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Most-read articles are from the articles published in 2022 during the last three month.

Review Article
Functional Movement Disorders: Updates and Clinical Overview
Jung E Park
J Mov Disord. 2024;17(3):251-261.   Published online July 1, 2024
DOI: https://doi.org/10.14802/jmd.24126
  • 1,345 View
  • 151 Download
AbstractAbstract PDF
Functional movement disorder (FMD) is a type of functional neurological disorder that is common but often difficult to diagnose or manage. FMD can present as various phenotypes, including tremor, dystonia, myoclonus, gait disorders, and parkinsonism. Conducting a clinical examination appropriate for assessing a patient with suspected FMD is important, and various diagnostic testing maneuvers may also be helpful. Treatment involving a multidisciplinary team, either outpatient or inpatient, has been found to be most effective. Examples of such treatment protocols are also discussed in this review. While recognition and understanding of the disorder has improved over the past few decades, as well as the development of treatments, it is not uncommon for patients and physicians to continue to experience various difficulties when dealing with this disorder. In this review, I provide a practical overview of FMD and discuss how the clinical encounter itself can play a role in patients’ acceptance of the diagnosis. Recent neuroimaging studies that aid in understanding the pathophysiology are also discussed.
Brief communication
COVID-19 Vaccine-Related Movement Disorders: A Systematic Review
Grace Elysse D. Angeles, Lowrence Precious C. Dichoso, Roland Dominic G. Jamora
J Mov Disord. 2024;17(3):322-327.   Published online March 19, 2024
DOI: https://doi.org/10.14802/jmd.24001
  • 2,051 View
  • 104 Download
  • 2 Comments
AbstractAbstract PDFSupplementary Material
Objective
Since the release of vaccines against coronavirus disease 2019 (COVID-19), there have been reports of vaccine-related neurologic complications. This study aimed to perform a descriptive systematic review of movement disorders associated with COVID-19 vaccines.
Methods
We described the demographics, clinical presentation, management, outcomes, and proposed pathomechanism of the patients. A systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A standardized tool was used to assess the quality of the cases.
Results
We identified 8 articles that met our inclusion criteria; these articles included 10 patients who developed movement disorders after vaccination. The majority were males (n = 8), with a median age of 64.5 years. The most common movement disorder was hemichorea. The rest presented with generalized chorea with myoclonus, cervical dystonia, and akathisia. Most patients respond to immunotherapy. The standardized tool used showed that most studies had a low risk of bias.
Conclusion
The reported incidence of vaccine-related movement disorders was low based on available published cases.
Review Article
Current Status and Future Perspectives on Stem Cell-Based Therapies for Parkinson’s Disease
Young Cha, Tae-Yoon Park, Pierre Leblanc, Kwang-Soo Kim
J Mov Disord. 2023;16(1):22-41.   Published online January 12, 2023
DOI: https://doi.org/10.14802/jmd.22141
  • 8,560 View
  • 532 Download
  • 15 Web of Science
  • 13 Crossref
AbstractAbstract PDF
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease, affecting 1%–2% of the population over the age of 65. As the population ages, it is anticipated that the burden on society will significantly escalate. Although symptom reduction by currently available pharmacological and/or surgical treatments improves the quality of life of many PD patients, there are no treatments that can slow down, halt, or reverse disease progression. Because the loss of a specific cell type, midbrain dopamine neurons in the substantia nigra, is the main cause of motor dysfunction in PD, it is considered a promising target for cell replacement therapy. Indeed, numerous preclinical and clinical studies using fetal cell transplantation have provided proof of concept that cell replacement therapy may be a viable therapeutic approach for PD. However, the use of human fetal cells remains fraught with controversy due to fundamental ethical, practical, and clinical limitations. Groundbreaking work on human pluripotent stem cells (hPSCs), including human embryonic stem cells and human induced pluripotent stem cells, coupled with extensive basic research in the stem cell field offers promising potential for hPSC-based cell replacement to become a realistic treatment regimen for PD once several major issues can be successfully addressed. In this review, we will discuss the prospects and challenges of hPSC-based cell therapy for PD.

Citations

Citations to this article as recorded by  
  • RNA-based controllers for engineering gene and cell therapies
    Kei Takahashi, Kate E Galloway
    Current Opinion in Biotechnology.2024; 85: 103026.     CrossRef
  • Precision Medicine in Parkinson's Disease Using Induced Pluripotent Stem Cells
    Min Seong Kim, Hyesoo Kim, Gabsang Lee
    Advanced Healthcare Materials.2024;[Epub]     CrossRef
  • A recent update on drugs and alternative approaches for parkinsonism
    Sneha Kispotta, Debajyoti Das, Shakti Ketan Prusty
    Neuropeptides.2024; 104: 102415.     CrossRef
  • Recent Research Trends in Neuroinflammatory and Neurodegenerative Disorders
    Jessica Cohen, Annette Mathew, Kirk D. Dourvetakis, Estella Sanchez-Guerrero, Rajendra P. Pangeni, Narasimman Gurusamy, Kristina K. Aenlle, Geeta Ravindran, Assma Twahir, Dylan Isler, Sara Rukmini Sosa-Garcia, Axel Llizo, Alison C. Bested, Theoharis C. Th
    Cells.2024; 13(6): 511.     CrossRef
  • Continuous immunosuppression is required for suppressing immune responses to xenografts in non-human primate brains
    Su Feng, Ting Zhang, Zhengxiao He, Wenchang Zhang, Yingying Chen, Chunmei Yue, Naihe Jing
    Cell Regeneration.2024;[Epub]     CrossRef
  • The role of neuroinflammation in neurodegenerative diseases: current understanding and future therapeutic targets
    Alhamdu Adamu, Shuo Li, Fankai Gao, Guofang Xue
    Frontiers in Aging Neuroscience.2024;[Epub]     CrossRef
  • Past, present, and future of cell replacement therapy for parkinson’s disease: a novel emphasis on host immune responses
    Tae-Yoon Park, Jeha Jeon, Young Cha, Kwang-Soo Kim
    Cell Research.2024; 34(7): 479.     CrossRef
  • Dopamine synthesis and transport: current and novel therapeutics for parkinsonisms
    Mary Dayne Sia Tai, Gloria Gamiz-Arco, Aurora Martinez
    Biochemical Society Transactions.2024; 52(3): 1275.     CrossRef
  • Experimental models of Parkinson's disease: Challenges and Opportunities
    Roshan Lal, Aditi singh, Shivam watts, Kanwaljit Chopra
    European Journal of Pharmacology.2024; 980: 176819.     CrossRef
  • The prospective role of mesenchymal stem cells in Parkinson's disease
    Pratima Tambe, Vaishali Undale, Avinash Sanap, Ramesh Bhonde, Nishant Mante
    Parkinsonism & Related Disorders.2024; : 107087.     CrossRef
  • Potential for Therapeutic-Loaded Exosomes to Ameliorate the Pathogenic Effects of α-Synuclein in Parkinson’s Disease
    David J. Rademacher
    Biomedicines.2023; 11(4): 1187.     CrossRef
  • Neural Stem Cell Therapies: Promising Treatments for Neurodegenerative Diseases
    Amir Gholamzad, Hadis Sadeghi, Maryam Azizabadi Farahani, Ali Faraji, Mahya Rostami, Sajad Khonche, Shirin Kamrani, Mahsa Khatibi, Omid Moeini, Seyed Armit Hosseini, Mohammadmatin Nourikhani, Mehrdad Gholamzad
    Neurology Letters.2023; 2(2): 55.     CrossRef
  • Should continuous dopaminergic stimulation be a standard of care in advanced Parkinson’s disease?
    Z. Pirtošek, V. Leta, P. Jenner, M. Vérin
    Journal of Neural Transmission.2023; 130(11): 1395.     CrossRef
Original Article
Umami and Other Taste Perceptions in Patients With Parkinson’s Disease
Priya Jagota, Nattida Chotechuang, Chanawat Anan, Teeraparp Kitjawijit, Chanchai Boonla, Roongroj Bhidayasiri
J Mov Disord. 2022;15(2):115-123.   Published online March 22, 2022
DOI: https://doi.org/10.14802/jmd.21058
  • 6,467 View
  • 237 Download
  • 4 Web of Science
  • 4 Crossref
AbstractAbstract PDF
Objective
Studies of taste perceptions in Parkinson’s disease (PD) patients have been controversial, and none of these studies have assessed umami taste. This study aimed to assess umami, along with the other 4 taste functions in PD patients.
Methods
Participants were tested for gustation using the modified filter paper disc method and olfaction using the modified Sniffin’ Stick-16 (mSS-16) test (only 14 culturally suitable items were used). A questionnaire evaluated patients’ subjective olfactory and gustatory dysfunction, taste preference, appetite, and food habits.
Results
A total of 105 PD patients and 101 age- and sex-matched controls were included. The body mass index (BMI) of PD patients was lower than that of controls (PD = 22.62, controls = 23.86, p = 0.028). The mSS-16 score was 10.7 for controls and 6.4 for PD patients (p < 0.001) (normal ≥ 9). Taste recognition thresholds (RTs) for sweet, salty, sour, bitter and umami tastes were significantly higher in PD, indicating poorer gustation. All taste RTs correlated with each other, except for umami. Most patients were unaware of their dysfunction. Patients preferred sweet, salty and umami tastes more than the controls. Dysgeusia of different tastes in patients was differentially associated with poorer discrimination of tastes, an inability to identify the dish and adding extra seasoning to food. BMI and mSS-16 scores showed no correlation in either patients or controls.
Conclusion
PD patients have dysgeusia for all five tastes, including umami, which affects their appetite and diet. Patients preferred sweet, salty and umami tastes. This information can help adjust patients’ diets to improve their nutritional status.

Citations

Citations to this article as recorded by  
  • The missing piece of the puzzle – The key role of the dietitian in the management of Parkinson's disease
    Richelle Flanagan, Carley Rusch, Fiona E. Lithander, Indu Subramanian
    Parkinsonism & Related Disorders.2024; 121: 106021.     CrossRef
  • Body mass index in patients with Parkinson’s disease: a systematic review
    Yinghui Li, Yumei Liu, Chuanning Du, Jun Wang
    Journal of Neurophysiology.2024; 131(2): 311.     CrossRef
  • Apnea behavior in early- and late-stage mouse models of Parkinson's disease: Cineradiographic analysis of spontaneous breathing, acute stress, and swallowing
    Lorena Roberta de Souza Mendes Kawamura, Max Sarmet, Priscila Sales de Campos, Sachiko Takehara, Yasuhiro Kumei, Jorge Luis Lopes Zeredo
    Respiratory Physiology & Neurobiology.2024; 323: 104239.     CrossRef
  • Gustatory dysfunction is related to Parkinson's disease: A systematic review and meta‐analysis
    Il‐Youp Kwak, Kyung Soo Kim, Hyun Jin Min
    International Forum of Allergy & Rhinology.2023; 13(10): 1949.     CrossRef
Review Articles
α-Synuclein: A Promising Biomarker for Parkinson’s Disease and Related Disorders
Taku Hatano, Ayami Okuzumi, Gen Matsumoto, Taiji Tsunemi, Nobutaka Hattori
J Mov Disord. 2024;17(2):127-137.   Published online April 9, 2024
DOI: https://doi.org/10.14802/jmd.24075
  • 2,947 View
  • 332 Download
  • 1 Crossref
AbstractAbstract PDF
Mutations in the SNCA gene, which encodes α-synuclein (α-syn), play a key role in the development of genetic Parkinson’s disease (PD). α-Syn is a major component of Lewy bodies in PD and glial cytoplasmic inclusions in multiple system atrophy (MSA). Rapid eye movement sleep behavior disorder patients often progress to PD, dementia with Lewy bodies, or MSA, which are collectively known as α-synucleinopathies. The loss of dopaminergic neurons with Lewy bodies precedes motor dysfunction in these diseases, but the mechanisms of neurodegeneration due to α-syn aggregation are poorly understood. Monitoring α-syn aggregation in vivo could serve as a diagnostic biomarker and help elucidate pathogenesis, necessitating a simple and accurate detection method. Seed amplification assays (SAAs), such as real-time quaking-induced conversion and protein misfolding cyclic amplification, are used to detect small amounts of abnormally structured α-syn protofibrils, which are central to aggregation. These methods are promising for the early diagnosis of α-synucleinopathy. Differences in α-syn filament structures between α-synucleinopathies, as observed through transmission electron microscopy and cryo-electron microscopy, suggest their role in the pathogenesis of neurodegeneration. SAAs may differentiate between subtypes of α-synucleinopathy and other diseases. Efforts are also being made to identify α-syn from blood using various methods. This review introduces body fluid α-syn biomarkers based on pathogenic α-syn seeds, which are expected to redefine α-synucleinopathy diagnosis and staging, improving clinical research accuracy and facilitating biomarker development.

Citations

Citations to this article as recorded by  
  • Selective detection of alpha synuclein amyloid fibrils by faradaic and non-faradaic electrochemical impedance spectroscopic approaches
    Hussaini Adam, Subash C.B. Gopinath, Hemavathi Krishnan, Tijjani Adam, Makram A. Fakhri, Evan T. Salim, A. Shamsher, Sreeramanan Subramaniam, Yeng Chen
    Bioelectrochemistry.2025; 161: 108800.     CrossRef
Fighting Against the Clock: Circadian Disruption and Parkinson’s Disease
Yen-Chung Chen, Wei-Sheng Wang, Simon J G Lewis, Shey-Lin Wu
J Mov Disord. 2024;17(1):1-14.   Published online November 21, 2023
DOI: https://doi.org/10.14802/jmd.23216
  • 3,428 View
  • 336 Download
AbstractAbstract PDF
Circadian disruption is being increasingly recognized as a critical factor in the development and progression of Parkinson’s disease (PD). This review aims to provide an in-depth overview of the relationship between circadian disruption and PD by exploring the molecular, cellular, and behavioral aspects of this interaction. This review will include a comprehensive understanding of how the clock gene system and transcription–translation feedback loops function and how they are diminished in PD. The article also discusses the role of clock genes in the regulation of circadian rhythms, as well as the impact of clock gene dysregulation on mitochondrial function, oxidative stress, and neuroinflammation, including the microbiota-gut-brain axis, which have all been proposed as being crucial mechanisms in the pathophysiology of PD. Finally, this review highlights potential therapeutic strategies targeting the clock gene system and circadian rhythm for the treatment of PD.
Adult-Onset Genetic Leukoencephalopathies With Movement Disorders
Mu-Hui Fu, Yung-Yee Chang
J Mov Disord. 2023;16(2):115-132.   Published online March 7, 2023
DOI: https://doi.org/10.14802/jmd.22127
  • 5,672 View
  • 429 Download
  • 1 Comments
AbstractAbstract PDF
Genetic leukoencephalopathies (GLEs) are a group of white matter abnormalities with heterogeneous radiological and phenotypic features. Although these conditions have mostly been described in children, adult-onset cases are increasingly recognized owing to the widespread use of neuroimaging and advances in molecular genetic testing. The disease course is often progressive with a varied spectrum of presentations, trapping neurologists in the dilemma of differential diagnosis. Movement disorders are among the most common symptoms, and their diversity makes diagnosis challenging. In this review, we focus on adult-onset GLEs with movement disorders and offer a step-by-step diagnostic approach by clarifying the phenomenology of movement, advising investigations for acquired causes, describing the clinical and radiological clues to each disease, emphasizing the limitations of advanced molecular testing, and discussing the future application of artificial intelligence. We provide a list summarizing the leukoencephalopathies associated with different categories of movement disorders. In addition to guiding clinicians on how to narrow the list of differential diagnoses with the tools currently available, another aim of this review is to emphasize the inevitable trend toward applying advanced technology in diagnosing these difficult diseases.
Original Article
Association Between Exposure to Particulate Matter and the Incidence of Parkinson’s Disease: A Nationwide Cohort Study in Taiwan
Ting-Bin Chen, Chih-Sung Liang, Ching-Mao Chang, Cheng-Chia Yang, Hwa-Lung Yu, Yuh-Shen Wu, Winn-Jung Huang, I-Ju Tsai, Yuan-Horng Yan, Cheng-Yu Wei, Chun-Pai Yang
J Mov Disord. 2024;17(3):313-321.   Published online June 18, 2024
DOI: https://doi.org/10.14802/jmd.24003
  • 1,166 View
  • 37 Download
AbstractAbstract PDF
Objective
Emerging evidence suggests that air pollution exposure may increase the risk of Parkinson’s disease (PD). We aimed to investigate the association between exposure to fine particulate matter (PM2.5) and the risk of incident PD nationwide.
Methods
We utilized data from the Taiwan National Health Insurance Research Database, which is spatiotemporally linked with air quality data from the Taiwan Environmental Protection Administration website. The study population consisted of participants who were followed from the index date (January 1, 2005) until the occurrence of PD or the end of the study period (December 31, 2017). Participants who were diagnosed with PD before the index date were excluded. To evaluate the association between exposure to PM2.5 and incident PD risk, we employed Cox regression to estimate the hazard ratio and 95% confidence interval (CI).
Results
A total of 454,583 participants were included, with a mean (standard deviation) age of 63.1 (9.9) years and a male proportion of 50%. Over a mean follow-up period of 11.1 (3.6) years, 4% of the participants (n = 18,862) developed PD. We observed a significant positive association between PM2.5 exposure and the risk of PD, with a hazard ratio of 1.22 (95% CI, 1.20–1.23) per interquartile range increase in exposure (10.17 μg/m3) when adjusting for both SO2 and NO2.
Conclusion
We provide further evidence of an association between PM2.5 exposure and the risk of PD. These findings underscore the urgent need for public health policies aimed at reducing ambient air pollution and its potential impact on PD.
Review Article
Multiple System Atrophy: Advances in Diagnosis and Therapy
Hirohisa Watanabe, Sayuri Shima, Yasuaki Mizutani, Akihiro Ueda, Mizuki Ito
J Mov Disord. 2023;16(1):13-21.   Published online December 20, 2022
DOI: https://doi.org/10.14802/jmd.22082
  • 5,191 View
  • 464 Download
  • 4 Web of Science
  • 4 Crossref
AbstractAbstract PDF
This review summarizes improvements in understanding the pathophysiology and early clinical symptoms of multiple system atrophy (MSA) and advancements in diagnostic methods and disease-modifying therapies for the condition. In 2022, the Movement Disorder Society proposed new diagnostic criteria to develop disease-modifying therapies and promote clinical trials of MSA since the second consensus was proposed in 2008. Regarding pathogenesis, cutting-edge findings have accumulated on the interactions of α-synuclein, neuroinflammation, and oligodendroglia with neurons. In neuroimaging, introducing artificial intelligence, machine learning, and deep learning has notably improved diagnostic accuracy and individual analyses. Advancements in treatment have also been achieved, including immunotherapy therapy against α-synuclein and serotonin-targeted and mesenchymal stem cell therapies, which are thought to affect several aspects of the disease, including neuroinflammation. The accelerated progress in clarifying the pathogenesis of MSA over the past few years and the development of diagnostic techniques for detecting early-stage MSA are expected to facilitate the development of disease-modifying therapies for one of the most intractable neurodegenerative diseases.

Citations

Citations to this article as recorded by  
  • A Blinded Evaluation of Brain Morphometry for Differential Diagnosis of Atypical Parkinsonism
    Kazuya Kawabata, Florian Krismer, Beatrice Heim, Anna Hussl, Christoph Mueller, Christoph Scherfler, Elke R. Gizewski, Klaus Seppi, Werner Poewe
    Movement Disorders Clinical Practice.2024; 11(4): 381.     CrossRef
  • The potential of phosphorylated α‐synuclein as a biomarker for the diagnosis and monitoring of multiple system atrophy
    Toufik Abdul‐Rahman, Ranferi Eduardo Herrera‐Calderón, Arjun Ahluwalia, Andrew Awuah Wireko, Tomas Ferreira, Joecelyn Kirani Tan, Maximillian Wolfson, Shankhaneel Ghosh, Viktoriia Horbas, Vandana Garg, Asma Perveen, Marios Papadakis, Ghulam Md Ashraf, Ath
    CNS Neuroscience & Therapeutics.2024;[Epub]     CrossRef
  • Delivering the diagnosis of multiple system atrophy: a multicenter survey on Japanese neurologists’ perspectives
    Miki Yoshitake, Atsuhiko Sugiyama, Takayoshi Shimohata, Nobuyuki Araki, Masahide Suzuki, Kazumoto Shibuya, Kengo Nagashima, Nobutaka Hattori, Satoshi Kuwabara
    BMC Neurology.2024;[Epub]     CrossRef
  • Clinical comparison of the 2008 and 2022 diagnostic criteria for early multiple system atrophy-cerebellar type
    Seoyeon Kim, Kyung Ah Woo, Jung Hwan Shin, Han-Joon Kim, Beomseok Jeon
    Clinical Autonomic Research.2024;[Epub]     CrossRef
Original Articles
High Levels of Mutant Huntingtin Protein in Tear Fluid From Huntington’s Disease Gene Expansion Carriers
Marlies Gijs, Nynke Jorna, Nicole Datson, Chantal Beekman, Cira Dansokho, Alexander Weiss, David E. J. Linden, Mayke Oosterloo
J Mov Disord. 2024;17(2):181-188.   Published online February 21, 2024
DOI: https://doi.org/10.14802/jmd.24014
  • 2,414 View
  • 224 Download
  • 1 Web of Science
  • 1 Crossref
AbstractAbstract PDFSupplementary Material
Objective
Huntington’s disease (HD) is an autosomal dominant, fully penetrant, neurodegenerative disease that most commonly affects middle-aged adults. HD is caused by a CAG repeat expansion in the HTT gene, resulting in the expression of mutant huntingtin (mHTT). Our aim was to detect and quantify mHTT in tear fluid, which, to our knowledge, has never been measured before.
Methods
We recruited 20 manifest and 13 premanifest HD gene expansion carriers, and 20 age-matched controls. All patients underwent detailed assessments, including the Unified Huntington’s Disease Rating Scale (UHDRS) total motor score (TMS) and total functional capacity (TFC) score. Tear fluid was collected using paper Schirmer’s strips. The level of tear mHTT was determined using single-molecule counting SMCxPRO technology.
Results
The average tear mHTT levels in manifest (67,223 ± 80,360 fM) and premanifest patients (55,561 ± 45,931 fM) were significantly higher than those in controls (1,622 ± 2,179 fM). We noted significant correlations between tear mHTT levels and CAG repeat length, “estimated years to diagnosis,” disease burden score and UHDRS TMS and TFC. The receiver operating curve demonstrated an almost perfect score (area under the curve [AUC] = 0.9975) when comparing controls to manifest patients. Similarly, the AUC between controls and premanifest patients was 0.9846. The optimal cutoff value for distinguishing between controls and manifest patients was 4,544 fM, whereas it was 6,596 fM for distinguishing between controls and premanifest patients.
Conclusion
Tear mHTT has potential for early and noninvasive detection of alterations in HD patients and could be integrated into both clinical trials and clinical diagnostics.

Citations

Citations to this article as recorded by  
  • Unveiling brain disorders using liquid biopsy and Raman spectroscopy
    Jeewan C. Ranasinghe, Ziyang Wang, Shengxi Huang
    Nanoscale.2024; 16(25): 11879.     CrossRef
Premonitory Urges Reconsidered: Urge Location Corresponds to Tic Location in Patients With Primary Tic Disorders
Jana Essing, Ewgeni Jakubovski, Nikolas Psathakis, Sinan N Cevirme, James F Leckman, Kirsten R Müller-Vahl
J Mov Disord. 2022;15(1):43-52.   Published online January 25, 2022
DOI: https://doi.org/10.14802/jmd.21045
  • 6,534 View
  • 230 Download
  • 11 Web of Science
  • 15 Crossref
AbstractAbstract PDFSupplementary Material
Objective
In patients with Tourette syndrome and other primary tic disorders (PTDs), tics are typically preceded by premonitory urges (PUs). To date, only a few studies have investigated the location and frequency of PUs, and contrary to clinical experience, the results suggest that PUs are not located in the same anatomic region as the tics. This study aimed to further explore PU location and frequency in detail, differentiating the kind and complexity of the corresponding tics, in a large sample of patients with PTD.
Methods
A total of 291 adult (≥ 18 years) patients with a confirmed diagnosis of chronic PTD were included. The study was conducted online, assement included tics and the general characterization of PUs and a sophisticated body drawing for locating PUs.
Results
We found that PUs were located in the same body area as, or in direct proximity to, the corresponding tic. Most frequently, PUs were located in the face and at the head (62.1%). Compared with simple tics, complex (motor and vocal) tics were more often preceded by a PU; but there was no difference in PU frequency observed between motor tics and vocal tics. PUs were more often experienced at the front than at the back of the body (73% vs. 27%), while there was no difference between the right and left sides (41.6% vs. 41.3%).
Conclusion
The strong association between PU and tic location further supports the hypothesis that PUs represent the core of PTD. Accordingly, future therapies should focus on treating PUs to achieve greater tic reduction.

Citations

Citations to this article as recorded by  
  • Door-To-Door Video-Enhanced Prevalence Study of Tourette Disorder Among African Americans
    Catherine Striley, Kevin J. Black, Natalie E. Chichetto, Lauren Vagelakos
    Evidence-Based Practice in Child and Adolescent Mental Health.2024; 9(2): 281.     CrossRef
  • Functional Tic‐Like Behaviors: A Common Comorbidity in Patients with Tourette Syndrome
    Kirsten R. Müller‐Vahl, Anna Pisarenko, Carolin Fremer, Martina Haas, Ewgeni Jakubovski, Natalia Szejko
    Movement Disorders Clinical Practice.2024; 11(3): 227.     CrossRef
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    Lisa Keenan, Jessica Bramham, Michelle Downes
    Developmental Neuropsychology.2024; 49(1): 39.     CrossRef
  • Premonitory Urge in Patients with Tics and Functional Tic‐like Behaviors
    Natalia Szejko, Julian Fletcher, Davide Martino, Tamara Pringsheim
    Movement Disorders Clinical Practice.2024; 11(3): 276.     CrossRef
  • A meta-analysis of transcranial magnetic stimulation in Tourette syndrome
    Elizabeth R. Steuber, Joseph F. McGuire
    Journal of Psychiatric Research.2024; 173: 34.     CrossRef
  • Sensory Phenomenon Assessment Scale: a new tool for assessment of tic-associated sensations
    Xianbin Wang, Yanlin Li, Liping Yu, Hui Xu, Anyi Zhang, Wenyan Zhang, Zhongliang Jiang, Yonghua Cui, Ying Li
    Frontiers in Psychiatry.2024;[Epub]     CrossRef
  • We've all been wrong about provisional tic disorder
    Sarah C. Grossen, Amanda L. Arbuckle, Emily C. Bihun, Jonathan M. Koller, David Y. Song, Angela M. Reiersen, Bradley L. Schlaggar, Deanna J. Greene, Kevin J. Black
    Comprehensive Psychiatry.2024; 134: 152510.     CrossRef
  • Validation and assessment of the self-injurious behavior scale for tic disorders (SIBS-T)
    Natalia Szejko, Heike große Schlarmann, Anna Pisarenko, Martina Haas, Valerie Brandt, Ewgeni Jakubovski, Kirsten R. Müller-Vahl
    Scientific Reports.2024;[Epub]     CrossRef
  • Premonitory Urge and Tic Severity, Comorbidities, and Quality of Life in Chronic Tic Disorders
    Valerie Brandt, Jana Essing, Ewgeni Jakubovski, Kirsten Müller‐Vahl
    Movement Disorders Clinical Practice.2023; 10(6): 922.     CrossRef
  • Motor awareness, volition, and the cortical neurophysiology of simple motor tics
    Aysegul Gunduz, Christos Ganos
    Clinical Neurophysiology.2023; 151: 130.     CrossRef
  • Tourette syndrome research highlights from 2022
    Andreas Hartmann, Per Andrén, Cyril Atkinson-Clément, Virginie Czernecki, Cécile Delorme, Nanette Marinette Monique Debes, Kirsten Müller-Vahl, Peristera Paschou, Natalia Szejko, Apostolia Topaloudi, Keisuke Ueda, Kevin J. Black
    F1000Research.2023; 12: 826.     CrossRef
  • Tourette syndrome research highlights from 2022
    Andreas Hartmann, Per Andrén, Cyril Atkinson-Clément, Virginie Czernecki, Cécile Delorme, Nanette Marinette Monique Debes, Kirsten Müller-Vahl, Peristera Paschou, Natalia Szejko, Apostolia Topaloudi, Keisuke Ueda, Kevin J. Black
    F1000Research.2023; 12: 826.     CrossRef
  • Clinical evaluation of premonitory urges in children and adolescents using the Chinese version of Individualized Premonitory Urge for Tics Scale
    Guanghua Che, Wenjing Ren, Joseph F. McGuire, Ping Li, Zhiruo Zhao, Jing Tian, Jinyuan Zhang, Yue Zhang
    Frontiers in Psychiatry.2023;[Epub]     CrossRef
  • Mass social media-induced illness presenting with Tourette-like behavior
    Carolin Fremer, Natalia Szejko, Anna Pisarenko, Martina Haas, Luise Laudenbach, Claudia Wegener, Kirsten R. Müller-Vahl
    Frontiers in Psychiatry.2022;[Epub]     CrossRef
  • Tics bei Erwachsenen
    Tina Rawish, Gesine Sallandt, Alexander Münchau
    NeuroTransmitter.2022; 33(12): 38.     CrossRef
Review Articles
GBA1 Variants and Parkinson’s Disease: Paving the Way for Targeted Therapy
Young Eun Huh, Tatiana Usnich, Clemens R. Scherzer, Christine Klein, Sun Ju Chung
J Mov Disord. 2023;16(3):261-278.   Published online June 12, 2023
DOI: https://doi.org/10.14802/jmd.23023
  • 4,076 View
  • 384 Download
  • 3 Web of Science
  • 3 Crossref
AbstractAbstract PDF
Glucosylceramidase beta 1 (GBA1) variants have attracted enormous attention as the most promising and important genetic candidates for precision medicine in Parkinson’s disease (PD). A substantial correlation between GBA1 genotypes and PD phenotypes could inform the prediction of disease progression and promote the development of a preventive intervention for individuals at a higher risk of a worse disease prognosis. Moreover, the GBA1-regulated pathway provides new perspectives on the pathogenesis of PD, such as dysregulated sphingolipid metabolism, impaired protein quality control, and disrupted endoplasmic reticulum-Golgi trafficking. These perspectives have led to the development of novel disease-modifying therapies for PD targeting the GBA1-regulated pathway by repositioning treatment strategies for Gaucher’s disease. This review summarizes the current hypotheses on a mechanistic link between GBA1 variants and PD and possible therapeutic options for modulating GBA1-regulated pathways in PD patients.

Citations

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  • A Comparative Biochemical and Pathological Evaluation of Brain Samples from Knock-In Murine Models of Gaucher Disease
    Makaila L. Furderer, Bahafta Berhe, Tiffany C. Chen, Stephen Wincovitch, Xuntian Jiang, Nahid Tayebi, Ellen Sidransky, Tae-Un Han
    International Journal of Molecular Sciences.2024; 25(3): 1827.     CrossRef
  • Towards a Global View of Parkinson's Disease Genetics
    Marzieh Khani, Catalina Cerquera‐Cleves, Mariam Kekenadze, Peter Wild Crea, Andrew B. Singleton, Sara Bandres‐Ciga
    Annals of Neurology.2024; 95(5): 831.     CrossRef
  • Exploring the Association between Cathepsin B and Parkinson’s Disease
    Changhao Lu, Xinyi Cai, Shilin Zhi, Xiaofen Wen, Jiaxin Shen, Tommaso Ercoli, Elena Rita Simula, Carla Masala, Leonardo A. Sechi, Paolo Solla
    Brain Sciences.2024; 14(5): 482.     CrossRef
Gastrointestinal Dysfunction in Parkinson’s Disease: Neuro-Gastroenterology Perspectives on a Multifaceted Problem
Ai Huey Tan, Kee Huat Chuah, Yuan Ye Beh, Jie Ping Schee, Sanjiv Mahadeva, Shen-Yang Lim
J Mov Disord. 2023;16(2):138-151.   Published online May 24, 2023
DOI: https://doi.org/10.14802/jmd.22220
  • 3,933 View
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  • 6 Web of Science
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AbstractAbstract PDF
Patients with Parkinson’s disease (PD) face a multitude of gastrointestinal (GI) symptoms, including nausea, bloating, reduced bowel movements, and difficulties with defecation. These symptoms are common and may accumulate during the course of PD but are often under-recognized and challenging to manage. Objective testing can be burdensome to patients and does not correlate well with symptoms. Effective treatment options are limited. Evidence is often based on studies in the general population, and specific evidence in PD is scarce. Upper GI dysfunction may also interfere with the pharmacological treatment of PD motor symptoms, which poses significant management challenges. Several new less invasive assessment tools and novel treatment options have emerged in recent years. The current review provides an overview and a practical approach to recognizing and diagnosing common upper and lower GI problems in PD, e.g., dyspepsia, gastroparesis, small bowel dysfunction, chronic constipation, and defecatory dysfunction. Management aspects are discussed based on the latest evidence from the PD and general populations, with insights for future research pertaining to GI dysfunction in PD.

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Original Article
Fatigue in Parkinson’s Disease Is Due to Decreased Efficiency of the Frontal Network: Quantitative EEG Analysis
Min Seung Kim, Sanguk Park, Ukeob Park, Seung Wan Kang, Suk Yun Kang
J Mov Disord. 2024;17(3):304-312.   Published online June 10, 2024
DOI: https://doi.org/10.14802/jmd.24038
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AbstractAbstract PDFSupplementary Material
Objective
Fatigue is a common, debilitating nonmotor symptom of Parkinson’s disease (PD), but its mechanism is poorly understood. We aimed to determine whether electroencephalography (EEG) could objectively measure fatigue and to explore the pathophysiology of fatigue in PD.
Methods
We studied 32 de novo PD patients who underwent EEG. We compared brain activity between 19 PD patients without fatigue and 13 PD patients with fatigue via EEG power spectra and graphs, including the global efficiency, characteristic path length, clustering coefficient, small-worldness, local efficiency, degree centrality, closeness centrality, and betweenness centrality.
Results
No significant differences in absolute or relative power were detected between PD patients without or with fatigue (all p > 0.02, Bonferroni-corrected). According to our network analysis, brain network efficiency differed by frequency band. Generally, the brain network in the frontal area for theta and delta bands showed greater efficiency, and in the temporal area, the alpha1 band was less efficient in PD patients without fatigue (p < 0.0001, p = 0.0011, and p = 0.0007, respectively, Bonferroni-corrected).
Conclusion
Our study suggests that PD patients with fatigue have less efficient networks in the frontal area than PD patients without fatigue. These findings may explain why fatigue is common in PD, a frontostriatal disorder. Increased efficiency in the temporal area in PD patients with fatigue is assumed to be compensatory. Brain network analysis using graph theory is more valuable than power spectrum analysis in revealing the brain mechanism related to fatigue.
Viewpoint
A Practical Guide for Clinical Approach to Patients With Huntington’s Disease in Korea
Chaewon Shin, Ryul Kim, Dallah Yoo, Eungseok Oh, Jangsup Moon, Minkyeong Kim, Jee-Young Lee, Jong-Min Kim, Seong-Beom Koh, Manho Kim, Beomseok Jeon
J Mov Disord. 2024;17(2):138-149.   Published online March 12, 2024
DOI: https://doi.org/10.14802/jmd.24040
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