Movement Disorders (revue)

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Etiological musculo‐skeletal factor in focal dystonia in a musician's hand: A case study of the right hand of a guitarist

Identifieur interne : 001086 ( Istex/Corpus ); précédent : 001085; suivant : 001087

Etiological musculo‐skeletal factor in focal dystonia in a musician's hand: A case study of the right hand of a guitarist

Auteurs : Joris N. A. L. Leijnse ; Mark Hallett

Source :

RBID : ISTEX:61449F1FC11275215D42FBBA20F6222C7795D523

English descriptors

Abstract

A case study is presented in which a focal hand dystonia seems to have developed in the right hand of a classical guitarist as a result of a neuromuscular peripheral defect caused by trauma. The trauma was a near total perforation of the first web space by a splinter. Healing was uneventful without apparent functional complications. Two years later the patient noticed difficulties in extending the index in playing, for which he received various unsuccessful treatments during seven years. However, we found more severe dystonic symptoms (cocontractions) in the thumb than in the index during playing, which correlated with an undiagnosed insufficiency in the flexor pollicis brevis (FPB). This defect allowed proposing a biomechanical analysis of compensations for diminished thumb control in playing, which would explain the dysfunction in the index in playing as overcompensation for the thumb problem. If this analysis is correct, the etiology of the case can be traced back to underlying multiarticular control problems in the thumb caused by an insufficient FPB. This defect was considered irrepairable. It was concluded that even with knowledge of the underlying cause, a potentially successful treatment of the dystonia might not exist in this case. The case would demonstrate that task‐specific hand dystonias can arise as overcompensations for (peripheral) neuro‐musculoskeletal defects. The case is illustrated by videos of playing and functional thumb tests. © 2007 Movement Disorder Society

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DOI: 10.1002/mds.21636

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ISTEX:61449F1FC11275215D42FBBA20F6222C7795D523

