Are dysautonomic and sensory symptoms present in early Parkinson’s disease?
Identifieur interne : 000351 ( Main/Corpus ); précédent : 000350; suivant : 000352Are dysautonomic and sensory symptoms present in early Parkinson’s disease?
Auteurs : O. Tysnes ; B. Müller ; J. P. LarsenSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 2010-07.
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Abstract
Tysnes O‐B, Müller B, Larsen JP. Are dysautonomic and sensory symptoms present in early Parkinson’s disease? Acta Neurol Scand: 2010: 122 (Suppl. 190): 72–77. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non‐motor symptoms have been increasingly connected to the disease although already described in James Parkinson’s ‘Essay on the shaking palsy’ from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non‐motor symptoms like dysautonomia, insomnia, day‐time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. Currently, the evidence for sensory and autonomic involvement in PD is reviewed with special focus on the early phase of the disease.
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DOI: 10.1111/j.1600-0404.2010.01380.x
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Are dysautonomic and sensory symptoms present in early Parkinson’s disease? Acta Neurol Scand: 2010: 122 (Suppl. 190): 72–77. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non‐motor symptoms have been increasingly connected to the disease although already described in James Parkinson’s ‘Essay on the shaking palsy’ from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non‐motor symptoms like dysautonomia, insomnia, day‐time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. Currently, the evidence for sensory and autonomic involvement in PD is reviewed with special focus on the early phase of the disease.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>O.‐B. Tysnes</name><affiliations><json:string>Department of Neurology, Haukeland University Hospital, Bergen, Norway</json:string><json:string>Institute for Clinical Medicine, University of Bergen, Bergen, Norway</json:string></affiliations></json:item><json:item><name>B. 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Are dysautonomic and sensory symptoms present in early Parkinson’s disease? Acta Neurol Scand: 2010: 122 (Suppl. 190): 72–77. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non‐motor symptoms have been increasingly connected to the disease although already described in James Parkinson’s ‘Essay on the shaking palsy’ from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non‐motor symptoms like dysautonomia, insomnia, day‐time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. 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Are dysautonomic and sensory symptoms present in early Parkinson’s disease? Acta Neurol Scand: 2010: 122 (Suppl. 190): 72–77. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non‐motor symptoms have been increasingly connected to the disease although already described in James Parkinson’s ‘Essay on the shaking palsy’ from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non‐motor symptoms like dysautonomia, insomnia, day‐time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. Currently, the evidence for sensory and autonomic involvement in PD is reviewed with special focus on the early phase of the disease.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>constipation</term></item><item><term>drooling</term></item><item><term>dysautonomia</term></item><item><term>hyposmia</term></item><item><term>pain</term></item><item><term>Parkinson’s disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/BA6CC49CD275EF410B20F6CA10D73A60E86EB414/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0404</doi><issn type="print">0001-6314</issn><issn type="electronic">1600-0404</issn><idGroup><id type="product" value="ANE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ACTA NEUROLOGICA SCANDINAVICA">Acta Neurologica Scandinavica</title></titleGroup></publicationMeta><publicationMeta level="part" position="07000"><doi origin="wiley">10.1111/ane.2010.122.issue-s190</doi><titleGroup><title type="specialIssueTitle">Selected Articles from the Annual Meeting of the Norwegian Neurological Association, Oslo, November 2009</title></titleGroup><numberingGroup><numbering type="journalVolume" number="122">122</numbering><numbering type="supplement">s190</numbering></numberingGroup><coverDate startDate="2010-07">July 2010</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="14" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.2010.01380.x</doi><idGroup><id type="unit" value="ANE1380"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Review Articles</title></titleGroup><copyright>© 2010 John Wiley & Sons A/S</copyright><eventGroup><event type="firstOnline" date="2010-06-02"></event><event type="publishedOnlineFinalForm" date="2010-06-02"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-06-03"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="72">72</numbering><numbering type="pageLast" number="77">77</numbering></numberingGroup><correspondenceTo>Ole‐Bjørn Tysnes, Department of Neurology, Haukeland University Hospital, N‐5021 Bergen, Norway
Tel.: +47 5597 5045
Fax: +47 5597 5165
