Schizophrenia

AQA - A Level Psychology - Schizophrenia

Diagnosing Schizophrenia

A: Two (or more) of symptoms each present for a significant portion of time during a 1 month period

B: Level of functioning below level achieved prior to onset

C: Continuous signs of disturbance for at least 6 months

D:

E:

F:

Schizophrenia Symptoms List

Delusions

Hallucinations

Disorganised Speech

Grossly disorganised or catatonic behaviour

Negative symptoms

Positive Symptoms

An excess or distortion of ‘normal dysfunction’

Delusions & Hallucinations

Negative Symptoms

Reduction or loss of ‘normal’ functioning

Avolition & Speech poverty

Reliability of Diagnosis: Key Concepts

Consistency of DSM and other tests

Test retest

Inter rater

Reliability of ICD and DSM Study

Cheniaux et al (2009)

2 psychiatrist independently diagnose 100 patients using DSM and ICD criteria

One doctor: 26 according to DSM and 44 according to ICD

Other: 13 according to DSM and 24 according to ICD

Reliability of Diagnosis: Evaluation

- Low inter rater reliability

- Cultural difference (Copeland)

H Temporal validity as in 1971

- Research of faking schizophrenia (Rosenhan)

Cultural differences in diagnosis reliability Research

Copeland (1971)

134 US & 194 British psychiatrists given description of patients

69% in US, 2% in UK

Validity of Diagnosis: Key Concepts

Accurate and meaningful
Measures what it intends to
Be distinct from other disorders

Issues:
Comorbidity
Symptom overlap
Gender bias
Culture bias

Validity of Diagnosis: Evaluation

- Gender bias (Broverman et al)
Either gender-biased criteria or clinicians holding stereotypes

- Symptom overlap (Read)
Leading to misdiagnosis

- Comorbidity
Schizophrenia often occurs alongside substance abuse, anxiety & depression
May be on condition (Buckley et al and Swets et al)

- Rosenhan Faking Schizophrenia ressearch

Faking Schizophrenia: Research

Rosenhan (1973)

‘Normal’ people presented to hospitals claiming auditory hallucinations (voices saying ‘empty’, ‘hollow’ and ‘dull’)

All diagnosed & admitted

No staff recognised lack of symptoms

Follow up:
Warned hospitals of ‘pseudopatients’
21% detection rate despite none presenting

Gender biased diagnosis research

Broverman et al

US clinicians: mentally healthy ‘adult’ behaviour = mentally healthy ‘male’ behaviour

Led to women being seen as less mentally healthy

Symptom Overlap Research

Read (2004)

Most people with schizophrenia have enough symptoms of other disorder that they could receive at least one other diagnosis

Comorbidity Research

Buckley et al (2009)
Estimated comorbid Depression in 50%, lifetime diagnosis of comorbid substance abuse in 47%

Swets et al (2014)
12% fulfilled diagnostic criteria for OCD
25% displayed significant OCD symptoms

Biological Explanations for Schizophrenia

Genetics

Neural Correlates

Dopamine hypothesis

Genetics as an Explanation: Key Concepts

Polygenic

A etiologically heterogeneous (different combinations of genes can lead to Sz)

Family Studies (Gottesman)

Twin Studies (Joseph)

Adoption Studies (Tienari et al)

Family Studies of Schizophrenia

Gottesman (1991)

Two biological parents with SZ: 46%

One schizophrenic parent: 13%

Siblings: 9%

General pop: 1%

Twin Studies of Schizophrenia

Identical twins: 47%

Fraternal twins: 17%

Joseph (2004)

MZ twins are treated more similarly, encounter more similar environments and experience more ‘identity confusion’ than DZ

Adoption Studies of Schizophrenia

Tienari et al (2000)

164 adoptees with schizophrenic biological mothers

5.8% in psychologically healthy families developed Vs 36.8% in dysfunctional families

2% of 197 control adoptees

Genetic Explanation: Evaluation

+ Research Support
Family Studies (Gottesman)
Twin Studies
H MZ treated more similarly (Joseph)
Adoption Studies (Tienari et al)
H in Finland

I/D: Fails to acknowledge nurture such as birth complications, childhood trauma
Genes alone cannot explain it

Dopamine Hypothesis: Key Concepts

Excess in certain regions

Positive symptoms

Hyperdopaminergia
High levels at subcortex
Excess of dopamine receptors in Broca’s area linked with speech poverty and auditory hallucinations

Hypodopaminergia
Low levels of dopamine in prefrontal cortex linked to negative symptoms

Dopamine Hypothesis: Evaluation

+ Research support
Drug therapy (L-Dopa raises dopamine and can cause schizophrenic type symptoms)
Post mortem (Seeman) revealed higher levels of dopamine receptors in brain
H Causal issue

- Individual differences
Drugs don't work for 1/3 patients
Suggests dopamine can’t explain all cases

