Particular types of lesions have differing effects on sensory nerve fibers. Compression of a nerve ablates mainly the function of large touch and pressure fibers and leaves the function of small pain, thermal, and autonomic fibers intact; lidocaine has the opposite effect. The effects of sustained pressure on a nerve for as long as 30 min, produces paresthesiae within a few minutes, followed by sensory loss—first of touch and vibration, then of cold, fast pain, heat, and slow pain, in that order and spreading centripetally. Physiologic studies have confirmed the theory of Lewis and colleagues that compression blocks the function of nerve fibers in order of their size. Release of the pressure results in postcompression paresthesia, which has been shown to arise from spontaneous activity that is generated along the myelinated nerve fibers from ectopic sites at a distance from the compression. Within seconds of releasing the pressure, there is an array of tingling, stinging, cramp-like sensations that reach maximum intensity in 90 to 120 s and slowly fade (Lewis et al). Sensory function is recovered in an order inverse to that in which it was lost. Similar spontaneous and ectopic discharges probably explain the paresthetic symptoms early in the acute demyelinating neuropathies, even before the appearance of sensory loss or numbness. It is worth emphasizing that these features of compression are not because of nerve ischemia, as commonly stated; instead, they result from reversible physiologic changes in the myelin and underlying axon.
Certain maneuvers for the provocation of positive sensory phenomena—e.g., the Tinel sign of tingling upon percussion of a regenerating peripheral nerve and the Phalen sign of paresthesia in the territory of the median nerve on wrist flexion—typify the susceptibility of a damaged nerve to pressure. In the case of a severed nerve, regeneration from the proximal end begins within days. The thin, regenerating sprouts are unusually sensitive to mechanical stimulation, which produces tingling, or the Tinel sign.
Diffuse Involvement of Nerves (Polyneuropathy) (See Table 8-3)
As most polyneuropathies affect mixed nerves, the sensory changes are accompanied by varying degrees of motor and reflex loss. Usually the sensory impairment is roughly symmetrical and the predominant symptoms are numbness and paresthesias. Because in most types of polyneuropathy the longest and largest axons are the most affected (“length dependent,” axonal neuropathy), sensory loss begins in, and is most severe over the feet and legs and, if the upper limbs are affected, over the hands. As the polyneuropathy progresses the margin of sensory loss “ascends,” meaning it moves proximally on the limbs. The term glove-and-stocking, employed to describe the distribution of sensory loss of polyneuropathy, draws attention to the predominantly distal pattern of involvement but does not convey that the change from normal to impaired sensation is characteristically gradual. (In psychogenic sensory loss, by contrast, the border between normal and absent sensation is usually sharply defined.) The abdomen, thorax, and face are spared in polyneuropathy except in the most severe cases, in which sensory changes may be found over the anterior thoracoabdominal escutcheon and around the mouth.