Schizophrenia

Diagnosis & Classification of Schizophrenia

AO1

Affects 1% of the population, more common males, city populations

Classification -identifying symptoms that go together

Diagnosis - use of the classification system to identify a disorder

DSM-5: 1 +ve symptom

ICD-11: 2 -ve symptoms

Positive symptoms (additional experiences): Hallucinations & delusions

Negative symptoms (loss of abilities): Speech poverty & avolition

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Neural Correlates of Schizophrenia

AO1

Abnormal levels of dopamine

Original hypothesis: High dopamine subcortex (hyperdopaminergia) = speech poverty & hallucinations

Updated hypothesis: Added low levels of dopamine (hypodopaminergia) in pre frontal cortex = -ve symptoms

AO3

+ Amphetamines mimic symptoms and antipsychotics reduce them. Both work on DA.

- Sz like symptoms in rats using amphetamines but apomorphine inc. DA and no symptoms

- Post mortem and scans show higher Glutamate and several candidate genes linked to G 

Treatment: Drug therapies

AO1

Typical: dopamine antagonists (block dopamine receptors), 1950s, Chlorpromazine, sedation effect = helps to calm when hospitalised

Atypical: Newer (1970s), Clozapine, less side effects, works on DA & serotonin and glutamate receptors, improves mood

Risperidone, 1990s, developed due to agranulocytosis risk of Clozapine. Binds more strongly so lower doses = less side effects

AO3

+ Thornley - 13 trials (1121 ppts), chlorpromazine = less symptoms

-Studies = short term

- Side effects: tardive dyskinesia

- Should not work according to updated DA theory

- Ethical issues with sedation

Interactionist approach to Schizophrenia

AO1

Diathesis-stress model: vulnerability + trigger

Meehl's (1962) model: Schizogene

Modern diathesis: Many genes involved, diathesis does not need to be genetic -could be ACEs

Modern stress: Stress can be psychological (e.g. parenting) or biological (cannabis use x7 increased risk - linked to DA)

Treatment: Anti-psychotic medication & CBT, UK have adopted this but US slower.

AO3

+ Tienari: adopted children with bio. sz mother. Higher sz with adoptive parents with high criticism, low empathy compared to controls.

- Original model: overly simplistic (Ripke 108 candidate genes)

+ Real world application: CBT & drug therapy most effective (Tarrier)

Reliability & Validity in diagnosis

AO1

Reliability = consistency

Inter-rater reliability: 2 clinicians

Test retest reliability: Over time

Validity = accuracy of diagnosis

Criterion validity: use of two manuals could produce different results

AO3

+ Good reliability: Osorio - +.97 inter rater & +.92 test retest

-Low validity: Cheniaux -100 ppts, diagnosis of 68 ICD and 39 DSM

- Comorbidity: Buckley -depression 50%, substance abuse 47%

- Gender bias: males diagnosed 1.4:1 to females

- Culture bias: Afro-Carribean men x10 more likely diagnosed

- Symptom overlap: hard to distinguish from bipolar

Psychological: Family Dysfunction

AO1

Schizophrenogenic mothers: psychodynamic, cold, rejecting and controlling (refrigerator mother). Leads to delusions. 

Double bind theory: Bateson, conflicting family communication, when 'wrong' love withdrawn. Leads to disorganised thinking. 

Expressed emotion: Relapse explanation. Criticism & hostility.  

AO3

+ Sz ppts more likely to have insecure attachments (Read)

- Lack of evidence for sz mother & double bind

- Social sensitivity: Parent blaming

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Treatments: Psychological Therapy

AO1

CBT: help to identify delusions & hallucinations, 20 sessions, helps to understand = normalising the experience, Turkington - paranoid client (mafia) reduced symptoms with CBT

Family therapy: reduce expressed emotions (anger, guilt)

Family become a therapeutic alliance = improve beliefs of sz & manage balance of support and living own life, Burbach's model (identify resources, unhelpful patterns, skills)

AO3 CBT

+ Jauhar: 34 studies of CBT for sz & significant effects

- Validity issues of research: CBT techniques & symptoms have been different. Hard to compare.

- CBT only manages symptoms not cures

AO3 Family

+ McFarlane: relapse rates reduced by 50-60%

+ Benefits the family - benefits beyond the patient: cost effective

Genetic Basis of Schizophrenia

AO1

Family studies: Gottesman 48% MZ twin, 17% DZ concordance rates

108 candidate genes (Ripke)

Polygenic & aetiologically heterogeneous

Mutation of parental DNA: +ve correlation paternal age and sz

AO3

+ Hilker: 33% MZ & 7% DZ

 - Incomplete explanation: 67% ppts past trauma - supports diathesis stress model

+ Real life application: genetic counselling 

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Psychological: Cognitive explanations

AO1

Dysfunctional thought process - lower levels in ventral striatum =

-ve symptoms

Frith: Meta-representation dysfunction - cannot recognise thoughts as own = hallucinations

Frith: Central control dysfunction - Derailment of thoughts as cannot suppress automatic responses = speech poverty

AO3

+ Dysfunctional thought: sz ppts took x2 as long to complete Stroop task (Stirling)

- Does dysfunctional thoughts lead to sz or vice versa?

- Psychological or biological? Dysfunctional thoughts may be genetic in origin

Token economies for Schizophrenia

AO1

Common in 1960s but UK decline in hospitalisation of sz ppts

Helps with personal care & social behaviour

Modifying = improves quality of life in institution and normalises behaviour to adopt back in the community

Tokens (coloured discs) given immediately with target behaviour

Tokens (secondary reinforcers) can be swapped for rewards (primary reinforcers) - based on operant conditioning

Most effective when ppts agree on rewards

AO3

+ Meta-analysis 7 studies 1999-2013 token economies = lower -ve symptoms & unwanted behaviour

- Small evidence bias & potential publishing bias

- Ethical issues: professionals hold the power

- More ethical alternatives e.g. art therapy

- Hard to implement in the community. Limited usefulness,