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Summary AQA A-level Psychology Schizophrenia Revision Notes

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This document is detailed revision notes with all you could ever need to know on the whole AQA A-level Psychology Schizophrenia topic, including AO1 and AO3 content. The notes are subdivided into the subtopics used by the textbook. They include the content from the textbook, which has been combined...

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Schizophrenia
Introduction to Schizophrenia
Diagnosis and classification
SZ: about 1% world at some point in life, more common in males, city-dwellers, lower
socio-economic groups, ages 15-35
Diagnosis done by identifying symptoms and deciding what disorder a person has.
2 major systems:
 WHO’s International Classification of Disease – ICD-10 (11)
 American Psychiatric Association’s Diagnostic and Statistical Manual – DSM-5
DSM says 1 positive symptom for at least 6 months needed for diagnosis, 2+ negative
symptoms for at least a month under ICD.
Subtypes:
- Paranoid SZ – powerful hallucinations and delusions
Both have dropped subtypes as too inconsistent.
Positive Symptoms
- Atypical symptoms in addition to normal experiences
Hallucinations = unusual sensory experiences, some relate to what senses picking up
in environment and others don’t e.g. voices heard talking to/commenting on a person,
often criticising, can be experienced in relation to any sense.
Delusions = paranoia, irrational beliefs, e.g. being important historical or political
figure, e.g. being persecuted by govt/aliens, e.g. having superpowers, e.g. under
external control, behaviour makes sense to them but seems bizarre to others,
majority not aggressive, more likely to be victims than perpetrators of violence, can
lead to aggression
Negative symptoms
- Loss to normal experiences
Speech poverty = changes in patterns of speech, reduction in amount and quality of
speech, sometimes delay in someone’s verbal responses during conversation, speech
disorganisation – speech becomes incoherent/changes topic mid-sentence (positive in
DSM-5) but SP negative
Avolition = apathy, difficult to begin/complete goal-directed activity, reduced
motivation, Andreasen: poor hygiene and grooming, lack of persistence in
work/education, lack of energy


Issues in diagnosis and classification
Good reliability

,Reliable = consistency - different diagnosing clinicians reach same diagnosis for same
individual (inter-rater reliability and same clinician reaches same diagnosis for same
individual on two occasions – test-retest reliability)
Before DSM-5 was low but improved
Osario et al.: good reliability in 180 individuals using DSM-5, pairs of interviewers had
IRR of +0.97 and TRR of +0.92.
More likely to accurately diagnose people, so they receive appropriate treatment
Low validity – criterion
Validity – if diagnosis represents something real and distinct from other disorders, if a
classification system measures what it claims to
Cheniaux et al.: 2 psychiatrists independently assessed same 100 clients under ICD-
10 and DSM-4 criteria – 68 diagnosed w ICD and 39 w DSM
Over- or under-diagnosed
However: Osario et al. – great agreement between clinicians when using two DSM
measures to diagnose SZ – criterion validity actually good within a single diagnostic
system
Co-morbidity
Calls into question validity of diagnosis/classification – might actually be single
condition and at least some people diagnosed w SZ may have unusual cases of
conditions e.g. depression.
SZ commonly diagnosed w others e.g. Buckley et al. – 50% of individuals diagnosed w
SZ also have depression, 47% with substance abuse, 23% with OCD, 29% with PTSD
Gender bias in diagnosis
Since 1980s men diagnosed more (ratio 1.4:1 Fischer and Buchanan) – women may
be less vulnerable than men but more likely women have closer relationships and get
support (Cotton et al.) – women w SZ function better than men.
Cotton et al.: women ‘function and cope’ better due to closer relationships – women
may be under-diagnosed
Women may not receive treatment and services that may benefit them
Culture bias in diagnosis
Some symptoms e.g. hearing voices have different meanings in different cultures e.g
Afro-Caribbean societies – communication from ancestors, A-Cs living in UK 9x as
likely to receive diagnosis (Pinto and Jones), although people in A-C countries are not –
not genetic vulnerability.
Diagnosis of clients by psychiatrists from different cultural background –
overinterpretation of symptoms in black British people (Escobar)
Symptom overlap
e.g. both SZ and bipolar disorder have positive symptoms (similar – Lichtenstein) e.g.
delusions and negative symptoms e.g. avolition.

, BP and SZ may just be variants of same condition – hard to distinguish so
classification, diagnosis and treatment are flawed



Biological explanations for SZ
Genetic bases of SZ
Family studies
Gottesman large-scale family study e.g. if aunt has SZ you have 2% chance, 9% if
sibling, 17% if DZ twin, 48% if MZ twin
*also share environment so correlation represents both
Candidate genes
Number of genes involved – polygenic
Most likely genes would be those coding for neurotransmitters e.g. dopamine
Ripke et al. – combined all previous data from genome-wide (whole human genome
not just genes) studies of SZ – genetic make-up of 38,000 people with SZ compared to
113,000 controls, 108 separate genetic variations found associated w increased risk of
SZ.
Aetiologically heterogenous – different combinations of factors inc. genetic variation
Mutation
Genetic origin in absence of family history
e.g. mutation in parental DNA, can be caused by radiation, poison or viral infection.
Positive correlations between paternal age (associated with increased risk of sperm
mutation) and risk of SZ, increasing from 0.7%w fathers under 25 to over 2% in
fathers over 50.



Evaluation
 Research support
o Gottesman: risk increases w genetic similarity to a family member w SZ
o Adoption study – Tienari et al. – 164 biological children of parents w SZ,
heightened risk even in adoptive family, 6.7% had SZ vs 2% from 197-
person control group
o Often ‘selectively placed’ in environments similar to biological
o Hilker et al. – concordance rate of 33% for identical twins and 7% for non-
identical
o Genes only increase don’t cause with certainty
 Ignores environmental factors – incomplete explanation
o Inc. biological e.g. birth complications (Morgan et al.) and smoking THC-
rich cannabis in teenage years (Di Forti et al.), and psychological e.g.
childhood trauma

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