AQA A Level psychology - Paper 3 Schizophrenia

Classification of schizophrenia
1. Affects 1% of pop. at some point in life.
2. Diagnosis manual > DSM-V (US) = classification & description of >200 mental disorders, grouped on common features. ICD-11(Europe)(= recent update).
3. Positive symptoms = reflect excess or distortion of normal functioning.
  1. Hallucinations
    1. Bizarre, unreal perceptions of environment> auditory (hearing voices), visual (seeing lights/ objects) , olfactory (smelling things) or tactile (feelings of being touched) = all things that others do not experience.
  2. Delusions
    1. Bizarre , unreal beliefs > paranoia (being followed or spied on), delusions of grandeur (inflated beliefs on own power/importance) or delusions of reference (events in environment appear directly related to them).
  3. Disorganised speech
    1. Abnormal thought processes = can't organising thoughts = derailment (slip from one topic to another) & incoherent speech= gibberish > 'word salad'
  4. Grossly disorganised
    1. Inability or motivation to do/complete task> day-to-day difficulties = low interest in personal hygiene/ dress or act bizarrely
      1. E.g. heavy clothes in summer
  5. catatonic behaviour
    1. Reduced reaction to immediate environment, rigid posture, aimless motor activity (movements)
4. Negative symptoms = reflect reduced or loss of normal functioning.
  1. Speech poverty (alogia)
    1. Lessened speech fluency & productivity (reflects blocked thoughts) = fewer words/ difficulty of spontaneous speech/ less complex syntax. > associated with long & earlier onset of illness.
  2. Avolition
    1. Reduced self-initiated involvement in available activities (e.g. can sit and do nothing for hours)
  3. Affective flattening
    1. Poor communication = Reduced range & intensity of emotional expression + deficit in paralinguistic features.
  4. Anhedonia
    1. Loss of interest in normally pleasurable stimuli = physical (no pleasure from food, bodily contact..), social (no pleasure from interacting with others).
    2. Sarkar et al. > physical anhedonia = more reliable symptom of schizophrenia [as social anhedonia overlaps with other disorders (e.g. depression).
5. Schiz. = Psychosis - severe mental disorder > impaired thoughts & emotion = loss of contact with external reality
6. Diagnosed between ages 15-35 > men & women affected equally.
Reliability & validity in diagnosis and classification
1. Reliability
  1. Diagnostic reliability = repeatability > test-retest reliability (clinicians reach same conclusions at different points in time) / inter-rater reliability (different clinicians reach same conclusions).
    1. Inter-rater reliability > measured by statistic = kappa score. 1 = perfect inter-rater agreement (same conclusions on diagnonsis) . 0 = no agreement (different conclusions). Kappa score ≥ 0.7 = good score.
      1. Regier at al. (2013) > DSM-V field trials - diagnosis of schizophrenia kappa score = 0.46.
  2. Cultural differences in diagnosis
    1. Research suggests> significant variation between countries when diagnosing schizophrenia = culture influences diagnostic process.
      1. Copeland (1971) > 134 US & 194 British psychiatrists given description of patient. 67% - US & 2% British psychiatrists diagnosed schizophrenia.
  3. = Consistency of measurements
2. Validity
  1. Gender bias in diagnosis
    1. Diagnosis accuracy = gender dependant
    2. Bias in diagnostic categories
      1. Boverman et al. (1970) US clinicians equated healthy 'adult' behaviour= healthy 'male' behaviour = androcentrism. = tendency for women to be seen as less mentally healthy.
  2. = Whether observed effect is genuine
  3. Symptom overlap
    1. Many pos./ neg. symptoms found in other disorders, eg. depression/ bipolar.
      1. Ellason & Ross (1995) > People with Dissociative identity disorder (DID) - have more schizophrenic symptoms than people diagnosed with schizoprenia
  4. Co-morbidity
    1. ≥ 2 conditions/disease co-occur in schizophrenic patient (substance abuse, anxiety, depression symptoms)
      1. Buckley et al. (2009) > 1/2 schizophrenic patients 50% = co-morbid depression & 47% = co-morbid substance abuse.
3. Evaluation of valitidty
  1. Gender bias support from research > Loring & Powell (1988) > randomly selected 290 male & female psychiastrists - given 2 case descriptions of patients' beh. Asked for judgement using standard diagnostic criteria. 'male'/ 'no gender descriptions' patient = 56% psychiatrists diagnosed schizophrenia. 'female' patient = 20% psychiatrists diagnosed schizophrenia. = diagnosis dependant on patients gender = gender bias = low internal validity.
