1
Q
What is schizophrenia?
A
A severe mental disorder where contact with reality & insight are impaired & characterised by hallucinations, delusions, avolition & speech poverty
2
Q
What are the 2 classification systems and how is schizophrenia classified?
A
- ICD-10 & DSM-5
- DSM-5 only needs 1 positive symptom for a diagnosis
- ICD-10 needs 2 or more negative symptoms
- ICD-10 recognises subtypes of schizophrenia: paranoid schizophrenia (powerful delusions), hebephrenic (negative symptoms) schizophrenia & catatonic
3
Q
What is the reliability of a diagnosis?
A
- Reliability refers to the consistency of diagnosis, including inter-rater reliability where the same diagnosis is made by two or more assessors
4
Q
What is the validity of a diagnosis?
A
- Validity is the extent to which the methods used to diagnose mental illness are accurate e.g. that the methods are able distinguish schizophrenia from other, similar disorders
5
Q
What is the difference between co-morbidity & symptom overlap?
A
- Symptom overlap: the extent to which the symptoms of one disorder are also present in a different disorder
- Co-morbidity: the extent to which two or more conditions occur together, calling into question the validity of diagnosis
6
Q
What are the strengths of diagnosing schizophrenia?
A
- Good reliability: a diagnosis = reliable when the same clinician reaches the same diagnosis for the same individual (inter-rater) & on two occasions (test-retest) - post DSM-5, reliability for schizo diagnosis had risen -> Osario et al reported excellent reliability in diagnosis of 180 individuals using DSM-5 (inter-rate of +.97 & test-retest of +.92)
7
Q
What are the issues with diagnosis & classification of schizophrenia?
A
- Comorbidity = extent to which two or more conditions occur together, calling into question the validity of diagnosis - Buckley et al. found that around half of all patients diagnosed with schizophrenia also had a diagnosis of depression - called into question the ability to tell the difference between the two & diagnose accurately -> could be that very severe depression can present as schizophrenia because it looks a lot like it (problems for classification)
- Gender bias: Since 1980s, men have been diagnosed with schizo more commonly than men (1.4:1 - Fischer & Buchanan) - could that be women are less genetically vulnerable but more likely that women are underdiagnosed as they have closer relationships -> more support (Cotton et al) -> schizophrenic women function better than men -> women don’t recieve right treatment
- Culture bias: some schizophrenic symptoms have different meanings in different cultures e.g. Haitians believe voices are communications from ancestors -> British Afro-Caribbeans are 9x mor likely to be diagnosed than white Brits (Pinto & Jones) yet people in African-Caribbean countries aren’t (rules out genetics) - due to culture bias in diagnosis by psychiatrists -> overinterpretation of symptoms in Black Brits (Esocbar)
- Symptom overlap: schizophrenia & bipolar disorder involve positive & negative symptoms - in terms of classification this implies schizo & bipolar disorder may not be 2 different conditions but variations of a single condition + in terms of diagnosis, it’s hard to distinguish the 2 + co-morbidity means schizo may not exist as a distinct condition -> flawed
8
Q
What are hallucinations?
A
When we perceive things around us that aren’t actually real e.g. hearing, feeling, or seeing things that aren’t there (can involve any of our 5 senses)
9
Q
What are delusions?
A
Firmly holding onto irrational beliefs about the world even when the evidence contradicts your beliefs
10
Q
What is avolition?
What are the 3 signs of avolition (Andreasen)
A
- When individuals feel a persistent lack of motivation or energy to complete their normal everyday tasks
- 3 signs: poor hygeine & grooming, lack of persistence in work or education, lack of energy
11
Q
What is speech poverty?
A
When people rarely speak & show a lack of spontaneous unprompted speech
12
Q
What is speech disorganisation?
