PSYA4: Schizophrenia


Clinical characteristics of schizophrenia

Schizophrenia = detachment from reality (psychotic episodes)
Symptoms divided into two types: (acording to the Diagnostic and Statistical Manual - DSM)

1. Positive  symptoms: (excess/distortion in normal functions)
(DSM-IVR: diagnosis requires at least one month - 2 or more positive symptoms)

  • Delusions (COGNITIVE, bizarre beliefs - e.g. paranoid or inflated)
  • Hallucinations (SENSORY, bizarre perceptions of environment usually auditory - also olfactory, tactile and visual)
  • Experiences of control/passivity (e.g. alien force)
  • Disordered thinking (inserted/withdrawn, broadcast, external forces - loosely associated speech)

2. Negative symptoms: (dimunution or loss of normal functions - low/absent positive symptoms)

  • Affective flattening(emotional expression)
  • Alogia(poverty of speech - fluency and productivity - blocked thought)
  • Avolution(goal-directed behaviour reduced, seclusion)
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Clinical characteristics of schizophrenia cont'd

No possibility of mood disorder (neurosis) or organic cause (e.g. drugs)

Lack insight (don't recognise they have a problem)

Types of schizophrenia: (affect symptoms)

  • Catatonic - 10% (disturbances of movement: reduce/increase/purposeless repetitive/mimicking/unusual positions)
  • Paranoid - 35-40%  (delusions of grandeur or persecution)
  • Residual - 20% (previous symptoms not present/diminished - no motivation/interest)
  • Disorganised - 10%(incoherent speech and thought, affective flattening)
  • Undifferentiated - 20% (variation of symptoms - don't fit into one)
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Issues: Reliability AO1

 Consistency of measuring instrument (e.g. DSM or ICD-10) - assessing severity of symptoms

1. Inter-rater reliability: two independent assessors - similar diagnoses

  • DSM-III (1980) - more reliable system of classifying psychiatric disorders (more agreement)

2. Test-retest reliability: separate tests - similar scores

  • Cognitive screening tests (e.g. RBANS) - degree of impairment
  • Wilks et al: two alternative forms (1-134 days) - correlation of scores high = 0.84
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Issues: Reliability AO2


Still little evidence - DSM-III used routinely with high reliability by mental health clinicians
(Whaley: +.11, Rosenhan:  abnormality and normality - situation not characteristics)

Cultural differences in diagnoses (Copeland - 194 British - 2% vs. 134 US - 69%)

Cheniaux et al: inter-rater reliability - DSM-IV and ICD-10 (above +.50 for both BUT ICD-10 criteria = more frequently)

Unreliable symptoms: only one symptom required ('bizarre') - i-r reliability of 50 US psychiatrists  = +.40 (Mojtabi and Nicolson)


Measures of cognitive functioning (vital): Prescott et al - meausures of attention and info. processing stable - 14 schizophrenics (6-month period)

NO OBJECTIVITY (no bio. test, e.g. blood, reliant on subjective interpretations)

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Issues: Validity AO1

Extent to which diagnosis reflects true nature of condition - something real and distinct 

Extent to which classification system measures what it claims to

Reliability and validity inextricably linked (cannot be valid if not reliable)

1. Issue of comorbidity: (two or more conditions co-occur) = common

  • Cormorbid depression (50%) and comorbid substance abuse (47%) - Buckley et al
  • Distinct? - difficulties in diagnosis of disorder and deciding treatment

2. Predictive validity (should predict outcome of a disorder - how people would develop and respond to treatment)

  • Rarely share same symptoms or outcomes
  • Bentall et al: 20% recover previous functioning, 10% significant and lasting improvement, 30% some improvement with intermittent relapses
  • Some never recover, many do

