Heart rate changes during freezing of gait in patients with Parkinson's disease
Identifieur interne : 001026 ( Main/Corpus ); précédent : 001025; suivant : 001027Heart rate changes during freezing of gait in patients with Parkinson's disease
Auteurs : Inbal Maidan ; Meir Plotnik ; Anat Mirelman ; Aner Weiss ; Nir Giladi ; Jeffrey M. HausdorffSource :
- Movement Disorders [ 0885-3185 ] ; 2010-10-30.
English descriptors
Abstract
Freezing of gait (FOG) is one of the most disabling symptoms that affect patients with Parkinson's disease (PD). Although the pathophysiology underlying FOG largely remains an enigma, several lines of evidence suggest that the autonomic nervous system might be involved. To this end, we tested the hypothesis that heart rate (HR) increases during FOG and, further, that HR increases just before FOG. To evaluate these hypotheses, 15 healthy older adults, 10 patients with PD who experienced FOG, and 10 patients who did not were studied. Patients with PD were tested during their “off” medication state. HR and HR variability were measured as subjects carried out tasks that frequently provoke FOG; 120 FOG episodes were evaluated. During FOG, HR increased (P = 0.001) by an average of 1.8 bpm, compared with HR measured before the beginning of FOG. HR also increased just before FOG, by 1 bpm (P < 0.0001). In contrast, during sudden stops and 180° turns, HR decreased by almost 2 bpm (P < 0.0001). HR variability was not associated with FOG. To our knowledge, these findings are the first to document the association of FOG to autonomic system activation, as manifested by HR dynamics. One explanation is that the changes in HR before and during FOG may be a sympathetic response that, secondary to limbic activation, contributes to the development of freezing. Although further studies are needed to evaluate these associations, the current results provide experimental evidence linking impaired motor blockades to autonomic nervous system function among patients with PD. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23280
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Hausdorff</name><affiliation><mods:affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</mods:affiliation></affiliation><affiliation><mods:affiliation>Harvard Medical School, Boston, Massachusetts, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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Although the pathophysiology underlying FOG largely remains an enigma, several lines of evidence suggest that the autonomic nervous system might be involved. To this end, we tested the hypothesis that heart rate (HR) increases during FOG and, further, that HR increases just before FOG. To evaluate these hypotheses, 15 healthy older adults, 10 patients with PD who experienced FOG, and 10 patients who did not were studied. Patients with PD were tested during their “off” medication state. HR and HR variability were measured as subjects carried out tasks that frequently provoke FOG; 120 FOG episodes were evaluated. During FOG, HR increased (P = 0.001) by an average of 1.8 bpm, compared with HR measured before the beginning of FOG. HR also increased just before FOG, by 1 bpm (P < 0.0001). In contrast, during sudden stops and 180° turns, HR decreased by almost 2 bpm (P < 0.0001). HR variability was not associated with FOG. To our knowledge, these findings are the first to document the association of FOG to autonomic system activation, as manifested by HR dynamics. One explanation is that the changes in HR before and during FOG may be a sympathetic response that, secondary to limbic activation, contributes to the development of freezing. Although further studies are needed to evaluate these associations, the current results provide experimental evidence linking impaired motor blockades to autonomic nervous system function among patients with PD. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Inbal Maidan MSc, PT</name><affiliations><json:string>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</json:string><json:string>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</json:string></affiliations></json:item><json:item><name>Meir Plotnik PhD</name><affiliations><json:string>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</json:string></affiliations></json:item><json:item><name>Anat Mirelman PhD</name><affiliations><json:string>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</json:string><json:string>Harvard Medical School, Boston, Massachusetts, USA</json:string></affiliations></json:item><json:item><name>Aner Weiss BS</name><affiliations><json:string>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</json:string></affiliations></json:item><json:item><name>Nir Giladi MD</name><affiliations><json:string>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</json:string><json:string>Department of Neurology, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</json:string></affiliations></json:item><json:item><name>Jeffrey M. Hausdorff PhD</name><affiliations><json:string>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</json:string><json:string>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</json:string><json:string>Harvard Medical School, Boston, Massachusetts, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gait</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>heart