Decrease in presynaptic inhibition on heteronymous monosynaptic Ia terminals in patients with Parkinson's disease.
Identifieur interne : 000333 ( Ncbi/Merge ); précédent : 000332; suivant : 000334Decrease in presynaptic inhibition on heteronymous monosynaptic Ia terminals in patients with Parkinson's disease.
Auteurs : H. Morita [Japon] ; M. Shindo ; S. Ikeda ; N. YanagisawaSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2000.
English descriptors
- KwdEn :
- Adult, Aged, Case-Control Studies, Electric Stimulation, Female, Gait Disorders, Neurologic (etiology), Gait Disorders, Neurologic (physiopathology), H-Reflex, Humans, Hypokinesia (etiology), Hypokinesia (physiopathology), Male, Middle Aged, Motor Neurons, Muscle Rigidity (etiology), Muscle Rigidity (physiopathology), Muscle, Skeletal (innervation), Muscle, Skeletal (physiopathology), Neural Inhibition, Neurons, Afferent, Parkinson Disease (complications), Parkinson Disease (physiopathology), Presynaptic Terminals, Synaptic Transmission, Tibial Nerve (physiopathology).
- MESH :
- complications : Parkinson Disease.
- etiology : Gait Disorders, Neurologic, Hypokinesia, Muscle Rigidity.
- innervation : Muscle, Skeletal.
- physiopathology : Gait Disorders, Neurologic, Hypokinesia, Muscle Rigidity, Muscle, Skeletal, Parkinson Disease, Tibial Nerve.
- Adult, Aged, Case-Control Studies, Electric Stimulation, Female, H-Reflex, Humans, Male, Middle Aged, Motor Neurons, Neural Inhibition, Neurons, Afferent, Presynaptic Terminals, Synaptic Transmission.
Abstract
Heteronymous Ia facilitation from the quadriceps to the soleus was studied to clarify central motor control through presynaptic inhibition (PSI) on Ia terminals of spinal motoneurons in Parkinson's disease.
PubMed: 11009187
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pubmed:11009187Le document en format XML
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<author><name sortKey="Morita, H" sort="Morita, H" uniqKey="Morita H" first="H" last="Morita">H. Morita</name>
<affiliation wicri:level="1"><nlm:affiliation>The Third Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.</nlm:affiliation>
<country xml:lang="fr">Japon</country>
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<author><name sortKey="Shindo, M" sort="Shindo, M" uniqKey="Shindo M" first="M" last="Shindo">M. Shindo</name>
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<author><name sortKey="Ikeda, S" sort="Ikeda, S" uniqKey="Ikeda S" first="S" last="Ikeda">S. Ikeda</name>
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<author><name sortKey="Yanagisawa, N" sort="Yanagisawa, N" uniqKey="Yanagisawa N" first="N" last="Yanagisawa">N. Yanagisawa</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Decrease in presynaptic inhibition on heteronymous monosynaptic Ia terminals in patients with Parkinson's disease.</title>
<author><name sortKey="Morita, H" sort="Morita, H" uniqKey="Morita H" first="H" last="Morita">H. Morita</name>
<affiliation wicri:level="1"><nlm:affiliation>The Third Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.</nlm:affiliation>
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<author><name sortKey="Shindo, M" sort="Shindo, M" uniqKey="Shindo M" first="M" last="Shindo">M. Shindo</name>
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<author><name sortKey="Ikeda, S" sort="Ikeda, S" uniqKey="Ikeda S" first="S" last="Ikeda">S. Ikeda</name>
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<author><name sortKey="Yanagisawa, N" sort="Yanagisawa, N" uniqKey="Yanagisawa N" first="N" last="Yanagisawa">N. Yanagisawa</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Case-Control Studies</term>
<term>Electric Stimulation</term>
<term>Female</term>
<term>Gait Disorders, Neurologic (etiology)</term>
<term>Gait Disorders, Neurologic (physiopathology)</term>
<term>H-Reflex</term>
<term>Humans</term>
<term>Hypokinesia (etiology)</term>
<term>Hypokinesia (physiopathology)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Motor Neurons</term>
<term>Muscle Rigidity (etiology)</term>
<term>Muscle Rigidity (physiopathology)</term>
<term>Muscle, Skeletal (innervation)</term>
<term>Muscle, Skeletal (physiopathology)</term>
<term>Neural Inhibition</term>
<term>Neurons, Afferent</term>
<term>Parkinson Disease (complications)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Presynaptic Terminals</term>
<term>Synaptic Transmission</term>
<term>Tibial Nerve (physiopathology)</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Disorders, Neurologic</term>
<term>Hypokinesia</term>
<term>Muscle Rigidity</term>
</keywords>
<keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Muscle, Skeletal</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Gait Disorders, Neurologic</term>
<term>Hypokinesia</term>
<term>Muscle Rigidity</term>
<term>Muscle, Skeletal</term>
<term>Parkinson Disease</term>
<term>Tibial Nerve</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Case-Control Studies</term>
<term>Electric Stimulation</term>
<term>Female</term>
<term>H-Reflex</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Motor Neurons</term>
<term>Neural Inhibition</term>
<term>Neurons, Afferent</term>
<term>Presynaptic Terminals</term>
<term>Synaptic Transmission</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Heteronymous Ia facilitation from the quadriceps to the soleus was studied to clarify central motor control through presynaptic inhibition (PSI) on Ia terminals of spinal motoneurons in Parkinson's disease.</div>
</front>
</TEI>
<pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11009187</PMID>
<DateCreated><Year>2001</Year>
<Month>01</Month>
<Day>09</Day>
</DateCreated>
<DateCompleted><Year>2001</Year>
<Month>01</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised><Year>2006</Year>
<Month>11</Month>
<Day>15</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN>
<JournalIssue CitedMedium="Print"><Volume>15</Volume>
<Issue>5</Issue>
<PubDate><Year>2000</Year>
<Month>Sep</Month>
</PubDate>
</JournalIssue>
<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
<ISOAbbreviation>Mov. Disord.</ISOAbbreviation>
</Journal>
<ArticleTitle>Decrease in presynaptic inhibition on heteronymous monosynaptic Ia terminals in patients with Parkinson's disease.</ArticleTitle>
<Pagination><MedlinePgn>830-4</MedlinePgn>
</Pagination>
<Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">Heteronymous Ia facilitation from the quadriceps to the soleus was studied to clarify central motor control through presynaptic inhibition (PSI) on Ia terminals of spinal motoneurons in Parkinson's disease.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">17 patients with Parkinson's disease and 36 control subjects participated in the study. Because the early part of facilitation reflects the degree of PSI, the extent of facilitation was quantified as the slope, within 0.8 msec of onset.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Heteronymous Ia facilitation in the patients was greater than in the age-matched control participants. PSI was negatively correlated with the walking speed of the patients. In the patients examined twice, lessening of bradykinesia was correlated to a decrease in PSI but not lessening of rigidity.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">These findings indicate that the degree of PSI is decreased and disturbance of the central control of PSI may relate to gait disturbance in Parkinson's disease.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Morita</LastName>
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<AffiliationInfo><Affiliation>The Third Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.</Affiliation>
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