Axonal injury or loss in the internal capsule and motor impairment in multiple sclerosis.

Abstract

IT HAS BECOME clear from results of animal¹ and human² studies that neurologic function can fully recover after acute inflammation, despite persistent demyelination. The mechanisms of recovery might include axonal adaptations such as the redistribution of sodium channels.^3,4 Thus, the focus of interest has recently been directed toward testing the hypothesis that axonal loss and damage are responsible for the persistent functional deficits found in multiple sclerosis (MS) (the axonal hypothesis).⁵