Journal of Movement Disorders

Case Report

Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis: Jae Young Joo, Dallah Yoo, Tae-Beom Ahn; J Mov Disord. 2022;15(1):66-70. Published online November 25, 2021; DOI: https://doi.org/10.14802/jmd.21115

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Movement disorders associated with glial fibrillary acidic protein (GFAP) autoantibodies have rarely been reported as ataxia or tremors. A 32-year-old man with headache and fever, initially diagnosed with viral meningoencephalitis, showed gradual improvement with empirical treatment. Two weeks after the illness, he suddenly developed orofacial, tongue, and neck dyskinesia accompanied by oculomotor abnormalities, which developed into severe generalized choreoballism. Brain magnetic resonance imaging (fluid-attenuated inversion recovery) showed signal hyperintensities in the bilateral globus pallidus interna. The clinical picture suggested an acute inflammatory trigger of secondary autoimmune encephalitis. The autoimmune antibody test was positive for GFAP, with the strongest reactivity in the cerebrospinal fluid (CSF) before treatment and decreased reactivity in serial CSF examinations during immunotherapy. Dyskinesia gradually improved to the extent that it could be controlled with only oral medications. This patient presented with parainfectious GFAP meningoencephalitis with distinctive clinical features and imaging findings.

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Relapsing Autoimmune GFAP Astrocytopathy: Case Report
Ekaterina O. Chekanova, Аlla А. Shabalina, Taras O. Simaniv, Rodion N. Konovalov, Larisa A. Dobrynina, Lyudmila A. Kalashnikova, Maria V. Gubanova, Maria N. Zakharova
Annals of Clinical and Experimental Neurology.2024; 17(4): 89. CrossRef
Comment on “Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis”
Byoung June Ahn, Kyum-Yil Kwon
Journal of Movement Disorders.2022; 15(2): 187. CrossRef
Re: Comment on “Parainfectious Anti-Glial Fibrillary Acidic Protein-Associated Meningoencephalitis”
Dallah Yoo, Tae-Beom Ahn
Journal of Movement Disorders.2022; 15(2): 189. CrossRef

Original Articles

Less Pulsatile Levodopa Therapy (6 Doses Daily) Is Associated with a Reduced Incidence of Dyskinesia: Mark M. Lin, Robert Laureno; J Mov Disord. 2019;12(1):37-42. Published online January 30, 2019; DOI: https://doi.org/10.14802/jmd.18046

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Abstract PDF

Objective
To evaluate whether less pulsatile levodopa therapy (LPT) can reduce the development of levodopa-induced dyskinesia (LID).
Methods
This is a retrospective cohort study of patients with Parkinson’s disease at the movement disorders clinic of Medstar Washington Hospital Center. The study was not blinded or randomized. Patients were seen between August 2002 and August 2018. During these years, we treated patients with less pulsatile (6 doses daily) levodopa treatment to reduce LID. Occurrence of LID was recorded.
Results
Ninety-five patients with Parkinson’s disease taking levodopa were divided into two groups: 1) patients who were initially managed on LPT or who switched from traditional therapy (TT) (n = 61) (mean disease duration: 7.7 ± 4.8 years, mean levodopa duration: 5.6 ± 4.5 years and mean observation time: 4.3 ± 3.4 years), and 2) patients on TT throughout the observation period or until they developed dyskinesia (n = 34) (mean disease duration: 8.3 ± 3.8 years, mean levodopa duration: 6.2 ± 4.2 years and mean observation time: 4.1 ± 3.4 years). Three of the 61 LPT patients developed dyskinesia during the observation period. One of the patients developed dyskinesia after being switched to pulsatile doses by another doctor. In the other two, dyskinesia was minimal. In contrast to this 4.9% cumulative incidence, dyskinesia occurred in 50% (17/34) of TT patients, an incidence similar to that in published data (p < 0.001).
Conclusion
Less pulsatile levodopa with 6 daily doses was associated with a low incidence of LID. Further study of this method of treatment is warranted.

