Effects of apomorphine and L-dopa on the parkinsonian bladder.
Identifieur interne : 001706 ( PubMed/Curation ); précédent : 001705; suivant : 001707Effects of apomorphine and L-dopa on the parkinsonian bladder.
Auteurs : B. Aranda [France] ; P. CramerSource :
- Neurourology and urodynamics [ 0733-2467 ] ; 1993.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : Apomorphine.
- chemical , therapeutic use : Levodopa.
- drug effects : Reflex, Abnormal, Urinary Bladder.
- drug therapy : Parkinson Disease.
- physiopathology : Parkinson Disease, Urinary Bladder.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged.
Abstract
Neurogenic bladder frequently occurs in Parkinson's disease. Detrusor hyperreflexia is a consequence of nigrostriatal dopamine depletion, whereas the cause of hyporeflexia remains unclear. We compared the results of cystometry and urethral profilometry with and without apomorphine (and L dopa) in 12 idiopathic parkinsonians with urinary disorders free of dopaminergic treatment. Whereas hyperreflexic patients improved with apomorphine, and to a lesser extent with L dopa, these drugs had no effect on hyporeflexic patients. These results confirm the role of dopaminergic lesions in the occurrence of bladder hyperreflexia and the possible implication of nondopaminergic lesions in the occurrence of hyporeflexia.
PubMed: 8330043
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Aranda</name><affiliation wicri:level="1"><nlm:affiliation>Department of Rehabilitation, Centre Hospitalier, Gonesse, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Rehabilitation, Centre Hospitalier, Gonesse</wicri:regionArea></affiliation></author><author><name sortKey="Cramer, P" sort="Cramer, P" uniqKey="Cramer P" first="P" last="Cramer">P. Cramer</name></author></analytic><series><title level="j">Neurourology and urodynamics</title><idno type="ISSN">0733-2467</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Apomorphine (pharmacology)</term><term>Female</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Reflex, Abnormal (drug effects)</term><term>Urinary Bladder (drug effects)</term><term>Urinary Bladder (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Reflex, Abnormal</term><term>Urinary Bladder</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term><term>Urinary Bladder</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neurogenic bladder frequently occurs in Parkinson's disease. Detrusor hyperreflexia is a consequence of nigrostriatal dopamine depletion, whereas the cause of hyporeflexia remains unclear. We compared the results of cystometry and urethral profilometry with and without apomorphine (and L dopa) in 12 idiopathic parkinsonians with urinary disorders free of dopaminergic treatment. Whereas hyperreflexic patients improved with apomorphine, and to a lesser extent with L dopa, these drugs had no effect on hyporeflexic patients. These results confirm the role of dopaminergic lesions in the occurrence of bladder hyperreflexia and the possible implication of nondopaminergic lesions in the occurrence of hyporeflexia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8330043</PMID><DateCreated><Year>1993</Year><Month>08</Month><Day>16</Day></DateCreated><DateCompleted><Year>1993</Year><Month>08</Month><Day>16</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0733-2467</ISSN><JournalIssue CitedMedium="Print"><Volume>12</Volume><Issue>3</Issue><PubDate><Year>1993</Year></PubDate></JournalIssue><Title>Neurourology and urodynamics</Title><ISOAbbreviation>Neurourol. Urodyn.</ISOAbbreviation></Journal><ArticleTitle>Effects of apomorphine and L-dopa on the parkinsonian bladder.</ArticleTitle><Pagination><MedlinePgn>203-9</MedlinePgn></Pagination><Abstract><AbstractText>Neurogenic bladder frequently occurs in Parkinson's disease. Detrusor hyperreflexia is a consequence of nigrostriatal dopamine depletion, whereas the cause of hyporeflexia remains unclear. We compared the results of cystometry and urethral profilometry with and without apomorphine (and L dopa) in 12 idiopathic parkinsonians with urinary disorders free of dopaminergic treatment. Whereas hyperreflexic patients improved with apomorphine, and to a lesser extent with L dopa, these drugs had no effect on hyporeflexic patients. These results confirm the role of dopaminergic lesions in the occurrence of bladder hyperreflexia and the possible implication of nondopaminergic lesions in the occurrence of hyporeflexia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aranda</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Rehabilitation, Centre Hospitalier, Gonesse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cramer</LastName><ForeName>P</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurourol Urodyn</MedlineTA><NlmUniqueID>8303326</NlmUniqueID><ISSNLinking>0733-2467</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>N21FAR7B4S</RegistryNumber><NameOfSubstance UI="D001058">Apomorphine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001058" MajorTopicYN="N">Apomorphine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012021" MajorTopicYN="N">Reflex, Abnormal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001743" MajorTopicYN="N">Urinary Bladder</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1993</Year><Month>1</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1993</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1993</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8330043</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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