- Nonmotor and Dopamine Transporter Change in REM Sleep Behavior Disorder by Olfactory Impairment
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Jee-Young Lee, Eun Jin Yoon, Yu Kyeong Kim, Chae Won Shin, Hyunwoo Nam, Jae Min Jeong, Han-Joon Kim, Beomseok Jeon
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J Mov Disord. 2019;12(2):103-112. Published online May 30, 2019
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DOI: https://doi.org/10.14802/jmd.18061
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Abstract
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.
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Citations
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- Neuropsychological Changes in Isolated REM Sleep Behavior Disorder: A Systematic Review and Meta-analysis of Cross-sectional and Longitudinal Studies
Caterina Leitner, Giada D’Este, Laura Verga, Shady Rahayel, Samantha Mombelli, Marco Sforza, Francesca Casoni, Marco Zucconi, Luigi Ferini-Strambi, Andrea Galbiati Neuropsychology Review.2024; 34(1): 41. CrossRef - Dopamine transporter positron emission tomography in patients with Alzheimer’s disease with Lewy body disease features
Sungwoo Kang, Seun Jeon, Young-gun Lee, Byoung Seok Ye Neurobiology of Aging.2024; 134: 57. CrossRef - Imaging Procedure and Clinical Studies of [18F]FP-CIT PET
Changhwan Sung, Seung Jun Oh, Jae Seung Kim Nuclear Medicine and Molecular Imaging.2024; 58(4): 185. CrossRef - Validation of the REM behaviour disorder phenoconversion-related pattern in an independent cohort
Beatrice Orso, Pietro Mattioli, Eun-Jin Yoon, Yu Kyeong Kim, Heejung Kim, Jung Hwan Shin, Ryul Kim, Claudio Liguori, Francesco Famà, Andrea Donniaquio, Federico Massa, David Vállez García, Sanne K. Meles, Klaus L. Leenders, Agostino Chiaravalloti, Matteo Neurological Sciences.2023; 44(9): 3161. CrossRef - Neurofilament light chain and cardiac MIBG uptake as predictors for phenoconversion in isolated REM sleep behavior disorder
Don Gueu Park, Ju Yeong Kim, Min Seung Kim, Mi Hee Kim, Young-Sil An, Jaerak Chang, Jung Han Yoon Journal of Neurology.2023; 270(9): 4393. CrossRef - Longitudinal evolution of cortical thickness signature reflecting Lewy body dementia in isolated REM sleep behavior disorder: a prospective cohort study
Jung Hwan Shin, Heejung Kim, Yu Kyeong Kim, Eun Jin Yoon, Hyunwoo Nam, Beomseok Jeon, Jee-Young Lee Translational Neurodegeneration.2023;[Epub] CrossRef - Brain olfactory‐related atrophy in isolated rapid eye movement sleep behavior disorder
Kyung Ah Woo, Heejung Kim, Eun Jin Yoon, Jung Hwan Shin, Hyunwoo Nam, Beomseok Jeon, Yu Kyeong Kim, Jee‐Young Lee Annals of Clinical and Translational Neurology.2023; 10(12): 2192. CrossRef - Monoaminergic Degeneration and Ocular Motor Abnormalities in De Novo Parkinson's Disease
Kyung Ah Woo, Joo Hong Joun, Eun Jin Yoon, Chan Young Lee, Beomseok Jeon, Yu Kyeong Kim, Jee‐Young Lee Movement Disorders.2023; 38(12): 2291. CrossRef - Altered cerebral perfusion and microstructure in advanced Parkinson’s disease and their associations with clinical features
Zhaoxi Liu, Yiwei Zhang, Han Wang, Dan Xu, Hui You, Zhentao Zuo, Feng Feng Neurological Research.2022; 44(1): 47. CrossRef - Brain Neuroimaging of Rapid Eye Movement Sleep Behavior Disorder in Parkinson’s Disease: A Systematic Review
Rafail Matzaras, Kuangyu Shi, Artemios Artemiadis, Panagiotis Zis, Georgios Hadjigeorgiou, Axel Rominger, Claudio L.A. Bassetti, Panagiotis Bargiotas Journal of Parkinson's Disease.2022; 12(1): 69. CrossRef - Odor Identification by Parkinson’s Disease Patients Tested by Using Sniffin’ Sticks versus Natural Spices
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Ryul Kim, Heejung Kim, Yu Kyeong Kim, Eun Jin Yoon, Hyun Woo Nam, Beomseok Jeon, Jee‐Young Lee Movement Disorders.2022; 37(10): 2099. CrossRef - Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression
Ryul Kim, Jee‐Young Lee, Yu Kyeong Kim, Heejung Kim, Eun Jin Yoon, Jung Hwan Shin, Dallah Yoo, Hyunwoo Nam, Beomseok Jeon Movement Disorders.2021; 36(8): 1889. CrossRef - Parkinson Disease-Related Brain Metabolic Patterns and Neurodegeneration in Isolated REM Sleep Behavior Disorder
Jung Hwan Shin, Jee-Young Lee, Yu-Kyeong Kim, Eun Jin Yoon, Heejung Kim, Hyunwoo Nam, Beomseok Jeon Neurology.2021;[Epub] CrossRef - Retina Thickness as a Marker of Neurodegeneration in Prodromal Lewy Body Disease
Jee‐Young Lee, Jeeyun Ahn, Sohee Oh, Joo Young Shin, Yu Kyeong Kim, Hyunwoo Nam, Beomseok Jeon Movement Disorders.2020; 35(2): 349. CrossRef - Serum TNF-α and neurodegeneration in isolated REM sleep behavior disorder
Ryul Kim, Jee-Young Lee, Han-Joon Kim, Yu Kyeong Kim, Hyunwoo Nam, Beomseok Jeon Parkinsonism & Related Disorders.2020; 81: 1. CrossRef - Longitudinal change in dopamine transporter availability in idiopathic REM sleep behavior disorder
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- Amantadine and the Risk of Dyskinesia in Patients with Early Parkinson’s Disease: An Open-Label, Pragmatic Trial
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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
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J Mov Disord. 2018;11(2):65-71. Published online May 30, 2018
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DOI: https://doi.org/10.14802/jmd.18005
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10,152
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260
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12
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15
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Abstract
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.
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