Visual and auditory evoked potentials in early onset parkinson's disease and their relationship to cerebrospinal fluid monoamine metabolites
Identifieur interne : 001992 ( Istex/Corpus ); précédent : 001991; suivant : 001993Visual and auditory evoked potentials in early onset parkinson's disease and their relationship to cerebrospinal fluid monoamine metabolites
Auteurs : Muthane ; P. Satishchandra ; M. N. SubhashSource :
- Movement Disorders [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
Abstract
We studied visual (VEP) and brainstem auditory (BAEP) evoked potential changes in 23 patients with early onset Parkinson's disease (EOPD) to establish the nature of the changes as well as their relationship to dopaminergic (DA) and serotonergic (5‐HT) disturbances, as determined by cerebrospinal fuid levels of homovanillic acid (HVA) and 5‐hydroxyindoleacetic acid (5‐HIAA). We also compared these parameters between the young onset (YOPD) and juvenile Parkinsonism (JP), the two subgroups of EOPD, to look for any possible differences between the two. In EOPD, the mean P100 latency of the VEP was significantly prolonged compared to controls (p < 0.001). However, within EOPD the evoked potential parameters were not significantly different between YOPD and the JP subgroups. P100 latency was abnormal in six patients (YOPD: 5, JP:1) (26%). Six patients (YOPD: 3, JP:3) (26%) had abnormal BAEP. A significant negative correlation (r: −0.89, p <1%) was observed between the P100 latency and CSF HVA levels. No correlation was observed between the BAEP interpeak latencies and either CSF HVA or 5‐HIAA levels. This study suggests that VEP and BAEP abnormalities do occur in EOPD (in both YOPD and JP), and that the prolongation of P100 latency is secondary to DA deficiency as in PD. The cause of BAEP abnormalities in EOPD. There was no correlation between the VEP or BAEP changes to either the age at onset or duration of EOPD.
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DOI: 10.1002/mds.870080316
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ISTEX:56E020AA28F1DDBFD6E8EABF4972AC68B84E71C7Le document en format XML
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We also compared these parameters between the young onset (YOPD) and juvenile Parkinsonism (JP), the two subgroups of EOPD, to look for any possible differences between the two. In EOPD, the mean P100 latency of the VEP was significantly prolonged compared to controls (p < 0.001). However, within EOPD the evoked potential parameters were not significantly different between YOPD and the JP subgroups. P100 latency was abnormal in six patients (YOPD: 5, JP:1) (26%). Six patients (YOPD: 3, JP:3) (26%) had abnormal BAEP. A significant negative correlation (r: −0.89, p <1%) was observed between the P100 latency and CSF HVA levels. No correlation was observed between the BAEP interpeak latencies and either CSF HVA or 5‐HIAA levels. This study suggests that VEP and BAEP abnormalities do occur in EOPD (in both YOPD and JP), and that the prolongation of P100 latency is secondary to DA deficiency as in PD. The cause of BAEP abnormalities in EOPD. 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We also compared these parameters between the young onset (YOPD) and juvenile Parkinsonism (JP), the two subgroups of EOPD, to look for any possible differences between the two. In EOPD, the mean P100 latency of the VEP was significantly prolonged compared to controls (p > 0.001). However, within EOPD the evoked potential parameters were not significantly different between YOPD and the JP subgroups. P100 latency was abnormal in six patients (YOPD: 5, JP:1) (26%). Six patients (YOPD: 3, JP:3) (26%) had abnormal BAEP. A significant negative correlation (r: −0.89, p >1%) was observed between the P100 latency and CSF HVA levels. No correlation was observed between the BAEP interpeak latencies and either CSF HVA or 5‐HIAA levels. This study suggests that VEP and BAEP abnormalities do occur in EOPD (in both YOPD and JP), and that the prolongation of P100 latency is secondary to DA deficiency as in PD. The cause of BAEP abnormalities in EOPD. 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We also compared these parameters between the young onset (YOPD) and juvenile Parkinsonism (JP), the two subgroups of EOPD, to look for any possible differences between the two. In EOPD, the mean P100 latency of the VEP was significantly prolonged compared to controls (p < 0.001). However, within EOPD the evoked potential parameters were not significantly different between YOPD and the JP subgroups. P100 latency was abnormal in six patients (YOPD: 5, JP:1) (26%). Six patients (YOPD: 3, JP:3) (26%) had abnormal BAEP. A significant negative correlation (r: −0.89, p <1%) was observed between the P100 latency and CSF HVA levels. No correlation was observed between the BAEP interpeak latencies and either CSF HVA or 5‐HIAA levels. This study suggests that VEP and BAEP abnormalities do occur in EOPD (in both YOPD and JP), and that the prolongation of P100 latency is secondary to DA deficiency as in PD. The cause of BAEP abnormalities in EOPD. 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N.</givenNames><familyName>Subhash</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IN" type="organization"><unparsedAffiliation>Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, India</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IN" type="organization"><unparsedAffiliation>Department of Neurochemistry, National Institute of Mental Health and Neurosciences, Bangalore, India</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, College of Physicians and Surgeons, Columbia‐Prebyterian Medical Center, New York, New York, U.S.A.