Does ageing aggravate parkinsonian disability?
Identifieur interne : 001745 ( PubMed/Curation ); précédent : 001744; suivant : 001746Does ageing aggravate parkinsonian disability?
Auteurs : J. Blin [France] ; B. Dubois ; A M Bonnet ; M. Vidailhet ; M. Brandabur ; Y. AgidSource :
- Journal of neurology, neurosurgery, and psychiatry [ 0022-3050 ] ; 1991.
English descriptors
- KwdEn :
- Age Factors, Aged, Disability Evaluation, Female, Humans, Levodopa (therapeutic use), Male, Middle Aged, Motor Neurons (drug effects), Motor Neurons (physiology), Muscles (innervation), Neurologic Examination, Parkinson Disease (diagnosis), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Retrospective Studies.
- MESH :
- chemical , therapeutic use : Levodopa.
- diagnosis : Parkinson Disease.
- drug effects : Motor Neurons.
- drug therapy : Parkinson Disease.
- innervation : Muscles.
- physiology : Motor Neurons.
- physiopathology : Parkinson Disease.
- Age Factors, Aged, Disability Evaluation, Female, Humans, Male, Middle Aged, Neurologic Examination, Retrospective Studies.
Abstract
The influence of age of onset of Parkinson's disease on the severity and the pattern of motor symptoms was investigated by comparing the motor scores with and without levodopa therapy in two groups of patients divided according to age of onset (early less than 50, late greater than 60 years) and matched for disease duration (n = 69 in each group, Study I). The baseline score, that is, the motor disability of patients when off levodopa, was similar in the early- and late- onset groups. In contrast, the residual motor score, assessed when the effect of levodopa treatment was maximum and stable, was significantly higher in the late onset group. When the two groups of patients were matched, in addition, for their residual motor score, (n = 54 in each group, Study II), no difference was observed between the early and late onset groups, except for gait disorder which was more severe in older patients. These results suggest that age of onset mainly affects the response to levodopa therapy, because it may increase the prevalence of non-dopaminergic lesions of the brain, including those responsible for gait disorders.
PubMed: 1955894
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<author><name sortKey="Bonnet, A M" sort="Bonnet, A M" uniqKey="Bonnet A" first="A M" last="Bonnet">A M Bonnet</name>
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<series><title level="j">Journal of neurology, neurosurgery, and psychiatry</title>
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<term>Disability Evaluation</term>
<term>Female</term>
<term>Humans</term>
<term>Levodopa (therapeutic use)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Motor Neurons (drug effects)</term>
<term>Motor Neurons (physiology)</term>
<term>Muscles (innervation)</term>
<term>Neurologic Examination</term>
<term>Parkinson Disease (diagnosis)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Retrospective Studies</term>
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<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Levodopa</term>
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<keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Neurons</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Muscles</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Neurons</term>
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<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term>
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<term>Aged</term>
<term>Disability Evaluation</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
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<front><div type="abstract" xml:lang="en">The influence of age of onset of Parkinson's disease on the severity and the pattern of motor symptoms was investigated by comparing the motor scores with and without levodopa therapy in two groups of patients divided according to age of onset (early less than 50, late greater than 60 years) and matched for disease duration (n = 69 in each group, Study I). The baseline score, that is, the motor disability of patients when off levodopa, was similar in the early- and late- onset groups. In contrast, the residual motor score, assessed when the effect of levodopa treatment was maximum and stable, was significantly higher in the late onset group. When the two groups of patients were matched, in addition, for their residual motor score, (n = 54 in each group, Study II), no difference was observed between the early and late onset groups, except for gait disorder which was more severe in older patients. These results suggest that age of onset mainly affects the response to levodopa therapy, because it may increase the prevalence of non-dopaminergic lesions of the brain, including those responsible for gait disorders.</div>
</front>
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<ArticleTitle>Does ageing aggravate parkinsonian disability?</ArticleTitle>
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<Abstract><AbstractText>The influence of age of onset of Parkinson's disease on the severity and the pattern of motor symptoms was investigated by comparing the motor scores with and without levodopa therapy in two groups of patients divided according to age of onset (early less than 50, late greater than 60 years) and matched for disease duration (n = 69 in each group, Study I). The baseline score, that is, the motor disability of patients when off levodopa, was similar in the early- and late- onset groups. In contrast, the residual motor score, assessed when the effect of levodopa treatment was maximum and stable, was significantly higher in the late onset group. When the two groups of patients were matched, in addition, for their residual motor score, (n = 54 in each group, Study II), no difference was observed between the early and late onset groups, except for gait disorder which was more severe in older patients. These results suggest that age of onset mainly affects the response to levodopa therapy, because it may increase the prevalence of non-dopaminergic lesions of the brain, including those responsible for gait disorders.</AbstractText>
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<CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 1978 May;35(5):261-3</RefSource>
<PMID Version="1">646679</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1979 Oct;6(4):355-9</RefSource>
<PMID Version="1">554525</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Rev Neurol (Paris). 1985;141(5):413-5</RefSource>
<PMID Version="1">4048732</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurology. 1990 Jan;40(1):38-41</RefSource>
<PMID Version="1">2296380</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurology. 1987 Sep;37(9):1539-42</RefSource>
<PMID Version="1">3627454</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurol Neurosurg Psychiatry. 1988 Feb;51(2):244-9</RefSource>
<PMID Version="1">3346689</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurology. 1989 Sep;39(9):1187-90</RefSource>
<PMID Version="1">2771070</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Adv Neurol. 1987;45:469-72</RefSource>
<PMID Version="1">3825727</PMID>
</CommentsCorrections>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000367" MajorTopicYN="N">Age Factors</DescriptorName>
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