Medium latency stretch reflexes in young-onset Parkinson's disease and MPTP-induced parkinsonism
Identifieur interne : 002384 ( Main/Exploration ); précédent : 002383; suivant : 002385Medium latency stretch reflexes in young-onset Parkinson's disease and MPTP-induced parkinsonism
Auteurs : B. R. Bloem [Pays-Bas] ; D. J. Beckley [États-Unis] ; J. G. Van Dijk [Pays-Bas] ; A. H. Zwinderman [Pays-Bas] ; M. P. Remler [États-Unis] ; J. W. Langston [États-Unis] ; R. A. C. Roos [Pays-Bas]Source :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1993.
Abstract
It is still unclear why components of the phasic stretch reflex are increased in Parkinson's disease (PD). To study the role of aging, we assessed medium latency (ML) stretch reflexes in 19 Parkinson patients (8 with young-onset PD, 11 with late-onset PD) and 23 normal subjects (10 young, 13 old). To assess the contribution of supraspinal dopaminergic influences, we also studied 5 young parkinsonian patients with a selective central dopamine deficiency induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). ML responses were recorded from the medial gastrocnemius muscle which was stretched by 4° toe-up rotations of a platform upon which subjects were standing. ML responses were significantly enhanced in late-onset patients compared with older controls. In contrast, ML responses did not differ between young-onset patients and young controls. This observation could be attributed to the significantly different influence of age on ML-amplitudes in patients and controls. Thus, ML-amplitudes declined with age in controls, whereas they increased with age in PD possibly because older patients were more severely affected than younger patients. Thus, the difference between young-onset and late-onset PD seems to be related to the opposite effects of increasing age and disease severity in patients and controls. ML-amplitudes did not differ between patients with MPTP-induced parkinsonism, patients with young-onset PD and controls, suggesting that supraspinal dopaminergic systems are not critically involved in control of ML responses. This result also indicates that the severity effect in PD may be related to disruption of non-dopaminergic pathways which occurs in late-onset, but not young-onset patients. In conclusion, we postulate that lesions in non-dopaminergic systems in older Parkinson patients contribute to enhancement of ML responses, and possibly other late occurring stretch reflexes as well.
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DOI: 10.1016/0022-510X(94)90203-8
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Bloem</name><affiliation wicri:level="1"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology and Clinical Neurophysiology, University Hospital Leiden, P.O, Box 9600, 2300 RC Leiden</wicri:regionArea><wicri:noRegion>2300 RC Leiden</wicri:noRegion></affiliation></author><author><name sortKey="Beckley, D J" sort="Beckley, D J" uniqKey="Beckley D" first="D. J." last="Beckley">D. J. Beckley</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, School of Medicine, University of California, Davis, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Van Dijk, J G" sort="Van Dijk, J G" uniqKey="Van Dijk J" first="J. G." last="Van Dijk">J. G. Van Dijk</name><affiliation wicri:level="1"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology and Clinical Neurophysiology, University Hospital Leiden, P.O, Box 9600, 2300 RC Leiden</wicri:regionArea><wicri:noRegion>2300 RC Leiden</wicri:noRegion></affiliation></author><author><name sortKey="Zwinderman, A H" sort="Zwinderman, A H" uniqKey="Zwinderman A" first="A. H." last="Zwinderman">A. H. Zwinderman</name><affiliation wicri:level="3"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Medical Statistics, State University Leiden, Leiden</wicri:regionArea><placeName><settlement type="city">Leyde</settlement><region nuts="2" type="province">Hollande-Méridionale</region></placeName></affiliation></author><author><name sortKey="Remler, M P" sort="Remler, M P" uniqKey="Remler M" first="M. P." last="Remler">M. P. Remler</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, School of Medicine, University of California, Davis, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Langston, J W" sort="Langston, J W" uniqKey="Langston J" first="J. W." last="Langston">J. W. Langston</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>The California Parkinson's Foundation, San Jose, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Roos, R A C" sort="Roos, R A C" uniqKey="Roos R" first="R. A. C." last="Roos">R. A. C. Roos</name><affiliation wicri:level="1"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology and Clinical Neurophysiology, University Hospital Leiden, P.O, Box 9600, 2300 RC Leiden</wicri:regionArea><wicri:noRegion>2300 RC Leiden</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">123</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="52">52</biblScope><biblScope unit="page" to="58">58</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">26305F5409D0EBE6BB9FAF8D12716788BD9565B4</idno><idno type="DOI">10.1016/0022-510X(94)90203-8</idno><idno type="PII">0022-510X(94)90203-8</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It is still unclear why components of the phasic stretch reflex are increased in Parkinson's disease (PD). To study the role of aging, we assessed medium latency (ML) stretch reflexes in 19 Parkinson patients (8 with young-onset PD, 11 with late-onset PD) and 23 normal subjects (10 young, 13 old). To assess the contribution of supraspinal dopaminergic influences, we also studied 5 young parkinsonian patients with a selective central dopamine deficiency induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). ML responses were recorded from the medial gastrocnemius muscle which was stretched by 4° toe-up rotations of a platform upon which subjects were standing. ML responses were significantly enhanced in late-onset patients compared with older controls. In contrast, ML responses did not differ between young-onset patients and young controls. This observation could be attributed to the significantly different influence of age on ML-amplitudes in patients and controls. Thus, ML-amplitudes declined with age in controls, whereas they increased with age in PD possibly because older patients were more severely affected than younger patients. Thus, the difference between young-onset and late-onset PD seems to be related to the opposite effects of increasing age and disease severity in patients and controls. ML-amplitudes did not differ between patients with MPTP-induced parkinsonism, patients with young-onset PD and controls, suggesting that supraspinal dopaminergic systems are not critically involved in control of ML responses. This result also indicates that the severity effect in PD may be related to disruption of non-dopaminergic pathways which occurs in late-onset, but not young-onset patients. In conclusion, we postulate that lesions in non-dopaminergic systems in older Parkinson patients contribute to enhancement of ML responses, and possibly other late occurring stretch reflexes as well.</div></front></TEI><affiliations><list><country><li>Pays-Bas</li><li>États-Unis</li></country><region><li>Californie</li><li>Hollande-Méridionale</li></region><settlement><li>Leyde</li></settlement></list><tree><country name="Pays-Bas"><noRegion><name sortKey="Bloem, B R" sort="Bloem, B R" uniqKey="Bloem B" first="B. R." last="Bloem">B. R. Bloem</name></noRegion><name sortKey="Roos, R A C" sort="Roos, R A C" uniqKey="Roos R" first="R. A. C." last="Roos">R. A. C. Roos</name><name sortKey="Van Dijk, J G" sort="Van Dijk, J G" uniqKey="Van Dijk J" first="J. G." last="Van Dijk">J. G. Van Dijk</name><name sortKey="Zwinderman, A H" sort="Zwinderman, A H" uniqKey="Zwinderman A" first="A. H." last="Zwinderman">A. H. Zwinderman</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Beckley, D J" sort="Beckley, D J" uniqKey="Beckley D" first="D. J." last="Beckley">D. J. Beckley</name></region><name sortKey="Langston, J W" sort="Langston, J W" uniqKey="Langston J" first="J. W." last="Langston">J. W. Langston</name><name sortKey="Remler, M P" sort="Remler, M P" uniqKey="Remler M" first="M. P." last="Remler">M. P. Remler</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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