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Cortical lesions in multiple sclerosis: inflammation versus neurodegeneration

Hans Lassmann
DOI: http://dx.doi.org/10.1093/brain/aws260 2904-2905 First published online: 13 October 2012

Demyelinated lesions in the cerebral cortex and cortical atrophy have recently been recognized as important components of multiple sclerosis pathology. Although it has consistently been recognized in studies on the pathology of multiple sclerosis that demyelination may not only affect white matter but also the cortex and deep grey matter nuclei (Brownell and Hughes, 1962; Lumsden, 1970; Kidd et al., 1999; Cifelli et al., 2002), only the application of modern techniques for immunocytochemical detection of myelin antigen has revealed its extent, particularly in patients who died during the progressive stage of the disease (Peterson et al., 2001; Kutzelnigg et al., 2005). Three types of cortical lesions have been identified: combined cortico/subcortical lesions, perivascular intracortical lesions and band-like subpial lesions, which affect the cerebral cortex over several adjacent gyri and sulci (Bo et al., 2003a). In particular, the subpial lesions can be very extensive, affecting >60% of the cortical ribbon in the cerebrum (Kutzelnigg et al., 2005), the cerebellum (Kutzelinigg et al., 2007) and the hippocampus (Geurts et al., 2007).

In the early descriptions of cortical lesions in patients with progressive disease, it was emphasized that they differ from white matter lesions by the absence of perivascular and parenchymal infiltrates of T- and B-lymphocytes, vascular inflammation and blood–brain barrier …