4.3.5 - Drug therapy for schizophrenia

Medication and symptom management

A treatment can make a voice less intense without removing every difficulty in a person's life. Antipsychotic medication is used both to reduce psychotic symptoms during an episode and to lower the chance of relapse. To evaluate it, we need to connect receptor action to benefits, recognise effects in other pathways and ask which outcomes trials actually measured.

Antipsychotics are usually most effective for positive symptoms, such as hallucinations and delusions. Some drugs have calming or sedating effects relatively quickly, while improvement in hallucinations and delusional thinking is assessed over days or weeks; response varies. They can be prescribed during an acute episode and may also be used as maintenance treatment to reduce the risk of relapse.

The core biological idea is that many antipsychotics reduce the effect of dopamine in the brain. Dopamine is involved in reward, attention, movement and emotional salience. If dopamine activity in some pathways is too high, neutral events may feel unusually important or threatening, which can contribute to delusions and hallucinations. Blocking some dopamine activity can therefore reduce the intensity of psychotic experiences.

For exam purposes, do not write "antipsychotics cure schizophrenia". A better sentence is: antipsychotics can reduce the intensity of psychotic symptoms and help prevent relapse, but they do not remove all symptoms for everyone and they can cause significant side effects.

The two categories AQA names are:

Typical antipsychotics

Typical antipsychotics act mainly through dopamine receptor blockade, with benefits and risks that depend on the pathway affected.

Chlorpromazine is a first-generation example introduced in the 1950s. Its availability expanded the treatment options for psychosis. Changes in hospital care also depended on wider social policy and community support, so they cannot be attributed to medication alone.

Chlorpromazine works mainly as a D2 dopamine receptor antagonist. By blocking D2 receptors, especially in dopamine pathways linked to positive symptoms, it reduces dopamine transmission. In AO1 terms, this is why typical antipsychotics are most often linked to reduced hallucinations and delusions.

Chlorpromazine also has a sedating effect. This can be helpful when a person is extremely distressed, frightened or agitated during an acute episode. For example, if Maya is admitted to hospital because she believes voices are ordering strangers to harm her, a doctor may prescribe an antipsychotic to reduce agitation first, then monitor whether her delusions and hallucinations reduce over the following days or weeks.

The same dopamine blockade that can help symptoms can also create problems. Dopamine is involved in movement control, especially in motor pathways involving the basal ganglia. When typical antipsychotics block dopamine outside the therapeutic target pathways, they can cause extrapyramidal side effects.

Typical antipsychotic side effects can include drowsiness, dizziness, dry mouth, constipation, weight gain, tremors, stiffness, muscle spasms and tardive dyskinesia. A rare but serious reaction is neuroleptic malignant syndrome, which can involve high temperature, muscle rigidity, confusion and autonomic instability. You do not need to diagnose these conditions, but you should be able to use them in AO3 to explain why drug therapy involves a cost-benefit decision.

The evaluation point is not simply "side effects are bad". A stronger point is that side effects reduce appropriateness and effectiveness. If a patient feels sedated, gains weight, develops tremors or fears long-term movement problems, they may stop taking medication. Stopping suddenly can increase relapse risk, so side effects can indirectly reduce the success of the treatment.

Atypical antipsychotics

Atypical antipsychotics differ in their receptor effects and side-effect profiles, so the category does not identify one uniformly safer drug.

Atypical antipsychotics were developed to keep the benefits of antipsychotic medication while reducing the more severe motor side effects associated with older typical drugs. The most important examples for AQA are clozapine and risperidone.

Clozapine is a special case. It affects several receptor systems, including dopamine and serotonin, and has established value for treatment-resistant schizophrenia. NICE guidance states that adults whose schizophrenia has not responded adequately to at least two antipsychotic drugs, including at least one non-clozapine second-generation drug, should be offered clozapine after appropriate clinical review. This makes clozapine a strong AO3 point: atypical antipsychotics are not just "newer"; some can be clinically important when standard treatment has failed.

The major drawback is safety. Clozapine can cause serious adverse effects, including severe constipation, weight gain and, most famously, agranulocytosis, a dangerous fall in white blood cells. Because of this, people taking clozapine need regular blood monitoring. This is why clozapine is usually reserved for cases where other antipsychotics have not worked well enough.

Risperidone is another atypical antipsychotic. It acts on dopamine and serotonin receptors and can be taken in oral form or, in some cases, as a long-acting injection. Risperidone is useful because it shows the more realistic modern view of atypical drugs: they may have advantages over many typical antipsychotics, but they are not automatically better for every patient. Risperidone can still cause side effects such as weight gain, hormonal effects and movement problems, especially at higher doses or for some individuals.

This matters for AO2. Suppose Jay has distressing auditory hallucinations but is terrified of needles and has previously stopped medication because of tremors. A psychiatrist should not simply choose "the strongest drug". NICE guidance emphasises shared decision-making, likely benefits, possible side effects and what side effects the person is most willing to tolerate. Drug therapy is therefore a biological treatment, but its success depends on psychological and practical factors too.