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JMD : Journal of Movement Disorders

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2 "Chae Won Shin"
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Original Articles
Nonmotor and Dopamine Transporter Change in REM Sleep Behavior Disorder by Olfactory Impairment
Jee-Young Lee, Eun Jin Yoon, Yu Kyeong Kim, Chae Won Shin, Hyunwoo Nam, Jae Min Jeong, Han-Joon Kim, Beomseok Jeon
J Mov Disord. 2019;12(2):103-112.   Published online May 30, 2019
DOI: https://doi.org/10.14802/jmd.18061
  • 4,747 View
  • 179 Download
  • 8 Citations
AbstractAbstract PDFSupplementary Material
Objective
It is unclear whether the decline in dopamine transporters (DAT) differs among idiopathic rapid eye movement sleep behavior disorder (iRBD) patients with different levels of olfactory impairment. This study aimed to characterize DAT changes in relation to nonmotor features in iRBD patients by olfactory loss.
Methods
This prospective cohort study consisted of three age-matched groups: 30 polysomnography-confirmed iRBD patients, 30 drug-naïve Parkinson’s disease patients, and 19 healthy controls without olfactory impairment. The iRBD group was divided into two groups based on olfactory testing results. Participants were evaluated for reported prodromal markers and then underwent 18F-FP-CIT positron emission tomography and 3T MRI. Tracer uptakes were analyzed in the caudate, anterior and posterior putamen, substantia nigra, and raphe nuclei.
Results
Olfactory impairment was defined in 38.5% of iRBD patients. Mild parkinsonian signs and cognitive functions were not different between the two iRBD subgroups; however, additional prodromal features, constipation, and urinary and sexual dysfunctions were found in iRBD patients with olfactory impairment but not in those without. Tracer uptake showed significant group differences in all brain regions, except the raphe nuclei. The iRBD patients with olfactory impairment had uptake reductions in the anterior and posterior putamen, caudate, and substantia nigra (p < 0.016 in all, adjusted for age), which ranged from 0.6 to 0.8 of age-normative values. In contrast, those without olfactory impairment had insignificant changes in all regions ranging above 0.8.
Conclusion
There was a clear distinction in DAT loss and nonmotor profiles by olfactory status in iRBD.
Amantadine and the Risk of Dyskinesia in Patients with Early Parkinson’s Disease: An Open-Label, Pragmatic Trial
Aryun Kim, Young Eun Kim, Ji Young Yun, Han-Joon Kim, Hui-Jun Yang, Woong-Woo Lee, Chae Won Shin, Hyeyoung Park, Yu Jin Jung, Ahro Kim, Yoon Kim, Mihee Jang, Beomseok Jeon
J Mov Disord. 2018;11(2):65-71.   Published online May 30, 2018
DOI: https://doi.org/10.14802/jmd.18005
  • 6,810 View
  • 214 Download
  • 12 Citations
AbstractAbstract PDFSupplementary Material
Objective
We examined whether amantadine can prevent the development of dyskinesia.
Methods
Patients with drug-naïve Parkinson’s disease (PD), younger than 70 years of age and in the early stage of PD (Hoehn and Yahr scale < 3), were recruited from April 2011 to December 2014. The exclusion criteria included the previous use of antiparkinsonian medication, the presence of dyskinesia, significant psychological disorders, and previous history of a hypersensitivity reaction. Patients were consecutively assigned to one of 3 treatment groups in an open label fashion: Group A-1, amantadine first and then levodopa when needed; Group A-2, amantadine first, dopamine agonist when needed, and then levodopa; and Group B, dopamine agonist first and then levodopa when needed. The primary endpoint was the development of dyskinesia, which was analyzed by the Kaplan-Meier survival rate.
Results
A total of 80 patients were enrolled: Group A-1 (n = 27), Group A-2 (n = 27), and Group B (n = 26). Twenty-four patients were excluded from the analysis due to the following: withdrawal of amantadine or dopamine agonist (n = 9), alternative diagnosis (n = 2), withdrawal of consent (n = 1), and breach in the protocol (n = 12). After exclusion, 5 of the 56 (8.93%) patients developed dyskinesia. Patients in Group A-1 and A-2 tended to develop dyskinesia less often than those in Group B (cumulative survival rates of 0.933, 0.929, and 0.700 for A-1, A-2, and B, respectively; p = 0.453).
Conclusion
Amantadine as an initial treatment may decrease the incidence of dyskinesia in patients with drug-naïve PD.

JMD : Journal of Movement Disorders