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Volume 3(2); October 2010
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Review Articles
Leucine-Rich Repeat Kinase 2-Linked Parkinson’s Disease: Clinical and Molecular Findings
Udhaya Kumari, Eng-King Tan
J Mov Disord. 2010;3(2):25-31.
  • 15,312 View
  • 106 Download
  • 3 Crossref
AbstractAbstract PDF

Mutations in Leucine-rich repeat kinase 2 (LRRK2) gene are the most common cause of sporadic and familial late onset Parkinson’s disease (PD). The G2019S common mutation has been identified about 1% of sporadic cases and 4–7% of familial cases. Over 50 variants have since been identified in LRRK2, and at least 7 of these are confirmed to be pathogenic. In addition to pathogenic mutations, several common polymorphisms in the LRRK2 gene (G2385R and R1628P) have been identified that may explain up to 10% of sporadic PD in Asian populations. LRRK2 is a large complex multidomain protein with 2,527-amino-acid and the molecular weight is 286 kDa. LRRK2 multidomain protein consists of a catalytic core domain, kinase domain and a number of putative protein-protein interaction domains. LRRK2 mutations found in PD families, including the G2019S and I2020T mutations show increased intrinsic kinase activity, when assessed with myelin basic protein as substrate. The modification of LRRK2 GTPase and kinase activity affecting residues in the ROC, COR and mitogen-activated protein kinase kinase kinases domains is believed to lead to neuronal cell death, but the pathways involved remain unclear. A number of in vivo models in C. elegans, D. melanogaster and mice have been developed to study the patho/physiological function of LRRK2. Based on current literature, a toxic gain of function in LRRK2 kinase activity is a possible pathophysiologic mechanism and thus inhibition of kinase activity in experimental models offers a potential therapeutic strategy for LRRK2-linked PD.


Citations to this article as recorded by  
  • Structural Insights and Development of LRRK2 Inhibitors for Parkinson’s Disease in the Last Decade
    Gunjan Thakur, Vikas Kumar, Keun Woo Lee, Chungkil Won
    Genes.2022; 13(8): 1426.     CrossRef
  • Sequential screening nominates the Parkinson's disease associated kinase LRRK2 as a regulator of Clathrin-mediated endocytosis
    George R. Heaton, Natalie Landeck, Adamantios Mamais, Mike A. Nalls, Jonathon Nixon-Abell, Ravindran Kumaran, Alexandra Beilina, Laura Pellegrini, Yan Li, Kirsten Harvey, Mark R. Cookson
    Neurobiology of Disease.2020; 141: 104948.     CrossRef
  • Target Engagement in Lead Generation
    Timothy B. Durham, Maria-Jesus Blanco
    Bioorganic & Medicinal Chemistry Letters.2015;[Epub]     CrossRef
X-Linked Dystonia Parkinsonism: Clinical Phenotype, Genetics and Therapeutics
Raymond L. Rosales
J Mov Disord. 2010;3(2):32-38.
  • 43,477 View
  • 366 Download
  • 28 Crossref
AbstractAbstract 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.


