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PD – Antimuscarinic Cognitive Impairment — SCE Neurology MCQ

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ModerateMovement DisordersPD – Antimuscarinic Cognitive ImpairmentSCE Neurology

A 60-year-old man with PD develops urinary urgency and frequency. His post-void residual is 40 mL (normal). Urodynamics confirm detrusor overactivity. His neurologist starts an antimuscarinic (solifenacin). After 4 weeks he develops confusion and worsening cognitive function. What is the most likely explanation?

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Correct answer: A — Antimuscarinic-induced cognitive impairment — centrally acting antimuscarinics can worsen cognition in PD patients who are already vulnerable to cholinergic dysfunction

PD patients have progressive cholinergic neuronal loss (nucleus basalis of Meynert), making them particularly vulnerable to the cognitive effects of antimuscarinic drugs. Centrally acting antimuscarinics (oxybutynin is the worst offender; solifenacin, tolterodine have intermediate risk) can cause confusion, delirium, and worsening of cognition. Mirabegron (beta-3 agonist) and trospium (a quaternary amine that poorly crosses the BBB) are safer alternatives in PD patients. A: The temporal relationship to starting solifenacin is key. C: Solifenacin has central anticholinergic effects. D: UTI should be excluded but antimuscarinic effect is more likely given timing. E: No levodopa dose change.

Reference: NICE NG71; BNF – Antimuscarinic Bladder Drugs