Skip Navigation
Skip to contents

JMD : Journal of Movement Disorders

OPEN ACCESS
SEARCH
Search

Search

Page Path
HOME > Search
8 "Dyskinesia"
Filter
Filter
Article category
Keywords
Publication year
Authors
Funded articles
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
  • 4,370 View
  • 288 Download
  • 2 Web of Science
  • 3 Crossref
AbstractAbstract PDFSupplementary Material
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.

Citations

Citations to this article as recorded by  
  • 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
  • 9,322 View
  • 284 Download
  • 9 Web of Science
  • 9 Crossref
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • 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
  • Effects of Intracerebral Aminophylline Dosing on Catalepsy and Gait in an Animal Model of Parkinson’s Disease
    Érica de Moraes Santos Corrêa, Gustavo Christofoletti, Albert Schiaveto de Souza
    International Journal of Molecular Sciences.2024; 25(10): 5191.     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
  • 9,475 View
  • 254 Download
  • 11 Web of Science
  • 14 Crossref
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  
  • 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
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
  • 8,079 View
  • 190 Download
  • 7 Web of Science
  • 7 Crossref
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • 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
  • 8,748 View
  • 174 Download
  • 6 Web of Science
  • 5 Crossref
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • Tongue dystonia as CIS and presenting symptom of multiple sclerosis
    Farid Shamlou, Narges Ebrahimi, Ahmad Chitsaz
    Neuroimmunology Reports.2024; 5: 100191.     CrossRef
  • The Pathogenesis of Paroxysmal Kinesigenic Dyskinesia: Current Concepts
    Zi‐yi Li, Wo‐tu Tian, Xiao‐jun Huang, Li Cao
    Movement Disorders.2023; 38(4): 537.     CrossRef
  • Recommendations for the diagnosis and treatment of paroxysmal kinesigenic dyskinesia: an expert consensus in China
    Li Cao, Xiaojun Huang, Ning Wang, Zhiying Wu, Cheng Zhang, Weihong Gu, Shuyan Cong, Jianhua Ma, Ling Wei, Yanchun Deng, Qi Fang, Qi Niu, Jin Wang, Zhaoxia Wang, You Yin, Jinyong Tian, Shufen Tian, Hongyan Bi, Hong Jiang, Xiaorong Liu, Yang Lü, Meizhen Sun
    Translational Neurodegeneration.2021;[Epub]     CrossRef
  • Les mouvements anormaux : mise au point
    M. Béreau, C. Tranchant
    La Revue de Médecine Interne.2018; 39(8): 641.     CrossRef
  • Lesion correlates of secondary paroxysmal dyskinesia in multiple sclerosis
    Kilian Fröhlich, Klemens Winder, Ralf A. Linker, Konstantin Huhn, Tobias Engelhorn, Arnd Dörfler, De-Hyung Lee, Stefan Schwab, Frank Seifert
    Journal of Neurology.2018; 265(10): 2277.     CrossRef
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
  • 20,708 View
  • 87 Download
  • 4 Web of Science
  • 4 Crossref
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • Rhabdomyolysis secondary to severe tic fits
    Ka Loong Kelvin Au, Shannon Chiu, Irene A Malaty
    BMJ Case Reports.2021; 14(3): e239874.     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
  • 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
    Tai N. Tran, Trang N. N. Vo, Karen Frei, Daniel D. Truong
    Journal of Neural Transmission.2018; 125(8): 1109.     CrossRef
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
  • 62,832 View
  • 70 Download
  • 4 Crossref
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • The oral manifestations of Huntington's disease: A systematic review of prevalence
    Luciana Munhoz, Ashjan Qasim Jabbar, William José e Silva Filho, Aline Yukari Nagai, Emiko Saito Arita
    Oral Diseases.2023; 29(1): 62.     CrossRef
  • Orofacial Dyskinesia and Intractable Hiccups in a Patient with Varicella-zoster Virus Encephalomyelitis
    Akito Funatsu, Yohei Yamamoto, Midori Araki, Fumitoshi Aga, Hideki Mine
    Internal Medicine.2023; 62(1): 119.     CrossRef
  • Harmine prevents 3-nitropropionic acid-induced neurotoxicity in rats via enhancing NRF2-mediated signaling: Involvement of p21 and AMPK
    Mohamed Z. Habib, Mariane G. Tadros, Hadwa A. Abd-Alkhalek, Magda I. Mohamad, Dalia M. Eid, Fatma E. Hassan, Hend Elhelaly, Yasser el Faramawy, Sawsan Aboul-Fotouh
    European Journal of Pharmacology.2022; 927: 175046.     CrossRef
  • Management of Traumatic Ulcerations of Lips in a Case of Huntington’s Disease: A Novel Application of Essix Retainer
    Mohamed Iqbal J
    Journal of Indian Orthodontic Society.2021; 55(4): 415.     CrossRef
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
  • 18,640 View
  • 76 Download
  • 3 Crossref
AbstractAbstract 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.

Citations

Citations to this article as recorded by  
  • Factors associated with anticholinergic-induced oral-buccal-lingual dyskinesia in Parkinson’s disease
    Joonyoung Ha, Suk Yun Kang, Kyoungwon Baik, Young H. Sohn, Phil Hyu Lee, Min Seok Baek, Jin Yong Hong
    Journal of Movement Disorders.2024; 17(1): 109.     CrossRef
  • 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
    Clinical Neurology and Neurosurgery.2021; 202: 106480.     CrossRef
  • Treatment of Tardive Dyskinesia: A General Overview with Focus on the Vesicular Monoamine Transporter 2 Inhibitors
    Nicki Niemann, Joseph Jankovic
    Drugs.2018; 78(5): 525.     CrossRef

JMD : Journal of Movement Disorders Twitter