Finally, CBT is incorporated in preventionprogrammes in universal, indicated and selectedsamples. A recent review of school-based pro-grammes [18] indicated that they were effectivefor anxiety, with effect sizes ranging from small tolarge. That is significant because it demonstrates

that CBT can be used as a general tool and acrossa variety of settings.

CONCLUSION

Children’s cognitions about their social worldreflect developmental histories that shapebehaviour. CBT is concerned with how thesecognitive processes may be altered and, whenaltered, if there are consequential reductions inpsychiatric symptoms and improvements in socialfunctioning. Results from many clinical trials haveshown that CBT reliably improves outcomes inchildren; recent studies show that CBT should nolonger be considered only for more mild cases,and that the list of targeted disorders appropriatefor CBT is increasing. Additionally, CBT has beenshown to be as effective as, perhaps better than,and possibly a useful adjunct to, medication. Thesefindings are important for instilling confidencein recommending treatment for ill and distressedchildren and their families. A next step is todevelop increasingly efficient modes of delivery toimprove access to this effective form of treatment.

REFERENCES

[1] Elkin I, Gibbons RD, Shea MT et al. (1995) Initialseverity and differential treatment outcome in theNational Institute of Mental Health Treatment ofDepression Collaborative Research Program. Jour-nal of Consulting and Clinical Psychology 63, 841–7.

[2] Muris P. (2010) Anxiety-related reasoning biases inchildren and adolescents. In: Hadwin JA and FieldAP (eds), Information Processing Biases and Anxi-ety: A Developmental Perspective. Wiley-Blackwell,pp. 21–46.

[3] Orobia de Castro B, Veerman JW, Koops W, BoschJD, Monshouwer HJ. (2002) Hostile attribution ofintent and aggressive behaviour: A meta-analysis.Child Development 73, 916–34.

[4] Abela JRZ, Brozina K, Haigh EP. (2002) An exam-ination of the response styles theory of depressionin third- and seventh-grade children: A short-termlongitudinal study. Journal of Abnormal Child Psy-chology 30, 515–27.

[5] Crick N and Dodge KA. (1994) A review and refor-mulation of social information processing mecha-nisms in children’s social adjustment. PsychologicalBulletin 115, 74–101.

[6] Cobham VE, Dadds MR, Spence SH. (1998) Therole of parental anxiety in the treatment of child-hood anxiety. Journal of Consulting and ClinicalPsychology 66, 893–905.

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[7] Murray L, Creswell C, Cooper PJ. (2009) Thedevelopment of anxiety disorders in childhood:an integrative review. Psychological Medicine 39,1413–23.

[8] Murray L, Woolgar M, Cooper P, Hipwell A. (2001)Cognitive vulnerability to depression in 5-year-oldchildren of depressed mothers. Journal of ChildPsychology and Psychiatry 42, 891–99.

[9] Laible DJ and Thompson RA. (1998) Attachmentand emotional understanding in preschool children.Developmental Psychology 34, 1038–45.

[10] Kendall PC and Southam-Gerow MA. (1996) Long-term follow-up of a cognitive behavioural therapyfor anxiety-disordered youth. Journal of Consultingand Clinical Psychology 64, 724–30.

[11] The TADS team. (2007) The treatment for adoles-cents with depression study (TADS). Archives ofGeneral Psychiatry 64, 1132–44.

[12] Cohen JA, Deblinger E, Mannarino AP, Steer RA.(2004) A multisite, randomized controlled trial forchildren with sexual abuse-related PTSD symptoms.Journal of the American Academy of Child andAdolescent Psychiatry 43, 393–402.

[13] Smith P, Yule W, Perrin S, Trannah T, DalgleishT, Clark D. (2007) Cognitive behavioural therapyfor PTSD in children and adolescents: a preliminaryrandomized controlled trial. Journal of the Amer-ican Academy of Child and Adolescent Psychiatry46, 1051–61.

[14] The Pediatric OCD Treatment Study (POTS)Randomized Trial. (2004) Cognitive-behavior ther-

apy, sertraline, and their combination for childrenand adolescents with obsessive-compulsive disor-der. Journal of the American Medical Association292, 1969–76.

[15] Creswell C, Hentges F, Parkinson P, Sheffield P,Willetts L, Cooper PJ. (2010) Feasibility of guidedcognitive behaviour therapy (CBT) self-help orchildhood anxiety disorders in primary care. MentalHealth in Family Medicine 7, 49–57.

[16] Walkup JT, Albano AM, Piacentini J et al. (2008)Cognitive behavioral therapy, sertraline or a combi-nation in childhood anxiety. New England Journalof Medicine 359, 2753–66.

[17] Brent D, Emslie G, Clarke G et al. (2008) Switchingto another SSRI or to venlafaxine with or withoutcognitive behavioral therapy for adolescents withSSRI-resistant depression. Journal of the AmericanMedical Association 299, 901–13.

[18] Neil AL and Christensen H. (2009) Efficacy andeffectiveness of school-based prevention and earlyintervention programs for anxiety. Clinical Psychol-ogy Review 29, 208–15.

FURTHER READING

O’Connor TG and Creswell C. (2005) Cognitivebehavioural therapy (CBT) in developmental perspec-tive. In: Graham P (ed.), Cognitive-Behaviour Therapyfor Children and Families, 2nd edn. Cambridge: Cam-bridge University Press; pp. 25–47.

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43Parenting Programmes for ConductProblemsStephen Scott1 and Sajid Humayun2

1Institute of Psychiatry, King’s College London, Department of Child and Adolescent Psychiatry,London, UK2National Academy for Parenting Research, Institute of Psychiatry, King’s College London, London, UK

EVIDENCE LINKING PARENTING TO CHILDPSYCHOPATHOLOGY

The finding that parent–child relationship qualityis associated with aggressive behaviour, conductdisorder and delinquency is one of the mostwidely reported in the literature, repeatedly foundin large-scale epidemiological investigations,intensive clinical investigations and naturalisticstudies of diverse samples using a mixture ofmethods [1]. The sort of parenting behavioursassociated with these outcomes are high criticismand hostility, harsh punishment, inconsistentdiscipline, low warmth, low involvement, lowencouragement and poor supervision.

The link with depression, anxiety and otheremotional problems (e.g. somatic complaints,social withdrawal) is clear, although smaller thanthat found for disruptive outcomes [2]. There isalso a connection between parenting and qualityof a child’s peer relationships, mediated by socialcognitions and behavioural strategies learnedfrom interacting with parents (Box 43.1).

PROGRAMMES FOR CHILDREN BASEDON SOCIAL LEARNING THEORY

Programmes based on social learning theory haveevolved for more than 40 years and there is alarge evidence base. Most are aimed at antisocialbehaviour as their proximal target outcome. The


content and delivery of a typical programmeis shown in Box 43.1. Most basic programmestake 8–12 sessions, lasting 1.5–2 hours each.Full accounts of programmes are given by thedevelopers [3,4].

FORMAT OF A TYPICAL SOCIALLEARNING PROGRAMME

Teaching a child-centred approachThe first session covers play. Parents are asked tofollow the child’s lead rather than impose their ownideas. Instead of giving directions, teaching andasking questions during play, parents are instructedsimply to give a running commentary on theirchild’s actions. As soon as the parent complies, thepractitioner gives feedback. After 10–15 minutes,this directly supervised play ends and the parentis ‘debriefed’ for half an hour or more alone withthe clinician.

The second session involves elaboration of playskills. The previous week’s ‘homework’ of playingat home is discussed with the parent in consider-able detail. Often there are practical reasons fornot doing it (‘I have to look after the other children,I’ve got no help’) and parents are then encouragedto solve the problem and find ways around the dif-ficulty. For some parents there may be emotionalblocks (‘it feels wrong – no one ever played withme as a child’), which need to be overcome beforethey feel able to practise the homework.

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Box 43.1 Features of effective parenting programmes based on social learningtheory

Content

• Structured sequence of topics, introduced in set order during 10—12 weeks

• Curriculum includes play, praise, rewards, setting limits and discipline

• Parenting seen as a set of skills to be deployed in the relationship

• Emphasis on promoting sociable, self-reliant child behaviour and calm parenting

• Constant reference to parent’s own experience and predicament

• Theoretical basis informed by extensive empirical research and made explicit

• Plentiful practice, either live or role-played during sessions

• Homework set to promote generalization

• Accurate but encouraging feedback given to parent at each stage

• Self-reliance prompted (e.g. through giving parents tip sheets or book)

• Emphasis on parents’ own thoughts and feelings varies from little to considerable

• Detailed manual available to enable replicability

Delivery

• Strong efforts made to engage parents (e.g. home visits if necessary)

• Collaborative approach, typically acknowledging parents’ feelings and beliefs

• Difficulties normalized, humour and fun encouraged

• Parents supported to practise new approaches during session and through homework

• Parent and child can be seen together, or parents only seen in some group programmes

• Creche, good-quality refreshments, and transport provided if necessary

• Therapists supervised regularly to ensure adherence and to develop skills

After this discussion, live practice with the childis carried out. This time the parent is encouragedto go beyond describing the child’s behaviour andto make comments describing the child’s likelymood state (e.g. ‘you’re really trying hard makingthat tower’, or ‘that puzzle is making you really fedup’). This process has benefits for both the parentand the child. The parent gets better at observingthe fine details of the child’s behaviour, whichmakes them more sensitive to the child’s mood.The child gradually gets better at understandingand labelling his/her own emotional states.

Increasing desirable child behaviourPraise and rewards are covered here. The parentis required to praise their child for lots of simpleeveryday behaviours such as playing quietly on

their own, eating nicely, and so on. In this way thefrequency of desired behaviour increases. How-ever, many parents find this difficult. Usually, withdirectly coached practice, praise becomes easier.Later sessions go through the use of reward charts.

Imposing clear commandsA hallmark of ineffective parenting is a continu-ing stream of ineffectual, nagging demands for thechild to do something. Parents need to be taughtto reduce the number of demands, but make themmuch more authoritative. This is done throughaltering both the manner in which they are given,and what is said. The manner should be force-ful (standing over the child, fixing him/her in theeye, and in a clear firm voice giving the instruction).

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The emotional tone should be calm, without shout-ing and criticism. The content should be phraseddirectly (‘I want you to . . . ’). It should be specific(‘keep the sand in the box’) rather than vague (‘dobe tidy’). It should be simple (one action at a time,not a chain of orders), and performable immedi-ately. Commands should be phrased as what theparent does want the child to do, not as whatthe child should stop doing (‘please speak quietly’rather than ‘stop shouting’). Instead of threateningthe child with vague, dire consequences (‘you’regoing to be sorry you did that’), ‘when–then’ com-mands should be given (‘when you’ve laid thetable, then you can watch television’).

Reducing undesirable child behaviourConsequences for disobedience should be appliedas soon as possible. They must always be followedthrough: children quickly learn to calculate theprobability that consequences will be applied, andif a sanction is given only every third occasion, achild is being taught he/she can misbehave the restof the time. Simple logical consequences should bedevised and enforced for everyday situations (e.g.if a child refuses to eat dinner, there will be nopudding). The consequences should ‘fit the crime’,should not be punitive, and should not be longterm (e.g. no bike riding for a month), as this willlead to a sense of hopelessness in the child, whomay see no point in behaving well if it seems thereis nothing to gain. Consistency of enforcementis central.

Time-out from positive reinforcement remainsthe final ‘big one’ as a sanction for unacceptablebehaviour. The point here is to put the child ina place away from a reasonably pleasant context.Parents must resist responding to taunts and criesfrom the child during time-out, as this will reinforcethe child by giving attention. Time-out provides abreak for the adult to calm down also.

INTERVENTIONS WITH YOUTH

In adolescence somewhat different approaches arenecessary, with more emphasis on negotiation andclose supervision when the young person is out ofthe home. Also, whilst many components of pro-grammes based on social learning theory are incor-porated, additional elements may be required. Inparticular, there may need to be more of a focuson the wider systems around the youth, be they

the wider family, school or peer networks. Thusinterventions tend to be one of two types:family-based interventions or multicomponentinterventions.

Family-based interventionsBeing based on systemic family therapy theo-ries, family-based interventions typically attemptto alter the structure and functioning of the familyunit. The best known in the context of delinquencyis Functional Family Therapy (FFT) [5]. It isdesigned to be practicable and relatively inexpen-sive: 8–12 one-hour sessions are given in the familyhome, to overcome attendance problems commonin this client group; for more intractable cases,26–30 hours are offered, usually over 3 months.

There are three phases to treatment; the firstis the engagement and motivation phase. Herethe therapist works hard to enhance the percep-tion that change is possible. The aim is to keepthe family in treatment, and then to move on tofind what precisely the family wants. Techniquesinclude reframing, whereby positive attributes areenhanced (e.g. a mother who continually nagsmay be labelled as caring, upset and hurt). Thenext phase is not commenced until motivationis enhanced, negativity decreased, and a positivealliance established.

The second phase targets behaviour change.There are two main elements to this: communi-cation training and parent training. This stage isapplied flexibly according to family needs. Thus ifthere are two parents who continually argue andthis is impinging on the adolescent, the ‘maritalsubsystem’ will be addressed, using standard tech-niques. Parent training techniques are similar tothose found in standard approaches.

