MovDisordV3, PascalFrancis, Corpus, bibRecord, 000E00

Sensory Functions in Dystonia: Insights from Behavioral Studies

Identifieur interne : 000E00 ( PascalFrancis/Corpus ); précédent : 000D99; suivant : 000E01

Sensory Functions in Dystonia: Insights from Behavioral Studies

Auteurs : Michele Tinazzi ; Mirta Fiorio ; Antonio Fiaschi ; John C. Rothwell ; Kailash P. Bhatia

Source :

Movement disorders [ 0885-3185 ] ; 2009.

RBID : Pascal:09-0358930

Descripteurs français

Pascal (Inist)
- Dystonie, Pathologie du système nerveux, Discrimination, Rotation mentale.

English descriptors

KwdEn :
- Discrimination, Dystonia, Mental rotation, Nervous system diseases.

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0885-3185`
A03		`1`		`@0 Mov. disord.`
A05				`@2 24`
A06				`@2 10`
A08	`01`	`1`	`ENG`	`@1 Sensory Functions in Dystonia: Insights from Behavioral Studies`
A11	`01`	`1`		`@1 TINAZZI (Michele)`
A11	`02`	`1`		`@1 FIORIO (Mirta)`
A11	`03`	`1`		`@1 FIASCHI (Antonio)`
A11	`04`	`1`		`@1 ROTHWELL (John C.)`
A11	`05`	`1`		`@1 BHATIA (Kailash P.)`
A14	`01`			`@1 Department of Neurological and Vision Sciences, University of Verona @2 Verona @3 ITA @Z 1 aut. @Z 2 aut. @Z 3 aut.`
A14	`02`			`@1 Neurology Unit, Borgo Trento Hospital @2 Verona @3 ITA @Z 1 aut.`
A14	`03`			`@1 Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology @2 London @3 GBR @Z 4 aut. @Z 5 aut.`
A20				`@1 1427-1436`
A21				`@1 2009`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 20953 @5 354000187543670020`
A44				`@0 0000 @1 © 2009 INIST-CNRS. All rights reserved.`
A45				`@0 101 ref.`
A47	`01`	`1`		`@0 09-0358930`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Movement disorders`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 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.
C02	`01`	`X`		`@0 002B17`
C02	`02`	`X`		`@0 002B17H`
C03	`01`	`X`	`FRE`	`@0 Dystonie @5 01`
C03	`01`	`X`	`ENG`	`@0 Dystonia @5 01`
C03	`01`	`X`	`SPA`	`@0 Distonía @5 01`
C03	`02`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 02`
C03	`02`	`X`	`ENG`	`@0 Nervous system diseases @5 02`
C03	`02`	`X`	`SPA`	`@0 Sistema nervioso patología @5 02`
C03	`03`	`X`	`FRE`	`@0 Discrimination @5 09`
C03	`03`	`X`	`ENG`	`@0 Discrimination @5 09`
C03	`03`	`X`	`SPA`	`@0 Discriminación @5 09`
C03	`04`	`X`	`FRE`	`@0 Rotation mentale @5 10`
C03	`04`	`X`	`ENG`	`@0 Mental rotation @5 10`
C03	`04`	`X`	`SPA`	`@0 Rotación mental @5 10`
C07	`01`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 37`
C07	`01`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 37`
C07	`01`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 37`
C07	`02`	`X`	`FRE`	`@0 Mouvement involontaire @5 38`
C07	`02`	`X`	`ENG`	`@0 Involuntary movement @5 38`
C07	`02`	`X`	`SPA`	`@0 Movimiento involuntario @5 38`
C07	`03`	`X`	`FRE`	`@0 Pathologie du muscle strié @5 39`
C07	`03`	`X`	`ENG`	`@0 Striated muscle disease @5 39`
C07	`03`	`X`	`SPA`	`@0 Músculo estriado patología @5 39`
C07	`04`	`X`	`FRE`	`@0 Trouble neurologique @5 41`
C07	`04`	`X`	`ENG`	`@0 Neurological disorder @5 41`
C07	`04`	`X`	`SPA`	`@0 Trastorno neurológico @5 41`
C07	`05`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 42`
C07	`05`	`X`	`ENG`	`@0 Cerebral disorder @5 42`
C07	`05`	`X`	`SPA`	`@0 Encéfalo patología @5 42`
C07	`06`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 43`
C07	`06`	`X`	`ENG`	`@0 Central nervous system disease @5 43`
C07	`06`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 43`
N21				`@1 257`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 09-0358930 INIST
ET :	Sensory Functions in Dystonia: Insights from Behavioral Studies
AU :	TINAZZI (Michele); FIORIO (Mirta); FIASCHI (Antonio); ROTHWELL (John C.); BHATIA (Kailash P.)
AF :	Department of Neurological and Vision Sciences, University of Verona/Verona/Italie (1 aut., 2 aut., 3 aut.); Neurology Unit, Borgo Trento Hospital/Verona/Italie (1 aut.); Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology/London/Royaume-Uni (4 aut., 5 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2009; Vol. 24; No. 10; Pp. 1427-1436; Bibl. 101 ref.
LA :	Anglais
EA :	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.
CC :	002B17; 002B17H
FD :	Dystonie; Pathologie du système nerveux; Discrimination; Rotation mentale
FG :	Syndrome extrapyramidal; Mouvement involontaire; Pathologie du muscle strié; Trouble neurologique; Pathologie de l'encéphale; Pathologie du système nerveux central
ED :	Dystonia; Nervous system diseases; Discrimination; Mental rotation
EG :	Extrapyramidal syndrome; Involuntary movement; Striated muscle disease; Neurological disorder; Cerebral disorder; Central nervous system disease
SD :	Distonía; Sistema nervioso patología; Discriminación; Rotación mental
LO :	INIST-20953.354000187543670020
ID :	09-0358930

