HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Murakami, K. Articles by Mano, T. Search for Related Content PubMed PubMed Citation Articles by Murakami, K. Articles by Mano, T.

Skin sympathetic nerve activity in acquired idiopathic generalized anhidrosis

Fourth Department of Internal Medicine (Drs. Murakami, Sobue, and Mitsuma), Aichi Medical University, Aichi; the Murakami Medical Clinic (Dr. Murakami), Aichi; and the Department of Autonomic and Behavioral Neurosciences, Division of Higher Nervous Function (Drs. Iwase and Mano), Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.

We recorded skin sympathetic nerve activity (SSNA) microneurographically from the right tibial nerve of a patient with acquired idiopathic generalized anhidrosis (AIGA). The patient did not show any spontaneous sweating or pilocarpine- and nicotine-induced sweat response. Histopathologic examination showed degenerated eccrine glands associated with surrounding inflammatory cellular infiltration. Electrical nerve stimulation produced a two-peak pattern of SSNA reflex discharge representing sudomotor and vasoconstrictor components. The frequency of spontaneous SSNA bursts (burst rate), presumably of a sudomotor nature, at the ambient temperature of 25 ^°C was significantly higher than in a healthy control subject and was further increased at a temperature of over 38 ^°C. Thus, sudomotor sympathetic nerve activity is well preserved or even increased in AIGA. We conclude that anhidrosis of AIGA results from the generalized sweat gland dysfunction rather than decreased sympathetic outflow to the skin.

Address correspondence and reprint requests to Dr. Ken Murakami, The Fourth Department of Internal Medicine, Aichi Medical University, Nagakute, Aichi 480-11, Japan.

Supported by grants from the Ministry of Health and Welfare of Japan.

Received May 14,1992. Accepted for publication in final form October 9, 1992.

This article has been cited by other articles:

				V Donadio, P Montagna, M Nolano, P Cortelli, C Misciali, G Pierangeli, V Provitera, A Casano, A Baruzzi, and R Liguori Generalised anhidrosis: different lesion sites demonstrated by microneurography and skin biopsy J. Neurol. Neurosurg. Psychiatry, April 1, 2005; 76(4): 588 - 591. [Abstract] [Full Text] [PDF]

				M. Asahina, A. Suzuki, N. Tamura, T. Yoshida, and T. Hattori Acquired generalized anhidrosis associated with lymphocytic infundibuloneurohypophysitis Neurology, November 9, 2004; 63(9): 1752 - 1752. [Full Text] [PDF]

				Y. Nakazato, N. Tamura, A. Ohkuma, K. Yoshimaru, and K. Shimazu Idiopathic pure sudomotor failure: Anhidrosis due to deficits in cholinergic transmission Neurology, October 26, 2004; 63(8): 1476 - 1480. [Abstract] [Full Text] [PDF]

				K. Yamamoto, G. Sobue, S. Iwase, M. Nagamatsu, T. Mano, and T. Mitsuma Skin sympathetic nerve activity in Guillain-Barre syndrome: a microneurographic study J. Neurol. Neurosurg. Psychiatry, October 1, 1997; 63(4): 537 - 540. [Abstract] [Full Text] [PDF]