The neuroscience and phenomenology of sensory loss

Abstract

Historically deafferentation has been seen in the context of a late effect of syphilis, (before the spirochaete's effects were largely killed off by antibiotics, at least in Western societies). One of the consequences of the chronic late stage of the disease is atrophy of the dorsal columns of the spinal cord, leading to loss of the tracts carrying touch and proprioception. This in turn led to the characteristic broad based staggering gait and uncontrolled ataxic movements. Dispassionate accounts of the consequences of this may have been made more difficult by the fact that with ataxia comes intractable lightning pains1. That such deafferentiation could arise from other peripheral and central causes of loss of proprioception was less clear2.