I/D: Biological reductionism
Only Focuses on one neurotransmitter but many are involved

Neural Correlates: Key Concepts

Ventricular Space - up to 30% larger

Ventral Striatum - linked to avolition (involved in anticipation of a reward)

Superior temporal gyrus & anterior cingulate gyrus - reduced activity linked to auditory hallucinations

Amygdala - smaller → loss of emotion (affective flattening)

Prefrontal cortex - lower activity → delusions and disorganised thoughts

Neural Correlates: Evaluation

+ Empirical evidence
MRIs allowed living brain images rather than just post mortems
H Findings are inconsistent

- Correlational evidence
Don’t know whether abnormalities predispose sz or clinical symptoms cause these changes

Typical Antipsychotics: Key Concepts

First generation (1950s)

Dopamine antagonist (acts against dopamine)

Binds to but doesn’t stimulate receptors

Also have sedation effect

Kapur et al : 60-75% of D2 receptors in mesolimbic pathway must be blocked to be effective
This means similar number of D2 receptors in other part must be blocked → side effects

Typical Antipsychotic Example

Chlorpromazine

Atypical Antipsychotic: Key Concepts

Second generation

Target dopamine and serotonin reducing depression & anxiety

Temporarily block D2 receptors

Strong affinity for serotonin receptors, lower affinity for D2 receptors

Lower side effect risks
Beneficial effect on negative symptoms & cognitive functioning
Suitable for treatment resistant

Atypical Antipsychotic Example

Clozapine

Drug Therapy: Evaluation

+ Research support for effectiveness
Thornley (2003)
Meltzer (2012)
H only looks at short term effects and not reduced severity of psychosis

- Side effects
Typical - dizziness, weight gain, tardive dyskinesia (involuntary facial movement) Neuroleptic Malignant Syndrome → delirium, coma
Leads to avoidance of treatments

I/D:
Focuses on nature, treating purely biological
More effective as an interactionist approach (meds & therapy)

Psychological Explanations for Schizophrenia

Family Dysfunction

Cognitive Explanations (Dysfunctional Thought Processing

Family Dysfunction Explanations

Schizophrenogenic Mother

Double Bind Theory

Expressed Emotion

Schizophrenogenic Mother: Key Concepts

Cold, rejecting and controlling

Family climate of tension and secrecy
→ distrust → paranoid delusions → schizophrenia

Double Bind Theory: Key Concepts

Contradictory messages from parents (claims to love but also be disgusted)

Messages invalidate each other

Prevents develop of internal coherent reality

Manifests as symptoms (flattened effect, withdrawal etc.)

Expressed Emotion: Key Concepts

Level of emotion expressed towards patient

Family talks about patients in hostile manner or way that indicates emotional over involvement

Most likely to affect relapse rates (Linszen et al - 4x more likely to relapse)

Lower tolerance for intense interactions, Negative climate leads to stress beyond impaired coping mechanisms

Family Dysfunction Explanations: Evaluation

+ Support for childhood traumas
Read et al: SZ disproportionately more likely to have insecure attachment
H Inconclusive evidence for schizophrenogenic Mother
Based on clinical observations of SZ patients and informal assessments not empirical evidence

- Social sensitivity
Leads to parents blaming, particularly mothers

I/D: Nuture
Focus exclusively on nurture side
Theories (schizophrenogenic mother & double Bind) give disorder as direct result of stressors
Ignore biological
Should use diathesis stress interactionist approach

Cognitive Explanations

Dysfunctional Thought Processing

Metarepresentation → hallucinations

Central control dysfunction → speech poverty

Egocentric bias → delusions

Excessive auditory focus → hallucinations

Dysfunctional Thought Processing: Key Concepts

Reduced thoughts processing in ventral striatum → negative symptoms

Reduced processing of info in temporal gyrus → hallucinations

Metarepresentation

Ability to reflect on thoughts & behaviours

Dysfunction disrupts ability to recognise thoughts as ourselves rather than others

Explains auditory hallucainations and delusions like thought insertions

Central Control Dysfunction

Ability to suppress automatic responses triggered by other thoughts

→ Speech poverty & thought dysfunction

Egocentric Bias

Individual sees themselves as central to events

→ jumps to false conclusions

Cognitive Explanations: Evaluation

+ Research support of cognitive tasks (Stirling)

I/D: Reductionist
Only explains what currently happens to produce symptoms
Not initial cause (Distal such as genes & family)

Research Support Cognitive Tasks Study

Stirling

Compared performance on range of cognitive tasks (Stroop etc) in 30 with sz and 30 without

People with sz toook longer to complete

Cognitive Behaviour Therapy: Key Concepts

CBTp

Identify and correct faulty interpretations

Trace origins of symptoms
Study content of delusions and consider ways of testing validity
Coping strategies (positive self talk etc)

Cognitive Behaviour Therapy: Evaulation

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