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<caption> Segment 1.Case, slow playing, right hand. The index does not properly extend to pluck the strings. Strong agonistic‐antagonistic cocontractions in the thumb with hyperflexion of the IP joint in static posture. When the thumb plucks a string, the cocontractions become significantly less or disappear. When the index plucks strings while keeping contact with the thumb, the fingertips of thumb and index remain forcefully pressed to together. When the thumb strikes a string, contact with the index is easily released and the thumb can well strike the string. In the occasion that the thumb does keep contact with the index during thumb stroke, the contact forces are visibly low. Segment 2.Case, fast playing, right hand. Neither index nor thumb has significant dystonic symptoms. Playing is very fast and finger strokes are regular. However, thumb movements are jerky. Thumb strokes originate mainly at the CMC1, with the thumb moving as a stick, with a large trajectory component perpendicular to the plane of the strings. Hesitations in playing are caused by thumb, not index. Segment 3.When the right hand thumb is flexed with active Flexor Pollicis Longus, i.e., with an actively flexing IP joint, the MCP joint can be normally flexed. Segment 4.Test of function of Flexor Pollicis Brevis (FPB): MCP1 flexion with relaxed IP joint. Part 1 (left hand): Normal MCP1 flexion, indicating normal FPB function. Part 2 (right hand): Impossibility to flex the MCP1 joint without cocontracting Flexor and Extensor Pollicis Longus. </caption>
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<p>A case study is presented in which a focal hand dystonia seems to have developed in the right hand of a classical guitarist as a result of a neuromuscular peripheral defect caused by trauma. The trauma was a near total perforation of the first web space by a splinter. Healing was uneventful without apparent functional complications. Two years later the patient noticed difficulties in extending the index in playing, for which he received various unsuccessful treatments during seven years. However, we found more severe dystonic symptoms (cocontractions) in the thumb than in the index during playing, which correlated with an undiagnosed insufficiency in the flexor pollicis brevis (FPB). This defect allowed proposing a biomechanical analysis of compensations for diminished thumb control in playing, which would explain the dysfunction in the index in playing as overcompensation for the thumb problem. If this analysis is correct, the etiology of the case can be traced back to underlying multiarticular control problems in the thumb caused by an insufficient FPB. This defect was considered irrepairable. It was concluded that even with knowledge of the underlying cause, a potentially successful treatment of the dystonia might not exist in this case. The case would demonstrate that task‐specific hand dystonias can arise as overcompensations for (peripheral) neuro‐musculoskeletal defects. The case is illustrated by videos of playing and functional thumb tests. © 2007 Movement Disorder Society</p>
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<title>Etiological musculo‐skeletal factor in focal dystonia in a musician's hand: A case study of the right hand of a guitarist</title>
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<title>Case Study</title>
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<title>Etiological musculo‐skeletal factor in focal dystonia in a musician's hand: A case study of the right hand of a guitarist</title>
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<name type="personal">
<namePart type="given">Joris N.A.L.</namePart>
<namePart type="family">Leijnse</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Laboratory for Clinical Biomechanics and Reconstructive Surgery of Hand and Upper Limb, Department of Mechanical Engineering, Speed School for Engineering & Price Institute for Surgical Research, Department of Surgery, University of Louisville, Louisville, Kentucky, USA</affiliation>
<description>Correspondence: Assistant Professor of Research, Department of Mechanical Engineering, 200 Sackett Hall, University of Louisville, Louisville, KY 40292</description>
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<name type="personal">
<namePart type="given">Mark</namePart>
<namePart type="family">Hallett</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Human Motor Control Section, NINDS, National Institutes of Health, Bethesda, Maryland, USA</affiliation>
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<dateIssued encoding="w3cdtf">2007-09-15</dateIssued>
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<abstract lang="en">A case study is presented in which a focal hand dystonia seems to have developed in the right hand of a classical guitarist as a result of a neuromuscular peripheral defect caused by trauma. The trauma was a near total perforation of the first web space by a splinter. Healing was uneventful without apparent functional complications. Two years later the patient noticed difficulties in extending the index in playing, for which he received various unsuccessful treatments during seven years. However, we found more severe dystonic symptoms (cocontractions) in the thumb than in the index during playing, which correlated with an undiagnosed insufficiency in the flexor pollicis brevis (FPB). This defect allowed proposing a biomechanical analysis of compensations for diminished thumb control in playing, which would explain the dysfunction in the index in playing as overcompensation for the thumb problem. If this analysis is correct, the etiology of the case can be traced back to underlying multiarticular control problems in the thumb caused by an insufficient FPB. This defect was considered irrepairable. It was concluded that even with knowledge of the underlying cause, a potentially successful treatment of the dystonia might not exist in this case. The case would demonstrate that task‐specific hand dystonias can arise as overcompensations for (peripheral) neuro‐musculoskeletal defects. The case is illustrated by videos of playing and functional thumb tests. © 2007 Movement Disorder Society</abstract>
<note type="funding">Dystonia Medical Research Foundation, Chicago, IL () [http://www.dystonia‐foundation.org]</note>
<note type="funding">University of Louisville, Louisville, Kentucky, USA</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>dystonia</topic>
<topic>focal</topic>
<topic>hand</topic>
<topic>musician</topic>
<topic>guitarist</topic>
<topic>overuse</topic>
<topic>biomechanics</topic>
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<title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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<title>Mov. Disord.</title>
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<note type="content"> This article includes supplementary video clips, available online at http://www.interscience.wiley.com/jpages/0885–3185/suppmatSupporting Info Item: Segment 1.Case, slow playing, right hand. The index does not properly extend to pluck the strings. Strong agonistic‐antagonistic cocontractions in the thumb with hyperflexion of the IP joint in static posture. When the thumb plucks a string, the cocontractions become significantly less or disappear. When the index plucks strings while keeping contact with the thumb, the fingertips of thumb and index remain forcefully pressed to together. When the thumb strikes a string, contact with the index is easily released and the thumb can well strike the string. In the occasion that the thumb does keep contact with the index during thumb stroke, the contact forces are visibly low. Segment 2.Case, fast playing, right hand. Neither index nor thumb has significant dystonic symptoms. Playing is very fast and finger strokes are regular. However, thumb movements are jerky. Thumb strokes originate mainly at the CMC1, with the thumb moving as a stick, with a large trajectory component perpendicular to the plane of the strings. Hesitations in playing are caused by thumb, not index. Segment 3.When the right hand thumb is flexed with active Flexor Pollicis Longus, i.e., with an actively flexing IP joint, the MCP joint can be normally flexed. Segment 4.Test of function of Flexor Pollicis Brevis (FPB): MCP1 flexion with relaxed IP joint. Part 1 (left hand): Normal MCP1 flexion, indicating normal FPB function. Part 2 (right hand): Impossibility to flex the MCP1 joint without cocontracting Flexor and Extensor Pollicis Longus. - </note>
<subject>
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<topic>Brief Report</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>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>22</number>
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<detail type="issue">
<caption>no.</caption>
<number>12</number>
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<start>1803</start>
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<identifier type="DOI">10.1002/mds.21636</identifier>
<identifier type="ArticleID">MDS21636</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Movement Disorder Society</accessCondition>
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