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CONCISEDIAGNOSIS REVIEW AND TREATMENT FOR CLINICIANS OF HYPERHIDROSIS Hyperhidrosis: Evolving Therapies for a Well-Established Phenomenon JOHN H. EISENACH, MD; JOHN L. D. ATKINSON, MD; AND ROBERT D. FEALEY, MD The socially embarrassing disorder of excessive sweating, or cause for the increased sweating and endeavor to remove it; hyperhidrosis, and its treatment options are gaining widespread attention. In order of frequency, palmar-plantar, palmar-axillary, 2) to check or modify the amount of secretion itself; and 3) isolated axillary, and craniofacial hyperhidrosis are distinct disor- to relieve any secondary dermatitis or other complications ders of sudomotor regulation. A common link among these disor- that may arise.” ders is an excessive, nonthermoregulatory sweat response often to emotional stimuli in body regions influenced by the anterior cingulate cortex as opposed to the thermoregulatory sweat response regulated by the preoptic-anterior hypothalamus. Diagno- DEFINITIONS sis of these mechanistically ambiguous disorders is primarily from patient history and physical examination, whereas results of labo- The condition that results when the sudomotor system ratory studies performed with indicator powder reveal the distribu- (which controls sweat output) functions excessively in iso- tion and severity of resting hyperhidrosis and document the integ- lation with no apparent cause is termed primary or essential rity of thermoregulatory sweating. Treatment options lie on a continuum based on the severity of hyperhidrosis and the risks hyperhidrosis. It is imperative to differentiate this condi- and benefits of therapy. In general, therapy begins with antiperspi- tion from secondary hyperhidrosis, which can be associ- rants or anticholinergics. Iontophoresis is available for palmar- ated categorically with infection, malignancy, neurologic plantar and axillary hyperhidrosis. Botulinum toxin type A or local excision/curettage is effective for isolated axillary hyperhidrosis and endocrine disorders, spinal cord injury, and miscella- not responsive to topical application of aluminum chloride. Endo- neous causes (Table 1).6 An important contemporary cause, scopic thoracic sympathectomy may be used for severe cases of terrorism-related chemical warfare agents (such as organo- palmar-plantar and palmar-axillary hyperhidrosis. No sole therapy of choice has emerged for craniofacial sweating. The long-term phosphate compounds that inhibit acetylcholinesterase, sequelae of hyperhidrosis and its treatment also are discussed. similar to agricultural pesticides), must be included in this 7 Mayo Clin Proc. 2005;80(5):657-666 list. Primary hyperhidrosis is classified as focal or general- BT-A = botulinum toxin type A; CH = compensatory hyperhidrosis; ETS = ized on the basis of the stimulus and site of neuromodula- endoscopic thoracic sympathectomy; TST = thermoregulatory sweat test tion. The exaggerated sweating response to emotional or sensory stimuli probably originates in the anterior cingulate frontal cortex as opposed to thermoregulatory sweat- xcessive sweating, or hyperhidrosis, is a socially em- ing, which is primarily regulated by the preoptic-anterior Ebarrassing disorder that may seem trivial to the general hypothalamus.8 Focal hyperhidrosis most commonly af- public because of its falsely perceived rarity; however, fects the palms (Figure 1, top) and soles. Excess sweating hyperhidrosis is being recognized increasingly, and its in these areas is called palmar-plantar hyperhidrosis. Iso- treatment options are gaining widespread attention.1-3 Both lated axillary hyperhidrosis affects only the underarms and ancient and modern medicine have been perplexed by this may coexist with palmar-plantar hyperhidrosis. Finally, entity. Of sweating, Hippocrates used the term hidroa, and least common, there is isolated supranormal sweating which was translated from Greek into Latin and English as of the face (craniofacial hyperhidrosis), which may be sudamina. Both terms gave rise to the present use of hidro- provoked by heat, emotion, or spicy foods (gustatory hy- sis and sudomotor function.4 Nearly 100 years ago, perhidrosis). This disorder is difficult for patients to hide, Meachen5 described hyperhidrosis and 3 therapeutic goals especially if the facial skin forms a darkened hue called that have withstood time: “…1) To seek out the underlying chromhidrosis. From the Department of Anesthesiology (J.H.E.), Department of Neurologic EPIDEMIOLOGY Surgery (J.L.D.A.), and Department of Neurology (R.D.F.), Mayo Clinic College of Medicine, Rochester, Minn. A recent survey in the United States suggests that the A question-and-answer section appears at the end of this article. prevalence of primary (essential) hyperhidrosis