Journal of Movement Disorders

Original Article

Clinical Profile and Genetic Composition of Patients With Juvenile Parkinsonism From a Single Tertiary Care Center in India: Madathum Kuzhiyil Farsana, Vikram V Holla, Prashant Phulpagar, Nitish Kamble, Babylakshmi Muthusamy, Ravi Yadav, Pramod Kumar Pal; J Mov Disord. 2026;19(1):19-30. Published online August 19, 2025; DOI: https://doi.org/10.14802/jmd.25132

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Abstract PDF: Objective
Studies outlining the genetic architecture of Parkinson’s disease in India are sparse, and juvenile parkinsonism is underrepresented in the literature. The objective was to study the clinical, therapeutic, and genetic profiles of patients with juvenile parkinsonism and to correlate their phenotypic–genotypic characteristics.
Methods
This retrospective chart review was conducted in patients with suspected genetically mediated juvenile parkinsonism (onset ≤21 years) who underwent genetic testing at a tertiary care center in India from 2015–2024. The available phenotypic–genotypic characteristics were evaluated and compared between Gene (+) and Gene (-) patients.
Results
Forty patients (22 males, 55.0%) with juvenile parkinsonism were included, with mean ages at onset and presentation of 15.85±4.96 years and 26.37±10.11 years, respectively. The mean duration of illness was 10.43±10.49 years. A positive family history was present in 40.0% of the participants, and consanguinity was present in 45%. Bradykinesia was the most common motor symptom (95.0%), and cognitive impairment was the most common nonmotor symptom (17.5%). Pathogenic/likely pathogenic variants were identified in 27 patients (67.5%), with variants in PRKN being the most common (n=8 patients), followed by those in PLA2G6 (n=7 patients). Gene (+) patients had significantly more severe disease with a better levodopa response and more frequent familial consanguinity, oculomotor abnormalities, motor fluctuations, and dyskinesia. Compared with PARK-PRKN patients, PARK-PLA2G6 patients had significantly more dystonia, gaze restriction, and pyramidal signs and more severe disease at presentation, with a lower levodopa equivalent daily dose and fewer motor fluctuations.
Conclusion
More than two-thirds (67.5%) of the juvenile parkinsonism patients in our cohort had an underlying monogenic cause. PARK-PRKN, PARK-PLA2G6, and PARK-SYNJ1 are the common causes of genetically mediated juvenile parkinsonism in India.

Brief communication

Clinico-Genetic Profiles of Seven Patients With PINK1-Related Parkinson’s Disease: A Case Series From a Tertiary Care Centre in India and a Review of the Literature: Aravind Gunasekaran, Vikram V Holla, Prashant Phulpagar, Sneha D Kamath, Nitish Kamble, Ravi Yadav, Babylakshmi Muthusamy, Pramod Kumar Pal; J Mov Disord. 2024;17(4):436-441. Published online September 19, 2024; DOI: https://doi.org/10.14802/jmd.24157

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Objective
Recessive variants in the PINK1 gene are known causes of early-onset Parkinson’s disease (EOPD). To describe the clinical features and genetic profiles of patients with PINK1-related Parkinson’s disease (PARK-PINK1) mutations.
Methods
We conducted a retrospective chart review of the demographic, clinical and genetic details of patients from our database carrying biallelic PINK1 variants.
Results
A total of 7 patients whose median age at onset was 33 years (range: 20–49) were recruited. All had asymmetrical onset, tremors were present in 4 patients, abnormal posturing was present in 2 patients, and slowness was present in 1 patient. The parkinsonism phenotype was noted in 6 patients (with dystonia in four) and isolated dystonia in one. Among the 6 patients with parkinsonism, five had rest tremors, all had good levodopa responses, and four had motor fluctuations with choreiform dyskinesia. Exome sequencing revealed biallelic pathogenic/likely pathogenic variants, five of which were novel.
Conclusion
PARK-PINK1 presents as an EOPD with tremor-predominant phenotype, good levodopa-responsiveness, early motor fluctuation and dyskinesia. We describe five novel variants in PINK1 gene.

Citations

Citations to this article as recorded by

Genetic Sketch of Parkinson’s Disease in India
Suvorit S Bhowmick, Soaham D Desai
Annals of Indian Academy of Neurology.2025; 28(4): 495. CrossRef

Original Articles

Phenotypic Spectrum of Progressive Supranuclear Palsy: Clinical Study and Apolipoprotein E Effect: Amina Nasri, Ikram Sghaier, Anis Neji, Alya Gharbi, Youssef Abida, Saloua Mrabet, Amina Gargouri, Mouna Ben Djebara, Imen Kacem, Riadh Gouider; J Mov Disord. 2024;17(2):158-170. Published online January 30, 2024; DOI: https://doi.org/10.14802/jmd.23178

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Abstract PDF

Objective
Progressive supranuclear palsy (PSP) is a rare neurodegenerative disorder encompassing several phenotypes with various motor and cognitive deficits. We aimed to study motor and cognitive characteristics across PSP phenotypes and to assess the influence of apolipoprotein E (APOE) gene variants on PSP phenotypic expression.
Methods
In this 20-year cross-sectional study, we retrospectively reviewed the charts of all patients classified as PSP patients and recategorized them according to phenotype using the Movement Disorder Society criteria (2017). Phenotypes were divided into three subgroups, Richardson’s syndrome (PSP-RS), PSP-cortical (PSP with predominant frontal presentation [PSP-F] + PSP with predominant speech/language disorder [PSP-SL] + PSP with predominant corticobasal syndrome [PSP-CBS]) and PSP-subcortical (PSP with predominant parkinsonism [PSP-P] + PSP with progressive gait freezing [PSP-PGF] + PSP with predominant postural instability [PSP-PI] + PSP with predominant ocular motor dysfunction [PSP-OM] + PSP with cerebellar ataxia [PSP-C] + PSP with primary lateral sclerosis [PSP-PLS]), based on clinical presentation during the first 3 years after symptom onset, which defines the early disease stage. Clinical and neuropsychological assessment data were collected. Genotyping of APOE was performed using restriction fragment length polymorphism polymerase chain reaction and verified by Sanger sequencing.
Results
We included 112 PSP patients comprising 10 phenotypes classified into 48 PSP-RS, 34 PSP-cortical (PSP-CBS, 17.6%; PSP-F, 9.4%; PSP-SL, 8.2%) and 30 PSP-subcortical (PSP-P, 11.6%; PSP-PI, 8%; PSP-OM, 2.7%; PSP-PGF, 1.8%; PSP-C, 1.8%; PSP-PLS, 0.9%) subgroups. PSP-RS patients were older at disease onset (p = 0.009) and had more akinetic-rigid and levodopa-resistant parkinsonism (p = 0.006), while PSP-cortical patients had more tremors and asymmetric and/or levodopa-responsive parkinsonism (p = 0.025). Cognitive domains were significantly less altered in the PSP-subcortical subgroup. Overall, PSP-APOEε4 carriers developed parkinsonism earlier (p = 0.038), had earlier oculomotor dysfunction (p = 0.052) and had more altered cognitive profiles. The APOEε4 allele was also associated with a younger age of parkinsonism onset in the PSP-RS phenotype group (p = 0.026).
Conclusion
This study demonstrated the wide phenotypic spectrum of PSP among Tunisians. Disease onset and akinetic-rigid and levodopa-resistant parkinsonism were the hallmarks of the PSP-RS phenotype, while milder cognitive impairment was characteristic of the PSP-subcortical subgroup. The APOEε4 allele was associated with earlier parkinsonism and oculomotor dysfunction and seemed to play a role in defining a more altered cognitive profile in PSP patients.

