Dopaminergic hallucinations — MRCPsych Paper A MCQ

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ModerateNeurophysiology and neurochemistryDopaminergic hallucinationsMRCPsych Paper A

A 72-year-old man with Parkinson's disease develops formed visual hallucinations shortly after an increase in his co-careldopa dose. He remains alert and oriented, without fluctuating attention, and assessment identifies no infective or metabolic trigger. Which pharmacological change most directly accounts for the hallucinations?

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Correct answer: E — Increased central dopamine receptor stimulation

The correct answer is E. Levodopa crosses into the brain and is decarboxylated to dopamine, so dose escalation increases central dopamine receptor stimulation. The close temporal link to dose increase, preserved attention and orientation, and exclusion of infective or metabolic causes point to a dopaminergic drug effect rather than delirium. UK product information attributes levodopa-related mental disturbances to increased brain dopamine and lists hallucinations as an adverse effect, and NICE advises reviewing and reducing dopaminergic medicines that trigger hallucinations. Central muscarinic blockade causes confusion and hallucinations, but with anticholinergic drugs, not levodopa. NMDA antagonism, 5-HT2A agonism and kappa-opioid agonism generate perceptual disturbance in other pharmacological contexts (ketamine, psychedelics, kappa agonists) but are not the mechanism of a co-careldopa dose-related reaction.

Reference: electronic Medicines Compendium, Sinemet (co-careldopa) 12.5 mg/50 mg Tablets, SmPC sections 4.4 and 5.1 — https://www.medicines.org.uk/emc/product/1654/smpc (supported by NICE NG71, Parkinson's disease in adults, 2017: https://www.nice.org.uk/guidance/ng71/chapter/recommendations)