A
- Speech becomes incoherent or the speaker changes topic mid sentence
- Classified in DSM-5 as a positive symptom
13
Q
What are the positive symptoms of schizophrenia? (define positive symptoms)
A
- Symptoms that involve abnormal, additional experiences that people don’t normally have
- E.g. hallucinations, delusions, speech disorganisation
14
Q
What are the negative symptoms of schizophrenia? (define negative symptoms)
A
- Symptoms that involve absence of usual experiences that people normally have
- E.g. avolition, speech poverty
15
Q
What are the 2 psychological explanations for schizophrenia?
A
- Family dysfunction
- Cognitive
16
Q
What is the family dysfunction explanation (psychological)?
A
- Abnormal processes within a family such as poor communication, cold parenting & high levels of expressed emotion which can be risk factors for the onset/maintenance of schizophrenia
17
Q
What is the schizophrengenic mother element of family dysfunction?
A
- Psychodynamic explanation proposed by Fromm-Reichmann based on patient’s childhood accounts
- Mother = cold, controlling, rejecting
- Family climate marked by tension & secrecy
- Leads to distrust & later paranoid delusions
18
Q
What is the double-bind hypothesis element of family dysfunction?
A
- Bateson et al (1972)
- Communicative style marked by contradictory or unclear messages from parents
- Children who frequently receive contradictory messages from parents -> schizophrenia
- Child fears trapped in situations where they fear doing the wrong thing + can’t seek clarification
- Getting it wrong results in withdrawal of love -> creates an understanding of the world as confusing
19
Q
What is the expressed emotion explanation element of family dysfunction?
A
- Negative EE is the level of negative emotion towards the patient by the carer e.g. hostility, anger, emotional over-involvement, verbal criticism
- Serious source of stress: can trigger a schizophrenic episode in someone genetically vulnerable or a relapse
20
Q
What are the 2 cognitive explanations as part of the psychological explanations for schizophrenia?
A
- Metarepresentation dysfunction
- Central control dysfunction
21
Q
What is dysfunctional thinking as a cognitive explanation for schizophrenia?
A
- Schizophrenia is characterised by disruption to normal thought processing
- Reduced thought processing in the ventral straitum is associated with negative symptoms
- Reduced processing of information in the temporal & cingulate gyri is associated with hallucinations
22
Q
What is the ‘metarepresentation dysfunction’ as a cognitive explanation?
A
- The ability to reflect on thoughts & behaviours - allows us insight into our own intentions & goals + allows us to interpret the actions of others
- Dysfunction in metarepresenation disrupts our ability to recognise our own actions & thoughts as being carried out by ourselves rather than someone else
- Would explain hallucinations of hearing voices & delusions like thought insertion
23
Q
What is the ‘central control dysfuntion’ as a cognitive explanation?
A
- Frith et al also identified issues with the cognitive ability to suppress automatic responses while we perform deliberate actions
- Speech poverty & thought disorder could result from inability to suppress automatic thoughts & speech triggered by other thoughts
- E.g. schizophrenics tend to experience a derailment of thoughts
24
Q
What are the strengths of family dysfunction? (A03)
A
- Research support: a review by Read et al found schizophrenic adults are likely to have insecure attachment, particularly type D or C & found that 69% of women & 59% of male schizophrenics have a history with physical and/or sexual abuse
- Accounts for environmental influences: psychological explanations (e.g., family dysfunction) consider the impact of childhood experiences, stress, & faulty thinking - provides a more holistic approach than purely biological models, making it more comprehensive
25
What are the strengths of family dysfunction? (A03)
- Poor evidence base for any of the explanations: plenty evidence that childhood family-based stress is associated with adult schizophrenia but none to support the importance of traditional family-based theories e.g. double bind, schizophrenogenic mother - both theories are based on clinical observations of schizophrenics & informal assessments of mothers' personalities (no systematic evidence)
- Correlational evidence: while research links family dysfunction & faulty cognition to schizophrenia, correlation ≠ causation - other factors (e.g. genetics) may be responsible → cannot establish cause & effect
26
What are the strengths of cognitive explanations for schizophrenia? (A03)
- Research support: Stirling et al compared performance on a range of cognitive tasks in 30 schizophrenics & a control of 30, including the Stroop task - ppts had to name the font-colours of colour words so have to suppress the tendency to read words aloud → schizophrenics took twice as long as predicted → this means that the cognitive processes of people with schizo are impaired
- Led to successful therapies: cognitive models have led to CBT - helps patients challenge their delusions & hallucination → high real-world application → improves treatment options beyond medication
27
What are the weaknesses of cognitive explanations for schizophrenia? (A03)
- A proximal explanation: they explain what is happening now to produce symptoms compared to distal explanations which focus on what initially caused the condition (distal = genetic & family dysfunction explanations) -> this explanation doesn't address well how genetic variation or childhood trauma may lead to problems with metarepresentation or central control -> partial explanation
- Cause & effect issue: cognitive dysfunction is often observed after diagnosis, making it unclear whether it causes schizophrenia or is a symptom -> reduces scientific credibility as it can't establish causation
- Ignores biological factors: cognitive explanations fail to account for dopamine imbalances, genetic influences, & neural abnormalities - a biopsychosocial approach would be more holistic & complete
28
What are the 3 element to the genetic basis of schizophrenia?
