Typical antipsychotics | AQA A-Level Psychology Revision

For 7182 specification, first teach in September 2025

AQA A-Level Psychology | Free Revision Notes

Estimated study time: 60 minutes

Typical antipsychotics are biological treatments used to reduce symptoms of schizophrenia. These Typical antipsychotics A-Level Psychology revision notes explain how drugs such as chlorpromazine reduce dopamine activity by blocking receptor sites.

Typical antipsychotics are generally more effective against positive symptoms such as hallucinations and delusions than negative symptoms such as avolition. Their use must be evaluated by balancing symptom reduction against side effects, adherence, relapse and ethical concerns. The current AQA specification requires knowledge of both typical and atypical antipsychotic drug therapy.

Learning Objectives 🎯

By the end of this revision page, you should be able to:

• Explain how typical antipsychotics are administered and used.

• Explain the action of dopamine antagonists at the synapse.

• Link typical antipsychotics to the dopamine hypothesis.

• Explain why the drugs are generally more effective against positive symptoms.

• Distinguish effectiveness from appropriateness.

• Evaluate typical antipsychotics using evidence, side effects and ethical considerations.

Revision Notes 📚

Typical antipsychotics A-Level Psychology revision overview

Antipsychotics are drugs used to reduce or manage symptoms associated with psychosis.

Psychosis can involve experiences such as:

• Hallucinations.

• Delusions.

• Disturbed thinking.

• Disorganised behaviour.

The AQA specification distinguishes between:

1. Typical antipsychotics

2. Atypical antipsychotics

Typical antipsychotics are the older or first-generation class.

They are commonly described as dopamine antagonists because they reduce dopamine activity by blocking dopamine receptor sites.

The best-known example used in A-Level Psychology is:

chlorpromazine

AQA directly assessed the mechanism in 2024. The correct explanation was that typical antipsychotics block dopamine receptor sites.

What does “typical” mean?

The word typical does not mean:

• Ordinary.

• Weak.

• Suitable for everyone.

• The most frequently prescribed drug in every situation.

It refers to the older class of conventional antipsychotic drugs developed before newer atypical drugs.

Typical antipsychotics are also known as:

• First-generation antipsychotics.

• Conventional antipsychotics.

• Neuroleptic drugs.

The terms describe a class of medication rather than one individual drug.

Chlorpromazine

What is chlorpromazine?

Chlorpromazine is a typical antipsychotic used to manage symptoms of schizophrenia and other psychotic conditions.

Its main antipsychotic action is usually explained through:

• Blocking dopamine receptor sites.

• Reducing dopamine transmission.

• Decreasing the effect of dopamine on postsynaptic neurons.

Chlorpromazine has historically been especially important because it helped transform the treatment of psychosis.

Before effective antipsychotic medication, some people experiencing severe psychosis required:

• Long-term hospitalisation.

• Extensive supervision.

• Physical restraint.

• Highly restrictive care.

Medication made it possible for many people to experience reduced symptoms and live outside long-term institutions. AQA recognises this historical transformation as an important evaluation point.

Chlorpromazine does not remove dopamine

It is inaccurate to say that chlorpromazine:

• Destroys dopamine.

• Removes all dopamine from the brain.

• Stops the brain making dopamine.

• Prevents dopamine reuptake.

Instead, it occupies or blocks some dopamine receptor sites.

Dopamine may still be released into the synapse, but its ability to stimulate the postsynaptic neuron is reduced.

How typical antipsychotics are administered

Typical antipsychotics may be administered in different forms.

Tablets or liquid medication

The person may take the drug orally each day.

Advantages

• Non-invasive.

• Dosage can be adjusted.

• The person can take the medication at home.

• Treatment can be stopped or changed under medical supervision.

Limitations

• The person must remember to take each dose.

• Medication can be deliberately or accidentally missed.

• Side effects may lead to discontinuation.

• Symptoms may make adherence difficult.

Injection

Medication may be given by injection.

This can be useful where:

• Rapid clinical management is required.

• Oral medication cannot be taken.

• The individual has difficulty following an oral regimen.

Injection is more invasive and may raise concerns about:

• Consent.

• Distress.

• Control.

• The professional’s power over the person.

Depot injection

A depot injection releases medication gradually over an extended period.

This means that the person does not need to take a tablet every day.

Possible advantages

• Reduces accidental missed doses.

• Provides more stable medication delivery.

• Makes adherence easier to monitor.

• May lower relapse associated with abruptly stopping medication.

Possible limitations

• Once injected, the drug cannot be removed immediately.

• Side effects may continue until the dose wears off.

• The person may experience the treatment as controlling.

• Informed consent remains essential.

📌 Exam precision: The method of administration is not the same as the biological mechanism. A depot injection describes how the drug enters the body. Dopamine-receptor blockade describes how it works.

How typical antipsychotics work

Synaptic transmission

A synapse is the small gap between two neurons.

Normal dopamine transmission can be simplified as follows:

1. An electrical impulse reaches the presynaptic neuron.

2. Dopamine is released into the synaptic cleft.

3. Dopamine crosses the synapse.

4. It binds with dopamine receptors on the postsynaptic neuron.

5. The postsynaptic neuron is stimulated.

Typical antipsychotics interfere with stage 4.

Dopamine antagonism

An antagonist is a substance that reduces the action of a neurotransmitter.

Typical antipsychotics act mainly as dopamine antagonists.

The process is:

1. The antipsychotic reaches the brain.

2. Its molecules occupy dopamine receptor sites.

3. Dopamine has fewer available receptors to bind with.

4. Postsynaptic stimulation is reduced.

5. Activity in relevant dopamine pathways decreases.

6. Positive symptoms may become less severe.

The treatment pathway can be remembered as:

receptor blockade → reduced dopamine action → reduced positive symptoms

D2 receptor blockade

Typical antipsychotics particularly block D2 dopamine receptors.

D2 receptors are one type of receptor that responds to dopamine.

When chlorpromazine occupies these receptors:

• Dopamine cannot bind as readily.

