[Gait disorders in Parkinson's disease: and pathophysiological approaches].
Identifieur interne : 000955 ( PubMed/Checkpoint ); précédent : 000954; suivant : 000956[Gait disorders in Parkinson's disease: and pathophysiological approaches].
Auteurs : C. Moreau [France] ; S. Cantiniaux ; A. Delval ; L. Defebvre ; J-P AzulaySource :
- Revue neurologique [ 0035-3787 ] ; 2010.
English descriptors
- KwdEn :
- Acoustic Stimulation, Biomechanical Phenomena, Cognition Disorders (physiopathology), Cognition Disorders (psychology), Gait (physiology), Gait Disorders, Neurologic (etiology), Gait Disorders, Neurologic (physiopathology), Humans, Parkinson Disease (physiopathology), Parkinson Disease (psychology), Temporal Lobe (physiopathology).
- MESH :
- etiology : Gait Disorders, Neurologic.
- physiology : Gait.
- physiopathology : Cognition Disorders, Gait Disorders, Neurologic, Parkinson Disease, Temporal Lobe.
- psychology : Cognition Disorders, Parkinson Disease.
- Acoustic Stimulation, Biomechanical Phenomena, Humans.
Abstract
Gait disorders and axial symptoms are the main therapeutic challenges in advanced Parkinson's disease (PD). Gait disorders in PD are characterized by spatial and temporal dysfunction. Gait hypokinesia is the first to appear and is responsible for the decrease in velocity. A good sensitivity to the levodopa is well established. Morris et al. [Morris ME, Iansek R, Matyas TA, Summers JJ. Ability to modulate walking cadence remains intact in Parkinson's disease. J Neurol Neurosurg Psychiatry 1994a;57(12):1532-4; Morris ME, Iansek R, Matyas TA, Summers JJ. The pathogenesis of gait hypokinesia in Parkinson's disease. Brain 1994b;117(Pt. 5):1169-81; Morris ME, Iansek R, Matyas TA, Summers JJ. Stride length regulation in Parkinson's disease. Brain 1996;119:551-68] demonstrated that the ability to modulate walking cadence remains intact in PD, and could correspond to a compensatory mechanism. More advanced disease stages of the disease are characterized by abnormal temporal parameters (such as stride length variability, stride time variability and cadence elevation) which are unresponsive to levodopa therapy and may be correlated with the occurrence of falls and freezing of gait (FOG). Lastly, postural instability also results in falls and is poorly responsive to levodopa. A link between gait impairment and frontal disorders has recently been suggested. After a few years of evolution, paradoxical episodic phenomena are described: festination ("hastening gait" with rapid small, short steps) and FOG (involuntary and sudden cessation of gait). Both symptoms are often incapacitating for PD patients, because of their resultant loss of independence and their poor response to levodopa therapy. Kinematical studies of FOG revealed a decrease in velocity, stride length and an exponential increase in cadence, prior to a FOG episode. New approaches (functional MRI, wavelets...) should offer new perspectives concerning these disabling symptoms.
