Journal of Neurology

, Volume 255, Supplement 1, pp 12–18

Interplay between mechanisms of damage and repair in multiple sclerosis

Article

DOI: 10.1007/s00415-008-1003-7

Cite this article as:
Stadelmann, C. & Brück, W. J Neurol (2008) 255(Suppl 1): 12. doi:10.1007/s00415-008-1003-7

Abstract

The neuropathology of multiple sclerosis is characterised by focal damage to white matter. However, tissue damage is also present in the cortical grey matter, with a particularly high prevalence of cortical demyelination being observed in secondary progressive and primary progressive forms of the disease. The presence of meningeal B-cell follicle-like structures, which frequently appear during the secondary progressive phase of disease, may be involved in the formation of these subpial cortical lesions. Diffuse white matter inflammation accompanied by axonal damage can also be observed in normal appearing white matter and, again, this is more prominent in chronic progressive forms of multiple sclerosis than in acute stages of disease. Axonal damage is a particularly important component of the pathology of multiple sclerosis and appears to be a critical determinant of clinical outcome. Axons appear to become vulnerable to injury as a result of loss of their myelin sheaths. Remyelination represents an important mechanism of tissue repair in multiple sclerosis and already occurs at an early stage of lesion development and in both white and grey matter lesions. The extent of remyelination appears to be greater in cortical lesions and in lesions further from the ventricles. There is important heterogeneity between patients in terms of the extent of remyelination, which may reflect underlying differences in pathogenetic mechanisms between patients.

Key words

Multiple sclerosis neuropathology inflammation axonal damage remyelination demyelination 

Copyright information

© Steinkopff-Verlag 2008

Authors and Affiliations

  1. 1.Georg-August-Universität Göttingen, Abteilung NeuropathologieGöttingenGermany

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