Skin potential recordings can be used to detect sympathetic sudomotor deficit in the peripheral neuropathies and central autonomic disorders (57,58). The recording electrodes are commonly electrode pairs 1 cm in diameter applied to the dorsal and ventral surfaces of the foot, the hand, or thigh. The stimulus might be an inspiratory gasp, a cough, a loud noise, or an electric shock. The sources of the skin potential are the sweat gland and the epidermis (59). A reasonable interpretation of studies in mammals, including humans, is that a component of the skin potential (early fast changes) is related to sweating, but that the later changes are because of skin potential changes. The latter can occur in patients who have congenital absence of sweat glands (60-63). The major advantage of the method is its simplicity so that it can be used in any electromyography (EMG) lab. The disadvantages are its enormous variability and the tendency of the responses to habituate, although claims for low coefficient of variation have appeared, and attempts have been made to reduce variability by using magnetic stimulation (64). The responses vary with the recording system, composition of the electrolyte paste, stimulus frequency, age, temperature, stress, status of central structures, and the effects of hormones and drugs (65). Following peripheral nerve section, skin potentials are no longer obtainable in the affected dermatome on direct and reflex stimulations. There was usually associated hypothermia and anhidrosis. Following sympathectomy, skin potentials are also lost, but only temporarily, returning in 4-6 months (66).
Skin potential recordings to detect sympathetic sudomotor deficit in the peripheral neuropathies and central autonomic deficits have been popularized (58). There is general agreement that a loss of SSR is abnormal. There is some controversy concerning whether a reduction of skin potential and a change in latency are reliable abnormalities (67). There is some evidence that unmyelinated fibers conduct without slowing or not at all (68). The test has been reported to correlate well with QSART (69), but in our experience is often present when QSART is clearly impaired. Potentials are reported to become reduced with aging (70).
SSR has been utilized in the evaluation of the peripheral neuropathies, especially diabetic neuropathy (71,72). The SSR deficit in amplitude and volume is reported to worsen with increasing duration of diabetes and correlates with sweatspot values (64) and clinical neuropathy (73). Both amplitude reduction and latency prolongation were seen and abnormalities may precede clinical neuropathy (73). In patients with well-established neuropathy, SSR in the foot is abnormal or absent in the majority of patients (72,74). For instance, in a study of 72 patients with diabetes with electrophysiologically confirmed sensorimotor peripheral neuropathy, SSR was absent in 83%. Statistically significant correlation was found between the Valsalva test abnormality, the degree of peripheral neuropathy, and the SSR (74). Its sensitivity and specificity to detect early abnormalities or improvement in clinical trials have not been established.
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