Imaging gait disorders in parkinsonism: a review
Identifieur interne : 002A58 ( Main/Corpus ); précédent : 002A57; suivant : 002A59Imaging gait disorders in parkinsonism: a review
Auteurs : Audrey Maillet ; Pierre Pollak ; Bettina DebûSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2012-10.
Abstract
Gait difficulties—including freezing of gait—are frequent and disabling symptoms of advanced Parkinson's disease and other parkinsonian syndromes. They respond poorly to current medical and surgical treatments, making patient management very difficult. The underlying pathophysiology remains largely unknown. The late onset of levodopa resistance of Parkinson's disease gait abnormalities has been suggested to result from the progressive extension of the degenerative process to non-dopaminergic structures involved in locomotion, such as cortico-frontal and brainstem networks. Deficiencies in other neurotransmission systems, involving acetylcholine, serotonin or norepinephrine, have also been evoked. Neuroimaging tools appear well suited to decipher the cerebral substrates of parkinsonian gait disorders and their modulation by dopaminergic medication or deep brain stimulation. Here the main functional and metabolic neuroimaging studies aimed at identifying these cerebral networks are reviewed, in both healthy subjects and parkinsonian patients. After a brief overview of the physiology and pathophysiology of gait control, the methodology, main results and limits of the studies published to date are examined. The most promising methods to examine gait difficulties and their response to currently available treatments are then discussed.
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DOI: 10.1136/jnnp-2012-302461
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type="abstract">Gait difficulties—including freezing of gait—are frequent and disabling symptoms of advanced Parkinson's disease and other parkinsonian syndromes. They respond poorly to current medical and surgical treatments, making patient management very difficult. The underlying pathophysiology remains largely unknown. The late onset of levodopa resistance of Parkinson's disease gait abnormalities has been suggested to result from the progressive extension of the degenerative process to non-dopaminergic structures involved in locomotion, such as cortico-frontal and brainstem networks. Deficiencies in other neurotransmission systems, involving acetylcholine, serotonin or norepinephrine, have also been evoked. Neuroimaging tools appear well suited to decipher the cerebral substrates of parkinsonian gait disorders and their modulation by dopaminergic medication or deep brain stimulation. Here the main functional and metabolic neuroimaging studies aimed at identifying these cerebral networks are reviewed, in both healthy subjects and parkinsonian patients. After a brief overview of the physiology and pathophysiology of gait control, the methodology, main results and limits of the studies published to date are examined. The most promising methods to examine gait difficulties and their response to currently available treatments are then discussed.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>Audrey Maillet</name><affiliations><json:string>Université Joseph Fourier, Grenoble I, Grenoble, France</json:string><json:string>INSERM, Grenoble Institut des Neurosciences, INSERM-UJF-CEA-CHU U836, Grenoble, France</json:string><json:string>E-mail: amaillet@chu-grenoble.fr</json:string></affiliations></json:item><json:item><name>Pierre Pollak</name><affiliations><json:string>Université Joseph Fourier, Grenoble I, Grenoble, France</json:string><json:string>INSERM, Grenoble Institut des Neurosciences, INSERM-UJF-CEA-CHU U836, Grenoble, France</json:string><json:string>Centre Hospitalier Universitaire (CHU), Service de Neurologie, Grenoble, France</json:string><json:string>Hôpitaux Universitaires de Genève, Genève, Switzerland</json:string></affiliations></json:item><json:item><name>Bettina Debû</name><affiliations><json:string>Université Joseph Fourier, Grenoble I, Grenoble, France</json:string><json:string>INSERM, Grenoble Institut des Neurosciences, INSERM-UJF-CEA-CHU U836, Grenoble, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Movement disorders</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Editor's choice</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Gait difficulties—including freezing of gait—are frequent and disabling symptoms of advanced Parkinson's disease and other parkinsonian syndromes. 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After a brief overview of the physiology and pathophysiology of gait control, the methodology, main results and limits of the studies published to date are examined. 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After a brief overview of the physiology and pathophysiology of gait control, the methodology, main results and limits of the studies published to date are examined. 