AQA A Level Psychology 3.3.5 Schizophrenia Exam Questions

About AQA A Level Psychology 3.3.5 Schizophrenia

Schizophrenia is one of the Option 2 choices on AQA A Level Paper 3, Issues and Options. You learn how schizophrenia is classified using positive and negative symptoms, and the problems of reliability and validity in diagnosis, including co-morbidity, culture bias, gender bias and symptom overlap. You then study biological explanations (genetics, the dopamine hypothesis and neural correlates), psychological explanations (family dysfunction and cognitive explanations), and treatments including drug therapy, CBT, family therapy and token economies. The topic ends with the interactionist approach and the diathesis-stress model. It builds on Psychopathology and Biopsychology and gives strong examples for the nature-nurture and reductionism debates.

What you need to know

• Classification Positive symptoms are additional experiences such as hallucinations and delusions; negative symptoms are a loss of usual abilities such as speech poverty and avolition. Diagnosis uses DSM-5 or ICD-10, which differ in how many symptoms are needed.
• Reliability and validity Inter-rater reliability can be low; Cheniaux et al. (2009) found psychiatrists diagnosed more patients using ICD than DSM. Validity issues include co-morbidity, symptom overlap with bipolar disorder, culture bias and gender bias.
• Biological explanations Family studies show risk rises with genetic relatedness (Gottesman, 1991, about 48% for MZ twins and 17% for DZ twins). The dopamine hypothesis links hyperdopaminergia in subcortical areas to positive symptoms and hypodopaminergia in the prefrontal cortex to negative symptoms. Neural correlates include reduced ventral striatum activity linked to avolition.
• Psychological explanations Family dysfunction includes the schizophrenogenic mother, the double-bind theory (Bateson et al., 1956) and high expressed emotion. Cognitive explanations involve dysfunctional thought processing, such as faulty metarepresentation and central control (Frith et al.).
• Drug therapy Typical antipsychotics such as chlorpromazine are dopamine antagonists; atypical antipsychotics such as clozapine and risperidone act on dopamine and serotonin and have fewer side effects such as tardive dyskinesia.
• Psychological therapies and management CBT helps patients understand and challenge delusions and hallucinations; family therapy reduces expressed emotion; token economies use secondary reinforcers to manage behaviour in institutions.
• Interactionist approach The diathesis-stress model says a genetic vulnerability combined with environmental stressors triggers schizophrenia; treatment often combines antipsychotics with CBT.

Common mistakes in 3.3.5 Schizophrenia

• Calling negative symptoms 'bad' symptoms; negative symptoms are a loss of normal functioning, positive symptoms are additions to normal experience.
• Stating that high dopamine explains all symptoms; the revised hypothesis links low prefrontal dopamine to negative symptoms.
• Describing token economies as a cure; they manage behaviour and do not treat the underlying symptoms.
• Confusing reliability (agreement between clinicians) with validity (whether the diagnosis measures a real, distinct disorder).
• Writing that MZ concordance of 48% proves schizophrenia is genetic; if it were wholly genetic the concordance would be 100%.

Try three 3.3.5 Schizophrenia exam-style questions