Pain sensitivity and clinical progression in Parkinson's disease.
Identifieur interne : 001078 ( PubMed/Corpus ); précédent : 001077; suivant : 001079Pain sensitivity and clinical progression in Parkinson's disease.
Auteurs : Veit Mylius ; Juliane Brebbermann ; Helena Dohmann ; Isabel Engau ; Wolfgang H. Oertel ; Jens C. MöllerSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Analysis of Variance, Disease Progression, Electric Stimulation, Electromyography, Female, Humans, Hyperalgesia (etiology), Male, Middle Aged, Pain (etiology), Pain Measurement, Pain Threshold (physiology), Parkinson Disease (complications), Questionnaires, Reflex (physiology), Somatosensory Disorders (etiology), Spinal Cord (physiopathology).
- MESH :
- complications : Parkinson Disease.
- etiology : Hyperalgesia, Pain, Somatosensory Disorders.
- physiology : Pain Threshold, Reflex.
- physiopathology : Spinal Cord.
- Adult, Aged, Aged, 80 and over, Analysis of Variance, Disease Progression, Electric Stimulation, Electromyography, Female, Humans, Male, Middle Aged, Pain Measurement, Questionnaires.
Abstract
Pain sensitivity in Parkinson's disease is known to be altered in an L-dopa-dependent manner with increased spinal nociception and experimental pain perception in the medication-defined "off" state. As Parkinson's disease-related pain can be an early symptom in Parkinson's disease, the present study aimed to investigate experimental pain sensitivity and spinal nociception during clinical progression. The nociceptive flexion reflex as a marker of spinal nociception as well as electrical and heat pain thresholds were assessed during the medication-defined "off" state in 29 patients with Parkinson's disease divided into 3 severity groups (according to their Unified Parkinson's Disease Rating Scale motor score) and compared with 27 healthy elderly subjects. Parkinson's disease-related pain was also quantified. Data provided evidence that spinal nociception and pain sensitivity are preserved during the early phase of Parkinson's disease. Following increased spinal nociception (F(1,36) = 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F(1,34) = 5.397, P = .014; F(1,34) = 6.038, P = 0.053), whereas spinal nociception further increased (F(1,34) = 5.397, P < .001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. Because Parkinson's disease-related pain is correlated with experimental pain sensitivity these 2 observations likely reflect a causal relation.
DOI: 10.1002/mds.23825
PubMed: 21766333
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pain sensitivity and clinical progression in Parkinson's disease.</title><author><name sortKey="Mylius, Veit" sort="Mylius, Veit" uniqKey="Mylius V" first="Veit" last="Mylius">Veit Mylius</name><affiliation><nlm:affiliation>Department of Neurology, Philipps University, Marburg, Germany. mylius@med.uni-marburg.de</nlm:affiliation></affiliation></author><author><name sortKey="Brebbermann, Juliane" sort="Brebbermann, Juliane" uniqKey="Brebbermann J" first="Juliane" last="Brebbermann">Juliane Brebbermann</name></author><author><name sortKey="Dohmann, Helena" sort="Dohmann, Helena" uniqKey="Dohmann H" first="Helena" last="Dohmann">Helena Dohmann</name></author><author><name sortKey="Engau, Isabel" sort="Engau, Isabel" uniqKey="Engau I" first="Isabel" last="Engau">Isabel Engau</name></author><author><name sortKey="Oertel, Wolfgang H" sort="Oertel, Wolfgang H" uniqKey="Oertel W" first="Wolfgang H" last="Oertel">Wolfgang H. Oertel</name></author><author><name sortKey="Moller, Jens C" sort="Moller, Jens C" uniqKey="Moller J" first="Jens C" last="Möller">Jens C. Möller</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="doi">10.1002/mds.23825</idno><idno type="RBID">pubmed:21766333</idno><idno type="pmid">21766333</idno><idno type="wicri:Area/PubMed/Corpus">001078</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Pain sensitivity and clinical progression in Parkinson's disease.</title><author><name sortKey="Mylius, Veit" sort="Mylius, Veit" uniqKey="Mylius V" first="Veit" last="Mylius">Veit Mylius</name><affiliation><nlm:affiliation>Department of Neurology, Philipps University, Marburg, Germany. mylius@med.uni-marburg.de</nlm:affiliation></affiliation></author><author><name sortKey="Brebbermann, Juliane" sort="Brebbermann, Juliane" uniqKey="Brebbermann J" first="Juliane" last="Brebbermann">Juliane Brebbermann</name></author><author><name sortKey="Dohmann, Helena" sort="Dohmann, Helena" uniqKey="Dohmann H" first="Helena" last="Dohmann">Helena Dohmann</name></author><author><name sortKey="Engau, Isabel" sort="Engau, Isabel" uniqKey="Engau I" first="Isabel" last="Engau">Isabel Engau</name></author><author><name sortKey="Oertel, Wolfgang H" sort="Oertel, Wolfgang H" uniqKey="Oertel W" first="Wolfgang H" last="Oertel">Wolfgang H. Oertel</name></author><author><name sortKey="Moller, Jens C" sort="Moller, Jens C" uniqKey="Moller J" first="Jens C" last="Möller">Jens C. Möller</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="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Analysis of Variance</term><term>Disease Progression</term><term>Electric Stimulation</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Hyperalgesia (etiology)</term><term>Male</term><term>Middle Aged</term><term>Pain (etiology)</term><term>Pain Measurement</term><term>Pain Threshold (physiology)</term><term>Parkinson Disease (complications)</term><term>Questionnaires</term><term>Reflex (physiology)</term><term>Somatosensory Disorders (etiology)</term><term>Spinal Cord (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Hyperalgesia</term><term>Pain</term><term>Somatosensory Disorders</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Pain Threshold</term><term>Reflex</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Spinal Cord</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Analysis of Variance</term><term>Disease Progression</term><term>Electric Stimulation</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Pain Measurement</term><term>Questionnaires</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pain sensitivity in Parkinson's disease is known to be altered in an L-dopa-dependent manner with increased spinal nociception and experimental pain perception in the medication-defined "off" state. As Parkinson's disease-related pain can be an early symptom in Parkinson's disease, the present study aimed to investigate experimental pain sensitivity and spinal nociception during clinical progression. The nociceptive flexion reflex as a marker of spinal nociception as well as electrical and heat pain thresholds were assessed during the medication-defined "off" state in 29 patients with Parkinson's disease divided into 3 severity groups (according to their Unified Parkinson's Disease Rating Scale motor score) and compared with 27 healthy elderly subjects. Parkinson's disease-related pain was also quantified. Data provided evidence that spinal nociception and pain sensitivity are preserved during the early phase of Parkinson's disease. Following increased spinal nociception (F(1,36) = 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F(1,34) = 5.397, P = .014; F(1,34) = 6.038, P = 0.053), whereas spinal nociception further increased (F(1,34) = 5.397, P < .001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. Because Parkinson's disease-related pain is correlated with experimental pain sensitivity these 2 observations likely reflect a causal relation.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">21766333</PMID><DateCreated><Year>2011</Year><Month>10</Month><Day>24</Day></DateCreated><DateCompleted><Year>2012</Year><Month>03</Month><Day>05</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>12</Issue><PubDate><Year>2011</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Pain sensitivity and clinical progression in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>2220-5</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23825</ELocationID><Abstract><AbstractText>Pain sensitivity in Parkinson's disease is known to be altered in an L-dopa-dependent manner with increased spinal nociception and experimental pain perception in the medication-defined "off" state. As Parkinson's disease-related pain can be an early symptom in Parkinson's disease, the present study aimed to investigate experimental pain sensitivity and spinal nociception during clinical progression. The nociceptive flexion reflex as a marker of spinal nociception as well as electrical and heat pain thresholds were assessed during the medication-defined "off" state in 29 patients with Parkinson's disease divided into 3 severity groups (according to their Unified Parkinson's Disease Rating Scale motor score) and compared with 27 healthy elderly subjects. Parkinson's disease-related pain was also quantified. Data provided evidence that spinal nociception and pain sensitivity are preserved during the early phase of Parkinson's disease. Following increased spinal nociception (F(1,36) = 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F(1,34) = 5.397, P = .014; F(1,34) = 6.038, P = 0.053), whereas spinal nociception further increased (F(1,34) = 5.397, P < .001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. 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ValidYN="Y"><LastName>Möller</LastName><ForeName>Jens C</ForeName><Initials>JC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>07</Month><Day>15</Day></ArticleDate></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="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000369">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000704">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D018450">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004558">Electric Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004576">Electromyography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006930">Hyperalgesia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010146">Pain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010147">Pain Measurement</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017288">Pain Threshold</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011795">Questionnaires</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012018">Reflex</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020886">Somatosensory Disorders</DescriptorName><QualifierName MajorTopicYN="Y" 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