DMCA
Distribution of multiple sclerosis (1998)
| Citations: | 180 - 3 self |
BibTeX
@MISC{Compston98distributionof,
author = {Alastair Compston and Alasdair Coles},
title = {Distribution of multiple sclerosis},
year = {1998}
}
Share
 |
 |
 |
 |
||
OpenURL
Abstract
Multiple sclerosis is primarily an infl ammatory disorder of the brain and spinal cord in which focal lymphocytic infi ltration leads to damage of myelin and axons. Initially, infl ammation is transient and remyelination occurs but is not durable. Hence, the early course of disease is characterised by episodes of neurological dysfunction that usually recover. However, over time the pathological changes become dominated by widespread microglial activation associated with extensive and chronic neurodegeneration, the clinical correlate of which is progressive accumulation of disability. Paraclinical investigations show abnormalities that indicate the distribution of infl ammatory lesions and axonal loss (MRI); interference of conduction in previously myelinated pathways (evoked electrophysiological potentials); and intrathecal synthesis of oligoclonal antibody (examination by lumbar puncture of the cerebrospinal fl uid). Multiple sclerosis is triggered by environmental factors in individuals with complex genetic-risk profi les. Licensed disease modifying agents reduce the frequency of new episodes but do not reverse fi xed defi cits and have questionable eff ects on the long-term accumulation of disability and disease progression. We anticipate that future studies in multiple sclerosis will provide a new taxonomy on the basis of mechanisms rather than clinical empiricism, and so inform strategies for improved treatment at all stages of the disease.
Keyphrases
multiple sclerosis new episode clinical correlate infl ammatory disorder chronic neurodegeneration intrathecal synthesis long-term accumulation remyelination occurs oligoclonal antibody evoked electrophysiological potential questionable eff ect disease progression widespread microglial activation pathological change environmental factor lumbar puncture infl ammatory lesion improved treatment spinal cord early course paraclinical investigation future study focal lymphocytic infi ltration clinical empiricism axonal loss inform strategy neurological dysfunction fi xed defi cits new taxonomy cerebrospinal fl uid infl ammation progressive accumulation complex genetic-risk profi le