rate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autonomic nervous system</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>freezing of gait</value></json:item></subject><articleId><json:string>MDS23280</json:string></articleId><language><json:string>eng</json:string></language><abstract>Freezing of gait (FOG) is one of the most disabling symptoms that affect patients with Parkinson's disease (PD). Although the pathophysiology underlying FOG largely remains an enigma, several lines of evidence suggest that the autonomic nervous system might be involved. To this end, we tested the hypothesis that heart rate (HR) increases during FOG and, further, that HR increases just before FOG. To evaluate these hypotheses, 15 healthy older adults, 10 patients with PD who experienced FOG, and 10 patients who did not were studied. Patients with PD were tested during their “off” medication state. HR and HR variability were measured as subjects carried out tasks that frequently provoke FOG; 120 FOG episodes were evaluated. During FOG, HR increased (P = 0.001) by an average of 1.8 bpm, compared with HR measured before the beginning of FOG. HR also increased just before FOG, by 1 bpm (P > 0.0001). In contrast, during sudden stops and 180° turns, HR decreased by almost 2 bpm (P > 0.0001). HR variability was not associated with FOG. To our knowledge, these findings are the first to document the association of FOG to autonomic system activation, as manifested by HR dynamics. One explanation is that the changes in HR before and during FOG may be a sympathetic response that, secondary to limbic activation, contributes to the development of freezing. Although further studies are needed to evaluate these associations, the current results provide experimental evidence linking impaired motor blockades to autonomic nervous system function among patients with PD. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1608</abstractCharCount><pdfWordCount>5722</pdfWordCount><pdfCharCount>34486</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>257</abstractWordCount></qualityIndicators><title>Heart rate changes during freezing of gait in patients with Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>25</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>9</total><last>2354</last><first>2346</first></pages><issn><json:string>0885-3185</json:string></issn><issue>14</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23280</json:string></doi><id>6E5D5E50D419FD31DBB5C62B2889C07A09D21EAF</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6E5D5E50D419FD31DBB5C62B2889C07A09D21EAF/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6E5D5E50D419FD31DBB5C62B2889C07A09D21EAF/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6E5D5E50D419FD31DBB5C62B2889C07A09D21EAF/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Heart rate changes during freezing of gait in patients with Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*The funding agencies were not involved with data collection, data analysis, or manuscript preparation.</note><note type="content">*Potential conflict of interest: The authors have no competing interests to disclose.</note><note>The European Commission in the context of FP6 projects DAPHNet - No. fet‐018474‐2;</note><note>SENSACTION‐AAL - No. infso‐ist‐045622;</note><note>The National Parkinson Foundation</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Heart rate changes during freezing of gait in patients with Parkinson's disease</title><author><persName><forename type="first">Inbal</forename><surname>Maidan</surname></persName><roleName type="degree">MSc, PT</roleName><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</affiliation></author><author><persName><forename type="first">Meir</forename><surname>Plotnik</surname></persName><roleName type="degree">PhD</roleName><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation></author><author><persName><forename type="first">Anat</forename><surname>Mirelman</surname></persName><roleName type="degree">PhD</roleName><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Harvard Medical School, Boston, Massachusetts, USA</affiliation></author><author><persName><forename type="first">Aner</forename><surname>Weiss</surname></persName><roleName type="degree">BS</roleName><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation></author><author><persName><forename type="first">Nir</forename><surname>Giladi</surname></persName><roleName type="degree">MD</roleName><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Department of Neurology, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</affiliation></author><author><persName><forename type="first">Jeffrey M.