Revise Explanations of schizophrenia for Cambridge 9990 (1.1.2)

Biological explanations propose that schizophrenia is rooted in physiological factors. The genetic explanation is supported by substantial evidence from family, twin, and adoption studies. For instance, Gottesman's (1991) large-scale review found a 48% concordance rate for monozygotic (MZ) twins, who share 100% of their genes, compared to just 17% for dizygotic (DZ) twins. This suggests a strong genetic vulnerability, though it is not 100%, indicating other factors must be involved. This vulnerability is believed to be polygenic. Neural correlates are abnormalities in brain structure or function associated with schizophrenia. For example, many patients show enlarged ventricles (fluid-filled cavities), implying a loss of brain tissue. Reduced grey matter in areas like the temporal and frontal lobes is also a common finding, linked to cognitive and negative symptoms.

The dopamine hypothesis is a key biochemical explanation, suggesting that schizophrenia is caused by abnormal levels of the neurotransmitter dopamine. The original theory proposed hyperdopaminergia (an excess of dopamine) in subcortical brain areas, which was linked to positive symptoms like hallucinations and delusions. Evidence for this came from the effectiveness of typical antipsychotics (e.g., chlorpromazine), which act as dopamine antagonists and reduce these symptoms. However, this failed to explain negative symptoms. The revised hypothesis suggests a more complex picture: hypodopaminergia (a deficit of dopamine) in the prefrontal cortex is responsible for negative and cognitive symptoms, alongside the original hyperdopaminergia in the subcortex. This provides a more comprehensive explanation for the varied symptom profile of the disorder.

Psychological explanations focus on the influence of family dynamics. The concept of 'Expressed Emotion' (EE) is a prominent theory, describing a family communication style characterised by high levels of criticism, hostility, and emotional over-involvement. While not seen as a cause, high EE is a robust predictor of relapse in patients recovering from schizophrenia. Earlier, more controversial theories include the 'schizophrenogenic mother' (Fromm-Reichmann, 1948), which described a cold, rejecting, and controlling mother figure thought to induce schizophrenia in her child. Another is the double-bind theory (Bateson et al., 1956), which posits that children who repeatedly receive contradictory messages from parents may struggle to develop a coherent construction of reality, leading to symptoms like disorganised thinking and paranoid delusions. These earlier theories are now largely discredited.

The cognitive approach explains schizophrenia through dysfunctional thought processes. Frith et al. (1992) identified two key cognitive deficits. The first is a failure of 'metarepresentation', which is the ability to reflect on our own thoughts and intentions. A breakdown in this process can lead to an inability to distinguish between internal thoughts and external stimuli, explaining auditory hallucinations (mistaking inner speech for an external voice) and delusions of control. The second deficit is a lack of 'central control', the ability to suppress automatic or irrelevant thoughts and actions. This can account for symptoms like disorganised speech and thought disorder, as the individual is unable to inhibit automatic associations and focus on the intended topic. These deficits are not a cause, but an explanation of the mechanisms behind the symptoms.