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Early onset Parkinson's disease</keyword><keyword xml:id="kwd2">Young onset Parkinson's disease</keyword><keyword xml:id="kwd3">Juvenile parkinsonism</keyword><keyword xml:id="kwd4">Parkinson's disease</keyword><keyword xml:id="kwd5">Evoked potentials</keyword><keyword xml:id="kwd6">Monoamine metabolites</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We studied visual (VEP) and brainstem auditory (BAEP) evoked potential changes in 23 patients with early onset Parkinson's disease (EOPD) to establish the nature of the changes as well as their relationship to dopaminergic (DA) and serotonergic (5‐HT) disturbances, as determined by cerebrospinal fuid levels of homovanillic acid (HVA) and 5‐hydroxyindoleacetic acid (5‐HIAA). We also compared these parameters between the young onset (YOPD) and juvenile Parkinsonism (JP), the two subgroups of EOPD, to look for any possible differences between the two. In EOPD, the mean P<sub>100</sub> latency of the VEP was significantly prolonged compared to controls (p < 0.001). However, within EOPD the evoked potential parameters were not significantly different between YOPD and the JP subgroups. P<sub>100</sub> latency was abnormal in six patients (YOPD: 5, JP:1) (26%). Six patients (YOPD: 3, JP:3) (26%) had abnormal BAEP. A significant negative correlation (r: −0.89, p <1%) was observed between the P<sub>100</sub> latency and CSF HVA levels. No correlation was observed between the BAEP interpeak latencies and either CSF HVA or 5‐HIAA levels. This study suggests that VEP and BAEP abnormalities do occur in EOPD (in both YOPD and JP), and that the prolongation of P<sub>100</sub> latency is secondary to DA deficiency as in PD. The cause of BAEP abnormalities in EOPD. There was no correlation between the VEP or BAEP changes to either the age at onset or duration of EOPD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Visual and auditory evoked potentials in early onset parkinson's disease and their relationship to cerebrospinal fluid monoamine metabolites</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>EARLY ONSET PARKINSON'S AND EVOKED POTENTIALS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Visual and auditory evoked potentials in early onset parkinson's disease and their relationship to cerebrospinal fluid monoamine metabolites</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Muthane</namePart><affiliation>Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, India</affiliation><affiliation>Department of Neurology, College of Physicians and Surgeons, Columbia‐Prebyterian Medical Center, New York, New York, U.S.A.</affiliation><description>Correspondence: Department of Neurology, 310 Black Building, 650 West 168th Street, New York, NY 10032, U.S.A</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Satishchandra</namePart><affiliation>Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. N.</namePart><namePart type="family">Subhash</namePart><affiliation>Department of Neurochemistry, National Institute of Mental Health and Neurosciences, Bangalore, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">reviewArticle</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="tables">1</extent><extent unit="references">12</extent></physicalDescription><abstract lang="en">We studied visual (VEP) and brainstem auditory (BAEP) evoked potential changes in 23 patients with early onset Parkinson's disease (EOPD) to establish the nature of the changes as well as their relationship to dopaminergic (DA) and serotonergic (5‐HT) disturbances, as determined by cerebrospinal fuid levels of homovanillic acid (HVA) and 5‐hydroxyindoleacetic acid (5‐HIAA). We also compared these parameters between the young onset (YOPD) and juvenile Parkinsonism (JP), the two subgroups of EOPD, to look for any possible differences between the two. In EOPD, the mean P100 latency of the VEP was significantly prolonged compared to controls (p < 0.001). However, within EOPD the evoked potential parameters were not significantly different between YOPD and the JP subgroups. P100 latency was abnormal in six patients (YOPD: 5, JP:1) (26%). Six patients (YOPD: 3, JP:3) (26%) had abnormal BAEP. A significant negative correlation (r: −0.89, p <1%) was observed between the P100 latency and CSF HVA levels. No correlation was observed between the BAEP interpeak latencies and either CSF HVA or 5‐HIAA levels. This study suggests that VEP and BAEP abnormalities do occur in EOPD (in both YOPD and JP), and that the prolongation of P100 latency is secondary to DA deficiency as in PD. The cause of BAEP abnormalities in EOPD. There was no correlation between the VEP or BAEP changes to either the age at onset or duration of EOPD.</abstract><subject lang="en"><genre>Keywords</genre><topic>Early onset Parkinson's disease</topic><topic>Young onset Parkinson's disease</topic><topic>Juvenile parkinsonism</topic><topic>Parkinson's disease</topic><topic>Evoked potentials</topic><topic>Monoamine metabolites</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Review</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>344</start><end>348</end><total>5</total></extent></part></relatedItem><identifier type="istex">56E020AA28F1DDBFD6E8EABF4972AC68B84E71C7</identifier><identifier type="DOI">10.1002/mds.870080316</identifier><identifier type="ArticleID">MDS870080316</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1993 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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