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Vanderbilt Autonomic Dysfunction Center

QSART Testing

What is the purpose of QSART testing?

Sweat tests evaluate a particular part of the autonomic nervous system. The brain increases sweating by directing an increase in sympathetic nervous system traffic to sweat glands in the skin. The chemical messenger, acetylcholine, is released and acts on the sweat glands to stimulate the production of sweat. 

The QSART is a special form of sweat test. It tests the ability of sympathetic nerve terminals in the skin to release acetylcholine and increase sweat production.  If the patient has a loss of sympathetic nerve terminals, he/she will not produce sweat in this test. However, if the patient has a central (brain) abnormality that prevents them from producing sweat in response to increasing temperature, they will still produce sweat during QSART testing and have normal test results. Because of this, the results of this test help distinguish between sympathetic cholinergic failure from loss of nerve terminals and failure that results from misregulation of of sympathetic nerve traffic.

How is the test performed?

The skin on the leg and wrist is wiped with acetone, then alcohol and dried, cleaning the skin in preparation for the test.  Four electrodes filled with acetylcholine are placed on three areas of the leg and one area on the wrist. A mild electrical current called iontophoresis is then applied to help the drug stimulate the sweat glands. This evokes sweating at the site, but it also allows the body to release its own acetylcholine, resulting in sweat production at nearby sites. The sweat response is measured. The test takes approximately 45 minutes.

What are the expected results for a patient with POTS?

If a person has a loss of sympathetic nerve terminals that release acetylcholine, applying the patches would not lead to increased sweating. By this sort of neuropharmacologic test, doctors can distinguish sympathetic cholinergic failure due to loss of cholinergic terminals from failure due to abnormal regulation of sympathetic nerve traffic to intact cholinergic terminals.

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