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Year : 2019  |  Volume : 2  |  Issue : 2  |  Page : 37-38

Poststroke movement disorders: One etiology many phenotypes


Department of Neurology, Govind Ballabh Pant Institute of Postgraduate Medical Education and Research, New Delhi, India

Date of Web Publication13-Aug-2019

Correspondence Address:
Prof. Sanjay Pandey
Department of Neurology, Govind Ballabh Pant Institute of Postgraduate Medical Education and Research, Academic Block, Room No. 507, New Delhi 110002
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AOMD.AOMD_10_19

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How to cite this article:
Chouksey A, Pandey S. Poststroke movement disorders: One etiology many phenotypes. Ann Mov Disord 2019;2:37-8

How to cite this URL:
Chouksey A, Pandey S. Poststroke movement disorders: One etiology many phenotypes. Ann Mov Disord [serial online] 2019 [cited 2019 Dec 9];2:37-8. Available from: http://www.aomd.in/text.asp?2019/2/2/37/264357



Poststroke movement disorder (PSMD) represents a heterogeneous subgroup of secondary movement disorders. They constitute around 22% of all the secondary causes of movement disorders.[1] PSMDs are one of the important but still an underrated cause of poststroke morbidity. Few studies that have studied PSMDs suggest that only 1%–4% of the strokes are followed by the appearance of abnormal movements.[2] However, this figure seems to underestimate the actual frequency of PSMDs as they are either often overlooked in an emergency setting due to masking by the overwhelming stroke symptoms or sometimes missed because of their transient or short-lasting nature and spontaneous resolution after stroke. PSMDs may present as either hyperkinetic or hypokinetic movements. Various phenomenology that have been described after vascular event include tremor, chorea-ballism, dystonia, athetosis, myoclonus, ataxia,  Parkinsonism More Details, and stereotypy.[3],[4],[5] The delay between the stroke and the onset of the abnormal movement is highly variable and it may reflect the time taken by the neuronal plasticity for the partial recovery of motor function and the formation of pathological circuitry due to maladaptive plasticity.

The various mechanisms that have been proposed to be underlying the origin of PSMDs include the changes in neuronal membrane excitability, the loss of perilesional GABAergic inhibition, the enhanced glutamatergic transmission, and the postischemic synaptic plasticity that contributes to the brain reorganization following the stroke. This also leads to unmasking or disinhibition of preexisting functionally silent synapses around the lesion, so the neuronal networks that are not primarily involved in stroke become progressively activated.[6],[7] Thus, the recovery from motor stroke is associated with different patterns of functional reorganization of the brain in different individuals depending on both the site of the subcortical lesion and the somatotopic organization of the pyramidal tract.[8] During the poststroke remodeling phase, increased activity is observed in the contralesional hemisphere along with reduced interhemispheric inhibition, which results in increased cortical excitability and better functional recovery at the cost of the appearance of abnormal movements.[9] Recent studies on stroke have focused on developing the novel strategies to improve the motor recovery following stroke by facilitating the adaptive brain plasticity and reducing the effect of maladaptive plasticity. Transcranial magnetic stimulation of the motor cortex is one of such tools that are under investigation for their utility in the treatment of the PSMDs.

PSMDs differ from their non-stroke-related counterparts in terms of their clinical profile, natural history, anatomical structures involved, prognosis, and treatment. The major factors that seem to play a role in deciding the phenomenology of PSMDs include the age of the patient, type of stroke, and location of the lesion. Alarcón et al.,[2] in their study of 56 patients with PSMD, found that dystonia was the most common movement observed in the younger age group, whereas chorea was more common in older patients with stroke. In their systematic review of 284 patients with PSMD, Suri et al.[10] observed that parkinsonism, chorea, and dystonia were the most commonly observed movements in patients with ischemic stroke, whereas dystonia, tremor, and myoclonus (15%) were more frequent in patients with hemorrhagic stroke. In the Lausanne Stroke Registry, basal ganglia (44%) followed by thalamic involvement (37%) were the most common site of lesion in patients with PSMD.[11] The most common site of isolated lesions causing dystonia is putamen followed by caudate, pallidum, thalamus, and the midbrain.[12] Hemichorea has been most commonly associated with lesions affecting the lentiform nucleus or the thalamus, whereas poststroke hemiballism occurs mostly due to an ischemic lesion in the contralateral subthalamic nucleus. Vascular parkinsonism is most commonly seen with lesions in the basal ganglia (mainly striatum or lentiform nucleus). Lesions in the posterior thalamus or lesions interrupting the dentato-rubro-thalamic pathways are the most likely culprit for the development of poststroke tremor.[13] It has been observed that the same movement disorder can be caused by lesions involving the different structures of the brain, and the lesion of the same structure can produce different types of abnormal movement in different patients. Therefore, it is difficult to precisely predict the location of the lesion based on the phenomenology of PSMD.

Despite the recent advances in this field, there are many questions that remain unanswered such as the reason behind the absence of strict anatomical or clinical correlate between the location of the lesion and phenomenology of PSMD. It is also not known that what factors predispose an individual to develop these PSMDs as not all the patients with stroke involving these critical structures develop PSMD. Furthermore, the variable duration of latency between the stroke and appearance of abnormal movement makes it difficult to convincingly attribute the damage caused by the stroke as a sole cause of these movements. There is no established therapeutic recommendation for the management of PSMD due to lack of conclusive evidence for the efficacy of available pharmacological agents in different PSMDs. Thus, these caveats in the understanding of the pathogenesis and the management of the PSMD need to be addressed in future studies. Further research will help to decipher more precisely the mechanism of neuroplasticity responsible for PSMD.

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Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Netravathi M, Pal PK, Indira DB A clinical profile of 103 patients with secondary movement disorders: Correlation of etiology with phenomenology. Eur J Neurol 2012;19:226-33.  Back to cited text no. 1
    
2.
Alarcón F, Zijlmans JC, Dueñas G, Cevallos N Post-stroke movement disorders: Report of 56 patients. J Neurol Neurosurg Psychiatry 2004;75:1568-74.  Back to cited text no. 2
    
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Suri R, Rodriguez-Porcel F, Donohue K, Jesse E, Lovera L, Dwivedi AK, et al. Post-stroke movement disorders: The clinical, neuroanatomic, and demographic portrait of 284 published cases. J Stroke Cerebrovasc Dis 2018;27:2388-97.  Back to cited text no. 10
    
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Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J Hyperkinetic movement disorders during and after acute stroke: The Lausanne Stroke Registry. J Neurol Sci 1997;146:109-16.  Back to cited text no. 11
    
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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. 12
    
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Nowak DA, Seidel B, Reiner B Tremor following ischemic stroke of the posterior thalamus. J Neurol 2010;257:1934-6.  Back to cited text no. 13
    




 

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