Primary focal hyperhidrosis Primary focal hyperhidrosis Authors C Christopher Smith, MD David Pariser, MD Section Editors Robert P Dellavalle, MD, PhD, MSPH Mark V Dahl, MD Deputy Editor Abena O Ofori, MD Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Oct 2013. | This topic last updated: Aug 14, 2012.

INTRODUCTION — Hyperhidrosis (excessive sweating) is a common condition rarely due to significant underlying pathology that may have serious social, emotional, and professional consequences.

The diagnosis and treatment of primary focal hyperhidrosis is reviewed here. Night sweats and menopausal hot flashes are discussed separately. (See "Approach to the patient with night sweats" and "Menopausal hot flashes" .)

DEFINITION — Hyperhidrosis is the secretion of sweat in amounts greater than physiologically needed for thermoregulation. It is most commonly a chronic idiopathic (primary) condition; however, secondary medical conditions or medications should be excluded. Idiopathic hyperhidrosis localized to certain areas of the body is called primary focal hyperhidrosis. Primary focal hyperhidrosis usually affects the axillae, palms, and soles.

A consensus panel suggested the following diagnostic criteria for primary focal hyperhidrosis [ 1 ]:

• Focal, visible, excessive sweating of at least six months duration without apparent cause plus at least two of the following characteristics:

• Bilateral and relatively symmetric • Impairs daily activities • At least one episode per week • Onset before age 25 • Family history of idiopathic hyperhidrosis • Focal sweating stops during sleep

SYMPTOMS — Patients with primary focal hyperhidrosis generally develop symptoms in childhood or adolescence that persist throughout life. Patients have focal symptoms most often localized to the palms, soles, and axillae [ 2-4 ]. Less commonly, primary focal hyperhidrosis may affect the scalp and face, or other sites [ 4 ]. While primary focal hyperhidrosis is made worse by heat or emotional stimuli, it is not considered a psychological disorder.

Patients with axillary hyperhidrosis report skin maceration and staining of clothes. Palmar hyperhidrosis often leads to a fear of shaking hands and soiling of papers, and patients may have difficulty with work or recreational tasks that require a dry grip. Patients report that hyperhidrosis often results in social problems on both a private and professional level.

Hyperhidrosis is associated with an increased incidence of other cutaneous disorders. In a retrospective case-control study involving 387 patients with primary focal hyperhidrosis, patients with hyperhidrosis were more likely to suffer from dermatophytosis, pitted keratolysis, and viral warts at the sites of hyperhidrosis [ 4 ]. In addition, atopic dermatitis and other eczematous dermatitides were present at a greater frequency in subjects with hyperhidrosis. The reason for this association is unknown; one theory is that hyperhidrosis is an exacerbating factor for dermatitis [ 4 ].

EPIDEMIOLOGY AND ETIOLOGY — Hyperhidrosis prevalence estimates range from 1 to 3 percent of the population [ 5,6 ]. [ 3 ].

A study of patients with primary palmar hyperhidrosis who had been treated with thoracoscopic sympathectomy found that 49 of 58 patients and none of 20 controls reported a family history of hyperhidrosis [ 7 ] suggests a genetic component to the disease.

PATHOGENESIS — Sweating assists thermoregulation, skin hydration, and fluid and electrolyte balance. Three types of sweat glands, eccrine and apocrine, and apoeccrine glands have been described in humans [ 8 ]. Eccrine sweat glands are responsible for hyperhidrosis, although apoeccrine glands might play a role in axillary hyperhidrosis [ 9 ].

The primary function of eccrine sweat glands is thermoregulation, with cooling resulting from evaporation of eccrine sweat. Eccrine sweat glands are located throughout the body, but they are found in greatest quantity in the palms, soles, and (to a lesser degree) axillae. Sweating on the face, chest, and back is generally due to heat stimuli, while sweating of the palms and soles is due to emotional stress. The axillae have eccrine, apocrine, and apoeccrine glands. Thermal sweating can occur throughout the day, but emotional sweating (palms, soles, and to some degree axillae) stops while sleeping [ 10,11 ].

