Acute movement disorders with bilateral basal ganglia lesions in uremia
Identifieur interne : 002067 ( Istex/Corpus ); précédent : 002066; suivant : 002068Acute movement disorders with bilateral basal ganglia lesions in uremia
Auteurs : Wang ; Peter Brown ; Andrew J. LeesSource :
- Movement Disorders [ 0885-3185 ] ; 1998-11.
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Abstract
Acute and subacute extrapyramidal movement disorders are rarely reported in uremic patients. We report three such cases with basal ganglia lesions. All three had advanced renal failure with high serum creatinine levels. One of the patients had a history of ischemic heart disease and acute pulmonary edema with hypoxemia. Another patient had experienced arterial hypotension during previous hemodialysis. The third had prominent metabolic acidosis. One of the patients developed generalized dyskinesias, whereas the other two developed gait disturbances. Neuroimaging studies in all three cases showed bilateral changes in the basal ganglia. The natural history was self‐limiting with gradual improvement. Diminution of the basal ganglia lesions was demonstrated on follow‐up imaging in two of the three cases. We conclude that acute or subacute movement disorders with bilateral basal ganglia lesions may occur in uremia. Hypoperfusion with global brain ischemia and selective vulnerability of the basal ganglia to uremic toxins may account for these lesions.
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DOI: 10.1002/mds.870130615
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Hypoperfusion with global brain ischemia and selective vulnerability of the basal ganglia to uremic toxins may account for these lesions.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Wang MD</name><affiliations><json:string>Department of Neurology, Shin Kong Wu Ho‐Su Memorial Hospital, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>Peter Brown MD</name><affiliations><json:string>The National Hospital for Neurology and Neurosurgery, and MRC Human Movement and Balance Unit, Institute of Neurology, Queen Square, London, England</json:string></affiliations></json:item><json:item><name>Andrew J. Lees MD, Frcp</name><affiliations><json:string>The National Hospital for Neurology and Neurosurgery, Institute of Neurology, Queen Square, London, England</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Movement disorder</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Uremia</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Acute and subacute extrapyramidal movement disorders are rarely reported in uremic patients. We report three such cases with basal ganglia lesions. All three had advanced renal failure with high serum creatinine levels. One of the patients had a history of ischemic heart disease and acute pulmonary edema with hypoxemia. Another patient had experienced arterial hypotension during previous hemodialysis. The third had prominent metabolic acidosis. One of the patients developed generalized dyskinesias, whereas the other two developed gait disturbances. Neuroimaging studies in all three cases showed bilateral changes in the basal ganglia. The natural history was self‐limiting with gradual improvement. Diminution of the basal ganglia lesions was demonstrated on follow‐up imaging in two of the three cases. We conclude that acute or subacute movement disorders with bilateral basal ganglia lesions may occur in uremia. 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We report three such cases with basal ganglia lesions. All three had advanced renal failure with high serum creatinine levels. One of the patients had a history of ischemic heart disease and acute pulmonary edema with hypoxemia. Another patient had experienced arterial hypotension during previous hemodialysis. The third had prominent metabolic acidosis. One of the patients developed generalized dyskinesias, whereas the other two developed gait disturbances. Neuroimaging studies in all three cases showed bilateral changes in the basal ganglia. The natural history was self‐limiting with gradual improvement. Diminution of the basal ganglia lesions was demonstrated on follow‐up imaging in two of the three cases. We conclude that acute or subacute movement disorders with bilateral basal ganglia lesions may occur in uremia. Hypoperfusion with global brain ischemia and selective vulnerability of the basal ganglia to uremic toxins may account for these lesions.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>A videotape accompanies this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Acute movement disorders with bilateral basal ganglia lesions in uremia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>BILATERAL BASAL GANGLIA LESIONS IN UREMIA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Acute movement disorders with bilateral basal ganglia lesions in uremia</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Wang</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Shin Kong Wu Ho‐Su Memorial Hospital, Taipei, Taiwan</affiliation><description>Correspondence: The Department of Neurology, Shin Kong Wu Ho‐Su Memorial Hospital, 95, Wen Chang Road, Shih Lin District, Taipei, Taiwan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Brown</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>The National Hospital for Neurology and Neurosurgery, and MRC Human Movement and Balance Unit, Institute of Neurology, Queen Square, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew J.</namePart><namePart type="family">Lees</namePart><namePart type="termsOfAddress">MD, Frcp</namePart><affiliation>The National Hospital for Neurology and Neurosurgery, Institute of Neurology, Queen Square, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-11</dateIssued><dateCaptured encoding="w3cdtf">1998-03-03</dateCaptured><dateValid encoding="w3cdtf">1998-07-12</dateValid><copyrightDate encoding="w3cdtf">1998</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="references">34</extent></physicalDescription><abstract lang="en">Acute and subacute extrapyramidal movement disorders are rarely reported in uremic patients. We report three such cases with basal ganglia lesions. All three had advanced renal failure with high serum creatinine levels. One of the patients had a history of ischemic heart disease and acute pulmonary edema with hypoxemia. Another patient had experienced arterial hypotension during previous hemodialysis. The third had prominent metabolic acidosis. One of the patients developed generalized dyskinesias, whereas the other two developed gait disturbances. Neuroimaging studies in all three cases showed bilateral changes in the basal ganglia. The natural history was self‐limiting with gradual improvement. Diminution of the basal ganglia lesions was demonstrated on follow‐up imaging in two of the three cases. We conclude that acute or subacute movement disorders with bilateral basal ganglia lesions may occur in uremia. Hypoperfusion with global brain ischemia and selective vulnerability of the basal ganglia to uremic toxins may account for these lesions.</abstract><note type="content">*A videotape accompanies this article.</note><subject lang="en"><genre>Keywords</genre><topic>Basal ganglia</topic><topic>Movement disorder</topic><topic>Uremia</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. 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