J Neurol Sci 2003 Feb 15;206(2):187-91
Lassmann H.
Division of Neuroimmunology, Brain Research Institute, University of
Vienna, Spitalgasse 4, A-1090, Vienna, Austria
Recent data suggest that the mechanisms of demyelination and tissue damage in multiple sclerosis (MS) are heterogenous.
In this review, evidence is discussed, which show that in a subset of multiple sclerosis patients the central nervous system (CNS) lesions show profound similarities to tissue alterations found in acute white matter stroke, thus suggesting that a hypoxia-like metabolic injury is a pathogenetic component in a subset of inflammatory brain lesions.
Both, vascular pathology as well as metabolic
disturbances induced by toxins of activated macrophages and microglia may
be responsible for such lesions in multiple sclerosis.