Abstract
Dapsone produces a potentially reversible toxic neuropathy, with its primary effect on the soma and axons of motor neurons as opposed to myelin. There is very little evidence to suggest involvement of sensory axons in most cases; if present, it would appear minimal. A "dying back" of motor axons is postulated to produce the clinical features of primarily distal weakness and wasting. Recovery appears to occur via axon regeneration and peripheral sprouting. The sporadic occurrence of this neuropathy may be due to slow acetylation of dapsone in some patients.
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