Eccrine glands are innervated by the sympathetic nervous system but utilize acetylcholine as the primary neurotransmitter. Thermal and emotional sweating are controlled by different regions of the brain. Thermal sweating is controlled by the hypothalamus via the thermosensitive preoptic sweat center, while emotional sweating is regulated by the cerebral cortex. A sympathetic signal is carried to endocrine glands via cholinergic autonomic neurons. In patients with primary focal hyperhidrosis, the sweat glands are usually histologically and functionally normal. Rather, the cause of hyperhidrosis appears to be an abnormal or exaggerated central response to normal emotional stress.

DIFFERENTIAL DIAGNOSIS — Patients with primary focal hyperhidrosis generally have hyperhidrosis involving the face, palms, soles, and axillae. Generalized sweating suggests an etiology other than primary focal hyperhidrosis. The most common cause of generalized sweating is excessive heat. Generalized hyperhidrosis can be due to systemic diseases or medications. Unlike primary focal hyperhidrosis, patients with generalized, secondary hyperhidrosis usually present as adults and report sweating that occurs both while awake and sleeping. A history of generalized hyperhidrosis requires a careful evaluation for systemic causes. The differential diagnosis for generalized hyperhidrosis is similar to the differential diagnosis of night sweats. (See "Approach to the patient with night sweats" .) One should evaluate for signs and symptoms of an infectious cause such as tuberculosis [ 12 ], HIV [ 13 ], or endocarditis; a malignant etiology such as lymphoma [ 14,15 ]; or an endocrinopathy such as carcinoid syndrome [ 16 ], pheochromocytoma [ 17 ], or hyperthyroidism [ 18 ].

Medications should be carefully reviewed as many can cause generalized sweating ( table 1 ).

While menopause is a common cause of excessive sweating, clinicians should perform a careful history and examination before concluding that excessive sweating in a woman of perimenopausal age is due to hot flashes. (See "Menopausal hot flashes" .)

Other causes of excessive sweating include:

• Patients with previous spinal cord injuries may occasionally develop episodes of diffuse sweating long after their injury. These sweating episodes can be due to an autonomic dysreflexia, orthostatic hypotension, or a post-traumatic syringomyelia. Hyperhidrosis attributed to autonomic dysreflexia is caused by an exaggerated autonomic response to normal stimuli such as bowel and bladder distention or skin irritation. In addition to sweating of the face, neck, and trunk, patients generally have flushing of the face and a throbbing headache. Their spinal cord lesion is usually at or above the sixth thoracic level. A post-traumatic syringomyelia may occur months to years after the development of paraplegia from a spinal cord injury of any level. The syrinx may develop above or below the level of the transection and may be associated with progressive numbness of the hyperhidrotic areas [ 10,11 ]. • Gustatory sweating (mild sweating around the lips, nose, and forehead) occurs normally with the consumption of hot, spicy foods. However, pathologic gustatory sweating may be caused by sympathetic nerve damage, either due to invasion (such as a Pancoast tumor), or by sympathectomy (see below). It can also be due to a diabetic neuropathy, herpes zoster of the preauricular region, or misdirection of autonomic nerve fibers following parotid surgery (Frey's syndrome) [ 10,11 ].

TREATMENT — Primary focal hyperhidrosis can lead to significant social and employment distress. While many effective therapies exist, they are often associated with difficult side effects. It is important to understand the patient's goals and expectations and to carefully counsel the patient on available treatments, as well as their limitations and complications.

Topical therapy — Most commercially available over-the-counter antiperspirants contain a low-dose metal salt (usually aluminum) that physically obstructs the opening of sweat gland ducts. These over-the-counter products are only successful in treating patients with very mild symptoms. In patients who do not respond to over-the-counter antiperspirants, prescription strength antiperspirants such as 20 percent aluminum chloride in ethanol (Drysol) or 6.25 percent aluminum tetrachloride (Xerac) may provide adequate therapy for patients with mild to moderate axillary, palmar, or plantar hyperhidrosis (though they are generally more successful in treatment of axillary than palmar or plantar hyperhidrosis) [ 19,20 ]. These antiperspirants are thought to work by mechanically obstructing the eccrine sweat gland ducts or by causing atrophy of the secretory cells [ 21 ].

Prescription strength antiperspirants should be applied nightly until improvement is noted; significant improvement may be noted within one week. The interval between applications can then be gradually lengthened, with once weekly applications typically needed for maintenance therapy [ 22 ].