Citations

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Motor and non-motor features in progressive supranuclear palsy: the impact of microtubule associated protein tau haplotypes among a Tunisian cohort
Youssef Abida, Ikram Sghaier, Amira Souissi, Alya Gharbi, Amina Nasri, Oumeyma Belkehia, Imen Kacem, Amina Gargouri-Berrachid, Riadh Gouider
Journal of Neural Transmission.2026; 133(3): 423. CrossRef
Progressive Supranuclear Palsy—A Global Review
Prashanth Lingappa Kukkle, Rosy Neupane, Alexandar Pantelyat, Anne‐Marie Wills, Ed Jabbari, Elise G.P. Dopper, Gabor G. Kovacs, Gunther Hoglinger, Ikuko Aiba, Irene Litvan, Jacky Ganguly, Jennifer L. Whitwell, Jinghong Ma, Kigocha Okeng’O, Ryuji Skakibara
Movement Disorders Clinical Practice.2026; 13(3): 611. CrossRef
The Spectrum of Cognitive Impairment in Atypical Parkinsonism Syndromes: A Comprehensive Review of Current Understanding and Research
Kurt A. Jellinger
Diseases.2025; 13(2): 39. CrossRef
Pathomechanisms of neuropsychiatric disturbances in atypical parkinsonian disorders: a current view
Kurt A. Jellinger
Journal of Neural Transmission.2025; 132(4): 495. CrossRef
A possible role of Apolipoprotein E in Idiopathic Generalized Epilepsy
Maria Kabbage, Saloua Mrabet, Maha Mounadi, Alya Gharbi, Amal Atrous, Istabrak Abdelkefi, Amina Gargouri-Berrechid, Riadh Gouider
Epilepsy & Behavior.2025; 172: 110554. CrossRef
Comorbid pathologies and their impact on progressive supranuclear palsy: current view
Kurt A. Jellinger
Journal of Neural Transmission.2025;[Epub] CrossRef
Differences in neuropsychological performance across clinical variants of progressive supranuclear palsy
Elizabeth A. Boots, Stephen D. Weigand, Nha Trang Thu Pham, Farwa Ali, Heather M. Clark, Julie A. Stierwalt, Hugo Botha, Sarah M. Boland, Yehkyoung C. Stephens, Keith A. Josephs, Jennifer L. Whitwell, Mary M. Machulda
Journal of the International Neuropsychological Society.2025; 31(5-6): 384. CrossRef
Clinical and molecular predictors of survival among atypical parkinsonian syndromes in a North African tertiary referral center
Ikram Sghaier, Amina Nasri, Amal Atrous, Youssef Abida, Alya Gharbi, Amira Souissi, Saloua Mrabet, Mouna Ben Djebara, Imen Kacem, Amina Gargouri-Berrechid, Riadh Gouider
Journal of the Neurological Sciences.2024; 464: 123155. CrossRef

Comparative Olfactory Profiles in Parkinson’s Disease and Drug-Induced Parkinsonism: In Hee Kwak, Young Eun Kim, Suk Yun Kang, Joong Seob Lee, Jeongjae Lee, Min Seung Kim, Dong A Yea, Hyeo-il Ma; J Mov Disord. 2024;17(1):64-70. Published online October 6, 2023; DOI: https://doi.org/10.14802/jmd.23105

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Abstract PDF Supplementary Material

Objective
Drug-induced parkinsonism (DIP) is a frequently encountered diagnostic possibility when considering Parkinson’s disease (PD). While olfactory dysfunction is a common clinical feature in PD, the comparison of olfactory function between the two conditions remains insufficient. This study aimed to compare olfactory function, including threshold, discrimination, and identification (TDI) profiles, between PD and DIP.
Methods
Consecutive patients with drug-naïve PD (n = 78) or DIP (n = 31) confirmed through dopamine transporter imaging were enrolled in this study. The YSK olfactory function (YOF) test, composed of TDI domains culturally familiar odorants to Koreans, was administered to all patients.
Results
In the study population, patients with DIP were significantly older than patients with PD. Over 70% of patients in each group had hyposmia or anosmia, and there was no significant difference in the occurrence of olfactory dysfunction between the two groups. In addition, there were no differences in the total YOF score and threshold score between the two groups. Meanwhile, the PD group had a significantly lower discrimination and identification score than the DIP group after adjusting for age, sex, the existence of diabetes, disease duration, and cognitive function.
Conclusion
This study demonstrated that detailed olfactory profiles are different in PD and DIP, even though olfactory dysfunction can be observed in both conditions.

Citations

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Olfactory dysfunction as potential biomarker in neurodegenerative diseases: a narrative review
Nicolas De Cleene, Katarína Schwarzová, Samuel Labrecque, Clancy Cerejo, Atbin Djamshidian, Klaus Seppi, Beatrice Heim
Frontiers in Neuroscience.2025;[Epub] CrossRef
Alpha-synuclein pathology and Parkinson’s disease-related olfactory dysfunctions: an update on preclinical models and therapeutic approaches
Jancy Nixon Abraham, Devesh Rawat, Priyadharshini Srikanth, Lisni P. Sunny, Nixon M. Abraham
Mammalian Genome.2025; 36(2): 444. CrossRef
Prevalence and clinical impact of alpha-synuclein pathology in idiopathic normal pressure hydrocephalus: Insights from RT-QuIC assay
Je kook Yu, Hye Joung Choi, Dongwoo Kim, Pham Hong Ngoc, In Hee Kwak, Huu Dat Nguyen, Trung Nguyen Thanh, Suk Jun Song, Jeongjae Lee, Hyeo-il Ma, Young Eun Kim
Parkinsonism & Related Disorders.2025; 136: 107857. CrossRef
Case Report: Practical approach to differentiating juvenile parkinsonism of genetic cause and drug-induced parkinsonism in adolescents: a case series and literature review
Ioana Grigore, Lăcrămioara Ionela Butnariu, Thomas Gabriel Schreiner, Vasile Valeriu Lupu, Ancuta Lupu, Ludmila Darie, Cătălin Prăzaru, Elena Țarcă, Setalia Popa, Ecaterina Grigore
Frontiers in Genetics.2025;[Epub] CrossRef
Peripheral inflammatory markers and clinical phenotypes reflecting the impact of diabetes on Parkinson's disease
In Hee Kwak, Hyeo-il Ma, Yun Joong Kim, Hye-Mi Noh, Jeongjae Lee, Je Kook Yu, Young Eun Kim
Journal of Parkinson’s Disease.2025; 15(8): 1431. CrossRef

Case Report

Rapid-Onset Dystonia and Parkinsonism in a Patient With Gaucher Disease: Ellen Hertz, Grisel Lopez, Jens Lichtenberg, Dietrich Haubenberger, Nahid Tayebi, Mark Hallett, Ellen Sidransky; J Mov Disord. 2023;16(3):321-324. Published online June 13, 2023; DOI: https://doi.org/10.14802/jmd.23074

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Abstract PDF Supplementary Material

Biallelic mutations in GBA1 cause the lysosomal storage disorder Gaucher disease, and carriers of GBA1 variants have an increased risk of Parkinson’s disease (PD). It is still unknown whether GBA1 variants are also associated with other movement disorders. We present the case of a woman with type 1 Gaucher disease who developed acute dystonia and parkinsonism at 35 years of age during a recombinant enzyme infusion treatment. She developed severe dystonia in all extremities and a bilateral pill-rolling tremor that did not respond to levodopa treatment. Despite the abrupt onset of symptoms, neither Sanger nor whole genome sequencing revealed pathogenic variants in ATP1A3 associated with rapid-onset dystonia-parkinsonism (RDP). Further examination showed hyposmia and presynaptic dopaminergic deficits in [18F]-DOPA PET, which are commonly seen in PD but not in RDP. This case extends the spectrum of movement disorders reported in patients with GBA1 mutations, suggesting an intertwined phenotype.

Citations

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Emerging Molecular‐Genetic Families in Dystonia: Endosome‐Autophagosome‐Lysosome and Integrated Stress Response Pathways
Nicole Calakos, Michael Zech
Movement Disorders.2025; 40(1): 7. CrossRef
Long‐Read Sequencing: The Third Generation of Diagnostic Testing for Dystonia
Thomas Wirth, Kishore R. Kumar, Michael Zech
Movement Disorders.2025; 40(6): 1009. CrossRef
Phenotypic consequences of GBA1 pathological variant R463C (p.R502C)
Emory Ryan, Samantha Nishimura, Grisel Lopez, Nahid Tayebi, Ellen Sidransky
American Journal of Medical Genetics Part A.2024;[Epub] CrossRef
In vitro study of ATP1A3 p.Ala275Pro mutant causing alternating hemiplegia of childhood and rapid-onset dystonia-parkinsonism
Dan-dan Ruan, Jing Zou, Li-sheng Liao, Ming-dong Ji, Ruo-li Wang, Jian-hui Zhang, Li Zhang, Mei-zhu Gao, Qian Chen, Hong-ping Yu, Wen Wei, Yun-fei Li, Hong Li, Fan Lin, Jie-wei Luo, Xin-fu Lin
Frontiers in Neuroscience.2024;[Epub] CrossRef

Review Articles

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

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Abstract 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.

