Journal of Movement Disorders

Hyeyoung Park

4 Articles

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

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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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Investigation of the Long-Term Effects of Amantadine Use in Parkinson’s Disease
Sangmin Park, Jung Hwan Shin, Seung Ho Jeon, Chan Young Lee, Han-Joon Kim, Beomseok Jeon
Journal of Movement Disorders.2023; 16(2): 224. CrossRef
Polypharmazie bei der Behandlung von Parkinsonsymptomen: eine Nutzen-Risiko Abwägung
J. Bedarf, I. Csoti, H. Herbst, P. Urban, D. Woitalla, U. Wüllner
DGNeurologie.2023; 6(6): 504. CrossRef
Role of glutamate receptor complex in the organism. Ligands of NMDA receptors in neurodegenerative processes – a modern state of the problem
Vladimir D. Dergachev, Ekaterina E. Yakovleva, Eugenii R. Bychkov, Levon B. Piotrovskiy, Petr D. Shabanov
Reviews on Clinical Pharmacology and Drug Therapy.2022; 20(1): 17. CrossRef
Effect of glycine transporter 1 inhibition with bitopertin on parkinsonism and L-DOPA induced dyskinesia in the 6-OHDA-lesioned rat
Imane Frouni, Woojin Kang, Dominique Bédard, Sébastien Belliveau, Cynthia Kwan, Shadi Hadj-Youssef, Élodie Bourgeois-Cayer, Leanne Ohlund, Lekha Sleno, Adjia Hamadjida, Philippe Huot
European Journal of Pharmacology.2022; 929: 175090. CrossRef
Amantadine in the treatment of Parkinson’s disease. New opportunities in the context of COVID-19
E.A. Katunina
Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova.2021; 121(4): 101. CrossRef
Current Knowledge on the Background, Pathophysiology and Treatment of Levodopa-Induced Dyskinesia—Literature Review
Michał Hutny, Jagoda Hofman, Aleksandra Klimkowicz-Mrowiec, Agnieszka Gorzkowska
Journal of Clinical Medicine.2021; 10(19): 4377. CrossRef
Neuroinflammation and blood–brain barrier disruption following traumatic brain injury: Pathophysiology and potential therapeutic targets
Suraj Sulhan, Kristopher A. Lyon, Lee A. Shapiro, Jason H. Huang
Journal of Neuroscience Research.2020; 98(1): 19. CrossRef
Emerging drugs for the treatment of L-DOPA-induced dyskinesia: an update
Sohaila AlShimemeri, Susan H Fox, Naomi P Visanji
Expert Opinion on Emerging Drugs.2020; 25(2): 131. CrossRef
Pharmacological Treatment of Early Motor Manifestations of Parkinson Disease (PD)
Michelle Ann C. Sy, Hubert H. Fernandez
Neurotherapeutics.2020; 17(4): 1331. CrossRef
Gut Microbiota Approach—A New Strategy to Treat Parkinson’s Disease
Jing Liu, Fei Xu, Zhiyan Nie, Lei Shao
Frontiers in Cellular and Infection Microbiology.2020;[Epub] CrossRef
Viewpoint: Developing drugs for levodopa‐induced dyskinesia in PD: Lessons learnt, what does the future hold?
Susan H. Fox, Jonathan M. Brotchie
European Journal of Neuroscience.2019; 49(3): 399. CrossRef
Polypharmacy in Parkinson’s disease: risks and benefits with little evidence
I. Csoti, H. Herbst, P. Urban, D. Woitalla, U. Wüllner
Journal of Neural Transmission.2019; 126(7): 871. CrossRef
Activation of mGlu2/3 receptors, a novel therapeutic approach to alleviate dyskinesia and psychosis in experimental parkinsonism
Imane Frouni, Adjia Hamadjida, Cynthia Kwan, Dominique Bédard, Vaidehi Nafade, Fleur Gaudette, Stephen G. Nuara, Jim C. Gourdon, Francis Beaudry, Philippe Huot
Neuropharmacology.2019; 158: 107725. CrossRef
Can therapeutic strategies prevent and manage dyskinesia in Parkinson’s disease? An update
Valentina Leta, Peter Jenner, K. Ray Chaudhuri, Angelo Antonini
Expert Opinion on Drug Safety.2019; 18(12): 1203. CrossRef

Survival of Korean Huntington’s Disease Patients: Han-Joon Kim, Chae-Won Shin, Beomseok Jeon, Hyeyoung Park; J Mov Disord. 2016;9(3):166-170. Published online September 21, 2016; DOI: https://doi.org/10.14802/jmd.16022

