Abstract
In the last few years, there has been an increased appreciation of the apparently primary role of neuronal and axonal injury in the pathogenesis of multiple sclerosis (MS) [1, 2]. This has been driven to a significant degree by the results of proton magnetic resonance (MR) spectroscopy (1H-MRS) studies, which have emphasized that substantial neuroaxonal damage occurs inside the demyelinating lesions as well as in the normal-appearing white matter (NAWM) and gray matter (GM) of the brain of patients with MS [2, 3]. All this has been confirmed pathologically [1, 4, 5] and has led to a reconsideration of the role of axonal damage in MS [6].
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