Citations to this article as recorded by  
  • A scoping review on the diagnosis and treatment of X-linked dystonia-parkinsonism
    Anisah Hayaminnah D. Alonto, Roland Dominic G. Jamora
    Parkinsonism & Related Disorders.2024; 119: 105949.     CrossRef
  • Taf1 knockout is lethal in embryonic male mice and heterozygous females show weight and movement disorders
    Elisa M. Crombie, Andrea J. Korecki, Karen Cleverley, Bethany A. Adair, Thomas J. Cunningham, Weaverly Colleen Lee, Tess C. Lengyell, Cheryl Maduro, Victor Mo, Liam M. Slade, Ines Zouhair, Elizabeth M. C. Fisher, Elizabeth M. Simpson
    Disease Models & Mechanisms.2024;[Epub]     CrossRef
  • Progressive Decline in Voice and Voice-Related Quality of Life in X-Linked Dystonia Parkinsonism
    Sungjin A. Song, Criscely L. Go, Patrick B. Acuna, Jan Kristopher Palentinos De Guzman, Nutan Sharma, Phillip C. Song
    Journal of Voice.2023; 37(1): 134.     CrossRef
  • X-linked dystonia parkinsonism: epidemiology, genetics, clinical features, diagnosis, and treatment
    Hok Leong Chin, Chia-Yi Lin, Oscar Hou-In Chou
    Acta Neurologica Belgica.2023; 123(1): 45.     CrossRef
  • Basal Ganglia Atrophy as a Marker for Prodromal X‐Linked Dystonia‐Parkinsonism
    Henrike Hanssen, Cid C. E. Diesta, Marcus Heldmann, Jackson Dy, Jeffrey Tantianpact, Julia Steinhardt, Rosanna Sauza, Hans T. S. Manalo, Andreas Sprenger, Charles Jourdan Reyes, Raphael Tuazon, Björn‐Hergen Laabs, Aloysius Domingo, Raymond L. Rosales, Chr
    Annals of Neurology.2023; 93(5): 999.     CrossRef
  • Oculomotor abnormalities indicate early executive dysfunction in prodromal X-linked dystonia-parkinsonism (XDP)
    Renana Mertin, Cid Diesta, Norbert Brüggemann, Raymond L. Rosales, Henrike Hanssen, Ana Westenberger, Julia Steinhardt, Marcus Heldmann, Hans T. S. Manalo, Jean Q. Oropilla, Christine Klein, Christoph Helmchen, Andreas Sprenger
    Journal of Neurology.2023; 270(9): 4262.     CrossRef
  • Endemic parkinsonism: clusters, biology and clinical features
    Katerina Menšíková, John C. Steele, Raymond Rosales, Carlo Colosimo, Peter Spencer, Annie Lannuzel, Yoshikazu Ugawa, Ryogen Sasaki, Santiago Giménez-Roldán, Radoslav Matej, Lucie Tuckova, Dominik Hrabos, Kristyna Kolarikova, Radek Vodicka, Radek Vrtel, Mi
    Nature Reviews Neurology.2023; 19(10): 599.     CrossRef
  • Elucidating Hexanucleotide Repeat Number and Methylation within the X-Linked Dystonia-Parkinsonism (XDP)-Related SVA Retrotransposon in TAF1 with Nanopore Sequencing
    Theresa Lüth, Joshua Laβ, Susen Schaake, Inken Wohlers, Jelena Pozojevic, Roland Dominic G. Jamora, Raymond L. Rosales, Norbert Brüggemann, Gerard Saranza, Cid Czarina E. Diesta, Kathleen Schlüter, Ronnie Tse, Charles Jourdan Reyes, Max Brand, Hauke Busch
    Genes.2022; 13(1): 126.     CrossRef
  • Prodromal X‐Linked Dystonia‐Parkinsonism is Characterized by a Subclinical Motor Phenotype
    Julia Steinhardt, Henrike Hanssen, Marcus Heldmann, Andreas Sprenger, Björn‐Hergen Laabs, Aloysius Domingo, Charles Jourdan Reyes, Jannik Prasuhn, Max Brand, Raymond Rosales, Thomas F. Münte, Christine Klein, Ana Westenberger, Jean Q. Oropilla, Cid Diesta
    Movement Disorders.2022; 37(7): 1474.     CrossRef
  • A Community-based study on the prevalence and predisposing factors of Parkinson’s disease in Barangay Mangilag Sur, Quezon Province, Philippines
    Raymond L. Rosales, Mary Camille E. Rosales, Danica Jane S.J. Robles, Ron Christian Neil T. Rodriguez, Nadia Beatrice S. Romana, Joseph Mariuz B. Rosales, Gerardo B. Salazar, Richelle Ann S. Santiano
    Clinical Parkinsonism & Related Disorders.2022; 7: 100169.     CrossRef
  • Retroelement-derived RNA and its role in the brain
    Taylor A. Evans, Jennifer Ann Erwin
    Seminars in Cell & Developmental Biology.2021; 114: 68.     CrossRef
  • Behandlungsstrategien bei oromandibulärer Dystonie
    Kazuya Yoshida
    Fortschritte der Neurologie · Psychiatrie.2021; 89(11): 562.     CrossRef
  • X-linked dystonia Parkinsonism: crossing a new threshold
    Arlene R. Ng, Roland Dominic G. Jamora, Raymond L. Rosales
    Journal of Neural Transmission.2021; 128(4): 567.     CrossRef
  • A Cross-Cultural Validation of the Filipino and Hiligaynon Versions of the Parts IIIB (Non-Motor Features) and IV (Activities of Daily Living) of the X-Linked Dystonia-Parkinsonism– MDSP Rating Scale
    Richelle Ann S. Santiano, Raymond L. Rosales
    Clinical Parkinsonism & Related Disorders.2021; 5: 100100.     CrossRef