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Reduced Plasma Levodopa Fluctuations with More Frequent Administration of a Novel Carbidopa/Levodopa Functionally Scored Tablet
Thomas N. Chase, Ahmad AL‐Sabbagh, Minako Koga, Kathleen Clarence‐Smith
Clinical Pharmacology in Drug Development.2024; 13(4): 380. CrossRef
Dopamine D1 Agonists: First Potential Treatment for Late-Stage Parkinson’s Disease
Mechelle M. Lewis, Lauren J. Van Scoy, Sol De Jesus, Jonathan G. Hakun, Paul J. Eslinger, Julio Fernandez-Mendoza, Lan Kong, Yang Yang, Bethany L. Snyder, Natalia Loktionova, Sridhar Duvvuri, David L. Gray, Xuemei Huang, Richard B. Mailman
Biomolecules.2023; 13(5): 829. CrossRef
Classification of l-DOPA pharmacokinetics shapes and creating a predictive model
Noriko Nishikawa, Hirtotaka Iwaki, Yohei Mukai, Yuji Takahashi
Parkinsonism & Related Disorders.2023; 114: 105798. CrossRef
Personalized Medicine Approach in Treating Parkinson’s Disease, Using Oral Administration of Levodopa/Carbidopa Microtablets in Clinical Practice
Helga María Grétarsdóttir, Erik Widman, Anders Johansson, Dag Nyholm
Journal of Personalized Medicine.2021; 11(8): 720. 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
Pallidal versus subthalamic nucleus deep brain stimulation for levodopa‐induced dyskinesia
Shi‐Ying Fan, Kai‐Liang Wang, Wei Hu, Robert S. Eisinger, Alexander Han, Chun‐Lei Han, Qiao Wang, Shimabukuro Michitomo, Jian‐Guo Zhang, Feng Wang, Adolfo Ramirez‐Zamora, Fan‐Gang Meng
Annals of Clinical and Translational Neurology.2020; 7(1): 59. CrossRef
A Stage-Based Approach to Therapy in Parkinson’s Disease
Claudia Carrarini, Mirella Russo, Fedele Dono, Martina Di Pietro, Marianna G. Rispoli, Vincenzo Di Stefano, Laura Ferri, Filomena Barbone, Michela Vitale, Astrid Thomas, Stefano Luca Sensi, Marco Onofrj, Laura Bonanni
Biomolecules.2019; 9(8): 388. CrossRef
The Gut Microbiome: A Therapeutically Targetable Site of Peripheral Levodopa Metabolism
Eoin Mulroy, Kailash P. Bhatia
Movement Disorders Clinical Practice.2019; 6(7): 547. CrossRef

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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Abstract PDF Supplementary 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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Sangmin Park, Jung Hwan Shin, Seung Ho Jeon, Chan Young Lee, Han-Joon Kim, Beomseok Jeon
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Polypharmazie bei der Behandlung von Parkinsonsymptomen: eine Nutzen-Risiko Abwägung
J. Bedarf, I. Csoti, H. Herbst, P. Urban, D. Woitalla, U. Wüllner
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Vladimir D. Dergachev, Ekaterina E. Yakovleva, Eugenii R. Bychkov, Levon B. Piotrovskiy, Petr D. Shabanov
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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
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Michelle Ann C. Sy, Hubert H. Fernandez
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Jing Liu, Fei Xu, Zhiyan Nie, Lei Shao
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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
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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
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Can therapeutic strategies prevent and manage dyskinesia in Parkinson’s disease? An update
Valentina Leta, Peter Jenner, K. Ray Chaudhuri, Angelo Antonini
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Case Reports

A Patient with Recurrent Dyskinesia and Hyperpyrexia Syndrome: Min Seok Baek, Hyung Woo Lee, Chul Hyoung Lyoo; J Mov Disord. 2017;10(3):154-157. Published online July 14, 2017; DOI: https://doi.org/10.14802/jmd.17022

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Abstract PDF

Dyskinesia hyperpyrexia syndrome is a rare medical emergency in Parkinson’s disease. It is characterized by continuous dyskinesia associated with hyperthermia, rhabdomyolysis, and alteration of the mental state. We present the case of a 74-year-old woman who presented with recurrent dyskinesia hyperpyrexia syndrome. Although some provocation factors and clinical manifestations seem to be shared with parkinsonism hyperpyrexia syndrome, a clear distinction in management should be considered.