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A rare case of adult-onset vanishing white matter leukoencephalopathy with movement disorder, expressing homozygous EIF2B3 and PRKN pathogenic variants
Bashar Kamal Ali Douden, Yazan Mohammad Abdullah Abufara, Mahmood Fayez Ali Aldrabeeh, Naela Ramadan Mohammad Tell, Ismail Abudaya
BMC Neurology.2025;[Epub] CrossRef

Movement Disorders Associated With Radiotherapy and Surgical Procedures: Bharath Kumar Surisetti, Shweta Prasad, Vikram Venkappayya Holla, Nitish Kamble, Ravi Yadav, Pramod Kumar Pal; J Mov Disord. 2023;16(1):42-51. Published online January 12, 2023; DOI: https://doi.org/10.14802/jmd.22092

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Abstract PDF

Occasionally, movement disorders can occur following interventional procedures including but not limited to radiotherapy, dental procedures, and cardiac, cerebral and spinal surgeries. The majority of these disorders tend to be unexpected sequelae with variable phenomenology and latency, and they can often be far more disabling than the primary disease for which the procedure was performed. Owing to poor knowledge and awareness of the problem, delays in diagnosing the condition are common, as are misdiagnoses as functional movement disorders. This narrative review discusses the phenomenology, pathophysiology, and potential treatments of various movement disorders caused by interventional procedures such as radiotherapy and neurological and non-neurological surgeries and procedures.

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Delayed Holm’s tremor complicated by contralateral midbrain metastasis: A nigrostriatal subtype
Sang-Won Yoo, Hyochun Lee, Joong-Seok Kim
Neurological Sciences.2025; 46(5): 2329. CrossRef
Cancer-related movement disorders: A scoping review and diagnostic approach
Laura E Schroeder, Ethan Snow, Casandra Chen, Amy Addo, Nahid Mohammadzadeh, Lawrence Recht, Saud Alhusaini
Neuro-Oncology Practice.2025; 12(6): 970. CrossRef
Myoclonus: an update
Betsy Thomas, Steven J. Frucht
Current Opinion in Neurology.2024; 37(4): 421. CrossRef
Biofeedback Endurance Training for Gait Rehabilitation in Parkinson’s Disease: a Non-Randomized Controlled Study
Olga V. Guseva, Natalia G. Zhukova
Bulletin of Rehabilitation Medicine.2023; 22(6): 21. CrossRef

Case Report

Nearly Abolished Dopamine Transporter Uptake in a Patient With a Novel FBXO7 Mutation: Eun Young Kim, Seon Young Kim, Youngduk Seo, Chaewon Shin; J Mov Disord. 2022;15(3):269-272. Published online July 26, 2022; DOI: https://doi.org/10.14802/jmd.22006

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Mutations in the F-box only protein 7 (FBXO7) gene are the cause of autosomal recessive parkinsonian-pyramidal syndrome. Herein, we report a patient with a novel FBXO7 mutation with a unique clinical presentation. A 43-year-old male visited our hospital with complaints of progressing gait disturbance since a generalized tonic clonic seizure. There were no past neurological symptoms or familial disorders. Neurological examination revealed bradykinesia, masked face, stooped posture, parkinsonian gait, and postural instability. The bilateral uptake by dopamine transporters was nearly abolished, as determined by N-(3-[18F]fluoropropyl)- 2β-carbon ethoxy-3β-(4-iodophenyl) nortropane positron emission tomography (18F-FP-CIT PET). Next-generation sequencing revealed a heterozygous c.1066_1069delTCTG (p.Ser356ArgfsTer56) frameshift variant and a heterozygous c.80G>A (p.Arg27His) missense variant of the FBXO7 gene. The patient’s specific clinical features, medication-refractory parkinsonism and seizures further broaden the spectrum of FBXO7 mutations. The nearly abolished dopamine transporter uptake identified by 18F-FP-CIT PET is frequently found in patients with FBXO7 mutations, which is different from the usual rostrocaudal gradient that is observed in patients with Parkinson’s disease.

Citations

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FBXO7 Pathogenic Variants in Early‐Onset Parkinsonism: Insights from a Neuroimaging Perspective and Review of the Literature
Erdi Şahin, Bedia Samanci, Gül Yalçın Çakmaklı, Ebba Lohmann, Gamze Güven, Ebru Erzurumluoğlu Gökalp, Ayşegül Gündüz, Ayşe Nazlı Başak, Sibel Ertan, Bülent Elibol, Başar Bilgiç, Haşmet Hanağası
Movement Disorders Clinical Practice.2025; 12(11): 1972. CrossRef
Imaging Procedure and Clinical Studies of [18F]FP-CIT PET
Changhwan Sung, Seung Jun Oh, Jae Seung Kim
Nuclear Medicine and Molecular Imaging.2024; 58(4): 185. CrossRef
Study of an FBXO7 patient mutation reveals Fbxo7 and PI31 co‐regulate proteasomes and mitochondria
Sara Al Rawi, Lorna Simpson, Guðrún Agnarsdóttir, Neil Q. McDonald, Veronika Chernuha, Orly Elpeleg, Massimo Zeviani, Roger A. Barker, Ronen Spiegel, Heike Laman
The FEBS Journal.2024; 291(12): 2565. CrossRef
The characteristics of FBXO7 and its role in human diseases
Yeling Zhong, Jinyun Li, Meng Ye, Xiaofeng Jin
Gene.2023; 851: 146972. CrossRef

Brief communication

Movement Disorders Resulting From Bilateral Basal Ganglia Lesions in End-Stage Kidney Disease: A Systematic Review: Kah Hui Yap, Nurul Husna Baharudin, Abdul Halim Abdul Gafor, Rabani Remli, Shen-Yang Lim, Wan Asyraf Wan Zaidi, Shahrul Azmin, Shahizon Azura Mohamed Mukari, Raihanah Abdul Khalid, Norlinah Mohamed Ibrahim; J Mov Disord. 2022;15(3):258-263. Published online May 26, 2022; DOI: https://doi.org/10.14802/jmd.21185

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Objective
The basal ganglia (BG) are susceptible to fluctuations in blood urea levels, sometimes resulting in movement disorders. We described patients with end-stage kidney disease (ESKD) presenting with movement disorders associated with bilateral BG lesions on imaging.
Methods
We report four patients and systematically reviewed all published cases of ESKD presenting with movement disorders and bilateral BG lesions (EBSCOhost and Ovid).
Results
Of the 72 patients identified, 55 (76.4%) were on regular dialysis. Parkinsonism was the most common movement disorder (n = 39; 54.2%), followed by chorea (n = 24; 33.3%). Diabetes mellitus (n = 51; 70.8%) and hypertension (n = 16; 22.2%) were the most common risk factors. Forty-three (59.7%) were of Asian ethnicity. Complete clinical resolution was reported in 17 (30.9%) patients, while 38 (69.1%) had incomplete clinical resolution with relapse. Complete radiological resolution occurred in 14 (34.1%) patients.
Conclusion
Movement disorders associated with BG lesions should be recognized as a rare and potentially reversible metabolic movement disorder in patients with ESKD.

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Irreversible Diabetic Striatopathy in Reversible Diabetes
Subhankar Chatterjee, Alak Pandit, Samya Sengupta, Shambaditya Das, Ritwik Ghosh, Souvik Dubey
JCEM Case Reports.2025;[Epub] CrossRef

Case Report

Dystonia Responsive to Dopamine: POLG Mutations Should Be Considered If Sensory Neuropathy Is Present: Jessica Qiu, Kishore Raj Kumar, Eloise Watson, Kate Ahmad, Carolyn M. Sue, Michael W. Hayes; J Mov Disord. 2021;14(2):157-160. Published online May 26, 2021; DOI: https://doi.org/10.14802/jmd.20159

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The POLG gene encodes mitochondrial DNA polymerase, and mutations in this gene cause a spectrum of disorders related to mitochondrial DNA depletion or deletion. Dystonia has only rarely been reported as an early and prominent manifestation of POLG mutations. We report a case of a 30-year-old male presenting with lower limb dystonia with peripheral neuropathy and demonstrate that the dystonia was levodopa responsive (with video findings). Whole-genome sequencing revealed biallelic variants in the POLG gene: a known pathogenic variant [NM_001126131.2:c.2209G>C (p.Gly737Arg)] and a novel likely pathogenic variant [NM_001126131.2:c.3305A>C (p.Gln1102Pro)]. A genetic diagnosis was made before the appearance of more readily recognizable features of mitochondrial disease, allowing us to avoid invasive tissue biopsies or potentially deleterious treatments, such as sodium valproate. A POLG-related disorder should be suspected in cases of dystonia with peripheral neuropathy, and this diagnosis may have implications for further investigations and management.

