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Table of Contents
Year : 2019  |  Volume : 2  |  Issue : 3  |  Page : 140

Reply: Dystonia and asterixis in acute thalamic infarct

Department of Neurology, Dispur Hospital, Guwahati, Assam, India

Date of Submission11-Oct-2019
Date of Acceptance12-Oct-2019
Date of Web Publication04-Dec-2019

Correspondence Address:
Dr. Neelav Sarma
Department of Neurology, Dispur Hospital, Guwahati 781006, Assam.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/AOMD.AOMD_25_19

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How to cite this article:
Sarma N. Reply: Dystonia and asterixis in acute thalamic infarct. Ann Mov Disord 2019;2:140

How to cite this URL:
Sarma N. Reply: Dystonia and asterixis in acute thalamic infarct. Ann Mov Disord [serial online] 2019 [cited 2021 Oct 18];2:140. Available from: https://www.aomd.in/text.asp?2019/2/3/140/272288

Dear Editor,

The author(s) have very nicely elucidated the proposed mechanisms responsible for causing dystonia and asterixis following thalamic lesions by explaining both the phenomena arising from the involvement of a single region of the thalamus. Their remarks on pathophysiology of asterixis following thalamic lesion are fully agreed on. Post stroke asterixis has been described following involvement of areas that maintain postural tone, which include thalamus, basal ganglia, cerebellum, frontoparietal cortex and brainstem.[1],[2] Our patient also had an infarct involving the occipital cortex, raising the question whether that has any bearing with the generation of asterixis. A South Korean study comprising 30 patients of poststroke asterixis found concomitant occipital lobe involvement in some of their patients; it, however, concluded that occipital lobe involvement has no role to play in the generation of asterixis.[2]

Similarly, the pathophysiological mechanisms responsible for the generation of dystonia have been well described by the authors(s), as explained by the loss of inhibitory influence on thalamus from basal ganglia, leading to increased excitatory influence of cortex by thalamus causing dystonia. However, a few more points deserve consideration while discussing the role of thalamus in the generation of dystonia. Two important nuclei, namely the centromedian nucleus of thalamus and the pedunculopontine nucleus (PPN) in pons, have regulatory effect on the thalamus. Although the centromedian nucleus has a direct influence by inhibiting the cortico-striato-pallido-thalamo-cortical loop, the PPN affects the thalamus by modulating the activity of centromedian nucleus as well as the ventrolateral nucleus.[3] Lesioning of the thalamus can affect the fibers of these modulating pathways, and hence increase the stimulating activity of thalamus to cortex. These influences occur independently of the described direct and indirect pathways that involve the basal ganglia.

Finally, if both asterixis and dystonia arise from stroke involving the same region, it will be interesting to discuss why the former resolves over a short period, whereas the latter persists. One explanation could be a bilateral control of postural tone by supratentorial structures, resulting in quick recovery of asterixis.[2] Secondary neuronal changes, such as transsynaptic neuronal degeneration, ephaptic transmission, remyelinisation, and neuroplasticity, may be responsible for the persistence of dystonia.[1]

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There are no conflicts of interest.

  References Top

Mehanna R, Jankovic J. Movement disorders in cerebrovascular disease. Lancet Neurol 2013;12:597-608.  Back to cited text no. 1
Kim JS. Asterixis after unilateral stroke: Lesion location of 30 patients. Neurology 2001;56:533-6.  Back to cited text no. 2
Gupta N, Pandey S. Post-thalamic stroke movement disorders: A systematic review. Eur Neurol 2018;79:303-14.  Back to cited text no. 3


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