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Abstract PDF

Objective
The survival of Huntington’s disease (HD) patients is reported to be 15–20 years. However, most studies on the survival of HD have been conducted in patients without genetic confirmation with the possible inclusion of non-HD patients, and all studies have been conducted in Western countries. The survival of patients with HD in East Asia, where its prevalence is 10–50-fold lower compared with Western populations, has not yet been reported.
Methods
Forty-seven genetically confirmed Korean HD patients from independent families were included in this retrospective medical record review study.
Results
The mean age at onset among the 47 patients was 46.1 ± 14.0 years. At the time of data collection, 25 patients had died, and these patients had a mean age at death of 57.8 ± 13.7 years. The Kaplan-Meier estimate of the median survival from onset in the 47 patients was 14.5 years (95% confidence interval: 12.3–16.6). None of the following factors were associated with the survival time in the univariate Cox regression analysis: gender, age at onset, normal CAG repeat size, mutant CAG repeat size, and the absence or presence of non-motor symptoms at onset.
Conclusion
This is the first Asian study on survival in HD patients. Survival in Korean HD patients may be shorter than that reported for Western populations, or at least is in the lower range of expected survival. A larger longitudinal observation study is needed to confirm the results found in this study.

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Analysis of HTT CAG repeat expansion among healthy individuals and patients with chorea in Korea
Ryul Kim, Moon-Woo Seong, Bumjo Oh, Ho Seop Shin, Jee-Soo Lee, Sangmin Park, Mihee Jang, Beomseok Jeon, Han-Joon Kim, Jee-Young Lee
Parkinsonism & Related Disorders.2024; 118: 105930. CrossRef
Increased 10-Year Prevalence of Huntington’s Disease in South Korea: An Analysis of Medical Expenditure Through the National Healthcare System
Chan Young Lee, Jun-soo Ro, Hyemin Jung, Manho Kim, Beomseok Jeon, Jee-Young Lee
Journal of Clinical Neurology.2023; 19(2): 147. CrossRef
Clustering and prediction of disease progression trajectories in Huntington's disease: An analysis of Enroll-HD data using a machine learning approach
Jinnie Ko, Hannah Furby, Xiaoye Ma, Jeffrey D. Long, Xiao-Yu Lu, Diana Slowiejko, Rita Gandhy
Frontiers in Neurology.2023;[Epub] CrossRef
Survival in Huntington’s disease and other young‐onset dementias
Samantha M. Loi, Paraskevi Tsoukra, Emily Sun, Zhibin Chen, Pierre Wibawa, Maria di Biase, Sarah Farrand, Dhamidhu Eratne, Wendy Kelso, Andrew Evans, Mark Walterfang, Dennis Velakoulis
International Journal of Geriatric Psychiatry.2023;[Epub] CrossRef
Functional Intercellular Transmission of miHTT via Extracellular Vesicles: An In Vitro Proof-of-Mechanism Study
Roberto D. V. S. Morais, Marina Sogorb-González, Citlali Bar, Nikki C. Timmer, M. Leontien Van der Bent, Morgane Wartel, Astrid Vallès
Cells.2022; 11(17): 2748. CrossRef
Huntington's disease: Mortality and risk factors in an Australian cohort
Emily Sun, Matthew Kang, Pierre Wibawa, Vivian Tsoukra, Zhibin Chen, Sarah Farrand, Dhamidhu Eratne, Wendy Kelso, Andrew Evans, Mark Walterfang, Dennis Velakoulis, Samantha M. Loi
Journal of the Neurological Sciences.2022; 442: 120437. CrossRef
Huntington’s disease in Turkey: genetic counseling, clinical features, and outcome
Yesim Sucullu Karadag, Busranur Erozan Cavdarli, Rabia Nazik Yuksel
Neurological Research.2021; 43(5): 381. CrossRef
Validation of diagnostic codes and epidemiologic trends of Huntington disease: a population-based study in Navarre, Spain
Esther Vicente, Ainara Ruiz de Sabando, Fermín García, Itziar Gastón, Eva Ardanaz, María A. Ramos-Arroyo
Orphanet Journal of Rare Diseases.2021;[Epub] CrossRef
Epidemiology of Huntington disease in Cyprus: A 20‐year retrospective study
C.A. Demetriou, A. Heraclides, C. Salafori, G.A. Tanteles, K. Christodoulou, Y. Christou, E. Zamba‐Papanicolaou
Clinical Genetics.2018; 93(3): 656. CrossRef
Population-specific genetic modification of Huntington's disease in Venezuela
Michael J. Chao, Kyung-Hee Kim, Jun Wan Shin, Diane Lucente, Vanessa C. Wheeler, Hong Li, Jared C. Roach, Leroy Hood, Nancy S. Wexler, Laura B. Jardim, Peter Holmans, Lesley Jones, Michael Orth, Seung Kwak, Marcy E. MacDonald, James F. Gusella, Jong-Min L
PLOS Genetics.2018; 14(5): e1007274. CrossRef

