Notes · PsychologyUK · A-Levels

Schizophrenia

This optional topic examines schizophrenia, a severe mental disorder that disrupts thinking, perception and emotion. It covers the classification and symptoms of schizophrenia and the reliability and validity of its diagnosis, the biological and psychological explanations of its causes, the drug and psychological therapies used to treat it, and the argument for an interactionist, diathesis-stress approach. It is one of the three choices in the second option block of Paper 3.

6 sections~19 min reading time3 competenciesLevel Standard 1 · Advanced 5

T·121212 / 17

Exam profile

AO1 · Describe the classification, symptoms, explanations and therapies for schizophreniaAO2 · Apply the explanations and therapies to novel case materialAO3 · Evaluate the reliability and validity of diagnosis, the explanations and the treatments

Operators:describeexplainapplyevaluatediscuss

basic level

This is a full A-Level (A2) optional topic, not part of AS; on Paper 3 students study one topic from this option block (Schizophrenia, Eating behaviour or Stress).

higher level

The full A-Level requires description, application and evaluation of the biological and psychological explanations and treatments, and an argument for interactionism.

Depth

Text

Contents · 6 sections

Schizophrenia

Classification and symptoms of schizophrenia#

StandardAQA 7182 3.3.5DfE GCE Psychology - classification of schizophrenia

Positive and negative symptoms of schizophrenia

Fig. 1Symptoms are classified as positive (added experiences) or negative (reduced functions).

Schizophrenia is a serious mental disorder affecting about 1% of people, characterised by a loss of contact with reality. It is diagnosed using classification systems - the ICD (International Classification of Diseases) and the DSM (Diagnostic and Statistical Manual) - which list the symptoms that must be present. The two systems differ slightly (the DSM requires at least one positive symptom, whereas the ICD allows a diagnosis on two or more negative symptoms), a difference that becomes important when evaluating the reliability of diagnosis.

Symptoms are divided into positive and negative. Positive symptoms are additional experiences beyond ordinary existence - things added to normal functioning. Hallucinations are unusual sensory experiences with no basis in reality (most commonly hearing voices). Delusions are irrational beliefs held with strong conviction, such as delusions of persecution (believing one is being plotted against) or of grandeur (believing one has special powers or identity).

Negative symptoms are the loss or reduction of normal functions. Speech poverty (alogia) is a reduction in the amount and quality of speech, sometimes with a delay in verbal responses. Avolition is a severe reduction in motivation to carry out goal-directed activities, so the person loses interest and drive and may sit inactive for long periods. Negative symptoms are often more disabling in the long term and less responsive to treatment than positive symptoms.

Understanding the symptoms matters because they underpin both diagnosis and treatment. The distinction between positive and negative symptoms links to the biological explanations (different symptoms are associated with different patterns of dopamine activity) and to treatment (some drugs target positive symptoms more effectively than negative ones). Being able to identify a described experience as a specific positive or negative symptom is a common exam requirement.

Worked example

Classifying symptoms

A person reports hearing a voice commenting on their actions, holds an unshakeable belief that MI5 is monitoring them, and no longer washes or leaves the house. Classify each symptom.

The voice
Hearing a voice with no external source is a hallucination - a positive symptom.
The belief about MI5
An irrational, firmly held belief of persecution is a delusion - a positive symptom.
The self-neglect
No longer washing or leaving the house reflects avolition (loss of motivation) - a negative symptom.

Result: Two positive symptoms (a hallucination and a delusion) and one negative symptom (avolition).

Typical mistakes

Classifying avolition or speech poverty as positive symptoms - they are negative (reduced functioning).
Confusing hallucinations (false perceptions) with delusions (false beliefs).

Active revision

For each, state whether it is a positive or negative symptom: hearing voices; a lack of motivation to get dressed; believing one is being followed by spies.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for psychology (Department for Education) · AQA A-level Psychology 7182 specification (AQA)

Reliability and validity of diagnosis#

AdvancedAQA 7182 3.3.5DfE GCE Psychology - reliability and validity in diagnosis

Reliability of diagnosis means consistency: whether different clinicians reach the same diagnosis for the same person (inter-rater reliability) and whether the same clinician would diagnose the same way on different occasions. Reliability is undermined by the fact that the ICD and DSM use different criteria, so the same patient may be diagnosed with schizophrenia under one system but not the other, and by cultural differences in how symptoms are interpreted.