The third and final phase is generalization. Herethe goal is to get the improvements made in afew specific situations to generalize to other simi-lar family situations and to the wider community.For example, to help the youth and family nego-tiate positively with community agencies such asschool and to help them get the resources theyneed. Sometimes this latter goal may require thetherapist to be a case manager for the family.

Multicomponent interventionsThese attempt to target multiple risk factors inmultiple domains, with the best known being Mul-tisytemic Therapy (MST) [6]. The initial focus of

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MST is an assessment that will identify the youth’sdifficulties in relation to the wider environment.Difficulties are understood as a reaction to aspecific context, not seen as necessarily intrinsicdeficits. At the same time strengths will be identi-fied that can be used as levers for positive change.These may be in the young person, the parents, thewider family, peers, the school or the community.

Interventions are designed to promote respon-sible behaviour and decrease irresponsiblebehaviour with the aim of helping the youthbecome independent and develop prosocial lifeskills. They will be focused in the present and beaction oriented with well-defined specific goals.This requires daily or weekly efforts by familymembers, which enables frequent practice of newskills, positive feedback for efforts made and rapididentification of non-adherence to treatment.

Intervention effectiveness is evaluated con-tinually with the intervention team assumingresponsibility for overcoming barriers to suc-cessful outcomes. Whilst the way the therapy isdelivered is closely controlled, the precise natureof moment-to-moment interaction is not tightlyprescribed. In a sense MST is a set of operatingprinciples that draw on the evidence for what-ever works – e.g. cognitive–behavioural therapy(CBT), close monitoring and supervision – ratherthan one specific therapy.

EFFECTIVENESS

Social learning approachesSystematic reviews and meta-analyses of studiesusually with ‘no treatment controls’ confirm thatthese approaches work well for antisocial chil-dren aged 3–10 years [7]. Mean effect sizes acrossstudies vary from around 0.4 to 1.0 according tooutcome, thus showing good effectiveness.

Youth interventionsAdolescents are generally found to do less wellin parenting programmes for antisocial behaviour.However, studies on adolescents generally havethe most severe, persistent cases. When cases ofsimilar severity are compared directly there is noage effect [8]. The results for FFT and MST arereasonably impressive, at least in the USA [9,10].Whilst evaluations outside the USA are eitherlacking or mixed there are currently UK trials ofthese interventions underway.

MEDIATORS OF CHANGE

In recent years, researchers have begun to inves-tigate the factors that mediate outcome. Thisresearch helps to identify the ‘active ingredient’of therapy. Both reductions in negative parent-ing (critical, harsh and ineffective practices) [11]and increases in positive parenting [12] have beenshown to mediate a reduction in child symptoms.

DISSEMINATION: THE ROLEOF THERAPIST SKILL

Therapist performance can be divided into threeparts: the alliance, which could be defined as howwell, both personally and collaboratively, the clientand therapist get on together; fidelity or adherenceto specific components of a model, which concernsthe extent to which the therapist follows the actionsprescribed in the manual; and the skill or compe-tence with which the therapist carries out the tasks(i.e. how well the therapist performs the actions).A meta-analysis of youth studies found that thealliance contributed on average an effect size of0.21 standard deviations to outcome; this findingheld across treatment types, and across youth, par-ent and family approaches [13]. In a trial underregular clinical conditions [14], therapist skill hada large effect on child outcomes – the worst thera-pist made outcomes slightly worse. These findingshave major implications for service delivery, sincethey suggest that at least for multi-problem, clini-cal cases a high level of therapist skill is required,and staff training will need to reflect this.

CONCLUSION

The best parenting programmes incorporateempirical findings from developmental studies andare effective in using these to alter dimensions ofparenting, which in turn improve child outcomes.In future, better assessments of parenting areneeded so that programmes can be tailored tospecific needs rather than ‘one size fits all’.

REFERENCES

[1] Denham S, Workman E, Cole P et al. (2000) Pre-diction of externalizing behaviour problems fromearly to middle childhood: the role of parentalsocialisation and emotion expression. Developmen-tal Psychopathology 12, 23–45.

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[2] Wood J, McLeod B, Sigman M et al. (2003) Par-enting and childhood anxiety: theory, empiricalfindings, and future directions. Journal of ChildPsychology and Psychiatry 44, 134–51.

[3] Markie-Dadds C and Sanders M. (2006) Self-directed triple P (positive parenting programme) formothers with children at-risk of developing conductproblems. Behavioural and Cognitive Psychother-apy 34, 259–75.

[4] Webster-Stratton C and Reid J. (2003) The incred-ible years parenting program. In: Kazdin A andWeisz J (eds), Evidence-Based Psychotherapies forChildren and Adolescents. New York: GuilfordPress, 224–40.

[5] Sexton TL and Alexander JF. (2000) FunctionalFamily Therapy. Washington, DC: U.S. Departmentof Justice.

[6] Henggeler SW, Rowland MD, Randall J et al. (1999)Home-based multisystemic therapy as an alternativeto the hospitalization of youths in psychiatric crisis:clinical outcomes. Journal of the American Academyof Child and Adolescent Psychiatry 38, 1331–9.

[7] Maughan B, Denita R, Christiansen E et al. (2005)Behavioural parent training as a treatment for exter-nalizing behaviours and disruptive behaviour disor-ders: a meta-analysis. School Psychology Review 34,267–86.

[8] Ruma PR, Burke R, Thompson RW. (1996) Groupparent training: is it effective for children of all ages?Behaviour Therapy 27, 159–69.

[9] Woolfenden SR, Williams K, Peat J. (2001) Fam-ily and parenting interventions in children andadolescents with conduct disorder and delin-quency aged 10-17. Cochrane Database of Sys-tematic Reviews Issue 2. Art. No.: CD003015; doi:10.1002/14651858.CD003015.

[10] Littell JH. (2005) Lessons from a systematic reviewof effects of multisystemic therapy. Children andYouth Services Review 27, 445–63.

[11] Beauchaine T, Webster-Stratton C, Reid J. (2005)Mediators, moderators and predictors of 1-yearoutcomes among children treated for early-onsetproblems: a latent growth curve analysis. Journal ofConsulting and Clinical Psychology 75, 371–88.

[12] Gardner F, Burton J, Klimes I. (2006) Randomisedcontrolled trial of a parenting intervention in thevoluntary sector for reducing child conduct prob-lems: outcomes and mechanisms of change. Journalof Child Psychology and Psychiatry 47, 1123–32.

[13] Shirk S and Karver M. (2003) Prediction of treat-ment outcome from relationship variables in childand adolescent therapy: a meta-analytic review.Journal of Consulting and Clinical Psychology 71,452–64.

[14] Scott S, Spender Q, Doolan M et al. (2001) Mul-ticentre controlled trial of parenting groups forchildhood antisocial behaviour in clinical practice.British Medical Journal 323, 1–7.

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Systemic and family approaches to intervention

44Systemic and Family Approachesto InterventionPhilip MessentTower Hamlets Child and Adolescent Mental Health Service, London, UK

INTRODUCTION

The word ‘systemic’ holds many meanings thathave changed and evolved over time accordingto historical and political contexts [1]. With prac-tice ever-changing and evolving, approaches thathave been researched are unlikely to be at the cut-ting edge of practice. As Carr [2] notes, mostof the approaches researched thus far belongto modernist early systemic approaches ratherthan to later postmodern approaches that are lessamenable to manualizing and randomized con-trolled trials (RCTs). Modernism here refers to therationalist, materialist and reductionist view thatan objective understanding of a shared, universaland measurable reality is achievable. In contrastpostmodernist approaches see our understandingof the world as tentative and provisional, elabo-rated by individuals within particular communities.Such approaches are inherently sceptical about theuniversal applicability of any treatment approach.

Research trials assessing the effectiveness offamily-based approaches to common problemsexhibited by children and young people haverecently been reviewed [2]. Here I focus on themost promising approaches, before noting evi-dence of treatment effectiveness of more recentpostmodernist practices drawn from a differentresearch tradition.


EXTERNALIZING DISORDERS

Attention deficit hyperactivitydisorder (ADHD)Systemic interventions for ADHD comprisingsessions with families, school staff and youngpeople, are best offered as elements of multimodalprogrammes involving stimulant medication [3],with systemic interventions playing an increasinglyimportant role in the longer term [4]. Familytherapy for ADHD focuses on helping familiesto develop patterns of organization conduciveto effective child management: a high level ofparental cooperation; clear intergenerationalboundaries; warm, supportive family relation-ships; clear communication and clear, moderatelyflexible rules, roles and routines [5].

Conduct problems in adolescenceWoolfenden et al. [6] found that family-basedinterventions were more effective than routinetreatment – falling on a continuum of care extend-ing from Functional Family Therapy through moreintensive Multi-Systemic Therapy (MST), to veryintensive treatment foster care. The first two ofthese approaches are discussed elsewhere in thisvolume (see Chapter 43), so I will only discuss herethe third and most intensive of these interventions,Multi-Dimensional Treatment Foster Care.

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Multi-Dimensional Treatment Foster Care(MDTFC): This approach aims to help adoles-cents with pervasive conduct problems and theirfamilies by linking both to a new and positivefamilial system: a treatment foster family. It aimsto modify problem-maintaining factors in allsystems by placing the adolescent temporarilywithin a foster family in which the foster parentshave been trained to use behavioural strategiesto modify the youngster’s deviant behaviour. Thegoal is to avoid long-term separation so that astherapeutic progress is made, adolescents spendmore time with their natural family. Chamberlainand Smith [7] in a review of two studies foundthat compared with care in a group home fordelinquents, this treatment approach reducedrunning away from placement, rearrest rate andself-reported violent behaviour. Benefits were dueto improvements in parents’ skills for managingadolescents in a consistent, fair and non-violentway, and to reductions in adolescents’ involvementwith ‘deviant’ peers, with cost savings of $40,000per case in juvenile justice and crime victim costs.

It is clear that the family-based interventionsdescribed in Wolfenden et al. [6] can be effectivewith adolescents in contact with juvenile justice sys-tems. The authors note, however, a lack of RCTsfor family and parenting interventions for childrenand adolescents with conduct disorders, who havehad no contact with juvenile justice systems [6]. Inaddition they point out that in the studies enteringinto their review, there was insufficient evidence ofbeneficial effects on problem behaviour, parentalmental health, family functioning and peer rela-tions. Long-term follow-up on adult outcomes wasnot available.

Transferability of treatment approaches: Thetransferability to a UK setting of these mul-tidimensional systemic treatment approachesdeveloped in the USA has yet to be established.In a London borough trial of MDTFC the projectteam had great difficulty with respect to two treat-ment protocol conditions: recruiting two-parentfoster families and persuading adolescents to giveup their mobile phones. Holmes et al. [8], however,have reported some early positive findings fromthis British trial: the social care costs incurred bythe sample children in the first 6 months of thepilot study were about 15% less than those theyhad incurred in the 6 months prior to entry.

All of these treatment approaches are labourintensive: treatment foster care is offered for aperiod of up to a year, followed by an ongo-ing multisystemic intervention. During a time ofreductions in public services in the UK, evidencedrawn from current RCTs will need to providecompelling evidence of effectiveness to justify suchcostly investment.

Substance misuse in adolescenceLiddle [9] found that family therapy with youngpeople who misuse substances was more effectivethan routine individual or group psychotherapiesin engaging and retaining them in therapy, and inimproving psychological, educational and familyadjustment. Liddle’s version of multidimensionalfamily therapy involves assessment and interven-tion in four areas:

• the adolescent as an individual and a member ofa family and peer network;

• the parent(s) – both as individual adults andtheir roles as mother, father or caregiver;

• the family environment and family relationships,as manifested in day-to-day family transactionalpatterns;

• extrafamilial sources of influence such as peers,school and juvenile justice.

Interventions are made within and coordinatedacross domains, with progress in one area orwith one person having implications for others.Individual meetings with parent(s) and teenagerset the stage for family sessions, and familymeetings may offer content and new outcomes totake to meetings with juvenile justice or schoolpersonnel. Liddle emphasizes that this approachwas developed and tested as a treatment systemrather than a one-size-fits-all approach [10]. Thatis, as a system offering different versions of aclinical model that vary according to factors suchas clinical sample characteristics (e.g. older versusyounger adolescents), and treatment parameters(e.g. type of clinical setting).

EMOTIONAL PROBLEMS

AnxietySystematic reviews (e.g. Ref. [11]) show thata family-based treatment for anxiety disordersis at least as effective as individual cognitive–behavioural therapy (CBT) in alleviating

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symptoms of anxiety, and more effective whereparents also have anxiety disorders, and inimproving the quality of family functioning.

EncopresisIn a narrative review of 42 studies McGrath etal. [12] found that multimodal programmes involv-ing medical assessments and intervention followedby behavioural family therapy were effective for43–75% of cases. Effective behavioural familytherapy involves psycho-education coupled with areward programme. There is some evidence [13]that a narrative approach is more effective thana behavioural one. In the former, child symptomsare ‘externalized’, that is, they are talked aboutin such a way that they are no longer seen as‘belonging’ to the child. This can help children feelless blamed and stigmatized and more in control.In a retrospective study of 108 children withsoiling problems the 54 who were treated usingan externalizing approach did better than childrenreceiving a standard behavioural intervention,with parents rating the externalizing interventionas much more helpful.