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Presentation, Treatment, and Outcome of a First Stroke-like Episode in a Carrier of the Compound Heterozygous Variants c.695G_A and c.2209G_C in POLG: A Case Report
Dominik Zieglgänsberger, Josef Finsterer
Cureus.2025;[Epub] CrossRef
Genome sequencing reanalysis increases the diagnostic yield in dystonia
Avi Fellner, Gurusidheshwar M. Wali, Neil Mahant, Bianca R. Grosz, Melina Ellis, Ramesh K. Narayanan, Karl Ng, Ryan L. Davis, Michel C. Tchan, Katya Kotschet, Dennis Yeow, Laura I. Rudaks, Sue-Faye Siow, Gautam Wali, Con Yiannikas, Matthew Hobbs, Joseph C
Parkinsonism & Related Disorders.2024; 124: 107010. CrossRef
Possible EIF2AK2‐Associated Stress‐Related Neurological Decompensation with Combined Dystonia and Striatal Lesions
Sophie E. Waller, Hugo Morales‐Briceño, Laura Williams, Shekeeb S. Mohammad, Avi Fellner, Kishore R. Kumar, Michel Tchan, Victor S.C. Fung
Movement Disorders Clinical Practice.2022; 9(2): 240. CrossRef
Movement disorders and neuropathies: overlaps and mimics in clinical practice
Francesco Gentile, Alessandro Bertini, Alberto Priori, Tommaso Bocci
Journal of Neurology.2022; 269(9): 4646. CrossRef
Transgenic Mice for the Translational Study of Neuropathic Pain and Dystonia
Damiana Scuteri, Kengo Hamamura, Chizuko Watanabe, Paolo Tonin, Giacinto Bagetta, Maria Tiziana Corasaniti
International Journal of Molecular Sciences.2022; 23(15): 8580. CrossRef
An overview of the pharmacotherapeutics for dystonia: advances over the past decade
O. Abu-hadid, J. Jimenez-Shahed
Expert Opinion on Pharmacotherapy.2022; 23(17): 1927. CrossRef
Exploitation of Thermal Sensitivity and Hyperalgesia in a Mouse Model of Dystonia
Damiana Scuteri, Laura Rombolà, Silvia Natoli, Antonio Pisani, Paola Bonsi, Kengo Hamamura, Giacinto Bagetta, Paolo Tonin, Maria Tiziana Corasaniti
Life.2021; 11(9): 985. CrossRef

Review Article

Manganese and Movement Disorders: A Review: Dinkar Kulshreshtha, Jacky Ganguly, Mandar Jog; J Mov Disord. 2021;14(2):93-102. Published online April 6, 2021; DOI: https://doi.org/10.14802/jmd.20123

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Abstract PDF

Scientific and technological advances achieved with industrial expansion have led to an ever-increasing demand for heavy metals. This demand has, in turn, led to increased contamination of soil, water and air with these metals. Chronic exposure to metals may be detrimental not only to occupational workers but also to the nonoccupational population exposed to these metals. Manganese (Mn), a commonly used heavy metal, is an essential cofactor for many enzymatic processes that drive biological functions. However, it is also a potential source of neurotoxicity, particularly in the field of movement disorders. The typical manifestation of Mn overexposure is parkinsonism, which may be difficult to differentiate from the more common idiopathic Parkinson’s disease. In addition to environmental exposure to Mn, other potential etiologies causing hypermanganesemia include systemic health conditions, total parenteral nutrition and genetic mutations causing Mn dyshomeostasis. In this review, we critically analyze Mn and discuss its sources of exposure, pathophysiology and clinical manifestations. We have highlighted the global public health impact of Mn and emphasize that movement disorder specialists should record a detailed social and occupational history to ensure that a toxic etiology is not misdiagnosed as a neurodegenerative disease. In the absence of a definite therapeutic option, early diagnosis and timely institution of preventive measures are the keys to managing its toxic effects.

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Analysis of toxic and radiotoxic heavy metals in some cereal grains consumed in Türkiye and assessment of potential health risk
Şeref Turhan, Ergin Murat Altuner, Aslı Kurnaz, Kenan Akyol, Aybaba Hançerlioğulları, Aydan Altıkulaç
Journal of Food Composition and Analysis.2026; 151: 108958. CrossRef
Longitudinal changes in pallidal index and their associations with urinary manganese and CaNa₂EDTA chelation
Tuğba Akkale, Nuriye Kayalı Şendur, Süleyman Filiz, Nilüfer Merve Çelik
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Original Article

Association between Olfactory Deficit and Motor and Cognitive Function in Parkinson’s Disease: Han Soo Yoo, Seok Jong Chung, Yang Hyun Lee, Byoung Seok Ye, Young H. Sohn, Phil Hyu Lee; J Mov Disord. 2020;13(2):133-141. Published online April 6, 2020; DOI: https://doi.org/10.14802/jmd.19082

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303 Download
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Abstract PDF Supplementary Material

Objective
To investigate whether baseline olfactory dysfunction in Parkinson’s disease (PD) patients is associated with baseline and longitudinal motor and cognitive function.
Methods
We recruited 228 drug-naïve PD patients who were followed for a mean of 6 years. Patients underwent the Cross-Cultural Smell Identification Test (CCSIT), a neuropsychological test, and N-(3-[18F]fluoropropyl)-2β-carbomethoxy-3β-(4-iodophenyl) nortropane positron emission tomography within 6 months of the baseline evaluation. Olfactory dysfunction was categorized as normosmia (CCSIT score ≥ 9), hyposmia (CCSIT score 5–8), and anosmia (CCSIT score ≤ 4). During the follow-up period, we investigated changes in the levodopa-equivalent dose (LED) and the occurrence of wearing-off, levodopa-induced dyskinesia, and dementia.
Results
Among the PD patients, 80.7% were hyposmic at the time of diagnosis, and 26.1% were anosmic. Baseline olfactory dysfunction was not associated with either initial parkinsonian motor symptoms or with the longitudinal LED increment and motor complications. Meanwhile, the anosmic group had lower baseline scores on the Korea version of the Boston Naming Test and Stroop color reading test than the normosmic and hyposmic groups. The anosmic group exhibited a higher rate of conversion to dementia than the normosmic [adjusted hazard ratio (HR) 3.99, 95% confidence interval (CI) 1.08–14.72] and hyposmic (adjusted HR 2.48, 95% CI 1.15–5.32) PD groups, regardless of baseline motor deficits and cognitive status.
Conclusion
Baseline olfactory dysfunction was not associated with motor deficits and complications, but it was associated with cognitive dysfunction and prognosis, suggesting that severe olfactory impairment may reflect early cortical involvement, probably in the frontotemporal region, and rapid spreading of Lewy body pathology.

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Review Articles

Oro-Pharyngeal Dysphagia in Parkinson’s Disease and Related Movement Disorders: Miseon Kwon, Jae-Hong Lee; J Mov Disord. 2019;12(3):152-160. Published online September 30, 2019; DOI: https://doi.org/10.14802/jmd.19048

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1,352 Download
61 Web of Science
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Abstract PDF Supplementary Material

Oro-pharyngeal dysphagia is a common symptom in patients with Parkinson’s disease (PD) and related disorders, even in their early stage of diseases. Dysphagia in these patients has been underdiagnosed, probably due to poor the self-awareness of the conditions and the underuse of validated tools and objective instruments for assessment. The early detection and intervention of dysphagia are closely related to improving the quality of life and decreasing the mortality rate in these patients. The purpose of this paper is to give an overview of the characteristics of dysphagia, including the epidemiology, pathophysiology, and clinical symptomatology, in patients with PD compared with other parkinsonian disorders and movement disorders. The management of dysphagia and future research directions related to these disorders are also discussed.

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Pseudobulbar Affect in Parkinsonian Disorders: A Review: Mathew Hakimi, Carine W. Maurer; J Mov Disord. 2019;12(1):14-21. Published online January 30, 2019; DOI: https://doi.org/10.14802/jmd.18051

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373 Download
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Abstract PDF

Pseudobulbar affect (PBA) is a neurological symptom of inappropriate and uncontrollable laughter or crying that occurs secondary to a variety of neurological conditions, including parkinsonian disorders. PBA is a socially and emotionally debilitating symptom that has been estimated to affect 3.6% to 42.5% of the population with Parkinson’s disease. While indexing measures and treatment options for PBA have been extensively studied in neurological conditions such as amyotrophic lateral sclerosis and multiple sclerosis, there has been considerably less attention given in the literature to PBA in parkinsonian disorders. The purpose of this review is to discuss the pathophysiology of PBA, its prevalence and impact on quality of life in parkinsonian disorders, and the treatment options currently available. Areas requiring further study, including the development of standardized, cross-culturally validated methods of symptom assessment, and evidence-based studies exploring the efficacy of current treatment options in parkinsonian disorders, are also highlighted.

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Abnormal Eye Movements in Parkinsonism and Movement Disorders: Ileok Jung, Ji-Soo Kim; J Mov Disord. 2019;12(1):1-13. Published online January 30, 2019; DOI: https://doi.org/10.14802/jmd.18034

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Abstract PDF Supplementary Material

Abnormal eye movements are commonly observed in movement disorders. Ocular motility examination should include bedside evaluation and laboratory recording of ocular misalignment, involuntary eye movements, including nystagmus and saccadic intrusions/oscillations, triggered nystagmus, saccades, smooth pursuit (SP), and the vestibulo-ocular reflex. Patients with Parkinson’s disease (PD) mostly show hypometric saccades, especially for the selfpaced saccades, and impaired SP. Early vertical saccadic palsy is characteristic of progressive supranuclear palsy-Richardson’s syndrome. Patients with cortico-basal syndrome typically show a delayed onset of saccades. Downbeat and gaze-evoked nystagmus and hypermetric saccades are characteristic ocular motor findings in ataxic disorders due to cerebellar dysfunction. In this review, we discuss various ocular motor findings in movement disorders, including PD and related disorders, ataxic syndromes, and hyperkinetic movement disorders. Systemic evaluation of the ocular motor functions may provide valuable information for early detection and monitoring of movement disorders, despite an overlap in the abnormal eye movements among different movement disorders.

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Case Report

A Patient with Myotonic Dystrophy Type 1 Presenting as Parkinsonism: Ji-Hyun Choi, Jee-Young Lee, Han-Joon Kim, Beomseok Jeon; J Mov Disord. 2018;11(3):145-148. Published online September 30, 2018; DOI: https://doi.org/10.14802/jmd.18028

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Abstract PDF: The current body of literature contains 5 reports of myotonic dystrophy (DM) with parkinsonism: 4 reports of DM type 2 and 1 report of clinically suspected DM type 1. To date, there have been no genetically proven cases of DM type 1 with parkinsonism. Here, we report the first case of genetically proven DM type 1 and parkinsonism that developed ahead of muscle symptoms with bilateral putaminal, presynaptic dopaminergic deficits on imaging. A 54-year-old female patient presented with bradykinesia, axial and bilateral limb rigidity, stooped posture, and hypomimia, which did not respond to levodopa. At age 56, she developed neck flexion weakness. Examination showed bilateral facial weakness, percussion and grip myotonia, and electromyography confirmed myotonic discharges. A genetic study of DM type 1 showed a DMPK mutation. At age 58, gait freezing, postural instability, and frequent falling developed and did not respond to increasing doses of levodopa. At age 59, the patient died from asphyxia.

Review Article

Tau Positron Emission Tomography Imaging in Degenerative Parkinsonisms: Chul Hyoung Lyoo, Hanna Cho, Jae Yong Choi, Young Hoon Ryu, Myung Sik Lee; J Mov Disord. 2018;11(1):1-12. Published online January 23, 2018; DOI: https://doi.org/10.14802/jmd.17071

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Abstract PDF

In recent years, several radiotracers that selectively bind to pathological tau proteins have been developed. Evidence is emerging that binding patterns of in vivo tau positron emission tomography (PET) studies in Alzheimer’s disease (AD) patients closely resemble the distribution patterns of known neurofibrillary tangle pathology, with the extent of tracer binding reflecting the clinical and pathological progression of AD. In Lewy body diseases (LBD), tau PET imaging has clearly revealed cortical tau burden with a distribution pattern distinct from AD and increased cortical binding within the LBD spectrum. In progressive supranuclear palsy, the globus pallidus and midbrain have shown increased binding most prominently. Tau PET patterns in patients with corticobasal syndrome are characterized by asymmetrical uptake in the motor cortex and underlying white matter, as well as in the basal ganglia. Even in the patients with multiple system atrophy, which is basically a synucleinopathy, ¹⁸F-flortaucipir, a widely used tau PET tracer, also binds to the atrophic posterior putamen, possibly due to off-target binding. These distinct patterns of tau-selective radiotracer binding in the various degenerative parkinsonisms suggest its utility as a potential imaging biomarker for the differential diagnosis of parkinsonisms.

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Claire Sexton, Heather Snyder, Dirk Beher, Adam L. Boxer, Pat Brannelly, Jean‐Pierre Brion, Luc Buée, Angela M. Cacace, Gaël Chételat, Martin Citron, Sarah L. DeVos, Kristophe Diaz, Howard H. Feldman, Bess Frost, Alison M. Goate, Michael Gold, Bradley Hym
Alzheimer's & Dementia.2022; 18(5): 988. CrossRef
18F‐Florzolotau Tau Positron Emission Tomography Imaging in Patients with Multiple System Atrophy–Parkinsonian Subtype
Feng‐Tao Liu, Xin‐Yi Li, Jia‐Ying Lu, Ping Wu, Ling Li, Xiao‐Niu Liang, Zi‐Zhao Ju, Fang‐Yang Jiao, Ming‐Jia Chen, Jing‐Jie Ge, Yi‐Min Sun, Jian‐Jun Wu, Tzu‐Chen Yen, Jian‐Feng Luo, Chuantao Zuo, Jian Wang
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Imaging pathological tau in atypical parkinsonisms: A review
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Case Reports

‘Hummingbird’ Sign in a Patient with Guam Parkinsonism-Dementia Complex: Tianrong Yeo, Louis CS Tan; J Mov Disord. 2017;10(3):145-148. Published online August 8, 2017; DOI: https://doi.org/10.14802/jmd.17025

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Abstract PDF Supplementary Material

We present a case of a 71-year-old male Chamorro patient from Guam who presented with progressive supranuclear palsy (PSP)-Richardson’s syndrome. Considering his strong family history of parkinsonism and a PSP phenotype, he was clinically diagnosed with Guam parkinsonism-dementia complex (PDC). Magnetic resonance imaging (MRI) of the brain revealed prominent midbrain atrophy with preserved pontine volume, forming the ‘hummingbird’ sign, which has not been described before in Guam PDC. Molecular analysis of the chromosome 9 open reading frame 72 gene (C9orf72) showed only 6 GGGGCC repeats. We discuss the clinico-pathological similarities and differences between PSP and Guam PDC, and highlight the topography of neuropathological changes seen in Guam PDC to explain the appearance of the ‘hummingbird’ sign on MRI.

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Discriminative pattern of reduced cerebral blood flow in Parkinson’s disease and Parkinsonism-Plus syndrome: an ASL-MRI study
Lina Cheng, Xiaoyan Wu, Ruomi Guo, Yuzhou Wang, Wensheng Wang, Peng He, Hanbo Lin, Jun Shen
BMC Medical Imaging.2020;[Epub] CrossRef
Tauopathy and Movement Disorders—Unveiling the Chameleons and Mimics
Jacky Ganguly, Mandar Jog
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Suspected Perinatal Depression Revealed to be Hereditary Diffuse Leukoencephalopathy with Spheroids: Josefine Blume, Robert Weissert; J Mov Disord. 2017;10(1):59-61. Published online December 27, 2016; DOI: https://doi.org/10.14802/jmd.16050

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Abstract PDF Supplementary Material

Early motor symptoms of neurodegenerative diseases often appear in combination with psychiatric symptoms, such as depression or personality changes, and are in danger of being misdiagnosed as psychogenic in young patients. We present the case of a 32-year-old woman who presented with rapid-onset depression, followed by a hypokinetic movement disorder and cognitive decline during pregnancy. Genetic testing revealed a mutation in the colony-stimulating factor 1 receptor gene, which led to the diagnosis of hereditary diffuse leukoencephalopathy with spheroids. Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is probably an under-recognized disease. HDLS should be considered in patients with rapidly progressing parkinsonian symptoms and dementia accompanied by white matter lesions.

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CSF1R -related leukoencephalopathy
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Original Articles

Clinical Features Indicating Nigrostriatal Dopaminergic Degeneration in Drug-Induced Parkinsonism: Seung Ha Lee, Han Kyeol Kim, Young Gun Lee, Chul Hyoung Lyoo, Sung Jun Ahn, Myung Sik Lee; J Mov Disord. 2017;10(1):35-39. Published online December 27, 2016; DOI: https://doi.org/10.14802/jmd.16045

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Abstract PDF Supplementary Material

Objective
Patients with drug-induced parkinsonism (DIP) may have nigrostriatal dopaminergic degeneration. We studied the clinical features that may indicate nigrostriatal dopaminergic degeneration in patients with DIP.
Methods
Forty-one DIP patients were classified into normal and abnormal [¹⁸F] FP-CIT scan groups. Differences in 32 clinical features and drug withdrawal effects were studied.
Results
Twenty-eight patients had normal (Group I) and 13 patients had abnormal (Group II) scans. Eight patients of Group I, but none of Group II, had taken calcium channel blockers (p = 0.040). Three patients of Group I and six of Group II had hyposmia (p = 0.018). After drug withdrawal, Group I showed greater improvement in Unified Parkinson’s Disease Rating Scale total motor scores and subscores for bradykinesia and tremors than Group II. Only hyposmia was an independent factor associated with abnormal scans, but it had suboptimal sensitivity.
Conclusion
None of the clinical features were practical indicators of nigrostriatal dopaminergic degeneration in patients with DIP.

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Comparative Olfactory Profiles in Parkinson’s Disease and Drug-Induced Parkinsonism
In Hee Kwak, Young Eun Kim, Suk Yun Kang, Joong Seob Lee, Jeongjae Lee, Min Seung Kim, Dong A Yea, Hyeo-il Ma
Journal of Movement Disorders.2024; 17(1): 64. CrossRef
Retinal Thickness and Its Interocular Asymmetry Between Parkinson’s Disease and Drug-Induced Parkinsonism
Wool Suh, Sung Uk Baek, Jungsu S. Oh, Seung Yeon Seo, Jae Seung Kim, You Mie Han, Min Seung Kim, Suk Yun Kang
Journal of Korean Medical Science.2023;[Epub] CrossRef
Gait abnormalities and non-motor symptoms predict abnormal dopaminergic imaging in presumed drug-induced Parkinsonism
Whitley W. Aamodt, Jacob G. Dubroff, Gang Cheng, Betty Taylor, Stephanie Wood, John E. Duda, James F. Morley
npj Parkinson's Disease.2022;[Epub] CrossRef
Acute dopamine receptor blockade in substantia nigra pars reticulata: a possible model for drug-induced Parkinsonism
Verónica Alejandra Cáceres-Chávez, Ricardo Hernández-Martínez, Jesús Pérez-Ortega, Marco Arieli Herrera-Valdez, Jose J. Aceves, Elvira Galarraga, José Bargas
Journal of Neurophysiology.2018; 120(6): 2922. CrossRef
Neuroimaging in Parkinson's disease: focus on substantia nigra and nigro-striatal projection
Daniela Frosini, Mirco Cosottini, Duccio Volterrani, Roberto Ceravolo
Current Opinion in Neurology.2017; 30(4): 416. CrossRef

Movement Disorders in Non-Wilsonian Hepatic Cirrhotic Patients: The Subgroup Analysis of Various Phenotypes and Associated Risk Factors: Kulthida Methawasin, Piyanant Chonmaitree, Chatchawan Wongjitrat, Suthee Rattanamongkolgul, Thanin Asawavichienjinda; J Mov Disord. 2016;9(2):104-113. Published online March 28, 2016; DOI: https://doi.org/10.14802/jmd.15047

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Abstract PDF

Objective
The aim of this subgroup analysis was to identify the risk factors associated with the development of various movement disorder phenotypes.
Methods
Eighty-three non-Wilsonian cirrhotic patients with abnormal movements were allocated into the following groups: intention tremor, bradykinesia, Parkinsonism, and abnormal ocular movements. These movement types were considered the primary outcomes as there was a sufficient sample size. Researchers took into consideration the gender, etiologies of cirrhosis, cirrhosis-related complications, hepatic encephalopathy, medical illness, and some neurological deficits as potential factors associated with these movement disorders.
Results
The male gender (p = 0.002) and alcoholic cirrhosis (p = 0.005) were significant factors for the prevalence of intention tremors. In bradykinesia, hepatic encephalopathy was highly statistically significant (p < 0.001), and females more commonly developed bradykinesia (p = 0.04). The Parkinsonism features in this study were confounded by hyperlipidemia (p = 0.04) and motor or sensory deficits (p = 0.02). Jerky pursuits and a horizontal nystagmus were detected. Jerky pursuits were significantly related to hepatic encephalopathy (p = 0.003) and bradykinesia, but there were no factors associated with the prevalence of nystagmus other than an intention tremor.
Conclusions
The association of alcoholic cirrhosis with the development of intention tremor indicates that the persistent cerebellar malfunction in cirrhotic patients is due to alcohol toxicity. The slowness of finger tapping and jerky pursuit eye movements are significantly associated with hepatic encephalopathy. Thus, further studies are needed to evaluate the diagnostic value of these two signs for an early detection of mild hepatic encephalopathy.

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Unveiling the link: hepatitis C virus and Parkinson’s disease
Rasha Eletreby, Eman Elhady, Shaimaa Shaheen, Iman Hamza, Ahmed Hashem
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Review Article

Clinical Approach to Progressive Supranuclear Palsy: Helen Ling; J Mov Disord. 2016;9(1):3-13. Published online January 25, 2016; DOI: https://doi.org/10.14802/jmd.15060

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Abstract PDF

Sixty years ago, Steele, Richardson and Olszewski designated progressive supranuclear palsy (PSP) as a new clinicopathological entity in their seminal paper. Since then, in addition to the classic Richardson’s syndrome (RS), different clinical phenotypic presentations have been linked with this four-repeat tauopathy. The clinical heterogeneity is associated with variability of regional distribution and severity of abnormal tau accumulation and neuronal loss. In PSP subtypes, the presence of certain clinical pointers may be useful for antemortem prediction of the underlying PSP-tau pathology. Midbrain atrophy on conventional MRI correlates with the clinical phenotype of RS but is not predictive of PSP pathology. Cerebrospinal fluid biomarkers and tau ligand positron emission tomography are promising biomarkers of PSP. A multidisciplinary approach to meet the patients’ complex needs is the current core treatment strategy for this devastating disorder.

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Case Report

Creutzfeldt-Jakob Disease in a Tertiary Care Hospital in Thailand: A Case Series and Review of the Literature: Praween Lolekha, Ahmed Rasheed, Chutanat Yotsarawat; J Mov Disord. 2015;8(3):136-140. Published online September 10, 2015; DOI: https://doi.org/10.14802/jmd.15014

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Abstract PDF

Creutzfeldt-Jakob Disease (CJD) is an incurable and inevitably fatal neurodegenerative disorder. Although CJD has a worldwide distribution, there are no official statistics on CJD in Thailand. A diagnosis of CJD is suspected when a patient develops rapidly progressive dementia with myoclonus. However, CJD may be mistaken for a variety of illnesses because its initial presentation frequently consists of non-specific symptoms. Here, we examined cases of sporadic CJD (sCJD) from Thammasat University Hospital (a tertiary care hospital in Thailand) between January 1, 2012 and December 31, 2014. Three cases of probable and possible sCJD were collected. All cases presented with rapidly progressive cognitive dysfunction accompanied by spontaneous myoclonus. Classical electroencehalography changes and typical abnormal MRI features were observed. All of the cases died within a period of 8 months. None of the patients underwent brain biopsy. Our findings raise questions about the prevalence of CJD in Thailand, which needs further study.