Validity of diagnosis means accuracy: whether the diagnosis of schizophrenia is measuring a real, distinct disorder. Several problems threaten validity. Co-morbidity is the presence of two or more conditions at once (schizophrenia often co-occurs with depression or substance abuse), which makes it hard to be sure schizophrenia is a separate condition rather than part of a broader problem. Symptom overlap means schizophrenia and other disorders (such as bipolar disorder) share symptoms, so distinguishing them is difficult - which raises the question of whether they are genuinely separate disorders.

Culture and gender bias also threaten valid diagnosis. There is evidence that people of some ethnic backgrounds are diagnosed with schizophrenia at higher rates in Western countries, which may reflect clinician bias or the misinterpretation of culturally normal experiences (such as hearing the voice of an ancestor) as symptoms. Gender bias appears in evidence that men are diagnosed more often than women, possibly because women's better interpersonal functioning masks their symptoms and leads to under-diagnosis.

These issues are evaluated by weighing the evidence. Rosenhan's classic 'being sane in insane places' study, in which healthy 'pseudopatients' were admitted to psychiatric hospitals and their normal behaviour interpreted through the lens of their diagnosis, is often cited as evidence of poor validity and the power of labelling. Later revisions of the DSM have improved inter-rater reliability by tightening the criteria, but the persistence of co-morbidity, symptom overlap and cultural and gender bias means the validity of the diagnosis remains a live issue - and a rich source of AO3 evaluation.

Worked example

Diagnosing a validity problem

A patient meets some criteria for both schizophrenia and bipolar disorder, and also has a diagnosis of depression. Explain the two validity problems illustrated here.

Identify symptom overlap
Meeting criteria for both schizophrenia and bipolar disorder shows symptom overlap - shared symptoms make it hard to tell the two disorders apart.
Identify co-morbidity
Also having depression shows co-morbidity - two conditions present at once, blurring whether schizophrenia is a separate condition.
Draw the conclusion
Both undermine the validity of the schizophrenia diagnosis, since it is unclear that a single, distinct disorder is being accurately identified.

Result: Symptom overlap and co-morbidity both cast doubt on whether the diagnosis validly identifies a distinct disorder.

Typical mistakes

Confusing reliability (do clinicians agree?) with validity (is it a real, distinct disorder?).
Confusing co-morbidity (two conditions together) with symptom overlap (shared symptoms between disorders).

Active revision

Explain how co-morbidity and symptom overlap each threaten the validity of a diagnosis of schizophrenia.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for psychology (Department for Education) · AQA A-level Psychology 7182 specification (AQA)

Biological explanations: genetics and the dopamine hypothesis#

AdvancedAQA 7182 3.3.5DfE GCE Psychology - biological explanations for schizophrenia

Genetic risk of schizophrenia

Fig. 2Risk rises with genetic closeness - from about 1% in the general population to about 48% for an identical twin (Gottesman's figures).

The genetic explanation says schizophrenia is inherited: it runs in families, and the closer the genetic relationship to a person with schizophrenia, the greater the risk. Gottesman's family studies illustrate this - the concordance rate rises from about 1% in the general population to about 9% for siblings and about 48% for identical (monozygotic) twins. Schizophrenia is polygenic (many genes each add a small risk) and the identified candidate genes are largely those involved in neurotransmitter function. Adoption studies (children of mothers with schizophrenia adopted into healthy families still show raised rates) help separate genes from the shared family environment.

The dopamine hypothesis proposes that schizophrenia is associated with abnormal activity of the neurotransmitter dopamine. The original version emphasised hyperdopaminergia - too much dopamine activity, or too many/too sensitive D2 receptors, in subcortical (mesolimbic) areas such as Broca's area - which was linked to the positive symptoms such as hallucinations. Support came from the fact that amphetamines (which increase dopamine) can induce schizophrenia-like symptoms, while antipsychotic drugs (which block dopamine) reduce them.

