Pathophysiological concepts of restless legs syndrome
Identifieur interne : 001E33 ( Istex/Corpus ); précédent : 001E32; suivant : 001E34Pathophysiological concepts of restless legs syndrome
Auteurs : Walter Paulus ; Pascal Dowling ; Roselyne Rijsman ; Karin Stiasny-Kolster ; Claudia Trenkwalder ; Al De WeerdSource :
- Movement Disorders [ 0885-3185 ] ; 2007-07-30.
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- KwdEn :
Abstract
Pathophysiological concepts of restless legs syndrome (RLS) are based mainly on neuroimaging and on neurophysiological data. Furthermore treatment effects contribute essentially to the present understanding of the disease, unless the genetic progress expected in the near future will clarify substantially open issues. The concept agreed on assumes a dysfunction of the dopaminergic system, possibly on the level of striatal and/or spinal dopamine receptors, and the A11 neuron group localized in the hypothalamus as an integrated part of the system. These neurons modulate spinal excitability, alterations of which in turn affect sensory processing predominantly of leg afferents in brain stem structures. Neurophysiologically excitability alterations can be measured by a variety of methods such as determination of pain thresholds, H‐reflex testing, and quantitative sensory testing. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21533
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ISTEX:6719F1AC8FF041437899AE0C7B5CBCA794B9DF99Le document en format XML
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Furthermore treatment effects contribute essentially to the present understanding of the disease, unless the genetic progress expected in the near future will clarify substantially open issues. The concept agreed on assumes a dysfunction of the dopaminergic system, possibly on the level of striatal and/or spinal dopamine receptors, and the A11 neuron group localized in the hypothalamus as an integrated part of the system. These neurons modulate spinal excitability, alterations of which in turn affect sensory processing predominantly of leg afferents in brain stem structures. 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Furthermore treatment effects contribute essentially to the present understanding of the disease, unless the genetic progress expected in the near future will clarify substantially open issues. The concept agreed on assumes a dysfunction of the dopaminergic system, possibly on the level of striatal and/or spinal dopamine receptors, and the A11 neuron group localized in the hypothalamus as an integrated part of the system. These neurons modulate spinal excitability, alterations of which in turn affect sensory processing predominantly of leg afferents in brain stem structures. Neurophysiologically excitability alterations can be measured by a variety of methods such as determination of pain thresholds, H‐reflex testing, and quantitative sensory testing. © 2007 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Pathophysiological concepts of restless legs syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Pathophysiological Concepts of RLS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Pathophysiological concepts of restless legs syndrome</title></titleInfo><name type="personal"><namePart type="given">Walter</namePart><namePart type="family">Paulus</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurophysiology, University of Göttingen, Göttingen, Germany</affiliation><description>Correspondence: Department of Clinical Neurophysiology, University of Göttingen, Robert Koch Str. 40, D‐37075 Göttingen, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pascal</namePart><namePart type="family">Dowling</namePart><namePart type="termsOfAddress">MPhil</namePart><affiliation>Department of Clinical Neurophysiology, University of Göttingen, Göttingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roselyne</namePart><namePart type="family">Rijsman</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Clinical Neurophysiology and Sleepcenter. 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Furthermore treatment effects contribute essentially to the present understanding of the disease, unless the genetic progress expected in the near future will clarify substantially open issues. The concept agreed on assumes a dysfunction of the dopaminergic system, possibly on the level of striatal and/or spinal dopamine receptors, and the A11 neuron group localized in the hypothalamus as an integrated part of the system. These neurons modulate spinal excitability, alterations of which in turn affect sensory processing predominantly of leg afferents in brain stem structures. Neurophysiologically excitability alterations can be measured by a variety of methods such as determination of pain thresholds, H‐reflex testing, and quantitative sensory testing. © 2007 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>restless legs</topic><topic>pathophysiology</topic><topic>spinal</topic><topic>dopamine</topic><topic>opiate</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><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>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1451</start><end>1456</end><total>6</total></extent></part></relatedItem><identifier type="istex">6719F1AC8FF041437899AE0C7B5CBCA794B9DF99</identifier><identifier type="DOI">10.1002/mds.21533</identifier><identifier type="ArticleID">MDS21533</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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