Psychotic Disorders of Later Life

Epidemiology, Classification, Treatment

and Prognosis

Background

• Term ‘paranoid’ still in popular use, but incorrectly applied

• Refers to symptoms, personality types or syndromes

• Can be qualitatively or quantitatively different from ‘normal’

• KRAEPILIN: Association of paranoid symptoms with sensitive pre-morbid personalities (Sensitive Beziehungswahn- Krestchmer)

• Freud: Proposed that origin was unconscious from defence mechanisms of denial and

projection

Paranoid states/Delusional disorders

• Psychotic disorders without PRIMARY mood-related, schizophreniform or organic basis

• Characterised by acute/chronic course with self-referential delusions, frequently fixed, elaborated and systematised

• ‘Delusional disorder’ replaces ‘paranoid state’ in ICD-10

• Derived from concept of ‘paranoia’ (KAHLBAUM 1863)

‘A primary delusional system remaining unchanged for years’

• Modern concepts of delusional disorder are broadly in keeping with this

Paranoid personality disorder

• Equates with ‘sensitive’ personality

• DSMIII-R defines it as: Pervasive tendency to interpret actions of

others as deliberately demeaning/threatening

Expects to be exploited/harmed by others Questions loyalty of friends Reads threats/insults into neutral actions Bears grudges over altercations Reluctant to confide in others for fear of

being betrayed Easily offended/angered by slights Questions fidelity of spouse/sexual

partners

Late-onset psychotic disorders• KRAEPILIN (1912): Chronic fantastic

delusions and hallucinations noted preservation of personality, lack of thought disorder and preservation of volition that distinguished it from schizophrenia

• Originally thought to hold an intermediate position between schizophrenia and paranoia

• ROTH (1955): ‘Late paraphrenia’. Well-organised system of paranoid delusions with/without auditory hallucinations with preservation of personality and affective response

• FISH (1960): ‘Senile schizophrenia’

• POST (1966): ‘Persistent persecutory states of the elderly’

• ICD-9 (1970s): Paraphrenia

• ICD-10 (1990 TO DATE): Persistent delusional disorder

PROBLEMS WITH CLASSIFICATION

• Important to distinguish late-onset delusional disorders from people with schizophrenia who have become older

• American classificatory systems have used age cut-off as 45 compared with 60/65 in British systems

• Earlier classifications included mood disorder, personality disorder and symptoms of schizophrenia in definitions

• Often difficult to establish clinical picture such as age of onset because, by definition, sufferers often less amenable to interview

• Approximately 15%. 7% and 5% of people with a lifetime history of schizophrenia will develop the disorder after the ages of 45, 60 and 65 respectively

Epidemiology

• Late-onset delusional disorders have a prevalence of between 2 and 4% of psychiatric disorders for over-65s in the community

• Incidence studies rare, but one study found incidence of between 17 and 26 per 100,000

• Aetiological associations encompass personality characteristics, genetic factors, physical impairment and organic brain disease

Pre-morbid personality

• Greater likelihood of paranoid/schizoid personality disorder

• Persistent delusional disorder may represent an accentuation of pre-existing paranoid personality disorder

• Schizoid personality disorder characterised by:

PERVASIVE INDIFFERENCE TO SOCIAL RELATIONS

DECREASED RANGE OF EMOTIONAL EXPRESSION

‘ECCENTRIC’, ‘ALOOF’, ‘COLD’

INDIFFERENT TO PRAISE/CRITICISM

LACK OF CLOSE FRIENDS/CONFIDANTES

Genetic factors

• Some evidence for genetic loading (Kay 1972)

• However, methodological problems include:

Variability in diagnostic criteriaUnreliable information on

family pedigree Overinclusiveness of psychotic phenomena

• Late-onset makes genetic studies problematic

• HLA sub-types show some heritability in persistent delusional disorder (HLA B37) [Naguib et al 1987]

Socio-demographic factors• Early postulated associations with un-

married status and low fertility (Post 1966), subsequent studies have not confirmed this (Kay and Roth 1961)

• Social isolation has a consistent association with persistent delusional disorder, suggested as a consequence of maladaptive personality traits (Kay 1972), BUT social isolation of onset in later life also implicated (Almeida et al 1995)

• Excess of females with persistent delusional disorder (Ranges from 3:1 to 45:2). Not simply a reflection of later onset of psychotic disorder in women. Theories include an excess of Dopamine receptors in older women and delayed onset of psychotic disorder through early use of coping mechanisms