The hypothesis was later revised to include hypodopaminergia - too little dopamine activity in the prefrontal cortex - which was linked to the negative and cognitive symptoms such as avolition. The updated hypothesis therefore proposes different dopamine abnormalities in different brain regions producing different symptoms, which is a more nuanced account than the original.

The biological explanations are evaluated as well supported but incomplete. The genetic evidence (twin and adoption studies) is strong, and the dopamine hypothesis is supported by the action of the drugs. However, concordance in identical twins is well below 100%, so genes alone cannot cause schizophrenia (the environment must contribute). The dopamine hypothesis is challenged by the fact that some newer antipsychotics act on other neurotransmitters (such as serotonin) yet still work, and by uncertainty about whether abnormal dopamine is a cause or an effect of schizophrenia. This incompleteness is what motivates the interactionist, diathesis-stress approach covered later.

The dopamine hypothesis

Fig. 3The revised dopamine hypothesis: too much subcortical dopamine underlies positive symptoms; too little prefrontal dopamine underlies negative symptoms.

Worked example

Reasoning from concordance rates

Identical twins show about 48% concordance and non-identical twins about 17%. Explain what this comparison suggests and its main limitation.

Compare the rates
Identical twins (100% shared genes) show far higher concordance than non-identical twins (about 50% shared genes), suggesting a genetic contribution.
Note the shortfall
Even identical twins are concordant only about 48% of the time, not 100%.
Interpret
If schizophrenia were purely genetic, identical-twin concordance would be 100%; the gap shows environmental factors also contribute, supporting a diathesis-stress rather than purely genetic model.

Result: The twin comparison supports a genetic vulnerability, but the sub-100% concordance shows the environment is also involved.

Typical mistakes

Saying identical-twin concordance is 100% - it is around 48%, which shows the environment also matters.
Treating the dopamine hypothesis as only 'too much dopamine' - the revised version includes too little in the prefrontal cortex.

Active revision

Explain how twin studies provide evidence for a genetic basis of schizophrenia, and why they do not prove genes are the sole cause.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for psychology (Department for Education) · AQA A-level Psychology 7182 specification (AQA)

Psychological explanations: family dysfunction and cognition#

AdvancedAQA 7182 3.3.5DfE GCE Psychology - psychological explanations for schizophrenia

Family dysfunction and expressed emotion

Fig. 4Dysfunctional family communication, especially high expressed emotion, is a source of stress linked to symptoms and relapse.

Family dysfunction explanations locate the cause of schizophrenia in abnormal patterns of communication and relationships within the family. Three ideas are named. The schizophrenogenic mother (from psychodynamic theory) is a cold, controlling and rejecting mother who creates a family climate of tension and secrecy that may lead to schizophrenia. The double-bind theory (Bateson) suggests that children who repeatedly receive contradictory messages from a parent (where they are punished whatever they do, and cannot comment on the contradiction) come to see the world as confusing and dangerous, which may be reflected in disorganised thinking. Expressed emotion (EE) is a family communication style involving high levels of criticism, hostility and emotional over-involvement directed at the person with schizophrenia; high EE is a serious source of stress that is strongly linked to relapse.

The cognitive explanation focuses on the faulty thought processing that accompanies schizophrenia. Frith identified dysfunctional thought processing, such as problems with metarepresentation (the ability to reflect on our own thoughts and behaviour, whose failure could explain hallucinations and thought insertion) and with central control (the ability to suppress automatic responses, whose failure could explain disorganised speech and thought). On this view the characteristic symptoms are the outward signs of underlying cognitive deficits.

Importantly, the family-dysfunction and cognitive explanations describe different kinds of cause. Family dysfunction points to the social environment as a source of the stress that triggers or worsens the disorder, while the cognitive explanation describes the internal information-processing that produces the symptoms - and the two can be combined (cognitive deficits may have a biological origin but be worsened by a stressful family environment).

The psychological explanations are evaluated for evidence and for their sensitivity. Expressed emotion has strong support as a predictor of relapse, and family-based therapies that reduce EE improve outcomes, giving the explanation real-world value. However, the schizophrenogenic-mother and double-bind ideas are dated, hard to test, and were socially damaging in wrongly blaming (particularly) mothers for the disorder. The cognitive explanation has good support (people with schizophrenia do show the predicted processing deficits) but is criticised for describing the proximate cognitive mechanism rather than the ultimate cause - it does not by itself say where the cognitive deficits come from, which is where the biological explanations and the interactionist approach come in.

