Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by He, F.
Right arrow Articles by Zhang, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by He, F.
Right arrow Articles by Zhang, C.
NEUROLOGY 1995;45:2178-2183
© 1995 American Academy of Neurology

Delayed dystonia with striatal CT lucencies induced by a mycotoxin (3-nitropropionic acid)

Fengsheng He, MD, Shoulin Zhang, MD, Fangyi Qian, MD and Chaoli Zhang, MD

From the Institute of Occupational Medicine (Drs. He and S. Zhang), Chinese Academy of Preventive Medicine; and Beijing 514 Hospital (Drs. Qian and C. Zhang), Beijing, China.
Received January 26, 1994. Accepted in final form April 12, 1995.
Address correspondence and reprint requests to Dr. Fengsheng He, Institute of Occupational Medicine, Chinese Academy of Preventive Medicine, 29 Nan Wei Road, 100050 Beijing, P.R. China.

We describe a clinical syndrome of delayed dystonia in children subsequent to initial gastrointestinal symptoms and acute noninflammatory encephalopathy.The syndrome was caused by the ingestion of mildewed sugarcane containing the Arthrinium-produced mycotoxin, 3-nitropropionic acid (3-NPA). In the severely affected patients, intoxication usually was heralded by coma, with dystonia appearing 7 to 40 days after recovery from the coma. The dystonia was manifested as choreoathetosis, torsion spasms, or painful paroxysmal spasms of the extremities and was neither progressive nor reversible. CTs of the dystonic patients consistently showed bilateral hypodensities in the lenticular nuclei. The pathogenesis of the selective lenticular lesions induced by 3-NPA is not yet clear.

NEUROLOGY 1995;45: 2178-2183




This article has been cited by other articles:


Home page
 J. Neurosci.Home page
G. W. Kim, Y. Gasche, S. Grzeschik, J.-C. Copin, C. M. Maier, and P. H. Chan
Neurodegeneration in Striatum Induced by the Mitochondrial Toxin 3-Nitropropionic Acid: Role of Matrix Metalloproteinase-9 in Early Blood-Brain Barrier Disruption?
J. Neurosci., September 24, 2003; 23(25): 8733 - 8742.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
K. L. Gabrielson, B. A. Hogue, V. A. Bohr, A. J. Cardounel, W. Nakajima, J. Kofler, J. L. Zweier, E. R. Rodriguez, L. J. Martin, N. C. de Souza-Pinto, et al.
Mitochondrial Toxin 3-Nitropropionic Acid Induces Cardiac and Neurotoxicity Differentially in Mice
Am. J. Pathol., October 1, 2001; 159(4): 1507 - 1520.
[Abstract] [Full Text]

Home page
 J. Neurosci.Home page
P. Narasimhan, R. Sklar, M. Murrell, R. A. Swanson, and F. R. Sharp
Methylmalonyl-CoA Mutase Induction by Cerebral Ischemia and Neurotoxicity of the Mitochondrial Toxin Methylmalonic Acid
J. Neurosci., November 15, 1996; 16(22): 7336 - 7346.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1995 by AAN Enterprises, Inc.