Small-amplitude cortical myoclonus in Parkinson's disease: physiology and clinical observations.
Identifieur interne : 003A28 ( PubMed/Corpus ); précédent : 003A27; suivant : 003A29Small-amplitude cortical myoclonus in Parkinson's disease: physiology and clinical observations.
Auteurs : John N. Caviness ; Charles H. Adler ; Thomas G. Beach ; Kristi L. Wetjen ; Richard J. CaselliSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2002.
English descriptors
- KwdEn :
- Aged, Cerebral Cortex (physiopathology), Dominance, Cerebral (physiology), Electroencephalography, Electromyography, Evoked Potentials, Motor (physiology), Evoked Potentials, Somatosensory (physiology), Female, Humans, Male, Mental Status Schedule, Middle Aged, Motor Neurons (physiology), Muscle, Skeletal (innervation), Myoclonus (diagnosis), Myoclonus (physiopathology), Neurologic Examination, Parkinson Disease (diagnosis), Parkinson Disease (physiopathology), Reaction Time (physiology), Signal Processing, Computer-Assisted, Somatosensory Cortex (physiopathology).
- MESH :
- diagnosis : Myoclonus, Parkinson Disease.
- innervation : Muscle, Skeletal.
- physiology : Dominance, Cerebral, Evoked Potentials, Motor, Evoked Potentials, Somatosensory, Motor Neurons, Reaction Time.
- physiopathology : Cerebral Cortex, Myoclonus, Parkinson Disease, Somatosensory Cortex.
- Aged, Electroencephalography, Electromyography, Female, Humans, Male, Mental Status Schedule, Middle Aged, Neurologic Examination, Signal Processing, Computer-Assisted.
Abstract
We studied the occurrence of small-amplitude myo- clonus in 20 idiopathic Parkinson's disease patients who had no evidence of dementia as defined by criteria in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition. Parkinson's disease was diagnosed by United Kingdom Brain Bank criteria, and clinical assessment was performed with the Unified Parkinson's Disease Rating Scale motor score, Hoehn and Yahr staging, and the Mini-Mental State Examination. Clinical assessment showed a range of mild-to-moderate disease severity. All patients underwent polygraphic electro-encephalographic-electromyographic (EMG) recording with back-averaging, somatosensory evoked potential testing, and attempted elicitation of long-latency EMG responses. Multichannel surface EMG recording during muscle activation showed irregular, multifocal, brief (<50 msec) myoclonus EMG discharges. Back-averaging consistently showed a focal, short-latency, electroencephalographic transient prior to the myoclonus EMG discharge. Cortical somatosensory evoked potential waves were not enlarged, and long-latency EMG responses at rest were not present. The small-amplitude myoclonus in such cases arises from an abnormal discharge from the sensorimotor cortex. The mechanism of this cortical myoclonus in Parkinson's disease has differences from the more common "cortical reflex myoclonus" physiology. Advanced parkinsonism is not a requirement for manifestation of this myoclonus type. Although the myoclonus occurred without dementia in these cases, its relationship to the subsequent development of cognitive impairment remains to be defined.
DOI: 10.1002/mds.10177
PubMed: 12210853
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pubmed:12210853Le document en format XML
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Wetjen</name></author><author><name sortKey="Caselli, Richard J" sort="Caselli, Richard J" uniqKey="Caselli R" first="Richard J" last="Caselli">Richard J. Caselli</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12210853</idno><idno type="pmid">12210853</idno><idno type="doi">10.1002/mds.10177</idno><idno type="wicri:Area/PubMed/Corpus">003A28</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Small-amplitude cortical myoclonus in Parkinson's disease: physiology and clinical observations.</title><author><name sortKey="Caviness, John N" sort="Caviness, John N" uniqKey="Caviness J" first="John N" last="Caviness">John N. Caviness</name><affiliation><nlm:affiliation>Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259, USA. jcaviness@mayo.edu</nlm:affiliation></affiliation></author><author><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H" last="Adler">Charles H. Adler</name></author><author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G" last="Beach">Thomas G. Beach</name></author><author><name sortKey="Wetjen, Kristi L" sort="Wetjen, Kristi L" uniqKey="Wetjen K" first="Kristi L" last="Wetjen">Kristi L. Wetjen</name></author><author><name sortKey="Caselli, Richard J" sort="Caselli, Richard J" uniqKey="Caselli R" first="Richard J" last="Caselli">Richard J. Caselli</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Cerebral Cortex (physiopathology)</term><term>Dominance, Cerebral (physiology)</term><term>Electroencephalography</term><term>Electromyography</term><term>Evoked Potentials, Motor (physiology)</term><term>Evoked Potentials, Somatosensory (physiology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Mental Status Schedule</term><term>Middle Aged</term><term>Motor Neurons (physiology)</term><term>Muscle, Skeletal (innervation)</term><term>Myoclonus (diagnosis)</term><term>Myoclonus (physiopathology)</term><term>Neurologic Examination</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (physiopathology)</term><term>Reaction Time (physiology)</term><term>Signal Processing, Computer-Assisted</term><term>Somatosensory Cortex (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Myoclonus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dominance, Cerebral</term><term>Evoked Potentials, Motor</term><term>Evoked Potentials, Somatosensory</term><term>Motor Neurons</term><term>Reaction Time</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term><term>Myoclonus</term><term>Parkinson Disease</term><term>Somatosensory Cortex</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Electroencephalography</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Mental Status Schedule</term><term>Middle Aged</term><term>Neurologic Examination</term><term>Signal Processing, Computer-Assisted</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied the occurrence of small-amplitude myo- clonus in 20 idiopathic Parkinson's disease patients who had no evidence of dementia as defined by criteria in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition. Parkinson's disease was diagnosed by United Kingdom Brain Bank criteria, and clinical assessment was performed with the Unified Parkinson's Disease Rating Scale motor score, Hoehn and Yahr staging, and the Mini-Mental State Examination. Clinical assessment showed a range of mild-to-moderate disease severity. All patients underwent polygraphic electro-encephalographic-electromyographic (EMG) recording with back-averaging, somatosensory evoked potential testing, and attempted elicitation of long-latency EMG responses. Multichannel surface EMG recording during muscle activation showed irregular, multifocal, brief (<50 msec) myoclonus EMG discharges. Back-averaging consistently showed a focal, short-latency, electroencephalographic transient prior to the myoclonus EMG discharge. Cortical somatosensory evoked potential waves were not enlarged, and long-latency EMG responses at rest were not present. The small-amplitude myoclonus in such cases arises from an abnormal discharge from the sensorimotor cortex. The mechanism of this cortical myoclonus in Parkinson's disease has differences from the more common "cortical reflex myoclonus" physiology. Advanced parkinsonism is not a requirement for manifestation of this myoclonus type. Although the myoclonus occurred without dementia in these cases, its relationship to the subsequent development of cognitive impairment remains to be defined.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">12210853</PMID><DateCreated><Year>2002</Year><Month>09</Month><Day>04</Day></DateCreated><DateCompleted><Year>2002</Year><Month>11</Month><Day>20</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>17</Volume><Issue>4</Issue><PubDate><Year>2002</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Small-amplitude cortical myoclonus in Parkinson's disease: physiology and clinical observations.</ArticleTitle><Pagination><MedlinePgn>657-62</MedlinePgn></Pagination><Abstract><AbstractText>We studied the occurrence of small-amplitude myo- clonus in 20 idiopathic Parkinson's disease patients who had no evidence of dementia as defined by criteria in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition. Parkinson's disease was diagnosed by United Kingdom Brain Bank criteria, and clinical assessment was performed with the Unified Parkinson's Disease Rating Scale motor score, Hoehn and Yahr staging, and the Mini-Mental State Examination. Clinical assessment showed a range of mild-to-moderate disease severity. All patients underwent polygraphic electro-encephalographic-electromyographic (EMG) recording with back-averaging, somatosensory evoked potential testing, and attempted elicitation of long-latency EMG responses. Multichannel surface EMG recording during muscle activation showed irregular, multifocal, brief (<50 msec) myoclonus EMG discharges. Back-averaging consistently showed a focal, short-latency, electroencephalographic transient prior to the myoclonus EMG discharge. Cortical somatosensory evoked potential waves were not enlarged, and long-latency EMG responses at rest were not present. The small-amplitude myoclonus in such cases arises from an abnormal discharge from the sensorimotor cortex. The mechanism of this cortical myoclonus in Parkinson's disease has differences from the more common "cortical reflex myoclonus" physiology. Advanced parkinsonism is not a requirement for manifestation of this myoclonus type. Although the myoclonus occurred without dementia in these cases, its relationship to the subsequent development of cognitive impairment remains to be defined.</AbstractText><CopyrightInformation>Copyright 2002 Movement Disorder Society</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Caviness</LastName><ForeName>John N</ForeName><Initials>JN</Initials><AffiliationInfo><Affiliation>Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259, USA. jcaviness@mayo.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adler</LastName><ForeName>Charles H</ForeName><Initials>CH</Initials></Author><Author ValidYN="Y"><LastName>Beach</LastName><ForeName>Thomas G</ForeName><Initials>TG</Initials></Author><Author ValidYN="Y"><LastName>Wetjen</LastName><ForeName>Kristi L</ForeName><Initials>KL</Initials></Author><Author ValidYN="Y"><LastName>Caselli</LastName><ForeName>Richard J</ForeName><Initials>RJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002540">Cerebral Cortex</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004292">Dominance, Cerebral</DescriptorName><QualifierName MajorTopicYN="N" 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