3. Positive or negative symptoms: Klosterkoetter et al (+ve more useful - obvious)

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Issues: Validity AO2

1. Comorbidity (implications for treatment methods)

  • Poor functioning less the result of the psychiatric disorder - more to do with untreated comorbid physical disorders - Weber et al (many comorbid non-psychiatric diagnoses  - medical problems - lower standards of medical care - paranoia)
  • High risk for suicide (major cause - comorbid depression): 1% (schizophrenia) to 40%  (comorbid mood disorder)

2.Cultural relativism and variations in diagnoses - ethnicity and misdiagnosis

  • Asian counties vs. Arabic (emotion) - knowledge of cultural relativism needed
  • African-Caribbean (higher rates in UK) - Harrison et al (8x higher than whites) - social factors BUT cultural differences (language, mannerisms, clinicians and patients)

3. Symptoms

  • Found in many other disorders = invalid (Ellason and Ross - dissociative identity disorder, DID)
  • Not a discrete disorder - spectrum of psychotic symptoms (assumes mental disorders are different, but 5 types of schizophrenia with diverse symptoms)
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Biological explanations: genetic factors

1. Family studies (whether bio. relatives similarly affected more than non-bio. = genetic)

  • E.g Gottesman: more common among bio. relatives, esp. more closely related (2 schizophrenic parents - 46%, 1 - 13%, siblings - 9%)

Research: appears to run in families = genetic BUT common rearing patterns/non-hereditary (e.g. expressed emotion - negative emotional climate - stress beyong coping mechanisms = trigger)

2. Twin studies (relative contributions - genetic and environmental influences - MZ and DZ)

  • Joseph (meta-analysis): concordance - MZ (40.4%), DZ (7.4%) = EMPIRICISM
  • More methodologically sound ('blind' diagnoses): lower CR for MZ (still higher)

Assumes environments of MZ and DZ are equivalent (CR due to genetics): Joseph - MZ treated more similarly (twins not individuals) = environmental differences

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Biological explanations: genetic factors

3. Adoption studies: (genetically related reared apart - separate genetic and environmental influences - difficulty with those sharing both), e.g. Tienari et al (Finland - methodologically sound):

  • 11/164 adoptees (6.7%) - bio. mother diagnosed with schizophrenia - also diagnosed
  • 4/197 control adoptees (2%) - non-schizophrenic mothers

Assumes adoptees are not selectively placed (adoptive parents no different to those of 'normal')

  • Joseph: Denmark and US - informed of genetic background
  • Kringlen: 'who would adopt those...'

Other EVs: may not be wanted - worsen symptoms (expressed emotion) = LACK OF CONTROL

Further evaluation:

Methodological issues - (broadening def. - incl. psychotic 'schizophrenic spectrum disorders'. E.g. Kety et al (first-degree relatives - no full schizophrenia) = SUBJECTIVE

Evolutionary perspective: maladaptive may be adaptive - 'group splitting hypothesis' (Stevens and Price)

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Biological expl: the dopamine hypothesis AO1

Bio-chemical explanation - EXCESS of neurotransmitters responsible for symptoms

  • Messages from pre-synaptic neurons (transmit dopamine) fire too easily/too often =EXCESS dopamine molecules
  • Abnormally high levels of D2 receptors on receiving neurons on receiving/post-synaptic neurons (more D binding, more neurons firing) = overly active
  • Lower level of enxyme (breaks down dopamine in synaptic gap) = transmission sucessively easier
  • Key role: guiding attention = attention-, perception-, thought-related problems (disordered thinking)
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Biological expl.: the dopamine hypothesis AO2

Evidence: drugs (rationale based on discovery...)

