Journal of Movement Disorders

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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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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Current directions in tau research: Highlights from Tau 2020
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
Movement Disorders.2022; 37(9): 1915. CrossRef
Imaging pathological tau in atypical parkinsonisms: A review
Anastassia M. Mena, Antonio P. Strafella
Clinical Parkinsonism & Related Disorders.2022; 7: 100155. CrossRef
Integrated 18F-T807 Tau PET, Structural MRI, and Plasma Tau in Tauopathy Neurodegenerative Disorders
Cheng-Hsuan Li, Ta-Fu Chen, Ming-Jang Chiu, Ruoh-Fang Yen, Ming-Chieh Shih, Chin-Hsien Lin
Frontiers in Aging Neuroscience.2021;[Epub] CrossRef
Dual-Phase 18F-FP-CIT PET in Corticobasal Syndrome
Je Hong Min, Dong Gyu Park, Jung Han Yoon, Young Sil An
Clinical Nuclear Medicine.2019; 44(1): e49. CrossRef
Tau Positron-Emission Tomography in Former National Football League Players
Robert A. Stern, Charles H. Adler, Kewei Chen, Michael Navitsky, Ji Luo, David W. Dodick, Michael L. Alosco, Yorghos Tripodis, Dhruman D. Goradia, Brett Martin, Diego Mastroeni, Nathan G. Fritts, Johnny Jarnagin, Michael D. Devous, Mark A. Mintun, Michael
New England Journal of Medicine.2019; 380(18): 1716. CrossRef

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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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

Clinical Heterogeneity of Atypical Pantothenate Kinase-Associated Neurodegeneration in Koreans: Jae-Hyeok Lee, Jongkyu Park, Ho-Sung Ryu, Hyeyoung Park, Young Eun Kim, Jin Yong Hong, Sang Ook Nam, Young-Hee Sung, Seung-Hwan Lee, Jee-Young Lee, Myung Jun Lee, Tae-Hyoung Kim, Chul Hyoung Lyoo, Sun Ju Chung, Seong Beom Koh, Phil Hyu Lee, Jin Whan Cho, Mee Young Park, Yun Joong Kim, Young H. Sohn, Beom Seok Jeon, Myung Sik Lee; J Mov Disord. 2016;9(1):20-27. Published online January 25, 2016; DOI: https://doi.org/10.14802/jmd.15058

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Objective
Neurodegeneration with brain iron accumulation (NBIA) represents a group of inherited movement disorders characterized by iron accumulation in the basal ganglia. Recent advances have included the identification of new causative genes and highlighted the wide phenotypic variation between and within the specific NBIA subtypes. This study aimed to investigate the current status of NBIA in Korea.
Methods
We collected genetically confirmed NBIA patients from twelve nationwide referral hospitals and from a review of the literature. We conducted a study to describe the phenotypic and genotypic characteristics of Korean adults with atypical pantothenate kinase-associated neurodegeneration (PKAN).
Results
Four subtypes of NBIA including PKAN (n = 30), PLA2G6-related neurodegeneration (n = 2), beta-propeller protein-associated neurodegeneration (n = 1), and aceruloplasminemia (n = 1) have been identified in the Korean population. The clinical features of fifteen adults with atypical PKAN included early focal limb dystonia, parkinsonism-predominant feature, oromandibular dystonia, and isolated freezing of gait (FOG). Patients with a higher age of onset tended to present with parkinsonism and FOG. The p.R440P and p.D378G mutations are two major mutations that represent approximately 50% of the mutated alleles. Although there were no specific genotype-phenotype correlations, most patients carrying the p.D378G mutation had a late-onset, atypical form of PKAN.
Conclusions
We found considerable phenotypic heterogeneity in Korean adults with atypical PKAN. The age of onset may influence the presentation of extrapyramidal symptoms.