- Family studies
- Candidate genes
- Role of mutation
29
What is the 'family studies' element of the genetic basis of schizophrenia? (What study was conducted?)
- Family studies have confirmed that risk of schizophrenia increases in line with genetic similarity to a relative with the disorder
- Gottesman large scale study e.g someone with a schizophrenic parent had a 6% of developing it, increasing to 17% for fraternal twins & 48% for identical twins
- Although family members tend to share aspects of environment → this correlation supports both
30
What is the 'candidate genes' element of the genetic basis of schizophrenia?
- Early research believed 1 faulty gene caused/explained schizophrenia
- Schizophrenia is polygenic → Ripke et al combined all previous data from genome-wide studies of schizophrenia
- The genetic makeup of 37,000 schizophrenics was compared to 113,000 controls → 108 genetic separate variations were associated with slightly increased risk of schizophrenia
- Schizophrenia is aeteologically heterogenous too - different studies have identified different candidate genes
31
What is the 'role of mutation' element of the genetic basis of schizophrenia?
- Schizophrenia can also have a genetic origin in the absence of a family history of disorder
- Due to mutation in parental DNA, caused by radiation, poison or viral infection
- Evidence comes from positive correlations between paternal age & risk of schizo, increasing from 0.7% with fathers under 25 to 2% in fathers over 50
32
What is the original dopamine hypothesis? (Neural correlates)
- Based on the discovery that drugs used to treat schizophrenia cause symptoms similar to one's in Parkinson's (characterised by low DA)
- Schizophrenia may result from high DA (hyperdopaminergia) in subcortical brain areas
- Excess DA receptors in pathways from subcortex to Broca's -> speech poverty & hallucinations
33
What is the updated dopamine hypothesis?
