Drug therapy

Question 1

Outline the dopamine hypothesis- refer to the mesolimbic and mesocortical pathways in your answer.

Answer 1

Evidence has shown positive symptoms such as auditory hallucinations result from hyperdopaminergia. Excess D2 dopamine receptors lead to high levels of dopamine in the pathways from the subcortical areas to the Broca’s area. The mesolimbic pathway: between the VTA (ventral tegmental area) and the NA (nucleus accumbens) is affected here.

negative symptoms may result from hypodopaminergia. here, there is a dysfunction in the mesocortical pathway (between the ventral tegmental area and the cortex, causing low levels of dopamine here. E.g pre-frontal cortex causes inattention.

Question 2

Outline typical antipsychotics for the treatment of schizophrenia.

Answer 2

Typical antipsychotics: Developed in the 1950s, for example Chlorpromazine. They act as dopamine antagonists, attempting to reduce dopamine activity. They block dopamine receptors on post-synaptic neurons, meaning that less dopamine is transmitted across the synapse. They work on hyperdopaminergia and the mesolimbic pathway. This has the effect of reducing dopamine production, and reduces positive symptoms such as hallucinations. Drugs such as Chlorpromazine also have a sedative effect, meaning that they calm patients down and reduce anxiety. As the drugs block dopamine activity, they tend to have (sometime severe) side-effects.

Question 3

Outline atypical antipsychotics as a treatment for schizophrenia.

Answer 3

Atypical antipsychotics: Developed in the 1970s, as an attempt to find drugs with fewer severe side-effects than typical antipsychotics. An example is Clozapine which is used when other drugs have failed, due to the risk of agranulocytosis (a potentially fatal blood condition). Clozapine acts in a similar way to Chlorpromazine, but also acts on serotonin and glutamate receptors. The effect of this is, as well as reducing positive symptoms, the reduction of depression and anxiety, and the enhancement of mood. It is therefore prescribed when the patient is at risk of suicide. Can have serious side effects such as agranulocytosis.

Risperidone is another atypical antipsychotic, and is designed to be as effective as Clozapine without the risky side-effects. It binds to dopamine receptors more strongly than Clozapine, meaning it can be given in a smaller dose with the same effectiveness, and there is some evidence that it produces fewer side-effects.

Question 4

What are some of the strengths for using drug therapy to treat schizophrenia?

Answer 4

+ Research support for effectiveness: Thornley et al (2003) found in a meta-analysis that Chlorpromazine was associated with better functioning and reduced symptom severity than placebos, supporting that the drug does have a positive effect on schizophrenia patients.

+enhanced quality of life: for patients who can live independently /outside of institutional care; for family members.

+economic implications eg cost in relation to other treatments / hospitalisation; analysis of benefit re ability of patient to return to work.

Question 5

What are some of the limitations for using biological treatments for schizophrenia?

Answer 5

• need to assess long-term benefits – many studies focus on short-term effects only
• Antipsychotic drugs are weakened by the fact that they have severe side-effects. For example, some patients on typical antipsychotics develop tardive dyskinesia- a condition where there are uncontrollable facial tics. Even after stopping the use of the drug, this condition can persist. Other side effects are potentially fatal, for example agranulocytosis and neuroleptic malignant syndrome (NMS). Side effects are less severe where patients are taking a reduced dose, as many do today, but this can reduce the effectiveness of the drug as well. The severity of the side-effects is a weakness as patients will be reluctant to take them, or may even die as a result of the effect.
• The effectiveness of chlorpromazine may be questioned due to it’s sedative effect. We do not know if the sedative effect is what reduces symptoms or the dopamine antagonist effect is actually in play as the drug claims to do.