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Dyskinesia-hyperpyrexia syndrome in Parkinson's disease triggered by overdose of levodopa — a case report and literature review
Xiangnan Du, Xuemei Wang, Xiaokun Geng
Frontiers in Neurology.2024;[Epub] CrossRef
Case report: Reversible encephalopathy caused by dyskinesia-hyperpyrexia syndrome
Bohan Luo, Hainan Zhang, Lixia Qin
Frontiers in Neurology.2023;[Epub] CrossRef
Parkinsonism-Hyperpyrexia Syndrome and Dyskinesia-Hyperpyrexia Syndrome in Parkinson’s Disease: Two Cases and Literature Review
Jian-Yong Wang, Jie-Fan Huang, Shi-Guo Zhu, Shi-Shi Huang, Rong-Pei Liu, Bei-Lei Hu, Jian-Hong Zhu, Xiong Zhang
Journal of Parkinson's Disease.2022; 12(6): 1727. CrossRef
Dyskinesia-hyperpyrexia syndrome triggered by overdose of istradefylline: a case report
Shota Komori, Takashi Tsuboi, Masashi Suzuki, Tomohiko Nakamura, Masahisa Katsuno
Rinsho Shinkeigaku.2022; 62(8): 627. CrossRef
Dyskinesia-hyperpyrexia syndrome in Parkinson’s disease: a systematic review
Miao Wang, Wei Wang, Zhongbao Gao, Xi Yin, Tong Chen, Ziying Jiang, Zhenfu Wang
Clinical Autonomic Research.2021; 31(4): 529. CrossRef
Rhabdomyolysis Associated with Severe Levodopa-Induced Dyskinesia in Parkinson’s Disease: A Report of Two Cases and Literature Review
Yuvadee Pitakpatapee, Jindapa Srikajon, Tanita Sangpeamsook, Prachaya Srivanitchapoom
Tremor and Other Hyperkinetic Movements.2021;[Epub] CrossRef
Dyskinesia‐Hyperpyrexia Syndrome in Parkinson's Disease: A Heat Shock–Related Emergency?
Marianna Sarchioto, Valeria Ricchi, Marta Melis, Marcello Deriu, Roberta Arca, Maurizio Melis, Francesca Morgante, Giovanni Cossu
Movement Disorders Clinical Practice.2018; 5(5): 534. CrossRef

Paroxysmal Kinesigenic Dyskinesia as the Presenting and Only Manifestation of Multiple Sclerosis after Eighteen Months of Follow-Up: Marius Baguma, Michel Ossemann; J Mov Disord. 2017;10(2):96-98. Published online March 24, 2017; DOI: https://doi.org/10.14802/jmd.16055

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Abstract PDF

Other than tremor, movement disorders are uncommon in multiple sclerosis. Among these uncommon clinical manifestations, paroxysmal kinesigenic dyskinesia is the most frequently reported. It is characterized by episodic attacks of involuntary movements that are induced by repetitive or sudden movements, startling noise or hyperventilation. The diagnosis is essentially clinical and based on a good observation of the attacks. It is very easy to misdiagnose it. We describe the case of a young female patient who presented paroxysmal kinesigenic dyskinesia as the first and only clinical manifestation of multiple sclerosis, with no recurrence of attacks nor any other neurologic symptom after eighteen months of follow-up.

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Tongue dystonia as CIS and presenting symptom of multiple sclerosis
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Recommendations for the diagnosis and treatment of paroxysmal kinesigenic dyskinesia: an expert consensus in China
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Rhabdomyolysis Related to Dyskinesia in Parkinson’s Disease: Hesna Bekta, Orhan Deniz, adiye Temel, Hava Dnmez Keklikolu, ener Akyol; J Mov Disord. 2014;7(1):25-27. Published online April 30, 2014; DOI: https://doi.org/10.14802/jmd.14006

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Abstract PDF

Rhabdomyolysis is a life threatening syndrome. It accounts for an estimated 8% to 15% of cases of acute renal failure and is associated with a mortality rate of 5%. In movement disorders, various causes of rhabdomyolysis have been reported including status dystonicus, myoclonus, generalized chorea and parkinsonism-hyperprexia syndrome in Parkinson’s disease (PD). Levodopa-induced dyskinesia leading to rhabdomyolysis is a very rare phenomenon in PD. We report a case of 76 years old PD patient with dyskinesia and rhabdomyolysis.

