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Volume 6(2); October 2013
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Original Articles
Orthostatic and Supine Blood Pressures Are Associated with White Matter Hyperintensities in Parkinson Disease
Yoon-Sang Oh, Joong-Seok Kim, Kwang-Soo Lee
J Mov Disord. 2013;6(2):23-27.   Published online October 30, 2013
DOI: https://doi.org/10.14802/jmd.13006
  • 13,589 View
  • 94 Download
  • 41 Citations
AbstractAbstract PDF
Background and Purpose:

Several reports on the elderly population have suggested that orthostatic hypotension is associated with white matter hyperintensities (WMH); however, little information is available on patients with Parkinson’s disease (PD).

Methods:

We analyzed the association blood pressure profiles during tilt table testing with WMH scores in 117 patients with PD. WMH were rated using the semiquantitative visual rating system proposed by Scheltens et al.

Results:

The presence of orthostatic hypotension was associated with increasing tendency of WMH score and the blood pressure changes during tilting and supine blood pressure were positively correlated with increasing WMH score.

Conclusions:

This finding indicates that hemodynamic changes associated with orthostatic hypotension may be associated with white matter changes in patients with PD.

Citations

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    Seon-Min Lee, Mina Lee, Eun Ji Lee, Rae On Kim, Yongduk Kim, Kyum-Yil Kwon
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  • Arterial Blood Pressure Variability and Other Vascular Factors Contribution to the Cognitive Decline in Parkinson’s Disease
    Anna Pierzchlińska, Magdalena Kwaśniak-Butowska, Jarosław Sławek, Marek Droździk, Monika Białecka
    Molecules.2021; 26(6): 1523.     CrossRef
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    Na-Young Shin, Yae Won Park, Sang-Won Yoo, Ji-Yeon Yoo, Yangsean Choi, Jinhee Jang, Kook-Jin Ahn, Bum-soo Kim, Joong-Seok Kim
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    Jose-Alberto Palma, Gabriel Redel-Traub, Angelo Porciuncula, Daniela Samaniego-Toro, Patricio Millar Vernetti, Yvonne W. Lui, Lucy Norcliffe-Kaufmann, Horacio Kaufmann
    Parkinsonism & Related Disorders.2020; 75: 97.     CrossRef
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    Horacio Kaufmann, Jose‐Alberto Palma
    Movement Disorders Clinical Practice.2020; 7(6): 595.     CrossRef
  • White Matter Hyperintensities Mediate Impact of Dysautonomia on Cognition in Parkinson's Disease
    Mahsa Dadar, Seyed‐Mohammad Fereshtehnejad, Yashar Zeighami, Alain Dagher, Ronald B. Postuma, D. Louis Collins
    Movement Disorders Clinical Practice.2020; 7(6): 639.     CrossRef
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    Sang-Won Yoo, Eunkyeong Yun, Mirim Bang, Uicheul Yoon, Ji-Yeon Yoo, Kwang-Soo Lee, Na-Young Shin, Joong-Seok Kim
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  • Consensus statement on the definition of neurogenic supine hypertension in cardiovascular autonomic failure by the American Autonomic Society (AAS) and the European Federation of Autonomic Societies (EFAS)
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    Valeria Milazzo, Cristina Di Stefano, Fabrizio Vallelonga, Gabriele Sobrero, Maurizio Zibetti, Alberto Romagnolo, Aristide Merola, Alberto Milan, Alberto J. Espay, Leonardo Lopiano, Franco Veglio, Simona Maule
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  • Central hemodynamics and arterial stiffness in idiopathic and multiple system atrophy
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  • Cardiovascular Autonomic Dysfunction in Patients with Drug-Induced Parkinsonism
    Joong-Seok Kim, Dong-Woo Ryu, Ju-Hee Oh, Yang-Hyun Lee, Sung-Jin Park, Kipyung Jeon, Jong-Yun Lee, Seong Hee Ho, Jungmin So, Jin Hee Im, Kwang-Soo Lee
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    Dong-Woo Ryu, Joong-Seok Kim, Jee-Eun Lee, Jeong-Wook Park, Yoon-Sang Oh, Jae-Young An, Kwang-Soo Lee
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  • Microstructural integrity of white matter tracts amongst older fallers: A DTI study
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    Joong-Seok Kim, Si-Hoon Lee, Yoon-Sang Oh, Jeong-Wook Park, Jae-Young An, Hyun-Seok Choi, Kwang-Soo Lee
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  • Autonomic Nervous System Dysfunction in Patients With Parkinson Disease Having Depression
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    Andrew D. Robertson, Michelle A. Messner, Zahra Shirzadi, Galit Kleiner-Fisman, Joyce Lee, Julia Hopyan, Anthony E. Lang, Sandra E. Black, Bradley J. MacIntosh, Mario Masellis
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Growth Hormone Deteriorates the Functional Outcome in an Experimental Model of Huntington’s Disease Induced by 3-Nitropionic Acid
Jung-Eun Park, Soon-Tae Lee, Woo-Seok Im, Manho Kim
J Mov Disord. 2013;6(2):28-33.   Published online October 30, 2013
DOI: https://doi.org/10.14802/jmd.13007
  • 9,506 View
  • 60 Download
  • 1 Citations
AbstractAbstract PDF
Background and Purpose:

Growth hormone (GH) has been frequently used to control the aging process in healthy individuals, probably due to its slowing effect on senescence-associated degeneration. Mitochondrial dysfunction is related to the aging process, and one of the chemical models of Huntington’s disease is that it can be induced by mitochondrial toxin. To investigate the potential application of GH to modify the progression of Huntington’s disease (HD), we examined whether GH can protect the functional deterioration by striatal damage induced by 3-nitropropionic acid (3NP).

Methods:

3NP (63 mg/kg/day) was delivered to Lewis rats by osmotic pumps for five consecutive days, and the rats received intraperitoneal administration of GH or vehicle (saline) throughout the experiment. Neurological deficits and body weight were monitored. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test was performed to further determine the mitochondrial activity in cultured N18TG2 neuroblastoma cells in vitro.

Results:

3NP-treated rats showed progressive neurologic deficits with striatal damage. Application of GH accelerated behavioral deterioration, particularly between day 3 and day 5, resulting in reduced survival outcome. The body weights of rats given 3NP were decreased, but GH did not affect such decrease compared to the non-treated control group. The effect of GH on cultured neuronal cells was a decrease in the MTT absorbance, suggesting a lower number of cells in a dose dependent pattern.

Conclusions:

Those results suggest that application of GH to a 3NP-induced experimental model of HD deteriorates the progress of functional deficits, possibly disturbing mitochondrial activities.

Citations

Citations to this article as recorded by  
  • Tert-buthylhydroquinone pre-conditioning exerts dual effects in old female rats exposed to 3-nitropropionic acid
    Alejandro Silva-Palacios, Ana L. Colín-González, Stefanie P. López-Cervantes, Cecilia Zazueta, Armando Luna-López, Abel Santamaría, Mina Königsberg
    Redox Biology.2017; 12: 610.     CrossRef
Case Reports
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
  • 16,955 View
  • 60 Download
  • 5 Citations
AbstractAbstract 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.

Citations

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  • Toxicity of amantadine hydrochloride on cultured bovine cornea endothelial cells
    Po-Yen Lee, Yu-Hung Lai, Po-Len Liu, Ching-Chih Liu, Chia-Cheng Su, Fang-Yen Chiu, Wei-Chung Cheng, Shiuh-Liang Hsu, Kai-Chun Cheng, Li-Yi Chiu, Tzu-En Kao, Chia-Ching Lin, Yo-Chen Chang, Shu-Chi Wang, Chia-Yang Li
    Scientific Reports.2021;[Epub]     CrossRef
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    Santiago Perez-Lloret, Olivier Rascol
    Journal of Neural Transmission.2018; 125(8): 1237.     CrossRef
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    Merel S. Ekker, Sabine Janssen, Klaus Seppi, Werner Poewe, Nienke M. de Vries, Thomas Theelen, Jorik Nonnekes, Bastiaan R. Bloem
    Parkinsonism & Related Disorders.2017; 40: 1.     CrossRef
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    Ilona Csoti, Wolfgang H. Jost, Heinz Reichmann
    Journal of Neural Transmission.2016; 123(1): 3.     CrossRef
  • Amantadine Use as a Risk Factor for Corneal Edema: A Nationwide Cohort Study in Taiwan
    Po Yen Lee, Hung Pin Tu, Chang Ping Lin, Cheng Hsien Chang, Kai Chun Cheng, Chia Ching Lin, Shiuh Liang Hsu
    American Journal of Ophthalmology.2016; 171: 122.     CrossRef
Hot Cross Bun Sign Following Bilateral Pontine Infarction: A Case Report
Sook Young Roh, Hyun-soon Jang, Yoon Hee Kim
J Mov Disord. 2013;6(2):37-39.   Published online October 30, 2013
DOI: https://doi.org/10.14802/jmd.13009
  • 14,856 View
  • 103 Download
  • 8 Citations
AbstractAbstract PDF

The hot cross bun sign is characterized by cruciform T2 signal hyperintensity in the pons and has been reported to be a specific but not pathognomic for multiple system atrophy. It reflects degeneration of pontine neurons and transverse pontocerebellar fibers, regardless of the underlying pathogenic process. Here, we report a case of hot cross bun sign following bilateral pontine infarction due to Wallerian degeneration of the pontocerebellar fibers.

Citations

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  • The “hot cross bun sign” in patients with autoimmune cerebellar ataxia: A case report and literature review
    Mange Liu, Haitao Ren, Nan Lin, Ying Tan, Siyuan Fan, Hongzhi Guan
    Frontiers in Neurology.2022;[Epub]     CrossRef
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    Ansuya Kasavelu Naidoo, Cait‐Lynn Deanne Wells, Yashvir Rugbeer, Neil Naidoo
    Movement Disorders Clinical Practice.2022; 9(8): 1105.     CrossRef
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    Elena Schlapakow, Vera C. Keil, Marie Paus, Cornelia Kornblum, Elke Hattingen, Thomas Klockgether
    Journal of Clinical Neuroscience.2020; 76: 238.     CrossRef
  • Various Diseases and Clinical Heterogeneity Are Associated With “Hot Cross Bun”
    Shuzhen Zhu, Hualing Li, Bin Deng, Jialing Zheng, Zifeng Huang, Zihan Chang, Yanjun Huang, Zhibo Wen, Yanran Liang, Mengjue Yu, Ling-Ling Chan, Eng-King Tan, Qing Wang
    Frontiers in Aging Neuroscience.2020;[Epub]     CrossRef
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    Christopher Way, David Pettersson, Amie Hiller
    Journal of Movement Disorders.2019; 12(1): 27.     CrossRef
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    Han-Joon Kim, Beomseok Jeon, Victor S.C. Fung
    Movement Disorders Clinical Practice.2017; 4(1): 12.     CrossRef
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    H. Ishikawa, N. Kawada, A. Taniguchi, K. Odachi, A. Mizutani, M. Asahi, H. Tomimoto
    Acta Neurologica Scandinavica.2016; 133(5): 398.     CrossRef
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    Han-Joon Kim, Beom S. Jeon, Kurt A. Jellinger
    Journal of Neurology.2015; 262(8): 1801.     CrossRef

JMD : Journal of Movement Disorders