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Original Articles
A prospective study on post-thalamic stroke Holmes tremor with analysis of semiology, lesion topography and treatment outcomes
Amlan Kusum Dutta, Adreesh Mukherjee, Sudeshna Malakar, Atanu Biswas
Received May 12, 2023  Accepted October 20, 2023  Published online October 20, 2023  
DOI: https://doi.org/10.14802/jmd.23095    [Accepted]
  • 241 View
  • 13 Download
AbstractAbstract PDF
Introduction
Holmes tremor (HT) comprises rest, postural and intention tremor subtypes, usually involving both proximal and distal musculature. Perturbations of nigro-striatal pathways might be fundamental in the pathogenesis of HT along with the cerebello-thalamic connections.
Methods
Nine patients with HT phenotype secondary to thalamic stroke were included. Epidemiological, and clinical records were obtained. Structural and functional brain imaging were done with magnetic resonance imaging (MRI) or computed tomography (CT) and positron emission tomography (PET) respectively. Levodopa was administered in sequentially increasing dosage, with various other drugs in case of inadequate response. Longitudinal follow-up was done for at least three months. The essential tremor rating assessment (TETRAS) scale was used for assessment.
Results
The mean latency from stroke to tremor onset was 50.4 ± 30.60 days (range 21-90 days). Dystonia was the most frequently associated hyperkinetic movement (88.8%). Tremor was bilateral in 22.2% of participants. Clinical response was judged based on reduction of TETRAS score by a prefixed value (≥ 30%), pertaining to which 55.5% (n=5) subjects were classified as responders and rest as non-responders. The responders showed improvement with significantly lower doses of levodopa than remaining (240 ± 54.7 mg vs 400 ± 40.8 mg; p=0.012).
Conclusion
Although levodopa is useful in HT, augmenting the dosage of levodopa beyond a certain point might not add to appreciable clinical benefit. Topography of vascular lesions within the thalamus might additionally influence phenomenology of HT.
Hair Loss: A Well-Known Yet Understudied Symptom in Parkinson’s Disease Patients During Dopaminergic Therapy
Jungyeun Lee, Hwa Jung Ryu, Soon Young Hwang, Seong-Beom Koh
Received May 1, 2023  Accepted September 24, 2023  Published online September 26, 2023  
DOI: https://doi.org/10.14802/jmd.23088    [Epub ahead of print]
  • 222 View
  • 28 Download
AbstractAbstract PDFSupplementary Material
Objective
Hair loss has been reported to occur during dopaminergic therapy in patients with Parkinson’s disease. The mechanism by which dopaminergic therapy induces hair loss is not well understood. Dopamine receptors are present in the hair follicle, where they regulate melanin production. However, the role of dopamine receptors in hair growth is still not well understood. This study aimed to evaluate the prevalence of hair loss and identify factors associated with complaints of hair loss in patients with Parkinson’s disease.
Methods
A cross-sectional design involving 495 Parkinson’s disease patients was applied to evaluate hair loss status. Patients completed a questionnaire, and scalp/hair examinations were performed. Patients with underlying conditions that could affect hair loss and those prescribed medications known to increase the risk of hair loss were excluded. Finally, 291 patients (58.8%) were included for analysis.
Results
Among the 495 patients, 138 (27.9%) reported hair loss. Interestingly, more than half of the patients who complained of hair loss (79 out of 138) did not utilize treatments such as hair products, massage, dietary modifications, or alopecia medications. Hair inspection by a single investigator revealed objective hair loss in 263 patients (53.1%). An analysis of factors associated with hair loss complaints showed that the intake of dopaminergic medications with a levodopa-equivalent daily dose > 448 mg was associated with complaints of hair loss.
Conclusion
Dopaminergic medication is associated with hair loss complaints in Parkinson’s disease patients.
Therapeutic Effect of Levodopa/Carbidopa/Entacapone on Sleep Disturbance in Patients with Parkinson’s Disease
Kye Won Park, Sungyang Jo, Seung Hyun Lee, Yun Su Hwang, Dagyo Lee, Ho-Sung Ryu, Sun Ju Chung
J Mov Disord. 2020;13(3):205-212.   Published online September 9, 2020
DOI: https://doi.org/10.14802/jmd.20055
  • 6,983 View
  • 263 Download
  • 9 Citations
AbstractAbstract PDF
Objective
To investigate the efficacy of levodopa/carbidopa/entacapone (LCE) at bedtime for treating sleep disturbance in patients with Parkinson’s disease (PD) with motor fluctuations.
Methods
Participants included 128 PD patients with motor fluctuations. All patients were assessed for motor, nonmotor, and sleep-specific symptoms using the United Parkinson’s Disease Rating Scale (UPDRS), the Korean version of the Nonmotor Symptom Scale, the Parkinson’s Disease Sleep Scale (PDSS), the Epworth Sleepiness Scale, and the Rapid Eye Movement Sleep Behavior Disorder Screening Questionnaire (RBDSQ). We compared the baseline characteristics of patients with sleep disturbance (PDSS score < 120) and those without sleep disturbance (PDSS score ≥ 120). Thirty-nine patients with sleep disturbance who agreed to take LCE at bedtime completed 3-month follow-ups. We analyzed changes in the scores of motor, nonmotor, and sleep symptom scales over the 3 months.
Results
PD patients with sleep disturbance were at more advanced disease stages and had more severe motor, nonmotor, and sleep symptoms than those without sleep disturbance. Patients who took LCE at night showed improvements in motor (UPDRS part III, p = 0.007) and sleep symptoms (total PDSS, p < 0.001). Sleep features that benefitted from LCE included not only nocturnal motor components but also insomnia (PDSS items 2 and 3, p = 0.005 and p < 0.001) and rapid eye movement behavior disorder (PDSS item 6, p = 0.002; and RBDSQ, p < 0.001).
Conclusion
The use of LCE at bedtime may be a useful treatment for sleep disturbance in advanced PD patients with motor fluctuations.