is 2.8%, Individual reprints of this article are not available. Address correspondence to with approximately one half (1.4%) of these individuals John H. Eisenach, MD, Department of Anesthesiology, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905 (e-mail: eisenach.john projected to have axillary hyperhidrosis and one sixth @mayo.edu). (0.5%) projected to have sweating that is intolerable or 9 © 2005 Mayo Foundation for Medical Education and Research interferes with daily activities. Epidemiological data spe- Mayo Clin Proc. • May 2005;80(5):657-666 • www.mayoclinicproceedings.com 657 For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings. DIAGNOSIS AND TREATMENT OF HYPERHIDROSIS TABLE 1. Categories of Secondary Hyperhidrosis Category Pathogenesis Features Chronic infection Tuberculosis, brucellosis Night sweats Neuroendocrine Pheochromocytoma Paroxysmal sweating, sudomotor cholinergic activation malignancy from excess catecholamines; responds to anticholinergics Endocrinologic Thyrotoxicosis, diabetes mellitus Paroxysmal sweating, increased metabolism and increased sensitivity of nerve fibers to epinephrine; thyrotoxicosis responds to β-blockade Malignancy Leukemia, lymphoma, renal cell Night sweats, pruritus; may respond to plasmapheresis or carcinoma, Castleman disease histamine2 receptor antagonists Neurologic diseases Acromegaly, carcinoid syndrome, Paroxysmal sweating; pontine ischemia may damage diencephalic epilepsy, basilar decending inhibitory fibers artery occlusion–pontine ischemia Biochemical agents Acetylcholinesterase inhibitors, Responsive to removal of stimulus, anticholinergics chemical warfare, pesticides Spinal cord injury Autonomic dysreflexia, orthostatic Can occur months to years after injury to spinal cord hypotension, posttraumatic syringomyelia Miscellaneous Anxiety, hypoglycemia, menopause cific to palmar hyperhidrosis are sparse, but this condition ways diurnal, is controlled by the anterior cingulate cortex, affects an estimated 0.6% to 1.0% of the Western popula- and its distribution is limited usually to the face, axillas, tion.10 The prevalence of severe palmar hyperhidrosis var- palms, and soles.8 Both higher centers descend to synapse ies geographically and has been described as endemic in on the intermediolateral cell column neurons of the spinal Southeast Asia, where it affects up to 3% of the popula- cord. From there, myelinated preganglionic sympathetic tion.10,11 This high prevalence in Southeast Asia can be seen nerves exit the cord via the ventral roots and enter the in the staggering group sizes (1167-9988 patients) in sev- segmental paravertebral sympathetic ganglia or course up eral outcome studies of thoracoscopic sympathectomy.12-14 and down the sympathetic chain and enter paraverterbral On review of these and other large-scale reports,12-17 several ganglia at other levels. Unmyelinated postganglionic sym- conclusions can be drawn. Of patients with severe hyper- pathetic fibers exit the ganglion and rejoin the segmental hidrosis presenting for surgery, most have palmar-plantar spinal nerve or plexus, eventually innervating pilomotor hyperhidrosis, 15% to 20% have combined palmar-axillary (hair follicles), sudomotor (sweat glands), and vascular hyperhidrosis, 5% to 10% have isolated axillary hyper- effectors of the skeletal muscle and skin of the trunk and hidrosis, and less than 5% have craniofacial hyperhidrosis. limbs. Hyperhidrosis is heritable in autosomal dominant fashion Sudomotor nerves release acetylcholine onto the musca- with variable penetrance; a recent study on allelic probabil- rinic cholinergic receptors of the sweat glands (Figure 2). ity estimates that a child of a parent with palmar hyper- There are 2 million to 5 million sweat glands in the body, hidrosis has a likelihood of phenotypic expression of 0.28, and they are anatomically and functionally differentiated meaning the child has an approximate 25% chance of de- into eccrine and apocrine. Developed in utero, eccrine veloping hyperhidrosis.18 Most large studies report that sweat glands are ubiquitous in skin but are heavily concen- 25% to 50% of patients with palmar hyperhidrosis have a trated in the forehead, scalp, axillas, palms, and soles.19 family history of the disorder. No other risk factors are Glabrous or hairless skin (palms, soles, lips) is rich in arte- known to cause primary hyperhidrosis. riovenous anastomoses (bypass conduits between arteri- oles and venules) that are richly innervated by sympathetic vasoconstrictor nerves.20 Thus, in addition to emotional MECHANISMS sweating, glabrous skin is a source of thermoregulation and Understanding why patients have supranormal sweating of heat release. In the dermis, eccrine gland secretory coils the

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