DOI: 10.1016/j.neurol.2009.05.010
PubMed: 19616816
Affiliations:
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Cantiniaux</name></author><author><name sortKey="Delval, A" sort="Delval, A" uniqKey="Delval A" first="A" last="Delval">A. Delval</name></author><author><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. 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Moreau</name><affiliation wicri:level="3"><nlm:affiliation>Service de neurologie et pathologie du mouvement, hôpital Roger-Salengro, CHRU, 59037 Lille cedex, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Service de neurologie et pathologie du mouvement, hôpital Roger-Salengro, CHRU, 59037 Lille cedex</wicri:regionArea><placeName><region type="region" nuts="2">Hauts-de-France</region><region type="old region" nuts="2">Nord-Pas-de-Calais</region><settlement type="city">Lille</settlement></placeName></affiliation></author><author><name sortKey="Cantiniaux, S" sort="Cantiniaux, S" uniqKey="Cantiniaux S" first="S" last="Cantiniaux">S. Cantiniaux</name></author><author><name sortKey="Delval, A" sort="Delval, A" uniqKey="Delval A" first="A" last="Delval">A. Delval</name></author><author><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. Defebvre</name></author><author><name sortKey="Azulay, J P" sort="Azulay, J P" uniqKey="Azulay J" first="J-P" last="Azulay">J-P Azulay</name></author></analytic><series><title level="j">Revue neurologique</title><idno type="ISSN">0035-3787</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acoustic Stimulation</term><term>Biomechanical Phenomena</term><term>Cognition Disorders (physiopathology)</term><term>Cognition Disorders (psychology)</term><term>Gait (physiology)</term><term>Gait Disorders, Neurologic (etiology)</term><term>Gait Disorders, Neurologic (physiopathology)</term><term>Humans</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (psychology)</term><term>Temporal Lobe (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Disorders, Neurologic</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gait</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cognition Disorders</term><term>Gait Disorders, Neurologic</term><term>Parkinson Disease</term><term>Temporal Lobe</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Cognition Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acoustic Stimulation</term><term>Biomechanical Phenomena</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gait disorders and axial symptoms are the main therapeutic challenges in advanced Parkinson's disease (PD). Gait disorders in PD are characterized by spatial and temporal dysfunction. Gait hypokinesia is the first to appear and is responsible for the decrease in velocity. A good sensitivity to the levodopa is well established. Morris et al. [Morris ME, Iansek R, Matyas TA, Summers JJ. Ability to modulate walking cadence remains intact in Parkinson's disease. J Neurol Neurosurg Psychiatry 1994a;57(12):1532-4; Morris ME, Iansek R, Matyas TA, Summers JJ. The pathogenesis of gait hypokinesia in Parkinson's disease. Brain 1994b;117(Pt. 5):1169-81; Morris ME, Iansek R, Matyas TA, Summers JJ. Stride length regulation in Parkinson's disease. Brain 1996;119:551-68] demonstrated that the ability to modulate walking cadence remains intact in PD, and could correspond to a compensatory mechanism. More advanced disease stages of the disease are characterized by abnormal temporal parameters (such as stride length variability, stride time variability and cadence elevation) which are unresponsive to levodopa therapy and may be correlated with the occurrence of falls and freezing of gait (FOG). Lastly, postural instability also results in falls and is poorly responsive to levodopa. A link between gait impairment and frontal disorders has recently been suggested. After a few years of evolution, paradoxical episodic phenomena are described: festination ("hastening gait" with rapid small, short steps) and FOG (involuntary and sudden cessation of gait). Both symptoms are often incapacitating for PD patients, because of their resultant loss of independence and their poor response to levodopa therapy. Kinematical studies of FOG revealed a decrease in velocity, stride length and an exponential increase in cadence, prior to a FOG episode. New approaches (functional MRI, wavelets...) should offer new perspectives concerning these disabling symptoms.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19616816</PMID><DateCreated><Year>2010</Year><Month>02</Month><Day>22</Day></DateCreated><DateCompleted><Year>2010</Year><Month>04</Month><Day>30</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0035-3787</ISSN><JournalIssue CitedMedium="Print"><Volume>166</Volume><Issue>2</Issue><PubDate><Year>2010</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Revue neurologique</Title><ISOAbbreviation>Rev. Neurol. (Paris)</ISOAbbreviation></Journal><ArticleTitle>[Gait disorders in Parkinson's disease: and pathophysiological approaches].