Treatment of progressive supranuclear palsy and corticobasal degeneration.
Identifieur interne : 001381 ( Ncbi/Merge ); précédent : 001380; suivant : 001382Treatment of progressive supranuclear palsy and corticobasal degeneration.
Auteurs : Anthony E. Lang [Canada]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- Amantadine (therapeutic use), Cerebral Cortex (pathology), Cholinesterase Inhibitors (therapeutic use), Corpus Striatum (pathology), Dopamine Agents (therapeutic use), Dopamine Agonists (therapeutic use), Dystonia (drug therapy), Dystonia (pathology), Globus Pallidus (pathology), Humans, Indans (therapeutic use), Levodopa (therapeutic use), Nerve Degeneration (drug therapy), Nerve Degeneration (pathology), Piperidines (therapeutic use), Substantia Nigra (pathology), Supranuclear Palsy, Progressive (drug therapy).
- MESH :
- chemical , therapeutic use : Amantadine, Cholinesterase Inhibitors, Dopamine Agents, Dopamine Agonists, Indans, Levodopa, Piperidines.
- drug therapy : Dystonia, Nerve Degeneration, Supranuclear Palsy, Progressive.
- pathology : Cerebral Cortex, Corpus Striatum, Dystonia, Globus Pallidus, Nerve Degeneration, Substantia Nigra.
- Humans.
Abstract
Success in treating patients with progressive supranuclear palsy and corticobasal degeneration remains exceedingly low. This finding probably relates to the widespread distribution of the pathological changes that account for the varied and complex spectrum of clinical manifestations. Dopaminergic drugs are regularly used for the parkinsonian features; however, these rarely result in more than modest benefit, and when better or sustained responses are obtained, as sometimes occurs in progressive supranuclear palsy, the clinical features are atypical and diagnosis is often delayed or not made in life. A variety of other treatments have been used in both disorders, sometimes directed at other specific features such as dystonia or myoclonus, and these treatments will be reviewed. Greater success in treating these disorders will require advances in our understanding of their cause(s) or the pathogenetic mechanisms underlying the neurodegenerative processes. The similarities in the molecular pathology of these four-repeat tauopathies suggests that important advances in the management of one will have a definite impact on the treatment of the other.
DOI: 10.1002/mds.20545
PubMed: 16092096
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pubmed:16092096Le document en format XML
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Lang</name><affiliation wicri:level="1"><nlm:affiliation>Toronto Western Hospital, Movement Disorders Clinic, Ontario, Canada. lan@uhnres.utoronto.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Hospital, Movement Disorders Clinic, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="doi">10.1002/mds.20545</idno><idno type="RBID">pubmed:16092096</idno><idno type="pmid">16092096</idno><idno type="wicri:Area/PubMed/Corpus">002F31</idno><idno type="wicri:Area/PubMed/Curation">002F31</idno><idno type="wicri:Area/PubMed/Checkpoint">002F25</idno><idno type="wicri:Area/Ncbi/Merge">001381</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Treatment of progressive supranuclear palsy and corticobasal degeneration.</title><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name><affiliation wicri:level="1"><nlm:affiliation>Toronto Western Hospital, Movement Disorders Clinic, Ontario, Canada. lan@uhnres.utoronto.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Hospital, Movement Disorders Clinic, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></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="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amantadine (therapeutic use)</term><term>Cerebral Cortex (pathology)</term><term>Cholinesterase Inhibitors (therapeutic use)</term><term>Corpus Striatum (pathology)</term><term>Dopamine Agents (therapeutic use)</term><term>Dopamine Agonists (therapeutic use)</term><term>Dystonia (drug therapy)</term><term>Dystonia (pathology)</term><term>Globus Pallidus (pathology)</term><term>Humans</term><term>Indans (therapeutic use)</term><term>Levodopa (therapeutic use)</term><term>Nerve Degeneration (drug therapy)</term><term>Nerve Degeneration (pathology)</term><term>Piperidines (therapeutic use)</term><term>Substantia Nigra (pathology)</term><term>Supranuclear Palsy, Progressive (drug therapy)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Amantadine</term><term>Cholinesterase Inhibitors</term><term>Dopamine Agents</term><term>Dopamine Agonists</term><term>Indans</term><term>Levodopa</term><term>Piperidines</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dystonia</term><term>Nerve Degeneration</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebral Cortex</term><term>Corpus Striatum</term><term>Dystonia</term><term>Globus Pallidus</term><term>Nerve Degeneration</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Success in treating patients with progressive supranuclear palsy and corticobasal degeneration remains exceedingly low. This finding probably relates to the widespread distribution of the pathological changes that account for the varied and complex spectrum of clinical manifestations. Dopaminergic drugs are regularly used for the parkinsonian features; however, these rarely result in more than modest benefit, and when better or sustained responses are obtained, as sometimes occurs in progressive supranuclear palsy, the clinical features are atypical and diagnosis is often delayed or not made in life. A variety of other treatments have been used in both disorders, sometimes directed at other specific features such as dystonia or myoclonus, and these treatments will be reviewed. Greater success in treating these disorders will require advances in our understanding of their cause(s) or the pathogenetic mechanisms underlying the neurodegenerative processes. The similarities in the molecular pathology of these four-repeat tauopathies suggests that important advances in the management of one will have a definite impact on the treatment of the other.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">16092096</PMID><DateCreated><Year>2005</Year><Month>08</Month><Day>15</Day></DateCreated><DateCompleted><Year>2005</Year><Month>12</Month><Day>13</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>20 Suppl 12</Volume><PubDate><Year>2005</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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A variety of other treatments have been used in both disorders, sometimes directed at other specific features such as dystonia or myoclonus, and these treatments will be reviewed. Greater success in treating these disorders will require advances in our understanding of their cause(s) or the pathogenetic mechanisms underlying the neurodegenerative processes. The similarities in the molecular pathology of these four-repeat tauopathies suggests that important advances in the management of one will have a definite impact on the treatment of the other.</AbstractText><CopyrightInformation>Copyright 2005 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Anthony E</ForeName><Initials>AE</Initials><AffiliationInfo><Affiliation>Toronto Western Hospital, Movement Disorders Clinic, Ontario, Canada. lan@uhnres.utoronto.ca</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><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><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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