schizophrenia “a slow fire burning” dr c christie
TRANSCRIPT
Schizophrenia
“A Slow Fire Burning”
Dr C Christie
General
Schizophrenia is a major psychotic disorder Chronic debilitating illness Devastating effects on all aspects of patient’s life Comprehensive and continuous lifelong treatment Heterogeneous disorder Variation in presentation Clinical diagnosis No single symptom pathognomonic of 295
3 Symptom clusters
Positive symptoms – hallucinations and delusions
Disorganised thought, behaviour and speech
Negative symptomsAffective flattening, alogia, anhedonia and
avolition
History
Kraeplin (1856 – 1926) termed dementia precox (early onset of cognitive decline)
Bleuler (1857 – 1939) used term schizophrenia.
Schism between thought, emotion and behaviour
Does NOT mean split personality
DSM IV
A. Characteristic symptoms (2 or more)Delusions, hallucinations, disorganised speech
Grossly disorganised or catatonic behaviour
Negative symptoms
B. Social/occupational dysfunction
C. Duration: 6 months
D. Exclude schizoaffective and mood disorder
E. Exclude GMC and substances
F. Exclude pervasive developmental disorder (autism)
Subtypes
Disorganised Paranoid Catatonic Undifferentiated Residual
Epidemiology
1% prevalenceRisk increased if first degree relatives
have the disorderRisk increased if person is single,
industrialised nation, in lower SE class, urban, problems in utero, perinatal problems, born in winter, recent stressful life event
Age and Sex. M = F
Males
Present at earlier age
Peak in early 20’s
Poorer premorbid personality and social adjustment
Females
Peaks in late 20’s and 30’s
Better prognosis
Fewer admissions, shorter length of stay
Mortality and morbidity
Mortality twice that of general populationSuicide high, 50% attempt10 -15% successfulHigher risk of dying a violent deathGMC present needs to be vigorously
diagnosed and treated
Substance Abuse
Co-morbidity of substance abuse and schizophrenia very common
30 – 50% alcohol abuse15 – 25% cannabisNicotine!
Genetics
Sibling of schiz patient 8%Dizygotic twin 12%Child of one schiz parent 12%Both parents with schiz 40%Monozygotic twin 47%
Cultural and socioeconomic
Found in all cultures and socio-economic groups
In developing countries prognosis and outcome better
Related to stronger family/social supportHomelessness and 295 linkedDownward drift and deinstitutionalisation
Biological factors/ structural
Changes in limbic system, basal ganglia and frontal cortex
Enlarged lateral and third ventriclesReduction in cortical volumeCytoarchitextural abnormalities of
amygdala,hippocampus and parahippocampal gyrus
Neuroimaging
Abnormal PET scans,shows deranged glucose utilisation/cerebral blood flow when challenged with psychological task, hypoactivity of frontal lobes and intellectual testing may show deficits
Is 295 a neurodevelopmental disorder only manifesting later in life with microanatomical cortical dysgenesis?
Neurochemistry
Neurochemical abnormalities central Models have been hypothesised using drug
induced psychotic models Dopamine hypothesis: hyperdopaminergia is
main protagonist Drugs that reduce firing of mesolimbic
dopamine neurons have antipsychotic effect Drugs that stimulate dopamine increase
psychosis
Neurochemistry
Hypothesis revised Low prefrontal dopamine causes deficit,
negative symptomsExcessive dopamine activity in
mesolimbic dopamine neurons cause positive symptoms
Dopamine AND serotonin
Atypical neuroleptics act as 5HT2 and
Dopamine antagonists5HT2a, 5HT2c antagonism, 5HT1a
agonismCholinergic, muscarinic, GABA and
glutamate mediated actions modulate antipsychotic drug action
Clinical features/Acute phase
Behaviour and appearance – normal, perplexed, sudden behavioural changes
Speech – vague, concrete, bizarre, pressure, poverty, word salad, neologisms
Range of affect – blunted Auditary hallucinations common Voices often derogatory and refer to patient in
3rd person Delusions Insight is reduced
Chronic Phase
Psychotic symptoms may be less severeSymptoms persist in attenuated formNegative symptoms may predominate
Delirium Schizophreniform
disorder Schizoaffective
disorder Delusional disorder Brief psychotic
disorder
Bipolar mood disorder
Substance induced psychotic disorder
Psychosis secondary to GMC – TLE, epilepsy
Course and prognosis
10 -15% have a good prognosis20 – 30% lead reasonably normal lives40 – 60% poor outcome with chronic
deteriorating courseParanoid subtype best prognosisDisorganised subtype worst prognosis
Course and prognosis
Symptoms begin in adolescenceMay have prodrome diagnosed in
retrospectEach relapse followed by deteriorationPositive symptoms may become less
severe over timePsychosis is toxic for the brain!
