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, 6 mths
ICD-11: 2 -ve symptoms, 1 mth
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) = leads to hallucinations
Updated hypothesis: Added low levels of dopamine (hypodopaminergia) in pre frontal cortex = -ve symptoms
Enlarged ventricles - fluid filled pockets in the brain
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
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Treatment: Drug therapies
AO1
Typical: dopamine antagonists (block dopamine receptors), 1950s, Chlorpromazine, sedation effect = helps to calm when hospitalised. Side effects - tardive dyskinesia
Atypical: Newer (1970s), Clozapine, less side effects but agranulocytosis, 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
Issues with symptom overlap, culture and gender bias
AO3
+ Good reliability: Osorio - +.97 inter rater & +.92 test retest
-Low criterion 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 x9 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 (two conflicting messages received at the same time), when 'wrong' love withdrawn. Leads to disorganised thinking.
Expressed emotion: Relapse explanation. Critical and hostile or emotional over involvement.
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 genetic variations (Ripke)
Polygenic & aetiologically heterogeneous
Mutation of paternal 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 processing - lower levels of thought processing 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
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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,
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