</forename><surname>Hausdorff</surname></persName><roleName type="degree">PhD</roleName><note type="correspondence"><p>Correspondence: Laboratory for Gait and Neurodynamics, Tel Aviv Sourarsky Medical Center, 6 Weizmann Street, Tel Aviv 64239, Israel</p></note><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</affiliation><affiliation>Harvard Medical School, Boston, Massachusetts, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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Although the pathophysiology underlying FOG largely remains an enigma, several lines of evidence suggest that the autonomic nervous system might be involved. To this end, we tested the hypothesis that heart rate (HR) increases during FOG and, further, that HR increases just before FOG. To evaluate these hypotheses, 15 healthy older adults, 10 patients with PD who experienced FOG, and 10 patients who did not were studied. Patients with PD were tested during their “off” medication state. HR and HR variability were measured as subjects carried out tasks that frequently provoke FOG; 120 FOG episodes were evaluated. During FOG, HR increased (P = 0.001) by an average of 1.8 bpm, compared with HR measured before the beginning of FOG. HR also increased just before FOG, by 1 bpm (P < 0.0001). In contrast, during sudden stops and 180° turns, HR decreased by almost 2 bpm (P < 0.0001). HR variability was not associated with FOG. To our knowledge, these findings are the first to document the association of FOG to autonomic system activation, as manifested by HR dynamics. One explanation is that the changes in HR before and during FOG may be a sympathetic response that, secondary to limbic activation, contributes to the development of freezing. Although further studies are needed to evaluate these associations, the current results provide experimental evidence linking impaired motor blockades to autonomic nervous system function among patients with PD. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>gait</term></item><item><term>heart rate</term></item><item><term>autonomic nervous system</term></item><item><term>freezing of gait</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-01-03">Received</change><change when="2010-05-05">Registration</change><change when="2010-10-30">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6E5D5E50D419FD31DBB5C62B2889C07A09D21EAF/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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href="file:MDS.MDS23280.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="41"></count><count type="wordTotal" number="6921"></count></countGroup><titleGroup><title type="main" xml:lang="en">Heart rate changes during freezing of gait in patients with Parkinson's disease<link href="#fn1"></link><link href="#fn2"></link></title><title type="short" xml:lang="en">Heart Rate Changes During Freezing of Gait</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Inbal</givenNames><familyName>Maidan</familyName><degrees>MSc, PT</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Meir</givenNames><familyName>Plotnik</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af4"><personName><givenNames>Anat</givenNames><familyName>Mirelman</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Aner</givenNames><familyName>Weiss</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af3"><personName><givenNames>Nir</givenNames><familyName>Giladi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2 #af4" corresponding="yes"><personName><givenNames>Jeffrey M.</givenNames><familyName>Hausdorff</familyName><degrees>PhD</degrees></personName><contactDetails><email>jhausdor@tasmc.health.gov.il</email><email>jhausdor@bidmc.harvard.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IL" type="organization"><unparsedAffiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IL" type="organization"><unparsedAffiliation>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="IL" type="organization"><unparsedAffiliation>Department of Neurology, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Harvard Medical School, Boston, Massachusetts, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">gait</keyword><keyword xml:id="kwd3">heart rate</keyword><keyword xml:id="kwd4">autonomic nervous system</keyword><keyword xml:id="kwd5">freezing of gait</keyword></keywordGroup><fundingInfo><fundingAgency>The European Commission in the context of FP6 projects DAPHNet</fundingAgency><fundingNumber>fet‐018474‐2</fundingNumber></fundingInfo><fundingInfo><fundingAgency>SENSACTION‐AAL</fundingAgency><fundingNumber>infso‐ist‐045622</fundingNumber></fundingInfo><fundingInfo><fundingAgency>The National Parkinson Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Freezing of gait (FOG) is one of the most disabling symptoms that affect patients with Parkinson's disease (PD). Although the pathophysiology underlying FOG largely remains an enigma, several lines of evidence suggest that the autonomic nervous system might be involved. To this end, we tested the hypothesis that heart rate (HR) increases during FOG and, further, that HR increases just before FOG. To evaluate these hypotheses, 15 healthy older adults, 10 patients with PD who experienced FOG, and 10 patients who did not were studied. Patients with PD were tested during their “off” medication state. HR and HR variability were measured as subjects carried out tasks that frequently provoke FOG; 120 FOG episodes were evaluated. During FOG, HR increased (<i>P</i> = 0.001) by an average of 1.8 bpm, compared with HR measured before the beginning of FOG. HR also increased just before FOG, by 1 bpm (<i>P</i> < 0.0001). In contrast, during sudden stops and 180° turns, HR decreased by almost 2 bpm (<i>P</i> < 0.0001). HR variability was not associated with FOG. To our knowledge, these findings are the first to document the association of FOG to autonomic system activation, as manifested by HR dynamics. One explanation is that the changes in HR before and during FOG may be a sympathetic response that, secondary to limbic activation, contributes to the development of freezing. Although further studies are needed to evaluate these associations, the current results provide experimental evidence linking impaired motor blockades to autonomic nervous system function among patients with PD. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>The funding agencies were not involved with data collection, data analysis, or manuscript preparation.</p></note><note xml:id="fn2"><p>Potential conflict of interest: The authors have no competing interests to disclose.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Heart rate changes during freezing of gait in patients with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Heart Rate Changes During Freezing of Gait</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Heart rate changes during freezing of gait in patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Inbal</namePart><namePart type="family">Maidan</namePart><namePart type="termsOfAddress">MSc, PT</namePart><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Meir</namePart><namePart type="family">Plotnik</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anat</namePart><namePart type="family">Mirelman</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Harvard Medical School, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Aner</namePart><namePart type="family">Weiss</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nir</namePart><namePart type="family">Giladi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Department of Neurology, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeffrey M.</namePart><namePart type="family">Hausdorff</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Movement Disorders Unit, Department of Neurology, Tel‐Aviv Sourasky Medical Center, Tel‐Aviv, Israel</affiliation><affiliation>Department of Physical Therapy, Sackler Faculty of Medicine, Tel‐Aviv University, Tel‐Aviv, Israel</affiliation><affiliation>Harvard Medical School, Boston, Massachusetts, USA</affiliation><description>Correspondence: Laboratory for Gait and Neurodynamics, Tel Aviv Sourarsky Medical Center, 6 Weizmann Street, Tel Aviv 64239, Israel</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-10-30</dateIssued><dateCaptured encoding="w3cdtf">2010-01-03</dateCaptured><dateValid encoding="w3cdtf">2010-05-05</dateValid><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">3</extent><extent unit="tables">2</extent><extent unit="references">41</extent><extent unit="words">6921</extent></physicalDescription><abstract lang="en">Freezing of gait (FOG) is one of the most disabling symptoms that affect patients with Parkinson's disease (PD). Although the pathophysiology underlying FOG largely remains an enigma, several lines of evidence suggest that the autonomic nervous system might be involved. To this end, we tested the hypothesis that heart rate (HR) increases during FOG and, further, that HR increases just before FOG. To evaluate these hypotheses, 15 healthy older adults, 10 patients with PD who experienced FOG, and 10 patients who did not were studied. Patients with PD were tested during their “off” medication state. HR and HR variability were measured as subjects carried out tasks that frequently provoke FOG; 120 FOG episodes were evaluated. During FOG, HR increased (P = 0.001) by an average of 1.8 bpm, compared with HR measured before the beginning of FOG. HR also increased just before FOG, by 1 bpm (P < 0.0001). In contrast, during sudden stops and 180° turns, HR decreased by almost 2 bpm (P < 0.0001). HR variability was not associated with FOG. To our knowledge, these findings are the first to document the association of FOG to autonomic system activation, as manifested by HR dynamics. One explanation is that the changes in HR before and during FOG may be a sympathetic response that, secondary to limbic activation, contributes to the development of freezing. Although further studies are needed to evaluate these associations, the current results provide experimental evidence linking impaired motor blockades to autonomic nervous system function among patients with PD. © 2010 Movement Disorder Society</abstract><note type="content">*The funding agencies were not involved with data collection, data analysis, or manuscript preparation.</note><note type="content">*Potential conflict of interest: The authors have no competing interests to disclose.</note><note type="funding">The European Commission in the context of FP6 projects DAPHNet - No. fet‐018474‐2; </note><note type="funding">SENSACTION‐AAL - No. infso‐ist‐045622; </note><note type="funding">The National Parkinson Foundation</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>gait</topic><topic>heart rate</topic><topic>autonomic nervous system</topic><topic>freezing of gait</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</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>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>14</number></detail><extent unit="pages"><start>2346</start><end>2354</end><total>9</total></extent></part></relatedItem><identifier type="istex">6E5D5E50D419FD31DBB5C62B2889C07A09D21EAF</identifier><identifier type="DOI">10.1002/mds.23280</identifier><identifier type="ArticleID">MDS23280</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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