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Review Article

¹²³I-Metaiodobenzylguanidine Myocardial Scintigraphy in Lewy Body-Related Disorders: A Literature Review: Eun Joo Chung, Sang Jin Kim; J Mov Disord. 2015;8(2):55-66. Published online May 31, 2015; DOI: https://doi.org/10.14802/jmd.15015

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Abstract PDF

Lewy body-related disorders are characterized by the presence of Lewy bodies and Lewy neurites, which have abnormal aggregations of α-synuclein in the nigral and extranigral areas, including in the heart. 123I-metaiodobenzylguanidine (MIBG) scintigraphy is a well-known tool to evaluate cardiac sympathetic denervation in the Lewy body-related disorders. MIBG scintigraphy showed low uptake of MIBG in the Lewy body-related disorders, including Parkinson’s disease, dementia with Lewy bodies, pure autonomic failure and rapid eye movement sleep behavior disorder. This review summarizes previous results on the diagnostic applications of MIBG scintigraphy in Lewy body-related disorders.

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Joong-Seok Kim, Hyung-Eun Park, Yoon-Sang Oh, In-Uk Song, Dong-Won Yang, Jeong-Wook Park, Kwang-Soo Lee
Journal of the Neurological Sciences.2015; 357(1-2): 173. CrossRef
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Case Report

Amantadine Induced Corneal Edema in a Patient with Primary Progressive Freezing of Gait: Young Eun Kim, Ji Young Yun, Hui-Jun Yang, Han-Joon Kim, Mee Kum Kim, Won Ryang Wee, Beom S. Jeon; J Mov Disord. 2013;6(2):34-36. Published online October 30, 2013; DOI: https://doi.org/10.14802/jmd.13008

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Abstract PDF

Amantadine is commonly used for Parkinsonism. However amantadine can induce adverse corneal reaction. Here we report a patient with primary progressive freezing of gait who had severe corneal edema associated with amantadine, which was reversible after discontinuation of the amantadine. This report alerts neurologists for this reversible but potentially critical corneal edema in patients with Parkinsonism who are receiving amantadine.

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Review Article

New Perspective on Parkinsonism in Frontotemporal Lobar Degeneration: Hee Kyung Park, Sun J. Chung; J Mov Disord. 2013;6(1):1-8.; DOI: https://doi.org/10.14802/jmd.13001

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Abstract PDF

Frontotemporal dementia (FTD) is the second most common type of presenile dementia. Three clinical prototypes have been defined; behavioral variant FTD, semantic dementia, and progressive nonfluent aphasia. Progressive supranuclear palsy, corticobasal degeneration, and motor neuron disease may possess clinical and pathological characteristics that overlap with FTD, and it is possible that they may all belong to the same clinicopathological spectrum. Frontotemporal lobar degeneration (FTLD) is a clinicopathological syndrome that encompasses a heterogenous group of neurodegenerative disorders. Owing to the advancement in the field of molecular genetics, diagnostic imaging, and pathology, FTLD has been the focus of great interest. Nevertheless, parkinsonism in FTLD has received relatively less attention. Parkinsonism is found in approximately 20–30% of patients in FTLD. Furthermore, parkinsonism can be seen in all FTLD subtypes, and some patients with familial and sporadic FTLD can present with prominent parkinsonism. Therefore, there is a need to understand parkinsonism in FTLD in order to obtain a better understanding of the disease. With regard to the clinical characteristics, the akinetic rigid type of parkinsonism has predominantly been described. Parkinsonism is frequently observed in familial FTD, more specifically, in FTD with parkinsonism linked to chromosome 17q (FTDP-17). The genes associated with parkinsonism are microtubule associated protein tau (MAPT), progranulin (GRN or PGRN), and chromosome 9 open reading frame 72 (C9ORF72) repeat expansion. The neural substrate of parkinsonism remains to be unveiled. Dopamine transporter (DAT) imaging revealed decreased uptake of DAT, and imaging findings indicated atrophic changes of the basal ganglia. Parkinsonism can be an important feature in FTLD and, therefore, increased attention is needed on the subject.

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Case Reports

Apparently Ipsilateral Parkinsonism in a Patient with Chronic Subdural Hematoma: Tae Hwan Roh, Dokyung Lee, Il Ki Hong, Deog Yoon Kim, Tae-Beom Ahn; J Mov Disord. 2012;5(1):18-20.; DOI: https://doi.org/10.14802/jmd.12005

11,254 View
73 Download
1 Crossref

Abstract PDF

Symptomatic parkinsonism secondary to ipsilateral lesion is rarely reported. Although the contribution of the contralateral lesions was assumed in some cases, the pathomechanism remains undetermined. Herein we report a patient with a subdural hematoma, who developed parkinsonism in the ipsilateral hemibody. Structural and functional imaging suggests the contralateral dopaminergic dysfunction as the major culprit of apparently ipsilateral parkinsonism.

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Secondary parkinsonism caused by chronic subdural hematomas owing to compressed cortex and a disturbed cortico–basal ganglia–thalamocortical circuit: illustrative case
Masao Fukumura, Sho Murase, Yuzo Kuroda, Kazutomo Nakazawa, Yasufumi Gon
Journal of Neurosurgery: Case Lessons.2021;[Epub] CrossRef

Cardiac ¹²³I-metaiodobenzylguanidine Scintigraphy in a Patient with Familial Parkinsonism with Parkin Gene Mutation: Young-Do Kim, In-Uk Song, Joong-Seok Kim, Sung-Woo Chung, Kwang-Soo Lee; J Mov Disord. 2010;3(2):42-44.; DOI: https://doi.org/10.14802/jmd.10011

15,130 View
60 Download
4 Crossref

Abstract PDF

A decreased cardiac ¹²³I-metaiodobenzylguanidine (¹²³I-MIBG) uptake has been used as a powerful tool to identify Lewy body disease, such as idiopathic parkinson’s disease (IPD). We performed cardiac ¹²³I-MIBG scintigraphy in patient with autosomal recessive juvenile parkinsonism (ARJP) with parkin gene mutation (PARK2). The findings showed normal cardiac ¹²³I-MIBG uptake. Therefore, although the clinical features of ARJP are sometimes quite similar to those of late-onset IPD, cardiac ¹²³I-MIBG scintigraphy may be used as a valuable tool to identify patients with IPD and to distinguish them from patients with other parkinsonian syndromes.

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Parkinsonism in spinocerebellar ataxia with axonal neuropathy caused by adult-onset COA7 variants: a case report
Shogo Ouchi, Kazuhiro Ishii, Kenjiro Kosaki, Hisato Suzuki, Mamiko Yamada, Toshiki Takenouchi, Akira Tamaoka
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α‐Synuclein Deposition in Sympathetic Nerve Fibers in Genetic Forms of Parkinson's Disease
Risa Isonaka, David S. Goldstein, William Zhu, Esther Yoon, Debra Ehrlich, Alice B. Schindler, Angela D. Kokkinis, Marya S. Sabir, Sonja W. Scholz, Sara Bandres‐Ciga, Cornelis Blauwendraat, Pedro Gonzalez‐Alegre, Grisel Lopez, Ellen Sidransky, Derek P. Na
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Cardiac sympathetic burden reflects Parkinson disease burden, regardless of high or low orthostatic blood pressure changes
Sang-Won Yoo, Joong-Seok Kim, Yoon-Sang Oh, Dong-Woo Ryu, Seunggyun Ha, Ji-Yeon Yoo, Kwang-Soo Lee
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Review Article

X-Linked Dystonia Parkinsonism: Clinical Phenotype, Genetics and Therapeutics: Raymond L. Rosales; J Mov Disord. 2010;3(2):32-38.; DOI: https://doi.org/10.14802/jmd.10009

