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Start Over Author "Tung-Sheng Shih" Journal european neurology
6 results on '"Tung-Sheng Shih"'

1. Diffuse White Matter Lesions in Carbon Disulfide Intoxication: Microangiopathy or Demyelination

Author

Chin Chang Huang, Tzu Chen Yen, Ho Yuan Chang, Tung-Sheng Shih, Hung Chou Kuo, Chi Jen Chen, and Mei Chuan Ku

Subjects
Male, Pathology, medicine.medical_specialty, Neural Conduction, Poison control, Neuropsychological Tests, Time, White matter, chemistry.chemical_compound, Evoked Potentials, Somatosensory, Occupational Exposure, parasitic diseases, Humans, Medicine, Neurotransmitter, Neurologic Examination, Tomography, Emission-Computed, Single-Photon, Brain Mapping, Carbon disulfide, Cerebellar ataxia, business.industry, Poisoning, Parkinsonism, Microangiopathy, Brain, food and beverages, Middle Aged, medicine.disease, Magnetic Resonance Imaging, Hyperintensity, Occupational Diseases, medicine.anatomical_structure, nervous system, Neurology, chemistry, Carbon Disulfide, Cerebrovascular Circulation, Neurology (clinical), medicine.symptom, Tomography, X-Ray Computed, business, Demyelinating Diseases
Abstract

Long-term exposure to carbon disulfide (CS2) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS2. The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T2-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS2 encephalopathy using brain MRI. In addition, the 99mTc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS2, possibly through microangiopathy. In addition, CS2 poisoning can be considered as one of the causes of chronic leukoencephalopathy.

Published
2003
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2. Contents, Vol 36, 1996

Author

G.A. Carlesimo, Stefano Paolucci, Massimo Conti, Paul Krack, Christian W. Hess, Emilio Di Maria, Jesús V. Sala-Lizárraga, Pierre Pollak, Matthias Sturzenegger, C. Caltagirone, L. Parnetti, Alberto Primavera, Alim-Louis Benabid, L. Fadda, Carlo Gandolfo, S. Lubich, Hiroaki Takahashi, Emilia Bellone, Christine Lawrence, Chun-Che Chu, Fumihito Yoshii, Gabriella Antonucci, Hisashi Yonezawa, Shinn-Kuang Lin, Regula S. Briellmann, Kenichi Tamura, Thomas Schaffner, Massimo Del Sette, Emberti Gialloreti, B.J. Sweeney, Yukito Shinohara, Hideo Tohgi, Fabio Bandini, Giovanni Abbruzzese, Joseph Ghika, Franco Ajmar, G. Gainotti, G. Marfia, Juan A. López-Andreu, C. Marra, Cinzia Calautti, Tung-Sheng Shih, Thierry Kuntzer, Marian Small, Simon Ellis, M.N. Rossor, Chin-Chang Huang, Anne D. Zurn, Vittoria M. Gianelli, José Salcedo-Vivó, Satoshi Takahashi, Wakoh Takahashi, R. Gallassi, Marco Traballesi, Leonardo Palombi, Paola Mandich, Josep Ferrís i Tortajada, Jack Tseng, Rou-Shayn Chen, Patrick Aebischer, U. Nocentini, Luca Pratesi, Carlo Loeb, Patricia Limousin, S. Lorusso, Mario Manto, Cinzia Finocchi, and Heinz A. Gerber

Subjects
Neurology, Neurology (clinical)
Published
1996
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3. Chronic carbon disulfide encephalopathy

Author

Tung-Sheng Shih, Rou-Shayn Chen, Chun-Che Chu, Shinn-Kuang Lin, and Chin-Chang Huang

Subjects
Male, Pathology, medicine.medical_specialty, Ultrasonography, Doppler, Transcranial, Encephalopathy, Computed tomography, Central nervous system disease, chemistry.chemical_compound, Occupational Exposure, parasitic diseases, medicine, Humans, Viscose, Carbon disulfide, Brain Diseases, medicine.diagnostic_test, business.industry, Magnetic resonance imaging, Electroencephalography, Middle Aged, medicine.disease, Magnetic Resonance Imaging, Cerebral Angiography, Occupational Diseases, Carotid Arteries, Neurology, chemistry, Carbon Disulfide, Angiography, Chronic Disease, Neurology (clinical), Radiology, business, Tomography, X-Ray Computed, Polyneuropathy
Abstract

To understand central nervous damage after long-term exposure to carbon disulfide (CS2), 10 patients who had polyneuropathy with various neuropsychiatric symptoms in a viscose rayon plant were studied. Clinical and laboratory examinations including electroencephalography (EEG), brain computed tomography (CT), brain magnetic resonance images (MRI), and carotid duplex sonography were carried out. Clinically, headache, unpleasant dreams, memory impairment, fatigue, anorexia and emotional lability were common in these patients while 2 patients had stroke episodes. EEGs were all normal. Brain CT scan showed mild cortical atrophy in 3 and low density lesions in the basal ganglia in 3. Brain MRI studies also disclosed mild cortical atrophy in 4 and multiple lesions involving the basal ganglia and corona radiata in 4. Carotid duplex sonography revealed mild atherosclerosis with plaques (20% stenosis) of extracranial vessels in 6. However there was no significant difference in flow velocities and flow volumes in the extracranial carotid arteries between patients and the normal controls. Interestingly, 2 patients had multiple brain lesions in the subcortical white matter but without strokes. In conclusion, encephalopathy with possible strokes may occur after chronic exposure to CS2, as well as polyneuropathy. The lesions usually involve the basal ganglia and subcortical white matter. Furthermore, MRI study may detect brain lesions particularly in the subcortical white matter areas before the occurrence of stroke.