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Typical pantothenate kinase-associated neurodegeneration caused by compound heterozygous mutations in PANK2 gene in a Chinese patient: a case report and literature review
Yilun Tao, Chen Zhao, Dong Han, Yiju Wei, Lihong Wang, Wenxia Song, Xiaoze Li
Frontiers in Neurology.2023;[Epub] CrossRef
The first Vietnamese patient who presented late onset of pantothenate kinase-associated neurodegeneration diagnosed by whole exome sequencing: A case report
Van Khanh Tran, Chi Dung Vu, Hai Anh Tran, Nguyen Thi Kim Lien, Nguyen Van Tung, Nguyen Ngoc Lan, Huy Thinh Tran, Nguyen Huy Hoang
Medicine.2023; 102(43): e34853. CrossRef
Genetic mutation spectrum of pantothenate kinase-associated neurodegeneration expanded by breakpoint sequencing in pantothenate kinase 2 gene
Dahae Yang, Sanghyun Cho, Sung Im Cho, Manjin Kim, Moon-Woo Seong, Sung Sup Park
Orphanet Journal of Rare Diseases.2022;[Epub] CrossRef
Long-Term Outcomes of Deep Brain Stimulation in Pantothenate Kinase-Associated Neurodegeneration-Related Dystonia
Kyung Ah Woo, Han-Joon Kim, Seung-Ho Jeon, Hye Ran Park, Kye Won Park, Seung Hyun Lee, Sun Ju Chung, Jong-Hee Chae, Sun Ha Paek, Beomseok Jeon
Journal of Movement Disorders.2022; 15(3): 241. CrossRef
Psychiatric symptoms in an adolescent reveal a novel compound heterozygous mutation of the PANK2 gene in the atypical PKAN syndrome
Luz María González Huerta, Sorina Gómez González, Jaime Toral López
Psychiatric Genetics.2021; 31(3): 95. CrossRef
Rational Design of Novel Therapies for Pantothenate Kinase–Associated Neurodegeneration
Nivedita Thakur, Thomas Klopstock, Suzanne Jackowski, Enej Kuscer, Fernando Tricta, Aleksandar Videnovic, Hyder A. Jinnah
Movement Disorders.2021; 36(9): 2005. CrossRef
Atypical Pantothenate Kinase-Associated Neurodegeneration with variable phenotypes in an Egyptian family
Ali S. Shalash, Thomas W. Rösler, Ibrahim Y. Abdelrahman, Hatem S. Abulmakarem, Stefanie H. Müller, Franziska Hopfner, Gregor Kuhlenbäumer, Günter U. Höglinger, Mohamed Salama
Heliyon.2021; : e07469. CrossRef
Treatment Responsiveness of Parkinsonism in Atypical Pantothenate Kinase‐Associated Neurodegeneration
Jeanne Feuerstein, Caroline Olvera, Michelle Fullard
Movement Disorders Clinical Practice.2020;[Epub] CrossRef
Diagnostic and clinical experience of patients with pantothenate kinase-associated neurodegeneration
Randall D. Marshall, Abigail Collins, Maria L. Escolar, H. A. Jinnah, Thomas Klopstock, Michael C. Kruer, Aleksandar Videnovic, Amy Robichaux-Viehoever, Colleen Burns, Laura L. Swett, Dennis A. Revicki, Randall H. Bender, William R. Lenderking
Orphanet Journal of Rare Diseases.2019;[Epub] CrossRef
Intrafamilial variability and clinical heterogeneity in a family with PLA2G6-associated neurodegeneration
Jong Kyu Park, Jinyoung Youn, Jin Whan Cho
Precision and Future Medicine.2019; 3(3): 135. CrossRef
On the complexity of clinical and molecular bases of neurodegeneration with brain iron accumulation
C. Tello, A. Darling, V. Lupo, B. Pérez‐Dueñas, C. Espinós
Clinical Genetics.2018; 93(4): 731. CrossRef
Looking Deep into the Eye-of-the-Tiger in Pantothenate Kinase–Associated Neurodegeneration
J.-H. Lee, A. Gregory, P. Hogarth, C. Rogers, S.J. Hayflick
American Journal of Neuroradiology.2018; 39(3): 583. CrossRef
Parkinson’s Disease and Metal Storage Disorders: A Systematic Review
Edward Botsford, Jayan George, Ellen Buckley
Brain Sciences.2018; 8(11): 194. CrossRef
Atypical pantothenate kinase-associated neurodegeneration: Clinical description of two brothers and a review of the literature
S. Mahoui, A. Benhaddadi, W. Ameur El Khedoud, M. Abada Bendib, M. Chaouch
Revue Neurologique.2017; 173(10): 658. CrossRef
Clinical rating scale for pantothenate kinase‐associated neurodegeneration: A pilot study
Alejandra Darling, Cristina Tello, María Josep Martí, Cristina Garrido, Sergio Aguilera‐Albesa, Miguel Tomás Vila, Itziar Gastón, Marcos Madruga, Luis González Gutiérrez, Julio Ramos Lizana, Montserrat Pujol, Tania Gavilán Iglesias, Kylee Tustin, Jean Pie
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Letter to the editor

Parkinsonism and Dementia Associated with Giant Virchow-Robin Spaces: Myung Sik Lee, Cheol Hyung Lyoo, Tae Sub Chung; J Mov Disord. 2015;8(2):106-107. Published online May 31, 2015; DOI: https://doi.org/10.14802/jmd.15013

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M.O. Iridoy, P. Clavero, T. Cabada, M.E. Erro
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Original Article

Current Status of Huntington’s Disease in Korea: A Nationwide Survey and National Registry Analysis: Hyun Sook Kim, Chul Hyoung Lyoo, Phil Hyu Lee, Sang Jin Kim, Mee Young Park, Hyeo-Il Ma, Jae Hyeok Lee, Sook Kun Song, Jong Sam Baik, Jin Ho Kim, Myung Sik Lee; J Mov Disord. 2015;8(1):14-20. Published online January 31, 2015; DOI: https://doi.org/10.14802/jmd.14038

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Objective Huntington’s disease (HD) is a rare neurological disorder, and its current status in Korea is not well investigated. This study aims to determine the prevalence and incidence of HD and to investigate the clinical features of HD patients in Korea.
Methods We estimated the crude prevalence and annual incidence of HD based on the databases of the Rare Diseases Registry (RDR) and the National Health Insurance (NHI). The clinical data of genetically confirmed HD patients was collected from 10 referral hospitals and analyzed.
Results The mean calculated annual incidence was 0.06 cases per 100,000 persons, and the mean calculated prevalence was 0.38 based on the NHI database. The estimated crude prevalence based on the RDR was 0.41. Of the sixty-eight HD patients recruited, the mean age of onset was 44.16 ± 14.08 years and chorea was most frequently reported as the initial symptom and chief complaint. The mean CAG repeat number of the expanded allele was 44.7 ± 4.8 and correlated inversely with the age of onset (p < 0.001). About two-thirds of the patients have a positive family history, and HD patients without positive family history showed a delay in onset of initial symptoms, a prolonged interval between initial symptom onset and genetic diagnosis and a delay in the age of genetic diagnosis.
Conclusions To the best of our knowledge, this is the first study to estimate the prevalence and incidence of HD in Korea and the largest HD series in the Asian population. Our analyses might be useful for further studies and large-scale investigations in HD patients.

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Dnyandev G. Gadhave, Vrashabh V. Sugandhi, Saurav Kumar Jha, Sopan N. Nangare, Gaurav Gupta, Sachin Kumar Singh, Kamal Dua, Hyunah Cho, Philip M. Hansbro, Keshav Raj Paudel
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Clinical and Genetic Characteristics Associated With Survival Outcome in Late-Onset Huntington’s Disease in South Korea
Yun Su Hwang, Sungyang Jo, Gu-Hwan Kim, Jee-Young Lee, Ho-Sung Ryu, Eungseok Oh, Seung-Hwan Lee, Young Seo Kim, Sun Ju Chung
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Sohee Jung, Gucheol Jung, Dayoung Kim, Jeeyoung Oh, Kyomin Choi
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Increased 10-Year Prevalence of Huntington’s Disease in South Korea: An Analysis of Medical Expenditure Through the National Healthcare System
Chan Young Lee, Jun-soo Ro, Hyemin Jung, Manho Kim, Beomseok Jeon, Jee-Young Lee
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Sarah A. O'Shea, Ludy C. Shih
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Case Reports

Psychogenic Balance Disorders: Is It a New Entity of Psychogenic Movement Disorders?: Jong Sam Baik, Myung Sik Lee; J Mov Disord. 2012;5(1):24-27.; DOI: https://doi.org/10.14802/jmd.12007

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Abstract PDF

The various reported psychogenic dyskinesias include tremor, dystonia, myoclonus, gait disorder, Parkinsonism, tics, and chorea. It is not easy to diagnose psychogenic movement disorders, especially in patients with underlying organic disease. We describe three patients with balance and/or posture abnormalities that occur when they stand up, start to move, or halt from walking, although their gaits are normal. One had an underlying unilateral frontal lobe lesion. All patients improved dramatically after receiving a placebo-injection or medication. These abnormal features differ from the previously reported features of astasia without abasia and of psychogenic gait disorders, including recumbent gait. We describe and discuss the patients’ unique clinical characteristics.

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Somatization in Parkinson's Disease: A systematic review
Danilo Carrozzino, Per Bech, Chiara Patierno, Marco Onofrj, Bo Mohr Morberg, Astrid Thomas, Laura Bonanni, Mario Fulcheri
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Functional movement disorders
Anita Barbey, Selma Aybek
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Neuroleptic Malignant Syndrome in a Patient with Corticobasal Degeneration: Myung Jun Lee, Chul Hyoung Lyoo, Myung Sik Lee; J Mov Disord. 2011;4(2):73-74.; DOI: https://doi.org/10.14802/jmd.11015

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Abstract PDF

Parkinson’s disease is a principal underlying disease of neuroleptic malignant syndrome (NMS) occurring in parkinsonian disorders, but NMS may occur in patients with progressive supranuclear palsy and multiple system atrophy. We report first patient with corticobasal degeneration (CBD) who developed NMS after abrupt reduction of antiparkinsonian medication and concurrent infection. It should be kept in mind that the prevention of infectious illness, which is common complication in parkinson-plus syndrome, is important, and dose reduction or withdrawal of anti-parkinsonian medications should be carefully performed even in the patients with CBD who are expected to be unresponsive to levodopa treatment.

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Diagnosis and Management of Progressive Corticobasal Syndrome
Claire Delpirou Nouh, Kyan Younes
Current Treatment Options in Neurology.2024; 26(7): 319. CrossRef

Oculogyric Crisis Associated with Disulfiram-Induced Pallidonigral Lesion: Jae Hyeok Lee, Chul Hyoung Lyoo, Jin Goo Lee, Myung Sik Lee; J Mov Disord. 2009;2(1):48-49.; DOI: https://doi.org/10.14802/jmd.09013

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Abstract PDF

We report a man who developed oculogyric crisis one month after disulfiram intoxication. Brain MRI showed lesions involving bilateral globus pallidus and left substantia nigra. In our patient, neuronal discharges from pathologically reorganized basal ganglia circuit to the mid-brain ocular motor center might lead to tonic deviation of the eyes.

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Oculogyric Crisis in a Wilson's Disease Patient
Ping Jin, Xiao‐Ming Fu, Yu Wang, Xin‐Feng Ma, Wen‐Long Ai, Ya‐Yun Xu, Bo Li, Qun‐Rong Ye, Gong‐Qiang Wang
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Delayed onset of impaired consciousness complicated with ketoacidosis after disulfiram overdose
Kohei Kakimoto, Mayu Hikone, Kazuhiro Sugiyama
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A Case of Genetically Confirmed Spinocerebellar Ataxia Type 8: Gyoungim Suh, Won Chan Kim, Myung Sik Lee; J Mov Disord. 2008;1(2):90-92.; DOI: https://doi.org/10.14802/jmd.08017

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Abstract PDF: Spinocerebellar ataxia type 8 patients typically have a slowly progressive, adult-onset ataxia. SCA8 is characterized by relatively pure cerebellar ataxia, which is caused by the expansion of combined CTA/CTG repeats on chromosome 13q21. We report a 58 years old woman with slowly progressive dysarthria, and gait ataxia. We performed genetic studies for SCA 1, 2, 3, 6, 7, 8, 17 and detected CTA/CTG repeat expansion in the SCA8 gene.

Original Articles

The Relationship Between Plasma Homocysteine Level and C677T MTHFR Genotype in Drug-Naive Patients With Idiopathic Parkinson’s Disease: Il Hyung Lee, Hyun Sook Kim, Ok Joon Kim, Won Chan Kim, Myung Sik Lee; J Mov Disord. 2008;1(2):71-74.; DOI: https://doi.org/10.14802/jmd.08013

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Abstract PDF: Backgrounds:
The cause of idiopathic Parkinson’s disease (IPD) is unknown, but reduced activity of complex I of the electron-transport chain has been implicated in the pathogenesis of IPD. Hyperhomocysteinemia is a well-established risk factor for cardiovascular and cerebrovascular diseases. However, recent evidence suggests that changes in the metabolic fate of homocysteine, leading to hyperhomocysteinemia, may also play a role in the pathophysiology of IPD.
Methods:
Age and sex-matched 41 drug-naive IPD patients (16 men and 25 women) and 161 healthy controls (66 men and 95 women) were included in this study. Their fasting plasma homocystein and folate level, and the genotypes of methylenetetrahydrofolate reductase (MTHFR) were analyzed.
Results:
The plasma level of homocysteine was higher in untreated IPD patients (12.0±2.9 μmol/L) compared to the controls (9.0±2.6 μmol/L) (p =0.001). The frequencies of MTHFR C677T genotypes were not different between patients (CC:CT:TT=7:23:11) and controls (CC:CT:TT=27:86:48) (p =0.930). The adjusted odds ratio of homocysteine was remarkable (adjusted OR=1.149, 95% confidential interval=1.66–2.28, p =0.004).
Conclusions:
IPD patients have higher plasma homocysteine level than healthy controls but MTHFR C667T genotype was not related to the homocysteine level. It can be suggested that increased plasma homocysteine level may contribute to the pathogenesis of IPD.

Relationship Between the Striatal and Cerebellar Glucose Metabolism and the Response to Levodopa Treatment in Patients With Multiple System Atrophy: Chul Hyoung Lyoo, Seung Hun Oh, Ki Ook Lee, Seung Yeob Lee, Young Hoon Ryu, Myung Sik Lee; J Mov Disord. 2008;1(1):26-32.; DOI: https://doi.org/10.14802/jmd.08005

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Abstract PDF: Introduction:
About two thirds of the patients with multiple system atrophy (MSA) do not respond to levodopa treatment. Postmortem pathological studies and one retrospective [¹⁸F]-deoxyglucose positron emission tomography (FDGPET) study attributed such poor response to the striatal degeneration. We prospectively investigated the relationship between levodopa responsiveness and the metabolic activities of the striatum and cerebellum in MSA patients.
Methods:
In 39 patients with MSA, the UPDRS motor score was assessed and two sets of timed motor tests were perform ed before and after the levodopa treatment. After quantitative FDG PET and baseline evaluation, treatment w as started with 3 tablets of Sinemet^® 25/250 mg a day. Clinical assessments were performed monthly for three months. Metabolic activities of the caudate, anterior putamen, posterior putamen, cerebellar cortex and cerebellar vermis were measured. We compared the measurements with mean percentage changes of motor function. Also, using statistical parametric mapping (SPM) analysis, we tried to find brain areas in which metabolism correlated with the clinical changes.
Results:
Mean percentage improvements of UPDRS motor scores w ere correlated with glucose metabolism in the posterior putamen and cerebellar vermis. The mean percentage improvements of performance in Purdue peg board test correlated with the glucose metabolism in the cerebellar cortex and vermis. In SPM analysis, cerebellar glucose metabolism correlated with the improvement of UPDRS motor score and the performance of two timed motor tests.
Conclusion:
The integrity of cerebellum, as well as posterior putamen, may be an important factor for showing the response to levodopa.

Falls and Physical Injuries in Patients With Parkinson’s Disease: Tae-Jin Song, Do Hyun Kim, Kwon-Duk Seo, Seung-Hun Oh, Chul Hyoung Lyoo, Myung Sik Lee; J Mov Disord. 2008;1(1):13-18.; DOI: https://doi.org/10.14802/jmd.08003

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1 Crossref

Abstract PDF

Background:

In Parkinson’s disease (PD), falls and subsequent physical injuries are frequent causes of morbidity and mortality. We investigated the characteristics of falls and physical injuries in Korean patients with PD.

Methods:

This study included 239 patients with PD. Using the medical records and interviews, we studied the characteristics of fall and its consequences retrospectively.

Results:

Among the 239 patients with PD, 129 (54.0%) patients had a history of fall. The mean interval between the disease onset and the first fall was 15.3 months. Among them, 83 patients (64.3%) fell more than twice. Eighty-six patients (66.7%) had physical injuries and 21 patients (15.3%) had fractures including 7 with hip fracture and 7 with arm fracture. Patients with physical injuries fell earlier and repetitively. They tended to fall during the night, toward lateral or posterior direction, and were unable to make protective hand movements.

Conclusions:

Elderly PD patients with long duration have a high risk of fall. To prevent the physical injuries, the clinicians should try to reduce the off time and advice the patients and caregivers to limit physical activities during the night.

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A retrospective study on the management of osteoporosis in Parkinson's disease – A single institution, preliminary study
Kwang-Kyoun Kim, Tae-Kyun Kim, Yougun Won, Won-Sub Sung
Osteoporosis and Sarcopenia.2015; 1(1): 59. CrossRef

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