Introduction to schizophrenia
Description:
1. Serious mental disorder affecting 1% of population. More common in males, city-
dwellers, and lower socio-economic groups.
2. Diagnosis and classification are interlinked. To diagnose we need to be able to
distinguish one disorder from another. Classification – identify symptoms that go
together - a disorder. Diagnosis –and use classification to identify disorder.
3. Two classification systems: DSM-5 (one positive symptom must be present), ICD-19
(two or more negative symptoms must be present).
4. Positive symptoms (additional experiences beyond those of ordinary existence).
Negative symptoms (loss of usual abilities and experience).
5. Positive: Hallucinations (distorted perceptions of real things, in relation to any sense,
e.g. seeing people who aren’t there). Delusions (make sense to them, bizarre to others,
e.g beliefs about being a very important person).
6. Negative: Speech poverty (reduce in amount and quality of speech, delay in verbal
responses), avolition (loss of motivation to carry out everyday tasks, and goal-directed
behaviours).
Evaluation:
1. + Of diagnosis = good reliability. Reliable diagnosis – consistent between clinicians
(inter-rater) and occasions (test-retest). Osorio reports good reliability for DSM-5,
inter-rater agreement +.97 and test-retest reliability of +9.2.
2. – Of diagnosis is low validity. Criterion validity = seeing whether different
procedures to assess same individuals arrive at the same diagnosis. Two psychiatrists
individually assessed same 100 clients. 68 diagnosed with ICD and 39 with DSM.
Either over- or under-diagnosed. Criterion validity low.
3. – Co-morbidity with other conditions. Commonly diagnosed with other conditions.
Buckley concluded schizophrenia is co-morbid with depression (50% of cases),
substance abuse (47%), or OCD (23%). May not exist as distinct condition.
4. – Gender bias. Men diagnosed more ratio of 1.4:1. Men more genetically vulnerable,
women have better social support masking symptoms. Some women not diagnosed so
miss out on helpful treatment.
5. – Culture bias. Hearing voices accepted in some cultures (e.g. Afro-Caribbean ’hear
voices’ from ancestors). Afro-Caribbean British men ten times more likely to be
diagnosed than white British men (overinterpretation from UK psychiatrists).
Discriminated against culturally biased diagnostic system.
6. – Symptom overlap, both schizophrenia and bipolar disorder involve delusions and
avolition, may be the same condition (classification issue), hard to distinguish from
one another (diagnosis issue). Schizophrenia may not exist as condition, if does hard
to diagnose.
Biological explanations for schizophrenia
Description:
1. Strong relationship between degree of genetic similarity and shared risk of
schizophrenia. Gottesman found someone with an aunt with schizophrenia have 2%
, chance of developing it, sibling (9%), 48% (MZ twin). Family share environment but
still indicates support for genetic view.
2. Schizophrenia = polygenic – requires several genes. Aetiologically heterogenous –
risk affected by different combinations. Ripke combined previous data from genome-
wide studies and found 108 separate genes associated with schizophrenia. Candidate
genes.
3. Schizophrenia can have genetic origin in absence of family history due to mutation in
parental DNA. Evidence comes from the corelation between paternal age (associated
with increased risk of sperm mutation as age increases – 0.75 fathers under 25 and 2%
over 50) and risk of schizophrenia.
4. Dopamine (DA) believed to be involved in schizophrenia because it is featured in
functioning of brain systems related to symptoms of schizophrenia.
5. Original DA hypothesis. High DA activity in subcortex (central areas of brain)
associated with hallucinations and poverty of speech (e.g. excess of DA receptors in
pathways linking from subcortex to Broca’s area). Explains specific symptoms e.g.
auditory hallucinations and poverty of speech.
6. Updated version. Hypodopaminergia linked to prefrontal cortex. Updated hypothesis
has added low levels of DA in prefrontal cortex (responsible for thinking) could
explain negative. Explains origins of abnormal DA – early stressful experiences and
genetic variations = more sensitive to subcortical hypodopaminergia.
Evaluation:
1. + Strong evidence base. Family studies show risk increases with genetic similarity.
33% concordance for MZ and 7% DZ twins. Adoption studies show child still at risk
even if they have parents with schizophrenia even if they grow up in an adoptive
family. Some people more vulnerable due to genes.
2. - Evidence for environment risk factors. Biological risk factors include birth
complications, smoking cannabis. Psychology risk factors include childhood trauma
(67% with schizophrenia) (38% matched controls) reported at least one childhood
trauma. Genes alone can’t provide complete explanation for schizophrenia.
3. + Support for DA in symptoms of schizophrenia. Amphetamines (increase DA)
worsen symptoms and induce symptoms in people without. Antipsychotic drugs
(reduce DA) and reduce intensity of symptoms. Some candidate genes act on the
product of DA or DA receptors.
4. - Evidence for a central role for glutamate. Post-mortem and scanning studies found
raised glutamate in people with schizophrenia. Several candidate genes believed to be
involved in glutamate production or processing. Strong case can be made for a role
for other neurotransmitters in schizophrenia.
Psychological explanations for schizophrenia
Description:
1. Fromm-Reichman – ‘schizophrenogenic mothers’. Cold, rejecting, controlling, create
a family climate of tension and secrecy leading to distrust and paranoid delusions and
schizophrenia.