DepressionEffective family-based interventions for childrenand adolescents with depression aim to decreasefamily stress and enhance social support withinthe family context through the facilitation of clearparent–child communication, the promotion offamily-based problem-solving, the disruption ofnegative critical parent–child interaction, and thepromotion of secure parent–child attachment. Ina multi-country study comparing psychodynamicindividual and family therapy interventions forchildren aged 9 to 15 years presenting withmoderate to severe depression, both approacheswere found to be effective [14]. Over 74% ofchildren in both groups were no longer clinicallydepressed at post-test, and 81% of the familytherapy group were also no longer clinicallydepressed at 6-month follow-up.

Attempted suicideFamily interventions have been found to improvethe adjustment of adolescents who have attemptedsuicide [15], while a version of MST adaptedfor such young people was more effective thanemergency hospitalization and treatment by a

multidisciplinary psychiatric team [16]. Effectiveapproaches begin with engaging young people andfamilies in an initial risk-assessment process, thendeveloping a clear plan for risk reduction involv-ing individual therapy for adolescents alongsidesystemic therapy for members of the family andsocial support networks. King et al. [17] describea manualized Youth-Nominated Support Teamapproach that involves the young person namingfour people to be part of their ‘support team’.This team, which might include individuals inschools, extended family or religious community,is encouraged to maintain weekly contact with theadolescent and themselves receive input aimed atfacilitating their understanding of the young per-son and their provision of appropriate support.Compared with psychotherapy and antidepressantmedication, this approach led to improvementsin the level of suicidal ideation for girls, butnot significantly for boys. The authors hypoth-esized that because female adolescents tend toperceive higher levels of social support than maleadolescents and are usually more satisfied withthe social support they receive from persons intheir lives, the enhanced support system involvedin the intervention would be particularly helpfulfor female subjects. Their research suggests thatoutside-the-family supports can be useful for sui-cidal adolescents because some parents of suicidalteenagers have significant difficulties of their ownthat interfere with their ability to be supportive.

EATING DISORDERS

Adolescent anorexia nervosaFamily therapy approaches here as described byEisler [18] involve firstly an ‘engagement’ phasemaking contact with each adolescent’s familymember and emphasizing a primary task of over-coming anorexia, rather than understanding itscauses; secondly helping the family to ‘challengethe symptoms’; thirdly as concerns around eatingrecede, exploring issues of individual and familydevelopment more broadly; and fourthly endingwith a discussion of future plans. Eisler notesalso [18] the usefulness of a multiple family dayprogramme where different families can meetand establish group cohesion in a supportiveatmosphere in which new solutions can be tried.

Eisler’s [18] systematic review of 11 family ther-apy trials for adolescent anorexia nervosa found

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that by the end of treatment between one-halfand two-thirds of participants had achieved ahealthy weight. At follow-up between 60% and90% had fully recovered. This contrasts with therates of relapse of 25–30% for first in-patientadmission and 55–75% for further admissions.This evidence is reflected in the National Institutefor Health and Clinical Excellence (NICE) guide-lines [19], which state that: ‘Family interventionsdirectly addressing the eating disorder should beoffered to children and adolescents with anorexianervosa’. Some caveats are noted by Eisler, how-ever, including the small number of studies, theirmethodological limitations, and that there is lit-tle research comparing family therapy with othertreatments. He notes, too, that systematic evalua-tions have largely been confined to family therapywith a strong ‘structural’ flavour [18].

BulimiaTwo trials of family therapy show it to be moreeffective than supportive therapy [20], and aseffective as CBT interventions [21] that also helpparents to work together to supervise the youngperson to break the binge–purge cycle.

A DIFFERENT SORT OF EVIDENCE

Narrative/postmodernist family therapists wouldargue that an exclusive reliance on knowledgedrawn from RCTs of manualized approaches totreatment ignores the more ‘local’ knowledge andexpertise in managing difficulties developed byclinicians, clients, families, services and commu-nities. This can be disempowering and unhelpfulto families. Fredman [22], in contrast, illustrateshow clinicians’ knowledge and expertise, com-bined with specific knowledge gained during thetherapeutic encounter, can help bereaved families.

An alternative method of gaining ‘practice-based evidence’ has been described by Young andCooper [23] whereby families who had receivedtherapy reviewed tapes of their own clinical ses-sions. Families were asked to stop the tape at‘meaningful moments’ and then interviewed. Thefollowing themes were generated:

• Family members commented upon the impor-tance of their therapist’s stance – e.g. a 14-year-old commented, ‘I liked hearing that she wasaccepting that if I didn’t want to answer a questionthen she would be fine with that. . .’.

• Giving people back their words: an 11-year-oldcommented that ‘with her reviewing the stuff Isaid, it just really helped me ‘cause it was in mybrain more. . .’.

• Externalizing conversations: a mother of an8-year-old said, ‘What she was doing in termsof how she was phrasing things, because she said‘‘the worry puts thoughts in your head. . .’’ andmy son was immediately saying, like echoing backwhat she was saying, ‘‘the worry does this. . .’’ soI was starting to feel that this was looking good.’[laughs].

Such action-based research can help ensurethat clinicians are attentive to the experience ofservice-users and that their practice is respon-sive and effective. It also acts as a counterweightto knowledge derived from the research on tri-als of manualized treatment approaches that haveformed the bulk of this chapter. This emphasis onwhat clinicians bring to their work and how theylearn and develop is an important complement tolessons about effectiveness drawn from larger scalequantitative studies. It has long been found that thespecific technique or approach used by therapistsis not as important in accounting for effective-ness as non-specific factors linked to the qualityof the relationship that is developed betweenclient (family) and therapist (as evidenced e.g. byChatoor and Krupnick’s [24] review of the lit-erature). The responsible and ethical systemicpractitioner will be able to draw from the researchknowledge base developed for the particular prob-lem areas described above, and continue to learn,from their practice with individual clients, whatcontributes to the development of relationshipsthat client families experience as helpful.

REFERENCES

[1] Fredman G. (2006) Working systemically with intel-lectual disability: why not? In: Baum S and Lyng-gaard H (eds) Intellectual Disabilities: A SystemicApproach. London: Karnac, pp. 1–20.

[2] Carr A. (2009) The effectiveness of family ther-apy and systemic interventions for child-focusedproblems. Journal of Family Therapy 31, 3–45.

[3] Hinshaw S, Klein R, Abikoff H. (2007) Childhoodattention-deficit hyperactivity disorder: nonphar-macological treatments and their combination withmedication. In: Nathan P and Gorman J (eds) AGuide to Treatments that Work, 3rd edn. New York:Oxford University Press, pp. 3–28.

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[4] Jensen P, Arnold L, Swanson J, Vitiello B, AbikoffH, Greenhill L. (2007) 3-year follow-up of theNIMH MTA Study. Journal of the AmericanAcademy of Child and Adolescent Psychiatry 46,989–1002.

[5] Anastopoulos A, Shelton TL, Barkley R. (2005)Family-based psychosocial treatments for childrenand adolescents with attention-deficit/hyperactivitydisorder. In: Hibbs E and Jensen P (eds) Psychoso-cial Treatments for Child and Adolescent Disorders:Empirically Based Strategies for Clinical Practice,2nd edn. Washington, DC: American PsychologicalAssociation, pp. 327–50.

[6] Woolfenden S, Williams K, Peat J. (2002) Familyand parenting interventions for conduct disorderand delinquency: a meta-analysis of randomisedcontrol trials. Archives of Diseases in Childhood 86,251–6.

[7] Chamberlain P and Smith D. (2003) Antisocialbehaviour and children and adolescents: The Ore-gon multidimensional treatment foster care model.In: Kazdin A and Weisz J (eds) Evidence BasedPsychotherapies for Children and Adolescents. NewYork: Guilford Press, pp. 281–300.

[8] Holmes L, Westlake D, Ward H. (2008) Calculat-ing and Comparing the Costs of MultidimensionalTreatment Foster Care, England (MTFCE): Reportto the Department for Children, Schools and Fam-ilies. Loughborough: Centre for Child and FamilyResearch, Loughborough University.

[9] Liddle H. (2004) Family-based therapies for ado-lescent alcohol and drug use: research contributionsand future research needs. Addiction 99, 76–92.

[10] Liddle H. (2010) Multidimensional Family Therapy:a science-based treatment system. Australian andNew Zealand Journal of Family Therapy 31, 133–48.

[11] Barmish A and Kendall P. (2005) Should parents beco-clients in cognitive-behavioural therapy for anx-ious youth? Journal of Clinical Child and AdolescentPsychology 34, 569–81.

[12] McGrath M, Mellon M and Murphy L. (2000)Empirically supported treatments in paediatric psy-chology: constipation and encopresis. Journal ofPaediatric Psychology 25, 225–54.

[13] Silver E, Williams A, Worthington F, Philips N.(1999) Family Therapy and soiling: an audit of exter-nalising and other approaches. Journal of FamilyTherapy 20, 413–22.

[14] Trowell J, Joffe I, Campbell J et al. (2007)Childhood depression: a place for psychotherapy: anoutcome study comparing individual psychody-namic psychotherapy and family therapy. EuropeanChild and Adolescent Psychiatry 16, 157–67.

[15] Harrington R, Kerfoot M, Dyer E et al. (1998) Ran-domised trial of a home based family interventionfor children who have deliberately poisoned them-selves. Journal of the American Academy of Childand Adolescent Psychiatry 37, 512–18.

[16] Huey S, Henggeler S, Rowland M et al. (2004) Mul-tisystemic therapy reduces attempted suicide in ahigh-risk sample. Journal of the American Academyof Child and Adolescent Psychiatry 43, 183–90.

[17] King C, Kramer A, Preuss L, Kerr D, Weisse L,Venkataraman S. (2006) Youth-nominated supportteam for Suicidal Adolescents (Version 1): A ran-domised control trial. Journal of Consulting andClinical Psychology 74, 199–206.

[18] Eisler I. (2005) The empirical and theoretical baseof family therapy and multiple family day therapyfor adolescent anorexia nervosa. Journal of FamilyTherapy 27, 104–13.

[19] NICE. (2004) Eating Disorders: Core Interventionsin the Treatment and Management of AnorexiaNervosa, Bulimia Nervosa and Related Eating Dis-orders. London: The British Psychological Societyand Gaskell.

[20] Le Grange D, Crosby R, Rathouz P, Leventhal B.(2007) A randomised control comparison of family-based treatment and supportive psychotherapy foradolescent bulimia nervosa. Archives of GeneralPsychiatry 64, 1049–56.

[21] Schmidt U, Lee S, Beecham J et al. (2007) Arandomised controlled trial of family therapy andcognitive behavioural therapy guided self-care foradolescents with bulimia nervosa and related disor-ders. American Journal of Psychiatry 164, 591–8.

[22] Fredman G. (1997) Death Talk: Conversations withChildren and Families. London: Karnac.

[23] Young K and Cooper S. (2008) Towards co-composing an evidence base: the narrative therapyrevisiting project. Journal of Systemic Therapies 27,67–83.

[24] Chatoor I and Krupnick J. (2001) The role ofnon-specific factors in treatment outcome of psy-chotherapy studies. European Child and AdolescentPsychiatry 10, S19–S25.

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45Psychotherapeutic Approaches: APsychodynamic PerspectiveEilis KennedyTavistock and Portman NHS Foundation Trust, London, UK

INTRODUCTION

An interest in applying psychoanalytic ideas totherapeutic work with children and adolescentsarose out of the thinking of Anna Freud andMelanie Klein, and received further impetusfrom work showing the impact upon children oftheir experiences of separation and loss duringthe Second World War [1]. Over time psycho-analytically informed therapeutic approacheshave expanded beyond individual work withthe child to include work with families, groups,parent–infant psychotherapy and parent/couplework. This chapter focuses on psychodynamicpsychotherapeutic approaches to children andadolescents presenting with a variety of emotionaland behavioural problems.

BASIC PREMISES OF A PSYCHODYNAMICAPPROACH

Key concepts guiding the therapeutic processinclude an interest in unconscious processes andthe ‘internal’ world of the child. Children’s playis thought to provide a window onto the child’sunconscious thoughts and feelings. The child’s playand behaviour is therefore used by the therapist tounderstand the child’s inner world [2]. Attunementto the child in order to be receptive to the minutiaeof what is being emotionally exchanged is one ofthe primary tasks [3]. The ability to gather finedetails regarding how the child responds to thesetting and relates to the therapist is essential.


Where possible the work is undertaken in aregular consistent setting. When working indi-vidually with young children the psychotherapistprepares a box for each child with suitable toys anddrawing materials to facilitate the child’s creativeplay, exploration and non-verbal communication.It is usual practice for the child’s parents/carers toattend parallel psychotherapeutic sessions.

The psychotherapeutic model is deeply embed-ded in a developmental approach to children’sdifficulties, and an excellent account of a psycho-analytic perspective on personality developmentfrom infancy to adolescence can be found inWaddell [4]. Increasingly, research from neu-roscience and developmental psychology isused to complement this model and enhanceunderstanding of work with children with neu-rodevelopmental disorders or those who haveexperienced severe maltreatment [5].

