Sensory functions in dystonia: Insights from behavioral studies
Identifieur interne : 002061 ( Main/Curation ); précédent : 002060; suivant : 002062Sensory functions in dystonia: Insights from behavioral studies
Auteurs : Michele Tinazzi [Italie] ; Mirta Fiorio [Italie, Royaume-Uni] ; Antonio Fiaschi [Italie] ; John C. Rothwell [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-07-30.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Animals, Behavior (physiology), DYT1 gene, Discrimination, Dystonia, Dystonia (complications), Dystonia (psychology), Humans, Mental rotation, Movement (physiology), Nervous system diseases, Sensation Disorders (etiology), dystonia, endophenotype, mental rotation, sensory system, temporal discrimination.
- MESH :
Abstract
The pathophysiology of primary dystonia is thought to involve dysfunction of the basal ganglia cortico‐striatal‐thalamo‐cortical motor circuits. In the past, emphasis was placed on the role of the basal ganglia in controlling movements; in more recent times, however, it has also become clear that they play an important part in sensory as well as cognitive functions. Here, we review evidence for dysfunction of sensory processing in patients with dystonia, and speculate that this may lead to abnormalities in a crucial role of the basal ganglia that links sensory information to appropriate motor output. Sensory function, particularly in the somatosensory domain, has been shown to be compromised in patients with primary dystonia, both in adult onset focal dystonia and in genetically characterized DYT1 dystonia. Given that nonaffected DYT1 gene carriers may show similar abnormalities to clinically affected individuals, sensory deficits could constitute a subclinical endophenotypic trait of disease that precedes overt clinical manifestations. Whether they can trigger primary dystonia or are an epiphenomenon is an issue warranting further study, but the fact that a number of different neurorehabilitative approaches explicitly manipulate somatosensory inputs to improve motor function suggests there may be a causal link between them. We believe that in future, randomized, blind and controlled studies in large patient populations should address this issue, providing efficient strategies to aid functional recovery, particularly in focal hand dystonia, where the available medical treatments offer little benefit. © 2009 Movement Disorder Society
Url:
DOI: 10.1002/mds.22490
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<front><div type="abstract" xml:lang="en">The pathophysiology of primary dystonia is thought to involve dysfunction of the basal ganglia cortico-striatal-thalamo-cortical motor circuits. In the past, emphasis was placed on the role of the basal ganglia in controlling movements; in more recent times, however, it has also become clear that they play an important part in sensory as well as cognitive functions. Here, we review evidence for dysfunction of sensory processing in patients with dystonia, and speculate that this may lead to abnormalities in a crucial role of the basal ganglia that links sensory information to appropriate motor output. Sensory function, particularly in the somatosensory domain, has been shown to be compromised in patients with primary dystonia, both in adult onset focal dystonia and in genetically characterized DYT1 dystonia. Given that nonaffected DYT1 gene carriers may show similar abnormalities to clinically affected individuals, sensory deficits could constitute a subclinical endophenotypic trait of disease that precedes overt clinical manifestations. Whether they can trigger primary dystonia or are an epiphenomenon is an issue warranting further study, but the fact that a number of different neurorehabilitative approaches explicitly manipulate somatosensory inputs to improve motor function suggests there may be a causal link between them. We believe that in future, randomized, blind and controlled studies in large patient populations should address this issue, providing efficient strategies to aid functional recovery, particularly in focal hand dystonia, where the available medical treatments offer little benefit.</div>
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<author><name sortKey="Tinazzi, Michele" sort="Tinazzi, Michele" uniqKey="Tinazzi M" first="Michele" last="Tinazzi">Michele Tinazzi</name>
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<author><name sortKey="Fiorio, Mirta" sort="Fiorio, Mirta" uniqKey="Fiorio M" first="Mirta" last="Fiorio">Mirta Fiorio</name>
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<author><name sortKey="Fiaschi, Antonio" sort="Fiaschi, Antonio" uniqKey="Fiaschi A" first="Antonio" last="Fiaschi">Antonio Fiaschi</name>
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<author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. Rothwell</name>
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<author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name>
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<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Sensory functions in dystonia: Insights from behavioral studies</title>
<author><name sortKey="Tinazzi, Michele" sort="Tinazzi, Michele" uniqKey="Tinazzi M" first="Michele" last="Tinazzi">Michele Tinazzi</name>
<affiliation wicri:level="1"><country xml:lang="fr">Italie</country>