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For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</copyright-statement><copyright-year>2012</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-83-986.pdf"></self-uri><abstract><p>Gait difficulties—including freezing of gait—are frequent and disabling symptoms of advanced Parkinson's disease and other parkinsonian syndromes. They respond poorly to current medical and surgical treatments, making patient management very difficult. The underlying pathophysiology remains largely unknown. The late onset of levodopa resistance of Parkinson's disease gait abnormalities has been suggested to result from the progressive extension of the degenerative process to non-dopaminergic structures involved in locomotion, such as cortico-frontal and brainstem networks. Deficiencies in other neurotransmission systems, involving acetylcholine, serotonin or norepinephrine, have also been evoked. Neuroimaging tools appear well suited to decipher the cerebral substrates of parkinsonian gait disorders and their modulation by dopaminergic medication or deep brain stimulation. Here the main functional and metabolic neuroimaging studies aimed at identifying these cerebral networks are reviewed, in both healthy subjects and parkinsonian patients. After a brief overview of the physiology and pathophysiology of gait control, the methodology, main results and limits of the studies published to date are examined. The most promising methods to examine gait difficulties and their response to currently available treatments are then discussed.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><partName>Review</partName><title>Imaging gait disorders in parkinsonism: a review</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><partName>Review</partName><title>Imaging gait disorders in parkinsonism: a review</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Audrey</namePart><namePart type="family">Maillet</namePart><affiliation>Université Joseph Fourier, Grenoble I, Grenoble, France</affiliation><affiliation>INSERM, Grenoble Institut des Neurosciences, INSERM-UJF-CEA-CHU U836, Grenoble, France</affiliation><affiliation>E-mail: amaillet@chu-grenoble.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Pollak</namePart><affiliation>Université Joseph Fourier, Grenoble I, Grenoble, France</affiliation><affiliation>INSERM, Grenoble Institut des Neurosciences, INSERM-UJF-CEA-CHU U836, Grenoble, France</affiliation><affiliation>Centre Hospitalier Universitaire (CHU), Service de Neurologie, Grenoble, France</affiliation><affiliation>Hôpitaux Universitaires de Genève, Genève, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bettina</namePart><namePart type="family">Debû</namePart><affiliation>Université Joseph Fourier, Grenoble I, Grenoble, France</affiliation><affiliation>INSERM, Grenoble Institut des Neurosciences, INSERM-UJF-CEA-CHU U836, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article"></genre><subject><genre>hwp-journal-coll</genre><topic>Editor's choice</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2012-10</dateIssued><dateCreated encoding="w3cdtf">2012-07-08</dateCreated><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Gait difficulties—including freezing of gait—are frequent and disabling symptoms of advanced Parkinson's disease and other parkinsonian syndromes. They respond poorly to current medical and surgical treatments, making patient management very difficult. The underlying pathophysiology remains largely unknown. The late onset of levodopa resistance of Parkinson's disease gait abnormalities has been suggested to result from the progressive extension of the degenerative process to non-dopaminergic structures involved in locomotion, such as cortico-frontal and brainstem networks. Deficiencies in other neurotransmission systems, involving acetylcholine, serotonin or norepinephrine, have also been evoked. Neuroimaging tools appear well suited to decipher the cerebral substrates of parkinsonian gait disorders and their modulation by dopaminergic medication or deep brain stimulation. Here the main functional and metabolic neuroimaging studies aimed at identifying these cerebral networks are reviewed, in both healthy subjects and parkinsonian patients. After a brief overview of the physiology and pathophysiology of gait control, the methodology, main results and limits of the studies published to date are examined. The most promising methods to examine gait difficulties and their response to currently available treatments are then discussed.</abstract><note type="footnotes">302263.</note><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID">jnnp</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>83</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>986</start></extent></part></relatedItem><identifier type="istex">7A900BC301A922DAB1582801E07D3E02863AE5C0</identifier><identifier type="DOI">10.1136/jnnp-2012-302461</identifier><identifier type="href">jnnp-83-986.pdf</identifier><identifier type="ArticleID">jnnp-2012-302461</identifier><identifier type="PMID">22773859</identifier><identifier type="Related-article-Href">10.1136/jnnp-2012-302263</identifier><identifier type="related-article-ID">RA1</identifier><identifier type="local">jnnp;83/10/986</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/7A900BC301A922DAB1582801E07D3E02863AE5C0/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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