THE EVIDENCE BASE FOR CHILDPSYCHOTHERAPY

The evidence base for psychodynamic childpsychotherapy is somewhat limited as randomizedcontrolled trials (RCTs) have been few in number.A 2004 systematic review identified 32 studies, not-ing that many had limitations of study design andsample size. Only five were RCTs and four werequasi-RCTs [6]. Though small in number, theselatter nine studies represent 33.3% of the totalreviewed – a proportion that compares favourablywith the 7.4% of experimental/quasi-experimental

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studies identified in an examination of theevidence base for treatments in child mental healthin general [7]. Recent research reviews includequalitative studies and those focusing on processas well as outcome research [8,9]. A NationalInstitute for Health Research (NIHR) multicentreRCT, comparing cognitive–behavioural therapy,short-term psychodynamic psychotherapy andspecialist clinical care, in the treatment of adoles-cents with major depression, is now underway (seethe NIHR website: http://www.hta.ac.uk/project/1731.asp).

EXAMPLES OF RESEARCH WITH CHILDRENAND YOUNG PEOPLE PRESENTING WITHVARIOUS CLINICAL PROBLEMS

Children who have experiencedabuse or neglectWhile not concerned with assessing the effects ofpsychodynamic interventions per se, an interestingbody of work undertaken by Hodges and Steele[10,11] illustrates that it is possible to assess andmeasure changes in the attachment representa-tions of children who have been adopted followingexperiences of abuse and neglect. Using a storystem technique, whereby children are presentedwith the beginning of a story relevant to theirexperiences and then asked to complete it, Hodgesand Steele demonstrated that the children’s por-trayal of attachment figures changed over a 2-yearfollow-up period to include more positive repre-sentations of attachment figures, although earliernegative representations still persisted alongsidethe more positive ones.

A research project by Trowell et al. [12], on theother hand, concentrates on assessing the effec-tiveness of two types of interventions for girlswho had been sexually abused. Using an RCTdesign, individual psychotherapy was comparedwith a psycho-educational group psychotherapeu-tic intervention. While both types of interventionwere found to be effective at substantially reducingpsychopathological symptoms, and participants inboth groups evidenced improved functioning, indi-vidual therapy led to a greater improvement insymptoms of post-traumatic stress disorder. Theauthors note that the small sample size, and thelack of a control group limit conclusions aboutchanges attributable to treatment.

Internalizing and externalizing disordersDisruptive behavioural disorders: There islimited intervention research in this area, though aretrospective study of the case notes of 763children attending the Anna Freud Centre foundpoorer outcomes for those diagnosed with conductor oppositional defiant disorders [13]. Outcomeswere, however, better for younger children andthose with mixed emotional and behaviouraldisorders.

Internalizing disorders: Research evidence heresuggests that children with depressive and/or anx-iety disorders respond positively to a psychody-namic therapeutic approach.

In a quasi-randomized 2-year follow-up of chil-dren aged 6–11 years with depressive or anxietydisorders, Muratori et al. [14] compared thoseassigned to either a time-limited psychodynamicpsychotherapy (PP) intervention condition or tocommunity services. The results of the study indi-cated that PP was effective in treating internaliz-ing disorders at the time of intervention and at6-month follow-up. A ‘sleeper’ effect for PP wasalso found at 2-year follow-up in so far as only chil-dren in the PP group moved into the non-clinicalrange on standardized assessments, while those inthe control group remained at the same level ofclinical severity.

A multicentre randomized trial comparedfocused individual psychodynamic therapy andparallel therapeutic work with parents (FIPP) witha systemic integrative family therapy approach(SIFT), in a sample of children aged 10–14 yearswho met criteria for major depressive disorderand/or dysthmia [15]. Significant reductions indisorder rates for both groups were found suchthat clinical depression had remitted in more than70% of participants in both types of intervention,and reductions in comorbid conditions wereevident. Improvements were persistent, with a6-month follow-up indicating that none of theFIPP participants remained depressed, comparedto 81% of SIFT participants, although the loss offour cases to follow-up in the SIFT group limitedassessment of effectiveness rates. While the finaloutcome of these interventions appears similar, adifferent pattern of responses was found. Familywork appeared to have highly effective initialimpact, whereas the response to individual workwas slower but possibly more sustained.

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Mixed diagnosesA number of studies have focused on childrenpresenting in middle childhood with a range ofdifficulties rather than belonging to a particulardiagnostic category. One randomized trial of suchchildren, aged 5–9 years, compared time-unlimitedor time-limited (12 sessions) psychodynamicallyoriented treatment with a minimal-contact controlgroup (four sessions) [16]. All groups showed sig-nificant improvements from pre-test to post-test,though changes in family functioning in the con-trol group were significantly greater than thosein the time-unlimited group. At 4-year follow-up,all three groups did well on a variety of outcomemeasures although the control group did ratherbetter, being the only group to report significantimprovements on severity of target problems andmeasures of family functioning. The researchersspeculate that the four-session ‘minimal contactcontrol’ group may have proved most effectivebecause the families’ own capacities for copingand resilience had been harnessed.

A further RCT compared the effectiveness ofstructural family therapy with individual psycho-dynamic child psychotherapy and a ‘recreational’control in boys aged 6–12 years presenting withmixed diagnoses [17]. Attrition was greatest inthe control group (43%) and greater in the fam-ily therapy group compared with the individualtherapy (16% vs 4%). Both family therapy andindividual psychodynamic therapy were equallyeffective in reducing behavioural and emotionalproblems on a variety of outcome measures thatincluded family systems and individual psycho-dynamic rating scales. Findings on measures offamily functioning were mixed: the control groupshowed no significant change; the family therapygroup improved; those receiving individual psy-chodynamic psychotherapy showed deteriorationat 1-year follow-up. This finding may possibly bebiased as an intention-to-treat analysis was notcarried out despite variable drop-outs in the threegroups, but it may also be attributable to the factthat the individual psychodynamic child therapywas undertaken in the absence of any parallel par-ent work, contrary to usual practice. The studyunderlines the importance of working with thewider family system in conjunction with individualwork with the child.

Young people with poorly controlled diabetesMoran and colleagues undertook a series of stud-ies assessing the effectiveness of psychoanalyticpsychotherapy for children with poorly controlleddiabetes [18,19]. A quasi-randomized study com-pared two groups, each containing 11 diabeticchildren with unstable insulin-dependent diabetes.Those in the treatment group received intensivepsychoanalytic psychotherapy (up to 3–4 times aweek) for an average of 15 weeks; those in thecontrol group received only routine psychologicalinput without individual psychotherapy. A signif-icant improvement in diabetic control was notedin the experimental group compared to controls,with 91% of participants in the treatment groupshowing a reduction in glycosylated haemoglobinin contrast to only 36% of controls. This improve-ment was maintained at 1-year follow-up.

As part of this study three children with dia-betes and growth retardation were studied, usinga single-case experimental design methodology; inall three cases there were gains in height overthe predicted height following psychotherapeutictreatment [19].

Long-term outcomesThe Anna Freud Centre long-term follow-upstudy:Adult outcome: In this study [20], the adultoutcome of 34 children who had received psy-chotherapeutic treatment at the Anna FreudCentre was compared with the outcome of 11of their untreated siblings. In general those whohad received treatment in childhood were foundto be functioning well, reporting low levels ofadversity, relatively few severe life events andgood health. They displayed adequate personalityfunctioning across a range of domains and a lowrate of personality disorders.

Interestingly while adversity in childhood wasgreater in the treated children, the untreated sib-lings were found to experience more negative lifeevents in adulthood. In relation to personality func-tioning, the entire sample appeared to be doingwell in the work domain. In the area of intimaterelationships those children successfully treated inchildhood appeared to be doing better than theiruntreated siblings.

Possible adverse effects of treatment were high-lighted in relation to attachment security. Whilea secure adult attachment status was common in

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those who had moved from poor functioning inchildhood to high functioning in adulthood, theattachment style of those who had been unsuccess-fully treated in their childhood was predominantlypreoccupied/entangled. Those children in the sam-ple who did not receive psychoanalytic treatmentwere found to be predominantly dismissing intheir adult attachment style. Treated participantsdemonstrated a balanced and accurate memory oftheir childhood experiences, though in contrast totheir siblings, their memories tended to be morepainful.

Patients’ perspectives: Another aspect of thisstudy assessed the perspective of the patient byexploring the memories of adults who were intherapy as children and examining the meaningparticipants gave to the experience of therapy inthe context of their later lives [21].

Two-thirds of participants were able to describesome aspect of the experience of child psychother-apy that had felt helpful at the time of treatment.Some were more confident about the positiveimpact than others. Several described how beingable to talk and ‘unburden’ themselves was help-ful. One described how the treatment provided a‘sort of canvas’ to ‘express myself in a way thatI wouldn’t necessarily have been able to talk toanyone else about these problems’. Some notedhow the therapist’s attention made them feel moreconfident and how therapy enabled them to copebetter.

Others questioned the potentially negativeimpact of the therapy. Some of their commentsincluded feelings that the therapy was ‘pointless’and had made no difference, or that it had setthem apart from others. As one observed ‘thelast thing I wanted was to feel different’. In someparticipants, this sense of being different createdor exacerbated a sense that they were somehow‘damaged’ and that there was ‘something wrong’with them.

POTENTIAL ADVERSE EFFECTSOF TREATMENT

In contrast to research on pharmacologicaltreatments there has been a tendency not to looksystematically for adverse effects of psychother-apeutic treatments. However, existing researchsuggests some potential adverse consequencesof treatment that would benefit from scrutiny in

future research. For example, there are indicationsthat individual psychotherapy undertaken in theabsence of concurrent parent/family work mayhave a negative impact on family functioning.There is a suggestion also that unsuccessfultreatment in childhood may result in a preoc-cupied/entangled attachment style in adulthood.In addition some adults who received treatmentin childhood describe how the treatment itselfcompounded a sense they had that there was‘something wrong with them’ and for some therewas an anxiety that it may have resulted in atendency to be overly introspective.

CONCLUSION

The application of psychoanalytic understandingto psychotherapeutic work with children has along tradition. Hopefully this work will continueto evolve and develop with the contribution of newinsights from large-scale treatment trials, develop-mental psychology and neuroscience.

REFERENCES

[1] Likerman M, Urban E. (2009) The roots of childand adolescent psychotherapy in psychoanalysis.In: Lanyado M and Horne A (eds), The Handbookof Child and Adolescent Psychotherapy: Psychoan-alytic Approaches, 2nd edn. London: Routledge,pp. 15–26.

[2] Lanyado M and Horne A. (2009) The therapeuticsetting and process. In: Lanyado M and Horne A(eds), The Handbook of Child and Adolescent Psy-chotherapy: Psychoanalytic Approaches, 2nd edn.London: Routledge, pp. 157–74.

[3] Hunter M. (2001) Psychotherapy with Young Peo-ple in Care: Lost and Found. Sussex: Brunner-Routledge.

[4] Waddell M. (2002) Inside Lives: Psychoanalysis andthe Development of the Personality, revised edn.London: Karnac.

[5] Music G. (2010) Nuturing Natures: Attachment andChildren’s Emotional, Sociocultural and BrainDevelopment. London: Psychology Press.

[6] Kennedy E. (2004) Child and Adolescent Psy-chotherapy: A Systematic Review of PsychoanalyticApproaches. London: North Central London Strate-gic Health Authority.

[7] Fonagy P, Target M, Cottrell D, Phillips J, Kurtz Z.(2002) What Works for Whom? A Critical Reviewof Treatments for Children and Adolescents. NewYork: Guilford Press.

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[8] Kennedy E and Midgley N. (2007) Process andOutcome Research in Child, Adolescent and Parent-Infant Psychotherapy: A Thematic Review. London:NHS London.

[9] Midgley N, Anderson J, Grainger E, Nesic-Vuckovic T, Urwin C. (2009) Child Psychotherapyand Research: New Directions, Emerging Findings.London: Routledge.

[10] Hodges J, Steele M. (2000) Effects of abuse onattachment representations; Narrative assessmentsof abused children. Journal of Child Psychotherapy26, 433–55.

[11] Hodges J, Steele M, Hillman S, Henderson K,Kaniuk J. (2003) Changes in attachment represen-tation over the first year of adoptive placement:narratives of maltreated children. Clinical ChildPsychology and Psychiatry 8, 351–68.

[12] Trowell J, Kolvin I, Weeramanthri T et al. (2002)Psychotherapy for sexually abused girls: psy-chopathological outcome findings and patterns ofchange. British Journal of Psychiatry 180, 234–47.

[13] Fonagy P and Target M. (1994) The efficacy of psy-choanalysis for children with disruptive disorders.Journal of the American Academy of Child andAdolescent Psychiatry 33, 45–55.

[14] Muratori F, Picchi L, Bruni G, Patarnello M,Romagnoli G. (2003) A two-year follow-up ofpsychodynamic psychotherapy for internalizing dis-orders in children. Journal of the American Academyof Child and Adolescent Psychiatry 42, 331–9.