Citations

Citations to this article as recorded by  
  • Opicapone versus entacapone: Head‐to‐head retrospective data‐based comparison of healthcare resource utilization in people with Parkinson's disease new to catechol‐O‐methyltransferase (COMT) inhibitor treatment
    Glynn Harrison‐Jones, Xiaocong Li Marston, Francesca Morgante, K. Ray Chaudhuri, Guillermo Castilla‐Fernández, Valentina Di Foggia
    European Journal of Neurology.2023; 30(10): 3132.     CrossRef
  • Management of REM sleep behavior disorder: an American Academy of Sleep Medicine systematic review, meta-analysis, and GRADE assessment
    Michael Howell, Alon Y. Avidan, Nancy Foldvary-Schaefer, Roneil G. Malkani, Emmanuel H. During, Joshua P. Roland, Stuart J. McCarter, Rochelle S. Zak, Gerard Carandang, Uzma Kazmi, Kannan Ramar
    Journal of Clinical Sleep Medicine.2023; 19(4): 769.     CrossRef
  • The real-life effect of catechol-O-methyltransferase inhibition on non-motor symptoms in levodopa-treated Parkinson’s disease: opicapone versus entacapone
    Valentina Leta, Daniel J. van Wamelen, Federico Aureli, Vinod Metta, Dhaval Trivedi, Pietro Cortelli, Carmen Rodriguez-Blazquez, Alexandra Rizos, K. Ray Chaudhuri
    Journal of Neural Transmission.2023; 130(7): 925.     CrossRef
  • Non-oral continuous drug delivery based therapies and sleep dysfunction in Parkinson’s disease
    P. Tall, M. A. Qamar, L. Batzu, V. Leta, C. Falup-Pecurariu, K. Ray Chaudhuri
    Journal of Neural Transmission.2023; 130(11): 1443.     CrossRef
  • Tenuigenin promotes non-rapid eye movement sleep via the GABAA receptor and exerts somnogenic effect in a MPTP mouse model of Parkinson's disease
    Di Zhang, Wenjing Zhang, Shumin Deng, Lu Liu, Hua Wei, Fenqin Xue, Hui Yang, Xiaomin Wang, Zheng Fan
    Biomedicine & Pharmacotherapy.2023; 165: 115259.     CrossRef
  • Neurological Insights into Sleep Disorders in Parkinson’s Disease
    Subramanian Thangaleela, Bhagavathi Sundaram Sivamaruthi, Periyanaina Kesika, Subramanian Mariappan, Subramanian Rashmi, Thiwanya Choeisoongnern, Phakkharawat Sittiprapaporn, Chaiyavat Chaiyasut
    Brain Sciences.2023; 13(8): 1202.     CrossRef
  • Real‐world considerations regarding the use of the combination of levodopa, carbidopa, and entacapone (Stalevo®) in Parkinson's disease
    Heinz Reichmann
    European Journal of Neurology.2023; 30(S2): 15.     CrossRef
  • The Home-Based Sleep Laboratory
    Yael Hanein, Anat Mirelman, Anat Mirelman, E. Ray Dorsey, Patrik Brundin, Bastiaan R. Bloem
    Journal of Parkinson's Disease.2021; 11(s1): S71.     CrossRef
  • Shudi Pingchan Decoction combined with repetitive transcranial magnetic stimulation in the treatment of Parkinson’s disease with sleep disorders
    Qing Ye, Xiqun Chen, Yuqing Hu, Jie Zhou, Chen Gao, Zhenguo Liu
    Traditional Medicine and Modern Medicine.2020; 03(02): 85.     CrossRef
Case Report
Dopa-Responsive Dystonia: A Male Patient Inherited a Novel GCH1 Deletion from an Asymptomatic Mother
Wendi Wang, Baozhong Xin, Heng Wang
J Mov Disord. 2020;13(2):150-153.   Published online March 18, 2020
DOI: https://doi.org/10.14802/jmd.19069
  • 5,142 View
  • 136 Download
  • 2 Citations
AbstractAbstract PDF
Dopa-responsive dystonia (DRD) is a complex genetic disorder with either autosomal dominant or autosomal recessive inheritance, with autosomal dominant being more frequent. Autosomal dominant DRD is known to be caused by mutations in the GCH1 gene, with incomplete penetrance frequently reported, particularly in males. Here, we report a male patient with DRD caused by exon 1 deletion in the GCH1 gene inherited from the asymptomatic mother. The patient had an atypical presentation, notably with no dystonia, and underwent extensive workup for a myriad of neuromuscular disorders before a low-dose L-dopa trial and confirmatory genetic testing were performed. Our experience with this family highlights an atypical presentation of DRD and prompts us to consider the genetic complexity of DRD.