• Dopamine transmission is reduced.

• Excessive stimulation in relevant pathways is lowered.

The drug therefore does not need to remove dopamine itself.

It reduces dopamine’s effect on the next neuron.

Typical antipsychotics and the dopamine hypothesis

The treatment links directly with dopamine activity and neural explanations.

The revised dopamine hypothesis proposes that positive symptoms are associated with excessive dopamine activity in some subcortical pathways.

Typical antipsychotics reduce this activity by blocking dopamine receptors.

The connection is:

excessive subcortical dopamine activity → hallucinations and delusionsD2 receptor blockade → reduced dopamine transmission → reduction in positive symptoms

Treatment as evidence for the dopamine hypothesis

When dopamine-blocking medication reduces hallucinations or delusions, this supports the idea that dopamine contributes to those symptoms.

The reasoning is:

1. The drug reduces dopamine activity.

2. Positive symptoms become less severe.

3. Dopamine activity is therefore likely to be involved.

However, this is supportive evidence rather than proof that excess dopamine was the original cause.

A treatment can interrupt a symptom-producing process without correcting the factor that first created the condition.

Which symptoms are treated most effectively?

Positive symptoms

Typical antipsychotics are particularly associated with reducing positive symptoms, including:

• Hallucinations.

• Delusions.

• Severe agitation linked with psychosis.

• Some forms of disorganised thought or behaviour.

These symptoms are reviewed in added and reduced psychological functioning.

Hallucinations

If excessive dopamine activity makes internally generated information unusually vivid or important, blocking dopamine receptors may reduce that abnormal stimulation.

The hallucination may then become:

• Less frequent.

• Less intense.

• Less distressing.

• Easier to ignore.

Delusions

If excessive dopamine activity causes neutral events to gain abnormal significance, receptor blockade may reduce this experience of excessive salience.

Delusional beliefs may become:

• Less intense.

• Less dominant.

• Less emotionally distressing.

• More open to alternative interpretation.

Medication does not necessarily cause a belief to disappear immediately.

Psychological support may still be needed to examine beliefs developed during the period of psychosis.

Negative symptoms

Typical antipsychotics are usually less effective against negative symptoms such as:

• Speech poverty.

• Avolition.

This fits the revised dopamine hypothesis because negative symptoms may involve reduced dopamine activity in cortical or reward-related regions.

Blocking dopamine receptors more widely is unlikely to correct an existing dopamine deficit.

It may sometimes make motivational or movement difficulties more noticeable.

AQA’s 2022 mark scheme identifies greater effectiveness for positive symptoms as an important evaluative point.

Symptom reduction is not the same as a cure

Typical antipsychotics are generally described as managing symptoms.

They do not necessarily:

• Remove genetic vulnerability.

• Reverse all neural differences.

• Change dysfunctional family communication.

• Resolve traumatic or stressful experiences.

• Teach coping strategies.

• Challenge established beliefs.

• Prevent every future episode.

A person may need to continue medication after symptoms improve to reduce the risk of relapse.

The treatment may therefore be:

• Acute, reducing current symptoms.

• Maintenance-based, reducing the likelihood of symptoms returning.

Acute treatment

Acute treatment is treatment given during a period of severe or rapidly worsening symptoms.

The aim may be to:

• Reduce hallucinations.

• Reduce delusional distress.

• Lower severe agitation.

• Improve safety.

• Enable further psychological treatment.

A person experiencing intense psychosis may initially struggle to take part in a demanding talking therapy.

Medication may reduce symptoms enough for them to engage more effectively with:

• challenging beliefs and interpretations 

• reducing family stress and improving communication 

Maintenance treatment

Maintenance treatment continues after the most severe symptoms have reduced.

Its purpose may be to:

• Prevent relapse.

• Maintain functioning.

• Reduce repeated hospital admission.

• Support community living.

• Allow psychological and social rehabilitation to continue.

Stopping medication suddenly may increase the risk of symptoms returning.

However, continuing treatment must be balanced against:

• Side effects.

• The person’s preferences.

• Previous relapse history.

• Effectiveness for that individual.

• The possibility of alternative treatments.

Adherence

What is adherence?

Adherence means following an agreed treatment plan.

For antipsychotic medication, this may involve:

• Taking the correct dose.

• Taking it at the agreed time.

• Continuing for the agreed period.

• Attending monitoring appointments.

• Reporting side effects.

Why adherence may be difficult

A person may stop medication because:

• Side effects are unpleasant.

• They feel better and believe it is no longer needed.

• They do not believe they are unwell.

• They forget doses.

• Their routine is disrupted.

• They dislike feeling controlled.

• They do not trust healthcare professionals.

• The medication does not seem effective.

The June 2024 examiner report noted that students often developed a side-effect criticism by explaining that unpleasant effects may lead people to discontinue treatment.

Adherence and relapse

If medication is effective but then discontinued, symptoms may return.

This can create a cycle:

treatment → improvement → medication stopped → relapse → readmission → treatment restarted

Repeated movement between hospital and community care is sometimes called a revolving-door pattern.

This raises questions about:

• Long-term effectiveness.

• Appropriateness.

• Support for adherence.

• Whether medication is being combined with psychological therapy.

Effectiveness and appropriateness

These terms should be distinguished clearly.

Effectiveness

Effectiveness asks:

Does the treatment produce its intended outcome?

Relevant outcomes include:

• Reduced hallucinations.

• Reduced delusions.

• Lower symptom scores.

• Fewer relapses.

• Fewer hospital admissions.

• Improved everyday functioning.

• Better quality of life.

Appropriateness

Appropriateness asks:

Is this treatment suitable and acceptable for this person?

Relevant considerations include:

• Side effects.

• Informed consent.

• Symptom profile.

• Physical health.

• Personal preferences.

• Ability to follow the regimen.

• Long-term risks and benefits.

• Availability of alternative treatments.

A drug can be effective but inappropriate.

