Long latency postural reflexes are under supraspinal dopaminergic control
Identifieur interne : 000621 ( Istex/Corpus ); précédent : 000620; suivant : 000622Long latency postural reflexes are under supraspinal dopaminergic control
Auteurs : Bloem ; Dennis J. Beckley ; Jeroen P. P. Van Vugt ; J. Gert Van Dijk ; Michael P. Remler ; J. William Langston ; Raymund A. C. RoosSource :
- Movement Disorders [ 0885-3185 ] ; 1995-09.
English descriptors
- KwdEn :
Abstract
Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.
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DOI: 10.1002/mds.870100509
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<front><div type="abstract" xml:lang="en">Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</div>
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<affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, School of Medicine, University of California, Davis</unparsedAffiliation>
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<affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</unparsedAffiliation>
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<keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword>
<keyword xml:id="kwd2">Posture</keyword>
<keyword xml:id="kwd3">Long latency reflexes</keyword>
<keyword xml:id="kwd4">Dopamine</keyword>
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<abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title>
<p>Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</p>
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<!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Long latency postural reflexes are under supraspinal dopaminergic control</title>
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<titleInfo type="abbreviated" lang="en"><title>LL REFLEXES IN HYPODOPAMINERGIC SYNDROMES</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Long latency postural reflexes are under supraspinal dopaminergic control</title>
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<name type="personal"><namePart type="termsOfAddress">Dr.</namePart>
<namePart type="family">Bloem</namePart>
<affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation>
<affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation>
<affiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</affiliation>
<description>Correspondence: Department of Neurology, University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands</description>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Dennis J.</namePart>
<namePart type="family">Beckley</namePart>
<affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Jeroen P. P.</namePart>
<namePart type="family">van Vugt</namePart>
<affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">J. Gert</namePart>
<namePart type="family">van Dijk</namePart>
<affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Michael P.</namePart>
<namePart type="family">Remler</namePart>
<affiliation>Department of Neurology, School of Medicine, University of California, Davis</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">J. William</namePart>
<namePart type="family">Langston</namePart>
<affiliation>The Parkinson's Institute, Sunnyvale, California, U.S.A.</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Raymund A. C.</namePart>
<namePart type="family">Roos</namePart>
<affiliation>Department of Neurology, University Hospital Leiden, The Netherlands</affiliation>
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<dateIssued encoding="w3cdtf">1995-09</dateIssued>
<dateValid encoding="w3cdtf">1995-02-15</dateValid>
<copyrightDate encoding="w3cdtf">1995</copyrightDate>
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<abstract lang="en">Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by “toe‐up” rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young‐onset Parkinson's disease, and 4 patients with MPTP‐induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4° amplitude, (b) 10 serial (predictable) perturbations of 10° amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10° amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a “default” response emerged that anticipated the 10° perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic‐induced parkinsonism and young‐onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP‐induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>Parkinson's disease</topic>
<topic>Posture</topic>
<topic>Long latency reflexes</topic>
<topic>Dopamine</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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<titleInfo type="abbreviated"><title>Mov. Disord.</title>
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<topic>Article</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>1995</date>
<detail type="volume"><caption>vol.</caption>
<number>10</number>
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<detail type="issue"><caption>no.</caption>
<number>5</number>
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<extent unit="pages"><start>580</start>
<end>588</end>
<total>9</total>
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<accessCondition type="use and reproduction" contentType="copyright">Copyright © 1995 Movement Disorder Society</accessCondition>
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