Citations

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  • Detection of Single-Nucleotide and Copy Number Defects Underlying Hyperphenylalaninemia by Next-Generation Sequencing
    Elisabetta Anna Tendi, Giovanna Morello, Maria Guarnaccia, Valentina La Cognata, Salvatore Petralia, Maria Anna Messina, Concetta Meli, Agata Fiumara, Martino Ruggieri, Sebastiano Cavallaro
    Biomedicines.2023; 11(7): 1899.     CrossRef
  • Study on Mechanism of Cumulative Directional Blasting of Brittle Karst Limestone in the Guizhou Province
    Jie Hu, Yiping Zhang, Chengcheng Fang, Yusong Miao, Xin Zhao, Dengguo Liu, José António Fonseca de Oliveira Correia
    Advances in Materials Science and Engineering.2023; 2023: 1.     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
  • 8,390 View
  • 275 Download
  • 7 Citations
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  
  • 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
  • 8,654 View
  • 246 Download
  • 14 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  
  • 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
Sleepiness and Depression in Parkinson’s Disease Patients Treated with Ropinirole and Levodopa
Suk Yun Kang, Ho-Sung Ryu, Mun-Kyung Sunwoo, Sang-Jin Kim, Jong-Sam Baik, Mee-Young Park, Hyung-Eun Park, Joong-Seok Kim, Kyum-Yil Kwon, Seong-Beom Koh, Young-Eun Kim, Mi-Kyong Lee, Jong-Min Kim, Sun Ju Chung, Young-Ho Sohn
J Mov Disord. 2017;10(3):123-129.   Published online September 22, 2017
DOI: https://doi.org/10.14802/jmd.17048
  • 8,465 View
  • 190 Download
  • 10 Citations
AbstractAbstract PDF
Objective
We aimed to investigate the effect of ropinirole on excessive daytime sleepiness (EDS) and depression in Parkinson’s disease (PD) with a large population.
Methods
We conducted a cross-sectional observational study at nine hospitals in Korea between April 24, 2013, and April 22, 2015. We analyzed the demographic and clinical features, other medical history, history of antiparkinsonian medication within 6 months, Hoehn and Yahr stage (HY stage), Unified Parkinson’s Disease Rating Scale (UPDRS) part II and III, Epworth Sleepiness Scale (ESS), and 30-item Geriatric Depression Scale (GDS-30).
Results
Four-hundred-thirteen patients with PD (mean age: 65.2 ± 9.0 years; men: 227 patients) were analyzed. Multivariate logistic regression analysis showed that age at examination, UPDRS II, and GDS-30 were independent risk factors for EDS and that sex, UPDRS II, and ESS were independent risk factors for depression.
Conclusion
Our large group study did not find any significant associations of ropinirole with EDS and depression in Korean PD patients.

Citations

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  • Associations between non-motor symptoms and patient characteristics in Parkinson’s disease: a multicenter cross-sectional study
    Remi Morimoto, Mutsumi Iijima, Yasuyuki Okuma, Keisuke Suzuki, Fumihito Yoshii, Shigeru Nogawa, Takashi Osada, Kazuo Kitagawa
    Frontiers in Aging Neuroscience.2023;[Epub]     CrossRef
  • Excessive Daytime Sleepiness in Parkinson’s Disease
    Hanshu Liu, Jingwen Li, Xinyi Wang, Jinsha Huang, Tao Wang, Zhicheng Lin, Nian Xiong
    Nature and Science of Sleep.2022; Volume 14: 1589.     CrossRef
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    Fei Feng, YingYing Cai, YanBing Hou, Ruwei Ou, Zheng Jiang, HuiFang Shang
    Parkinsonism & Related Disorders.2021; 85: 133.     CrossRef
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    Gianpaolo Maggi, Luigi Trojano, Paolo Barone, Gabriella Santangelo
    Neuropsychology Review.2021; 31(4): 643.     CrossRef
  • Longitudinal risk factors for developing depressive symptoms in Parkinson's disease
    Tarek Antar, Huw R. Morris, Faraz Faghri, Hampton L. Leonard, Mike A. Nalls, Andrew B. Singleton, Hirotaka Iwaki
    Journal of the Neurological Sciences.2021; 429: 117615.     CrossRef
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    Jiali Zhu, Min Chen
    Medicine.2021; 100(46): e27653.     CrossRef
  • Pramipexole regulates depression-like behavior via dopamine D3 receptor in a mouse model of Parkinson’s disease
    Shi-Zhuang Wei, Xiao-Yu Yao, Chen-Tao Wang, An-Qi Dong, Dan Li, Yu-Ting Zhang, Chao Ren, Jin-Bao Zhang, Cheng-Jie Mao, Fen Wang, Chun-Feng Liu
    Brain Research Bulletin.2021; 177: 363.     CrossRef
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    Mahino Fatima, Mir Hilal Ahmad, Saurabh Srivastav, Moshahid Alam Rizvi, A.C. Mondal
    Neurochemistry International.2020; 136: 104730.     CrossRef
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    Silvia Rota, Iro Boura, Lucia Batzu, Nataliya Titova, Peter Jenner, Cristian Falup-Pecurariu, K Ray Chaudhuri
    Expert Review of Neurotherapeutics.2020; 20(9): 953.     CrossRef
  • An Investigation on the Clinical Features and Neurochemical Changes in Parkinson's Disease With Depression
    Teng-Hong Lian, Peng Guo, Li-Jun Zuo, Yang Hu, Shu-Yang Yu, Li Liu, Zhao Jin, Qiu-Jin Yu, Rui-Dan Wang, Li-Xia Li, Ying-Shan Piao, Wei Zhang
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Case Reports
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
  • 20,201 View
  • 87 Download
  • 4 Citations
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

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  • 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
Thrombocytopenia Associated with Levodopa Treatment
Ku-Eun Lee, Hyun Seok Kang, Hyun-Jeung Yu, Sook Young Roh
J Mov Disord. 2013;6(1):21-22.
DOI: https://doi.org/10.14802/jmd.13005
  • 54,131 View
  • 71 Download
  • 2 Citations
AbstractAbstract PDF

There were few cases of thrombocytopenia associated with levodopa. Herein, we report a patient with Parkinson’s disease, who suffered thrombocytopenia related to long-term use of levodopa.

Citations

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  • High rates of blood transfusion associated with Parkinson’s disease
    Shane Shahrestani, Julian Gendreau, Ali R. Tafreshi, Nolan J. Brown, Khashayar Dashtipour
    Neurological Sciences.2022; 43(8): 4761.     CrossRef
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    Sheng-Che Chou, Chun-Hwei Tai, Sheng-Hong Tseng
    Scientific Reports.2022;[Epub]     CrossRef
Invited Review
Apomorphine and Levodopa Infusion Therapies for Advanced Parkinson’s Disease
Angelo Antonini
J Mov Disord. 2009;2(1):4-9.
DOI: https://doi.org/10.14802/jmd.09002
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AbstractAbstract PDF

Continuous infusion of levodopa or apomorphine provide constant dopaminergic stimulations are good alternatives to deep brain stimulation to control motor fluctuations in patients with advanced Parkinson’s disease (PD). Apomorphine provides motor benefit similar to dopamine, but its long-term use is limited by compliance, mostly injection site skin reactions. Administration of levodopa/carbidopa by continuous duodenal infusion allows replacement of all oral medications and permits achievement of a satisfactory therapeutic response paralleled by a reduction in motor complication severity. However, this procedure is more invasive than apomorphine as it requires a percutaneous endoscopic gastrostomy Clinical experience with infusions shows that continuous dopaminergic stimulation of dopaminergic medications reduces dyskinesia and widens the therapeutic window in advanced PD.

