Sensory disinhibition on passive movement in cervical dystonia
Identifieur interne : 001348 ( Istex/Corpus ); précédent : 001347; suivant : 001349Sensory disinhibition on passive movement in cervical dystonia
Auteurs : Mark Obermann ; Clemens Vollrath ; Armin De Greiff ; Elke R. Gizewski ; Hans-Christoph Diener ; Mark Hallett ; Matthias MaschkeSource :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
English descriptors
Abstract
The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23321
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<front><div type="abstract" xml:lang="en">The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</div>
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<keyword xml:id="kwd2">cervical dystonia</keyword>
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<keyword xml:id="kwd4">cortical disinhibition</keyword>
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<p>The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</p>
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<noteGroup><note xml:id="fn1"><p>Potential conflict of interest: Nothing to report.</p>
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<titleInfo type="abbreviated" lang="en"><title>Sensory Disinhibition on Passive Movement</title>
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<name type="personal"><namePart type="given">Mark</namePart>
<namePart type="family">Obermann</namePart>
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<affiliation>Department of Neurology, University of Duisburg‐Essen, Germany</affiliation>
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<abstract lang="en">The relevance of the sensory system in the pathophysiology of cervical dystonia (CD) has been discussed since the description of sensory tricks associated with this disorder. Our objective was to locate changes in somatosensory processing of patients with CD responding in a passive sensory task of body regions that are not affected by dystonic symptoms. We used functional magnetic resonance imaging (fMRI) in 17 patients with CD and 17 healthy controls performing a strictly passive 30‐degree forearm movement task with the left arm. TSUI and TWSTRS rating scales were used for clinical assessment. All patients were treated with botulinum neurotoxin type A (BoNT‐A; Dysport®). Patients with CD showed BOLD‐signal increase in the contralateral primary and secondary sensory cortex, the cingulate cortex and cerebellum bilaterally compared to healthy controls. We found a strong positive correlation of this activation with BoNT‐A dosage in the supplementary motor area (SMA) and a negative correlation with the TWSTRS in that same region. The observed sensory overactivation suggests a general disinhibition of the somatosensory system in CD as it was not limited to the motor‐system or the direct neuronal representation of the affected dystonic musculature alone. © 2010 Movement Disorder Society</abstract>
<note type="content">*Potential conflict of interest: Nothing to report.</note>
<subject lang="en"><genre>Keywords</genre>
<topic>focal dystonia</topic>
<topic>cervical dystonia</topic>
<topic>fMRI</topic>
<topic>cortical disinhibition</topic>
<topic>somatosensory system</topic>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
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<part><date>2010</date>
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