- Davis et al proposed cortical hypodopaminergia - abnormally low DA in the brain's cortex
- Low DA in the prefrontal cortex (controls thinking) could explain cognitive problems e.g. negative symptoms
- Also suggested that cortical hypo -> subcortical hyperdopaminergia
- Both genetic variations & early experience experiences of stress (psychological & physical) -> more sensitive to hypodopaminergia & subcortical hypodopaminergia as a result
34
What are the strengths of the genetic basis for schizophrenia? (A03)
- Research support: Gottesman = risk increases with genetic similarity to a family member + Tienari et al adoption study - biological children of schizophrenics are at heightened risk, even if growing up in adopted home + Hilker et al showed a 33% concordance for identical twins & 7% for non-identical
- Counter: Concordance rates not 100% -> environmental factors (e.g., stress, family dysfunction) also play a role
- Objective & Scientific: studies use brain imaging, genetic testing, & twin studies, which are replicable, measurable, & less open to bias compared to psychological explanation
- Genome-Wide Studies: modern research has identified specific candidate genes (e.g., the COMT, DRD4, DISC1 genes) linked to schizophrenia, improving scientific validity
35
What are the weaknesses of the genetic basis for schizophrenia? (A03)
- Environmental factors neglected: biological risk factors include birth complications (Morgan et al) & smoking THC-rich cannabis as a teen (Di Forti et al) - psychological risk factors include childhood trauma e.g. Morkved et al found that 67% people with schizophrenia reported at least 1 childhood trauma as opposed to 38% in a matched control
- Deterministic: implies individuals with schizophrenia-related genes will inevitably develop the disorder, ignoring free will & the role of environmental factors
- Nature vs Nurture: Twins share the same environment (especially MZ twins, who are often treated more similarly than DZ twins), making it hard to separate genetic vs environmental influences
36
What are the strengths of the neural correlates explanation for schizophrenia? (A03)
- Evidence for dopamine: amphetamines increase DA & worsen symptoms in schizophrenics & induce symptoms in people without (Curran et al) + antipsychotic drugs reduce DA activity & reduce intensity of symptoms + some candidate genes act on
the production of DA
- Controlled procedures: brain imaging studies are highly controlled & replicable, increasing internal validity & reliability
37
What are the weaknesses of the neural correlates explanation for schizophrenia? (A03)
- There is evidence for a central role of glutamate: post-mortem & live-scanning studies have consistently found raised levels of the NT glutamate in several brain regions of schizophrenics (McCutheon et al) + several candidate genes are thought to be involved in glutamate production (reductionist)
- Brain scans may show correlations, but not causation – we don’t know if neural abnormalities cause schizophrenia or are a result of it
- fMRI scans can be expensive & hard to interpret, & ppts may be on medication, which can affect brain activity
38
How are typical anti-psychotics prescribed for schizophrenia?
- Around since 1950s
- Example: Chlorpromazine
- Can be taken as tablets, syrup or injection
- If taken orally - must be daily & to a max dose of 1000mg but -> doses are usually much smaller for most & increased to a max between 400-800mg
- Typical prescribed doses have decreased over the past 50yrs
39
How do typical antagonists act as 'dopamine antagonists'?
- There is a strong association between the use of typical antipsychotics & DA hypothesis
- DA antagonists work by blocking DA receptors in synapses of the brain, reducing the action of DA
- Initially when taking chlorpromazine DA levels build, but then production is reduced
- DA hypothesis: this dopamine-antagonist effect normalises transmission in key brain areas, reducing hallucinations
40
How do typical antipsychotics have a sedation effect?
- Chlorpromazine is an effective sedative
- Related to its effect on histamine receptors - not fully understood how this -> sedation
- Chlorpromazine is also used to calm individuals with other conditions - often used when patients are highly anxious when first admitted to hospitals
- Syrup is absorbed faster - used for sedation
41
How are atypical anti-psychotics prescribed for schizophrenia?
- Used since the 1970s
- Aim was to maintain/improve the effectiveness of drugs suppressing the symptoms of psychosis & minimise side effects
- There are some atypical antipsychotics that we still don't know how they work
42
What is the history of clozapine & how does it work?
History:
- Developed in the 60s but first trialled in the 70s
- Withdrawn in the 70s following the deaths of some patients from a blood condition
- Remarketed as a treatment in the 80s when it was found more effective than typicals
- 300-450mg a day - fatal side effects (agranulocytosis)
How it works:
- Binds to DA receptors just like chlorpromazine + acts on serotonin & glutamate receptors
- This action helps improve mood & reduce depression & anxiety + may improve cognitive functioning
- Mood enhancing effect -> prescribed to suicide-risk patients
43
What is the history of risperidone & how does it work?
History:
- Around since the 90s
- Developed to produce a drug as effective as clozapine without serious side effects
- Can be taken as tablets or an injection (2wks)
- Start with an initial small dose then built up to a daily dose of 4-8mg (max 12mg)
How it works:
- Binds to DA & serotonin receptors
- Binds more strongly than clozapine -> more effective in smaller doses -> evidence suggests this causes less side effects
44
What are the strengths of antipsychotics as a treatment for schizophrenia? (A03)
- Evidence for effectiveness: Thornley et al reviewed studies comparing effects of chlorpromazine to control conditions - data from 13 trials & 1121 ppts showed that chlorpromazine was associated with better overall functioning than placebo + Meltzer's review concluded clozapine is effective in 30-50% of treatment cases where typicals have failed
- Counter: Many trials lack long-term follow-up – effectiveness tends to reduce over time, with high relapse rates when medication stops
- Practical application: Fast-acting and cost-effective treatment widely used in clinical practice + less expensive than therapy – improves quality of life & functioning
- Scientific credibility: based on DA hypothesis & clear neurochemical pathways – can be objectively tested
45
What are the weaknesses of antipsychotics as a treatment for schizophrenia? (A03)
- Serious side effects: typical antipsychotics are associated with dizziness, weight gain, sleepiness etc + long-term use -> tardive dyskinesia - caused by DA super-sensitivity & causes involuntary facial movements (blinking, grimacing etc) + worst side effect = NMS - caused when the drug blocks DA action in the hypothalamus -> high temp, comas -> can be fatal (estimates of its frequency 0.1%-2%)
- May treat symptoms not causes – doesn’t address psychological or environmental factors -> reductionist
46
47
What is CBT & how is it used to treat schizophrenia?
- A method for treating mental disorders based on cognitive & behavioural techniques + invloves working with a patient to address their thinking (cognitions) & by adjusting their own thinking, they can adjust their behaviour
- Takes place over 5-20 sessions
48
How does CBT help with schizophrenia?
- Helps a client make sense of how their irrational cognitions impact their feelings & behvaiour
- Understanding where symptoms come from can be helpful for those with auditory hallucinations - therapist can convince them the voice comes from a malfunctioning brain centre + can't hurt them
- Doesn't eliminate symptoms but can help them cope -> function adequately
- People hearing voices can be helped by teaching them that voice-hearing is an extension of the ordinary experience of thinking in words
- Delusions can be challenged by reality testing - if delusions are resistant, reality testing can still reduce associated anxiety/depression
49
What is family therapy?
- A psychological therapy carried out with all/some members of a family including identified patient
- Aim is to improve quality of interaction & communication within family & reduce stress at home
50
How does family therapy help with schizophrenia?
- Reduced negative emotions: aims to reduce levels of EE but especially negative emotions like anger & guilt -> stress (reducing stress is vital to reduce chance of relapse)
- Improve's family's ability to help: therapist encourages family members to form a therapeutic whereby they all agree on aims of therapy + improve families' beliefs about schizo + ensure family members achieve a balance between caring for the schizophrenic & maintaining their own lives
51
What was Burbach's proposed model of practice for family therapy?