  • Speech and swallowing deficits in X-Linked Dystonia-Parkinsonism
    Ana Luiza Zaninotto, Jan K. de Guzman, Kaila L. Stipancic, Bridget J. Perry, Melanie L. Supnet, Criscely Go, Nutan Sharma, Jordan R. Green
    Parkinsonism & Related Disorders.2021; 89: 105.     CrossRef
  • Tremor in Primary Monogenic Dystonia
    Sanjay Pandey, Sonali Bhattad, Shreya Dinesh
    Current Neurology and Neuroscience Reports.2021;[Epub]     CrossRef
  • Oromandibular Dystonia: A Clinical Examination of 2,020 Cases
    Laura M. Scorr, Stewart A. Factor, Sahyli Perez Parra, Rachel Kaye, Randal C. Paniello, Scott A. Norris, Joel S. Perlmutter, Tobias Bäumer, Tatiana Usnich, Brian D. Berman, Marie Mailly, Emmanuel Roze, Marie Vidailhet, Joseph Jankovic, Mark S. LeDoux, Ric
    Frontiers in Neurology.2021;[Epub]     CrossRef
  • Voice and swallowing dysfunction in X‐linked dystonia parkinsonism
    Phillip C. Song, Hoai Le, Patrick Acuna, Jan Kristopher Palentinos De Guzman, Nutan Sharma, Taylor N. Francouer, Marisela E. Dy, Criscely L. Go
    The Laryngoscope.2020; 130(1): 171.     CrossRef
  • Increased insula-putamen connectivity in X-linked dystonia-parkinsonism
    Anne J. Blood, Jeff L. Waugh, Thomas F. Münte, Marcus Heldmann, Aloysius Domingo, Christine Klein, Hans C. Breiter, Lillian V. Lee, Raymond L. Rosales, Norbert Brüggemann
    NeuroImage: Clinical.2018; 17: 835.     CrossRef
  • Altered glutamate response and calcium dynamics in iPSC-derived striatal neurons from XDP patients
    P. Capetian, N. Stanslowsky, E. Bernhardi, K. Grütz, A. Domingo, N. Brüggemann, M. Naujock, P. Seibler, C. Klein, F. Wegner
    Experimental Neurology.2018; 308: 47.     CrossRef
  • Eye movement deficits in X-linked dystonia-parkinsonism are related to striatal degeneration
    Andreas Sprenger, Henrike Hanssen, Imke Hagedorn, Jannik Prasuhn, Raymond L. Rosales, Roland Dominic G. Jamora, Cid C. Diesta, Aloysius Domingo, Christine Klein, Norbert Brüggemann, Christoph Helmchen
    Parkinsonism & Related Disorders.2018;[Epub]     CrossRef
  • Validation of a screening questionnaire for X‐linked dystonia parkinsonism: The first phase of the population‐based prevalence study of X‐linked dystonia parkinsonism in Panay
    Jose Danilo B Diestro, Paul Matthew D Pasco, Lillian V Lee
    Neurology and Clinical Neuroscience.2017; 5(3): 79.     CrossRef
  • Validation of the XDP–MDSP rating scale for the evaluation of patients with X-linked dystonia-parkinsonism
    Paul Matthew D. Pasco, Roland Dominic G. Jamora, Raymond L. Rosales, Cid Czarina E. Diesta, Arlene R. Ng, Rosalia A. Teleg, Criscely L. Go, Lillian Lee, Hubert H. Fernandez
    npj Parkinson's Disease.2017;[Epub]     CrossRef
  • Clinicopathological Phenotype and Genetics of X-Linked Dystonia–Parkinsonism (XDP; DYT3; Lubag)
    Toshitaka Kawarai, Ryoma Morigaki, Ryuji Kaji, Satoshi Goto
    Brain Sciences.2017; 7(7): 72.     CrossRef
  • Prevalence and Predisposing Factors of Parkinson Disease: A Community-Based Study In Barangay Mangilag Sur, Candelaria, Quezon: A Research Protocol
    Danica Jane S.J Robles, Ron Christian Neil T Rodriguez, Nadia Beatrice S Romana, Joseph Mariuz B Rosales, Mary Camille E Rosales, Gerardo B Salazar, Raymond L Rosales
    Journal of Medicine, University of Santo Tomas.2017; 1(1): 109.     CrossRef
  • Evidence of TAF1 dysfunction in peripheral models of X-linked dystonia-parkinsonism
    Aloysius Domingo, David Amar, Karen Grütz, Lillian V. Lee, Raymond Rosales, Norbert Brüggemann, Roland Dominic Jamora, Eva Cutiongco-dela Paz, Arndt Rolfs, Dirk Dressler, Uwe Walter, Dimitri Krainc, Katja Lohmann, Ron Shamir, Christine Klein, Ana Westenbe
    Cellular and Molecular Life Sciences.2016; 73(16): 3205.     CrossRef
  • Can a Positive Allosteric Modulation of GABAergic Receptors Improve Motor Symptoms in Patients with Parkinson’s Disease? The Potential Role of Zolpidem in the Treatment of Parkinson’s Disease
    Antonio Daniele, Francesco Panza, Antonio Greco, Giancarlo Logroscino, Davide Seripa
    Parkinson's Disease.2016; 2016: 1.     CrossRef
  • Introduction
    Erle C.H. Lim, Roongroj Bhidayasiri, Raymond L. Rosales, Ryuji Kaji
    Parkinsonism & Related Disorders.2011; 17: S1.     CrossRef
Original Article
Four Cases with Peripheral Trauma Induced Involuntary Movements
Eun Joo Chung, Sang Jin Kim, Won Yong Lee, Jong Seok Bae, Eung Gyu Kim, Sung Hwa Pang
J Mov Disord. 2010;3(2):39-41.
  • 9,525 View
  • 58 Download
  • 2 Crossref
AbstractAbstract PDF
Background and Purpose