Unfortunately, treatment with strong antiperspirants is often limited by skin irritation (especially in the axillary region). To reduce the risk of irritation, these products should be applied to dry skin between episodes of sweating. Ideally, it should be applied at bedtime when hyperhidrosis is at a minimum and washed off in the morning [ 22 ]. Others have recommended using a hair dryer to quickly dry the application, or to use baking soda powder in the morning to neutralize any remaining aluminum chloride [ 11 ]. Low potency corticosteroid creams (such as 2.5 percent hydrocortisone cream) can help alleviate the axillary irritation that frequently occurs.

A small trial found that topical glycopyrrolate 2 percent reduced forehead sweat production in patients with primary craniofacial or secondary gustatory hyperhidrosis [ 23 ]. Topical glycopyrrolate is only available through compounding pharmacies.

Medications — Although systemic therapies (anticholinergics, clonidine , beta-blockers, and benzodiazepines) can be effective for primary focal hyperhidrosis, concern regarding the potential adverse effects of systemic agents has inhibited the routine use of these therapies. Topical agents remain the initial treatment of choice for primary focal hyperhidrosis. (See 'Topical therapy' above.)

The most common anticholinergic agents prescribed for primary focal hyperhidrosis are glycopyrrolate and oxybutynin [ 24-26 ]. Glycopyrrolate is utilized more frequently than oxybutynin. However, only oxybutynin has been evaluated in a randomized trial.

• Glycopyrrolate – The use of oral glycopyrrolate for hyperhidrosis is supported by retrospective case series [ 25-27 ]. In one retrospective series in which 45 patients with primary hyperhidrosis (axillary, palmoplantar, generalized, or craniofacial) received treatment with glycopyrrolate alone (11 patients) or in combination with local therapies (34 patients), 67 percent of patients reported symptomatic improvement [ 26 ]. In addition, a retrospective study of 31 children with hyperhidrosis (mean age of 15 years) found that 71 percent achieved major improvement in symptoms during treatment with glycopyrrolate (with or without concomitant topical aluminum chloride) [ 28 ]. The children in this study were treated with an average total dose of 2 mg of glycopyrrolate per day. Typical doses for adults range from 1 to 2 mg once or twice daily (ie, 1 to 4 mg per day). • Oxybutynin – The efficacy of oxybutynin for hyperhidrosis was documented in a six- week randomized trial of 50 patients with palmar or axillary hyperhidrosis [ 29 ]. At six weeks, great or moderate improvement in symptoms occurred in 48 and 26 percent of patients treated with oxybutynin (2.5 mg per day for one week, 2.5 mg twice daily for two weeks, and 5 mg twice daily for three weeks), respectively. In contrast, great or moderate improvement was reported by 0 and 27 percent of patients treated with placebo, respectively. Uncontrolled studies performed by the same authors also support the efficacy of oxybutynin for facial, palmar, and axillary hyperhidrosis [ 30-32 ].

Potential adverse effects of anticholinergic agents include dry mouth (most common), blurred vision, headache, and urinary retention [ 25,28 ]. Although the side effects of glycopyrrolate and oxybutynin are often tolerable, discontinuation of glycopyrrolate may be necessary in up to one-third of treated patients [ 25 ]. Additional studies are necessary to confirm the long term efficacy and safety of anticholinergic drugs when utilized for this indication. Contraindications to these therapies are reviewed separately. (See "Glycopyrrolate (glycopyrronium): Drug information" and "Oxybutynin: Drug information" .)

As noted above, other drugs have been employed for the treatment of hyperhidrosis. Evidence for the efficacy of clonidine , an alpha-2 adrenergic agonist that reduces sympathetic outflow, for hyperhidrosis is limited to case reports and a small retrospective case series [ 26,33,34 ]. Reduced blood pressure is a potential adverse effect of this agent.

In patients with hyperhidrosis related to specific emotional events, beta-blockers or benzodiazepines may be useful in reducing the emotional stimulus that leads to the excessive sweating [ 22,35,36 ].

Iontophoresis — Iontophoresis is the introduction of ionized substances through intact skin by the application of direct current (also called electromotive drug administration or transdermal electromotive drug administration). The exact mechanism of action is unclear, but it is thought to temporarily block sweat glands [ 11,22 ]. Iontophoresis for hyperhidrosis is typically performed with tap water, and equipment is available for home use.

