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Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller

BACKGROUND: Manganese 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 abnormalit...

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Autores principales: Ghosh, Ritwik, Dubey, Souvik, Chatterjee, Subhankar, Ghosh, Mrinalkanti, Ray, Biman Kanti, Benito-León, Julián
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ubiquity Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7597573/
https://www.ncbi.nlm.nih.gov/pubmed/33178484
http://dx.doi.org/10.5334/tohm.537
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author Ghosh, Ritwik
Dubey, Souvik
Chatterjee, Subhankar
Ghosh, Mrinalkanti
Ray, Biman Kanti
Benito-León, Julián
author_facet Ghosh, Ritwik
Dubey, Souvik
Chatterjee, Subhankar
Ghosh, Mrinalkanti
Ray, Biman Kanti
Benito-León, Julián
author_sort Ghosh, Ritwik
collection PubMed
description BACKGROUND: Manganese 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 REPORT: We 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. DISCUSSION: This 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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spelling pubmed-75975732020-11-10 Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller Ghosh, Ritwik Dubey, Souvik Chatterjee, Subhankar Ghosh, Mrinalkanti Ray, Biman Kanti Benito-León, Julián Tremor Other Hyperkinet Mov (N Y) Case Report BACKGROUND: Manganese 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 REPORT: We 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. DISCUSSION: This 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. Ubiquity Press 2020-10-20 /pmc/articles/PMC7597573/ /pubmed/33178484 http://dx.doi.org/10.5334/tohm.537 Text en Copyright: © 2020 The Author(s) http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (CC-BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See http://creativecommons.org/licenses/by/4.0/.
spellingShingle Case Report
Ghosh, Ritwik
Dubey, Souvik
Chatterjee, Subhankar
Ghosh, Mrinalkanti
Ray, Biman Kanti
Benito-León, Julián
Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller
title Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller
title_full Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller
title_fullStr Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller
title_full_unstemmed Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller
title_short Hypermanganesemia Induced Chorea and Cognitive Decline in a Tea Seller
title_sort hypermanganesemia induced chorea and cognitive decline in a tea seller
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7597573/
https://www.ncbi.nlm.nih.gov/pubmed/33178484
http://dx.doi.org/10.5334/tohm.537
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