[15] Trowell J, Joffe I, Campbell J et al. (2007) Child-hood depression: a place for psychotherapy. An

outcome study comparing individual psychody-namic psychotherapy and family therapy. EuropeanChild and Adolescent Psychiatry 16, 157–67.

[16] Smyrnios K and Kirby R. (1993) Long term com-parison of brief versus unlimited psychodynamictreatments with children and their parents. Journalof Consulting and Clinical Psychology 61, 1020–7.

[17] Szapocznik J, Murray E, Scopetta M et al. (1989)Structural family versus psychodynamic child ther-apy for problematic Hispanic boys. Journal ofConsulting and Clinical Psychology 57, 571–8.

[18] Moran G, Fonagy P, Kurtz A, Bolton A, BrookC. (1991) A controlled study of the psychoanalytictreatment of brittle diabetes. Journal of the Amer-ican Academy of Child and Adolescent Psychiatry30, 926–35.

[19] Fonagy P and Moran C. (1990) Studies of the efficacyof child psychoanalysis. Journal of Consulting andClinical Psychology 58, 684–95.

[20] Schachter A, Target M. (2009) The adult outcome ofchild psychoanalysis: The Anna Freud Centre long-term follow-up study. In: Midgley N, Anderson J,Grainger E, Nesic-Vuckovic T (eds), Child Psy-chotherapy and Research: New Approaches, Emerg-ing Findings. London: Routledge, pp. 144–56.

[21] Midgley N, Target M, Smith J. (2006) The outcomeof child psychoanalysis from the patient’s point ofview: a qualitative analysis of a long-term follow-up study. Psychology and Psychotherapy – Theory,Research and Practice 79, 257–69.

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Paediatric psychopharmacology: special considerations

46Paediatric Psychopharmacology:Special ConsiderationsParamala J. Santosh and Rakendu SurenCentre for Interventional Paediatric Psychopharmacology, Department of Child and Adolescent MentalHealth, Great Ormond Street Hospital for Children NHS Trust, London, UK

INTRODUCTION

Problems of mental health and behaviour in chil-dren require a multidisciplinary approach, andoptimal treatment is multimodal. The number ofchildren in the USA taking prescription drugs foremotional and behavioural disturbances is growingdramatically and has given rise to multiple con-troversies, ranging from concerns over off-labeluse and long-term safety to debates about thesocietal value and cultural meaning of pharma-cological treatment of childhood behavioural andemotional disorders. More than 80% of the world-wide use of stimulant medications occurs in theUSA, and the use of antidepressants and antipsy-chotics is many times greater in the USA thanin other countries [1]. Variability in use reflectsdifferences in diagnostic systems, clinical practiceguidelines, drug regulation, health services orga-nization, availability and allocation of financialresources, and cultural attitudes towards child-hood behavioural and emotional disturbances [1].This chapter focuses on aspects of psychopharma-cology that have special relevance in children andadolescents; it provides relevant information aboutclasses of medication, rather than disorder-specifictreatment recommendations.

INFORMATION TO ASSIST JUDICIOUSPRESCRIBING

Apart from a thorough diagnostic assessment, thefollowing information is important:


• full medical history – current and past;• detailed medication history, including over-the-

counter medications;• history of substance misuse to ascertain potential

misuse liability and interactions with prescribedmedication;

• detailed family history, including history of men-tal illness, suicide, substance abuse, neurolog-ical/medical conditions (especially early-onsetcoronary artery disease), and the response ofthe family members to psychotropic medication.

MEDICATION AS PART OF A MULTIMODALTREATMENT PACKAGE

Treatment plans should be individualized accord-ing to the pattern of target symptoms and strengthsidentified in the evaluation. Treatment shouldtarget situations in which symptoms cause mostimpairment, and treatment progress should bemonitored by custom-designed target symptomscales or daily behavioural report cards. Thedesignation of a case manager is essential forchronically disabled individuals to coordinate thewide range of services necessary for their care andto ensure periodic diagnostic reassessments.

SYMPTOM-BASEDPHARMACOTHERAPEUTIC STRATEGY

As pharmacological treatment is symptom basedin most psychiatric conditions, it is useful to con-ceptualize it as described below [2].

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• Symptoms that require and are likely to respondto medication alone: inattention, impulsivity,hyperactivity, tics, obsessions, psychotic symp-toms, labile mood.

• Symptoms that are less likely to respond to med-ication alone, requiring both medication andpsychosocial interventions: aggression, rituals,self-injury, depression.

• Symptoms that are unlikely to respond to medica-tion and need specific remediation: skill deficitsin academic, social or sports domain.

THE ART OF PRESCRIBING MEDICATION

Besides the neurochemical effect of any givenagent, the response to medication also dependson an inherent ‘placebo response’, as well as thetherapeutic concordance achieved by obtainingagreement and acceptance of why the medicationis prescribed and what is the expected response.Rewards experienced from medication treatmentinclude improvement in symptoms, school perfor-mance and family relationships, and reduced levelof parenting stress. Identified costs include theimpact of adverse side effects, social stigma, lackof response, fears of addiction, and changes in thechild’s personality [3]. Acceptance of the diagnosisinfluences adherence while medication educationhas varying effects. Families’ attitudes, beliefs andperceptions about psychiatric illness and treatmentplay a large role in medication treatment deci-sions. A trusting relationship with the clinician hasa positive effect on adherence, but psychosocialtreatment alternatives are usually preferred. Withmaturation, adolescents have more influence ondecisions related to adherence [3].

The above characteristics are enhanced whenparents and patients feel understood, acceptthat treatment is necessary and agree with theprescriber regarding the need for the treatment,and when medication is started in small dosesusing the principles of minimum effective dose(MED). The MED is the minimum dose withwhich ‘acceptable’ improvement with minimalside effects is achieved. Medication should beinitiated in small doses (usually in doses that areone-eighth to one-sixth of the final anticipateddose), increasing the dosage after about every fivehalf-lives of the drug – in practice usually every3–7 days, over a period of 4–6 weeks – to identifythe MED [4].

USE OF NON-LICENSED PSYCHOTROPICMEDICATION

Most psychotropics – other than stimulants, ato-moxetine for attention-deficit hyperactivity disor-der (ADHD), and imipramine for enuresis – arenot licensed for use in children. Unlicensed psy-chotropics are not contraindicated in children, anddoctors can prescribe any medication approvedby the appropriate agency (e.g. the US Food andDrug Administration or the European MedicinesAgency), to any age group, if they believe thatthere is a reasonable clinical indication. Thus,licensing of medication constrains drug companiesbut leaves doctors free to prescribe unlicenseddrugs or to use licensed drugs for unlicensed indi-cations. The drug companies are not legally liableif any untoward reaction occurs in children treatedwithout their knowledge, using such non-licensedmedication. It is therefore important that the par-ents and patients (as appropriate) are given thisinformation as part of the informed consent.

FACTORS AFFECTINGPHARMACOTHERAPY IN CHILDREN

Understanding the pharmacokinetics and pharma-codynamics of drugs used in psychopharmacologyacross the paediatric age spectrum from infantsto adolescents represents a major challenge forclinicians. In paediatrics, treatment protocols useeither standard dose reductions for these drugsfor children below a certain age or use less con-ventional parameters such as weight for allometricdosing; the rationale behind this, however, is oftenlacking.

Absorption and hepatic metabolism: The rate ofabsorption is faster in children, and peak levelsare reached sooner. Hepatic metabolism is highestduring infancy and childhood (1–6 years), is abouttwice the adult rate in prepubertal children (6–10years), and is equivalent to that in adults by the ageof 15 years [5]. This is important clinically becauseyounger children may require higher doses (mg/kg)of hepatically metabolized medication, comparedwith older children and adults.

Fat distribution: Substantial fat stores slow theelimination of highly lipid-soluble drugs (e.g. fluox-etine and pimozide) from the body. Fat distribution

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varies in children, increasing during the first yearand gradually falling until puberty.

Protein-binding and volume of distribution: Thesediffer in children, affecting pharmacokinetics bymodifying the fraction of drug that is active(unbound) [6].

Incomplete maturation of neurotransmittersystem: The noradrenergic system does not fullydevelop anatomically and functionally until earlychildhood [7]. This may be one of the reasonsfor poor antidepressant response in childhooddepression.

Cardiotoxicity: The rates of maturation of thesympathetic and parasympathetic system vary,although vagal and sympathetic modulationsfollow a similar pattern. This may lead to accen-tuation of the relative loss of vagal modulationassociated with tricyclic antidepressants [8].

MEDICATIONS

The dose ranges of the majority of psychotropicsused in children and adolescents, with their mainindications, are shown in Table 46.1.

StimulantsStimulants have been used for decades and goodresearch evidence exists for their short-term usein ADHD. More recently, various stimulant deliv-ery systems have been developed – the osmoticcontrolled-release system (OROS), Concerta XL;the wax matrix-based beaded system, MetadateCD or Equasym XL; Focalin XL; the patch releasesystem, Daytrana, etc. – resulting in long-actingpreparations that make it possible to avoid theadministration of medication in school, reducingstigmatization and embarrassment.

The release systems and preparation of stim-ulants (proportion of immediate release vs slowrelease) allows the tailoring of the long-actingpreparations to suit individual children [9].Stimulants are contraindicated in schizophrenia,hyperthyroidism, cardiac arrhythmias, anginapectoris and glaucoma, and in patients with ahistory of hypersensitivity. Stimulants can be usedwith caution in hypertension, depression, tics

(or family history of Tourette syndrome), autismspectrum disorders, and severe mental retardation(Table 46.2).

AntipsychoticsSecond-generation antipsychotics (SGAs): Theseare prescribed most frequently, and include risperi-done, quetiapine, aripiprazole, olanzapine, ziprasi-done and amisulpride. They are dopamine receptorblockers (hence they reduce positive symptomsbut can produce extrapyramidal symptoms andhyperprolactinaemia) and 5HT-2A receptorblockers.

• Risperidone is the most used SGA; it is a potentdopamine D2 receptor blocker (hence produceshyperprolactinaemia) and can lead to extrapyra-midal symptoms.

• Quetiapine is an effective SGA with a moderateeffect on weight; it usually needs to be takenat least twice daily because of relatively weakreceptor binding.

• Ziprasidone is the only SGA that is weight neu-tral; however, it has a greater impact on cardiacrhythm and the QTc interval.

• Clozapine is used in those with resistant psy-choses or tardive dyskinesia, but can lead toneutropenia, sialorrhoea and significant weightgain.

• Olanzapine is used less in children and ado-lescents because of the propensity to weightgain and metabolic syndrome. Evidence fromadults suggests that clozapine, olanzapine andlow-potency conventional antipsychotics such aschlorpromazine are associated with an increasedrisk of insulin resistance, hyperglycaemia andtype 2 diabetes mellitus.

• Aripiprazole is a dopamine partial agonist ordopamine stabilizer and also has actions at 5HT-2A and D3 receptors, and partial agonism of5HT-1A receptors. Symptoms may improve inthe first week, but it is recommended to wait 4–6weeks to determine efficacy, owing to the phar-macokinetics of the drug. The mean eliminationhalf-life of aripiprazole is 75 hours, and 94 hoursfor the major metabolite, dihydro-aripiprazole.Little published evidence exists on its use inmanaging non-psychotic disruptive behaviour indevelopmental disorders, although clinical expe-rience suggests that very small doses (2–5 mgdaily) are sufficient (Table 46.3).

288


Table 46.1 Dose range of psychotropic medication used in children and adolescents.

Drug Dose range Target symptoms

Stimulants

Methylphenidate IR 5-60mg/day Inattention, hyperactivity, impulsivity, andbehavioural problems related to ADHD

Concerta XL 18-72mg/day

Equasym XL 10-60mg/day

Medikinet Retard 10-60mg/day

Dexamfetamine 2.5-40mg/day

Non-stimulant

Atomoxetine 1-1.2mg/kg body weight/day

Tricyclic antidepressants

Imipramine, desipramine <6 years: 10-20mg/day Bedwetting, hyperactivity, impulsivity,inattention

>6 years: 10-75mg/day

Clomipramine 10-200mg/day Obsessions, compulsions

SSRls

Fluoxetine

Fluvoxamine

Sertraline

Paroxetine

Citalopram

10-60mg/day

50-300mg/day

25-150mg/day

10-60mg/day

10-60mg/day

Depression (only fluoxetine approved),obsessions and compulsions (high doses maybe needed), self-injurious behaviour, andanxiety-related aggression in autism spectrumdisorder (low doses)

SNRI

Venlafaxine 37.5-150mg/day Symptoms of ADHD in adults

Antipsychotic medication High doses - psychosis, (hypo)mania

Haloperidol Pre-pubertal: 0.5-8mg/day Low doses (<1/3 of dose for psychosis) - tics,severe aggression and self-injury; risperidonein ASD with ADHD

Post-pubertal: 1-16mg/day

Clozapine∗ 50-600mg/day

Risperidone 0.25-6mg/day

Olanzapine 2.5-20mg/day

Quetiapine 25-300mg/day

Aripiprazole 1-15mg/day

Anti-epileptic medication Epilepsy, symptoms and prophylaxis of bipolarillness

Carbamazepine 5-10mg/litre (serum level)

Sodium valproate 50-100mg/litre (serum level)

Clonazepam 0.5-4mg/day Epilepsy, akathisia, sleep disorders


289



Drug Dose range Target symptoms

Other

Lithium carbonate 0.4-1.0 mEq/litre (serumlevel)

Bipolar disorder, aggression in the learningdisabled, augmentation in depression

Clonidine 0.05-0.4mg/day Hyperactivity, impulsivity, inattention,insomnia, tics, oppositionality, aggression inASD

Buspirone 10-45mg/day Anxiety, hyperactivity, aggression

Melatonin 0.5-9mg/day Sleep problems

Naltrexone 12.5-50mg/day Severe resistant self-injurious behaviour inASD

ADHD, attention-deficit hyperactivity disorder; ASD, autism spectrum disorder; SNRI, serotonin-norepinephrine reuptake inhibitor;SSRI, selective serotonin reuptake inhibitor.∗Only for psychosis and tardive dyskinesia.