    1. = some behavior seen as psychotic in males was not seen as psychotic in females.
  2. Problems with the validity = unsuitable treatment may be administered, sometimes on an involuntary basis = practical and ethical issues when selecting different types of treatment.
  3. Differences in prognosis (outcome forecast) - 20% recover from previous level of functioning, 10% achieve sig./lasting improvement, 30% some improvement + irregular relapses. = low predicitve validity of schiz. diagnosis.
4. Evaluation of reliability
  1. Inter-rater reliability issues when diagnosing schiz. > Rosenhan (1973) ON BEING SANE IN INSANE PLACES - PSEUDOPATIENTS (=fake patients) 'normal' ppl presented themselves to psychiatric hospitals in US - claimed hearing voice in head (pos. symptom) saying 'empty', 'hollow' & 'thud'. All diagnosed with schiz. & admitted into hospital. Throughout stay, no staff recognised ppl actually normal.
    1. Implications of this = led to stricter, better defined diagnosis of those with psychological disorders. DSM-III used in study> led to update DSM-V.
  2. Jakobsen et al. (2005) tested ICD- 10 (classification system commonly used in Europe) reliability. 100 Danish patients with psychosis history assessed using operational criteria - found concordance rate of 98% = high reliability of diagnosis using updated classification.
Psychological explanations for schizophrenia
1. Family dysfunction
  1. Double bind theory
    1. Gregory Bateson et al. (1956) child recieves frequent contradictory messages from parent(s) - e.g "Love you" (verbal affection) while squeezing ear (non-verbal hostility). = conflicting messages on different communicative levels.
      1. = confusion = prevents development of internally coherent construction of reality = in long-run forms schiz. symptoms (e.g. flattened effect/ withdrawal).
    2. Psychiatrist Laing > argued schiz. not disease & is reasonable response to insane world,
  2. Expressed emotion (EE)
    1. Negative emotional climate/ high degree of expressed emotions = family variable associated with schiz.
    2. EE = communication style - schiz. patient talked about in hostile manner by family members - indicating emotional over-involvement/ over-concern.
      1. Kuipers et al. (1983) found high EE relatives talk more, listen less.
    3. High EE level env. = likely influence to relapse rates (increases symptoms).
      1. Linszen at al. (1997) patient returning to high EE family = 4x more likely to relapse (than patient with low EE family).
    4. suggests schizophrenics - impaired coping mechanisms = low tolerance for intensive env. stimuli > particularly intense emotional comments/family interactions = arouse schiz. episode.
  3. = abnormal communication patterns within families
2. Cognitive explanations
  1. = dysfunctional thought processing
    1. more evident in patients displaying postitive symptoms (delusions/hallucinations)
  2. Cognitive explanations of delusions
    1. delusions = bizzarre beliefs
    2. IMPAIRED INSIGHT/ COG. PROCESSING
      1. unable to recognise cognitive distortions/ substitute more realistic explanations for events
        Beck & Rector (2005) Delusions in schiz. unaffected by 'reality testing' - patients unwilling/ unable to consider they may be wrong.
    3. FAULTY STIMULUS INTERPRETATION
      1. Experiences interpreted by inadequate information processing = formation of delusions
      2. Critical characteristic of delusional thinking = degree person perceives themselves as central component in events (egocentric bias) = jump to conclusions about external events.
        Relating irrelevant events to themselves = consequence of false conclusions.
        EXAMPLE - Muffled voices = critisisms. Flashes of lights = signal from God.
  3. Cognitive explanations of hallucinations
    1. hallucination = bizzarre perceptions
    2. Hallucinating ppl focus excessive attention on auditory stimuli = hyper vigilance > have higher expectancy for occurrence of voice than normal ppl.
      1. Aleman (2001) hallucination-prone have difficulty distinguishing between imagery & sensory-based perception> imagine sounds = self- generated auditory
    3. Baker & Morrison (198) Hallucinating patients with schiz. = more likely to misattribute source of self- generated auditory experience to external source than non-hallucinating schiz.
