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Original 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
  • 7,207 View
  • 224 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.

Citations

Citations to this article as recorded by  
  • 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
  • 13,616 View
  • 143 Download
  • 6 Citations
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • 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
  • 18,869 View
  • 215 Download
  • 14 Citations
AbstractAbstract PDFSupplementary 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.

Citations

Citations to this article as recorded by  
  • Genetic mutation spectrum of pantothenate kinase-associated neurodegeneration expanded by breakpoint sequencing in pantothenate kinase 2 gene
    Dahae Yang, Sanghyun Cho, Sung Im Cho, Manjin Kim, Moon-Woo Seong, Sung Sup Park
    Orphanet Journal of Rare Diseases.2022;[Epub]     CrossRef
  • Long-Term Outcomes of Deep Brain Stimulation in Pantothenate Kinase-Associated Neurodegeneration-Related Dystonia
    Kyung Ah Woo, Han-Joon Kim, Seung-Ho Jeon, Hye Ran Park, Kye Won Park, Seung Hyun Lee, Sun Ju Chung, Jong-Hee Chae, Sun Ha Paek, Beomseok Jeon
    Journal of Movement Disorders.2022; 15(3): 241.     CrossRef
  • Psychiatric symptoms in an adolescent reveal a novel compound heterozygous mutation of the PANK2 gene in the atypical PKAN syndrome
    Luz María González Huerta, Sorina Gómez González, Jaime Toral López
    Psychiatric Genetics.2021; 31(3): 95.     CrossRef
  • Rational Design of Novel Therapies for Pantothenate Kinase–Associated Neurodegeneration
    Nivedita Thakur, Thomas Klopstock, Suzanne Jackowski, Enej Kuscer, Fernando Tricta, Aleksandar Videnovic, Hyder A. Jinnah
    Movement Disorders.2021; 36(9): 2005.     CrossRef
  • Atypical Pantothenate Kinase-Associated Neurodegeneration with variable phenotypes in an Egyptian family
    Ali S. Shalash, Thomas W. Rösler, Ibrahim Y. Abdelrahman, Hatem S. Abulmakarem, Stefanie H. Müller, Franziska Hopfner, Gregor Kuhlenbäumer, Günter U. Höglinger, Mohamed Salama
    Heliyon.2021; : e07469.     CrossRef
  • Treatment Responsiveness of Parkinsonism in Atypical Pantothenate Kinase‐Associated Neurodegeneration
    Jeanne Feuerstein, Caroline Olvera, Michelle Fullard
    Movement Disorders Clinical Practice.2020;[Epub]     CrossRef
  • Diagnostic and clinical experience of patients with pantothenate kinase-associated neurodegeneration
    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
    Orphanet Journal of Rare Diseases.2019;[Epub]     CrossRef
  • 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
    Clinical Genetics.2018; 93(4): 731.     CrossRef
  • Looking Deep into the Eye-of-the-Tiger in Pantothenate Kinase–Associated Neurodegeneration
    J.-H. Lee, A. Gregory, P. Hogarth, C. Rogers, S.J. Hayflick
    American Journal of Neuroradiology.2018; 39(3): 583.     CrossRef
  • Parkinson’s Disease and Metal Storage Disorders: A Systematic Review
    Edward Botsford, Jayan George, Ellen Buckley
    Brain Sciences.2018; 8(11): 194.     CrossRef
  • 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
    Revue Neurologique.2017; 173(10): 658.     CrossRef
  • Clinical rating scale for pantothenate kinase-associated neurodegeneration: A pilot study
    Alejandra Darling, Cristina Tello, María Josep Martí, Cristina Garrido, Sergio Aguilera-Albesa, Miguel Tomás Vila, Itziar Gastón, Marcos Madruga, Luis González Gutiérrez, Julio Ramos Lizana, Montserrat Pujol, Tania Gavilán Iglesias, Kylee Tustin, Jean Pie
    Movement Disorders.2017; 32(11): 1620.     CrossRef
  • Missions of <italic>Journal of Movement Disorders</italic>
    Yun Joong Kim
    Journal of Movement Disorders.2016; 9(1): 1.     CrossRef
Letter to the editor
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
  • 12,479 View
  • 61 Download
  • 4 Citations
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Citations

Citations to this article as recorded by  
  • The Sudden Onset of Pure Parkinsonism Caused by Intracranial Dural Arteriovenous Fistulas
    Hitoshi Kawasaki, Risa Okuda, Ryu Yokoyama, Toshimasa Yamamoto
    Internal Medicine.2022; 61(7): 1059.     CrossRef
  • Reversible Parkinsonism and Rapidly Progressive Dementia Due to Dural Arteriovenous Fistula: Case Series and Literature Review
    Joshua Lai, Manraj K.S. Heran, A. Jon Stoessl, Peter A. Gooderham
    Movement Disorders Clinical Practice.2017; 4(4): 607.     CrossRef
  • Dementia and Parkinsonism-a Rare Presentation of Intracranial Dural Arteriovenous Fistulae
    Manoj Gopinath, Chinmay Nagesh, K Santhosh, ER Jayadevan
    Neurointervention.2017; 12(2): 125.     CrossRef
  • Straight sinus dural arteriovenous fistula presenting with reversible parkinsonism
    Jiali Pu, Xiaoli Si, Rong Ye, Baorong Zhang
    Medicine.2017; 96(49): e9005.     CrossRef

JMD : Journal of Movement Disorders