For example:

Chlorpromazine substantially reduces a person’s hallucinations, but severe movement-related side effects make continued treatment unsuitable.

A drug can also be appropriate but only moderately effective.

For example:

The person tolerates a low dose well, but only some symptoms improve.

Evaluating effectiveness

Evidence from chlorpromazine research

AQA identifies research comparing chlorpromazine with placebo and meta-analyses of chlorpromazine studies as relevant evidence when evaluating antipsychotic treatment.

Examples accepted by AQA include:

• Adams’ meta-analysis of chlorpromazine studies.

• Thornley’s comparison of chlorpromazine with placebo.

Such research generally supports the conclusion that chlorpromazine can reduce symptoms more effectively than inactive placebo treatment for many patients.

Why placebo comparisons are useful

A placebo is an inactive treatment designed to resemble the actual medication.

A placebo group helps researchers determine whether improvement results from:

• The pharmacological action of the drug.

• Expectations of improvement.

• Attention from healthcare professionals.

• Natural changes in symptoms.

• Passage of time.

If the drug group improves more than the placebo group, this strengthens the argument that the active medication produced an effect.

The placebo effect

The placebo effect occurs when expectations or the treatment context produce improvement despite the absence of an active ingredient.

People may improve because they:

• Expect to feel better.

• Receive increased attention.

• Feel reassured by treatment.

• Change their behaviour while being monitored.

A suitable placebo condition helps separate these effects from dopamine-receptor blockade.

Meta-analysis

A meta-analysis statistically combines results from several studies.

AQA directly identified meta-analysis as an appropriate way to combine evidence about drug effectiveness in the 2024 paper.

Strengths

• Produces a larger combined sample.

• Increases statistical power.

• Reduces reliance on one unusual study.

• Allows an overall treatment effect to be estimated.

• Can examine variation between studies.

Limitations

• Poor-quality original studies weaken the combined result.

• Studies may use different doses and outcome measures.

• Participants may have different symptom profiles.

• Unpublished negative findings may be missing.

• Combining highly different studies may conceal meaningful variation.

Relative effectiveness

Typical antipsychotics may be more effective for some outcomes than others.

More successful outcomes

They may reduce:

• Hallucinations.

• Delusions.

• Severe psychotic agitation.

• Immediate risk associated with severe symptoms.

Less successful outcomes

They may have less effect on:

• Avolition.

• Speech poverty.

• Cognitive difficulties.

• Social skills.

• Employment.

• Relationships.

• The causes of psychological distress.

A complete evaluation should therefore avoid saying simply:

“Typical antipsychotics work.”

Instead, ask:

• For which symptoms?

• For which patients?

• Over what period?

• Compared with what?

• At what cost?

Individual differences in effectiveness

Not every person responds in the same way.

Possible differences include:

• The dominant symptoms.

• Biological variation.

• Receptor sensitivity.

• Length of illness.

• Co-morbid conditions.

• Previous treatment.

• Medication adherence.

• Environmental stress.

• Psychological support.

One person may show a major reduction in hallucinations.

Another may show little improvement despite taking the same drug.

This means treatment effectiveness should be evaluated at both:

• Group level.

• Individual level.

Side effects

Why side effects occur

Dopamine is involved in functions beyond psychotic symptoms.

It contributes to:

• Movement.

• Motivation.

• Reward.

• Hormonal regulation.

• Cognitive functioning.

Typical antipsychotics do not block dopamine only in the pathway associated with positive symptoms.

They can also reduce dopamine action elsewhere.

This produces unwanted effects.

Commonly discussed side effects

AQA mark schemes identify examples including:

• Dry mouth.

• Weight gain.

• Muscle tremors.

Other movement-related effects may include:

• Muscle stiffness.

• Restlessness.

• Slowed movement.

• Involuntary movements.

The severity varies between drugs and individuals.

Movement-related side effects

Dopamine contributes to motor control.

Blocking dopamine receptors in movement-related pathways can produce effects resembling movement disorders.

The person may experience:

• Shaking.

• Stiffness.

• Difficulty initiating movement.

• Restlessness.

• Involuntary facial or body movements.

These effects can interfere with:

• Eating.

• Speaking.

• Walking.

• Working.

• Social interaction.

Tardive dyskinesia

Tardive dyskinesia involves persistent involuntary movements that may emerge following longer-term antipsychotic treatment.

Possible movements can affect:

• The face.

• Mouth.

• Tongue.

• Limbs.

The risk is important when balancing long-term benefits and harms.

Not every person develops this effect, but the possibility requires monitoring.

Sedation and reduced alertness

Some typical antipsychotics can make a person feel:

• Tired.

• Drowsy.

• Slowed down.

• Less alert.

Sedation may be useful temporarily when a person is severely agitated.

However, continuing sedation can reduce:

• Independence.

• Concentration.

• Employment or study.

• Social activity.

• Quality of life.

Symptom reduction achieved mainly by making a person heavily sedated would not necessarily represent meaningful recovery.

Weight gain and physical health

Weight gain may affect:

• Physical health.

• Self-esteem.

• Willingness to continue treatment.

• Long-term quality of life.

The clinical decision must therefore compare:

likely psychological benefit versus physical cost

Side effects and appropriateness

A side effect does not automatically mean a drug is inappropriate.

The decision depends on:

• Severity of the psychosis.

• Severity of the side effect.

• Availability of alternatives.

• Whether the side effect can be managed.

• The person’s preferences.

• Risk of untreated symptoms.

For example:

Mild dry mouth may be considered an acceptable cost if distressing hallucinations reduce substantially.

In contrast:

Severe persistent movement difficulties may outweigh a modest reduction in symptoms.

Appropriateness therefore involves a cost-benefit analysis.

Masking symptoms rather than treating causes

AQA accepts the criticism that drug therapy may mask symptoms rather than address the cause of schizophrenia.

Typical antipsychotics may reduce:

• Voices.

• Delusional intensity.

• Agitation.

They do not necessarily address:

• Dysfunctional interpretations.

