Many studies can’t randomly allocate pps to treatment / control group as participation in treatment
programmes decided by clinicians = mL patients regarded as best suited to family therapy are on
programme, accounting for their improvement
= TREATMENT BIAS (issue into effectiveness of therapy)
CONTEMPORARY STUDY
CARLSSON ET AL. (1999): NETWORK INTERACTIONS IN SZ -
THERAPEUTIC IMPLICATIONS
Aim: to review studies into relationship btw neurotransmitter levels (dopamine +
glutamate) on SZ symptoms
2 main “camps” in neurochemical explanations for SZ :
- Hyperdopaminergia
- Hypoglutamatergia
Drugs changing brain chemistry are leading treatment for SZ patients, but not effective
for every1
They acton reducing dopamine levels, but other neurotransmitters implicated in cause
of SZ = other drugs have to be tested for effectiveness
Most patients using antipsychotic medication complain abt impact side effects of drugs
have on their quality of life
Priority is to work to produce drugs that reduce relapse levels and negative side effects
Procedure: LITERATURE REVIEW OF RESEARCH + THEORY
Review research from variety of sources investigating neurochemical levels in those
diagnosed with sz and studies into drugs known to induce symptoms of psychosis
Cite evidence from brain scans providing further evidence to support view that high
dopamine levels related to psychosis
E.g. Abi-Dargham et al. (1998), Breier et al. (1997)
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