Iontophoresis is most often used for palmar or plantar hyperhidrosis, but a special axillary electrode can be used to treat axillary hyperhidrosis [ 37 ]. Still, treatment of the axillae is often less effective due to the difficulty of obtaining uniform contact of the electrode with the axillary skin. Although there are only limited data from randomized trials, iontophoresis appears to alleviate symptoms in approximately 85 percent of patients with palmar or plantar hyperhidrosis and is safe and simple to perform [ 38-41 ]. If tap water iontophoresis is ineffective, some authors recommend adding anticholinergic agents to the treatment trays [ 22 ].

While there are few side effects other than dry, cracked hands (which can be relieved with moisturizers), the biggest issue for patients with this treatment modality is generally the time required to perform the treatments. Initial treatment is generally 20 to 30 minutes per day; however, the frequency of treatments can often be reduced after only 10 to 15 treatments. While some studies have found that a reduction in sweating can be maintained with therapy every two weeks [ 38 ], some patients find that shorter duration treatments three times a week are required for maintenance. Botulinum toxin — Botulinum toxin A (BTX-A) blocks the release of neuronal acetylcholine from the presynaptic junction of both neuromuscular and cholinergic autonomic neurons. Botulinum toxin's effect at the neuromuscular junction has been used to treat conditions such as dystonia [ 42 ] and achalasia [ 43 ]. By blocking the release of acetylcholine, botulinum toxin can also temporarily reduce sweat production. Most studies have used one of two preparations of BTX-A: onabotulinumtoxinA (Botox) or abobotulinumtoxinA (Dysport). These two preparations have different dosing; 1 unit of onabotulinumtoxinA is equal to approximately 3 units of abobotulinumtoxinA [ 44 ]. US Food and Drug Administration (FDA) approval for botulinum toxin for hyperhidrosis is limited to onabotulinumtoxinA for axillary hyperhidrosis.

Axillary hyperhidrosis — Several studies have shown BTX-A to be particularly effective in the treatment of axillary hyperhidrosis [ 44-50 ]:

• In a randomized trial involving 320 patients with bilateral primary axillary hyperhidrosis, response rates after four weeks were significantly higher with onabotulinumtoxinA, 50 units per axilla, than placebo (94 versus 36 percent) [ 47 ]. After 16 weeks, 82 percent of the onabotulinumtoxinA group still had an effective response compared with 21 percent of the placebo group. Adverse events were similar in the two groups; however, more patients treated with onabotulinumtoxinA reported an increase in non-axillary sweating (5 versus 0 percent). • In a randomized trial involving 145 patients with primary axillary hyperhidrosis unresponsive to topical therapy with aluminum chloride, patients were injected with 200 units of abobotulinumtoxinA in one axilla and placebo in the other; after two weeks, the treatments were revealed, and the axilla that had been treated with placebo was injected with 100 units of abobotulinumtoxinA [ 44 ]. Two weeks after the initial injection, the rate of sweat production was significantly less on the side treated with abobotulinumtoxinA (24 versus 144 mg/min). Two weeks after the injection with 100 U, the rate of sweat production decreased from 144 to 32 mg/min. The mean reduction in sweating was greater with the 200 units injection (81.4 versus 76.5 percent). Twenty-six weeks after the initial injection, the rates of sweat production were still significantly lower than baseline in both axillae. No major adverse events were noted, and 92.4 percent were satisfied or completely satisfied with their results.

Although the above study found a statistically greater reduction in sweating with 200 units of abobotulinumtoxinA, it is not clear that this difference is clinically important. A study of 43 patients found no difference in the degree or duration of reduction in sweating with 100 or 200 units of abobotulinumtoxinA [ 51 ]. After 48 weeks, sweat production was the same in both groups and had returned nearly to baseline. A second injection at that point with either 100 units or 200 units of abobotulinumtoxinA again produced identical reductions in sweating; 48 weeks after the second injection sweat production was significantly lower than 48 weeks after the first injection.

Other studies have also shown continued efficacy for hyperhidrosis after several injections [ 46 ]. However, patients treated with BTX-A can develop antibodies, and when BTX-A has been used in other settings this has occasionally limited therapeutic effectiveness [ 52,53 ]. Palmar hyperhidrosis — The efficacy of BTX-A in the treatment of palmar hyperhidrosis has been demonstrated in several trials [ 54-58 ]:

• In a randomized trial in 19 patients with palmar hyperhidrosis, placebo was given in one hand and botulinum toxin in the other [ 55 ]. After four weeks, among the 17 patients not lost to follow-up, all rated the BTX-A injections a success, while only 12 percent rated the placebo injections a success. One patient had transient thenar weakness. • In a study of 20 patients with palmar hyperhidrosis who had not responded to topical and iontophoresis therapy, all developed anhidrosis by two weeks after therapy, with a continued reduction in sweating at least 12 months after therapy in all patients [ 54 ].