Links to Exploration step

Pascal:09-0358930

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">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><inist:fA14 i1="01"><s1>Department of Neurological and Vision Sciences, University of Verona</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Neurology Unit, Borgo Trento Hospital</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fiorio, Mirta" sort="Fiorio, Mirta" uniqKey="Fiorio M" first="Mirta" last="Fiorio">Mirta Fiorio</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurological and Vision Sciences, University of Verona</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fiaschi, Antonio" sort="Fiaschi, Antonio" uniqKey="Fiaschi A" first="Antonio" last="Fiaschi">Antonio Fiaschi</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurological and Vision Sciences, University of Verona</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. Rothwell</name>
<affiliation><inist:fA14 i1="03"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name>
<affiliation><inist:fA14 i1="03"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">09-0358930</idno>
<date when="2009">2009</date>
<idno type="stanalyst">PASCAL 09-0358930 INIST</idno>
<idno type="RBID">Pascal:09-0358930</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000E00</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">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><inist:fA14 i1="01"><s1>Department of Neurological and Vision Sciences, University of Verona</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Neurology Unit, Borgo Trento Hospital</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fiorio, Mirta" sort="Fiorio, Mirta" uniqKey="Fiorio M" first="Mirta" last="Fiorio">Mirta Fiorio</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurological and Vision Sciences, University of Verona</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fiaschi, Antonio" sort="Fiaschi, Antonio" uniqKey="Fiaschi A" first="Antonio" last="Fiaschi">Antonio Fiaschi</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurological and Vision Sciences, University of Verona</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. Rothwell</name>
<affiliation><inist:fA14 i1="03"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name>
<affiliation><inist:fA14 i1="03"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2009">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Discrimination</term>
<term>Dystonia</term>
<term>Mental rotation</term>
<term>Nervous system diseases</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dystonie</term>
<term>Pathologie du   système nerveux</term>
<term>Discrimination</term>
<term>Rotation mentale</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0>
</fA01>
<fA03 i2="1"><s0>Mov. disord.</s0>
</fA03>
<fA05><s2>24</s2>
</fA05>
<fA06><s2>10</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Sensory Functions in Dystonia: Insights from Behavioral Studies</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>TINAZZI (Michele)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>FIORIO (Mirta)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>FIASCHI (Antonio)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>ROTHWELL (John C.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>BHATIA (Kailash P.)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Neurological and Vision Sciences, University of Verona</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Neurology Unit, Borgo Trento Hospital</s1>
<s2>Verona</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
</fA14>
<fA20><s1>1427-1436</s1>
</fA20>
<fA21><s1>2009</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000187543670020</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2009 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>101 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>09-0358930</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17H</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Dystonie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Dystonia</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Distonía</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Pathologie du   système nerveux</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Discrimination</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Discrimination</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Discriminación</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Rotation mentale</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Mental rotation</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Rotación mental</s0>
<s5>10</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mouvement involontaire</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Movimiento involuntario</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Pathologie du muscle strié</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Striated muscle disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Músculo estriado patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>43</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>43</s5>
</fC07>
<fN21><s1>257</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 09-0358930 INIST</NO>
<ET>Sensory Functions in Dystonia: Insights from Behavioral Studies</ET>
<AU>TINAZZI (Michele); FIORIO (Mirta); FIASCHI (Antonio); ROTHWELL (John C.); BHATIA (Kailash P.)</AU>
<AF>Department of Neurological and Vision Sciences, University of Verona/Verona/Italie (1 aut., 2 aut., 3 aut.); Neurology Unit, Borgo Trento Hospital/Verona/Italie (1 aut.); Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology/London/Royaume-Uni (4 aut., 5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2009; Vol. 24; No. 10; Pp. 1427-1436; Bibl. 101 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17; 002B17H</CC>
<FD>Dystonie; Pathologie du   système nerveux; Discrimination; Rotation mentale</FD>
<FG>Syndrome extrapyramidal; Mouvement involontaire; Pathologie du muscle strié; Trouble neurologique; Pathologie de l'encéphale; Pathologie du   système nerveux central</FG>
<ED>Dystonia; Nervous system diseases; Discrimination; Mental rotation</ED>
<EG>Extrapyramidal syndrome; Involuntary movement; Striated muscle disease; Neurological disorder; Cerebral disorder; Central nervous system disease</EG>
<SD>Distonía; Sistema nervioso patología; Discriminación; Rotación mental</SD>
<LO>INIST-20953.354000187543670020</LO>
<ID>09-0358930</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PascalFrancis/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000E00 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000E00 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    MovDisordV3
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:09-0358930
   |texte=   Sensory Functions in Dystonia: Insights from Behavioral Studies
}}

This area was generated with Dilib version V0.6.23.
Data generation: Sun Jul 3 12:29:32 2016. Site generation: Wed Feb 14 10:52:30 2024

	Movement Disorders (revue)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Movement Disorders (revue)

Sensory Functions in Dystonia: Insights from Behavioral Studies

Sensory Functions in Dystonia: Insights from Behavioral Studies

Source :

Descripteurs français

English descriptors

Abstract

Notice en format standard (ISO 2709)

Format Inist (serveur)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri