to review studies into the relationship between levels of NT & SZ (dopamine & glutamate) - 2 existing explanations of what might be responsible for SZ
hyperdopaminergia (high levels of dopamine)
hypoglutamatergia (low levels of glutamate)
procedure - groups of studies
literature review which involved reviewing 33 previous studies on NT levels in patients with SZ - groups of studies looked at:
brain scan studies in SZ looking at dopamine activity in the brain
use of recreational drugs known to induce psychotic symptoms (e.g: PCP linked with psychosis, amphetamines which increase dopamine levels)
what are PET scans
involve injecting the patient with a radioactive tracer carried by the blood to the brain which concentrates around brain structures that are active
scan detects radioactivity and converts digital image of brain, highlighting areas in yellow and red
procedure - researchers evidence
researchers drew on evidence from studies into effectiveness of drugs used to treat SZ and mechanism of action it has on the brain to see which NT are associated with SZ
researchers discussed what kind of drugs can be produced without side effects to improve quality of life and improve compliance rates as patients complained about side effects
findings - drug use
amphetamine (increasing effects of dopamine) users - increases SZ like symptoms
PCP - linked to creating SZ like symptoms as it antagonies glutamate receptor NMDA receptors so PCP reduces action of glutamate in the brain which result in psychotic symptoms in users even more than amphetamine users
findings - glutamate
low levels of glutamate is linked to psychotic symptoms as glutamate is related in both positive/negative symptoms of SZ
low levels in the cerebral cortex = negative symptoms of SZ & low levels in the basal ganglia = positive symptoms
findings - thalamus
thalamus filters out information from sense - glutamate is dominant but if glutamate levels are low, thalamus cannot filter so leads to hyperarousal leading to positive symptoms of SZ
findings - effective treatments
studies shown that clozapine (reducing psychotic symptoms) has antidopaminergic (blocks activity of dopamine) and antiserotonergic (blocks activity of serotonin) functions so reduces level of both NT
conclusion
carlsson suggested that SZ may have different subtypes that could be caused by different NT such as glutamate not just dopamine
means there are implications for drug treatments as drug needs to be carefully targeted at particular NTs
further research still needed to develop drugs that treat SZ and avoid severe side effects
strength
draws from a large pool of 33 studies as secondary data to come up with results and conclusion
carlsson has a large sample size & dataset of patients of a rare MH disorder and allows studies to be collated & increase diversity of sample size so increasing generalisability of conclusions that multiple NT are linked to SZ
findings of the causes and suggestions for treatments of SZ is applicable to SZ patients and their therapists
weakness (counterpoint)
secondary data collected may include studies that have used old classification systems (e.g: DSM 3 to diagnose patients)
means results may not be true for updated classification systems
therefore, not valid for MH disorders at present time
strength
study could lead to development of new drugs - real life application
carlssons emphasis on serotonin & glutamate has pointed pharmaceutical businesses to consider serotonin antagonists and glutamate agonists to reduce symptoms of SZ
study can lead to new drugs with little side effects & high compliance rates to treat SZ
weakness
study not generalisable to humans
many of the studies used in review were based on animal research, such as animals being given NMDA antagonists
results from some of the studies may not be generalised to humans as our brain structures and NT are not identical