Adverse effects — Pain during injections is one of the most common complaints with this therapy. Whether being used for treatment of palmar or axillary hyperhidrosis, the application of botulinum toxin requires multiple, small-dose injections of the toxin. Multiple injections into sensitive areas such as the palms and soles are particularly painful for patients. In the study mentioned above, the 20 patients with palmar hyperhidrosis received an average of 26 injections (versus an average of 10 injections for axillary hyperhidrosis) [ 54 ].

Cryoanalgesia (refrigerant sprays or ice packs) or vibration anesthesia may be of some benefit in decreasing pain associated with injection [ 59-63 ]. Topical anesthetics have also been used in attempt to reduce pain [ 64 ], but may be poorly effective on the palms and soles where the thick stratum corneum may reduce drug penetration [ 65-67 ].

One additional complication commonly reported with use for palmar hyperhidrosis is the development of temporary weakness in the muscles of the thenar eminence. In the above study, 21 percent reported weakness that lasted an average of three weeks [ 54 ].

Surgery — For many years axillary hyperhidrosis was surgically treated with subcutaneous curettage or excision of the skin containing these eccrine glands. However, this procedure has a significant failure rate and is associated with permanent scarring and the risk of restricted arm movement [ 68 ]. Newer surgical techniques for excising axillary eccrine and apocrine sweat glands, such as minimally invasive suction curettage, may have improved outcomes and decreased morbidity [ 69 ], however larger long-term studies are needed [ 70 ].

The most commonly used surgical technique for treatment of upper extremity hyperhidrosis involves the interruption of the upper thoracic sympathetic chain (usually from the second to fourth thoracic ganglia). Numerous studies have shown endoscopic transthoracic sympathectomies (ETS) to be effective, but the potential for adverse effects, particularly the development of compensatory hyperhidrosis, precludes the use of ETS as first-line therapy [ 71-75 ]:

• A series of 850 patients with upper extremity hyperhidrosis was treated with bilateral endoscopic transthoracic sympathectomies [ 71 ]. After a median follow-up of 31 months, 98 percent of patients reported satisfactory results, with only 2 percent developing recurrent symptoms. There were no life-threatening complications. Horner's syndrome occurred in three cases. Compensatory sweating, primarily of the trunk, occurred in 55 percent of patients, but only 2 percent considered this to be as bothersome as their original hyperhidrosis symptoms. • In a review of 480 sympathectomies, there were no major complications requiring surgical reintervention and no postoperative deaths [ 73 ]. Initially, 95.5 percent were satisfied with the results of surgery. However, over time satisfaction waned; after a mean follow-up of 14.6 years, 66.7 percent were satisfied and 26.7 percent were partially satisfied despite a recurrence rate of only 1.5 percent. Patients with axillary hyperhidrosis without palmar involvement were the least satisfied. Compensatory and gustatory sweating, which occurred in 67.4 percent and 50.7 percent of patients, respectively were the most frequently stated reasons for dissatisfaction. • A study evaluating long-term results (median follow-up 3.8 years) in 125 patients who underwent ETS for treatment of upper limb hyperhidrosis found a much higher recurrence rate for axillary than palmar symptoms (65 versus 6.6 percent) [ 72 ]. Eighty-six percent developed compensatory sweating; however, 61 percent of these patients considered this only a minor disturbance, and only 6.3 percent of patients reported regret in having the surgery. Horner's syndrome occurred in three patients. • A study evaluating the severity of compensatory sweating in 158 patients who underwent bilateral sympathectomy received questionnaires back from 148 patients (94 percent) [ 76 ]. Compensatory sweating occurred in 89 percent of patients and was severe enough that patients often needed to change clothes during the day in 35 percent; 16 percent regretted having the surgery. Patients who had facial hyperhidrosis or blushing underwent surgery at the second thoracic ganglia; those who had palmar hyperhidrosis underwent surgery at the second and third thoracic ganglia; and those who had axillary hyperhidrosis underwent surgery at the second, third, and fourth thoracic ganglia. Compensatory sweating was more severe in the last group. The study could not distinguish whether this represented more severe compensatory sweating after more extensive sympathectomy or after sympathectomy performed in patients with axillary hyperhidrosis. • A retrospective review of 234 records of patients treated with ETS examined associations between the level of the sympathectomy and outcomes [ 77 ]. Although ETS for palmar hyperhidrosis is most commonly performed at a T2 or T3 level, similar efficacy was seen with T4-level ETS. Patients treated at a T4 level had less compensatory sweating than those with higher sympathectomies. • On a follow-up questionnaire in 180 patients who had undergone ETS (T2 or T2-3) for isolated facial blushing, compensatory and gustatory sweating were reported by 88 and 30 percent of patients, respectively [ 78 ]. Of those with compensatory sweating, in one-fourth it was severe enough to require changing clothes during the day.

