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Presynaptic dopamine depletion predicts levodopa-induced dyskinesia in de novo Parkinson disease

DC Field Value Language
dc.contributor.author선우문경-
dc.contributor.author손영호-
dc.contributor.author이지은-
dc.contributor.author이필휴-
dc.contributor.author함지현-
dc.contributor.author홍진용-
dc.date.accessioned2015-01-06T16:42:39Z-
dc.date.available2015-01-06T16:42:39Z-
dc.date.issued2014-
dc.identifier.issn0028-3878-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/98617-
dc.description.abstractObjective: To investigate whether the magnitude of presynaptic dopamine depletion is a risk factor for the development of levodopa-induced dyskinesia (LID) in Parkinson disease (PD) by quantitatively analyzing 18F-FP-CIT PET data. Methods: This retrospective cohort study enrolled a total of 127 drug-naive de novo patients with PD who completed 18F-FP-CIT PET scanning at their initial evaluation. The patients visited our outpatient clinic every 3–6 months and had been followed for a minimum of 2 years since beginning dopaminergic medication. The predictive power of the quantitatively analyzed 18F-FP-CIT uptake of striatal subregions and other clinical factors for the development of LID was evaluated using Cox proportional hazard models. Results: During a mean follow-up period of 3.4 years, 35 patients with PD (27.6%) developed LID. Patients with LID showed less dopamine transporter (DAT) activity in the putamen than did those without LID. Multivariate Cox proportional hazard models revealed that the DAT uptakes of the anterior putamen (hazard ratio [HR] 0.530; p = 0.032), posterior putamen (HR 0.302; p = 0.024), and whole putamen (HR 0.386; p = 0.022) were significant predictors of the development of LID, whereas DAT activities in the caudate and ventral striatum were not significantly correlated with the development of LID. In addition, younger age at onset of PD and higher dose of levodopa were also significant predictors of the development of LID. Conclusions: The present results provide convincing evidence that presynaptic dopaminergic denervation in PD plays a crucial role in the development of LID.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1597~604-
dc.relation.isPartOfNEUROLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAged-
dc.subject.MESHAntiparkinson Agents/adverse effects*-
dc.subject.MESHChi-Square Distribution-
dc.subject.MESHCohort Studies-
dc.subject.MESHCorpus Striatum/diagnostic imaging-
dc.subject.MESHCorpus Striatum/pathology-
dc.subject.MESHDopamine Plasma Membrane Transport Proteins/metabolism-
dc.subject.MESHDyskinesia, Drug-Induced/diagnostic imaging-
dc.subject.MESHDyskinesia, Drug-Induced/etiology*-
dc.subject.MESHDyskinesia, Drug-Induced/pathology*-
dc.subject.MESHFemale-
dc.subject.MESHHumans-
dc.subject.MESHLevodopa/adverse effects*-
dc.subject.MESHMagnetic Resonance Imaging-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHParkinson Disease/diagnostic imaging-
dc.subject.MESHParkinson Disease/drug therapy-
dc.subject.MESHPositron-Emission Tomography-
dc.subject.MESHPredictive Value of Tests-
dc.subject.MESHProportional Hazards Models-
dc.subject.MESHTropanes-
dc.titlePresynaptic dopamine depletion predicts levodopa-induced dyskinesia in de novo Parkinson disease-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Neurology (신경과학)-
dc.contributor.googleauthorJin Yong Hong-
dc.contributor.googleauthorJungsu S. Oh-
dc.contributor.googleauthorInjoo Lee-
dc.contributor.googleauthorMun Kyung Sunwoo-
dc.contributor.googleauthorJee Hyun Ham-
dc.contributor.googleauthorJi E. Lee-
dc.contributor.googleauthorYoung H. Sohn-
dc.contributor.googleauthorJae Seung Kim-
dc.contributor.googleauthorPhil Hyu Lee-
dc.identifier.doi10.1212/WNL.0000000000000385-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01935-
dc.contributor.localIdA01982-
dc.contributor.localIdA03270-
dc.contributor.localIdA04338-
dc.contributor.localIdA04442-
dc.contributor.localIdA03210-
dc.relation.journalcodeJ02340-
dc.identifier.eissn1526-632X-
dc.identifier.pmid24719485-
dc.identifier.urlhttp://www.neurology.org/content/82/18/1597.long-
dc.contributor.alternativeNameSunwoo, Mun Kyung-
dc.contributor.alternativeNameSohn, Young Ho-
dc.contributor.alternativeNameLee, Ji Eun-
dc.contributor.alternativeNameLee, Phil Hyu-
dc.contributor.alternativeNameHam, Jee Hyun-
dc.contributor.alternativeNameHong, Jin Yong-
dc.contributor.affiliatedAuthorSunwoo, Mun Kyung-
dc.contributor.affiliatedAuthorSohn, Young Ho-
dc.contributor.affiliatedAuthorLee, Phil Hyu-
dc.contributor.affiliatedAuthorHam, Jee Hyun-
dc.contributor.affiliatedAuthorHong, Jin Yong-
dc.contributor.affiliatedAuthorLee, Ji Eun-
dc.rights.accessRightsfree-
dc.citation.volume82-
dc.citation.number18-
dc.citation.startPage1597-
dc.citation.endPage604-
dc.identifier.bibliographicCitationNEUROLOGY, Vol.82(18) : 1597-604, 2014-
dc.identifier.rimsid38148-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers

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