Impaired habituation of long‐latency stretch reflexes of the wrist muscles in Huntington's disease
Identifieur interne : 003002 ( Istex/Corpus ); précédent : 003001; suivant : 003003Impaired habituation of long‐latency stretch reflexes of the wrist muscles in Huntington's disease
Auteurs : Abbruzzese ; D. Dall'Agata ; M. Morena ; L. Spadavecchia ; S. Rattod ; E. FavaleSource :
- Movement Disorders [ 0885-3185 ] ; 1990.
English descriptors
Abstract
Electromyographic responses to sudden wrist extension were recorded from the forearm and finger flexor muscles in 10 patients with Huntington's disease (HD) and in 10 normal controls. Stretch reflexes were characterized by a short‐latency (SL) and a long‐latency (LL) component both in patients and controls. Latency, duration, and size of the SL component were not different in the two groups, whereas the LL component was delayed in latency and reduced in size in HD patients. Increasing the stretch repetition rate from 0.1 to 0.4 cycles/s did not affect the SL component of either group, whereas the LL stretch reflex was reduced in size and duration in normal controls, but not in HD patients. These findings suggest an impairment of the “gain” mechanisms of the sole LL component, responsible for a desaturation of this component. This study supports the hypothesis that LL stretch reflexes are mediated by a transcortical long loop, possibly damaged in HD.
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DOI: 10.1002/mds.870050108
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<front><div type="abstract" xml:lang="en">Electromyographic responses to sudden wrist extension were recorded from the forearm and finger flexor muscles in 10 patients with Huntington's disease (HD) and in 10 normal controls. Stretch reflexes were characterized by a short‐latency (SL) and a long‐latency (LL) component both in patients and controls. Latency, duration, and size of the SL component were not different in the two groups, whereas the LL component was delayed in latency and reduced in size in HD patients. Increasing the stretch repetition rate from 0.1 to 0.4 cycles/s did not affect the SL component of either group, whereas the LL stretch reflex was reduced in size and duration in normal controls, but not in HD patients. These findings suggest an impairment of the “gain” mechanisms of the sole LL component, responsible for a desaturation of this component. This study supports the hypothesis that LL stretch reflexes are mediated by a transcortical long loop, possibly damaged in HD.</div>
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<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M.</namePart>
<namePart type="family">Morena</namePart>
<affiliation>Department of Neurology, University of Genoa, C.N.R., Genoa, Italy</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">L.</namePart>
<namePart type="family">Spadavecchia</namePart>
<affiliation>Institute of Cybernetics and Biophysics, C.N.R., Genoa, Italy</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S.</namePart>
<namePart type="family">Rattod</namePart>
<affiliation>Department of Neurology, University of Genoa, C.N.R., Genoa, Italy</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">E.</namePart>
<namePart type="family">Favale</namePart>
<affiliation>Department of Neurology, University of Genoa, C.N.R., Genoa, Italy</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre authority="originalCategForm">article</genre>
<originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place><placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">1990</dateIssued>
<copyrightDate encoding="w3cdtf">1990</copyrightDate>
</originInfo>
<language><languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
</language>
<physicalDescription><internetMediaType>text/html</internetMediaType>
<extent unit="figures">2</extent>
<extent unit="tables">2</extent>
<extent unit="references">16</extent>
</physicalDescription>
<abstract lang="en">Electromyographic responses to sudden wrist extension were recorded from the forearm and finger flexor muscles in 10 patients with Huntington's disease (HD) and in 10 normal controls. Stretch reflexes were characterized by a short‐latency (SL) and a long‐latency (LL) component both in patients and controls. Latency, duration, and size of the SL component were not different in the two groups, whereas the LL component was delayed in latency and reduced in size in HD patients. Increasing the stretch repetition rate from 0.1 to 0.4 cycles/s did not affect the SL component of either group, whereas the LL stretch reflex was reduced in size and duration in normal controls, but not in HD patients. These findings suggest an impairment of the “gain” mechanisms of the sole LL component, responsible for a desaturation of this component. This study supports the hypothesis that LL stretch reflexes are mediated by a transcortical long loop, possibly damaged in HD.</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>Stretch reflexes</topic>
<topic>Habituation</topic>
<topic>Huntington's disease</topic>
<topic>Long‐loop mechanisms</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>
<subject><genre>article category</genre>
<topic>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>1990</date>
<detail type="volume"><caption>vol.</caption>
<number>5</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>1</number>
</detail>
<extent unit="pages"><start>32</start>
<end>35</end>
<total>4</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">532F2122BD0BB8F4C0C2A4B121D7F5EE4F5C9BC0</identifier>
<identifier type="DOI">10.1002/mds.870050108</identifier>
<identifier type="ArticleID">MDS870050108</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 1990 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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