    4. hallucinations also result from poor 'reality testing' of external events
3. Evaluation of family dysfuntion
  1. Noll (2009) supportive/ low EE family - can help recovery & reduce anti-psychotic med. dependency = reduced likelihood of relapse
    1. Supports EE as factor affecting schizophrenic symptoms = real- world app. - healthy family setting can be used to aid recovery.
  2. Role of EE evidence in adoption studies > Tienari et al. (1994) adopted children with schiz. biological parents = more likely to develop schiz. (than those with non-schiz. biological parents). ONLY if adopted family disturbed.
    1. = disorder forms under certain env. conditions (e.g.disturbed family) = Genetic influence + env. conditions - both required
  3. Double bind theory support > Berger (1965) found schizophrenics = higher recall of double bind (contradictory) statements by mothers (than non- schizophrenics).
    1. Reliabililty is questionable - recall may be affetced by schizophrenia.
4. Evaluation of cognitive explanations
  1. NICE (2014) review of CBTp (involves evaluation of patients faulty beliefs)= found to be more effective in treating symptom severity & improving social functioning than anti-psychotic med.
    1. success shows dysfunctional thought processing/cognitions = key component of schiz.
  2. Reductionist explanation of schiz. - ignores other factors, e.g. neurochemical changes.
    1. Howes & Murray (2014) Intergrated model of schiz. - vulnerability factors (e.g. genes/birth complications..) + social stressors (e.g. social adversity) = sensitised dopamine system - increased dopamine release (combined with cog. processing bias = hallucinations.
      1. suggests combination of factors lead to schiz. symptoms
Drug therapy
1. Typical antipsychotics
  1. = first generation/conventional drugs - e.g. chlorpromazine
    1. combat positive symptoms = hallucinations & delusions > products of overactive dopamine system.
  2. HIGH AFFINITY FOR D₂ RECEPTORS
  3. Basic mechanism = reduce dopamine effects = reduced schiz. symptoms
  4. Dopamine ANTAGONISTS = bind to D₂ receptors in mesolimbic pathway > block dopamine actions = reduced stimulation in mesolimbic dopaminergic pathway (in brain) = eliminate hallucinations/delusions.
  5. Hallucinations & delusions usually diminish within few days BUT other symptoms may take several weeks
  6. Kapur et al. (2000) estimate 60% - 75% of D₂ receptors in mesolimbic dopamine pathway must be blocked for drugs to be effective = D₂ receptors in other areas of brain must also be blocked = undesirable side effects (extrapyramidal effects).
2. Atypical antipsychotics
  1. = second generation drugs, e.g. clozapine.
    1. combat positive symptoms & claimed to have some beneficial effects negative symptoms + cognitive impairments.
  2. HIGHER AFFINITY FOR SEROTONIN RECEPTOR [5-HT₂A] THAN D₂ RECEPTORS
  3. 3 main differences to typical drugs
    1. Lower risk of extrapyramidal side effects
      1. > due to ‘rapid disassociation’ (temporary occupation of D₂ receptors = allow normal dopamine transmission) = no movement problems as found with typical drugs
    2. Beneficial effect on (positive +) negative symptoms & cognitive impairment
    3. Suitable for treatment-resistant patients
3. antipsychotics
  1. Increase patients subjective wellbeing & helps them function as well as possible.
  2. Recommended as initial treatment for schiz. symptoms... after which clinicians combine meds & psychological therapy to manage disorder.
  3. Reduce positive symptoms in severely ill
  4. Help treat psychotic disorders, I,e, bipolar depression/scizoprenia.
  5. Developed following discovery of dopamine on 1952 - found to have effect on dopamine
  6. Antipsychotic action = reduce dopaminergic transmission = reduced action of dopamine neurotransmitter in areas of brain > associated with with symptoms of schiz. [DOPAMINE HYPOTHESIS - biological explanation]
4. Evaluation
  1. Support for antipsychotic effectiveness > Leucht et al. (2012) meta-analysis of 65 studies between 1959 & 2011 – 6000 patients. All pps stabilised on antipsychotics – then some pps taken off & placed on placebo & remaining pps stayed on regular antipsychotics > after 12 months - 64% on placebo relapsed & 27% on antipsychotic relapsed.
  2. Highly effective treatment for schiz. Symptoms = reduced relapse intensity and frequency/cheap/easy for patient to administer/non-time consuming > does not require regular visits to clinician for therapy = less dropout rate?