• Family stress.

• Social isolation.

• Trauma.

• Poverty.

• Genetic vulnerability.

• Reasons for treatment non-adherence.

The treatment may therefore manage the biological mechanism involved in symptoms without resolving the wider problem.

Counterargument

Reducing symptoms can still be extremely valuable.

If medication lowers severe hallucinations or delusions, the person may become better able to:

• Sleep.

• Communicate.

• Return home.

• Engage in therapy.

• Rebuild relationships.

• Manage everyday tasks.

Treating the immediate symptom does not become worthless simply because every original cause remains unresolved.

Treatment versus cure

Typical antipsychotics are more accurately described as treatments or management strategies than cures.

A cure would imply that:

• The underlying vulnerability has been removed.

• Treatment is no longer required.

• Symptoms will not return.

Antipsychotics often require continuing use, and relapse may occur after treatment ends.

A strong evaluation asks whether success is measured through:

• Short-term symptom suppression.

• Long-term recovery.

• Relapse prevention.

• Quality of life.

• Independent functioning.

Short-term and long-term effectiveness

Short-term benefits

Typical antipsychotics may:

• Reduce acute positive symptoms.

• Lower severe distress.

• Allow discharge from hospital.

• Enable psychological therapy.

• Reduce the need for restrictive care.

Long-term limitations

Long-term treatment may involve:

• Side effects.

• Discontinuation.

• Relapse.

• Reduced effectiveness for negative symptoms.

• Dependence on continuing medication.

• Repeated admission when treatment stops.

AQA identifies the distinction between short-term and long-term benefits and the possibility of relapse as relevant evaluation.

Historical value

Typical antipsychotics transformed the management of severe psychosis.

Before antipsychotic treatment

People with severe symptoms might experience:

• Long-term institutionalisation.

• Physical restraint.

• Limited independence.

• Fewer opportunities for community care.

Following the introduction of antipsychotics

Medication allowed many patients to:

• Experience fewer positive symptoms.

• Leave long-stay hospitals.

• Receive outpatient treatment.

• Live with family or independently.

• Engage with psychological support.

This historical effect is a significant practical strength.

Critical interpretation

Reduced hospitalisation does not prove complete recovery.

Community care without sufficient:

• Housing.

• Psychological therapy.

• Social support.

• Employment support.

• Physical-health monitoring.

may leave people isolated or vulnerable to relapse.

Medication needs to form part of a broader care plan.

Economic implications

Possible economic benefits

Typical antipsychotics may be relatively economical because:

• Drugs can be administered without lengthy therapy sessions.

• Medication may reduce hospital admission.

• Generic drugs can be inexpensive.

• One clinician can supervise medication for many patients.

• Symptom reduction may allow a return to employment or education.

Possible economic costs

Costs can include:

• Monitoring side effects.

• Treating physical complications.

• Repeated admission following relapse.

• Long-term prescriptions.

• Support where negative symptoms remain.

• Loss of work caused by sedation or side effects.

The 2022 examiner report warned that vague claims such as “drugs save time and money” were not creditworthy without a reasoned explanation.

A developed argument explains:

what becomes cheaper or quicker, for whom, and with what possible counter-cost

Ethical issues

Informed consent

A person should understand:

• What medication is being offered.

• Its intended benefits.

• Possible side effects.

• Available alternatives.

• What may happen if treatment is refused.

Severe psychosis can sometimes make informed decision-making difficult.

This creates tension between:

• Respecting autonomy.

• Protecting the person or others.

• Providing effective treatment.

Control

Medication may be used in circumstances where the person feels they have little choice.

AQA’s 2024 mark scheme identifies control as a relevant ethical issue in drug treatment.

Concerns may arise where:

• Treatment is compulsory.

• Medication is administered by injection.

• The person is not meaningfully involved in decisions.

• Sedation is used mainly to make behaviour easier to manage.

Chemical restraint

The term chemical restraint may be used when medication primarily controls behaviour rather than treating the person in their own interests.

This is ethically concerning because it prioritises:

• Institutional convenience.

• Staff control.

• Compliance.

over:

• Autonomy.

• Wellbeing.

• Meaningful recovery.

Medication prescribed to relieve severe distress is not automatically chemical restraint.

The issue concerns:

• Purpose.

• Dosage.

• Consent.

• Monitoring.

• Proportionality.

Right to refuse treatment

A competent patient may decide that:

• Side effects are intolerable.

• Another treatment is preferable.

• The benefits do not justify the costs.

Healthcare professionals may disagree with this decision, particularly where relapse risk is high.

Ethical treatment requires the person to be involved in decisions wherever possible.

Biological reductionism

Typical antipsychotics reflect a biological approach.

The treatment reduces complex experiences to neurotransmitter activity.

This can be useful because:

• Dopamine activity is measurable.

• The mechanism can be investigated scientifically.

• Precise drugs can be developed.

• Predictions about symptom reduction can be tested.

However, schizophrenia also involves:

• Beliefs.

• Relationships.

• Social conditions.

• Stress.

• Culture.

• Personal meaning.

Medication alone may therefore be biologically reductionist.

The strengths and weaknesses of this level of explanation are explored through biological and environmental levels of explanation.

Biological determinism

Drug treatment may encourage the view that symptoms are controlled entirely by brain chemistry.

This can reduce blame because schizophrenia is not treated as a personal weakness.

However, it may also create:

• Fatalism.

• Pessimism about recovery.

• Belief that psychological treatment is pointless.

• A passive patient role.

In practice, neural activity is influenced by:

• Stress.

• Learning.

• Relationships.

• Medication.

• Psychological therapy.

A biological treatment can be important without being the only useful intervention.

The medical model

Typical antipsychotics are consistent with the medical model.

The medical model treats schizophrenia as a condition involving:

• Identifiable symptoms.

• Biological dysfunction.

• Clinical diagnosis.

• Medical treatment.

Strengths

• Encourages systematic treatment.

• Reduces moral blame.

• Supports biological research.

