Amantadine sulphate in treating Parkinson's disease: Clinical effects, psychometric tests and serum concentrations
Identifieur interne : 000A14 ( Main/Corpus ); précédent : 000A13; suivant : 000A15Amantadine sulphate in treating Parkinson's disease: Clinical effects, psychometric tests and serum concentrations
Auteurs : M. Brenner ; A. Haass ; P. Jacobi ; K. SchimrigkSource :
- Journal of Neurology [ 0340-5354 ] ; 1989-03-01.
Abstract
Summary: Intravenous administration of amantadine has been shown to be a quick-acting and highly effective method of treating patients with Parkinson's disease. The duration of this therapeutic effect during long-term oral treatment has, however, remained controversial. Therefore, the effect of intravenous treatment was compared with long-term oral treatment over a period of 6 months. Clinical scores and psychometrically determined dexterity improved significantly during 10-day infusion therapy (200 mg amantadine sulphate/day). This improvement was successfully maintained by oral treatment (600 mg/day). A decrease in effectiveness was not observed. Reaction times were within the normal range for the age group involved and did not change significantly during the course of the study. Amantadine serum concentration during the infusion period ranged between 500 and 1000 μg/l and produced values nearly half as high as those obtained during oral treatment (600 mg/day). There was a constant relationship (quotient: 1.3) between serum and cerebrospinal fluid concentration. Considerable inter-individual variations were noted. A significant inter-individual correlation between serum concentration and clinical and psychological improvement was not discernible.
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DOI: 10.1007/BF00314331
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The duration of this therapeutic effect during long-term oral treatment has, however, remained controversial. Therefore, the effect of intravenous treatment was compared with long-term oral treatment over a period of 6 months. Clinical scores and psychometrically determined dexterity improved significantly during 10-day infusion therapy (200 mg amantadine sulphate/day). This improvement was successfully maintained by oral treatment (600 mg/day). A decrease in effectiveness was not observed. Reaction times were within the normal range for the age group involved and did not change significantly during the course of the study. Amantadine serum concentration during the infusion period ranged between 500 and 1000 μg/l and produced values nearly half as high as those obtained during oral treatment (600 mg/day). There was a constant relationship (quotient: 1.3) between serum and cerebrospinal fluid concentration. Considerable inter-individual variations were noted. A significant inter-individual correlation between serum concentration and clinical and psychological improvement was not discernible.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>M. Brenner</name><affiliations><json:string>Abteilungen für Neurologie, Universität des Saarlandes, D-6650, Homburg/Saar, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>A. Haass</name><affiliations><json:string>Abteilungen für Neurologie, Universität des Saarlandes, D-6650, Homburg/Saar, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>P. Jacobi</name><affiliations><json:string>Abteilungen für Medizinische Psychologie, Universität des Saarlandes, D-6650, Homburg/Saar, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>K. 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A decrease in effectiveness was not observed. Reaction times were within the normal range for the age group involved and did not change significantly during the course of the study. Amantadine serum concentration during the infusion period ranged between 500 and 1000 μg/l and produced values nearly half as high as those obtained during oral treatment (600 mg/day). There was a constant relationship (quotient: 1.3) between serum and cerebrospinal fluid concentration. Considerable inter-individual variations were noted. 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serum concentrations</ArticleTitle><ArticleCategory>Original Investigations</ArticleCategory><ArticleFirstPage>153</ArticleFirstPage><ArticleLastPage>156</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2004</Year><Month>8</Month><Day>25</Day></RegistrationDate><Received><Year>1988</Year><Month>6</Month><Day>10</Day></Received><Revised><Year>1988</Year><Month>11</Month><Day>28</Day></Revised><Accepted><Year>1988</Year><Month>12</Month><Day>13</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1989</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>415</JournalID><VolumeIDStart>236</VolumeIDStart><VolumeIDEnd>236</VolumeIDEnd><IssueIDStart>3</IssueIDStart><IssueIDEnd>3</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>M.</GivenName><FamilyName>Brenner</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>A.</GivenName><FamilyName>Haass</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><FamilyName>Jacobi</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>K.</GivenName><FamilyName>Schimrigk</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Abteilungen für Neurologie</OrgDivision><OrgName>Universität des Saarlandes</OrgName><OrgAddress><Postcode>D-6650</Postcode><City>Homburg/Saar</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Abteilungen für Medizinische Psychologie</OrgDivision><OrgName>Universität des Saarlandes</OrgName><OrgAddress><Postcode>D-6650</Postcode><City>Homburg/Saar</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Intravenous administration of amantadine has been shown to be a quick-acting and highly effective method of treating patients with Parkinson's disease. The duration of this therapeutic effect during long-term oral treatment has, however, remained controversial. Therefore, the effect of intravenous treatment was compared with long-term oral treatment over a period of 6 months. Clinical scores and psychometrically determined dexterity improved significantly during 10-day infusion therapy (200 mg amantadine sulphate/day). This improvement was successfully maintained by oral treatment (600 mg/day). A decrease in effectiveness was not observed. Reaction times were within the normal range for the age group involved and did not change significantly during the course of the study. Amantadine serum concentration during the infusion period ranged between 500 and 1000 μg/l and produced values nearly half as high as those obtained during oral treatment (600 mg/day). There was a constant relationship (quotient: 1.3) between serum and cerebrospinal fluid concentration. Considerable inter-individual variations were noted. A significant inter-individual correlation between serum concentration and clinical and psychological improvement was not discernible.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Amantadine sulphate</Keyword><Keyword>Parkinson's disease</Keyword><Keyword>Long-term oral treatment</Keyword><Keyword>Intravenous treatment</Keyword><Keyword>Serum concentration</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Amantadine sulphate in treating Parkinson's disease: Clinical effects, psychometric tests and serum concentrations</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Amantadine sulphate in treating Parkinson's disease: Clinical effects, psychometric tests and serum concentrations</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">M.</namePart><namePart type="family">Brenner</namePart><affiliation>Abteilungen für Neurologie, Universität des Saarlandes, D-6650, Homburg/Saar, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Haass</namePart><affiliation>Abteilungen für Neurologie, Universität des Saarlandes, D-6650, Homburg/Saar, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Jacobi</namePart><affiliation>Abteilungen für Medizinische Psychologie, Universität des Saarlandes, D-6650, Homburg/Saar, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Schimrigk</namePart><affiliation>Abteilungen für Neurologie, Universität des Saarlandes, D-6650, Homburg/Saar, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1988-06-10</dateCreated><dateIssued encoding="w3cdtf">1989-03-01</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Intravenous administration of amantadine has been shown to be a quick-acting and highly effective method of treating patients with Parkinson's disease. The duration of this therapeutic effect during long-term oral treatment has, however, remained controversial. Therefore, the effect of intravenous treatment was compared with long-term oral treatment over a period of 6 months. Clinical scores and psychometrically determined dexterity improved significantly during 10-day infusion therapy (200 mg amantadine sulphate/day). This improvement was successfully maintained by oral treatment (600 mg/day). A decrease in effectiveness was not observed. Reaction times were within the normal range for the age group involved and did not change significantly during the course of the study. Amantadine serum concentration during the infusion period ranged between 500 and 1000 μg/l and produced values nearly half as high as those obtained during oral treatment (600 mg/day). There was a constant relationship (quotient: 1.3) between serum and cerebrospinal fluid concentration. Considerable inter-individual variations were noted. 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