Striatopallidal and Thalamic Dystonia

Lehericy, Stéphane; Vidailhet, Marie; Dormont, Didier; Piérot, Laurent; Chiras, J.; Mazetti, Pilar; Marsault, C.; Agid, Yves

doi:10.1001/archneur.1996.00550030051022

Cited by 94 publications

(16 citation statements)

References 48 publications

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“…One case of segmental dystonia resembled Meige’s syndrome [92]. Dystonic spasm was reported in one case and myoclonic dystonia was reported in 5 cases [49, 72]. …”

Section: Resultsmentioning

confidence: 99%

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Post-Thalamic Stroke Movement Disorders: A Systematic Review

Gupta

Pandey²

2018

Eur Neurol

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Background: After a stroke, movement disorders are rare manifestations mainly affecting the deep structures of the brain like the basal ganglia (44%) and thalamus (37%), although there have been case studies of movement disorders in strokes affecting the cerebral cortex also. Summary: This review aims to delineate the various movement disorders seen in association with thalamic strokes and tries to identify the location of the nuclei affected in each of the described movement disorders. Cases were identified through a search of PubMed database using different search terms related to post-thalamic stroke movement disorders and a secondary search of references of identified articles. We reviewed 2,520 research articles and only 86 papers met the inclusion criteria. Cases were included if they met criteria for post-thalamic stroke movement disorders. Case-cohort studies were also reviewed and will be discussed further. Key Messages: The most common post-stroke abnormal movement disorder reported in our review was dystonia followed by hemiataxia. There was a higher association between ischaemic stroke and movement disorder. Acute onset movement disorders were more common than delayed. The posterolateral thalamus was most commonly involved in post-thalamic stroke movement disorders.

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“…One case of segmental dystonia resembled Meige’s syndrome [92]. Dystonic spasm was reported in one case and myoclonic dystonia was reported in 5 cases [49, 72]. …”

Section: Resultsmentioning

confidence: 99%

“…In our review, the centromedian nucleus was involved in 21 cases of dystonia. In the study of Lehericy et al [49], it was involved in all cases of thalamic dystonia. The centromedian nucleus is a part of the intralaminar nuclei that project to striatum and form the thalamostriate pathway [8].…”

Section: Discussionmentioning

confidence: 99%

Post-Thalamic Stroke Movement Disorders: A Systematic Review

Gupta

Pandey²

2018

Eur Neurol

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“…This hyperexcitability, however, is probably only an epiphenomenon which reflects the motor disorder in the cortex, basal ganglia, and probably thalamus, because the number of observations demonstrating the occurrence of dystonia in patients with thalamic lesions is increasing. 31 If the hypothesis is correct that the P22/ N30 complex and the N30 peak have their own generator located in the precentral cortex area (SMA and the dorsolateral prefrontal cortex), one might postulate that the lateralization of P22/N30 is caused by a relatively higher amplitude on the side contralateral to the direction of head deviation. On the contrary, when one common generator for the P22/N30 and N20/P25 would be considered, the hyperexcitability is present also in the postcen- * The side-to-side ratio of P22/N30 and N20/P25 amplitudes was calculated contralaterally/ipsilaterally according to the side of head deviation in patients (groups I and II) and healthy control subjects in group IV.…”

Section: Discussionmentioning

confidence: 99%

Lateralization of the P22/N30 precentral cortical component of the median nerve somatosensory evoked potentials is different in patients with a tonic or tremulous form of cervical dystonia

Kaňovský¹,

Streitová²,

Dufek³

et al. 1999

Mov. Disord.

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“…Multiple structural imaging studies also link limb dystonias with focal lesions of the thalamus (Cho and Samkoff, 2000; Ghika et al, 1994; Kim, 2001; Krystkowiak et al, 1998; Lee and Marsden, 1995; Lehericy et al, 2001; Lehericy et al, 1996; Miwa et al, 1996). The topography of lesions within the thalamus varies, with some occurring in subnuclei receiving information from the basal ganglia, and others receiving information from the cerebellum.…”

Section: A Reappraisal Of the Evidencementioning

confidence: 99%

The functional neuroanatomy of dystonia

Neychev

Gross

Lehericy

et al. 2011

Neurobiology of Disease

396

419

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Dystonia is a neurological disorder characterized by involuntary twisting movements and postures. There are many different clinical manifestations, and many different causes. The neuroanatomical substrates for dystonia are only partly understood. Although the traditional view localizes dystonia to basal ganglia circuits, there is increasing recognition that this view is inadequate for accommodating a substantial portion of available clinical and experimental evidence. A model in which several brain regions play a role in a network better accommodates the evidence. This network model accommodates neuropathological and neuroimaging evidence that dystonia may be associated with abnormalities in multiple different brain regions. It also accommodates animal studies showing that dystonic movements arise with manipulations of different brain regions. It is consistent with neurophysiological evidence suggesting defects in neural inhibitory processes, sensorimotor integration, and maladaptive plasticity. Finally, it may explain neurosurgical experience showing that targeting the basal ganglia is effective only for certain subpopulations of dystonia. Most importantly, the network model provides many new and testable hypotheses with direct relevance for new treatment strategies that go beyond the basal ganglia.

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Striatopallidal and Thalamic Dystonia

Abstract: These results suggest that striatopallidal and thalamic dystonia may have different pathophysiologic bases.

Cited by 94 publications

References 48 publications

Post-Thalamic Stroke Movement Disorders: A Systematic Review

Post-Thalamic Stroke Movement Disorders: A Systematic Review

Lateralization of the P22/N30 precentral cortical component of the median nerve somatosensory evoked potentials is different in patients with a tonic or tremulous form of cervical dystonia

The functional neuroanatomy of dystonia

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