• Provides a clear route to symptom management.

Limitations

• May overlook social context.

• Can place the patient in a passive role.

• May prioritise symptom suppression over personal recovery.

• Can encourage overreliance on medication.

Typical and atypical antipsychotics

Typical drugs should not be confused with newer broader-acting drug treatments.

Typical antipsychotics	Atypical antipsychotics
Older, first-generation drugs	Newer, second-generation drugs
Chlorpromazine is a key example	Clozapine and risperidone are common examples
Strong D2 dopamine-receptor blockade	Act on dopamine and often other neurotransmitter systems
Mainly effective against positive symptoms	May have a broader symptom profile
Greater concern about some movement-related effects	Different side-effect profile
Still effective for many patients	May be used when typical drugs are unsuitable

The full comparison belongs in the next lesson.

For this lesson, remember:

Typical antipsychotics primarily reduce dopamine activity by blocking receptor sites.

Combining treatments

Typical antipsychotics may be used alongside psychological treatments.

Medication and CBT

Medication may reduce the intensity of hallucinations or delusions.

CBT can then help the person:

• Examine beliefs.

• Consider alternative explanations.

• Develop strategies for responding to voices.

• Reduce distress.

This combination is developed in biological and psychological treatments working together.

Medication and family therapy

Medication may reduce current symptoms.

Family therapy may:

• Reduce expressed emotion.

• Improve communication.

• Support adherence.

• Reduce relapse-related stress.

Why combination may be more appropriate

Different treatments address different parts of the problem.

Treatment	Main focus
Typical antipsychotic	Dopamine activity and positive symptoms
CBT	Beliefs, interpretations and coping
Family therapy	Communication, stress and relapse
Combined treatment	Biological and psychosocial needs

Medication alone may be insufficient, but psychological therapy may also be difficult during severe untreated psychosis.

Applying typical antipsychotics

Scenario 1: positive symptoms

Caleb hears threatening voices and believes that strangers are following him. His psychiatrist prescribes chlorpromazine.

A developed explanation would state:

• Caleb experiences positive symptoms.

• Chlorpromazine is a typical antipsychotic.

• It acts as a dopamine antagonist.

• It blocks D2 receptor sites.

• Fewer dopamine molecules stimulate postsynaptic neurons.

• Reduced dopamine activity may lessen Caleb’s hallucinations and delusions.

Scenario 2: misunderstanding the mechanism

A student says that chlorpromazine prevents dopamine from being reabsorbed, so less dopamine is available.

This is incorrect.

Preventing reuptake would usually leave more neurotransmitter in the synapse.

The accurate explanation is:

Chlorpromazine blocks dopamine receptor sites and reduces dopamine’s effect on the postsynaptic neuron.

Scenario 3: side effects and adherence

Maya’s hallucinations become less severe after taking a typical antipsychotic, but she develops muscle tremors and stops taking it.

This illustrates:

• Some effectiveness against positive symptoms.

• A movement-related side effect.

• Reduced treatment appropriateness.

• Non-adherence.

• Increased risk of relapse after discontinuation.

Scenario 4: maintenance treatment

Tariq’s hallucinations have stopped, but his clinician recommends continuing medication.

The recommendation may be based on:

• Preventing symptoms from returning.

• Tariq’s previous relapse history.

• The treatment’s maintenance role.

However, continuing treatment should still involve:

• Reviewing side effects.

• Consulting Tariq.

• Considering dosage and alternatives.

• Monitoring long-term wellbeing.

Scenario 5: medication and negative symptoms

Asha’s delusions improve, but she remains unable to begin everyday tasks.

This pattern is consistent with:

• Typical antipsychotics being effective against a positive symptom.

• Limited effectiveness against avolition.

• Different neural mechanisms contributing to negative symptoms.

• A need for additional psychological or practical support.

Evaluating drug research

Randomised controlled trials

Participants may be randomly allocated to:

• A typical-antipsychotic group.

• A placebo group.

• An alternative-treatment group.

Random allocation helps distribute participant differences between groups.

These differences might include:

• Symptom severity.

• Age.

• Previous treatment.

• Motivation.

• Physical health.

Single-blind procedure

In a single-blind procedure, participants do not know whether they receive the active drug or placebo.

This reduces demand characteristics because expectations are less likely to differ between groups.

Double-blind procedure

In a double-blind procedure:

• Participants do not know their condition.

• The professionals assessing outcomes do not know the condition.

This reduces:

• Demand characteristics.

• Investigator effects.

• Biased symptom ratings.

AQA’s 2023 mark scheme accepted double-blind procedures as a way of reducing both participant expectations and investigator effects in antipsychotic research.

Standardisation

Researchers should standardise:

• Dosage schedules.

• Instructions.

• Assessment timing.

• Contact with professionals.

• Symptom-measurement procedures.

Standardisation increases reliability.

Problems with placebo studies

Placebo-controlled research can raise ethical questions.

If an effective treatment already exists, withholding it from someone with severe psychosis may expose them to:

• Distress.

• Risk.

• Functional deterioration.

Researchers may instead compare:

• A new drug with an existing drug.

• Standard treatment with an additional intervention.

• Different dosages.

Measuring treatment outcomes

Effectiveness should not be judged from one measure alone.

Symptom scales

Clinicians may rate:

• Hallucinations.

• Delusions.

• Negative symptoms.

• General functioning.

Strength

Produces standardised numerical data.

Limitation

Ratings may depend on clinical judgement.

Self-report

The person describes their:

• Symptoms.

• Distress.

• Side effects.

• Quality of life.

Strength

Captures the person’s own experience.

Limitation

Communication difficulties or fear of treatment changes may affect reporting.

Behavioural outcomes

Researchers may measure:

• Hospital readmission.

• Employment.

• Education.

• Independent living.

• Social activity.

These outcomes may be meaningful but are also influenced by housing, support and economic circumstances.

Relapse rates

Relapse provides an important long-term measure.

However, researchers must define relapse clearly, for example:

• Return of severe symptoms.