e‐mail: <email>obty@haukeland.no</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE1380.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Are dysautonomic and sensory symptoms present in early Parkinson’s disease?</title><title type="shortAuthors"><b>Tysnes et al.</b></title><title type="short"><b>Sensory and autonomic involvement in Parkinson’s disease</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>O.‐B.</givenNames><familyName>Tysnes</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a2"><personName><givenNames>B.</givenNames><familyName>Müller</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2 #a3 #a4"><personName><givenNames>J. P.</givenNames><familyName>Larsen</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="NO"><unparsedAffiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="NO"><unparsedAffiliation>Institute for Clinical Medicine, University of Bergen, Bergen, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="NO"><unparsedAffiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="NO"><unparsedAffiliation>The Norwegian Centre for Movement Disorders, Stavanger, Norway</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">constipation</keyword><keyword xml:id="k2">drooling</keyword><keyword xml:id="k3">dysautonomia</keyword><keyword xml:id="k4">hyposmia</keyword><keyword xml:id="k5">pain</keyword><keyword xml:id="k6">Parkinson’s disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Tysnes O‐B, Müller B, Larsen JP. Are dysautonomic and sensory symptoms present in early Parkinson’s disease? Acta Neurol Scand: 2010: 122 (Suppl. 190): 72–77. © 2010 John Wiley & Sons A/S.</p><p>Parkinson’s disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non‐motor symptoms have been increasingly connected to the disease although already described in James Parkinson’s ‘Essay on the shaking palsy’ from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non‐motor symptoms like dysautonomia, insomnia, day‐time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. Currently, the evidence for sensory and autonomic involvement in PD is reviewed with special focus on the early phase of the disease.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1" numbered="no"><p>Conflicts of interest: O‐BT has received fees from GlaxoSmithKline, Lundbeck, Orion Pharma, Pfizer and Boehringer. The remaining authors have declared no conflicts.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Are dysautonomic and sensory symptoms present in early Parkinson’s disease?</title></titleInfo><titleInfo type="abbreviated"><title>Sensory and autonomic involvement in Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Are dysautonomic and sensory symptoms present in early Parkinson’s disease?</title></titleInfo><name type="personal"><namePart type="given">O.‐B.</namePart><namePart type="family">Tysnes</namePart><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation><affiliation>Institute for Clinical Medicine, University of Bergen, Bergen, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Müller</namePart><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation><affiliation>Institute for Clinical Medicine, University of Bergen, Bergen, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. P.</namePart><namePart type="family">Larsen</namePart><affiliation>Institute for Clinical Medicine, University of Bergen, Bergen, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>The Norwegian Centre for Movement Disorders, Stavanger, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-07</dateIssued><copyrightDate encoding="w3cdtf">2010</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="figures">1</extent></physicalDescription><abstract lang="en">Tysnes O‐B, Müller B, Larsen JP. Are dysautonomic and sensory symptoms present in early Parkinson’s disease? Acta Neurol Scand: 2010: 122 (Suppl. 190): 72–77. © 2010 John Wiley & Sons A/S. Parkinson’s disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non‐motor symptoms have been increasingly connected to the disease although already described in James Parkinson’s ‘Essay on the shaking palsy’ from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non‐motor symptoms like dysautonomia, insomnia, day‐time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. Currently, the evidence for sensory and autonomic involvement in PD is reviewed with special focus on the early phase of the disease.</abstract><subject lang="en"><genre>Keywords</genre><topic>constipation</topic><topic>drooling</topic><topic>dysautonomia</topic><topic>hyposmia</topic><topic>pain</topic><topic>Parkinson’s disease</topic></subject><relatedItem type="host"><titleInfo><title>Acta Neurologica Scandinavica</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0001-6314</identifier><identifier type="eISSN">1600-0404</identifier><identifier type="DOI">10.1111/(ISSN)1600-0404</identifier><identifier type="PublisherID">ANE</identifier><part><date>2010</date><detail type="title"><title>Selected Articles from the Annual Meeting of the Norwegian Neurological Association, Oslo, November 2009</title></detail><detail type="volume"><caption>vol.</caption><number>122</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s190</number></detail><extent unit="pages"><start>72</start><end>77</end><total>6</total></extent></part></relatedItem><identifier type="istex">BA6CC49CD275EF410B20F6CA10D73A60E86EB414</identifier><identifier type="DOI">10.1111/j.1600-0404.2010.01380.x</identifier><identifier type="ArticleID">ANE1380</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 John Wiley & Sons A/S</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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