<wicri:regionArea>Department of Neurological and Vision Sciences, University of Verona, Verona</wicri:regionArea>
<wicri:noRegion>Verona</wicri:noRegion>
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<affiliation wicri:level="1"><country xml:lang="fr">Italie</country>
<wicri:regionArea>Neurology Unit, Borgo Trento Hospital, Verona</wicri:regionArea>
<wicri:noRegion>Verona</wicri:noRegion>
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<author><name sortKey="Fiorio, Mirta" sort="Fiorio, Mirta" uniqKey="Fiorio M" first="Mirta" last="Fiorio">Mirta Fiorio</name>
<affiliation wicri:level="1"><country xml:lang="fr">Italie</country>
<wicri:regionArea>Department of Neurological and Vision Sciences, University of Verona, Verona</wicri:regionArea>
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<affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Mirta Fiorio, Department of Neurological and Vision Sciences, Section of Rehabilitative Neurology, University of Verona, Via Casorati 43, 37131 Verona, ItalyKailash P. Bhatia, Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, WC1N 3BG</wicri:regionArea>
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<author><name sortKey="Fiaschi, Antonio" sort="Fiaschi, Antonio" uniqKey="Fiaschi A" first="Antonio" last="Fiaschi">Antonio Fiaschi</name>
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<wicri:regionArea>Department of Neurological and Vision Sciences, University of Verona, Verona</wicri:regionArea>
<wicri:noRegion>Verona</wicri:noRegion>
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<author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. Rothwell</name>
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<wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London</wicri:regionArea>
<placeName><settlement type="city">Londres</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Grand Londres</region>
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<author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name>
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<wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London</wicri:regionArea>
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<wicri:regionArea>Mirta Fiorio, Department of Neurological and Vision Sciences, Section of Rehabilitative Neurology, University of Verona, Via Casorati 43, 37131 Verona, ItalyKailash P. Bhatia, Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, WC1N 3BG</wicri:regionArea>
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<monogr></monogr>
<series><title level="j">Movement Disorders</title>
<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2009-07-30">2009-07-30</date>
<biblScope unit="vol">24</biblScope>
<biblScope unit="issue">10</biblScope>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Behavior (physiology)</term>
<term>DYT1 gene</term>
<term>Dystonia (complications)</term>
<term>Dystonia (psychology)</term>
<term>Humans</term>
<term>Movement (physiology)</term>
<term>Sensation Disorders (etiology)</term>
<term>dystonia</term>
<term>endophenotype</term>
<term>mental rotation</term>
<term>sensory system</term>
<term>temporal discrimination</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Dystonia</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Sensation Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Behavior</term>
<term>Movement</term>
</keywords>
<keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Dystonia</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Humans</term>
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<front><div type="abstract" xml:lang="en">The pathophysiology of primary dystonia is thought to involve dysfunction of the basal ganglia cortico‐striatal‐thalamo‐cortical motor circuits. In the past, emphasis was placed on the role of the basal ganglia in controlling movements; in more recent times, however, it has also become clear that they play an important part in sensory as well as cognitive functions. Here, we review evidence for dysfunction of sensory processing in patients with dystonia, and speculate that this may lead to abnormalities in a crucial role of the basal ganglia that links sensory information to appropriate motor output. Sensory function, particularly in the somatosensory domain, has been shown to be compromised in patients with primary dystonia, both in adult onset focal dystonia and in genetically characterized DYT1 dystonia. Given that nonaffected DYT1 gene carriers may show similar abnormalities to clinically affected individuals, sensory deficits could constitute a subclinical endophenotypic trait of disease that precedes overt clinical manifestations. Whether they can trigger primary dystonia or are an epiphenomenon is an issue warranting further study, but the fact that a number of different neurorehabilitative approaches explicitly manipulate somatosensory inputs to improve motor function suggests there may be a causal link between them. We believe that in future, randomized, blind and controlled studies in large patient populations should address this issue, providing efficient strategies to aid functional recovery, particularly in focal hand dystonia, where the available medical treatments offer little benefit. © 2009 Movement Disorder Society</div>
</front>
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