QSART evaluates postganglionic sudomotor function. It probably evaluates the distal ends of the postganglionic axon (50). The test is quantitative, reproducible, and noninvasive with a coefficient of variation of 8% (51). QSWEAT is the commercial counterpart, modeled after the Mayo Clinic system.
The neural pathway consists of an axon "reflex" mediated by the postganglionic sympathetic sudomotor axon. The axon terminal is activated by acetylcholine. The impulse travels antidromically, reaches a branch-point, then orthodromically to release acetyl-choline from nerve terminal. Acetylcholine traverses the neuroglandular junction and binds to M3 muscarinic receptors on eccrine sweat glands to evoke the sweat response (52). Acetylcholinesterase in subcutaneous tissue cleaves acetylcholine to acetate and choline, resulting in its inactivation and cessation of the sweat response. The test is usually done on one arm and three lead sites (37).
QSART recordings have been performed in many neuropathies including diabetic neuropathy (1). Distal sympathetic and vagal function were measured in 73 consecutive patients with diabetic neuropathy seen at the Mayo Autonomic Reflex Laboratory. Postganglionic sympathetic failure measured proximally within the foot occurred as commonly as vagal failure (58 and 55%, respectively) and occurred much more frequently than did OH (26%). This study found that distal sympathetic sudomotor failure and vagal failure occur with equal frequency when sensitive and quantitative recording methods are used. This pattern of distal sudomotor loss is the most common pattern seen in diabetes. It is often associated with the burning feet syndrome in diabetes and idiopathic neuropathies (53). There is a progressive loss of sweating with increasing duration and severity of neuropathy. Early on, there can be an exaggerated forearm (proximal) volume response (54).
QSART sweating is cholinergic. Of interest is that, during development sweating is under adrenergic control, with an adrenergic to cholinergic switch occurring, so that, in postnatal humans only 20% of sweating is under adrenergic control. There is some evidence that in neuropathic pain states, there may be a reversion back to predominantly adrenergic sweating (55). Whether that occurs in diabetic distal small fiber neuropathy is not known.
The thermoregulatory sweat test (TST) is a sensitive qualitative test of sudomotor function that provides important information on the pattern and distribution of sweat loss. The presence of sweating causes a change in the indicator from brown to a violet color. The subject is heated in a sweat cabinet (10,28). The value of the test can be enhanced and rendered semiquantitative by measuring the percent of anterior body surface anhidrosis (56).
Certain sweat patterns are recognizable in human diabetic neuropathy (28). Of 51 patients suspected of having neuropathy on the basis of a clinical examination, 48 (94%) had unequivocal abnormalities on the TST. Pathological loss of sweating occurred distally in 65%, segmentally in 25%, and only in isolated dermatomes in 25%; 78% of patients had a combination of two or more patterns. Global anhidrosis was noted in eight patients (16%), all of whom had profound autonomic neuropathy, and in the entire group, the percentage of body surface anhidrosis correlated with the degree of clinical dysau-tonomia (rank correlation coefficient = 0.77; p < 0.01). Major advantages of the method are its simplicity, sensitivity, the ability to recognize patterns of anhidrosis, including mixed patterns, and its semiquantitative nature. The disadvantages are its inability to distinguish between postganglionic, preganglionic, and central lesions, the discomfort, the qualitative nature of the information obtained, and the staining of clothing.
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