schizophrenia

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characteristics

positive symptoms- expreienced ontop of 'normsl behaviour'

- hallucinations

- delusions

negative symptoms- symptoms which stop people from demonstraing normal behaviour

alogia- poverty of speech

avolition- seems apathetic( little response)

anhedonia- in ability to react to pleasure

flatness of effect- express no emotion

catatonic behaviour- little or no movement, overly rapid repetitive behaviour, echopratia, bizarre contortions

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biological explanation 1- dopamine hypothesis

A)

ventral tegmental area (VTA)

nucleus accumbens (NAc)

too much dopamine either from neurons that fire to oftne or quickly cause overstimulation- this causes the positive symptoms of schizophrenia

B) the limbic system

consists of many structures which are responsible for;

- emotions 

- memory

-arousal

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dopamine receptor types

there are several subtypes of dopamine receptor (D1-5)

there spread in the cerebral cortex and in the limbic system, with D2 mainly limited to the limbic system

this distribution povides evidence that both limbic pathways play a role in schizophrenia

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evidence for dopamine link

•Treatment with antipsychotic drugs reduces neurotransmission, the level of dopamine, and reduces the POSITIVE symptoms of many with Sz.
•Conventionalantipsychotic drugs impact on D2 receptors specifically (Seeman & Lee 1975).
•Dopamine also is a major neurotransmitter in the mesocortical pathway that goes between the VTA and the frontal lobes in the cortex. •Toolittle dopamine in the D1 receptors produces cognitive impairments and the NEGATIVE symptoms of Sz (Davis et al 1991)
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evaluation

• over x300 scientists has reported that that there are 108 genetic loci associated with Sz. •This means that there are no obvious genes that can be said to cause Sz. •Any genetic basis for Sz is complex. •Dopamine levels are measured indirectly by the levels of metabolites (HVA or homovallinic acid) left in cerebrospinal fluid – via a lumbar puncture. •These metabolite levels may also be affected by: ▫Diet ▫Drug use •This means its very difficult to be confident about a link between dopamine and Sz based upon metabolites.
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twin studies

Gottesman & Shields (1982) – Used the Maudsley Twin Register. Found 58% (7 out of 12) twins shared Sz suggests that schizophrenia is inherited through genes. Studied 40 twins - the concordance rate for MZ twins is about 48% and only about 17% for DZ twins.

Cardno (1999) – Found a concordance rate of 40%  in MZ twins compared to a 5.3% one in DZ twins.

Also Cardno (2002) – found a concordance rate of 26.5% for MZ and 0% for DZ twins.

Torrey et al (1994) – If one twin develops Sz there is a 28% likelihood that the other will do too.

Benzel et al (2007) – Used gene-mapping and found that 3 gene variants interact to create a susceptibility to developing Sz.

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cause or effect?

•The Dopamine Hypothesis is that dopamine imbalances cause Sz. (D          Sz) •Sz could, however, be the cause of the dopamine imbalance? (Sz           D) • •Research using PET scans (Copolov & Crook 2000) has tried to examine this relationship, unsuccessfully!  
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drug treatment for dopamine works

•Phenothiazines bind to dopamine receptors and block the build up of dopamine. • •They reduce delusions and hallucinations. •

If they work, it would suggest dopamine is causal

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