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SCIENTIFIC LITERATURE · MED

Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller.

Tremor Other Hyperkinet Mov (N Y) · 2020-10-20

DOI: 10.5334/tohm.537PMID: 33178484

Open accessVideo-Audio Media; Research Support, Non-U.S. Gov't; Journal Article; Case Reports; Research Support, N.I.H., Extramural; case-reportOriginal source ↗

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The text below is the source article’s original abstract under a verified reuse license. cc by

BackgroundManganese associated neurotoxicity and neurodegeneration is quite rare yet established neurological disorder. This neurotoxic element has predilection for depositing in basal ganglia structures, manifesting mainly as parkinsonian and dystonic movement disorders with behavioral abnormalities.Case reportWe report a 40-year-old man who presented with a subacute onset bilateral, asymmetric hyperkinetic movement disorder (predominantly left sided chorea) with multi-domain cognitive impairment, dysarthria, and generalized rigidity. Clinical history and examination yielded multiple differential diagnoses including deposition and metabolic disorders, autoimmune and paraneoplastic encephalitis involving basal ganglia, and neurodegenerative disorders with chorea and cognitive impairment. However, magnetic resonance imaging was suggestive of paramagnetic substance deposition, which came out to be manganese after laboratory investigations. History, clinical examinations, and investigation results pointed towards a diagnosis of acquired hypermanganesemia due to over-ingestion of manganese containing substance (i.e., black tea). He was treated symptomatically and with chelation therapy (calcium disodium edetate). At the sixth month of follow-up, complete resolution of chorea, dysarthria and partial amelioration of rigidity were observed. His cognitive decline and behavioral abnormalities improved.DiscussionThis is probably the first reported case of acquired hypermanganesemia that presented as a combination of asymmetric chorea and cognitive dysfunction with atypical imaging characteristics. The clinical picture mimicked that of Huntington's disease. We highlight the potential deleterious effects of an apparently "benign" non-alcoholic beverage (i.e., black tea) on cerebral metabolism.

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