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Acute Onset Dystonia after Infarction of Premotor and Supplementary Motor Cortex

Objective Poststroke dystonia is the second most common movement disorder after chorea and often has a delayed manifestation. Lesions of the contralateral lenticular nucleus, particularly the putamen, have been implicated in the pathogenesis of dystonia. We present an unusual case of rapid onset of...

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Published in:	Journal of stroke and cerebrovascular diseases 2015-12, Vol.24 (12), p.2880-2882
Main Authors:	Dhakar, Monica B., MD, MS, Watson, Carla, MD, Rajamani, Kumar, MD
Format:	Article
Language:	English
Subjects:	Brain Infarction - complications Brain Infarction - pathology Cardiovascular Dystonia Dystonia - etiology Dystonia - pathology Female Humans Middle Aged Motor Cortex - pathology Neurology poststroke premotor cortex supplementary motor area
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container_title	Journal of stroke and cerebrovascular diseases
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creator	Dhakar, Monica B., MD, MS Watson, Carla, MD Rajamani, Kumar, MD
description	Objective Poststroke dystonia is the second most common movement disorder after chorea and often has a delayed manifestation. Lesions of the contralateral lenticular nucleus, particularly the putamen, have been implicated in the pathogenesis of dystonia. We present an unusual case of rapid onset of focal dystonia of the left upper extremity, which developed after infarction of the right premotor cortex (PMC) and the supplementary motor area (SMA). Method A retrospective chart review of the patient was performed. Results and Conclusion We propose that disruption of the afferents from PMC and SMA in the setting of chronic striatal abnormality can result in acute dystonia due to disinhibition of the thalamocortical circuit.
doi_str_mv	10.1016/j.jstrokecerebrovasdis.2015.09.016
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Lesions of the contralateral lenticular nucleus, particularly the putamen, have been implicated in the pathogenesis of dystonia. We present an unusual case of rapid onset of focal dystonia of the left upper extremity, which developed after infarction of the right premotor cortex (PMC) and the supplementary motor area (SMA). Method A retrospective chart review of the patient was performed. Results and Conclusion We propose that disruption of the afferents from PMC and SMA in the setting of chronic striatal abnormality can result in acute dystonia due to disinhibition of the thalamocortical circuit.</description><identifier>ISSN: 1052-3057</identifier><identifier>EISSN: 1532-8511</identifier><identifier>DOI: 10.1016/j.jstrokecerebrovasdis.2015.09.016</identifier><identifier>PMID: 26483154</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Brain Infarction - complications ; Brain Infarction - pathology ; Cardiovascular ; Dystonia ; Dystonia - etiology ; Dystonia - pathology ; Female ; Humans ; Middle Aged ; Motor Cortex - pathology ; Neurology ; poststroke ; premotor cortex ; supplementary motor area</subject><ispartof>Journal of stroke and cerebrovascular diseases, 2015-12, Vol.24 (12), p.2880-2882</ispartof><rights>National Stroke Association</rights><rights>2015 National Stroke Association</rights><rights>Copyright © 2015 National Stroke Association. 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source	ScienceDirect Freedom Collection 2022-2024
subjects	Brain Infarction - complications Brain Infarction - pathology Cardiovascular Dystonia Dystonia - etiology Dystonia - pathology Female Humans Middle Aged Motor Cortex - pathology Neurology poststroke premotor cortex supplementary motor area
title	Acute Onset Dystonia after Infarction of Premotor and Supplementary Motor Cortex
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