</ArticleTitle><Pagination><MedlinePgn>158-67</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neurol.2009.05.010</ELocationID><Abstract><AbstractText>Gait disorders and axial symptoms are the main therapeutic challenges in advanced Parkinson's disease (PD). Gait disorders in PD are characterized by spatial and temporal dysfunction. Gait hypokinesia is the first to appear and is responsible for the decrease in velocity. A good sensitivity to the levodopa is well established. Morris et al. [Morris ME, Iansek R, Matyas TA, Summers JJ. Ability to modulate walking cadence remains intact in Parkinson's disease. J Neurol Neurosurg Psychiatry 1994a;57(12):1532-4; Morris ME, Iansek R, Matyas TA, Summers JJ. The pathogenesis of gait hypokinesia in Parkinson's disease. Brain 1994b;117(Pt. 5):1169-81; Morris ME, Iansek R, Matyas TA, Summers JJ. Stride length regulation in Parkinson's disease. Brain 1996;119:551-68] demonstrated that the ability to modulate walking cadence remains intact in PD, and could correspond to a compensatory mechanism. More advanced disease stages of the disease are characterized by abnormal temporal parameters (such as stride length variability, stride time variability and cadence elevation) which are unresponsive to levodopa therapy and may be correlated with the occurrence of falls and freezing of gait (FOG). Lastly, postural instability also results in falls and is poorly responsive to levodopa. A link between gait impairment and frontal disorders has recently been suggested. After a few years of evolution, paradoxical episodic phenomena are described: festination ("hastening gait" with rapid small, short steps) and FOG (involuntary and sudden cessation of gait). Both symptoms are often incapacitating for PD patients, because of their resultant loss of independence and their poor response to levodopa therapy. Kinematical studies of FOG revealed a decrease in velocity, stride length and an exponential increase in cadence, prior to a FOG episode. New approaches (functional MRI, wavelets...) should offer new perspectives concerning these disabling symptoms.</AbstractText><CopyrightInformation>Copyright 2010. Published by Elsevier Masson SAS.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moreau</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Service de neurologie et pathologie du mouvement, hôpital Roger-Salengro, CHRU, 59037 Lille cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cantiniaux</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Delval</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Defebvre</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Azulay</LastName><ForeName>J-P</ForeName><Initials>JP</Initials></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Les troubles de la marche dans la maladie de Parkinson : problématique clinique et physiopathologique.</VernacularTitle><ArticleDate DateType="Electronic"><Year>2009</Year><Month>07</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Rev Neurol (Paris)</MedlineTA><NlmUniqueID>2984779R</NlmUniqueID><ISSNLinking>0035-3787</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000161" MajorTopicYN="N">Acoustic Stimulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001696" MajorTopicYN="N">Biomechanical Phenomena</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003072" MajorTopicYN="N">Cognition Disorders</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005684" MajorTopicYN="N">Gait</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020233" MajorTopicYN="N">Gait Disorders, Neurologic</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013702" MajorTopicYN="N">Temporal Lobe</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>64</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>03</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2009</Year><Month>05</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>05</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>7</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>7</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>5</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19616816</ArticleId><ArticleId IdType="pii">S0035-3787(09)00308-7</ArticleId><ArticleId IdType="doi">10.1016/j.neurol.2009.05.010</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Hauts-de-France</li><li>Nord-Pas-de-Calais</li></region><settlement><li>Lille</li></settlement></list><tree><noCountry><name sortKey="Azulay, J P" sort="Azulay, J P" uniqKey="Azulay J" first="J-P" last="Azulay">J-P Azulay</name><name sortKey="Cantiniaux, S" sort="Cantiniaux, S" uniqKey="Cantiniaux S" first="S" last="Cantiniaux">S. Cantiniaux</name><name sortKey="Defebvre, L" sort="Defebvre, L" uniqKey="Defebvre L" first="L" last="Defebvre">L. Defebvre</name><name sortKey="Delval, A" sort="Delval, A" uniqKey="Delval A" first="A" last="Delval">A. Delval</name></noCountry><country name="France"><region name="Hauts-de-France"><name sortKey="Moreau, C" sort="Moreau, C" uniqKey="Moreau C" first="C" last="Moreau">C. Moreau</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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