Schizophrenia Flashcards
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
Q
What are the strengths of family dysfunction? (A03)
A
- 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
Q
What are the strengths of cognitive explanations for schizophrenia? (A03)
A
- 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
Q
What are the weaknesses of cognitive explanations for schizophrenia? (A03)
A
- 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
Q
What are the 3 element to the genetic basis of schizophrenia?
A
- Family studies
- Candidate genes
- Role of mutation
29
Q
What is the ‘family studies’ element of the genetic basis of schizophrenia? (What study was conducted?)
A
- 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
Q
What is the ‘candidate genes’ element of the genetic basis of schizophrenia?
A
- 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
Q
What is the ‘role of mutation’ element of the genetic basis of schizophrenia?
A
- 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
Q
What is the original dopamine hypothesis? (Neural correlates)
A
- 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
Q
What is the updated dopamine hypothesis?
A
- 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
Q
What are the strengths of the genetic basis for schizophrenia? (A03)
A
- 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
Q
What are the weaknesses of the genetic basis for schizophrenia? (A03)
A
- 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
Q
What are the strengths of the neural correlates explanation for schizophrenia? (A03)
A
- 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
Q
What are the weaknesses of the neural correlates explanation for schizophrenia? (A03)
A
- 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
Q
How are typical anti-psychotics prescribed for schizophrenia?
A
- 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
Q
How do typical antagonists act as ‘dopamine antagonists’?
A
- 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
Q
How do typical antipsychotics have a sedation effect?
A
- 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
Q
How are atypical anti-psychotics prescribed for schizophrenia?
A
- 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
Q
What is the history of clozapine & how does it work?
A
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
Q
What is the history of risperidone & how does it work?
A
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
Q
What are the strengths of antipsychotics as a treatment for schizophrenia? (A03)
A
- 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
Q
What are the weaknesses of antipsychotics as a treatment for schizophrenia? (A03)
A
- 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
Q
A
47
Q
What is CBT & how is it used to treat schizophrenia?
A
- 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
Q
How does CBT help with schizophrenia?
A
- 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
Q
What is family therapy?
A
- 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
Q
How does family therapy help with schizophrenia?
A
- 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
Q
What was Burbach’s proposed model of practice for family therapy?
A
- 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
Q
What are the strengths of CBT as a treatment for schizophrenia? (A03)
A
- 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
Q
What are the weaknesses of CBT as a treatment for schizophrenia? (A03)
A
- 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
Q
What are the strengths of family therapy as a treatment for schizophrenia? (A03)
A
- 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
Q
What are the weaknesses of family therapy as a treatment for schizophrenia? (A03)
A
- 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
Q
What are token economies?
A
Reward systems used to manage maladaptive behaviour patterns due to extended periods of time in psychiatric hospitals
57
Q
How do token economies work?
A
- 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
Q
What is the rationale behind token economies?
A
- 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
Q
What is the theory behind token economies?
A
- 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
Q
What research has been carried into the development of token economies?
A
- 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
Q
What are the strengths of token economies being used as management for schizophrenia?
A
- 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
Q
What are the weaknesses of token economies being used as management for schizophrenia?
A
- 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
Q
What is the interactionist approach to schizophrenia?
A
- 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
Q
What is the diathesis-stress model?
A
- 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
Q
What is Meehl’s model of the diathesis-stress model?
A
- 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
Q
What is the modern understanding of diathesis in the diathesis-stress model?
A
- 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
Q
What is the modern understanding of stress in the diathesis-stress model?
A
- 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
Q
How does treatment work according to the interactionist model?
A
- 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
Q
What are the strengths of the interactionist approach to explaining/treating schizophrenia? (A03)
A
- 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
Q
What are the weaknesses of the interactionist approach to explaining/treating schizophrenia? (A03)
A
- 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
