The Treatment of Primary Focal Hyperhidrosis

Todd Wechter, BSc; Steven R. Feldman, MD, PhD; Sarah L. Taylor, MD, MPH


Skin Therapy Letter. 2019;24(1) 

In This Article

Abstract and Introduction


Primary focal hyperhidrosis is a relatively common disease that has a significant impact on afflicted patient's quality of life. The pathogenesis of the disease is thought to stem from increased cholinergic activity on eccrine sweat glands. Topical aluminum chloride based antiperspirants are good first-line agents for all affected body sites. Anticholinergic agents are emerging as effective topical alternatives. Iontophoresis passes an electrical current through the skin and is an excellent treatment option for palmoplantar disease. Botulinum toxin type A injections remain a mainstay second-line treatment. Local procedural advances including microwave thermolysis, laser therapy and focused ultrasound are emerging as safe and effective alternatives for refractory disease. Oral anticholinergics are generally well tolerated and can also be used for intractable disease. Last-line interventions include local surgical options and sympathectomy, though some patients may prefer permanent treatment. Further investigation of novel treatments as well as ways to optimize existing therapeutic options are needed.


Primary focal hyperhidrosis, characterized as sweating beyond what is needed for adequate thermoregulation, can have a dramatic effect on quality of life and has an estimated prevalence of 4.8% in the United States.[1,2] Primary focal disease differs from secondary hyperhidrosis in that it is located in discrete areas of the body (e.g. palms, soles, axilla, face or scalp) and is not induced by medications or other medical conditions.[3,4] While a complete understanding of the cause or causes of primary focal hyperhidrosis remains unknown, its pathogenesis is thought to be linked to the thermoregulatory center of the hypothalamus and the autonomic nervous system.[5] Post-ganglionic sympathetic cholinergic neurons release the neurotransmitter acetylcholine, which acts on eccrine sweat glands leading to sweat secretion.[6] Increased sympathetic activity on eccrine glands can be induced by either emotional or thermal stimuli.[7] Thus, potential treatment targets include the neurotransmitter, nerves, eccrine glands, and eccrine ducts (Figure 1).

Figure 1.

Proposed pathway of sweat production and sites of therapeutic intervention. A. Sympathectomy interrupts thoracic sympathetic outflow from the sympathetic chain. B. Botulinum toxin (BTX-A) injection prevents the release of acetylcholine (ACh) into the synapse. C. Topical and systemic anticholinergics competitively inhibit binding of ACh to muscarinic receptors on the eccrine sweat gland. D. Microwave thermolysis, laser therapy, focused ultrasound and local surgical interventions all damage and/or remove the eccrine sweat glands. E. Aluminum chloride antiperspirants precipitate and block the sweat gland duct.

There are many treatment options that exist for primary focal hyperhidrosis, which can be local or systemic and range from topical therapies to surgical management.[8] Disease severity, disease location, treatment cost, side effect profile and patient preference are all important considerations when deciding on therapeutic options.[8] Here, we review current and emerging treatment options for primary focal hyperhidrosis. We summarize our findings in Table 1 and then provide our treatment recommendations in Table 2.