Although peripheral trauma induced movement disorders have been rarely reported, diagnostic criteria for peripherally induced movement disorders (PIMD) have been established. Because preexisting subclinical movement disorders, or secondary gain for compensation and legal purposes are difficult to confirm, differential diagnosis for physicians still remains difficult.

Case Reports

We present four patients developed movement disorders after relatively various intervals after traffic accident. Three patients of them showed tremor and one patient presented propriospinal myoclonus. In this report, we investigate whether peripheral trauma can lead to movement disorders and describe the relationship between peripheral injury and movement disorders in four cases.


Injury was serious enough to develop involuntary abnormal movements with pain and the latency between injury and the onset of movements in all of cases was less than 1 year. Thus, our cases showed temporal and anatomical correlation between injury and the onset of movement disorder, strongly supporting the cause-and-effect relationship by previous diagnostic criteria for peripherally induced movement disorders.


Citations to this article as recorded by  
  • Early onset of propriospinal-like myoclonus in a child following a vertebral fracture
    Carlotta Facini, Marina Barsacchi, Benedetta Piccolo, Emanuela Claudia Turco, Francesco Pisani
    Neurology.2016; 87(9): 956.     CrossRef
  • Propriospinal myoclonus: The spectrum of clinical and neurophysiological phenotypes
    E. Antelmi, F. Provini
    Sleep Medicine Reviews.2014;[Epub]     CrossRef
Case Reports
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.
  • 12,951 View
  • 56 Download
  • 4 Crossref
AbstractAbstract 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.


