In the dopamine hypothesis of schizophrenia, the mesolimbic and mesocortical pathways are differentially affected. Which pairing of pathway-abnormality-symptom is CORRECT?

• A Mesocortical: hyperdopaminergia → positive symptoms
• B Nigrostriatal: hyperdopaminergia → EPS; Mesolimbic: hypodopaminergia → positive symptoms
• C Mesolimbic: hyperdopaminergia → positive symptoms; Mesocortical: hypodopaminergia → negative/cognitive symptoms ✓
• D Tuberoinfundibular: hyperdopaminergia → hyperprolactinaemia → positive symptoms

Explanation

The revised dopamine hypothesis proposes: (1) Mesolimbic pathway: excess dopamine (D2 receptor hyperactivation) → positive symptoms (delusions, hallucinations, disorganisation); and (2) Mesocortical pathway (to prefrontal cortex): deficient dopamine (D1 receptor hypoactivation) → negative and cognitive symptoms (avolition, alogia, impaired working memory). The nigrostriatal pathway: dopamine blockade by antipsychotics → EPS. The tuberoinfundibular pathway: dopamine blockade → elevated prolactin → galactorrhoea, amenorrhoea. This dual-pathway model explains why antipsychotics effectively treat positive symptoms (blocking mesolimbic D2) but may worsen negative/cognitive symptoms.

Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.

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