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Table of Contents
LETTERS TO THE EDITOR
Year : 2019  |  Volume : 2  |  Issue : 3  |  Page : 138-139

Comment: Dystonia and asterixis in acute thalamic infarct: Proposed mechanism


1 Department of Neurology, Federal University of Santa Maria, Santa Maria, Rio Grande do Sul, Brazil
2 Department of Medicine, Federal University of Santa Maria, Santa Maria, Rio Grande do Sul, Brazil

Date of Submission10-Sep-2019
Date of Decision11-Sep-2019
Date of Acceptance10-Oct-2019
Date of Web Publication04-Dec-2019

Correspondence Address:
Dr. Jamir Pitton Rissardo
Rua Roraima, Santa Maria, Rio Grande do Sul.
Brazil
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AOMD.AOMD_22_19

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How to cite this article:
Pitton Rissardo J, Fornari Caprara AL. Comment: Dystonia and asterixis in acute thalamic infarct: Proposed mechanism. Ann Mov Disord 2019;2:138-9

How to cite this URL:
Pitton Rissardo J, Fornari Caprara AL. Comment: Dystonia and asterixis in acute thalamic infarct: Proposed mechanism. Ann Mov Disord [serial online] 2019 [cited 2020 Apr 10];2:138-9. Available from: http://www.aomd.in/text.asp?2019/2/3/138/272285



Dear Editor,

We read an article in “Annals of Movement Disorders” with great interest, wherein Sarma and Mahanta[1] reported a case of an elderly man who presented with dystonic posturing of his left hand and ipsilateral intermittent jerks, suggestive of asterixis.

Dystonia is characterized by involuntary sustained muscle contractions, causing twisting and repetitive movements or abnormal postures. Also, it is the second most common movement disorder after a stroke, representing approximately one in every five cases. Asterixis could be described as negative myoclonus, caused by intermittent failure in maintaining sustained muscle contraction.[2]

We hypothesized that the concomitant occurrence of dystonia and asterixis probably occurred due to a lesion in the ventrolateral nucleus of the thalamus [Figure 1]. The pathophysiology of dystonia can be explained by the interruption in the cortico-striato-pallido-thalamo-cortical loop [Figure 1A]. A study by Mitchell et al.[3] described that a lesion in the pathways that lead to the thalamus might interrupt the direct and indirect pathways. However, the indirect pathway subactivity could probably predominate, and this disruption could increase the thalamocortical drive and eventually could lead to dystonia.[4]
Figure 1: Schematic diagram of the combined presentation of asterixis and dystonia

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On the contrary, the exact mechanism of generation of asterixis remains elusive since its first description [Figure 1B]. In this way, asterixis probably occurs secondary to lesions in the postural and tonic control such as the vestibulospinal, reticulospinal, and rubrospinal tracts.[5] These pathways are regulated by supratentorial structures such as the ventrolateral nucleus of the thalamus, which is the area where cerebellar–rubral and vestibulocerebellar fibers converge.[6] Furthermore, this hypothesis could be supported by a study conducted by Stell et al.,[7] which described an individual with a focal lesion in the ventrolateral nucleus of thalamus, who developed unilateral asterixis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sarma N, Mahanta A. Dystonia and asterixis in acute thalamic infarct. Ann Mov Dis 2019;2:78.  Back to cited text no. 1
    
2.
Bansil S, Prakash N, Kaye J, Wrigley S, Manata C, Stevens-Haas C, et al. Movement disorders after stroke in adults: A review. Tremor Other Hyperkinet Mov2012;2:pii.  Back to cited text no. 2
    
3.
Mitchell IJ, Luquin R, Boyce S, Clarke CE, Robertson RG, Sambrook MA, et al. Neural mechanisms of dystonia: Evidence from a 2-deoxyglucose uptake study in a primate model of dopamine agonist-induced dystonia. Mov Disord 1990;5:49-54.  Back to cited text no. 3
    
4.
Krystkowiak P, Martinat P, Defebvre L, Pruvo JP, Leys D, Destée A. Dystonia after striatopallidal and thalamic stroke: Clinicoradiological correlations and pathophysiological mechanisms. J Neurol Neurosurg Psychiatry 1998;65: 703-8.  Back to cited text no. 4
    
5.
Kim JS. Asterixis after unilateral stroke: Lesion location of 30 patients. Neurology 2001;56:533-6.  Back to cited text no. 5
    
6.
Masdeu JC, Gorelick PB. Thalamic astasia: Inability to stand after unilateral thalamic lesions. Ann Neurol 1988;23:596-603.  Back to cited text no. 6
    
7.
Stell R, Davis S, Carroll WM. Unilateral asterixis due to a lesion of the ventrolateral thalamus. J Neurol Neurosurg Psychiatry 1994;57:878-80.  Back to cited text no. 7
    


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