Table 46.2 Specific side effects of stimulants.

Side effect Precautions Comment

Seizure No evidence of decreasingseizure threshold; can be usedin well-controlled epilepsy

If seizures appear or worsen, change todexamfetamine; avoid atomoxetine

Growth retardation Reduced height and weightcentiles possible over time

Advisable not to start stimulants inchildren who are short or biologicallypredisposed to short stature

Cardiovascularproblems

Increases heart rate and bloodpressure - monitor regularly

High risk in those with structural cardiacdefects; monitor with ECG. AvoidAdderall in cardiac high-risk groups

Abuse potential Possible abuse of stimulants byothers with access

Self-initiated increase in dose byemotionally unstable patients withsubstance use disorders is possible, andshould be monitored; atomoxetine,bupropion or Concerta XL, (drug-deliverysystem makes it difficult to abuse) can beused

Psychotic symptoms Can induce or worsen psychoticexperience

Avoid in those who have first-degreerelatives with a psychotic disorder or inchildren who have psychotic orquasi-psychotic experiences;atomoxetine, tricyclic antidepressants,clonidine, bupropion or risperidone canbe used

ECG, electrocardiography.

290


Table 46.3 Specific side effects of selected psychotropic medication.

Drug Precautions Side effects

Non-stimulant

Atomoxetine(noradrenaline reuptakeinhibitor)

Contraindicated inhepatic impairment,glaucoma, uncontrolledseizures, or a history ofhypersensitivity to drug;use with caution inhypertension,tachycardia,cardiovascular problems,and patients with longQT interval or familyhistory of QTprolongation, orcerebrovascular disease

Growth retardation: reduction of two tothree percentiles in mean height, andsome weight loss

Seizure liability: not to be used in patientswith uncontrolled seizures, and should bediscontinued in those who develop or havean increased frequency of seizures

Cardiovascular: increases heart rate (byincreasing noradrenergic tone) and smallincrease in blood pressure; QT intervalprolongation

Suicide risk: monitor for signs ofdepression, suicidal thoughts andbehaviour∗

Liver dysfunction: severe liverinjury—rare. Abnormal liver enzymes aremore common. Discontinue on firstsymptom or sign of liver dysfunction, e.g.pruritus, dark urine, jaundice, right upperquadrant tenderness or unexplainedflu-like symptoms

Tricyclic antidepressants

Imipramine, amitriptyline,nortriptyline,desipramine,clomipramine

Use has declined due toconcerns of cardiacarrhythmias and casereports of sudden death

Cardiotoxicity, danger of accidental orintentional overdose, troublesomesedation, anticholinergic side effects,lowered seizure threshold

Newer antidepressants

SSRIS: fluoxetine,fluvoxamine, sertraline,paroxetine, citalopram,escitalopram

SNRI: venlafaxine

NRI: reboxetine,mirtazapine

It is currently advisedthat children oradolescents beingstarted on, or dose beingincreased of,antidepressants shouldbe monitored closely foremergence or worseningof suicidal ideation orbehaviour

Antidepressant-related suicidal ideationand behaviour: consistently there has beenincreased suicidal ideation with use ofantidepressants in childhood depression.This has to be balanced with genuinesuicidal risk in untreated severedepression†

Antidepressant-induced behaviouralactivation: increased motor activity,restlessness, excitability and impulsivitythat occurs usually early in treatment andmay be reduced by using the MEDprinciple; managed by reducing the dose,and with a benzodiazepine for a few days


291



Drug Precautions Side effects

Antipsychotic medication

FGAs: haloperidol,chlorpromazine

Monitor movementdisorders at baseline andregularly duringtreatment

Extrapyramidal side effects such astardive dyskinesia are more common inFGAs. Aripiprazole and clozapine areuseful in those who require antipsychoticsbut have developed tardive dyskinesia

SGAs: risperidone,olanzapine, quetiapine,aripiprazole, ziprasidone,clozapine

Monitor weight, waistcircumference, and BMIat baseline and every 6weeks; serum prolactin,fasting lipids, fastingcholesterol, fastingglucose, and liverfunction tests at baselineand every 6 months. Becautious if there is afamily history of obesity,dyslipidaemia,early-onsethypertension,cardiovascular disease,cerebrovascular accidentor diabetes

Hyperprolactinaemia: common withrisperidone and FGAs

Risk of weight gain and metabolicdysfunction:

High—clozapine, olanzapine

Moderate—risperidone, quetiapine

Low—amisulpride, aripiprazole,ziprasidone

Treatment of SGA-induced metabolicdysfunction: preventive healthy lifestylecounselling; regular monitoring of bodyweight and metabolic variables;cognitive-behavioural therapy andmotivational interviewing to addressunhealthy diet, physical inactivity, andsmoking; metformin therapy may becomenecessary in severe cases

FGA, first-generation antipsychotic; MED, minimum effective dose; NRI, norepinephrine reuptake inhibitor; SGA,second-generation antipsychotic; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRI, selective serotoninreuptake inhibitor.∗A black box warning exists as a result of analyses showing more frequent suicidal ideation in clinical trials ofchildren treated with atomoxetine [10].†In December 2003, the Committee on Safety of Medicines concluded that the evidence was adequate to establisheffectiveness only for fluoxetine in the treatment of depressive illness in children and adolescents, and advisedagainst the use of the other SSRIs [11]. The US Food and Drug Administration has insisted on black box warningsfor all SSRIs regarding the possibility of suicide-related behaviour as a side effect in children [12].

Mood stabilizersCarbamazepine, sodium valproate, lamotrigine,lithium carbonate and SGAs are mood stabilizers.

• Sodium valproate or valproic acid is the mostused mood stabilizer and is best avoided in girlsof child-bearing age due to its teratogenic effects,as well as possible side effect of polycystic ovar-ian disease.

• Lithium use warrants regular blood level moni-toring, which is often a problem in children.

• Lamotrigine is especially useful when significantdepressive symptoms exist in bipolar disorder.Valproic acid markedly increases the half-lifeof lamotrigine and the likelihood of developingsevere drug rashes including Stevens–Johnsonsyndrome. Lamotrigine is to be started at verylow doses (as low as 5 mg/day) and increasedslowly over a couple of months.

As antipsychotics, antidepressants and anti-manic agents are more closely associated with the

292


development of obesity and sexual/reproductiveadverse events in African American patients, prac-titioners need to carefully weigh the risks/benefitsof prescribing psychotropic agents to AfricanAmerican children, taking into considerationpre-existing/comorbid conditions or individualrisk factors for adverse reactions, especially whenmultiple medications are prescribed [13].

DRUG INTERACTIONS

Detailed reviews of the cytochrome P450 enzymesystem in children and guidelines for the predictionof drug–drug interactions are available [14,15].It is advisable to look through this list beforeprescribing concomitant medication. Terfenadine,ketoconazole, azetamazole and erythromycin, ifco-administered with selective serotonin reuptakeinhibitors, can in theory lead to cardiac arrhyth-mias. Fluvoxamine can significantly increaseclozapine levels; sodium valproate significantlyincreases lamotrigine levels, and imipraminewhen added to erythromycin can lead to toxicdelirium.

ETHICAL ISSUES IN PAEDIATRICPSYCHOPHARMACOLOGY

Research on psychopharmacological treatmentin children and adolescents is the subject ofongoing ethical discussion, as minors with mentaldisorders constitute a vulnerable patient group.Incentives for the conduct of clinical trials withchildren comparable to those contained in USlegislation are now provided in the EU. Researchto develop ‘me-too’ preparations (or drugs thatare just similar to already existing drugs) mayhave no significant benefit for children, but cancause research burden and detract from clinicallymore important projects by utilizing limitedinvestigator time and patient resources [16]. Theissues of avoiding undue influence from fundersand conflicts of interest remain a prominentconcern that can be solved by declaring conflictsand publishing all results of studies extensively.

CONCLUSION

Pharmacogenetic studies may bring more individ-ualized treatment approaches into child psychiatry

but they remain at present a promise for the future.Please see Chapter 41. A holistic biopsychoso-cial formulation and management of the child’sproblem is essential as psychopharmacotherapy isonly part of a package of care. Use of the MEDprinciple assists in titrating initial dose incrementsto the expected target dose based on treatmentresponse and emergent adverse effects. Paediatricpharmacovigilance for psychotropic agents andtrue long-term studies on efficacy and side effectsare essential. Evidence on treatment impact oncomorbid disorders, cost-effectiveness and impacton quality of life is sparse and urgently needs tobe addressed. Until such detailed data becomeavailable, it is safe to assume that paediatric pop-ulations are at least as, or more, vulnerable toadverse effects as adults.

REFERENCES

[1] Vitiello B. (2008) An international perspectiveon pediatric psychopharmacology. InternationalReview of Psychiatry 20, 121–6.

[2] Santosh PJ and Baird G. (1999) Psychopharma-cotherapy in children and adults with intellectualdisability. Lancet 354, 233–42.

[3] Hamrin V, McCarthy EM, Tyson V. (2010) Pediatricpsychotropic medication initiation and adherence:a literature review based on social exchange theory.Journal of Child and Adolescent Psychiatric Nursing23, 151–72.

[4] Santosh PJ. (2009) Medication for childrenand adolescents – current issues. In: Gelder M,Andreasen N, Lopez-Ibor J, Geddes J (eds), NewOxford Textbook of Psychiatry. Oxford: OxfordUniversity Press, pp. 1793–9 (Chapter 9.5.5).

[5] Bourin M and Couetoux du Tertre A. (1992)Pharmacokinetics of psychotropic drugs in chil-dren. Clinical Neuropharmacology 159(Suppl. 1),224A–25A.

[6] Paxton J and Dragunow M. (1993) Pharmacology.In: Werry J and Aman M (eds), Practitioner’s Guideto Psychoactive Drugs for Children and Adolescents.New York: Plenum, pp 23–50 (Chapter 2).

[7] Goldman-Rakic PS and Brown RM. (1982) Postna-tal development of monoamine content and synthe-sis in the cerebral cortex of rhesus monkeys. BrainResearch 256, 339–49.

[8] Mezzacappa E, Steingard R, Kindlon D, Saul P,Earls F. (1998) Tricyclic antidepressants and car-diac autonomic control in children and adolescents.Journal of the American Academy of Child andAdolescent Psychiatry 37, 52–9.

293


[9] Banaschewski T, Coghill D, Santosh P et al. (2006)Long-acting medications for the hyperkinetic disor-ders. A systematic review and European treatmentguideline. European Child and Adolescent Psychia-try 15, 476–95.

[10] Strattera (atomoxetine hydrochloride) Cap-sules: Detailed View: Safety Labeling ChangesApproved By FDA Center for Drug Eval-uation and Research (CDER) – July 2008.http://www.fda.gov/Safety/MedWatch/SafetyInformation/Safety-RelatedDrugLabelingChanges/ucm121836.htm (accessed 16 February 2011).

[11] Report of the CSM Expert Working Groupon the Safety of Selective Serotonin ReuptakeInhibitor Antidepressants. (2004) Committee onSafety of Medicines, http://www.mhra.gov.uk/home/groups/pl-p/documents/drugsafetymessage/con019472.pdf (accessed 17 June 2008).

[12] Food and Drug Administration. (2007) Antide-pressant use in Children, Adolescents andAdults. US FDA, http://www.fda.gov/Cder/drug/antidepressants/default.htm (accessed 17 June2008).

[13] Jerrell JM. (2010) Adverse events associated withpsychotropic treatment in African American chil-dren and adolescents. Journal of the National Med-ical Association 102, 375–83.

[14] Nemeroff CB, DeVane CL, Pollock BG. (1996)Newer antidepressants and the cytochrome P450system. American Journal of Psychiatry 153,311–20.

[15] Oesterheld JR, Shader RI. (1998) Cytochromes:a primer for child and adolescent psychiatrists.

Journal of the American Academy of Child andAdolescent Psychiatry 37, 447–50.

[16] Kolch M, Ludolph AG, Plener PL, Fangerau H,Vitiello B, Fegert JM. (2010) Safeguarding chil-dren’s rights in psychopharmacological research:ethical and legal issues. Current PharmaceuticalDesign 16, 2398–406.

FURTHER READING

Anonymous. (1992) Prescribing unlicensed drugs orusing drugs for unlicensed indications. Drug and Ther-apeutics Bulletin 30, 97–9.

