Biological explanation of schizophrenia

Family studies:

Gottesman (1991) found 48% concordance rate with MZ twins, 2% with aunts

Candidate jeans:

Ripke (2014) found 108 genetic variations were associated with developing sz, not just one gene (polygenetic)

High internal valdiity

Genetic evidence base, high validity from quantitative data

Environmental factors

Fromm-Reichmann (1948) schizophregenic mother: cold, rejecting, controlling, creates tension and paranoid delusions

The original dopamine hypothesis:

Seeman (1987) found drugs for schizophrenia caused symptoms similar to Parkinson’s (low dopamine) so, high dopamine must be implicated (Hyperdopaminergia in the subcortical areas of the brain). E.g. excess dopamine in Broca’s area, may associated with speech poverty.

The updated dopamine hypothesis:

Davis (1991) added hypodopamineriga (too low dopamine in the cortex). E.g. low dopamine in the prefrontal cortex (responsible for thinking) could explain cognitive issues (negative symptoms).

Cortical hypodopaminergia leads to subcortical hyperdopaminergia (both high and low levels of dopamine in different brain regions).

Neural support for dopamine

Tauscher (2014) found antipsychotic drugs reduce dopamine activity and also reduce the intensity of symptoms

Biologically determinist

Jauhar (2014) reviewed 34 studies of using CBT with SZ. Found there are small but significant effects on both positive and negative symptoms.