biological therapy for schizophrenia

• Typical antipsychotic drugs like chlorpromazine act as antagonists in the dopamine system and aim to reduce the action of dopamine. Dopamine antagonists work by blocking dopamine receptors in the action of dopamine. At first, dopamine levels build up after taking chlorpromazine, but then production is reduced. This normalises neurotransmission in key ares of the brain which reduce symptoms like hallucinations.
• the aim of developing newer antipsychotics was to maintain/improve on the effectiveness of drugs in suppressing the symptoms of psychosis and also minimise side effects. Clozapine binds to dopamine receptors as chlorpromazine does but it also acts on serotonin and glutamate receptors. This drug was more effective than typical antipsychotics as clozapine reduces depression and anxiety as well as improving cognitive functioning. It also improves mood, which is important as up to 50% of schizophrenics attempt suicide
• One strength of antipsychotics is evidence of their effectiveness. Thornley et al. reviewed data from 13 trials with 1121 participants and found that chlorpromazine was associated with better functioning and reduced symptom severity compared with placebo. There is also support for the benefits of atypical antipsychotics. Meltzer concluded that clozapine is more effective than typical antipsychotics, and that is is effective in 30-50% of treatment-resistant cases. This means that antipsychotics work.
• One limitation of antipsychotic drugs is the likelihood of side effects. Typical antipsychotics are associated with dizziness, agitation, sleepiness, weight gain etc. Log term use can lead to lip-smacking and grimacing due to dopamine super sensitivity. The most serious side effect is neuroleptic malignant syndrome cause by blocking dopamine action in the hypothalamus. This means that antipsychotics can do harm as well as good and individuals may avoid them
• One limitation of antipsychotics is that we don't know how they work. The use of most of these drugs is strongly tied up with the dopamine hypothesis and the idea that there are higher than usual levels of dopamine in the subcortex of people with SZ. But there is evidence that this may not be correct and that dopamine levels in other parts of the brain are too low rather than too high. If so, most antipsychotics may not be best treatment to opt for and perhaps some other factor is involves in their apparent success