Journal of Movement Disorders

Original Article

Nonmotor and Dopamine Transporter Change in REM Sleep Behavior Disorder by Olfactory Impairment: Jee-Young Lee, Eun Jin Yoon, Yu Kyeong Kim, Chae Won Shin, Hyunwoo Nam, Jae Min Jeong, Han-Joon Kim, Beomseok Jeon; J Mov Disord. 2019;12(2):103-112. Published online May 30, 2019; DOI: https://doi.org/10.14802/jmd.18061

8,206 View
215 Download
18 Web of Science
17 Crossref

Objective
It is unclear whether the decline in dopamine transporters (DAT) differs among idiopathic rapid eye movement sleep behavior disorder (iRBD) patients with different levels of olfactory impairment. This study aimed to characterize DAT changes in relation to nonmotor features in iRBD patients by olfactory loss.
Methods
This prospective cohort study consisted of three age-matched groups: 30 polysomnography-confirmed iRBD patients, 30 drug-naïve Parkinson’s disease patients, and 19 healthy controls without olfactory impairment. The iRBD group was divided into two groups based on olfactory testing results. Participants were evaluated for reported prodromal markers and then underwent 18F-FP-CIT positron emission tomography and 3T MRI. Tracer uptakes were analyzed in the caudate, anterior and posterior putamen, substantia nigra, and raphe nuclei.
Results
Olfactory impairment was defined in 38.5% of iRBD patients. Mild parkinsonian signs and cognitive functions were not different between the two iRBD subgroups; however, additional prodromal features, constipation, and urinary and sexual dysfunctions were found in iRBD patients with olfactory impairment but not in those without. Tracer uptake showed significant group differences in all brain regions, except the raphe nuclei. The iRBD patients with olfactory impairment had uptake reductions in the anterior and posterior putamen, caudate, and substantia nigra (p < 0.016 in all, adjusted for age), which ranged from 0.6 to 0.8 of age-normative values. In contrast, those without olfactory impairment had insignificant changes in all regions ranging above 0.8.
Conclusion
There was a clear distinction in DAT loss and nonmotor profiles by olfactory status in iRBD.

Citations

Citations to this article as recorded by

Neuropsychological Changes in Isolated REM Sleep Behavior Disorder: A Systematic Review and Meta-analysis of Cross-sectional and Longitudinal Studies
Caterina Leitner, Giada D’Este, Laura Verga, Shady Rahayel, Samantha Mombelli, Marco Sforza, Francesca Casoni, Marco Zucconi, Luigi Ferini-Strambi, Andrea Galbiati
Neuropsychology Review.2024; 34(1): 41. CrossRef
Dopamine transporter positron emission tomography in patients with Alzheimer’s disease with Lewy body disease features
Sungwoo Kang, Seun Jeon, Young-gun Lee, Byoung Seok Ye
Neurobiology of Aging.2024; 134: 57. 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
Validation of the REM behaviour disorder phenoconversion-related pattern in an independent cohort
Beatrice Orso, Pietro Mattioli, Eun-Jin Yoon, Yu Kyeong Kim, Heejung Kim, Jung Hwan Shin, Ryul Kim, Claudio Liguori, Francesco Famà, Andrea Donniaquio, Federico Massa, David Vállez García, Sanne K. Meles, Klaus L. Leenders, Agostino Chiaravalloti, Matteo
Neurological Sciences.2023; 44(9): 3161. CrossRef
Neurofilament light chain and cardiac MIBG uptake as predictors for phenoconversion in isolated REM sleep behavior disorder
Don Gueu Park, Ju Yeong Kim, Min Seung Kim, Mi Hee Kim, Young-Sil An, Jaerak Chang, Jung Han Yoon
Journal of Neurology.2023; 270(9): 4393. CrossRef
Longitudinal evolution of cortical thickness signature reflecting Lewy body dementia in isolated REM sleep behavior disorder: a prospective cohort study
Jung Hwan Shin, Heejung Kim, Yu Kyeong Kim, Eun Jin Yoon, Hyunwoo Nam, Beomseok Jeon, Jee-Young Lee
Translational Neurodegeneration.2023;[Epub] CrossRef
Brain olfactory‐related atrophy in isolated rapid eye movement sleep behavior disorder
Kyung Ah Woo, Heejung Kim, Eun Jin Yoon, Jung Hwan Shin, Hyunwoo Nam, Beomseok Jeon, Yu Kyeong Kim, Jee‐Young Lee
Annals of Clinical and Translational Neurology.2023; 10(12): 2192. CrossRef
Monoaminergic Degeneration and Ocular Motor Abnormalities in De Novo Parkinson's Disease
Kyung Ah Woo, Joo Hong Joun, Eun Jin Yoon, Chan Young Lee, Beomseok Jeon, Yu Kyeong Kim, Jee‐Young Lee
Movement Disorders.2023; 38(12): 2291. CrossRef
Altered cerebral perfusion and microstructure in advanced Parkinson’s disease and their associations with clinical features
Zhaoxi Liu, Yiwei Zhang, Han Wang, Dan Xu, Hui You, Zhentao Zuo, Feng Feng
Neurological Research.2022; 44(1): 47. CrossRef
Brain Neuroimaging of Rapid Eye Movement Sleep Behavior Disorder in Parkinson’s Disease: A Systematic Review
Rafail Matzaras, Kuangyu Shi, Artemios Artemiadis, Panagiotis Zis, Georgios Hadjigeorgiou, Axel Rominger, Claudio L.A. Bassetti, Panagiotis Bargiotas
Journal of Parkinson's Disease.2022; 12(1): 69. CrossRef
Odor Identification by Parkinson’s Disease Patients Tested by Using Sniffin’ Sticks versus Natural Spices
Florence Baert, Geertrui Vlaemynck, Jarissa Maselyne, Christophe Matthys, Seyed-Mohammad Fereshtehnejad
Parkinson's Disease.2022; 2022: 1. CrossRef
Brain Metabolic Correlates of Dopaminergic Denervation in Prodromal and Early Parkinson's Disease
Ryul Kim, Heejung Kim, Yu Kyeong Kim, Eun Jin Yoon, Hyun Woo Nam, Beomseok Jeon, Jee‐Young Lee
Movement Disorders.2022; 37(10): 2099. CrossRef
Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression
Ryul Kim, Jee‐Young Lee, Yu Kyeong Kim, Heejung Kim, Eun Jin Yoon, Jung Hwan Shin, Dallah Yoo, Hyunwoo Nam, Beomseok Jeon
Movement Disorders.2021; 36(8): 1889. CrossRef
Parkinson Disease-Related Brain Metabolic Patterns and Neurodegeneration in Isolated REM Sleep Behavior Disorder
Jung Hwan Shin, Jee-Young Lee, Yu-Kyeong Kim, Eun Jin Yoon, Heejung Kim, Hyunwoo Nam, Beomseok Jeon
Neurology.2021;[Epub] CrossRef
Retina Thickness as a Marker of Neurodegeneration in Prodromal Lewy Body Disease
Jee‐Young Lee, Jeeyun Ahn, Sohee Oh, Joo Young Shin, Yu Kyeong Kim, Hyunwoo Nam, Beomseok Jeon
Movement Disorders.2020; 35(2): 349. CrossRef
Serum TNF-α and neurodegeneration in isolated REM sleep behavior disorder
Ryul Kim, Jee-Young Lee, Han-Joon Kim, Yu Kyeong Kim, Hyunwoo Nam, Beomseok Jeon
Parkinsonism & Related Disorders.2020; 81: 1. CrossRef
Longitudinal change in dopamine transporter availability in idiopathic REM sleep behavior disorder
Jung Hwan Shin, Jee-Young Lee, Yu-Kyeong Kim, Sung-A Shin, Heejung Kim, Hyunwoo Nam, Beomseok Jeon
Neurology.2020;[Epub] CrossRef