Worked example

Applying the expressed-emotion explanation

After leaving hospital, a person with schizophrenia returns to a home where relatives are highly critical and over-involved, and soon relapses. Explain this using the family-dysfunction explanation.

Identify the family style
High criticism and emotional over-involvement are the markers of high expressed emotion (EE).
Link to stress
High EE is a serious and persistent source of stress for the person with schizophrenia.
Explain the relapse
Because stress can trigger or worsen symptoms, the stressful high-EE environment plausibly contributes to the relapse - a link with strong research support.

Result: The high-EE family environment acts as a stressor that plausibly precipitates the relapse.

Typical mistakes

Confusing double-bind (contradictory messages) with expressed emotion (a critical, hostile communication style).
Treating the cognitive explanation as identifying the ultimate cause - it describes the mechanism, not its origin.

Active revision

Explain how high expressed emotion in a family might contribute to relapse in a person with schizophrenia.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for psychology (Department for Education) · AQA A-level Psychology 7182 specification (AQA)

Biological and psychological therapies#

AdvancedAQA 7182 3.3.5DfE GCE Psychology - treatments for schizophrenia

Treatments for schizophrenia

Fig. 5Biological (drug) and psychological (CBTp, family therapy, token economy) treatments are usually combined.

Drug therapy is the main biological treatment and follows from the dopamine hypothesis. Typical antipsychotics (such as chlorpromazine) are dopamine antagonists that block D2 receptors, reducing dopamine activity and so reducing positive symptoms such as hallucinations; chlorpromazine also has a sedative effect. Atypical antipsychotics (such as clozapine and risperidone) were developed later to treat a wider range of symptoms with fewer side effects: they act on dopamine but also on other neurotransmitters such as serotonin, and clozapine is used for people who do not respond to other drugs (though it requires blood monitoring for a rare but dangerous side effect).

Cognitive behaviour therapy (CBTp) is a psychological treatment that helps the person make sense of and challenge their symptoms. It does not aim to remove hallucinations or delusions but to change how the person interprets and responds to them - for example, helping a patient to test a delusional belief against reality, or to see a voice as a product of their own mind rather than an external threat - which reduces the distress and disruption the symptoms cause.

Family therapy works with the whole family to improve communication and reduce expressed emotion. It aims to reduce the criticism, hostility and over-involvement that raise stress and provoke relapse, to improve the family's understanding of the disorder, and to support relatives so they can better help the patient. It is typically used alongside drug therapy and has good evidence for reducing relapse. The token economy is a form of behaviour management (not a cure) based on operant conditioning: desirable behaviours (such as self-care) are rewarded with tokens that can be exchanged for privileges, which helps manage behaviour and counter the effects of institutionalisation, particularly for negative symptoms.

The treatments are evaluated for effectiveness and appropriateness. Drug therapy is effective for positive symptoms, relatively cheap and allows many people to live in the community, but it treats symptoms rather than causes, has significant side effects (from movement disorders to, rarely, serious blood conditions), and raises ethical concerns about the use of powerful drugs and about consent. Psychological therapies (CBTp, family therapy) improve quality of life and reduce relapse and address the meaning of the illness, but require motivation and engagement and are usually used as an addition to, not a replacement for, medication. The strong consensus is that a combination of drug and psychological therapy - an interactionist approach - is most effective.

Worked example

Justifying a combined treatment

A patient's positive symptoms are controlled by medication but they still find voices distressing and their family is highly critical. Recommend a treatment plan and justify it.

Keep the medication
Antipsychotics are controlling the positive symptoms, so they should continue as the biological component.
Add CBTp
CBTp can help the patient reinterpret the voices as products of their own mind, reducing the distress the drugs do not fully address.
Add family therapy
Family therapy can reduce the high expressed emotion at home, lowering the stress that risks relapse - giving an interactionist plan that treats biology and environment together.

Result: A combined (interactionist) plan - medication plus CBTp plus family therapy - addresses symptoms, distress and family stress together.