  3. Typical antipsychotics extrapyramidal side effects (affects 50% of patients)– caused by blockage of 60-75% dopamine transmission > impact extrapyramidal brain region = responsible for motor activity = Parkinsonian/tremors/impaired motor activity
  4. Atypical antipsychotics metabolic side effects > Mareno et al. (2010-12) Study on 90 adolescents on atypical antipsychotics (for various diagnoses) found significant weight gain = on average 12 pounds in 70% of patients.
  5. Do not treat real cause & only treats symptoms > stopping medication will most likely result in relapse.
Cognitive behavioural therapy for psychosis (CBTp)
1. Developed to treat residual (pos. & neg.) schiz. symptoms (that persist despite use of antipsychotic med.) + improve patient’s functioning.
2. Evaluation
  1. Turner et al. (2014) significant effiectiveness in reducing positive symptoms (when compared with other psychosocial interventions).
  2. Meta-analysis can result in unreliable conclusions about CBTp effectiveness > as study quality not taken into account. E.g. some studies fail to randomly allocate pps to either CBTp or control condition.
    1. Juni et al. (2001) concluded methodologically weak trials = biased findings on CBTp effectiveness.
    2. Wykes et al. (2008) found that more rigorous (high quality) studies had weaker CBTp effects.
  3. Stafford et al. (2013) meta-analysis - CBT for those at risk of psychosis [risk ratio 0.54 at 95% confidence interval] shown to possibly delay/prevent transition to psychosis at 12 months.
3. Basic assumption of CBTp = ppl can have distorted beliefs = influence inappropriate feelings & behaviours.
  1. For schiz. these are dysfunctional thought processing = faulty interpretations of events = delusions
    1. CBTp used to help patient identify & correct faulty interpretations.
4. Aim of CBTp = help ppl establish links between thought, feelings/ actions & symptoms + general level of functioning.
  1. Monitoring own situation = patient better able to consider her ways of explaining why they feel/behave the way they do = reduced distress + improved functioning [ from more self-awareness & understanding].
5. Group sessions/ one-to-one.
6. NICE (National Institution for Health & Care Excellence) recommend at least 16 sessions for treating schiz.
7. Nature of CBTp
  1. Patients encouraged to trace symptoms to origins [to get idea of how they might have developed] + evaluate content of delusions/ hallucinations [to consider ways they can test validity of faulty beliefs = ‘reality testing’.
  2. Patient set behavioural assignments e.g. shower > improve general level of functioning.
  3. Patient develops own alternatives to previous maladaptive (inappropriate) beliefs > by looking for other explanations & coping strategies when assessing cause and effects & distorted thinking
8. Phases of CBTp
  1. Assessment
    1. Patient expresses thoughts about experiences to therapist + realistic goals for therapy set (patients current distress used as motivation for change)
  2. Engagement
    1. Therapist empathises with patients distress
  3. ABC model (Ellis)
    1. Activating events (A) that cause emotional & behavioural (B) consequences (C) to patient are explained > allows for unhealthy beliefs (e.g. ‘ppl won’t like me if I tell them about my voices’) to be rationalised, disputed and changed into healthy beliefs (e.g. ‘some may find it interesting’)
  4. Normalisation
    1. 1 in 4 ppl suffer from mental disorders > unusual experiences/delusions/hallucinations = reduces patients anxiety & isolation/less alienated & stigmatised = hope for their recovery.
  5. Critical collaborative analysis –
    1. Gentle questioning to help patient understand illogical deductions & conclusions – e.g. ‘If the voices are real, why can’t others here them ?’ (can result in no stress for patient if a non-judgemental atmosphere of trust and empathy is created between therapist and patient)
  6. Developing alternative explanations
    1. Patient develops other explanations for previously unhealthy assumptions
Family therapy
1. KEY STUDY : Pharoah at al. (2010) meta-analysis
  1. Procedure: Review of 53 published (RCTs = randomised controlled trial = random pps allocation) studies (2002-2010) conducted in Europe, Asia & North America > family therapy effectiveness - family therapy outcomes compared to 'standard' care (i.e, antipsychotic medication)
  2. Findings: MENTAL STATE = some studies reported improvement in family therapy patients compared to standard care patients BUT others did not. COMPLIANCE WITH MED. = Family therapy increased patient's medication compliance (correct following of medical advice). SOCIAL FUNCTIONING = Family therapy appeared to improve general functioning BUT did not have much of an effect on social functioning (e.g. living independently). REDUCED RELAPSE/READMISSION = Family therapy reduced risk of relapse and hospital admission during treatment & 2 yrs after.