  • Amphetamines (dopamine agonist - stimulate) - large doses = symptoms
  • Antipsychotics (e.g. chlorpromazine - D antagonists) - stimulation of D system, block D2 receptors = eliminates symptoms
  • Parkinson's disease:low D activity + too much L-doba (increases D) - schiz. symptoms

Schizophrenia or faulty chemicals (cause/effect): S may cause faulty chemicals (drugs infl. other systems?) = inconclusive. = LACKS CONTROL

Post-mortem studies: Falkai et al (more D recepters, increased density = EMPIRICISM) BUT drugs to block activity increase it (compensate - deficiency), e.g. Haracz - antipsychotics before death

Neuro-imaging: e.g. PET scans - more precise (previously measures of waste products). Lindstroem et al (L-dopa uptake quicker), Copolov and Crook (no convincing evidence) = LACKS EMPIRICISM

Dopamine not the sole cause - 25% don't respond well to medication (other abnormality) - Type 1 respond well, type 2 do not (effective for positive symptoms only)  

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Psychological expl: cognitive AO1

  • Initially biological factors (abnormal brain activity) - sensory experiences
  • Attempts to understand them - further features (interpretations of symptoms)
  • 'Faulty thinking': defective filtering mechanisms and processing systems - overwhelmed by sensory information (unable to process/interpret) = symptoms

Frith's model: unimportant info. gets into the conscious awareness - seen as important (e.g. auditory hallucinations - preconscious filter)

Hemsley's model: process of giving meaning to new sensory input using schemas breaks down (don't know what to attend to - highly relevant - internal speech/thoughts)

  • Turn to others to confirm validity - fail to cofirm (believe hiding truth + reject feedback)
  • Delusional belief of persecution/manipulation
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Psychological expl: cognitive AO2

Treatments based on this expl. improve outcome (e.g. CBT) = effective and appropriate (valid)

Integrates known genetic, environmental, psychosocial and cognitive factors = complete account

EMPIRICISM: (physical basis - cogn. deficits), Meyer-Lyndenberg et al (excess D - PFC and working memory), Neufeld (schiz. - longer to encode stimuli and STM problems)

RWA - treatment (Yellowlees et al - trialled machine producing virtual hallucinations - show they're not real. BUT no evidence of success yet

Doesn't explain cause only symptoms (can't explain why voices negative/abusive)

Only explains positive symptoms (delusions) not negative (alogia) = incomplete

Explains why symptoms vary between patients: differences in biology and cognitive schemas, attitudes and beliefs

Doesn't explain why men develop S in late teens/early 20s and women develop it in their late 20s/early 30s (may be hormonal/behavioural/cultural)

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Psychological expl: Behavioural

Learned from the environment (not mental illness with physical cause)

Operant conditioning: positively reinforced (attention/escape from real-world) or punished

Social learning theory: observes S being reinforced in e.g. parent = vicarious learning

Successful treatment based on this approach (e.g. Token Economy)

Research support: Wilder et al (unrelated topics ignored - bizarre vocalisations reduced - 30 sessions) - unlearned BUT improvement of delusion itself/feeling cannot speak about it AND on medication if in hospital

Cannot explain - no contact with schizophrenic but display symptoms/why it occurs late adolescence/early adulthood (different for male and female)

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Psychological expl.: socio-cultural - life events

Major stress factor - higher risk of schizophrenic episodes

Discrete stresses (e.g. death of close relative/break-up of relationship)

Brown and Birley: before - previous experience - twice as many stressful life events than control

Folloon et al: mechanisms (stress factors trigger S) unknown. High physiological arousal ***. with neurotransmitter changes thought to be involved

Research support: EMPIRICISM

  • Retrospective studies, e.g.Brown and Birley: 50% - stressful L.E. (3 weeks prior to relapse), 12% (9 weeks prior). Control: low, unchanging level (same period)
  • Prospective studies (L.E. in future) - Hirsch et al: L.E. - signif. cumulative contribution (12 months preceding) not more concentrated just prior to (challenges retrospective)

van Os et al: no link (L.E.s and onset) - not more likely (3m before). Prospective: major L.E. = lower likelihood

Evidence that supports link = correlational not causal (beginning of disorder = L.E.?)