• Readmission to hospital.

• Need for crisis treatment.

• Increase on a standardised symptom scale.

Different definitions can produce different results.

Attrition

Attrition occurs when participants leave a study before it ends.

Participants may withdraw because:

• The drug is ineffective.

• Side effects are severe.

• They do not wish to continue.

• Their symptoms worsen.

• They struggle to attend assessments.

If only people who complete treatment are analysed, the medication may appear more effective and acceptable than it really is.

Completer analysis

A completer analysis includes only participants who finish treatment.

This may exaggerate effectiveness because people experiencing the greatest problems have been excluded.

Intention-to-treat analysis

An intention-to-treat analysis includes participants in the groups to which they were originally assigned, even where they discontinue treatment.

This gives a more realistic estimate of how well the treatment works in ordinary clinical practice.

Publication bias

Publication bias occurs when studies with positive findings are more likely to be published than studies finding little or no benefit.

A review based mainly on published studies may therefore overestimate effectiveness.

Researchers conducting a meta-analysis should attempt to include:

• Published trials.

• Unpublished trials.

• Studies with positive and negative findings.

Symptom reduction and quality of life

A drug can lower a clinical symptom score while failing to improve the person’s everyday life.

For example:

• Voices reduce but severe sedation prevents work.

• Delusions lessen but movement side effects restrict social activity.

• Hospital admission falls but the person remains isolated.

• Positive symptoms improve while avolition remains severe.

A complete evaluation should therefore consider:

symptom change + side effects + functioning + the person’s own evaluation

Overall assessment of typical antipsychotics

Main strengths

• Can reduce severe positive symptoms.

• Supported by placebo-controlled and review evidence.

• Have major historical and practical value.

• May reduce hospitalisation.

• Can enable participation in psychological therapy.

• May help prevent relapse when treatment is continued.

• Biological mechanism is clearly testable.

Main limitations

• Less effective against many negative symptoms.

• Can produce significant side effects.

• Side effects may reduce adherence.

• Symptoms may return after discontinuation.

• They manage symptoms rather than every underlying cause.

• Individual responses vary.

• Treatment may raise issues of consent and control.

• Drug studies can be affected by attrition and publication bias.

• Medication alone may be biologically reductionist.

Balanced conclusion

Typical antipsychotics are neither:

• A useless chemical restraint in every case.

• A complete cure suitable for everyone.

They can be highly valuable when:

• Positive symptoms are severe.

• The person responds well.

• Side effects are monitored.

• Consent and preferences are respected.

• Medication is reviewed regularly.

• Psychological and social support are also available.

Hints from the Examiner Reports 💡

Examiner hint: Learn the drug mechanism precisely.

Typical antipsychotics:

block dopamine receptor sites

They do not prevent dopamine reuptake.

In the 2024 multiple-choice question, many students incorrectly selected an option stating that the drugs both blocked receptors and prevented reuptake.

Examiner hint: Do not write only that chlorpromazine “reduces dopamine”.

A developed answer should include:

1. Dopamine is released into a synapse.

2. Chlorpromazine occupies D2 receptor sites.

3. Dopamine cannot bind as readily.

4. Postsynaptic stimulation is reduced.

5. Positive symptoms may decrease.

Examiner hint: Match the content to the command word.

The 2022 question asked students only to evaluate antipsychotics. Students who spent substantial time describing drug action wasted time because the marks were entirely AO3.

Examiner hint: Avoid the unsupported statement:

“Drugs work.”

State:

• Which drug or drug class.

• Which symptoms improve.

• What comparison was made.

• What limitation remains.

Examiner hint: Develop side-effect points.

The 2024 examiner report noted that successful students often explained that side effects may lead to discontinuation. The full chain is:

side effect → treatment stopped → dopamine blockade ends → relapse risk increases

Examiner hint: AQA accepts dry mouth, weight gain and muscle tremors as examples of drug side effects. Name the effect and explain why it reduces appropriateness.

Examiner hint: Reason through time and cost.

Weak:

“Drugs are cheap and fast.”

Stronger:

“Medication can be administered without repeated lengthy therapy sessions and may reduce costly hospital admission. However, long-term prescribing and treatment of side effects create continuing costs.”

Examiner hint: When discussing effectiveness, distinguish:

• Positive from negative symptoms.

• Short-term symptom reduction from long-term relapse.

• Clinical symptom scores from everyday quality of life.

Examiner hint: Explain why a double-blind procedure is useful.

• Participants’ expectations are controlled.

• Assessors’ expectations are controlled.

• Differences in symptom ratings are therefore less likely to result from demand characteristics or investigator effects.

Examiner hint: Do not argue that successful drug treatment proves the dopamine hypothesis.

It supports dopamine involvement, but symptom improvement does not identify the original cause of schizophrenia.

Common Mistakes ⚠️

Mistake: Saying typical means commonly experienced

Why this is incorrect:

Typical refers to the older first-generation class of antipsychotic medication.

How to improve:

Use the terms “conventional” or “first-generation”.

Mistake: Saying chlorpromazine is an atypical antipsychotic

Why this is incorrect:

Chlorpromazine is a typical antipsychotic.

How to improve:

Remember:

chlorpromazine = conventional

Mistake: Saying typical antipsychotics increase dopamine

Why this is incorrect:

They reduce dopamine activity.

How to improve:

Describe them as dopamine antagonists.

Mistake: Saying typical antipsychotics prevent dopamine reuptake

Why this is incorrect:

Preventing reuptake would leave more dopamine in the synapse.

How to improve:

State that they block receptor sites.

Mistake: Saying the drug destroys dopamine receptors

Why this is incorrect:

The drug temporarily occupies or blocks receptor sites.

How to improve:

Use “receptor blockade” rather than “destruction”.

Mistake: Saying D2 receptors release dopamine

Why this is incorrect:

Dopamine is released by the presynaptic neuron and binds to receptors on another neuron.

How to improve:

Keep neurotransmitter release and receptor binding separate.

