Movement Disorders (revue)

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Dystonia Associated with pontomesencephalic lesions

Identifieur interne : 000704 ( Istex/Corpus ); précédent : 000703; suivant : 000705

Dystonia Associated with pontomesencephalic lesions

Auteurs : Thomas J. Loher ; Joachim K. Krauss

Source :

RBID : ISTEX:5AE656C80444F9C5976E28185FAF09785BA04E44

English descriptors

Abstract

Secondary dystonia is well known subsequent to lesions of the basal ganglia or the thalamus. There is evidence that brainstem lesions may also be associated with dystonia, but little is known about pathoanatomical correlations. Here, we report on a series of four patients with acquired dystonia following brainstem lesions. There were no basal ganglia or thalamic lesions. Three patients suffered tegmental pontomesencephalic hemorrhage and one patient diffuse axonal injury secondary to severe craniocerebral trauma. Dystonia developed with a delay of 1 to 14 months, at a mean delay of 6 months. The patients' mean age at onset was 33 years (range 4–56 years). All patients presented with hemidystonia combined with cervical dystonia, and two patients had craniofacial dystonia in addition. Three patients had postural or kinetic tremors. Dystonia was persistent in three patients, and improved gradually in one. There was little response to medical treatment. One patient with hemidystonia combined with cervical dystonia improved after thalamotomy. Overall, the phenomenology of secondary dystonia due to pontomesencephalic lesions is similar to that caused by basal ganglia or thalamic lesions. Structures involved include the pontomesencephalic tegmentum and the superior cerebellar peduncles. Such lesions are often associated with fatal outcome. While delayed occurrence of severe brainstem dystonia appears to be rare, it is possible that mild manifestations of dystonia might be ignored or not be emphasized in the presence of other disabling deficits. © 2008 Movement Disorder Society

Url:
DOI: 10.1002/mds.22196

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ISTEX:5AE656C80444F9C5976E28185FAF09785BA04E44

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<extent unit="references">37</extent>
<extent unit="words">5357</extent>
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<abstract lang="en">Secondary dystonia is well known subsequent to lesions of the basal ganglia or the thalamus. There is evidence that brainstem lesions may also be associated with dystonia, but little is known about pathoanatomical correlations. Here, we report on a series of four patients with acquired dystonia following brainstem lesions. There were no basal ganglia or thalamic lesions. Three patients suffered tegmental pontomesencephalic hemorrhage and one patient diffuse axonal injury secondary to severe craniocerebral trauma. Dystonia developed with a delay of 1 to 14 months, at a mean delay of 6 months. The patients' mean age at onset was 33 years (range 4–56 years). All patients presented with hemidystonia combined with cervical dystonia, and two patients had craniofacial dystonia in addition. Three patients had postural or kinetic tremors. Dystonia was persistent in three patients, and improved gradually in one. There was little response to medical treatment. One patient with hemidystonia combined with cervical dystonia improved after thalamotomy. Overall, the phenomenology of secondary dystonia due to pontomesencephalic lesions is similar to that caused by basal ganglia or thalamic lesions. Structures involved include the pontomesencephalic tegmentum and the superior cerebellar peduncles. Such lesions are often associated with fatal outcome. While delayed occurrence of severe brainstem dystonia appears to be rare, it is possible that mild manifestations of dystonia might be ignored or not be emphasized in the presence of other disabling deficits. © 2008 Movement Disorder Society</abstract>
<note type="content">*This article is part of the journal's online CME program. The CME activity including form, can be found online at http://www.movementdisorders.org/education/journalcme/</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>dystonia</topic>
<topic>brainstem</topic>
<topic>hemorrhage</topic>
<topic>trauma</topic>
<topic>tremor</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<note type="content"> Additional Supporting Information may be found in the online version of this article.</note>
<subject>
<genre>article category</genre>
<topic>Research Article</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>24</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>2</number>
</detail>
<extent unit="pages">
<start>157</start>
<end>167</end>
<total>11</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">5AE656C80444F9C5976E28185FAF09785BA04E44</identifier>
<identifier type="DOI">10.1002/mds.22196</identifier>
<identifier type="ArticleID">MDS22196</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Movement Disorder Society</accessCondition>
<recordInfo>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
</record>

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