2. Range of interventions aimed at schiz.'s family > schiz. guidance & management = psychoeducation
3. Evaluation
  1. Lobban et al. (2013) analysed studies & found positive impact on schiz. + family members > 60% of 50 family therapy studies reported sig. positive impact - e.g. coping/problem solving skills/relationship quality (including EE)
    1. HOWEVER poor methodology quality of studies = difficult to distinguish effective from ineffective interventions
  2. Economic benefits of family therapy - NICE review of family therapy studies > family therapy associated with sig. cost savings when offered to schizophrenics alogside standard (antipsychotic drugs) care.
    1. cost savings from lower hospitalisation/relapse rates (which fall during intervention + 24 months after)
  3. Methodological limitations - Pharoah et al. meta-analysis > some were chinese studies = Wu et al. > random allocation of pps stated but not used.
    1. + lack of double blind = observer bias when pps allocated > 10 /53 studies reported no form of blinding + 16/53 did not mention use
  4. Effetiveness of family therapy = increased patient medication compliance = correctly follow medical advice/regime = increased benefits from meds
4. NICE recommend family therapy (=priority when symptoms persist & high relapse risk) 'to all schizophrenics who are in contact with/live with family members'
5. Research shown> higher relapse rate in schiz. when family had high EE = high hostility & over-involvement
6. Nature of family therapy
  1. 3-12 months - atleast 10 sessions
  2. Aims to reduce family EE level = reduced emotional climate (e.g. less anger/guilt)
  3. Garety et al. (2008) estimate family therapy patients have 25% relapse rate & standard care patients have 50% relapse rate.
  4. Involves active participation of schizophrenic & family members = improves relationships as therapist encourages open discussion of problems & negotiation of potential solutions together = alliance formation
  5. Often used alongside drug treatment for patient + outpatient clinical care
Token economy & the management of schizophrenia
1. Token economy = form of behavioural (modification) therapy > clinican set target (desirable) behaviours (e.g. brushing hair/) believed to improve patient's engagement in daily activities.
2. Evaluation
  1. Corrigan (1991) Difficult administration of token economy to outpatients living in community> receive day treatment for few hrs/day. In psychiatric hospital setting - patients recieve 24 hr care = better control + monitoring in order to appropriately reward patients.
    1. positive results produced in outpatients = difficult to maintain beyond hospital env.
  2. Ethical concerns - to ensure effective reinforcement clinicans may strictly control primary reinforcers (e.g. food, privacy..) = basic human needs/ rights (to food, privacy...) violated through manipulation of token economy programme.
  3. Atthowe and Krasner (1968) Use of token economy to modify behaviour of chronic schizophrenics > significant increase in performed reinforced desirable behaviours + improved patient initiative, responsibility & social interaction.
  4. Dickerson et al. (2005) research support for token economy effectiveness in psychiatric setting > reviewed 13 studies (that use token economy to treat schizophrenia). 11/13 studies reported beneficial effects directly attributed to use of token economy
3. Assinging value to tokens
  1. Neutral token given 'value' through secondary reinforcement = token repeatedly paired with/immediately before reinforcing stimulus (e.g. watching movie/food/incentives..) = token acquired same reinforcing properties > can be used to modify behaviour
    1. classical conditioning
4. Reinforcing target behaviours
  1. Sran & Borrero (2010) Use of 'generalised' reinforcer in session (token can be exchanged for variety of privileges) = higher rates of target behaviours performed in sessions [than the use of token that can be excahnged for single privilege]
5. The 'trade'
  1. Kazdin (1977) Effectiveness of token economy decreases if more time passes between presentation of token & exchange for backup rewards (chosen by clinician)
  2. Frequent exchange periods (of tokens for privilege) = quicker patient reinforcement + increased target behaviour frequency
6. Token awarded when patient engages in target (desirable) behaviour & can later be exchanged for privileges (e.g.access to tv)
7. [Tokens paired with rewarding stimuli (privileges) = secondary reinforcement]
8. Ayllon & Azrin (1968) Token economy on female schiz. patient ward (many hospitalised for many yrs) > given 'one gift' plastic tokens for target behaviours (e.g. domestic chores). Tokens exchanged for privileges (e.g. watch movie). Use of token economy = dramatically increased desirable behaviours performed by patients each day.