Mistake: Saying typical antipsychotics cure schizophrenia

Why this is too strong:

Symptoms can return, and treatment does not remove every underlying influence.

How to improve:

Describe symptom management and relapse prevention.

Mistake: Saying the drugs are equally effective for all symptoms

Why this is inaccurate:

They are generally more successful against positive than negative symptoms.

How to improve:

Name the symptom being discussed.

Mistake: Saying the drug removes a delusion by proving it false

Why this is incorrect:

The drug reduces dopamine activity rather than directly challenging reasoning.

How to improve:

Link belief examination with CBT rather than receptor blockade.

Mistake: Treating sedation as evidence that psychosis has been cured

Why this is incorrect:

A quiet or sleepy patient may still experience symptoms.

How to improve:

Measure hallucinations, delusions, functioning and quality of life separately.

Mistake: Listing side effects without evaluation

Why this is incomplete:

A list does not explain the consequence.

How to improve:

Use:

side effect → impact on the person → impact on adherence or appropriateness

Mistake: Saying any side effect makes medication inappropriate

Why this is too absolute:

A mild side effect may be outweighed by a substantial reduction in severe symptoms.

How to improve:

Use a cost-benefit analysis.

Mistake: Claiming medication effectiveness proves dopamine caused schizophrenia

Why this is incorrect:

Treatment and cause are not logically identical.

How to improve:

State that the evidence supports dopamine involvement.

Mistake: Saying drug therapy treats the family environment

Why this is incorrect:

Antipsychotics act biologically.

How to improve:

Use family therapy for communication and expressed emotion.

Mistake: Saying placebo participants receive no treatment experience

Why this is incorrect:

They receive an inactive treatment that resembles the active drug.

How to improve:

Explain how placebo controls expectations.

Mistake: Saying double blind means participants take two drugs

Why this is incorrect:

It refers to who knows the treatment allocation.

How to improve:

State that neither participants nor assessors know the condition.

Mistake: Giving a vague cost criticism

Why this is incomplete:

The argument needs a clear source of cost.

How to improve:

Refer to prescription, monitoring, hospitalisation or treatment of side effects.

Mistake: Ignoring withdrawal from drug studies

Why this weakens evaluation:

People leaving because of side effects may disappear from the final results.

How to improve:

Discuss attrition and intention-to-treat analysis.

Mistake: Assuming continued medication is always forced

Why this is incorrect:

Many people agree to maintenance medication because it reduces relapse.

How to improve:

Evaluate consent and control using the circumstances of the individual case.

Exam-Style Questions ✍️

Questions

1. Name one typical antipsychotic used in the treatment of schizophrenia.[1 mark]

2. What is meant by saying that a typical antipsychotic is a dopamine antagonist?[2 marks]

3. Explain how blocking D2 receptors may reduce positive symptoms of schizophrenia.[4 marks]

4. Explain one difference between acute and maintenance use of typical antipsychotics.[4 marks]

5. A patient takes chlorpromazine and reports that the voices they hear have become less frequent. Their lack of motivation has not improved.

Explain this pattern using your knowledge of typical antipsychotics.[4 marks]

6. Kai’s delusions become less severe after taking a typical antipsychotic. He develops muscle tremors and decides to stop taking the medication.

Explain one issue concerning the appropriateness and one issue concerning the long-term effectiveness of Kai’s treatment.[6 marks]

7. Explain why the effectiveness of chlorpromazine provides support for the dopamine

hypothesis but does not prove that dopamine dysfunction originally caused schizophrenia.[4 marks]

8. Researchers compare a typical antipsychotic with a placebo. Neither the patients nor the clinicians assessing symptoms know which treatment each patient receives.

a) Name the experimental control described.[1 mark]

b) Explain how it improves the investigation.[4 marks]

9. Researchers obtain the following findings after six months:

Treatment group	Number who relapsed	Number who began treatment
Typical antipsychotic	18	60
Placebo	33	60

a) Calculate the relapse percentage in the typical-antipsychotic group.[2 marks]

b) Calculate the relapse percentage in the placebo group.[2 marks]

c) Explain one conclusion and one limitation of the findings.[4 marks]

10. Explain one strength and one limitation of typical antipsychotics as a treatment for schizophrenia.[6 marks]

11. Evaluate the appropriateness and effectiveness of typical antipsychotics in the treatment of schizophrenia.[8 marks]

12. Discuss typical antipsychotics as a treatment for schizophrenia. Refer to the following scenario in your answer.

Sofia experiences distressing voices and persecutory delusions. Chlorpromazine reduces these symptoms, but she becomes drowsy and develops muscle stiffness. She stops taking the tablets, and her symptoms later return. Her care team suggests a depot injection combined with psychological therapy.

[16 marks]

Answers and Mark Scheme

Question 1

Award one mark for:

• Chlorpromazine.

Credit another valid typical antipsychotic.

Question 2

Award up to two marks:

• An antagonist blocks or reduces the action of a neurotransmitter.

• A typical antipsychotic occupies dopamine receptor sites, reducing dopamine’s ability to stimulate the postsynaptic neuron.

Question 3

Award up to four marks:

• Dopamine is released into the synaptic cleft.

• It would normally bind to D2 receptors on the postsynaptic neuron.

• Typical antipsychotics occupy or block these receptor sites.

• Fewer dopamine molecules can activate the postsynaptic neuron.

• Dopamine transmission in relevant pathways is reduced.

• This may reduce positive symptoms such as hallucinations and delusions.

Question 4

Award up to four marks:

• Acute treatment is given during a current severe episode.

• It aims to reduce active symptoms such as hallucinations or delusions.

• Maintenance treatment continues after symptoms improve.

• Its main purpose is to reduce the risk of relapse.

• Maintenance treatment may continue for a longer period and requires consideration of long-term side effects and adherence.

Question 5

Award up to four marks:

• Voices are an auditory hallucination and therefore a positive symptom.

• Typical antipsychotics reduce dopamine activity by blocking D2 receptors.

