A major area of investigation in the neurosciences is directed at understanding the factors that participate in neurological deficits. In demyelinating diseases of the central nervous system (CNS), it has been assumed that demyelina-tion by itself contributes to functional deficits. Previous physiological studies demonstrated that demyelination in the CNS can result in conduction slowing and conduction block (McDonald and Sears, 1969). Such observations appeared sufficient to explain the majority of deficits in demyelinat-ing human diseases such as multiple sclerosis (MS). However, clinical and basic science observations have begun to challenge this hypothesis.
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