Introduction Multiple sclerosis (MS) is a chronic demyelinating disease affecting young adults and leading to significant disability. Although MS is presumed to derive from an autoimmune attack to myelin sheaths and oligodendrocytes, some evidence has recently accumulated to indicate that an axonal and synaptic pathology could accompany or even precede the central nervous system (CNS) autoimmune infiltration; for review see Geurts & Barkhof. In agreement with this idea, in chronic MS patients, together with the standard white matter lesions seen by brain imaging techniques, some degree of cortical and deep gray matter alterations have been found. The analysis of these gray matter lesions has shown a much less extensive inflammation and gliosis than in white matter lesions. Clearly, since gray matter is composed of neuronal cell bodies, dendrites, and synapses, these findings indicate an alteration of one or more of these neuronal structures in MS patients, which could then explain some of the contradictory clinical features of MS including the frequent association with cognitive disorders. Are these alterations of either synapses, axons, or dendrites a primary phenomenon or do they simply follow the immune attack? The former scenario would open a debate related to the real etiopathology of MS and the suitability of autoimmune myelitis as animal model of MS. The latter scenario would imply a sort of progression of the neuropathological damage initiated by the removal of myelin sheaths which alternatively might also derive from compensatory or plastic changes at the level of either upstream or downstream neuronal structures.
|Title of host publication||Multiple Sclerosis: Recovery of Function and Neurorehabilitation|
|Publisher||Cambridge University Press|
|Number of pages||7|
|ISBN (Print)||9780511781698, 9780521888325|
|Publication status||Published - Jan 1 2010|
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