Biological therapy

Cards (19)

  • The most common treatment for schizophrenia is the use of antipsychotic drugs.
  • Typical antipsychotics = the first generation of drugs for schizophrenia and other psychotic disorders, having been used since the 1950s. They work as dopamine antagonists and include chlorpromazine.
  • There is a strong association between the use of typical antipsychotics like chlorpromazine and the dopamine hypothesis.
  • Typical antipsychotics like chlorpromazine work by acting as antagonists in the dopamine system. Antagonists are chemicals which reduce the action of a neurotransmitter. Dopamine antagonists work by blocking dopamine receptors in the synapses of the brain, reducing the action of dopamine.
  • Initially when an individual begins taking chlorpromazine dopamine levels build up, but then its production is reduced. According to the dopamine hypothesis of schizophrenia this dopamine-antagonist effect normalises neurotransmission in key areas of the brain, reducing symptoms like hallucinations.
  • As well as having antipsychotic properties chlorpromazine is also an effective sedative. This is believed to be related to its effect on histamine receptors but it is not fully understood how this leads to sedation. Chlorpromazine is often used to calm individuals not only with schizophrenia but with other conditions. This has often been done when patients are first admitted to hospitals and are very anxious.
  • Atypical antipsychotics = drugs for schizophrenia developed after typical antipsychotics. Examples include clozapine and risperidone.
  • The aim in developing newer antipsychotics was to maintain or improve upon the effectiveness of drugs in suppressing the symptoms of psychosis and also minimises the side effects of the drugs used.
  • Clozapine was developed in the 1960s. It was withdrawn for a while in the 1970s following the deaths of some patients from a blood condition called agranulocytosis. However, in the 1980s, when it was discovered to be more effective than other typical antipsychotics, clozapine was remarketed as a treatment for schizophrenia to be used when other treatments failed. People taking clozapine have regular blood tests to ensure they are not developing agranulocytosis.
  • Clozapine binds to dopamine receptors in the same way that chlorpromazine does, but in addition it acts on serotonin and glutamate receptors. It is believed that this action helps improve mood and reduce depression and anxiety in patients, and that it may improve cognitive functioning.
  • The mood-enhancing effects of clozapine means that it is sometimes prescribed when an individual is considered at high risk of suicide. This is important as 30-50% of people with schizophrenia attempt suicide at some point.
  • Risperidone is a more recently developed atypical antipsychotic. It was developed in an attempt to produce a drug as effective as clozapine but without its serious side effects.
  • Like clozapine, risperidone is believed to bind to dopamine and serotonin receptors. Risperidone binds more strongly to dopamine receptors than clozapine and is therefore effective in much smaller doses than most antipsychotics. There is some evidence to suggest that this leads to fewer side effects than other antipsychotics.
  • There is a large body of evidence to support the idea that both typical and atypical antipsychotics are at least moderately effective in tackling the symptoms of schizophrenia. Thornley et al. reviewed studies comparing the effects of chlorpromazine to control conditions. Data from 13 trials with a total of 1121 participants showed that chlorpromazine was associated with better overall functioning and reduced symptom severity.
  • There is also evidence for the benefits of atypical antipsychotics. Meltzer concluded that clozapine is more effective than typical antipsychotics and other atypical antipsychotics, and that it is effective in 30-50% of treatment-resistant cases where typical antipsychotics have failed. This means that, as far as we can tell, antipsychotics work.
  • Healy has suggested serious flaws with evidence for effectiveness. Most studies are of short-term effects only and some successful trials have had their data published multiple times, exaggerating the size of the evidence base for positive effects. Also, because antipsychotics have powerful calming effects, it is easy to demonstrate they have some positive effect on people experiencing the symptoms of schizophrenia. This is not the same as saying they really reduce the severity of psychosis. This means the evidence base for antipsychotic effectiveness is less impressive than it first appears.
  • However, typical antipsychotics are associated with a range of side effects including dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. Long-term use can result in tardive dyskinesia, which is caused by dopamine super sensitivity and causes involuntary facial movements such as grimacing, blinking and lip-smacking.
  • The most serious side effect of antipsychotics is neuroleptic malignant syndrome (NMS). This is believed to be caused when the drug blocks dopamine action in the hypothalamus, an area of the brain associated with the regulation of a number of body systems. NMS results in high temperature, delirium and coma, and can be fatal. This means antipsychotics can do harm as well as good and individuals who experience these may avoid such treatments.
  • A limitation of antipsychotics is we do not know why they work. Our understanding of the mechanism by which antipsychotic drugs work is strongly tied up with the original dopamine hypothesis. However, we now know this original dopamine hypothesis is not a complete explanation for schizophrenia, and that dopamine levels in other parts of the brain are too low rather than too high. If this is true then most antipsychotics should not work. This means that at least some of the antipsychotics may not be the best treatment to opt for- perhaps some other factor is involved in their apparent success.