Citations to this article as recorded by  
  • 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
    BMC Neurology.2023;[Epub]     CrossRef
  • 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
    Movement Disorders.2021; 36(10): 2346.     CrossRef
  • 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
    npj Parkinson's Disease.2021;[Epub]     CrossRef
  • Normal ‘heart’ in Parkinson's disease: is this a distinct clinical phenotype?
    J.‐S. Kim, H.‐E. Park, I.‐S. Park, Y.‐S. Oh, D.‐W. Ryu, I.‐U. Song, Y.‐A. Jung, I. R. Yoo, H.‐S. Choi, P. H. Lee, K.‐S. Lee
    European Journal of Neurology.2017; 24(2): 349.     CrossRef
A Case of Juvenile Huntington Disease in a 6-Year-Old Boy
Jun-Sang Sunwoo, Soon-Tae Lee, Manho Kim
J Mov Disord. 2010;3(2):45-47.
  • 9,443 View
  • 65 Download
  • 5 Crossref
AbstractAbstract PDF

Huntington disease is a neurodegenerative disorder distinguished by the triad of dominant inheritance, choreoathetosis and dementia, usually with onset in the fourth and fifth decades. It is caused by an unstable cytosine-adenine-guanine (CAG) trinucleotide repeat expansion in the gene IT15 in locus 4p16.3. Juvenile HD that constitutes about 3% to 10% of all patients is clinically different from adult-onset form and characterized by a larger number of CAG repeats typically exceeding 60. We report a case of a 6-year-old boy with myoclonic seizure and 140 CAG repeats confirmed by molecular genetic analysis.


Citations to this article as recorded by  
  • Clinical Review of Juvenile Huntington’s Disease
    Mayke Oosterloo, Alexiane Touze, Lauren M. Byrne, Jannis Achenbach, Hande Aksoy, Annabelle Coleman, Dawn Lammert, Martha Nance, Peggy Nopoulos, Ralf Reilmann, Carsten Saft, Helen Santini, Ferdinando Squitieri, Sarah Tabrizi, Jean-Marc Burgunder, Oliver Qu
    Journal of Huntington's Disease.2024; 13(2): 149.     CrossRef
  • Drug-Resistant Epilepsy in Children with Juvenile Huntington's Disease: A Challenging Case and Brief Review
    Abdulhafeez M. Khair MD, Jessica Kabrt DO, Stephen Falchek MD
    Qatar Medical Journal .2020;[Epub]     CrossRef
  • Introducing an expanded CAG tract into the huntingtin gene causes a wide spectrum of ultrastructural defects in cultured human cells
    Ksenia N. Morozova, Lyubov A. Suldina, Tuyana B. Malankhanova, Elena V. Grigor’eva, Suren M. Zakian, Elena Kiseleva, Anastasia A. Malakhova, Hiroyoshi Ariga
    PLOS ONE.2018; 13(10): e0204735.     CrossRef
  • Tics as an initial manifestation of juvenile Huntington’s disease: case report and literature review
    Shi-Shuang Cui, Ru-Jing Ren, Ying Wang, Gang Wang, Sheng-Di Chen
    BMC Neurology.2017;[Epub]     CrossRef
  • Neuropathological Comparison of Adult Onset and Juvenile Huntington’s Disease with Cerebellar Atrophy: A Report of a Father and Son
    Caitlin S. Latimer, Margaret E. Flanagan, Patrick J. Cimino, Suman Jayadev, Marie Davis, Zachary S. Hoffer, Thomas J. Montine, Luis F. Gonzalez-Cuyar, Thomas D. Bird, C. Dirk Keene
    Journal of Huntington's Disease.2017; 6(4): 337.     CrossRef
A Case of Action-Induced Clonus that Mimicked Action Tremors and was Associated with Cervical Schwannoma
Young-Hee Sung, Ki-Hyung Park, Yeung-Bae Lee, Hyeon-Mi Park, Dong-Jin Shin
J Mov Disord. 2010;3(2):48-50.
  • 13,599 View
  • 46 Download
  • 1 Crossref
AbstractAbstract PDF

Clonus is the rhythmic muscle contraction which usually occurs in patients with lesions involving descending motor pathways. Sometimes, rhythmic oscillation of action induced clonus could be confused to action tremor. We report a case of action induced clonus associated with cervical schwannoma which was misdiagnosed as essential tremor. The patient had spasticity in all limbs with exaggerated tendon reflexes, and passive stretch-induced clonus. Imaging and histological examinations revealed a schwannoma extending from C2 to C7. The lesion was partially removed by surgery. Even though essential tremor is a common disease, clinician have to do sufficient neurologic examination considering differential diagnosis.