• Association with social class not informative

Sensory impairment

• Experimental hearing loss associated with paranoid symptoms and auditory hallucinations

• Hearing impairment present in upto 40% of people with persistent delusional disorder

• Earlier onset may be related to social isolation and suspiciousness

• Psychotic symptoms may be diminished after improving hearing

• Some limited evidence for an association with visual impairment

Organic brain disease

• Classically, late-onset psychotic disorders have been associated with Organic Brain Disease, but the majority of clinical longitudinal studies provided little evidence for a significant association

• Neuro-imaging studies HAVE found strong associations between persistent delusional disorder and cerebrovascular lesions, cortical atrophy and ventricular enlargement (Almeida et al 1995)

• A variety of neurological ‘soft signs’ have been associated with persistent delusional disorder (e.g. signs of extrapyramidal and frontal lobe damage)

Clinical features• Presence of elaborated/systematised delusions

is common in persistent delusional disorder

• Delusions of persecution/reference frequent. Sexual themes not uncommon. Passivity phenomena in up to 40%

• Relative preservation of personality/absence of ‘negative symptoms

• Auditory hallucinations can be conspicuous, but not essential for diagnosis (2nd/3rd person/olfactory/tactile)

• Depressive symptoms do not predominate clinical picture

• Some evidence for mild cognitive impairment associated with persistent delusional disorder. One study has found that greater number of psychotic symptoms associated with less severe cognitive impairment

• Influence of pre-occupation with psychotic symptoms, poor cooperation and side-effects of neuroleptic drugs have to be taken into account

Differential Diagnosis (What else could it be?)

• Severe depressive disorder: Delusions often have different content, e.g. nihilistic, worthlessness, guilt. Also, presence of other depressive symptoms and other clues in history/mental state examination

• Dementia: Delusions and hallucinations occur in up to 15% of sufferers, but cognitive impairment progressive and delusions more fleeting/fragmented

• Schizo-affective disorder: Presence of symptoms typical of both mood disorder and schizophrenia but core elaborated delusional system more prominent than mood-related symptoms

• Transient paranoid reactions/personality disorder/organic psychoses /drug-induced psychoses

Management

• More helpful to assess in person’s home, since delusions may be situation-specific

• Sufferers often known to neighbours, police, social services, other public bodies

• Rapport difficult to achieve initially

• Remediable factors such as hearing impairment may bring about significant reduction in severity of psychosis

• Social interventions may not be successful, particularly if life-long solitariness

• Hospital admission may result in ‘honeymoon period’

Drug Treatment• Placebo-controlled trials are rare

• Most studies of traditional neuroleptics have found improvement in psychotic symptoms (27% to 66%)

• Successful remission/partial remission more difficult to achieve than in patients with schizophrenia who have grown older

• Presence of accompanying physical illness, altered metabolism/receptor sensitivity, polypharmacy, variable compliance and cognitive impairment are all complicating factors

• Oral neuroleptics at 10 to 25% of conventional dose used

• Low dose depot neuroleptics beneficial (esp. compliance)

• Atypical neuroleptics minimise risk of extrapyramidal side-effects

Outcome

• Most people follow a chronic course; complete remission rare

• Marked reductions in psychotic symptoms, however, can be achieved

• Progression of cognitive impairment not as fast as in dementia

• Risk of tardive dyskinesia kept lower by smaller doses of neuroleptics/use of atypical antipychotics

• Most people kept on caseloads of community teams for considerable lengths of time in view of poor integration into community (i.e. problems with neighbours etc)

Reading List

•Articles

•Almeida, O.P., Howard, R.J., Levy, R., David, A.S. (1995) Psychotic states arising in later life. Psychopathology and nosology and The role of risk factors. British Journal of Psychiatry 166, 205-228

• Hymas, N., Naguib, B., Levy, R. (1989) Late paraphrenia: a follow-up study. International Journal of Geriatric Psychiatry 4, 23-29

•Howard, R., Almeida, O.P, Levy, R. (1994) Phenomenology, demography and diagnosis in late paraphrenia. Psychological Medicine 24, 397-410

BOOKS

•Naguib, M, & Levy, R. (1995) Paranoid states in the elderly and late paraphrenia. In Jacoby, R. & Oppenheimer, C. (Eds) Psychiatry in the elderly. Oxford University Press, Oxford

•Howard, R (1997) Drug treatments in paranoid states of the elderly. In: C Holmes and R Howard (Eds), Advances in Old Age Psychiatry: Chromosomes to Community Care. Wrightson Biomedical Publishing, London.