• They are generally more effective against positive symptoms.

• Lack of motivation may represent avolition, a negative symptom.

• Negative symptoms may involve reduced activity in other dopamine pathways and may respond less successfully to typical drugs.

Question 6

Award up to six marks.

Appropriateness:

• Muscle tremors are a side effect of the medication.

• They may interfere with Kai’s movement, comfort or quality of life.

• The treatment may therefore be less appropriate despite reducing delusions.

Long-term effectiveness:

• Stopping the medication ends the continuing dopamine-receptor blockade.

• Symptoms may return, reducing long-term effectiveness.

• Side effects have indirectly reduced effectiveness by producing non-adherence.

Question 7

Award up to four marks:

• Chlorpromazine blocks dopamine receptors.

• A reduction in symptoms after dopamine activity is reduced suggests dopamine is involved.

• This supports the biological explanation.

• However, a treatment can interrupt a symptom mechanism without correcting the original cause.

• Genetic vulnerability, stress or dysfunctional cognition might have initiated the condition.

• Drug effectiveness therefore does not prove that dopamine abnormality was the original cause.

Question 8a

Award one mark for:

• Double-blind procedure.

Question 8b

Award up to four marks:

• Patients do not know whether they receive the active drug or placebo.

• This reduces demand characteristics and expectancy effects.

• Assessing clinicians also do not know the condition.

• This reduces investigator effects or biased symptom ratings.

• Differences between groups are therefore more likely to reflect the drug’s active effect.

Question 9a

6018​×100=30%

Award:

• One mark for suitable working.

• One mark for 30%.

Question 9b

6033​×100=55%

Award:

• One mark for suitable working.

• One mark for 55%.

Question 9c

Award up to four marks.

Possible conclusion:

• Relapse was less frequent in the typical-antipsychotic group.

• The difference was 25 percentage points.

• This is consistent with the drug being more effective than placebo at preventing relapse.

Possible limitation:

• The figures do not show side effects or treatment withdrawals.

• The groups may have differed in adherence or initial severity.

• Relapse is only one measure of effectiveness.

• No inferential-test result is given, so statistical significance cannot be claimed.

Question 10

Award up to three marks for a developed strength and three marks for a developed limitation.

Possible strength:

Typical antipsychotics can reduce positive symptoms such as hallucinations and delusions. Placebo comparisons and meta-analytic evidence support the effectiveness of chlorpromazine, giving the treatment practical value.

Possible limitation:

Dopamine-receptor blockade can cause side effects such as muscle tremors. These may reduce quality of life and lead patients to stop treatment, increasing the risk of relapse and reducing long-term effectiveness.

Alternative creditworthy points include:

• Historical reduction in institutionalisation.

• Enabling psychological treatment.

• Limited effect on negative symptoms.

• Masking symptoms rather than treating causes.

• Ethical issues involving control.

• Individual differences.

• Attrition in drug research.

Question 11

A strong response should include:

• Evidence that chlorpromazine can reduce symptoms compared with placebo.

• Meta-analysis as a source of converging evidence.

• Greater effectiveness against positive symptoms.

• More limited effect on negative symptoms.

• Short-term symptom reduction.

• Maintenance treatment and relapse prevention.

• Symptoms returning following discontinuation.

• Side effects such as dry mouth, weight gain and muscle tremors.

• Side effects leading to non-adherence.

• Cost-benefit analysis for individual patients.

• Historical reduction in institutionalisation and physical restraint.

• Medication allowing engagement with psychological therapy.

• Drugs managing symptoms rather than every underlying cause.

• Individual differences in response.

• Ethical issues involving consent, injections and control.

• Short-term symptom scores versus quality of life.

• Attrition and publication bias in effectiveness research.

• Comparison with CBT, family therapy or atypical antipsychotics.

The 2022 antipsychotic question assessed evaluation only. A focused answer should therefore develop arguments rather than spend substantial time describing synaptic action.

Question 12

A strong response should include:

Knowledge and understanding

• Typical antipsychotics as first-generation drug treatments.

• Chlorpromazine.

• Dopamine-antagonist action.

• D2 receptor blockade.

• Reduced stimulation of postsynaptic neurons.

• Link with excessive subcortical dopamine.

• Greater effect on positive symptoms.

• Oral medication and depot injections.

• Acute and maintenance treatment.

Application

• Sofia’s voices are auditory hallucinations.

• Her belief that others intend to harm her is a persecutory delusion.

• Both are positive symptoms.

• Chlorpromazine blocks dopamine receptors and reduces dopamine activity.

• The reduction in hallucinations and delusions indicates some effectiveness.

• Drowsiness and muscle stiffness are side effects.

• These reduce appropriateness and quality of life.

• Side effects lead Sofia to stop the tablets.

• Discontinuation ends receptor blockade and is followed by relapse.

• A depot injection may improve adherence.

• The depot raises issues because the drug cannot be removed immediately.

• Psychological therapy could address beliefs, coping and wider causes.

Evaluation

• Evidence from placebo comparisons and meta-analyses supports chlorpromazine.

• Treatment effectiveness supports dopamine involvement but not original causation.

• Typical drugs are generally more effective for positive symptoms.

• Negative symptoms may remain.

• Side effects may outweigh benefits for some people.

• Side effects can indirectly reduce effectiveness through non-adherence.

• Treatment response varies between individuals.

• Drugs may mask symptoms without addressing psychological or social causes.

• Short-term improvement does not guarantee long-term recovery.

• Continued treatment may reduce relapse.

• Depot medication may support adherence but can feel controlling.

• Informed consent and autonomy are important.

• Historical benefits include reduced institutionalisation.

• Symptom reduction may allow engagement with CBT or family therapy.

• Medication alone may be biologically reductionist.

• Combined treatment may be more appropriate than relying solely on drugs.

Higher-level responses will distinguish effectiveness from appropriateness, apply each part of the scenario and reach a balanced judgement based on symptoms, side effects, adherence, ethics and long-term functioning.