Interactionist approach: Diathesis-stress model
1. Stress = environmental influence
2. Evalution
  1. Treatment implications/real-world app. > Known factors to interact with genetic vulnerability can be addressed - avoid additive effect of diathesis (genetics) + stress (env. factors)
    1. Borglum et al. (2014) Women with gene defect + infected with cytomegalovirus (type of virus) during pregnancy = higher risk to have child who develops schiz. (only if both mother & child have gene defect). Anti-viral medication during pregnancy = prevent onset of schiz. in offspring.
  2. Hammen (1992) argues maladaptive methods of coping with stress in childhood & throughout development = individual fails to develop effective coping skills = compromised resilience + higher vulnerability.
    1. Life = highly stressful & may trigger mental illness (e.g. schiz.) [mention psychiatrist Laing]
    2. = stress may not be key factor in triggering schiz. BUT may infact be individuals coping skills & how they react to stressors in env. that trigger schiz.
  3. Tienari et al. key study limitations > OPAS scale assessed adoptive family ONLY at one given point in time> does not reflect developmental changes (& how family conditions may have changed over time to produce/prevent schiz. onset)
  4. Urban environment not necessarily more stressful > Vassos et al. suggests living in densely populated urban env. = significant schiz. stress factor. HOWEVER Romans-Clarkson et al. found NO urban-rural differences in mental health [among women in New Zealand]
    1. Urbanisation as schiz. factor = highly simplistic. Cultural & gender differences (beta bias)> Women in New zealand non-representative of other cultures &/ males.
3. KEY STUDY: Tienari et al. (2004)
  1. PROCEDURE: Hopsital records of 20,000 women [admitted in Finnish psychiatric hospitals between 1960-79] checked. Sample collected = 145 high risk (with schiz. mother) adopted children & 158 low risk (non-schiz. mothers) adopted children > all assessed over 21 year period (longitudinal study)+ adoptive family assessed using OPAS
  2. FINDINGS: 14 from total 303 (= 145 high risk + 158 low risk) developed schiz. 11/14 from high risk group & 3/14 from low risk group. Low OPAS rating = healthy adoptive family > has protective effect from schiz. dev.. High OPAS rating = disturbed adoptive family = stressor >trigger schiz.
    1. Adoptive family stress = predictor of schiz. development
4. Diathesis = biological infleunce
5. Schizophrenia = result of biological & environmental influences
6. Family studies > People have varying vulnerability levels (high/low) to schiz. BUT going on to develop schizophrenia is determined by vulnerability (bio.) level + level of stress experienced through lifetime (env.)
7. Diathesis
  1. Genetics = determinant of schiz. vulnerability
  2. Twin studies > identical twin of schizophrenic = higher risk of developing schiz. than sibling/non-identical twin.
    1. Tienari et al. > adoptive relatives do NOT share increased risk as biological relaetives
  3. 50% of identical twins - where one is diagnosed with schiz. & other never meets diagnostic criteria for schiz.. This discordance rate suggests env. plays role (in schiz. dev.)
8. Stress
  1. Stressful life events (take many forms - e.g. childhood trauma/ living in highly urbanised area) = schiz. trigger
  2. Varese et al. (2012) children experienced severe trauma (=stressor) before age 16 = 3x more likely to develop schiz. in later life.
  3. Vassos et al. (2012) meta-analysis > most urban environments = 2.37x higher risk to develop schiz. than most rural environments.
    1. + Research suggests> higher urbanisation level associated with higher risk of developing different psychoses, including schiz.
      1. Urban env. = poorer/adverse living conditions
      2. HOWEVER > many ppl live in urban/densely populated areas BUT only few develop schiz. = urban env. is conditional to persons vulnerability level.
9. Additive nature of diathesis + stress
  1. Several ways combination of diathesis + stress lead to schiz. onset
    1. E.g. Highly vulnerable individual + minor stressor = schiz. / Low vulnerability individual + major stressor = schiz.
  2. Pre-supposed additivity = diathesis + stress combine to produce disorder (=schiz.)
Biological explanations for schizophrenia

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