55,571 View
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Abstract PDF

The clinical phenotype of X-Linked Dystonia Parkinsonism (XDP) is typically one that involves a Filipino adult male whose ancestry is mostly traced in the Philippine island of Panay. Dystonia usually starts focally in the lower limbs or oromandibular regions, then spreads to become generalized eventually. Parkinsonism sets in later into the disease and usually in combination with dystonia. /DYT3/ and /TAF1/ are the two genes associated with XDP. An SVA retrotransposon insertion in an intron of /TAF1/ may reduce neuron-specific expression of the /TAF1/ isoform in the caudate nucleus, and subsequently interfere with the transcription of many neuronal genes. Polypharmacy with oral benzodiazepines, anticholinergic agents and muscle relaxants leaves much to be desired in terms of efficacy. The medications to date that may appear beneficial, especially in disabling dystonias, are zolpidem, muscle afferent block with lidocaine-ethanol and botulinum toxin type A. Despite the few cases undergoing deep brain stimulation, this functional surgery has shown the greatest promise in XDP. An illustrative case of XDP in a family depicts the variable course of illness, including a bout of “status dystonicus,” challenges in therapy, reckoning with the social impact of the disease, and eventual patient demise. Indeed, there remains some gaps in understanding some phenomenological, genetic and treatment aspects of XDP, the areas upon which future research directions may be worthwhile.

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Norlinah Mohamed Ibrahim, Chin Hsien Lin
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Original Article

Autonomic Dysfunctions in Parkinsonian Disorders: Hyo-Jin Bae, Sang-Myung Cheon, Jae Woo Kim; J Mov Disord. 2009;2(2):72-77.; DOI: https://doi.org/10.14802/jmd.09019

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Abstract PDF

Background and Purpose:

Symptoms of autonomic dysfunctions are common in the patients with parkinsonian disorders. Because clinical features of autonomic dysfunctions are diverse, the comprehensive evaluation is essential for the appropriate management. For the appreciation of autonomic dysfunctions and the identification of differences, patients with degenerative parkinsonisms are evaluated using structured questionnaire for autonomic dysfunction (ADQ).

Methods:

Total 259 patients, including 192 patients with [idiopathic Parkinson’s disease (IPD, age 64.6 ± 9.6 years)], 37 with [multiple system atrophy (MSA, 62.8 ± 9.1)], 9 with [dementia with Lewy body (DLB, 73.9 ± 4.3)], and 21 with [progressive supranuclear palsy (PSP, 69.4 ± 9.6)]. The ADQ was structured for evaluation of the presence of symptoms and its severity due to autonomic dysfunction, covering gastrointestinal, urinary, sexual, cardiovascular and thermoregulatory domains. Patients were also evaluated for the orthostatic hypotension.

Results:

Although dementia with Lewy body (DLB) patients were oldest and duration of disease was longest in IPD, total ADQ scores of MSA and PSP (23.9 ± 12.6 and 21.1 ± 7.8) were significantly increased than that of IPD (15.1 ± 10.6). Urinary and cardiovascular symptom scores of MSA and gastrointestinal symptom score of PSP were significantly worse than those of IPD. The ratio of patient with orthostatic hypotension in IPD was 31.2% and not differed between groups (35.1% in MSA, 33.3% in DLB and 33.3% in PSP). But the systolic blood pressure dropped drastically after standing in patients with MSA and DLB than in patients with IPD and PSP.

Conclusions:

Patients with degenerative parkinsonism showed widespread symptoms of autonomic dysfunctions. The severity of those symptoms in patients with PSP were comparing to that of MSA patients and worse than that of IPD.

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Invited Review

Positron Emission Tomography in the Differential Diagnosis of Parkinsonism: Juha O Rinne; J Mov Disord. 2009;2(2):53-57.; DOI: https://doi.org/10.14802/jmd.09015

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Abstract PDF

Positron emission tomography (PET) studies on presynaptic dopaminergic function can reveal hypofunction in early Parkinson’s disease (PD) which may help in the early diagnosis especially in patients with mild symptoms. This hypofunction can be detected with fluorodopa (reflecting mainly aromatic amino acid decarboxylase activity of nigrostriatal terminals) or dopamine transporter ligands. These studies can also help to distinguish PD from essential tremor. However, investigations of presynaptic dopaminergic function are not useful in the differential diagnosis of parkinsonian syndromes. PET ligands, such as fluorodeoxyglucose (reflecting glucose metabolism) and dopamine receptor ligands, reflecting striatal neuronal function are better in this respect. Cardiac sympathetic function studies represent a new and interesting approach to improve differential diagnosis of parkinsonian syndromes but more studies are needed in larger patient populations with longer follow-up to evaluate the usefulness of these investigations. Multitracer approach combining ligands reflecting different aspects of dopaminergic neurotransmission and other physiological function will increase differential diagnostic accuracy.

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Case Report

Parkinsonsim due to a Chronic Subdural Hematoma: Bosuk Park, Sook Keun Song, Jin Yong Hong, Phil Hyu Lee; J Mov Disord. 2009;2(1):43-44.; DOI: https://doi.org/10.14802/jmd.09011

14,634 View
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Abstract PDF

Subdural hematoma is a rare cause of parkinsonism. We present the case of a 78-year-old man with right-side dominant parkinsonism about 3 months after a minor head injury. MRI reveals a chronic subdural hematoma on the left side with mildly displaced midline structures. The parkinsonian features were almost completely disappeared after neurosurgical evacuation of the hematoma without any anti-parkinson drug.

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Catherine Rojvirat, Gabriel R. Arismendi, Erin Feinstein, Maynard Guzman, Bruce A. Citron, Vedad Delic
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Secondary parkinsonism caused by chronic subdural hematomas owing to compressed cortex and a disturbed cortico–basal ganglia–thalamocortical circuit: illustrative case
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Original Article

Comparison of Cerebral Glucose Metabolism between Possible and Probable Multiple System Atrophy: Kyum-Yil Kwon, Jae Seung Kim, Ki Chun Im, Myoung Chong Lee, Sun Ju Chung; J Mov Disord. 2009;2(1):22-28.; DOI: https://doi.org/10.14802/jmd.09006

13,051 View
93 Download
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Abstract PDF

Background:

To investigate the relationship between presenting clinical manifestations and imaging features of multisystem neuronal dysfunction in MSA patients, using ¹⁸F-fluorodeoxyglucose positron emission tomography (¹⁸F-FDG PET).

Methods:

We studied 50 consecutive MSA patients with characteristic brain MRI findings of MSA, including 34 patients with early MSA-parkinsonian (MSA-P) and 16 with early MSA-cerebellar (MSA-C). The cerebral glucose metabolism of all MSA patients was evaluated in comparison with 25 age-matched controls. ¹⁸F-FDG PET results were assessed by the Statistic Parametric Mapping (SPM) analysis and the regions of interest (ROI) method.

Results:

The mean time from disease onset to ¹⁸F-FDG PET was 25.9±13.0 months in 34 MSA-P patients and 20.1±11.1 months in 16 MSA-C patients. Glucose metabolism of the putamen showed a greater decrease in possible MSA-P than in probable MSA-P (p=0.031). Although the Unified Multiple System Atrophy Rating Scale (UMSARS) score did not differ between possible MSA-P and probable MSA-P, the subscores of rigidity (p=0.04) and bradykinesia (p= 0.008) were significantly higher in possible MSA-P than in probable MSA-P. Possible MSA-C showed a greater decrease in glucose metabolism of the cerebellum than probable MSA-C (p=0.016).

Conclusions:

Our results may suggest that the early neuropathological pattern of possible MSA with a predilection for the striatonigral or olivopontocerebellar system differs from that of probable MSA, which has prominent involvement of the autonomic nervous system in addition to the striatonigral or olivopontocerebellar system.

Citations

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F-18 FP-CIT PET in Multiple System Atrophy of the Cerebellar Type: Additional Role in Treatment
Young Jin Jeong, Sang-Myung Cheon, Do-Young Kang, Jae Woo Kim
Contrast Media & Molecular Imaging.2017; 2017: 1. CrossRef
A systematic review of lessons learned from PET molecular imaging research in atypical parkinsonism
Flavia Niccolini, Marios Politis
European Journal of Nuclear Medicine and Molecular Imaging.2016; 43(12): 2244. CrossRef

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