Journal
CURRENT OPINION IN NEUROLOGY
Volume 14, Issue 3, Pages 289-298Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00019052-200106000-00005
Keywords
-
Categories
Funding
- Multiple Sclerosis Society [592] Funding Source: Medline
Ask authors/readers for more resources
Demyelination and inflammation both contribute to the neurological deficits characteristic of multiple sclerosis and Guillain-Barre syndrome. Conduction deficits attributable to demyelination are well known, but it is becoming clear that factors such as nitric oxide, endocaine, cytokines, and antiganglioside antibodies also play significant roles. Demyelination directly affects conduction and also causes changes in both the distribution and repertoire of expressed axolemmal ion channels, which in turn affect impulse propagation and can promote hyperexcitability. In conducting axons, sustained trains of impulses can produce intermittent conduction failure, and, in the presence of nitric oxide exposure, can also cause axonal degeneration. Other factors impairing impulse transmission include nodal widening, glutamate toxicity, and disturbances of both the blood-brain barrier and synaptic transmission. Curr Opin Neurol 14:289-298. (C) 2001 Lippincott Williams & Wilkins.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available