Discuss biological therapies for schizophrenia

(8+16) Another one of my weaker essays but can be useful for reference.

AO1 Drugs

Drugs that are effective in  treating most disturbing forms of psychotic illness, such as schizophrenia, are called antipsychotic drugs. There are convention antipsychotics and atypical antipsychotic drugs. The basic mechanism of conventional antipsychotic drugs is to reduce the effects of dopamine and so

reduce the symptoms of schizophrenia. Conventional antipsychotics and dopamine antagonists in that they bind to dopamine receptors but do not stimulate them, thus blocking their action. By reducing the stimulation of the dopamine system in the brain antipsychotic drugs such as chlorpromazine can eliminate the hallucinations and delusions. Atypical drugs also act on the dopamine system as they are thought to block serotonin receptors in the brain too. Kapur and Reminton however suggest that these drugs do not involve serotonin or other neurotransmitters, but only the dopamine system and the D2 receptors. They help by temporarily occupying the D2 receptors and then rapidly dissociating to allow normal dopamine transmission. It is thought that atypical drugs reduce side effects.

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Support for the effectiveness of these drugs has come from studying the relapse rates of people who take them alongside those who are taking a placebo, a fake drug. Davis et al (1980) looked at the results of 28 studies regarding relapse rates between typical antipsychotics and placebos, and found that people on a placebo were 55% more likely to relapse, whilst those on the drugs themselves were only 19% more likely to relapse. This clearly shows that antipsychotic drugs are effective in treating schizophrenia, as if they were not then we would not see such a low relapse rate in comparison to the placebos. The fact that they have significantly reduced this rate demonstrates that they combat the schizophrenic episodes with effectiveness. Yet, Ross and Read (2004) counter this conclusion and argue that it is illogical to state the drugs do effectively combat schizophrenia when compared to placebo’s, because 45% of people on the placebo’s did not relapse, which is still a significant number. This thus raises questions as to how effective the treatments actually are in comparison.

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Alongside this, Ross and Read take the argument into a wider context, and question the ethics of the studies Davis looked at. When putting a patient onto placebo’s, you are putting them into a drug withdrawal state, which means that the previously blocked dopamine system is suddenly overwhelmed by dopamine due to heightened sensitivity and an increased number of dopamine receptors. Not only does this make the comparison invalid, but it also raises ethical queries as we are essentially putting a patient back into their previous condition, causing their illness to get worse. Thus, the studies themselves can be criticised for being not only invalid, but highly unethical due to the fact that they place the patient in a pre-treatment state.

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Alongside this, Vaughn and Leff (1976) argue that antipsychotic drugs only help when you are in a hostile environment, as there was only a significant decrease of relapse rates while on such drugs in these conditions. In hostile environments, a patient has a 53% chance of relapsing if on typical antipsychotics, but a 92% chance of relapsing if on a placebo. However, when not in a hostile environment, these rates decrease to 15% for placebos and 12% for antipsychotic drugs. These immense difference immediately highlights to us that the environment a patient is in could play a bigger role in influencing treatment, thus making us question how effective they are alone.

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There is a consensus amongst psychiatrists that biological therapies alone cannot cure schizophrenia, because they simply target the symptoms and not the cause. Thus, psychological therapies are also used alongside such treatments.