Document Detail


Difference in neuropathogenetic mechanisms in human furious and paralytic rabies.
MedLine Citation:
PMID:  16226769     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Whereas paralysis is the hallmark for paralytic rabies, the precise pathological basis of paralysis is not known. It is unclear whether weakness results from involvement of anterior horn cells or of motor nerve fibers. There is also no conclusive data on the cause of the neuropathic pain which occurs at the bitten region, although it has been presumed to be related to sensory ganglionopathy. In this study, six laboratory-proven rabies patients (three paralytic and three furious) were assessed clinically and electrophysiologically. Our data suggests that peripheral nerve dysfunction, most likely demyelination, contributes to the weakness in paralytic rabies. In furious rabies, progressive focal denervation, starting at the bitten segment, was evident even in the absence of demonstrable weakness and the electrophysiologic study suggested anterior horn cell dysfunction. In two paralytic and one furious rabies patients who had severe paresthesias as a prodrome, electrophysiologic studies suggested dorsal root ganglionopathy. Postmortem studies in two paralytic and one furious rabies patients, who had local neuropathic pain, showed severe dorsal root ganglionitis. Intense inflammation of the spinal nerve roots was observed more in paralytic rabies patients. Inflammation was mainly noted in the spinal cord segment corresponding to the bite in all cases; however, central chromatolysis of the anterior horn cells could be demonstrated only in furious rabies patient. We conclude that differential sites of neural involvement and possibly different neuropathogenetic mechanisms may explain the clinical diversity in human rabies.
Authors:
Erawady Mitrabhakdi; Shanop Shuangshoti; Pongsak Wannakrairot; Richard A Lewis; Keiichiro Susuki; Jiraporn Laothamatas; Thiravat Hemachudha
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Publication Detail:
Type:  Case Reports; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-10-14
Journal Detail:
Title:  Journal of the neurological sciences     Volume:  238     ISSN:  0022-510X     ISO Abbreviation:  J. Neurol. Sci.     Publication Date:  2005 Nov 
Date Detail:
Created Date:  2005-10-31     Completed Date:  2005-12-20     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375403     Medline TA:  J Neurol Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  3-10     Citation Subset:  IM    
Affiliation:
Neurology Division, Department of Medicine, Chulalongkorn University Hospital, Rama 4 Road, Bangkok 10330, Thailand. erawady.M@chula.ac.th
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Demyelinating Diseases / pathology
Electrodiagnosis
Electromyography
Female
Ganglia, Spinal / pathology
Humans
Immunoglobulin G
Male
Middle Aged
Muscle, Skeletal / pathology,  physiopathology
Nerve Tissue / pathology*
Neural Conduction / physiology
Paralysis / pathology
Peripheral Nerves / pathology
Rabies / immunology,  pathology*
Spinal Cord / pathology
Chemical
Reg. No./Substance:
0/Immunoglobulin G

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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