Download Schizophrenia

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 symptoms
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Affective 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
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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
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Disorganised
Paranoid
Catatonic
Undifferentiated
Residual
Epidemiology
1% prevalence
 Risk increased if first degree relatives
have the disorder
 Risk increased if person is single,
industrialised nation, in lower SE class,
urban, problems in utero, perinatal
problems, born in winter, recent stressful
life event
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Age and Sex. M = F
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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 population
 Suicide high, 50% attempt
 10 -15% successful
 Higher risk of dying a violent death
 GMC present needs to be vigorously
diagnosed and treated

Substance Abuse
Co-morbidity of substance abuse and
schizophrenia very common
 30 – 50% alcohol abuse
 15 – 25% cannabis
 Nicotine!

Genetics
Sibling of schiz patient
 Dizygotic twin
 Child of one schiz parent
 Both parents with schiz
 Monozygotic twin

8%
12%
12%
40%
47%
Cultural and socioeconomic
Found in all cultures and socio-economic
groups
 In developing countries prognosis and
outcome better
 Related to stronger family/social support
 Homelessness and 295 linked
 Downward drift and deinstitutionalisation

Biological factors/ structural
Changes in limbic system, basal ganglia
and frontal cortex
 Enlarged lateral and third ventricles
 Reduction in cortical volume
 Cytoarchitextural 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?
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Neurochemistry
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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 symptoms
 Excessive dopamine activity in
mesolimbic dopamine neurons cause
positive symptoms

Dopamine AND serotonin
Atypical neuroleptics act as 5HT2 and
Dopamine antagonists
 5HT2a, 5HT2c antagonism, 5HT1a
agonism
 Cholinergic, muscarinic, GABA and
glutamate mediated actions modulate
antipsychotic drug action
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Clinical features/Acute phase
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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 severe
 Symptoms persist in attenuated form
 Negative symptoms may predominate
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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 prognosis
 20 – 30% lead reasonably normal lives
 40 – 60% poor outcome with chronic
deteriorating course
 Paranoid subtype best prognosis
 Disorganised subtype worst prognosis
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Course and prognosis
Symptoms begin in adolescence
 May have prodrome diagnosed in
retrospect
 Each relapse followed by deterioration
 Positive symptoms may become less
severe over time
 Psychosis is toxic for the brain!
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Good prognostic indicators
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Later onset
Female gender
Absent family hx
Marriage
Good pre-morbid
personality and
psychosocial
adjustment
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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
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General goals of treatment
Decrease frequency, severity and
psychosocial consequences of episodes
 Maximise psychosocial functioning
 Establish and maintain therapeutic
alliance
 Monitor patient status at regular intervals

Thorough initial workup
Rule out conditions that mimic 295
 Identify co-morbid conditions that
complicate diagnosis and treatment
 Establish baseline for monitoring course
of illness and response to treatment
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Acute phase management
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o
o
o
o
o
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HOSPITALISE IF:
Poses a threat to self or others
Unable to care for self
Co-morbidity
First episode
Substance abuse
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
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Duration of treatment - debate
First episode: 1 – 2 years of
maintenance
 Multiple episodes: minimum of 5 years
 Violent or aggressive behaviour or
suicide attempts need indefinite
treatment
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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
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Rehabilitation
Programmes emphasise social skills
training and vocational training
 NB for community based treatment
 Cognitive remediation can assist
recognition and treatment of cognitive
impairments
 Distractibility, memory problems, lack of
vigilance, limitations in planning and
decision making
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Individual psychotherapy
Supportive, reality orientated individual
therapy
 Individual and groups
 Teach coping and problem solving skills
 Psychotherapy is not a substitute for
medication and is helpful once
antipsychotics have started working
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Families
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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!
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References
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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.