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Biological therapies: antipsychotic medication AO1

Effective - treating most disturbing forms of psychotic illness

Helps them function as well as possible, increasing subjective well-being

Conventional antipsychotic drugs: (e.g. chlorpormazine)

  • Reduce effects of D + positive symptoms = D antagonists
  • Bind to D receptors (esp. D2) don't stimulate, block action
  • Effectiveness led to the D hypothesis
  • 10mg per day (break down 48-72 hours)

Atypical antipsychotic drugs: (e.g. clozapine)

  • Act on dopamine system + thought to block serotonin receptors (combat +ve and -ve symptoms)
  • BUT Kapur and Remington (only D system, D2 in particular - temporarily then rapidly dissociate - normal D transmission)
  • Dissociation = less side effects than conventional (e.g. tardive dyskinesia)
  • Combination: mood stabilisers (e.g. Lithium)/anti-depressants/ECT
  • Meltzer (1/3 no improvement with conventional - respond well)
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Biological therapies: antipsychotics medication AO

1. Conventional:


  • Effective in reducing symptoms (relapse rates - placebo vs. medication), e.g. Davis et al (p: 55%, d: 19%) BUT Ross and Read (placebo - drug withdrawal state)
  • Other important factors (Vaughn and Leff: hostile home env. (p: 92%, d: 53%), S(p: 15%, d: 12%)) = LACKS PREDICTABILITY  
  • Contradictory evidence (LT effectiveness) - Sampath et al (75% relapsed - switched to placebo, 33% - continued) BUT why 33%? Other causes not being treated.


  • Unpleasant, severe side-effects within a few weeks. LT: tardive dyskinesia (over 20% - on for over a year = irreversible 75%), e.g. Glenmullen (25yrs - 68%)
  • Motivational deficits: reduces motivation to look for solutions to alleviate stressors
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Bio. therapies: antipsychotics AO2

2. Atypical:

  • Tackle a broader range of symptoms
  • Leucht et al (m-a): superiority only moderate, 2 only 'slightly' more effective, other 2 no more so
  • Little EMPIRICAL support for treating -ve symptoms (Leucht et al: 2 'slightly' more, 1 'as ', 1 'slightly worse')


  • Less severe, fewer side-effects (e.g. tardive dyskinesia - 5% not 30%) - more likely to continue  BUT serious potential side effect (1-2% risk: reduction in white blood cells - life-threatening) BUT not with olanzapine
  • Individual differences (15% don't respond)

Biologically reductionist (only focuses on biological level) - complex mental disorder reduced to D

Symptoms not cause (INAPPROPRIATE) - prolonged use required (side-effects). Cost-benefit analysis -ve

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Biological therapies: ECT AO1

Historical origins: schizophrenia (then dementia praecox) rare in patients with epilepsy (seizures)

  • First studies disappointing (lower recovery rate) - Karagulla


1. Injected with short-acting barbiturate = unconscious

2. Nerve-blocking agent = paralysis (prevent contracting and fractures)

3. Electric current (0.6amps - 1/2 sec) - 2 scalp electrodes (bilateral/uni-lateral) = seizure (1 min - entire brain affected)

3-15 treatments

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Biological therapies: ECT AO2


Tharyan + Adams (m-a 26s): ECT vs. 'sham'/'simulated' ECT = more improved in real BUT no ev. over medium-/long-term AND antipsychotics better BUT combination =greater improvement (when rapid reduction required/limited response to medication alone)

American Psychiatric Association review: 19st. ECTvs.simulated = ECT no better/worse than antipsychotics BUT Indian study - no diff. ECT or simualted (36 patients)



Significant risks (incl. memory dysfunction, brain damage, death) - use declined (UK: '79-'99: by 59%)

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Psychological therapies: CBT AO1

Assumes - distorted perceptions and disordered thinking/faulty interpretations of cause and effect maladaptively influence behaviour

Aims to help identify and correct - challenging distorted beliefs (e.g. behaviour controlled by someone else)


