Psychology - Schizophrenia

how are symptoms classified in USA and UK?

• (USA) - DSM-5 → one positive symptom must be present for diagnosis

• (UK) - ICD-10 → two or more negative symptoms must be present for diagnosis

in which demographic is schizophrenia most prevalent

• affects 1% of population

• most common in males and lower socio-economic groups

what are positive symptoms + examples

• additional experiences that are beyond normal experiences

• hallucinations → additional sensory experiences such as distorted perceptions of real things, like hearing voices or seeing people

• delusions → irrational beliefs about themselves or the world

what are negative symptoms + examples

• loss of normal experiences and abilities

• speech poverty → loss in quality and quantity of verbal responses, can be positive if speech is excessively disorganised and individual wanders off the point

• avolition → loss of motivation to carry out everyday tasks like work, hobbies or hygiene, leading to low energy levels and unwillingness to carry out goal-orientated behaviour

strength of schizophrenia diagnoses

✅good reliability → diagnosis is consistent between occasions (test retest) and clinicians (inter-rater) e.g. Osario et al. reported excellent reliability for schizophrenia diagnosis using DSM5, with an inter-rater agreement of +0.97 and a test-retest reliability of +0.92

limitations of schizophrenia diagnoses

❌low validity → e.g. Chineaux et al. found low criterion validity as when 2 psychiatrists independently assessed the same 100 clients, 68 were diagnosed when using ICD and only 39 with DSM, meaning scz is either over or under diagnosed / ✅ has high criterion validity within single diagnostic system

❌high co-morbidity → schizophrenia is commonly diagnosed with other conditions, e.g. Buckley et al. found scz is co-morbid with depression (50% of cases), substance abuse(47% of cases) or OCD (23% of cases), ∴ it’s not a distinct condition

❌gender bias → men are diagnosed with scz more commonly than women as women present fewer negative symptoms and display symptoms like depression so are underdiagnosed + miss out on helpful treatment ∴ diagnosis is alpha biased + androcentric

❌culture biased → hearing voices may be accepted in Afro-Caribbean cultures, e.g. Afro-Caribbean men are 10x more likely to be diagnosed as schizophrenic than white British men as their symptoms are overinterpreted in UK ∴ they are misrepresented + discriminated by a culturally biased diagnostic system (imposed etic)

❌symptom overlap → e.g. both scz and bipolar experience delusions ∴ hard to distinguish & diagnose as it may not exist as a condition

AO1 for genetic basis of schizophrenia

• Gottesman et al. did large scale family studies → found concordance rate is higher in families (esp if family member is closely related) + chance of developing scz in individuals is: 2% if their aunt has it, 9% if their sibling has it & 48% if their identical twin has it

• schizophrenia is polygenic → meaning several candidate genes increase the risk of scz, e.g. Ripke et al. found 108 separate genes increase risk of scz

• scz is aetiologically heterogenous → risk is affected by different combinations in different people

• can be caused by genetic mutation

AO3 for genetic basis of schizophrenia

✅research support → Gottesman et al. shows risk increases w/ genetic similarity + found concordance rates are 48% for MZ twins and 17% for DZ twins ∴ supports genetic vulnerability, ↑ construct validity

❌ignores environmental risks → e.g. childhood trauma or in twin studies, MZ twins don’t have 100% concordance rate ∴ biologically reductionist + not complete explanation

AO1 for neural correlates of schizophrenia

• dopamine hypothesis → scz is due to dopamine imbalance in brain

• hyperdopaminergia → excess dopamine in speech centres like Broca’s area causes auditory hallucinations

• hypodopaminergia → low levels of dopamine in frontal cortex are linked to negative symptoms like avolition / speech poverty

• enlarged ventricles have been correlated with scz

• scz people have low quantities of glutamate (excitatory neurotransmitter) which is involved in attention, learning & memory

AO3 for neural correlates

✅research support → e.g. Leucht et al. did meta analysis of 212 studies & found that drug treatments that normalise dopamine levels were more effective than a placebo, ↑ validity of dopamine hypothesis

✅RWA → explaining scz at the basic chemical level has led to highly effective drug therapies, positive social + economic implications / ❌ biologically determinist can make sufferers feel disempowered and reliant on drug therapy

AO1 for family dysfunction (psychological explanation)

• schizophrenogenic mother (Fromm-Reichmann) → paranoid delusions result from a cold, controlling and rejecting mother & a passive mother, creating a tense environment which triggers psychotic thinking

• double blind theory (Bateson et al.) → child receives contradicting messages about what is expected from them + what is right and wrong, so they feel they can’t do the right thing, leading to disorganised thinking and delusions

• expressed emotion → the level of negative emotion expressed including: verbal criticism, over-involvement and hostility leading to relapse

AO3 for family dysfunction

✅research support linking FD to scz → Read et al. found adults with schizophrenia are disproportionately likely to have an insecure attachment (type C or D), ↑ construct validity + family dysfunction ↑ vulnerability