Clinical Heterogeneity of Atypical Pantothenate Kinase-Associated Neurodegeneration in Koreans: Jae-Hyeok Lee, Jongkyu Park, Ho-Sung Ryu, Hyeyoung Park, Young Eun Kim, Jin Yong Hong, Sang Ook Nam, Young-Hee Sung, Seung-Hwan Lee, Jee-Young Lee, Myung Jun Lee, Tae-Hyoung Kim, Chul Hyoung Lyoo, Sun Ju Chung, Seong Beom Koh, Phil Hyu Lee, Jin Whan Cho, Mee Young Park, Yun Joong Kim, Young H. Sohn, Beom Seok Jeon, Myung Sik Lee; J Mov Disord. 2016;9(1):20-27. Published online January 25, 2016; DOI: https://doi.org/10.14802/jmd.15058

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Abstract PDF Supplementary Material

Objective
Neurodegeneration with brain iron accumulation (NBIA) represents a group of inherited movement disorders characterized by iron accumulation in the basal ganglia. Recent advances have included the identification of new causative genes and highlighted the wide phenotypic variation between and within the specific NBIA subtypes. This study aimed to investigate the current status of NBIA in Korea.
Methods
We collected genetically confirmed NBIA patients from twelve nationwide referral hospitals and from a review of the literature. We conducted a study to describe the phenotypic and genotypic characteristics of Korean adults with atypical pantothenate kinase-associated neurodegeneration (PKAN).
Results
Four subtypes of NBIA including PKAN (n = 30), PLA2G6-related neurodegeneration (n = 2), beta-propeller protein-associated neurodegeneration (n = 1), and aceruloplasminemia (n = 1) have been identified in the Korean population. The clinical features of fifteen adults with atypical PKAN included early focal limb dystonia, parkinsonism-predominant feature, oromandibular dystonia, and isolated freezing of gait (FOG). Patients with a higher age of onset tended to present with parkinsonism and FOG. The p.R440P and p.D378G mutations are two major mutations that represent approximately 50% of the mutated alleles. Although there were no specific genotype-phenotype correlations, most patients carrying the p.D378G mutation had a late-onset, atypical form of PKAN.
Conclusions
We found considerable phenotypic heterogeneity in Korean adults with atypical PKAN. The age of onset may influence the presentation of extrapyramidal symptoms.

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Genetic mutation spectrum of pantothenate kinase-associated neurodegeneration expanded by breakpoint sequencing in pantothenate kinase 2 gene
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Long-Term Outcomes of Deep Brain Stimulation in Pantothenate Kinase-Associated Neurodegeneration-Related Dystonia
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Ali S. Shalash, Thomas W. Rösler, Ibrahim Y. Abdelrahman, Hatem S. Abulmakarem, Stefanie H. Müller, Franziska Hopfner, Gregor Kuhlenbäumer, Günter U. Höglinger, Mohamed Salama
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Treatment Responsiveness of Parkinsonism in Atypical Pantothenate Kinase‐Associated Neurodegeneration
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Randall D. Marshall, Abigail Collins, Maria L. Escolar, H. A. Jinnah, Thomas Klopstock, Michael C. Kruer, Aleksandar Videnovic, Amy Robichaux-Viehoever, Colleen Burns, Laura L. Swett, Dennis A. Revicki, Randall H. Bender, William R. Lenderking
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Intrafamilial variability and clinical heterogeneity in a family with PLA2G6-associated neurodegeneration
Jong Kyu Park, Jinyoung Youn, Jin Whan Cho
Precision and Future Medicine.2019; 3(3): 135. CrossRef
On the complexity of clinical and molecular bases of neurodegeneration with brain iron accumulation
C. Tello, A. Darling, V. Lupo, B. Pérez‐Dueñas, C. Espinós
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J.-H. Lee, A. Gregory, P. Hogarth, C. Rogers, S.J. Hayflick
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Parkinson’s Disease and Metal Storage Disorders: A Systematic Review
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Atypical pantothenate kinase-associated neurodegeneration: Clinical description of two brothers and a review of the literature
S. Mahoui, A. Benhaddadi, W. Ameur El Khedoud, M. Abada Bendib, M. Chaouch
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Dural Arteriovenous Fistula-Associated Reversible Parkinsonism with Presynaptic Dopaminergic Loss: Hang Rai Kim, Jee-Young Lee, Yu Kyeong Kim, Hyeyoung Park, Han-Joon Kim, Young-Je Son, Beom Seok Jeon; J Mov Disord. 2015;8(3):141-143. Published online September 10, 2015; DOI: https://doi.org/10.14802/jmd.15021

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