Correll CU and Carlson HE. (2006) Endocrine andmetabolic adverse effects of psychotropic medicationsin children and adolescents. Journal of the Ameri-can Academy of Child and Adolescent Psychiatry 45,771–91.

Martin A, Scahill L, Charney DS Leckman JF (eds).(2003) Paediatric Psychopharmacology – Principlesand Update. New York: Oxford University Press.

McVoy M and Findling R. (2009) Child and adoles-cent psychopharmacology update. Psychiatric Clinicsof North America 32, 111–33.

Stahl SM (ed.). Essential Psychopharmacology. Cam-bridge: Cambridge University Press.

van den Anker JN. (2010) Developmental pharmacol-ogy. Developmental Disabilities Research Reviews 16,233–8.

294

Index

Index

actioninfancy 19

adolescencecultural influences 15expressing grief in bereavement 93fostering resilience 78, 83

definition of resilience 79mobilizing resilience 81–2policy and practice 79–81

social and emotional development (SED) 57,59

social-cognitive development 62mentalizing 63–4mentalizing in mid-adolescence 64–5

adoption and fostering 100adopted from care 101–2foster children 100–1infancy 100treatment considerations 102–4

interventions for attachment difficulties 103adrenocorticotropic hormone (ACTH) 108affective social processes

infancy 19age of mother 5agreeableness 218aggression

conduct disorder 175, 176in the home 251problematic SED 60resulting from bereavement 92resulting from maltreatment 124sibling influences 10treatment 287

atypical antipsychotics 178buspirone 173buspirone 290


clonidine 290haloperidol 289lithium 290risperidone 145SSRIs 289

alcohol 202alcohol abuse 5alcohol use during pregnancy 155alkyl nitrate use 202allele, definition 27amphetamine use 202amygdala

impact of childhood mistreatment 121anger

first year of life 42–3anomalous parenting behaviours 88anorexia nervosa (AN) 194, 278–9

binge-purging subtype (AN-BP) 194restrictive subtype (AN-R) 194

anterior cingulate cortex (ACC) 123antisocial behaviour

maltreated children 117antisocial personality disorder (ASPD) 219anxiety 277–8

prevention programmes 75anxiety disorders 169, 173

aetiologygenetics 170life events 171neurobiology 171parent–child interactions 171social adversity 171temperament 170

assessment 171–2diagnosis 169–70epidemiology 170

295

Index

anxiety disorders (continued)prevention 173prognosis 172treatment 172

cognitive behavioural therapy (CBT) 172family therapy 173medication 173other psychotherapies 172–3

arginine vasopressin (AVP) 108aripiprazole 288, 289

bipolar disorder 212arousal

infancy 19array-based comparative genomic hybridization

(aCGH) 39–40Asperger syndrome 142Assessment Checklist for Children (ACC) 101

maltreated children 102atomoxetine

attention deficit hyperactivity disorder(ADHD) 156, 158

attachment 14–15attachment behaviour 85, 90

interventions 89fostered and adopted children 90, 103preventive 89–90

maltreated children 102variations in attachment

causes of variation 86–8consequences 89disorders 89normative patterns 86

attachment bond 85attachment theory

definition 85–6Attachment, Self-Regulation and Competency

(ARC) framework 103attention

infancy 18neuropsychological assessment 236, 240

attention deficit hyperactivity disorder (ADHD)143, 153

aetiology 154–5clinical course 159cognitive and neurobiological correlates 155diagnostic assessment 155

child information and observation 155–6information from parents 155key areas 155physical examination 156report from school 156

diagnostic classification 224–5, 226–7epidemiology 153–4management 156treatment 156

medication 156–7non-stimulants 158other interventions 159psychosocial interventions 158school interventions 158–9stimulants 157–8

attention skillsdevelopment from birth to five years 35–6

authoritarian parenting style 4authoritative parenting style 4autism spectrum disorders (ASDs) 141

aetiology 142assessment and investigation 144associated disorders 142course and prognosis 145diagnosis 142–3

parental concerns 143differential diagnosis 143–4management and intervention 144

medication 144–5practice points 145

prevalence 141–2avoidant personality disorder 220Avoidant type attachment 86, 87

base pair (bp), definition 27behavioural disorders 175, 178

aetiology 176–7definition 175epidemiology 176prevention and treatment 177–8subtyping 175–6

benzodiazepinesanxiety disorders 173

bereaved children 92, 95assessments

at death 96immediately after death 97longer term 98pre-death 96short term 97

expressing grief 92adolescence 93early childhood 92middle childhood 92–3

factors influencing outcome 94interventions

296

Index

help for parents 95needs of children 94role of professionals 95service for children 95theoretical and cultural influences 94

psychopathology 93resilience and positive outcomes 93understanding of death 92

Binge Eating Disorder (BED) 194biological influences see genetic and biological

influences on childrenbipolar disorder 210

see also depressionassessment 211clinical characteristics 210–11diagnostic classification 225–6diagnostic criteria 210differential diagnosis 211epidemiology 211longitudinal course and prognosis 211–12suicide risk 212treatment 212

acute phase 212–13depressive phase 213psychological treatments 213–14refractory cases 214

body mass index (BMI) 197, 198borderline personality disorder (BPD) 219Bowlby–Ainsworth model of attachment 14brain

impact of childhood mistreatment ondevelopment 121

amygdala and hippocampus 121corpus callosum and other white matter

122–3prefrontal cortex and cerebellum 121–2

impact of childhood mistreatment on function123

event-related potential (ERP) studies 123–4fMRI studies 123

regions involved in mentalizing 62–3Brazelton Behavioural Assessment Scale 70brothers and sisters see siblings, effect on

development 9bulimia nervosa (BN) 194, 279

non-purging subtype (BN-NP) 194purging subtype (BN-P) 194

bullying 6siblings 11

bupropion

attention deficit hyperactivity disorder(ADHD) 156

buspirone 290anxiety disorders 173

cannabis use 202carbamazepine 289catechol O-methyltransferase (COMT)


COMT gene 25cerebellum

impact of childhood mistreatment 121–2child abuse see maltreated childrenchild protection 119childcare, professional 5–6Children’s Yale–Brown Obsessive Compulsive

Scale (CY-BOCS) 162chronic fatigue syndrome (CFS) 148citalopram 289

somatization and somatoform disorders 151clomipramine 289

autism spectrum disorders (ASDs) 145obsessive–compulsive disorder (OCD) 165,

166clonazepam 289clonidine 290


clozapine 288, 289cocaine use 202cognitive behavioural therapy (CBT) 265, 269

adopted or fostered children 103anxiety 75anxiety disorders 172attention deficit hyperactivity disorder

(ADHD) 158basic premises 265–7

core steps 266key childhood cognitions 266

bereaved children 93depression 74developmental considerations 267eating disorders 199obsessive–compulsive disorder (OCD) 163–5recent advances 267–9stress 112substance misuse 206

cognitive developmentbirth to five years 36–9

community influences on children 6

297

Index

competitivenessmiddle childhood 58–9

complex condition, definition 27complicated traumatic grief (CTG) 93, 94comprehension strategies 48concerta XL 289conduct disorder (CD) 175

aetiology 176–7definition 175epidemiology 176prevention and treatment 177–8subtyping 175

configurations of risk 7conscientiousness 218copy-number variations (CNVs) 24

autism spectrum disorders (ASDs) 142definition 27

corpus callosum (CC)impact of childhood mistreatment 122–3

corticotropin-releasing hormone (CRH) 108co-sleeping 15crying

first year of life 42cultural influences on children 13, 16

see also ethnicityadolescence 15childhood and parenting across cultures

13–14development niche and ecocultural pathways

13infancy

attachment 14–15co-sleeping 15developmental stages 14neurobehavioural development 20–1parental involvement in play and learning

15mental health 15–16middle childhood 15

cytochrome P450 2D5 gene 263poor substrate metabolizers 263ultra-rapid substrate metabolizers 263

deficits in attention, motor skills and perception(DAMP) 143

deletion mutation, definition 27dependent personality disorder 220–1depression 187, 278

see also bipolar disorderaetiology 187–8diagnosis 189

epidemiology 187management 189managing associated comorbidities 189–90outcomes 189parental 4–5preventing relapse 190prevention programmes 74

desipramine 289development

birth to five years 32clinical decision-making and developmental

delay 37–8, 39developmental domains 33–9developmental examination 32–3diagnosis and management 40indicators of abnormal development 32,

37–8medical investigations 39–40physical examination 39

first year of life 41–2, 43–4crying 42fear 43smiling 42surprise, anger and sadness 42–3

developmental domains 33attention skills 35–6cognitive development 36–9drawing 34, 35gross motor 33imitating and copying cube models 34, 35language and communication 34, 36object concepts and relationships 34, 35play and social behaviour 34–5, 37visual, eye-hand coordination and problem

solving 34developmental examination 32

history-taking 32–3observation and interactive assessment 33

dexamfetamine 289attention deficit hyperactivity disorder

(ADHD) 156, 157diagnostic classification 224–5

ADHD 224–5, 226–7bipolar disorder 225–6current issues 226disruptive disorders 227progress 227self-injury 227

diploid number, definition 27disinhibited behaviour 102Disorganised type attachment 86, 87

298

Index

divorce of parents 5DNA 23–4

definition 27genomic regulation 24–5genomic variation 24

drug abuse 5dyslexia 134–5dyspraxia 143

eating disordersadolescence

assessment 197cognitive behavioural therapy (CBT) 199diagnosis and classification 194–5epidemiology and aetiology 195formulation 196future directions 199management 196medical aspects 197–8psychiatric aspects 198–9risk factors 195risk factors, high 196

infancy 128, 132assessment 130, 131diagnosis 129–30presentation 128–9risk evaluation 130–2treatment 132

Eating Disorders Examination (EDE) 195Eating Disorders Not Otherwise Specified

(EDNOS) 194ecstasy use 202education

maltreated children 117electroconvulsive therapy (ECT)

bipolar disorder 213emotional abuse of children 115emotional development see social and emotional

development (SED)encopresis 278epigenetic variation 26

definition 27equasym XL 289ethnicity 16

see also cultural influences on childrenmental health 15–16

event-related potential (ERP)maltreated children 123–4obsessive–compulsive disorder (OCD) 163,

165executive function

neuropsychological assessment 236–7, 243expressive language 46expressive SLI (E-SLI) 182expressive–receptive SLI (ER-SLI) 182extraversion 218eye movement desensitization and reprocessing

(EMDR)adopted or fostered children 103stress 112

family and systemic influences on children 3–4changing family patterns 5

separation and divorce 5single parents and step parents 5

childcare and schooling 5–6culture 13–14

parental involvement in play and learning 15parent and family characteristics 4–5siblings 8

adjustment 10development of social understanding 9–10individual relationships 9intervention programmes 11parent–child relationships 9peers 10–11

social and environmental factorsmultiple stressors 6–7neighbourhood and community contexts 6poverty and social disadvantage 6

family therapy assessment 255, 258definition 255general principles 256goals 256–7process 257–8research assessment tools 258types 255–6

family-focused therapy (FFT) 213fear

first year of life 43feeding disorders see eating disordersfluoxetine 289

anxiety disorders 173autism spectrum disorders (ASDs) 145depression 189somatization and somatoform disorders 151

fluvoxamine 289anxiety disorders 173obsessive–compulsive disorder (OCD) 166

fostering see adoption and fosteringfragile-X syndrome 142FRIENDS for life 75

299

Index

friendshipsrole of child’s siblings 10–11

Functional Family Therapy (FFT) 273

gene chip, definition 28gene, definition 27general ability

neuropsychological assessment 236generalised anxiety disorder 169genetic and biological influences on children 23,

27gene numbers 23–4genomic regulation mechanisms 24–5glossary of terms 27–9individual genome mapping 26–7sources of variation 24susceptibility to psychiatric disorders

epigenetic variation 26gene–environment interactions 25genome-wide association studies 25–6

genome, definition 28genome-wide association study, definition 28genotype, definition 28glue misuse 202

hallucinogen use 202haloperidol 289haploid number, definition 28headaches 148heterotypic continuity 85high-altitude adaptation through parental

practices 20–1hippocampus

impact of childhood mistreatment 121histrionic personality disorder 220Human Genome Project, definition 28hyperactivity 154hyperkinetic disorder 154hypothalamic–pituitary axis (HPA) 68

bereaved children 93psychophysiological response to stress 107, 108resilience 79

imipramine 289impulsivity 154inattention 154indels 24indicated prevention programmes 73indulgent parenting style 4infancy

adoption and fostering 100

cultural influencesattachment 14–15co-sleeping 15developmental stages 14parental involvement in play and learning 15

eating disorders 128, 132assessment 130, 131diagnosis 129–30presentation 128–9risk evaluation 130–2treatment 132

neurobehavioural development 18, 21capacities 18–19culture 20–1Mutual Regulation Model (MRM) 19–20

promoting mental healthassessment 69–70definition 68factors 69families with indicated additional needs 70–1importance of infancy 68–9universal interventions 70

social and emotional development (SED) 57social cognition 51–2

infant attachment classification profiles 87influences on children’s emotional and

behavioural development 3culture 13, 16

adolescence 15childhood and parenting across cultures

13–14development niche and ecocultural pathways

13infancy 14–15mental health 15–16middle childhood 15

family and systemic 3–4changing family patterns 5childcare and schooling 5–6parent and family characteristics 4–5social and environmental factors 6–7

genetic and biological 23, 27gene numbers 23–4genomic regulation mechanisms 24–5glossary of terms 27–9individual genome mapping 26–7sources of variation 24susceptibility to psychiatric disorders 25–6

siblings 8adjustment 10development of social understanding 9–10

300

Index

individual relationships 9intervention programmes 11parent–child relationships 9peers 10–11

inhibited behaviour 102insecure attachments 86, 87insertion mutation, definition 28interactive behaviour scales 87interventions, systemic and family approaches