Good prognostic indicators
Later onset Female gender Absent family hx Marriage Good pre-morbid
personality and psychosocial adjustment
Obvious precipitant Positive symptoms Good support
systems Mood symptoms with
family history of mood disorder
Management
Involve family and patient in active collaboration using integrated approach with pharmacologic, psychotherapeutic, psychosocial and rehabilitative measures
Need comprehensive and continuous treatment
At present NO CURE
General goals of treatment
Decrease frequency, severity and psychosocial consequences of episodes
Maximise psychosocial functioningEstablish and maintain therapeutic
allianceMonitor patient status at regular intervals
Thorough initial workup
Rule out conditions that mimic 295Identify co-morbid conditions that
complicate diagnosis and treatmentEstablish baseline for monitoring course
of illness and response to treatment
Acute phase management
HOSPITALISE IF:o Poses a threat to self or otherso Unable to care for selfo Co-morbidityo First episodeo Substance abuse o May need involuntary hospitalisation
Antipsychotics
Biological treatment the mainstay Typical antipsychotics – high potency –
haloperidol, low potency – chorpromazine Atypical antipsychotics – clozapine,
respiridone, olanzipine, quetiapine. Useful for negative symptoms, poor responders and patients prone to side effects
Choice of drug depends on age, physical status, co-existing medical problems
Drug treatment
60% of patients on antipsychotics for 6 weeks improve
If meds of well patient stopped 75% relapse in 6 – 24 months
First episode patients – 40 – 60% relapse during the year after episode if not on medication
Duration of treatment - debate
First episode: 1 – 2 years of maintenance
Multiple episodes: minimum of 5 yearsViolent or aggressive behaviour or
suicide attempts need indefinite treatment
Psychosocial treatment
Become ill during critical career forming years
Psychosocial interventions need to be integrated with psychopharmacological treatments
Focus on improving social functioning in the hospital, community, at home and at work
Rehabilitation
Programmes emphasise social skills training and vocational training
NB for community based treatmentCognitive remediation can assist
recognition and treatment of cognitive impairments
Distractibility, memory problems, lack of vigilance, limitations in planning and decision making
Individual psychotherapy
Supportive, reality orientated individual therapy
Individual and groupsTeach coping and problem solving skillsPsychotherapy is not a substitute for
medication and is helpful once antipsychotics have started working
Families
Grief with no end Teach family to recognise early signs of
relapse Psycho education to help families deal with
disease profile Blame should not be placed on patient for
pathology Families who are highly critical or
overprotective can increase relapse
Families
Group therapy enhances problem solving, goal planning, social interactions
and medication and side effect management
A lot more could be done for schizophrenics in our society!
References
Kaplan and Sadock’s Synopsis of Psychiatry eighth edition. pp 456 - 491 APA guidelines. Practice guideline for the
treatment of patients with Schizophrenia. Am Jnl Psychiatry 154: 4 April 1997 (supplement)
Carpenter WT, Buchanan RW. Schizophrenia. New England journal of Medicine. Vol 80, March 1983
Schizophrenia focus. The Lancet. Vol 346. Sept 9, 1995.