Schizophrenia: symptoms and diagnosis, biological explanations (dopamine, genetics) and psychological explanations, biological and psychological treatments, and the named schizophrenia studies.

What this dot point is asking

Edexcel wants you to describe the symptoms and diagnosis of schizophrenia, explain it biologically (dopamine and genetics) and psychologically, evaluate biological and psychological treatments, and use named studies as evidence. Schizophrenia is the lead disorder for clinical psychology, so it links directly to diagnosis, the medical model and research methods.

The answer

Symptoms and diagnosis

Diagnosis uses classification systems. The DSM-5 requires two or more characteristic symptoms (at least one being a positive symptom) present for a significant time over one month, with disturbance lasting six months. The ICD-11 is similar but historically recognised subtypes such as paranoid and catatonic schizophrenia. Diagnosis must be reliable (clinicians agree) and valid (it identifies a real, distinct disorder), both of which are challenged by the disorder's heterogeneity.

Biological explanations

The dopamine hypothesis is the central biological explanation.

Evidence for the dopamine hypothesis comes from drugs: typical antipsychotics block $D_2$ receptors and reduce positive symptoms, while amphetamines and L-dopa raise dopamine and can produce psychotic symptoms in healthy people. Post-mortem and PET studies report raised dopamine receptor density in some patients.

Genetic explanations propose an inherited vulnerability. Twin studies show higher concordance in monozygotic (MZ) twins (around 40 to 50 per cent) than dizygotic (DZ) twins (around 17 per cent), and family studies show that risk rises with genetic closeness (around 1 per cent in the general population but much higher for the child of two affected parents). Candidate genes are polygenic rather than a single gene.

Psychological explanations

Treatments

Biological treatment uses antipsychotic drugs. Typical antipsychotics (chlorpromazine) are dopamine antagonists that block $D_2$ receptors and reduce positive symptoms but carry serious side effects, notably tardive dyskinesia (involuntary movements). Atypical antipsychotics (clozapine, risperidone) act on dopamine and serotonin, target negative symptoms better and have fewer movement side effects, though clozapine risks agranulocytosis (a fall in white blood cells).

Psychological treatment uses CBT for psychosis (CBTp), which helps patients challenge and reframe delusional beliefs and cope with hallucinations, and family therapy, which reduces expressed emotion and relapse. Psychological treatments work best combined with medication, not instead of it.

Evaluation (GRAVE)

• Generalisability. Twin and drug studies often use specific clinical samples and Western diagnostic criteria, so findings may not generalise across cultures, where symptoms (such as hearing voices) are interpreted differently.
• Reliability. Diagnosis can be unreliable: clinicians do not always agree, and the disorder is heterogeneous, so two patients with the same label can have very different symptoms.
• Application. The dopamine hypothesis has clear real-world value: it underpins antipsychotic drug design, which has allowed many patients to live in the community rather than in institutions.
• Validity. Drug evidence is correlational, so it cannot prove that high dopamine causes symptoms. The delay between dopamine blockade (hours) and symptom relief (weeks) challenges a simple causal account.
• Ethics. Antipsychotics raise consent issues (patients lacking insight, depot injections) and have severe side effects, so treatment must balance benefit against harm.

Examples in context

Example 1. Carlsson and the antipsychotic evidence. Arvid Carlsson's work established that chlorpromazine and similar drugs reduce psychotic symptoms by blocking dopamine receptors, which became the foundation of the dopamine hypothesis. The clinical observation that drugs raising dopamine (amphetamines, L-dopa for Parkinson's disease) can produce hallucinations and paranoia in non-schizophrenic people gave converging support. However, the later success of clozapine, which is a relatively weak $D_2$ blocker but a strong serotonin antagonist and which helps treatment-resistant patients, showed that dopamine alone is an incomplete account and that serotonin and glutamate are also involved. This is the kind of named evidence Edexcel rewards when you evaluate the dopamine hypothesis.

Example 2. Tienari (2004) adoption study and gene-environment interaction. A Finnish adoption study followed adopted children of biological mothers with schizophrenia and a control group of adoptees with no family history. The children at genetic risk were significantly more likely to develop schizophrenia only when raised in families rated high in dysfunction and criticism, whereas a healthy family environment appeared protective. This is powerful evidence for the diathesis-stress model: a genetic vulnerability (diathesis) is expressed when triggered by an environmental stressor, integrating the biological and psychological explanations rather than treating them as rivals.

Try this

Q1. Outline the dopamine hypothesis of schizophrenia. [3 marks]

• Cue. Schizophrenia results from hyperactivity of dopamine at $D_2$ receptors in the mesolimbic pathway (positive symptoms); the revised version adds low prefrontal dopamine for negative symptoms.

Q2. Explain one strength and one limitation of antipsychotic drugs as a treatment. [4 marks]

• Cue. Strength: effective in reducing positive symptoms and easy to administer, allowing community living. Limitation: side effects such as tardive dyskinesia (typical) or agranulocytosis (clozapine), and they manage symptoms rather than curing the disorder.

Q3. Assess the view that schizophrenia is best explained by the diathesis-stress model. [8 marks]

• Cue. Use the less-than-100 per cent MZ concordance and Tienari's adoption study to argue genes create vulnerability but environmental stress triggers onset; weigh this against purely biological (dopamine, genetic) accounts that are reductionist and correlational.