Neuronal loss from the subthalamic nuclei in a patient with progressive chorea.
Identifieur interne : 004948 ( PubMed/Checkpoint ); précédent : 004947; suivant : 004949Neuronal loss from the subthalamic nuclei in a patient with progressive chorea.
Auteurs : J H Sinard [États-Unis] ; J C HedreenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1995.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Astrocytes (drug effects), Astrocytes (pathology), Brain (drug effects), Brain (pathology), Cell Count (drug effects), Cerebellar Diseases (chemically induced), Cerebellar Diseases (pathology), Chorea (chemically induced), Chorea (pathology), Epilepsy, Post-Traumatic (drug therapy), Epilepsy, Post-Traumatic (pathology), Humans, Male, Nerve Degeneration (drug effects), Nerve Degeneration (physiology), Neurologic Examination (drug effects), Phenytoin (adverse effects), Phenytoin (therapeutic use), Purkinje Cells (drug effects), Purkinje Cells (pathology), Thalamic Diseases (chemically induced), Thalamic Diseases (pathology), Thalamic Nuclei (drug effects), Thalamic Nuclei (pathology).
- MESH :
- chemical , adverse effects : Phenytoin.
- chemically induced : Cerebellar Diseases, Chorea, Thalamic Diseases.
- drug effects : Astrocytes, Brain, Cell Count, Nerve Degeneration, Neurologic Examination, Purkinje Cells, Thalamic Nuclei.
- drug therapy : Epilepsy, Post-Traumatic.
- pathology : Astrocytes, Brain, Cerebellar Diseases, Chorea, Epilepsy, Post-Traumatic, Purkinje Cells, Thalamic Diseases, Thalamic Nuclei.
- physiology : Nerve Degeneration.
- chemical , therapeutic use : Phenytoin.
- Aged, Aged, 80 and over, Humans, Male.
Abstract
We present a case of an 80-year-old man who developed a seizure disorder at age 66 and was treated with chronic phenytoin. In the last 3 years of his life, he developed multiple neurological deficits, including bilateral chorea, ataxic gait, sensory neuropathy, and progressive dementia. After death from pneumonia, autopsy examination of the patient's brain was most remarkable for a selective loss of neurons from both subthalamic nuclei and Purkinje cell loss in the cerebellum. This pattern of injury is consistent with a toxic process and does not fit previously characterized pathological syndromes known to be associated with movement disorders or dementia or both. Phenytoin has been shown to cause choreiform movements, peripheral neuropathy, and cognitive decline in some patients, but the pathological basis for these changes has not been elucidated. The patient's chorea was very likely the result of neuronal loss in the subthalamic nuclei, but causes for his dementia and neuropathy were not found. The pathological findings may represent either an unusual form of chronic phenytoin toxicity or a previously undescribed primary degenerative brain syndrome.
DOI: 10.1002/mds.870100313
PubMed: 7651448
Affiliations:
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In the last 3 years of his life, he developed multiple neurological deficits, including bilateral chorea, ataxic gait, sensory neuropathy, and progressive dementia. After death from pneumonia, autopsy examination of the patient's brain was most remarkable for a selective loss of neurons from both subthalamic nuclei and Purkinje cell loss in the cerebellum. This pattern of injury is consistent with a toxic process and does not fit previously characterized pathological syndromes known to be associated with movement disorders or dementia or both. Phenytoin has been shown to cause choreiform movements, peripheral neuropathy, and cognitive decline in some patients, but the pathological basis for these changes has not been elucidated. The patient's chorea was very likely the result of neuronal loss in the subthalamic nuclei, but causes for his dementia and neuropathy were not found. The pathological findings may represent either an unusual form of chronic phenytoin toxicity or a previously undescribed primary degenerative brain syndrome.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">7651448</PMID><DateCreated><Year>1995</Year><Month>09</Month><Day>28</Day></DateCreated><DateCompleted><Year>1995</Year><Month>09</Month><Day>28</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><Issue>3</Issue><PubDate><Year>1995</Year><Month>May</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neuronal loss from the subthalamic nuclei in a patient with progressive chorea.</ArticleTitle><Pagination><MedlinePgn>305-11</MedlinePgn></Pagination><Abstract><AbstractText>We present a case of an 80-year-old man who developed a seizure disorder at age 66 and was treated with chronic phenytoin. In the last 3 years of his life, he developed multiple neurological deficits, including bilateral chorea, ataxic gait, sensory neuropathy, and progressive dementia. After death from pneumonia, autopsy examination of the patient's brain was most remarkable for a selective loss of neurons from both subthalamic nuclei and Purkinje cell loss in the cerebellum. This pattern of injury is consistent with a toxic process and does not fit previously characterized pathological syndromes known to be associated with movement disorders or dementia or both. Phenytoin has been shown to cause choreiform movements, peripheral neuropathy, and cognitive decline in some patients, but the pathological basis for these changes has not been elucidated. The patient's chorea was very likely the result of neuronal loss in the subthalamic nuclei, but causes for his dementia and neuropathy were not found. The pathological findings may represent either an unusual form of chronic phenytoin toxicity or a previously undescribed primary degenerative brain syndrome.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sinard</LastName><ForeName>J H</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hedreen</LastName><ForeName>J C</ForeName><Initials>JC</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS29484</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, 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MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009410">Nerve Degeneration</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009460">Neurologic Examination</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010672">Phenytoin</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011689">Purkinje Cells</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013786">Thalamic Diseases</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013787">Thalamic Nuclei</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1995</Year><Month>5</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1995</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1995</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">7651448</ArticleId><ArticleId IdType="doi">10.1002/mds.870100313</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Connecticut</li></region></list><tree><noCountry><name sortKey="Hedreen, J C" sort="Hedreen, J C" uniqKey="Hedreen J" first="J C" last="Hedreen">J C Hedreen</name></noCountry><country name="États-Unis"><region name="Connecticut"><name sortKey="Sinard, J H" sort="Sinard, J H" uniqKey="Sinard J" first="J H" last="Sinard">J H Sinard</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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