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The neuroscience and phenomenology of sensory loss

Jonathan Cole


Introduction

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 pains.1 That such deafferentation could arise from other peripheral and central causes of loss of proprioception was less clear.2
This chapter will consider neurological causes of haptic sensory loss, from peripheral diseases leading to losses of large myelinated sensory nerve fibres alone to more central conditions including dorsal column loss and cortical damage. Perhaps the purest form of loss of movement and position sensation and cutaneous touch is seen in large fibre peripheral neuronopathy. This syndrome was first described by Schaumburg and colleagues in 1980 [1].3 Since then a number of different causes has been found, though their original post infective one remains the paradigm and, being non-progressive, has allowed the most long-term study and an understanding of the importance of afferents in haptic function. The chapter will therefore end with an analysis of function in subjects with this syndrome.
Before this, however, will be given a short précis of how sensation is now tested, a century after Head’s techniques (see Chapter 3).
This chapter will consider neurological causes of haptic sensory loss, from peripheral diseases leading to losses of large myelinated sensory nerve fibres alone to more central conditions including dorsal column loss and cortical damage. Perhaps the purest form of loss of movement and position sensation and cutaneous touch is seen in large fibre peripheral neuronopathy. This syndrome was first described by Schaumburg and colleagues in 1980 [1].3 Since then a number of different causes has been found, though their original post infective one remains the paradigm and, being non-progressive, has allowed the most long-term study and an understanding of the importance of afferents in haptic function. The chapter will therefore end with an analysis of function in subjects with this syndrome. Before this, however, will be given a short précis of how sensation is now tested, a century after Head’s techniques (see Chapter 3).

The testing of somatic sensation

When sensation was tested by Henry Head at the turn of the 19th and 20th century it took so long and was so detailed that such a schedule would have been impossible clinically. Faster techniques became accepted. Light touch was tested with cotton wool gently stroked across the skin, pain using a pin or hypodermic syringe needle, temperature with a cold metal object and movement and position sense by small movements of the digits, either fingers or toes. Two point discrimination did require special retractors and higher cortical sensation was sometime tested via the drawing of numbers on the outstretched palm and rarely by placing an object in the hand for manipulation in a manner Head would have recognised.
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