276eating disorders

anorexia nervosa (AN) 278–9bulimia nervosa (BN) 279

emotional problemsanxiety 277–8depression 278encopresis 278suicidal behaviour 278

externalizing disordersADHD 276adolescent conduct problems 276adolescent substance misuse 277multi-dimensional treatment foster care

(MDTFC) 277transferability of treatment approach

277nature of evidence 279

IQautism spectrum disorders (ASDs) 143neuropsychological assessment 234–5

ketamine use 202

lamotrigine 292language 45

see also literacy disorders; specific languageimpairment (SLI)

atypical development 48–9development from birth to five years 34, 36future directions for study 49milestones of speech and language

development 47neuropsychological assessment 236, 239phases of development 47–8processes and components of development

45–7large families, effect on children 5late talkers 48learning

cultural influencesparental involvement in play and learning 15

Life Story Book 103literacy disorders see also language

acquiring literacy skills 135assessment 137–8

diagnostic components 138identification 137

definition 134–5nature of impairment 135–6preschool to adolescence 136

risk factors 136teaching techniques 138–9

lithium carbonate 290, 292looked-after children (LAC) 100–1

maltreated children 102, 114, 119–20brain function differences 123

event-related potential (ERP) studies 123–4fMRI studies 123

clinical implications 124–5epidemiology 114harm to the child 116–17

antisocial behaviour 117educational progress and employment 117mechanisms 116mental health 117

impact on brain development 121amygdala and hippocampus 121corpus callosum and other white matter

122–3prefrontal cortex and cerebellum 121–2

intervention 118aims 118child protection 119immediate treatment 118–19treatment for the effects and future

prevention 119recognizing maltreatment 117–18

tiers of concern 118role of genetic influences 124social and family factors 114–16types of maltreatment 114, 115

maternal sensitivity scales 88maternal smoking during pregnancy 155medication

attention deficit hyperactivity disorder(ADHD) 156–7

autism spectrum disorders (ASDs) 144–5obsessive–compulsive disorder (OCD) 165–6psychotropic 261

national differences in prescription policies261–2

301

Index

medication (continued)somatization and somatoform disorders 151stress 112

medikinet retard 289memory

neuropsychological assessment 236, 238mental health

cultural influences on children 15–16maltreated children 117

mental health, promotingchildhood 72

anxiety prevention programmes 75depression prevention programmes 74future developments and challenges 75–6

prevention programmes 72–4infancy

assessment 69–70definition 68factors 69families with indicated additional needs

70–1importance 68–9universal interventions 70

mental state examination (MSE) 247metatonin 290methylation (genes), definition 28methylphenidate 289

attention deficit hyperactivity disorder(ADHD) 156, 157

microarray, definition 28middle childhood

cultural influences 15social and emotional development 56, 57, 58–9

addressing problems 60consequences of problems 60

migraine headaches 148modafinil


monoamine oxidase A (MAOA)MAOA gene 25, 124

aggression resulting from maltreatment 124mothers, young 5motor skills

development from birth to five years 33, 34neuropsychological assessment 236, 242

multi-dimensional treatment foster care(MDTFC) 277

Multisystemic Therapy (MST) 273–4mutation, definition 28Mutual Regulation Model (MRM) 19–20

naltrexone 290narcissistic personality disorder 220neglect of children 115neighbourhood influences on children 6neurobehavioural development in infancy 18, 21

capacities 18–19culture 20–1Mutual Regulation Model (MRM) 19–20

neuropsychological assessment 229, 233, 234, 237informal 233information gathering 230issues 230

environmental influences 230informal observations 230–1, 232setting and task characteristics 231–2

justification 234–5knowledge base and competencies 230, 231measurement considerations 235

developmental 235failure route 235psychometrics 235–6

necessity 234specialist assessment 236

attention 236, 240executive function 236–7, 243general ability 236language 236, 239memory 236, 238motor skills 236, 242social cognition 237spatial ability 236, 241

theoretical backgroundassessment 229child neuropsychological assessment model

230developmental model 229–30

neuroticism 218NICU (Neonatal Intensive Care Unit) Network

Neurobehavioural Scale (NNNS) 19nucleotide, definition 28

obsessive–compulsive disorder (OCD)aetiology 162assessment

comorbidities 163differential diagnosis 162distress of obsessions and compulsions 163phenomenology of obsessions and

compulsions 162prevalence 161prognosis and ongoing care 166

302

Index

symptoms 161threshold of ordinary rituals 162treatment 163

medication 165–6NICE stepped-care model 164understanding 163

obsessive–compulsive personality disorder(OCPD) 221

olanzapine 288, 289bipolar disorder 212

openness 218opiate use 202oppositional defiant disorder (ODD) see

behavioural disordersoxycarbazepine

bipolar disorder 212

panic disorder 170paranoid personality disorder 219parenting 3–4

adoption and fostering 103anomalous parenting behaviours 88changing family patterns 5

separation and divorce 5single parents and step parents 5

characteristics of parent and family 4–5childcare and schooling 5–6cultural influences 13–14

parental involvement in play and learning 15relationships with and among siblings 9styles of parenting 4

parenting programmes for conduct problems 274effectiveness

social learning approaches 274youth interventions 274

evidence linking parenting to childpsychopathology 271

mediators of change 274role of therapist skill 274social learning theory 271

child-centred approach 271–2features 272imposing clear commands 272–3increasing desirable child behaviour 272reducing undesirable child behaviour 273

youth interventions 273family-based 273multicomponent 273–4

paroxetine 289participatory action research (PAR) project 80–1perceptual reasoning (PR) factor 235

personalitychildhood traits with adult outcomes 217–18definition 217development 217

personality disorder 221assessment

antisocial personality disorder (ASPD) 219avoidant personality disorder 220borderlinel personality disorder (BPD) 219childhood personality 218dependent personality disorder 220–1diagnostic issues 218–19histrionic personality disorder 220narcissistic personality disorder 220obsessive–compulsive personality disorder

(OCPD) 221paranoid personality disorder 219personality disorder not otherwise specified

(NOS) 221schizoid personality disorder 219schizotypal personality disorder 219

definitionspersonality 217temperament 217

personality disorder not otherwise specified(NOS) 221

pharmacogenetics, definition 28pharmacogenomics

beyond CYP2D6 263–4cytochrome P450 2D5 gene 263

poor substrate metabolizers 263ultra-rapid substrate metabolizers 263

definition 262future expectations 264

phenotype, definition 28phobias 170physical abuse of children 115play

cultural influencesparental involvement in play and learning 15

development from birth to five years 34–5, 37middle childhood 58

polymorphisms 24Positive Parenting Programme 177post-traumatic stress disorder (PTSD)

children bereaved by parent murder or suicide93

mistreatment during childhoodimpact on hippocampus 121

stress response 109poverty 6

303

Index

prefrontal cortex (PFC) 62–3impact of childhood mistreatment 121–2mentalizing in adolescents 63–4

preschoolsocial and emotional development (SED) 57

psychiatric disorder assessmentchildren and adolescent interviews 246–8

mental state examination (MSE) 247observations 246

constructing a formulation 249family interviews 246necessity 245other sources of information 249parent/carer interviews 248

important information 248physical examination and investigations 248–9scope 245–6

psychological assessment 251, 253biopsychosocial model 252–3

main systems 252models 251–2psychological testing 253–4

psychological first aid 112psychometric testing

interpretation of scores 235–6reliability and validity 235

psychopharmacology, special paediatricconsiderations 286, 293

art of medication prescription 287drug interactions 293ethical issues 293factors in children 287

absorption and hepatic metabolism 287cardiotoxicity 288fat distribution 287–8incomplete maturation of neurotransmitter

system 288protein binding and distribution volume 288

judicious prescribing 286medications 288

antipsychotics 288mood regulators 292–3non-stimulants 291stimulants 288, 290

multimodal treatment package 286non-licensed psychotropic medication 287symptom-based strategy 286–7

psychotherapeutic approaches 281, 284basic premises of psychodynamic approach 281evidence base 281–2potential adverse effects of treatment 284

research examplesabuse or neglect 282long-term outcomes 283–4mixed diagnoses 283

psychotropic medication 261national differences in prescription policies

261–2

quetiapine 288, 289bipolar disorder 212

reactive attachment disorders (RADs) 89reading comprehension 135reading problems see literacy disordersrearrangement (chromosomes), definition 29receptive language 46relaxation therapy 151resilience 79

bereaved children 93mobilizing 81

project implementation 82project summary 81–2

policy and practice 79–81Resistant type attachment 86, 87ribosome, definition 29risperidone 288, 289

bipolar disorder 212rivalry

middle childhood 58–9RNA 24–5

definition 29

sadnessfirst year of life 42–3

schizoaffective disorder (SA) 214schizoid personality disorder 219schizotypal personality disorder 219school-based prevention programmes 74schools 6secure attachments 86, 87selective prevention programmes 73selective serotonin reuptake inhibitors (SSRIs)

anxiety disorders 173autism spectrum disorders (ASDs) 145bipolar disorder 213depression 189obsessive–compulsive disorder (OCD) 165–6somatization and somatoform disorders 151stress 112

separation anxiety disorder 169separation of parents 5

304

Index

sertraline 289anxiety disorders 173obsessive–compulsive disorder (OCD) 166

sexual abuse of children 115Short OCD Screener (SOCS) 161siblings, effect on development 8

adjustment 10bullying 11development of social understanding 9–10individual relationships 9intervention programmes 11parent–child relationships 9peers 10–11

single parents 5single-nucleotide polymorphisms (SNPs) 24

definition 29sisters and brothers see siblings, effect on

development 9sleep

states in infancy 19small inferring RNA (siRNA) 29smiling

first year of life 42smoking 202smoking, maternal 155sociability of humans 62–3social and emotional development (SED)

contributing factors 59positive 59problematic 59–60

middle years 56addressing problems 60consequences of problems 60

preschool 56–8social cognition 51

individual differences 53–4origins 54

infancy 51–2neuropsychological assessment 237young children 52–3

social disadvantage 6social interactions

first year of life 41–2, 43–4crying 42fear 43smiling 42surprise, anger and sadness 42–3

social learning theory 271typical format

child-centred approach 271–2features 272

imposing clear commands 272–3increasing desirable child behaviour 272reducing undesirable child behaviour 273

social phobia 169–70social skills training


social understandingrole of siblings 9–10

sodium valproate 289, 292bipolar disorder 212

somatization and somatoform disorders 147associated features

comorbidity 148educational concerns 149family factors 149personality features 148precipitating factors 148

clinical characteristics 147–8diagnostic assessment 149differential diagnosis 150future directions 152prevention 152referral to mental health clinics 150treatment effectiveness 151treatment effectiveness

legal considerations 151treatment planning 150

family work 151medication 151programme 150school 150–1

spatial abilityneuropsychological assessment 236, 241

specific language impairment (SLI) 135aetiology 181

biological bases 181cognitive bases 182environmental influences 182

associated developmental problems 183–4definition 180–1developmental progression of language skills

183distinctive features 182–3implications 184types 182

middle childhood 182specific learning difficulty (SLD) 234step parents 5stress

assessment 110–11

305

Index

stress (continued)trauma interview 111

definition 107developmental issues 108differential diagnosis 111epidemiology and history 109management and treatment 111

immediate measures 111psychopathology 110psychophysiological response 107

delayed reaction to an event 107–8longer-term effects 108, 109

reactions in children 109–10risk and resilience 109

substance misuse 201, 207aetiology 203

comorbid mental health problems 203assessment 203–5

investigations 206mental and physical examination 205–6protective factors 205risk factors 205

classification and interventions 204consequences and features 203definition 201–3epidemiology 201treatment 206

evidence base 206–7role of CAMHS 207

suicidal behaviour 278assessment 191bipolar disorder 212course 191epidemiology 190management 191precipitating factors 190–1predisposing factors 190prevention 192

risk associated with self-harm 191treatment 191–2

surprisefirst year of life 42–3

systems biology, definition 29

temperamentdefinition 217

tension headaches 148, 151threat appraisal 171threat attention 171tobacco use 202toddlerhood 14

social and emotional development (SED) 57translation (genetics), definition 29tricyclic antidepressants (TCAs)


somatization and somatoform disorders 151Tummy Time 21Turner syndrome 142

uninvolved parenting style 4universal prevention programmes 73

venlafaxinedepression 189, 289

Webster–Stratton Incredible Years Programme177

Wechsler Intelligence Scale for Children(WISC-IV) 234–5

well-being see mental health, promotingword recognition 135

young mothers 5

ziprasidone 288

306

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