Typical mistakes

Saying CBTp removes hallucinations - it changes how the person interprets and copes with them.
Treating the token economy as a cure - it is behaviour management, not a treatment of the disorder.

Active revision

Compare drug therapy and CBT as treatments for schizophrenia, referring to effectiveness and appropriateness.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for psychology (Department for Education) · AQA A-level Psychology 7182 specification (AQA)

The interactionist approach and the diathesis-stress model#

AdvancedAQA 7182 3.3.5DfE GCE Psychology - the interactionist approach

The diathesis-stress model of schizophrenia

Fig. 6Schizophrenia develops only when a vulnerability (diathesis) meets an environmental trigger (stressor); the vulnerability alone is not enough.

The interactionist approach argues that schizophrenia is best explained not by biology or by psychology alone but by their interaction, and it is formalised in the diathesis-stress model. A diathesis is a vulnerability - originally seen as purely genetic, but now understood to include biological factors (such as prenatal risks) and psychological ones (such as early trauma). A stressor is an environmental trigger - which may be psychological (a dysfunctional family, a stressful life event) or biological (such as cannabis use, now regarded as a possible stressor that can trigger onset in vulnerable people).

The model's central claim is that neither the diathesis nor the stressor alone is sufficient to produce schizophrenia: the disorder develops only when a person who carries the vulnerability also experiences the stressor. This explains why one identical twin can develop schizophrenia and the other not, despite sharing the same genes - only one encountered the necessary stressor. Modern versions treat both diathesis and stress as matters of degree, so a large vulnerability may need only a small stressor, and vice versa.

The interactionist model has direct implications for treatment: because both biological and psychological factors contribute, the most effective treatment combines both - antipsychotic medication (addressing the biological diathesis) together with psychological therapies such as CBTp and family therapy (addressing the psychological stressors). Treating only one side is less effective, which fits the evidence that combined treatment gives the best outcomes.

The interactionist approach is evaluated as the most complete account. Its strength is that it accounts for the evidence better than any single explanation - it accommodates the genetic and dopamine findings, the family and cognitive findings, and the sub-100% twin concordance, and it explains why combined treatment works best. Its limitation is that the model is quite general (the exact nature of the diathesis and the stressor, and how they interact, is still being worked out), and demonstrating a true interaction (rather than two separate additive causes) is methodologically difficult. Even so, it is now the dominant framework for understanding schizophrenia.

Worked example

Applying the diathesis-stress model

A young man with a family history of schizophrenia develops the disorder after a period of heavy cannabis use and family conflict, while his cousin with the same family history, living calmly, does not. Explain this using the model.

Identify the shared diathesis
Both men share a genetic vulnerability (diathesis) from the family history.
Identify the differing stressors
Only the young man experienced significant stressors - heavy cannabis use and family conflict; his cousin did not.
Apply the model
Because schizophrenia requires both a diathesis and a stressor, the young man - who met both - develops it, while the cousin, with the vulnerability but no stressor, does not.

Result: The shared vulnerability plus differing stressors explains why only the young man develops schizophrenia.

Typical mistakes

Treating the diathesis as only genetic - modern versions include biological and psychological vulnerabilities.
Saying either the diathesis or the stressor alone causes schizophrenia - the model requires both.

Active revision

Explain how the diathesis-stress model accounts for why only one of two identical twins develops schizophrenia.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for psychology (Department for Education) · AQA A-level Psychology 7182 specification (AQA)

References & sources

Sources

Department for Education

GCE AS and A level subject content for psychology

AQA

AQA A-level Psychology 7182 specification

Schizophrenia

6 sections~19 min reading time3 competenciesLevel Standard 1 · Advanced 5

Schizophrenia

Key points

Classifying symptoms

Key points

Diagnosing a validity problem

Key points

Reasoning from concordance rates

Key points

Applying the expressed-emotion explanation

Key points

Justifying a combined treatment

Key points

Applying the diathesis-stress model

Sources

Schizophrenia

Key points

Classifying symptoms

Key points

Diagnosing a validity problem

Key points

Reasoning from concordance rates

Key points

Applying the expressed-emotion explanation

Key points

Justifying a combined treatment

Key points

Applying the diathesis-stress model

Sources