Published
1996

4. Contents Vol. 50, 2003

Author

Theodor Landis, Ayako Nakano, Tung-Sheng Shih, D Cologno, P. Bertholon, Sándor Túri, D. Michel, Chin-Chang Huang, Soichiro Mochio, Nobuaki Horiuchi, Anne Cosson, Iris Spitzer, Gilles Capellier, M. Rieks, Masakazu Sugino, T.H. Leoh, Takao Mitsui, Toshiaki Hanafusa, Patrick Lemounaud, Eugeniu Revenco, Takuya Nishina, Elisabeth Vidry, Nils Brune, Gian Camillo Manzoni, Toshiyuki Ikemoto, Y.L. Lo, Fumiharu Kimura, C. Martin, Laurent Tatu, Hung-Chou Kuo, Miriam Juschka, Eric Berger, S. Fook-Chong, S. Nurjannah, Ryuichi Yamasaki, Julien Bogousslavsky, Fabrice Vuillier, Kiyoharu Inoue, Faouzi Belahsen, Masayo Morita, Sebastian Schimrigk, Olaf Blanke, Horst Przuntek, Hisayoshi Oka, Krisztina Bencsik, Shuichi Miyazaki, Tzu-Chen Yen, Eszter Karg, Ho-Yuan Chang, Hideto Nakajima, Mei-Chuan Ku, Y.E. Tan, Orhan Aktas, Volker Hoffmann, Lucien Rumbach, Thierry Moulin, Y.F. Dan, Chi-Jen Chen, J.C. Antoine, Denis Sablot, László Vécsei, Akira Shimizu, Masayuki Yoshioka, Péter Klivényi, Dieter Pöhlau, Sizue Ohtsuka, and Makoto Kunishige

Subjects
Neurology, Neurology (clinical)
Published
2003
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5. Subject Index Vol. 36, 1996

Author

Thierry Kuntzer, Emilio Di Maria, Jesús V. Sala-Lizárraga, Chin-Chang Huang, G.A. Carlesimo, Alim-Louis Benabid, Yukito Shinohara, L. Fadda, Fabio Bandini, Regula S. Briellmann, Josep Ferrís i Tortajada, Hideo Tohgi, Tung-Sheng Shih, Giovanni Abbruzzese, Chun-Che Chu, Emilia Bellone, B.J. Sweeney, Rou-Shayn Chen, G. Gainotti, G. Marfia, Emberti Gialloreti, Cinzia Calautti, Satoshi Takahashi, M.N. Rossor, Jack Tseng, Massimo Conti, Wakoh Takahashi, Patrick Aebischer, Franco Ajmar, R. Gallassi, José Salcedo-Vivó, C. Marra, Hiroaki Takahashi, Simon Ellis, Carlo Gandolfo, Leonardo Palombi, L. Parnetti, Shinn-Kuang Lin, Paola Mandich, Christine Lawrence, Paul Krack, Anne D. Zurn, Christian W. Hess, Gabriella Antonucci, Hisashi Yonezawa, Massimo Del Sette, Joseph Ghika, Pierre Pollak, Matthias Sturzenegger, Alberto Primavera, C. Caltagirone, Stefano Paolucci, Mario Manto, Cinzia Finocchi, Heinz A. Gerber, Marco Traballesi, U. Nocentini, Kenichi Tamura, S. Lubich, Fumihito Yoshii, Carlo Loeb, Patricia Limousin, Thomas Schaffner, Juan A. López-Andreu, Marian Small, Vittoria M. Gianelli, S. Lorusso, and Luca Pratesi

Subjects
Cognitive science, Index (economics), Neurology, Subject (documents), Neurology (clinical), Psychology, Cognitive psychology
Published
1996
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6. Diffuse White Matter Lesions in Carbon Disulfide Intoxication: Microangiopathy or Demyelination.

Author

Mei-Chuan Ku, Takao, Chin-Chang Huang, Hung-Chou Kuo, Tzu-Chen Yen, Chi-Jen Chen, Tung-Sheng Shih, and Ho-Yuan Chang

Subjects
DEMYELINATION, MAGNETIC resonance imaging, PHOTONS, TOMOGRAPHY, ATAXIA
Abstract

Long-term exposure to carbon disulfide (CS[sub 2] ) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS[sub 2] . The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T[sub 2] -weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS[sub 2] encephalopathy using brain MRI. In addition, the [sup 99m] Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS[sub 2] , possibly through microangiopathy. In addition, CS[sub 2] poisoning can be considered as one of the causes of chronic leukoencephalopathy.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2003
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