❌parental blaming → can cause extra stress for parents already seeing their child experience schizophrenia & taking responsibility for their care ∴ socially sensitive & controversial but may be worth it for potential benefits like showing attachment in childhood affect vulnerability to scz

AO1 for cognitive explanations of schizophrenia

• dysfunctional thought processing → lower levels of thought processing in some areas of the brain suggest cognition is impaired, e.g. in the ventral striatum which is associated w/ negative symptoms

• faulty metarepresentation → (MR is the ability to reflect on thoughts and behaviours) schizophrenics don’t have cognitive ability to recognise thoughts as their own leading to hallucinations & delusions

• central control dysfunction → (CC the ability to supress automatic responses while performing deliberate actions) derailment of thoughts occur as each word triggers an automatic association they can’t supress

what is the attention deficit theory

a faulty attention system cannot filter preconscious thoughts, causing delusions

AO3 for cognitive explanations

✅research support for dysfunctional thought processing → e.g. Stirling et al. compared cognitive tests (stroop task) in schizophrenic and non-schizophrenic people & found scz people took twice as long to name font colours, suggesting scz have impaired cognitive processes + ↑ construct validity

❌doesn’t explain cause of schizophrenia → cognitive approach explain symptoms e.g. faulty metarepresentation causes delusions & hallucinations, but the abnormal cognition is probably partly genetic and the result of abnormal biological brain development ∴ biological approach may better explain causes + incomplete explanation

(biological therapy ao1) what are antipsychotics

antipsychotics control symptoms of psychosis and can be injected or taken in pill form

what are typical antipsychotics

• developed in the 1950s, e.g. chlorpromazine

• only treat positive symptoms but have severe side effects

• work as dopamine antagonists by blocking dopamine receptors at the synapse in the brain to reduce the action of dopamine + have sedation effect to calm anxious patients

what are atypical antipsychotics

• newer drugs developed in 1970s & onwards, e.g. clozapine & risperidone (more effective as it binds to dopamine receptors stronger)

• treat negative and positive symptoms with reduced side effects

• works by blocking dopamine, serotonin & glutamate receptors + improves mood reducing suicide in scz people by up to 50%

AO3 for biological therapy for schizophrenia

✅research support → e.g. Leucht et al. did meta analysis of 212 studies & found that drug treatments that normalise dopamine levels were more effective than a placebo, ∴ drug treatments e.g. clozapine that target dopamine system are effective in reducing symptoms

✅RWA → drug therapies help scz people manage symptoms and are cheaper compared to providing hospital treatment or one-to-one psychological therapies ∴ has positive social + economic implications

❌side effects → e.g. typical antipsychotics can cause dizziness or weight gain, & long term use can cause dopamine super-sensitivity + neuroleptic malignant syndrome can be fatal when dopamine action is blocked in hypothalamus ∴ antipsychotics can do harm as well as good

❌don’t address causes → e.g. they only supress symptoms like hallucinations by blocking dopamine receptors, so don’t treat underlying problem which may be cognitive, ∴ psychological therapy (CBT) may be more suitable

what are psychological therapies + treatment for schizophrenia

• cognitive behavioural therapy

• family therapy

• token economies

what is cognitive behavioural therapy

• CBT → identifies and changes clients’ irrational thoughts

• clients are helped make sense of how their delusions and hallucinations impact their behaviour

• normalisation involves explaining that hearing voices is an ordinary experience

what is a case example for CBT

• Turkington et al. (2004) treated a paranoid client who believed the Mafia were plotting to kill him

• he acknowledged the client’s anxiety and explained that there were other less frightening possibilities and gently challenged the client’s evidence for his belief in the Mafia explanation

how may a cognitive behavioural therapist help treat a patient

• identify and challenge irrational beliefs by logically disputing (Ellis’ abcDE model) the reality of the faulty cognitions (delusions), then cognitively reconstructing those beliefs into alternatives (effect)

• reality testing → demonstrating that irrational thoughts (delusions and hallucinations) are not real

• give strategies to help counter irrational thoughts

AO3 for CBT

✅evidence for effectiveness → Jauhar et al. (2014) reviewed 34 studies of CBT on schizophrenia and concluded there is evidence for significant effects on symptoms + another study (Pontillo et al. (2016)) found reductions in auditory hallucinations ∴ people can seek help to effectively manage their symptoms + social implications + economic implications

❌CBT is not a cure → scz is a biological condition so CBT can only improve ability to live by dealing with symptoms / ✅ but studies show CBT significantly reduce positive and negative symptoms meaning it may be partial cure

what is family therapy

• aims to reduce levels of expressed emotion like anger and guilt, which cause stress, to reduce likelihood of relapse

• the treatment is family centred, intended to change their behaviour (& the scz individuals behaviour) & improve their beliefs towards schizophrenia

• the family is educated on symptoms via psychoeducation and develops techniques to reduce conflict and improve communication + problem-solving skills

what is Burbach’s (2018) model of practice

• phases 1 & 2 → share information and identify resources family can offer

• phases 3 & 4→ learn mutual understanding and look at unhelpful patterns of interaction

