Acute movement disorders with bilateral basal ganglia lesions in uremia.
Identifieur interne : 004305 ( PubMed/Corpus ); précédent : 004304; suivant : 004306Acute movement disorders with bilateral basal ganglia lesions in uremia.
Auteurs : H C Wang ; P. Brown ; A J LeesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1998.
English descriptors
- KwdEn :
- Acute Disease, Anoxia (complications), Basal Ganglia Diseases (etiology), Basal Ganglia Diseases (therapy), Diabetic Nephropathies (complications), Diabetic Nephropathies (therapy), Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Movement Disorders (etiology), Movement Disorders (therapy), Renal Dialysis, Uremia (complications).
- MESH :
- complications : Anoxia, Diabetic Nephropathies, Uremia.
- etiology : Basal Ganglia Diseases, Movement Disorders.
- therapy : Basal Ganglia Diseases, Diabetic Nephropathies, Movement Disorders.
- Acute Disease, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Renal Dialysis.
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.
DOI: 10.1002/mds.870130615
PubMed: 9827621
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pubmed:9827621Le document en format XML
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Brown</name></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9827621</idno><idno type="pmid">9827621</idno><idno type="doi">10.1002/mds.870130615</idno><idno type="wicri:Area/PubMed/Corpus">004305</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Acute movement disorders with bilateral basal ganglia lesions in uremia.</title><author><name sortKey="Wang, H C" sort="Wang, H C" uniqKey="Wang H" first="H C" last="Wang">H C Wang</name><affiliation><nlm:affiliation>Department of Neurology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.</nlm:affiliation></affiliation></author><author><name sortKey="Brown, P" sort="Brown, P" uniqKey="Brown P" first="P" last="Brown">P. Brown</name></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Disease</term><term>Anoxia (complications)</term><term>Basal Ganglia Diseases (etiology)</term><term>Basal Ganglia Diseases (therapy)</term><term>Diabetic Nephropathies (complications)</term><term>Diabetic Nephropathies (therapy)</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Movement Disorders (etiology)</term><term>Movement Disorders (therapy)</term><term>Renal Dialysis</term><term>Uremia (complications)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Anoxia</term><term>Diabetic Nephropathies</term><term>Uremia</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Movement Disorders</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Diabetic Nephropathies</term><term>Movement Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acute Disease</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Renal Dialysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9827621</PMID><DateCreated><Year>1999</Year><Month>02</Month><Day>17</Day></DateCreated><DateCompleted><Year>1999</Year><Month>02</Month><Day>17</Day></DateCompleted><DateRevised><Year>2004</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>13</Volume><Issue>6</Issue><PubDate><Year>1998</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Acute movement disorders with bilateral basal ganglia lesions in uremia.</ArticleTitle><Pagination><MedlinePgn>952-7</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>H C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Department of Neurology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brown</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Lees</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></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="D000208">Acute Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000860">Anoxia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001480">Basal Ganglia Diseases</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000628">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003928">Diabetic Nephropathies</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000628">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008279">Magnetic Resonance Imaging</DescriptorName></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="D009069">Movement Disorders</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000628">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006435">Renal Dialysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014511">Uremia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>11</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>11</Month><Day>25</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>11</Month><Day>25</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9827621</ArticleId><ArticleId IdType="doi">10.1002/mds.870130615</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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