- Starts with sharing basic info + providing emotional & practical support
- Phase 2: identifying resources -including what certain family members can/can't offer
- Phase 3 aims to encourage mutual understanding + create a safe space for the family to express feelings
- Phase 4: identifying unhelpful patterns of interaction
- Phase 5: skills training e.g. stress management techniques
- Phase 6: relapse prevention planning
- Phase 7: maintenance for the future
52
What are the strengths of CBT as a treatment for schizophrenia? (A03)
- Evidence of effectiveness: Jauhar et al reviewed 34 studies of using CBT with schizo concluding evidence for small but significant effects on positive & negative symptoms + Pontillo et al found reductions in frequency & severity of auditory hallucinations + clinical advice from NICE recommends CBT
- Counter: Publication bias may distort findings- studies showing positive effects are more likely to be published than null or negative results -> overestimates CBT’s effectiveness
- Targeted approach: helps individuals understand & manage their symptoms (e.g. challenging delusional beliefs) - gives them more control -> supports free will – encourages active participation & insight
- No side effects: unlike antipsychotics, CBT has no biological side effects - often preferred by patients long-term + ethically preferable – respects autonomy & well-being
- Counter: Requires significant time & effort from the patient - CBT may lead to frustration or fatigue, particularly in patients with cognitive deficits → therapy might be abandoned
53
What are the weaknesses of CBT as a treatment for schizophrenia? (A03)
- Quality of evidence: wide range of techniques & symptoms included in studies - Thomas points out that different studies use different CBT techniques & people with different combos of positive & negative symptoms -> the overall benefits of CBT likely conceal a wide variety of effects of different CBT techniques on different symptoms
- Limited effectiveness: CBT is more effective for those with insight &mild/moderate symptoms - less so for severely disorganised or paranoid patients -> idiographic approach might be more suitable – CBT is not a one-size-fits-all
- Hard to measure: improvements in delusional thinking or distress are subjective – harder to quantify than symptom reduction in drug therapy -> challenges scientific credibility – lacks objectivity & standardisation
- Time-consuming: requires regular attendance & motivation – dropout rates can be high -> practical limitations – less accessible than drug treatments
54
What are the strengths of family therapy as a treatment for schizophrenia? (A03)
- Evidence for effectiveness: McFarlane concluded family therapy was consistently most effective treatment for schizophrenia + relapse rates found to be reduced by 50-60% + using family therapy as mental health first starts to decline is promising + clinical advice from NICE recommends it
- Cost-effective in the long-term: reduces relapses & rehospitalisation, saving NHS resources over time - Counter: Short-term costs are high, requiring trained therapists & several sessions → may not be viable for overstretched services
- Addresses family environment (a known relapse trigger): helps reduce EE, improving the home setting to prevent relapse
- Counter: Success may depend on family willingness & dynamics – not all families are motivated, available
55
What are the weaknesses of family therapy as a treatment for schizophrenia? (A03)
- Benefits to whole family: a review by Lobban & Barrowclough concluded these effects are important as families provide the bulk of the care to schizophrenics - family therapy strengthens the functioning of a whole family -> lessens negative impact of schizo on other family members + strengthens ability of family to support schizophrenic
- Individual differences: family therapy assumes family is part of the solution, but for some patients, it may be the source of stress -> not universally appropriate
- Subjective outcomes: many outcomes (e.g., family cohesion, emotional expression) rely on self-report or observation, which can be biased or difficult to quantify
56
What are token economies?
Reward systems used to manage maladaptive behaviour patterns due to extended periods of time in psychiatric hospitals
57
How do token economies work?
- Tokens are given to patients immediately after they have carried out a desirable behaviour
- Delays reduce effectiveness & target behaviours are decided on an individual basis
- Tokens have no value in themselves but can be exchanged for tangible rewards e.g. sweets, magazines
58
What is the rationale behind token economies?
- Institutionalisation -> bad habits e.g. struggling to maintain good hygiene
- Matson et al identified 3 categories of institutional behaviour tackled by token economies:
1. Personal care
2. Condition-related
3. Social behaviour
- Behaviour modification isn't a cure but has 2 huge benefits:
1. Improves life within the hospital setting
2. Makes it easier to adapt back to life in the community after a day in hospital
59
What is the theory behind token economies?
- An example of behaviour modification - a behavioural therapy based on operant condititoning
- Tokens are secondary reinforcers - have no value in themselves + gain their power through being paired with a primary reinforcer (rewards)
- Tokens can be exchanged for a range of primary RFs -> powerful = generalised reinforcers
- Generally happens at the start of the programme - administered together
60
What research has been carried into the development of token economies?
- Ayllon & Nazrin - Ward of women with schizophrenia
- Carrying out a task e.g. making a bed -> token
- Swap for a gift/privelege
- Resulting in the number of tasks increasing
- Use has decreased recently due to a change of care routines (growth of community-base care), but also ethical issues (restricting rewards to people with mental health disorders)
61
What are the strengths of token economies being used as management for schizophrenia?