• phases 5, 6 & 7 → relapse prevention and maintenance + stress management techniques

AO3 for family therapy

✅evidence for effectiveness → McFlarne (2016) found family therapy reduced relapse rates by 50-60% + NICE (National Institute for health and Care Excellence) recommends family therapy ∴ helps manage symptoms + social implications

✅benefits the whole family → therapy is not just for the benefit of scz patient but also the families that provide the bulk of care for the person + it reduces negative impact of scz on the family so strengthens their ability to give support, ↓ relapse ∴ uses holistic approach, increasing overall effectiveness by addressing needs of both patient and their support network

who developed token economies

• Allyon and Azrin (1968)

what are token economies

• based on operant conditioning, where tokens are used as positive reinforcement

• tokens (secondary reinforcers) are given immediately after desirable target behaviour which are determined based on knowledge of the person because delayed rewards are less effective

• tokens have no value themselves and are swapped for rewards (primary reinforcers) e.g. a film

what categories of institutional behaviour can be tackled using token economies & benefits of them

• Matson et al. (2016) → personal care, condition related behaviours (e.g. apathy - no motivation) and social behaviour

• improves quality of life + normalises behaviour by encouraging normal behaviours, making it easier for individuals adapt back into society

AO3 for token economies

✅evidence of effectiveness → Glowacki et al. (2016) identified 7 studies in hospital settings showing a reduction in negative symptoms and a decline in frequency of unwanted behaviours as a result of token economies ∴ token economies can successfully reinforce adaptive behaviours + improve day-to-day life in controlled environment / ❌ evidence lacks external validity as hospitals are highly structured and controlled so positive effects of token economies cant be generalised to real world + evidence from only 7 studies (small sample), so may be subject to file draw problem - a bias to only publishing positive findings, ↓ pop. validity as its not representative of how token economies affect scz people symptoms

❌ethical issues → involve controlling and manipulating behaviour through rewards + restricting availability of pleasures to people who don’t behave as desired so very ill people already experiencing distressing symptoms have a worse time, ↓ autonomy and ↑ potential for coercion ∴ benefits of token economy may be outweighed by costs as can result in short term reduction in QoL

❌better alternatives to token economies → e.g. art therapy is a high-gain, low-risk to managing symptoms with no ethical concerns as patients maintain greater personal control w/ no ethical concerns while still offering therapeutic benefits ∴ token economies seen as less favourable

outline the interactionist approach to explaining schizophrenia

• schizophrenia caused by the interaction of biological and social factors

• diathesis stress model states both genetic vulnerability (diathesis) and a trigger (stressful negative experiences like family dysfunction) are needed to develop schizophrenia

outline the original diathesis stress model

• Meehl’s model stated diathesis was entirely due to a single ‘schizogene’ (biological)

• he argued someone without the gene wouldn’t develop schizophrenia no matter how much stress they were exposed to

• stress was limited to environmental factors like dysfunctional parenting (e.g. schizophrenogenic mother)

outline the modern diathesis stress model

• diathesis is due to many genes that cause vulnerability not a single ‘schizogene’, as schizophrenia is polygenic

• diathesis doesn’t have to be genetic, it could be psychological trauma affecting brain development

• stress can be psychological (e.g. parenting) or biological (e.g. cannabis use) which interferes with dopamine system

AO3 for interactionist approach to expalaining schizophrenia

✅research support → Gottesman et al. found concordance rates are 48% for MZ twins and 17% for DZ twins ∴ suggests there are genetic factors, however the concordance rate is less than 100% for MZ twins so there must be an interaction with environmental factors, ↑ construct validity

❌original diathesis stress model is oversimplistic → diathesis isn’t a single ‘schizogene’, multiple genes increase vulnerability (polygenic) + stress includes biological factors, Houston et al. found cannabis (biological, affects dopamine balance) is a trigger & sexual trauma is a diathesis ∴ there are multiple factors, biological and psychological affecting diathesis and stress

❌uncertainty in the approach → the mechanism by which a psychological event triggers a biological response resulting in symptoms is still uncertain, reducing confidence in the interactionist approach as a full explanation for schizophrenia, ∴ more research may be needed, ↓ validity

outline treatment according to the interactionist model

• as there are both psychological and biological aspects to development, CBT and drug therapy are combined (e.g. used more in UK compared to US)

• biological treatments allow them to reduce symptoms to engage in psychological therapies + CBT gives sufferers cognitive skills to change their underlying faulty cognitions

AO3 for treatment according to interactionist approach

✅RWA → Tarrier et al. (2004) randomly allocated 315 ppt to 3 groups, drugs + CBT, drugs + counselling or a control of just drugs & found patients in the combined treatment had lower symptom levels than those in the control, so interactionist approach has practical usefulness as its more useful than using antipsychotics alone, ↑ ecological validity

❌side effects + expensive → treatment includes antipsychotic drugs which have unpleasant side effects, which may reduce quality of life, while CBT has a high financial cost of one-to-one support from a trained therapist ∴ social and economic implications