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Brain, Vol. 126, No. 4, 751-752, April 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg070

Editorial

A function of myelin is to protect axons from subsequent injury: implications for deficits in multiple sclerosis

Moses Rodriguez1

1 Department of Neurology and Immunology, Mayo Medical and Graduate School, Rochester, MN, USA

The first 10% of the full text of this article appears below.

Once it was thought that the mechanism for development of permanent neurological deficits in multiple sclerosis was understood. Demyelination, the pathological hallmark of the multiple sclerosis lesion, was the culprit. Elegant physiological studies demonstrated that demyelination results in conduction slowing and, in particular, conduction block (McDonald and Sears, 1969Go). These observations appeared sufficient to explain the majority of deficits in multiple sclerosis. However, clinical observations began to challenge this hypothesis. With the development of MRI, clinicians saw patients with extensive white matter lesion load with minimal or no neurological deficits. Pathological studies demonstrated that lesions observed by MRI . . . [Full Text of this Article]


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S. Chandran, D. Hunt, A. Joannides, C. Zhao, A. Compston, and R. J.M Franklin
Myelin repair: the role of stem and precursor cells in multiple sclerosis
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[Abstract] [Full Text] [PDF]