- Evidence of effectiveness: Glowacki et al imeta-analysis of 7 high quality studies conducted between 1999-2013 on the effectiveness of TES for people with chronic mental health issues - in a hospital setting -> all showed a reduction in negative symptoms & decline in frequency of unwanted behaviours -> high value
- Empirical support: Allyon & Azrin found increased desirable behaviours (e.g. hygiene, social interaction) using tokens in institutional settings
- Counter: Lacks generalisability – conducted in a highly controlled hospital setting, not reflective of real-life environments
- Ease of use: simple to implement by staff; doesn't require specialist training like CBT or family therapy
- Counter: Success depends on staff consistency – if staff are not well-trained or consistent, the system breaks down.
62
What are the weaknesses of token economies being used as management for schizophrenia?
- Ethical issues: gives professionals lots of power to control behaviour of patient - imposition of norms on an individual -> problematic if issues aren't approached sensitively - restriction on personal freedoms + patients with the most distressing symptoms could have an even worse time due to removal of small pleasures -> led to legal action taken by patients' relatives -> decline of use of TES
- Limited real-world application: TES are most effective in institutional settings – rarely used outside of hospitals, limiting external validity.
- Short-term effects: behaviour often improves during treatment, but relapse is common once tokens are removed or after discharge
- Individual differences: not all patients respond equally – some may lack the cognitive awareness or motivation to engage with the token system
63
What is the interactionist approach to schizophrenia?
- An approach that recognises a variety of contributing factors in the development of schizophrenia
- Biological factors = genetic vulnerability, neurological abnormalities
- Social = poor quality family interactions
- Psychological = stress from life events, daily hassels
64
What is the diathesis-stress model?
- Diathesis = vulnerability
- Stress = negative experience
- Both are needed to develop the condition
- One or more underlying factors make a person vulnerable but stress triggers
65
What is Meehl's model of the diathesis-stress model?
- Vulnerability (diathesis) was seen as entirely genetic (single gene)
- Schizogene -> Schizotypic personality - one characteristic is sensitivity to stress
- No schizo gene -> no sensitivity to stress -> no schizophrenia
- Chronic stress through childhood - presence of schizophrengenic mother -> schizo
66
What is the modern understanding of diathesis in the diathesis-stress model?
- Schizophrenia is polygenic (Ripke et al)
- Vulnerability (diathesis) can also be caused by psychological trauma
- Early childhood trauma e.g. abuse, could even alter the developing brain (Read et al - neurodevelopmental model) - HPA could become overactive -> more vulnerable to stress
67
What is the modern understanding of stress in the diathesis-stress model?
- Originally stress was seen as psychological in nature - particular in relation to parenting
- Now considered anything that risks triggering schizo
- Cannabis-use (Houston et al) -> 7x more likely developing schizophrenia - interferes with DA system
- Most people don't develop schizo after cannabis-use as they lack the requisite vulnerability
68
How does treatment work according to the interactionist model?
- Model acknowledges biological & psychological factors
- Associated w/ combining antipsychotics & CBT
- Turkington et al points out it's possible to believe in biological causes of schizo & use CBT to relieve psychological symptoms - but requires adopting an interactionist approach
- Standard practice in the UK to treat schizophrenics w/ both antipsychotics & CBT
- In the US there is a history of conflict between biological & psychological schizo models
69
What are the strengths of the interactionist approach to explaining/treating schizophrenia? (A03)
- Comprehensive & holistic: considers both nature (genes, brain structure) & nurture (environmental stressors), which aligns with the complexity of schizophrenia
- Counter: May be difficult to pinpoint which factor (biological or psychological) is most influential for treatment, reducing predictive validity
70
What are the weaknesses of the interactionist approach to explaining/treating schizophrenia? (A03)
- Individual differences: not all patients benefit equally from combined treatments – effectiveness may vary by subtype, symptom severity, or personal insight
- Not falsifiable: hard to test the interaction precisely – can't isolate variables ethically (e.g., induce trauma or withhold treatment