  • Trusting/respectful relationship
  • Trace back to origins (idea of how developed - patterns/triggers)
  • Evaluates content of delusions/voices - how to test validity (show not real - challenge beliefs - change irrational thinking)
  • Behavioural assignments/homework and role play (general functioning)
  • Develop alternatives to previous maladaptive beliefs (coping strategies and alt.expl)

Outcome studies: measure effectiveness of treatment compared to accepted form for condition

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Pyschological therapies: CBT AO2


Outcome studies: CBT vs. antipsychotics (fewer hallucinations and delusions, greater functioning)

  • Drury et al (reduced +ve symptoms and recovery time by 25-50%), Kuipers et al: lower patient drop-out rates BUT self-report and therapist interpretation = SUBJECTIVE (could measure D levels)
  • Gould et al (all 7 in m-a: statistically signif. decrease - +ve symptoms), Lewis et al (first episode - shortens length BUT 18 months - same relapse rate as none = ST solution)
  • Most studies - patients treated with antipsychotics as well (usually so - drugs calm D levels) - effects due to CBT or other therapies?


  • Generates less distressing explanations rather than eliminating (-ve symptoms may be useful, e.g. increased medication, prevent worsening +ve symptoms) - alleviating
  • Not everyone with S benefits from CBT, e.g. Kingdon and Kirshen (e.g. older)
  • Palliative treatment not a cure (symptoms not cause) - LT improvement due to cogn. remodelling or client-therapist relationship (may relapse after)
  • All of the blame on the patient
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Psychological therapies: Token Economy AO1

Behaviourist therpay - operant conditioning ('behaviour modification technique')

Modify directly observable behaviours + motivate to behave socially desirable ways

3 steps:

1. Identify the undesirable/maladaptive behaviour

2. Identifying reinforcers maintaining behaviour (bizarre behaviour repated due to reinforcement)

3. Reconstructing environment - behaviour no longer reinforced (less likely to repeat)

Desired 'normal' behaviour = positive reinforcement (tokens - exchancheable for larger reward/privilege)

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Psychological therapies: Token Economy AO2


Significant improvements (self-care and desirable behaviour) even chronic institutional schizophrenics, e.g. Ost et al (0/5 had to be readmitted in 1yr follow-up BUT less than 50% + small sample), Ayllon and Azrin (from 5 to 40 chores per day)

Tokens must be given immediately after desired behaviour (longer interval = association less likely)

Lack EV: not continued in real world (no longer reinforced), e.g. Katzin and Bootzin (not permanent) - symptom not cause


Ethical issues: makes behaviour more acceptable to others - not helping (desired behaviour = SUBJECTIVE)

Not appropriate today (community treatment at home - lack surveillance)

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Psychological therapies: Family Intervention AO1

1970s: family env. potential role in influencing course of schizophrenia

High levels of criticism, hostility/over involvement = more frequent relapses than less expressive home env.

Aim: attempt to make family life less stressful = reduce re-hospitalisation


  • Alliance with relatives who care for the person
  • Reducing emotional climate and burden of care
  • Enhancing ability to anticipate/solve problems
  • Maintaining reasonable expectations (of behaviour) among family members
  • Reducing expressions of anger and guilt
  • Encouraging appropraite limits and some separation when needed

Used in conjunction with drug treatment and outpatient clinical care

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Psychological therapies: Family Intervention AO2


Effectiveness (NICE: m-a, 32 studies of 2500 patients) - compared to standard care alone = reduced hospital admissions and severity (during and up to 24m after). Relapse: 26% vs 50%

Why effective? Pharoah et al: improving clinical outcomes (mental state, social functioning) - more to do with increase in medical compliance


NICE review: cost savings (+ standard care). Offset - reduced hospitalisation costs. Relapse rates reduced for signif. period.

Cultural limitations: most evidence from outside UK (esp. China). NICE: may differ across countries (clinical practices vary) - rates may not be applicable to UK

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