PSYA4: Schizophrenia
- Created by: Kimberleypaige
- Created on: 20-05-15 16:36
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- Disordered thinking (inserted/withdrawn, broadcast, external forces - loosely associated speech)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)
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)
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
Issues: Reliability AO2
Inter-rater:
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)
Test-retest:
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)
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)
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)
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
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)
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)
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)
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
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)
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)
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.?)
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)
Biological therapies: antipsychotics medication AO
1. Conventional:
Effectiveness:
- 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.
Appropriateness:
- 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
Bio. therapies: antipsychotics AO2
2. Atypical:
Effectiveness:
- 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')
Appropriatenesss:
- 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
Biological therapies: ECT AO1
Historical origins: schizophrenia (then dementia praecox) rare in patients with epilepsy (seizures)
- First studies disappointing (lower recovery rate) - Karagulla
Procedure:
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
Biological therapies: ECT AO2
Effectiveness:
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)
= SOME EMPIRICISM
Appropriateness:
Significant risks (incl. memory dysfunction, brain damage, death) - use declined (UK: '79-'99: by 59%)
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)
Techniques:
- 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
Pyschological therapies: CBT AO2
Effectiveness:
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?
Appropriateness:
- 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
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)
Psychological therapies: Token Economy AO2
Affectiveness:
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
Appropriateness:
Ethical issues: makes behaviour more acceptable to others - not helping (desired behaviour = SUBJECTIVE)
Not appropriate today (community treatment at home - lack surveillance)
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
Strategies:
- 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
Psychological therapies: Family Intervention AO2
Effectiveness:
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
Appropriateness:
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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