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Rhabdomyolysis secondary to severe tic fits
Ka Loong Kelvin Au, Shannon Chiu, Irene A Malaty
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Rhabdomyolysis Associated with Severe Levodopa-Induced Dyskinesia in Parkinson’s Disease: A Report of Two Cases and Literature Review
Yuvadee Pitakpatapee, Jindapa Srikajon, Tanita Sangpeamsook, Prachaya Srivanitchapoom
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Assessment of plasma creatine kinase as biomarker for levodopa-induced dyskinesia in Parkinson’s disease
Anna Delamarre, François Tison, Qin Li, Monique Galitzky, Olivier Rascol, Erwan Bezard, Wassilios G. Meissner
Journal of Neural Transmission.2019; 126(6): 789. CrossRef
Levodopa-induced dyskinesia: clinical features, incidence, and risk factors
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Oromandibular Dyskinesia as the Initial Manifestation of Late-Onset Huntington Disease: Dong-Seok Oh, Eun-Seon Park, Seong-Min Choi, Byeong-Chae Kim, Myeong-Kyu Kim, Ki-Hyun Cho; J Mov Disord. 2011;4(2):75-77.; DOI: https://doi.org/10.14802/jmd.11016

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Abstract PDF

Huntington’s disease (HD) is a neurodegenerative disorder characterized by a triad of choreoathetosis, dementia and dominant inheritance. The cause of HD is an expansion of CAG trinucleotide repeats in the HD gene. Typical age at onset of symptoms is in the 40s, but the disorder can manifest at any time. Late-onset (≥ 60 years) HD is clinically different from other adult or juvenile onset HD and characterized by mild motor problem as the initial symptoms, shorter disease duration, frequent lack of family history, and relatively low CAG repeats expansion. We report a case of an 80-year-old female with oromandibular dyskinesia as an initial manifestation of HD and 40 CAG repeats.

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Luciana Munhoz, Ashjan Qasim Jabbar, William José e Silva Filho, Aline Yukari Nagai, Emiko Saito Arita
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Akito Funatsu, Yohei Yamamoto, Midori Araki, Fumitoshi Aga, Hideki Mine
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Original Article

Anticholinergic Agents Can Induce Oromandibular Dyskinesia: Hee-Young Shin, Won Tae Yoon, Won Yong Lee; J Mov Disord. 2009;2(2):69-71.; DOI: https://doi.org/10.14802/jmd.09018

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Abstract PDF

Background and Purpose:

Oromandibular dyskinesia (OMD) can occur spontaneously or they can be induced by the conventional dopamine receptor antagonists. Anticholinergic medications have rarely been reported to cause OMD in parkinsonian or non-parkinsonian patients.

Methods:

We analyzed the clinical features of two parkinsonian and one non-parkinsonian patients who experienced OMD after anticholinergic medication.

Results:

Each patient of our cases developed oromandibular symptoms in the temporal regions that were related to the addition of anticholinergic agents, and the symptoms were relieved following the discontinuation of the causative anticholinergic drugs. In one of our case, levodopa alone did not cause dyskinesia but augmented dyskinesia associated with anticholinergics.

Conclusions:

Here we report two parkinsonian and one non-parkinsonian patients with OMD induced by the use of anticholinergic agents. In our cases, we could not find any other precipitating or actual secondary causes for the OMD symptoms in our patients. Furthermore, the fact that the OMD in our cases were ameliorated with cessation of anticholinergics suggests that it may be anticholinergic-induced.

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Joonyoung Ha, Suk Yun Kang, Kyoungwon Baik, Young H. Sohn, Phil Hyu Lee, Min Seok Baek, Jin Yong Hong
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Impact of anticholinergic drugs withdrawal on motor function in patients with Parkinson’s disease
Yasaman Saeedi, Maryam Ghadimi, Mohammad Rohani, Maziar Emamikhah, Gholamali Shahidi, Mehdi Moghaddasi, Seyed Amir Hassan Habibi
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