Rapid Cognitive Decline and Myoclonus: A Reversible Case of Bismuth Toxicity With a Therapeutic Chelation Paradigm

Bismuth neurotoxicity is a rare but potentially reversible cause of encephalopathy resulting from systemic accumulation of bismuth. Clinical manifestations may mimic rapidly progressive neurodegenerative or prion disorders. A 75‐year‐old man with chronic bismuth subsalicylate use presented with progressive confusion, gait instability, and generalized myoclonus. Extensive evaluation, including cerebrospinal fluid analysis, autoimmune encephalopathy testing, electroencephalography, and brain magnetic resonance imaging, was unrevealing. Serum bismuth concentration was markedly elevated at 319 μg/L (reference range 0–9 μg/L), confirming bismuth toxicity. Bismuth was discontinued, and the patient underwent sequential chelation therapy with dimercaprol and N‐acetylcysteine followed by oral succimer. Clinical improvement paralleled declining serum and urine bismuth concentrations, with complete recovery of cognition and gait within 4 weeks. This case illustrates a reversible toxic mimic of rapidly progressive neurodegenerative disease. Chronic bismuth exposure should be considered in patients presenting with unexplained encephalopathy and myoclonus, particularly when initial investigations are unrevealing. Recognition of this rare entity may prevent misdiagnosis and allow complete neurological recovery through timely withdrawal of the offending agent and targeted treatment.