Citations to this article as recorded by  
  • Wrist clonus mimicking as action-induced tremors: an important clinical lesson
    Bhawna Sharma, Raghavendra Bakki Sannegowda, Kadam Nagpal, Rahul Jain
    BMJ Case Reports.2012; : bcr2012006804.     CrossRef
Preserved Glucose Metabolism of Deep Cerebellar Nuclei in a Case of Multiple System Atrophy with Predominant Cerebellar Ataxia: F-18 Fluorodeoxyglucose Positron Emission Tomography Study
Oh Dae Kwon, Chang-Seok Ki
J Mov Disord. 2010;3(2):51-53.
  • 20,069 View
  • 36 Download
AbstractAbstract PDF

The cerebellar glucose metabolism of multiple system atrophy with predominant cerebellar ataxia (MSA-C) is known to be decreased but is not defined among areas of cerebellum. We encountered a 54-year-old man who developed dizziness and progressive ataxia followed by urinary incontinence and orthostatic hypotension, all of those symptoms progressed relentlessly and the symptoms responded poorly to levodopa therapy. Visual analysis and statistical parametric mapping analysis of F-18 fluorodeoxyglucose positron emission tomography showed hypometabolism of both cerebellar hemisphere, severe at cortical area, and pons. There was clear sparing of deep cerebellar nuclei. Our report, as we know, shows the first case of preserved glucose metabolism of deep cerebellar nuclei relative to cerebellar cortex in an MSA-C patient.

Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated with Pramipexole in a Patient with Parkinson’s Disease
Yoonjae Choi, Jeong Jin Park, Na Young Ryoo, So-Hyun Kim, Changseok Song, Im-Tae Han, Chang-Gi Hong, Choong Kun Ha, Seong Hye Choi
J Mov Disord. 2010;3(2):54-56.
  • 28,477 View
  • 101 Download
  • 4 Crossref
AbstractAbstract PDF

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can be caused by a variety of drugs. Dopaminergic drugs might enhance the secretion of the antidiuretic hormone arginine vasopressin by reducing γ-amino butyric acid release through the dopaminergic receptor in supraoptic nucleus. A 75-year-old woman with Parkinson’s disease developed asthenia, delirium, aggravated parkinsonian symptoms, and hypotonic hyponatremia along with the diagnostic criteria for SIADH during dose escalation of pramipexole. After pramipexole withdrawal, these symptoms disappeared, and sodium levels returned to normal values. The serum sodium levels of patients receiving pramipexole should be monitored, especially during dose escalation.


Citations to this article as recorded by  
  • Syndrome of Inappropriate Antidiuretic Hormone Secretion as a Presentation of Untreated Parkinson’s Disease
    Karim Ali, Yaseen Najjar, Swati Mehta , Geovani Faddoul
    Cureus.2023;[Epub]     CrossRef
  • Is Restless Legs Syndrome De Facto Thyroid Disease?
    Szymon Suwała, Jakub Rzeszuto, Rafał Glonek, Magdalena Krintus, Roman Junik
    Biomedicines.2022; 10(10): 2502.     CrossRef
  • Levodopa-carbidopa intestinal gel is an option in Parkinson’s disease with hyponatremia induced by dopamine agonists
    Marina Picillo, Vincenzo Canoro, Giulio Cicarelli, Roberto Erro, Paolo Barone
    Neurological Sciences.2020; 41(11): 3361.     CrossRef
  • Liquid Levodopa/Carbidopa: Old Solution, Forgotten Complication
    Nirosen Vijiaratnam, Shuli Cheng, Kelly Lucinda Bertram, David Richard Williams
    Journal of Movement Disorders.2017; 10(3): 164.     CrossRef

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