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Schizophrenia 3

Biological Explanations for Schizophrenia

3 main biological factors genetics, abnormal dopamine functioning and neural correlates
Genetic explanation No single gene responsible but several genes increase individual vulnerability to developing schizophrenia.
Types of genetic research (2) Twin, family and adoption studies to assess concordance rates in related people, Gene-mapping looking for common genetic material in sufferers.
Gottesman and Shields (1976) Reviewed twin studies, 75-91% concordance for MZ twins with severe forms. Suggests genetics important in chronic forms.
Kety and Ingraham (1992) Prevalence rates were X10 higher in genetic than adopted relatives of schizophrenics-suggests genetics greater role than environmental factors.
Gurling et al (2006) Using gene mapping PCM1 gene implicated in susceptibility for schizophrenia
Schizophrenia working group of the Psychiatric Genomics consortium (2014) Found genetic variations associated with developing schizophrenia were higher in brain and immune system, showing link between immune system and schizophrenia and supporting biological causation.
Avramopoulos et al (2013) Support idea that schizophrenia is not single disease but set of related disorders; patients with neuregulin signalling variants more hallucinations but less impairment. Patients without this particular variation have different symptoms.
Evaluation genetic explanations: gene mapping possible to develop tests to identify high risk individuals but raises socially sensitive and ethical concerns.
Evaluation genetic explanations: diathesis-stress genetic study findings provide evidence for diathesis-stress model. Predisposition inherited but environmental triggers determine whether an individual develops schizophrenia
Genetic Evaluation points gene mapping possibilities, supports diathesis-stress, twin studies bias genetic explanations, sample sizes, MZ data, environmental factors.
Evaluation genetic explanations: Hedgecoe (2001) Scientists have used twin and adoption studies in a biased way to prioritise genetic explanations.
Evaluation genetic explanations: Leo (2006) Kety's adoption study had small sample size so generalisation is difficult. Many biological relatives with schizophrenia were distant relatives.
Evaluation genetic explanations: MZ twins If genes alone responsible concordance rates between MZ twins would be 100%. Twin studies provide wide range of estimates from 58 to 11%.
Evaluation genetic explanations: Sorri et al (2004) longitudinal study, compared adoptees whose biological mothers did/did not have schizophrenia. Also looked at rearing styles. Adoptees with high genetic risk more sensitive to non-healthy rearing patterns. Suggests environmental factors also important.
Evaluation genetic explanations: Twin studies and environmental considerations Twin studies suggest genetic factor in disease onset but don't consider influence of social class, and socio-psychological factors between twins or shared environmental influences
Development of dopamine hypothesis Antipsychotic drugs that lessened symptoms seemed to work by decreasing dopamine activity. Plus Dopamine releasing drug L-dopa creates schizophrenic symptoms in non schizophrenics.
Dopamine function Increases rate of firing of neurons during synapse which increases communication between neurones.
Snyder (1976) Dopamine hypothesis Abnormal levels of the neurotransmitter and hormone dopamine is linked to onset of disorder. Too much dopamine released during synapse can lead to onset.
Davis et al (1991) updated theory updated theory as high dopamine levels not found in all schizophrenics and clozapine is an effective drug even though it has little dopamine-blocking activity. Genetic factors probably linked to faulty dopaminergic systems.
Davis et al (1991), dopamine levels Suggested high dopamine levels in mesolimbic dopamine system are associated with positive symptoms. High levels in mesocortical dopamine system associated with negative symptoms.
Randrup and Munkvad (1966) Created schizophrenic -like behaviour in rats with amphetamines, which activate dopamine production; reversed effects by giving drugs that inhibit dopamine release.
Iversen (1979) Post mortems on people with schizophrenia found excess dopamine in the limbic system.
Kessler et al (2003) PET and MRI scans compared people with/without schizophrenia. Those with schizophrenia had elevated dopamine receptor levels in certain brain areas.
Javitt (2007) Showed that Ketamine induced schizophrenic symptoms by blocking neurotransmission at glutamate receptors which leads to abnormal dopamine system functioning - supports glutamate/dopamine connection in disorder onset.
Dopamine hypothesis evaluation: Inconclusive evidence and simplistic hypothesis. Inconclusive evidence as no consistent difference in dopamine levels between those with/without schizophrenia. Over simplistic, several neurotransmitters involved, such as glutamate and serotonin.
Dopamine hypothesis points: Inconclusive evidence, over-simplistic, other neurotransmitters also involved, pharmaceutical profits, positive symptoms, disorder effect, slow recovery,
Dopamine hypothesis evaluation: Healy (2000) pharmaceutical companies keen to promote dopamine theory as would make huge profits from making anti-schizophrenic drugs that inhibit dopamine production.
Dopamine hypothesis evaluation: slow recovery, effect not cause. Cannot explain why people given neuroleptic drugs recover slowly when drug has instant effect on dopamine levels. Different biochemistry may be effect not cause of the disorder.
Dopamine hypothesis evaluation: positive symptoms Dopamine associated more with positive symptoms, so may only contribute to some aspects of the disorder. Or could be different types of schizophrenia only some linked to dopamine.
Lloyd et al (1984) dopamine evaluation If dopamine is causative factor it may be indirect and mediated by environmental factors.
Neural correlates abnormalities of structure and function is specific brain areas is linked to schizophrenia
Evidence for neural correlates Originally post-mortems on brains, now functional Magnetic Resonance Imagery (MRI) images brain in action so can compare with non-sufferers.
Linking neural correlates to genetics Are brain abnormalities caused by genetic factors or the disorder? Compare family members with/without scizophrenia
Johnstone et al(1976) Schizophrenics had enlarged ventricles suggesting linked to loss of brain tissue.
Weyandt (2006) Enlarged ventricles are associated with negative symptoms only, suggests enlarged ventricles cannot explain all aspects of schizophrenia.
Boos et al (2012) MRI scans on 155 schizophrenics, 186 siblings and 122 non-related schizophrenics. Schizophrenics had decreased grey matter density and cortical thinning. Suggests brain tissue differences are an effect of having disorder rather than due to genetic factors
Tilo et al (2001) fMRI scan to 6 schizophrenics/ 6 non schizophrenics looking and speaking about Rorschach ink blots. Severity of thought disorder negatively related to activity level in Wernicke brain area- supporting idea of abnormal functioning in specific brain areas.
Evaluation neural correlates: ventricles some but not all schizophrenics have enlarged ventricles, so not support link to brain tissue loss. Schizophrenics not responding to medication mainly have enlarged ventricles so maybe long term disorder leads to brain damage not caused by it.
Evaluation neural correlates: environmental factors Environmental factors such as stress/substance abuse may also damage brain tissue so must consider them also.
Evaluation neural correlates: Ho et al (2003) Longitudinal study, re-scanned patients after 3 years, saw brain damage in recent onset patients which worsened over time (even when on medication), especially frontal lobes, correlated with increase in symptom severity.
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