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

12,482 View
432 Download
11 Web of Science
6 Crossref

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.

Citations

Citations to this article as recorded by

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 Article

Reorganization of the Human Somatosensory Cortex in Hand Dystonia: Maria Jose Catalan, Kenji Ishii, William Bara-Jimenez, Mark Hallett; J Mov Disord. 2012;5(1):5-8.; DOI: https://doi.org/10.14802/jmd.12002

9,382 View
57 Download
2 Crossref

Abstract PDF

Background and Purpose:

Abnormalities of finger representations in the somatosensory cortex have been identified in patients with focal hand dystonia. Measuring blood flow with positron emission tomography (PET) can be use to demonstrate functional localization of receptive fields.

Methods:

A vibratory stimulus was applied to the right thumb and little finger of six healthy volunteers and six patients with focal hand dystonia to map their receptive fields using H₂¹⁵O PET.

Results:

The cortical finger representations in the primary somatosensory cortex were closer to each other in patients than in normal subjects. No abnormalities were found in secondary somatosensory cortex, but the somatotopy there is less well distinguished.

Conclusions:

These data confirm prior electrophysiological and functional neuroimaging observations showing abnormalities of finger representations in somatosensory cortex of patients with focal hand dystonia.

Citations

Citations to this article as recorded by

Laminar VASO fMRI in focal hand dystonia patients
Laurentius Huber, Panagiotis Kassavetis, Omer Faruk Gulban, Mark Hallett, Silvina G. Horovitz
Dystonia.2023;[Epub] CrossRef
Sensory Alterations in Patients with Isolated Idiopathic Dystonia: An Exploratory Quantitative Sensory Testing Analysis
Lejla Paracka, Florian Wegner, Christian Blahak, Mahmoud Abdallat, Assel Saryyeva, Dirk Dressler, Matthias Karst, Joachim K. Krauss
Frontiers in Neurology.2017;[Epub] CrossRef

Case Report

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.; DOI: https://doi.org/10.14802/jmd.10014

20,413 View
37 Download

Abstract 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.

Original Articles

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

10,825 View
86 Download
2 Crossref

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

Citations to this article as recorded by

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

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

10,823 View
56 Download

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.

First
Prev
Page of 1
Next
Last

Search