Citations

Citations to this article as recorded by  
  • Safety and tolerability of long-term apomorphine infusion in advanced Parkinson's disease: an Indian multi-center (APO-IND) experience
    Vinod Metta, Rajinder K. Dhamija, Lucia Batzu, Rukmini Mrudula, Natuva Sai Sampath Kumar, Arunan S., Cristian Falup-Pecurariu, Carmen Rodriguez-Blazquez, Vinay Goyal, Prashanth L.K., Kalyan Bhattacharya, Suresh Kumar, Kallol Ray Chaudhuri, Rupam Borgohain
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  • A Randomized Trial Assessing the Safety, Pharmacokinetics, and Efficacy During Morning Off of AZ‐009
    Eva Thijssen, Jonas den Heijer, David Puibert, Laurence Moss, Mingzu Lei, David Hasegawa, Kyo Keum, Ken Mochel, Mohammed Ezzeldin Sharaf, Tom Alfredson, Wenxiang Zeng, Emilie van Brummelen, Tatjana Naranda, Geert Jan Groeneveld
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  • Why do ‘OFF’ periods still occur during continuous drug delivery in Parkinson’s disease?
    Silvia Rota, Daniele Urso, Daniel J. van Wamelen, Valentina Leta, Iro Boura, Per Odin, Alberto J. Espay, Peter Jenner, K. Ray Chaudhuri
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    Nicki Niemann, Andrew Billnitzer, Joseph Jankovic
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  • Subcutaneous apomorphine in advanced Parkinson’s disease and its use in Indian population
    Vinod Metta, Rupam Borgohain, Prashanth L Kukkle, Rukmini Mridula, Pankaj Agarwal, Asha Kishore, Vinay Goyal, Ray Chaudhuri
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  • Platinum/Graphene Oxide Coated Microfabricated Arrays for Multinucleus Neural Activities Detection in the Rat Models of Parkinson’s Disease Treated by Apomorphine
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  • Apomorphine en perfusion sous-cutanée continue dans la maladie de Parkinson : le point de vue clinique
    S. Drapier, M. Auffret, M. Vérin, P. Sauleau
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Original Article
Relationship Between the Striatal and Cerebellar Glucose Metabolism and the Response to Levodopa Treatment in Patients With Multiple System Atrophy
Chul Hyoung Lyoo, Seung Hun Oh, Ki Ook Lee, Seung Yeob Lee, Young Hoon Ryu, Myung Sik Lee
J Mov Disord. 2008;1(1):26-32.
DOI: https://doi.org/10.14802/jmd.08005
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AbstractAbstract PDF
Introduction:

About two thirds of the patients with multiple system atrophy (MSA) do not respond to levodopa treatment. Postmortem pathological studies and one retrospective [18F]-deoxyglucose positron emission tomography (FDGPET) study attributed such poor response to the striatal degeneration. We prospectively investigated the relationship between levodopa responsiveness and the metabolic activities of the striatum and cerebellum in MSA patients.

Methods:

In 39 patients with MSA, the UPDRS motor score was assessed and two sets of timed motor tests were perform ed before and after the levodopa treatment. After quantitative FDG PET and baseline evaluation, treatment w as started with 3 tablets of Sinemet® 25/250 mg a day. Clinical assessments were performed monthly for three months. Metabolic activities of the caudate, anterior putamen, posterior putamen, cerebellar cortex and cerebellar vermis were measured. We compared the measurements with mean percentage changes of motor function. Also, using statistical parametric mapping (SPM) analysis, we tried to find brain areas in which metabolism correlated with the clinical changes.

Results:

Mean percentage improvements of UPDRS motor scores w ere correlated with glucose metabolism in the posterior putamen and cerebellar vermis. The mean percentage improvements of performance in Purdue peg board test correlated with the glucose metabolism in the cerebellar cortex and vermis. In SPM analysis, cerebellar glucose metabolism correlated with the improvement of UPDRS motor score and the performance of two timed motor tests.

Conclusion:

The integrity of cerebellum, as well as posterior putamen, may be an important factor for showing the response to levodopa.


JMD : Journal of Movement Disorders