Characteristics of the sequence effect in Parkinson's disease.
Identifieur interne : 001703 ( PubMed/Corpus ); précédent : 001702; suivant : 001704Characteristics of the sequence effect in Parkinson's disease.
Auteurs : Suk Yun Kang ; Toshiaki Wasaka ; Ejaz A. Shamim ; Sungyoung Auh ; Yoshino Ueki ; Grisel J. Lopez ; Tetsuo Kida ; Seung-Hyun Jin ; Nguyet Dang ; Mark HallettSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Cross-Over Studies, Disability Evaluation, Disease Progression, Female, Humans, Levodopa (pharmacology), Levodopa (therapeutic use), Male, Middle Aged, Movement (drug effects), Movement (physiology), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Psychomotor Performance (drug effects), Psychomotor Performance (physiology), Severity of Illness Index, Transcranial Magnetic Stimulation (methods).
- MESH :
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug effects : Movement, Psychomotor Performance.
- methods : Transcranial Magnetic Stimulation.
- physiology : Movement, Psychomotor Performance.
- physiopathology : Parkinson Disease.
- therapy : Parkinson Disease.
- Aged, Cross-Over Studies, Disability Evaluation, Disease Progression, Female, Humans, Male, Middle Aged, Severity of Illness Index.
Abstract
The sequence effect (SE) in Parkinson's disease (PD) is progressive slowing of sequential movements. It is a feature of bradykinesia, but is separate from a general slowness without deterioration over time. It is commonly seen in PD, but its physiology is unclear. We measured general slowness and the SE separately with a computer-based, modified Purdue pegboard in 11 patients with advanced PD. We conducted a placebo-controlled, four-way crossover study to learn whether levodopa and repetitive transcranial magnetic stimulation (rTMS) could improve general slowness or the SE. We also examined the correlation between the SE and clinical fatigue. Levodopa alone and rTMS alone improved general slowness, but rTMS showed no additive effect on levodopa. Levodopa alone, rTMS alone, and their combination did not alleviate the SE. There was no correlation between the SE and fatigue. This study suggests that dopaminergic dysfunction and abnormal motor cortex excitability are not the relevant mechanisms for the SE. Additionally, the SE is not a component of clinical fatigue. Further work is needed to establish the physiology and clinical relevance of the SE. © 2010 Movement Disorder Society.
DOI: 10.1002/mds.23251
PubMed: 20669182
Links to Exploration step
pubmed:20669182Le document en format XML
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Shamim</name></author><author><name sortKey="Auh, Sungyoung" sort="Auh, Sungyoung" uniqKey="Auh S" first="Sungyoung" last="Auh">Sungyoung Auh</name></author><author><name sortKey="Ueki, Yoshino" sort="Ueki, Yoshino" uniqKey="Ueki Y" first="Yoshino" last="Ueki">Yoshino Ueki</name></author><author><name sortKey="Lopez, Grisel J" sort="Lopez, Grisel J" uniqKey="Lopez G" first="Grisel J" last="Lopez">Grisel J. Lopez</name></author><author><name sortKey="Kida, Tetsuo" sort="Kida, Tetsuo" uniqKey="Kida T" first="Tetsuo" last="Kida">Tetsuo Kida</name></author><author><name sortKey="Jin, Seung Hyun" sort="Jin, Seung Hyun" uniqKey="Jin S" first="Seung-Hyun" last="Jin">Seung-Hyun Jin</name></author><author><name sortKey="Dang, Nguyet" sort="Dang, Nguyet" uniqKey="Dang N" first="Nguyet" last="Dang">Nguyet Dang</name></author><author><name sortKey="Hallett, Mark" sort="Hallett, Mark" uniqKey="Hallett M" first="Mark" last="Hallett">Mark Hallett</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.23251</idno><idno type="RBID">pubmed:20669182</idno><idno type="pmid">20669182</idno><idno type="wicri:Area/PubMed/Corpus">001703</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Characteristics of the sequence effect in Parkinson's disease.</title><author><name sortKey="Kang, Suk Yun" sort="Kang, Suk Yun" uniqKey="Kang S" first="Suk Yun" last="Kang">Suk Yun Kang</name><affiliation><nlm:affiliation>Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1428, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Wasaka, Toshiaki" sort="Wasaka, Toshiaki" uniqKey="Wasaka T" first="Toshiaki" last="Wasaka">Toshiaki Wasaka</name></author><author><name sortKey="Shamim, Ejaz A" sort="Shamim, Ejaz A" uniqKey="Shamim E" first="Ejaz A" last="Shamim">Ejaz A. 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Lopez</name></author><author><name sortKey="Kida, Tetsuo" sort="Kida, Tetsuo" uniqKey="Kida T" first="Tetsuo" last="Kida">Tetsuo Kida</name></author><author><name sortKey="Jin, Seung Hyun" sort="Jin, Seung Hyun" uniqKey="Jin S" first="Seung-Hyun" last="Jin">Seung-Hyun Jin</name></author><author><name sortKey="Dang, Nguyet" sort="Dang, Nguyet" uniqKey="Dang N" first="Nguyet" last="Dang">Nguyet Dang</name></author><author><name sortKey="Hallett, Mark" sort="Hallett, Mark" uniqKey="Hallett M" first="Mark" last="Hallett">Mark Hallett</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Cross-Over Studies</term><term>Disability Evaluation</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Levodopa (pharmacology)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Movement (drug effects)</term><term>Movement (physiology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Psychomotor Performance (drug effects)</term><term>Psychomotor Performance (physiology)</term><term>Severity of Illness Index</term><term>Transcranial Magnetic Stimulation (methods)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Movement</term><term>Psychomotor Performance</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Transcranial Magnetic Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Movement</term><term>Psychomotor Performance</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Cross-Over Studies</term><term>Disability Evaluation</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The sequence effect (SE) in Parkinson's disease (PD) is progressive slowing of sequential movements. It is a feature of bradykinesia, but is separate from a general slowness without deterioration over time. It is commonly seen in PD, but its physiology is unclear. We measured general slowness and the SE separately with a computer-based, modified Purdue pegboard in 11 patients with advanced PD. We conducted a placebo-controlled, four-way crossover study to learn whether levodopa and repetitive transcranial magnetic stimulation (rTMS) could improve general slowness or the SE. We also examined the correlation between the SE and clinical fatigue. Levodopa alone and rTMS alone improved general slowness, but rTMS showed no additive effect on levodopa. Levodopa alone, rTMS alone, and their combination did not alleviate the SE. There was no correlation between the SE and fatigue. This study suggests that dopaminergic dysfunction and abnormal motor cortex excitability are not the relevant mechanisms for the SE. Additionally, the SE is not a component of clinical fatigue. Further work is needed to establish the physiology and clinical relevance of the SE. © 2010 Movement Disorder Society.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20669182</PMID><DateCreated><Year>2010</Year><Month>10</Month><Day>08</Day></DateCreated><DateCompleted><Year>2011</Year><Month>01</Month><Day>26</Day></DateCompleted><DateRevised><Year>2015</Year><Month>08</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>13</Issue><PubDate><Year>2010</Year><Month>Oct</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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Levodopa alone and rTMS alone improved general slowness, but rTMS showed no additive effect on levodopa. Levodopa alone, rTMS alone, and their combination did not alleviate the SE. There was no correlation between the SE and fatigue. This study suggests that dopaminergic dysfunction and abnormal motor cortex excitability are not the relevant mechanisms for the SE. Additionally, the SE is not a component of clinical fatigue. 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