2. Bateson - a child regularly trapped in situations where they fear doing the wrong
thing, receive conflicting messages about what is wrong, cannot express their feelings
Description:
1. Serious mental disorder affecting 1% of population. More common in males, city-
dwellers, and lower socio-economic groups.
2. Diagnosis and classification are interlinked. To diagnose we need to be able to
distinguish one disorder from another. Classification – identify symptoms that go
together - a disorder. Diagnosis –and use classification to identify disorder.
3. Two classification systems: DSM-5 (one positive symptom must be present), ICD-19
(two or more negative symptoms must be present).
4. Positive symptoms (additional experiences beyond those of ordinary existence).
Negative symptoms (loss of usual abilities and experience).
5. Positive: Hallucinations (distorted perceptions of real things, in relation to any sense,
e.g. seeing people who aren’t there). Delusions (make sense to them, bizarre to others,
e.g beliefs about being a very important person).
6. Negative: Speech poverty (reduce in amount and quality of speech, delay in verbal
responses), avolition (loss of motivation to carry out everyday tasks, and goal-directed
behaviours).
Evaluation:
1. + Of diagnosis = good reliability. Reliable diagnosis – consistent between clinicians
(inter-rater) and occasions (test-retest). Osorio reports good reliability for DSM-5,
inter-rater agreement +.97 and test-retest reliability of +9.2.
2. – Of diagnosis is low validity. Criterion validity = seeing whether different
procedures to assess same individuals arrive at the same diagnosis. Two psychiatrists
individually assessed same 100 clients. 68 diagnosed with ICD and 39 with DSM.
Either over- or under-diagnosed. Criterion validity low.
3. – Co-morbidity with other conditions. Commonly diagnosed with other conditions.
Buckley concluded schizophrenia is co-morbid with depression (50% of cases),
substance abuse (47%), or OCD (23%). May not exist as distinct condition.
4. – Gender bias. Men diagnosed more ratio of 1.4:1. Men more genetically vulnerable,
women have better social support masking symptoms. Some women not diagnosed so
miss out on helpful treatment.
5. – Culture bias. Hearing voices accepted in some cultures (e.g. Afro-Caribbean ’hear
voices’ from ancestors). Afro-Caribbean British men ten times more likely to be
diagnosed than white British men (overinterpretation from UK psychiatrists).
Discriminated against culturally biased diagnostic system.
6. – Symptom overlap, both schizophrenia and bipolar disorder involve delusions and
avolition, may be the same condition (classification issue), hard to distinguish from
one another (diagnosis issue). Schizophrenia may not exist as condition, if does hard
to diagnose.
Biological explanations for schizophrenia
Description:
1. Strong relationship between degree of genetic similarity and shared risk of
schizophrenia. Gottesman found someone with an aunt with schizophrenia have 2%
, chance of developing it, sibling (9%), 48% (MZ twin). Family share environment but
still indicates support for genetic view.
2. Schizophrenia = polygenic – requires several genes. Aetiologically heterogenous –
risk affected by different combinations. Ripke combined previous data from genome-
wide studies and found 108 separate genes associated with schizophrenia. Candidate
genes.
3. Schizophrenia can have genetic origin in absence of family history due to mutation in
parental DNA. Evidence comes from the corelation between paternal age (associated
with increased risk of sperm mutation as age increases – 0.75 fathers under 25 and 2%
over 50) and risk of schizophrenia.
4. Dopamine (DA) believed to be involved in schizophrenia because it is featured in
functioning of brain systems related to symptoms of schizophrenia.
5. Original DA hypothesis. High DA activity in subcortex (central areas of brain)
associated with hallucinations and poverty of speech (e.g. excess of DA receptors in
pathways linking from subcortex to Broca’s area). Explains specific symptoms e.g.
auditory hallucinations and poverty of speech.
6. Updated version. Hypodopaminergia linked to prefrontal cortex. Updated hypothesis
has added low levels of DA in prefrontal cortex (responsible for thinking) could
explain negative. Explains origins of abnormal DA – early stressful experiences and
genetic variations = more sensitive to subcortical hypodopaminergia.
Evaluation:
1. + Strong evidence base. Family studies show risk increases with genetic similarity.
33% concordance for MZ and 7% DZ twins. Adoption studies show child still at risk
even if they have parents with schizophrenia even if they grow up in an adoptive
family. Some people more vulnerable due to genes.
2. - Evidence for environment risk factors. Biological risk factors include birth
complications, smoking cannabis. Psychology risk factors include childhood trauma
(67% with schizophrenia) (38% matched controls) reported at least one childhood
trauma. Genes alone can’t provide complete explanation for schizophrenia.
3. + Support for DA in symptoms of schizophrenia. Amphetamines (increase DA)
worsen symptoms and induce symptoms in people without. Antipsychotic drugs
(reduce DA) and reduce intensity of symptoms. Some candidate genes act on the
product of DA or DA receptors.
4. - Evidence for a central role for glutamate. Post-mortem and scanning studies found
raised glutamate in people with schizophrenia. Several candidate genes believed to be
involved in glutamate production or processing. Strong case can be made for a role
for other neurotransmitters in schizophrenia.
Psychological explanations for schizophrenia
Description:
1. Fromm-Reichman – ‘schizophrenogenic mothers’. Cold, rejecting, controlling, create
a family climate of tension and secrecy leading to distrust and paranoid delusions and
schizophrenia.
2. Bateson - a child regularly trapped in situations where they fear doing the wrong
thing, receive conflicting messages about what is wrong, cannot express their feelings