Thoracic sympathetic clipping is an alternative to permanent severing of the sympathetic nerve [ 79-82 ]. The results of a prospective study of 727 patients treated with thorascopic sympathetic clipping for hyperhidrosis or facial flushing support the efficacy of the procedure for hyperhidrosis and suggest that some patients who develop postoperative compensatory sweating benefit from reversal of the procedure via clip removal [ 81 ]. In the study, 15 out of 31 patients (48 percent) followed after a reversal procedure reported a substantial reduction in compensatory sweating. Additional studies are necessary to evaluate efficacy, safety, and reversibility of sympathetic clipping in hyperhidrosis. Microwave energy — Early studies suggest that microwave energy can be utilized to destroy eccrine glands and relieve hyperhidrosis in the axilla [ 83-85 ]. In a randomized trial of 120 adults with primary axillary hyperhidrosis who were given one to three treatments with a microwave energy device (n = 81) or a sham device (n = 39), patients treated with the microwave device were more likely to notice a subjective reduction in the severity of axillary hyperhidrosis 30 days after treatment than patients in the sham treatment group (89 versus 54 percent) [ 85 ]. The difference in favor of active treatment remained statistically significant for up to six months.

In addition, more patients in the active group achieved at least a 50 or 75 percent reduction in a gravimetric measurement of sweat production through six months after treatment. However, this difference was only statistically significant for patients who achieved ≥75 percent improvement at the 30 day time point (62 versus 39 percent).

The most common side effects of treatment were altered skin sensation (median duration 25 days, range 4 to 225 days), discomfort, and other local reactions. Additional studies are necessary to determine the role of microwave energy devices in the treatment of hyperhidrosis.

SUMMARY AND RECOMMENDATIONS — Individuals with primary focal hyperhidrosis typically have excessive sweating of the palms, soles, and axillae and can suffer significant psychological, social, educational, and occupational consequences.

Patients with generalized hyperhidrosis not limited to the palms, soles, and axillae are likely to have hyperhidrosis secondary to medications or a systemic illness, and the evaluation is similar to that done for night sweats. (See "Approach to the patient with night sweats" .)

When choosing treatments for primary focal hyperhidrosis, the patient's goals in therapy should be understood, and the side effects associated with each therapy should be carefully discussed. Conservative measures should be tried before progressing to more invasive treatments. The severity and location of hyperhidrosis helps guide the choice of therapies:

• Patients with mild to moderately severe axillary, palmar, or plantar hyperhidrosis should initially be treated with topical agents such as aluminum chloride hexahydrate in alcohol. Skin irritation is common but may be managed by applying the preparation on dry skin at bedtime and washing it off in the morning; irritated skin can also be treated with 2.5 percent hydrocortisone cream. (See 'Topical therapy' above.) • Systemic therapies such as beta-blockers or benzodiazepines may be useful in treating symptoms directly related to emotional stress. Anticholinergic drugs and clonidine can be helpful for hyperhidrosis, but the use of these agents may be complicated by side effects. (See 'Medications' above.) • Palmar and plantar hyperhidrosis can be treated effectively with iontophoresis, but treatments can be time consuming. (See 'Iontophoresis' above.) • Axillary hyperhidrosis can be effectively treated with botulinum toxin (BTX). Palmar and plantar hyperhidrosis can also be treated with BTX, but the injections are quite painful on the hands and feet, and a significant percentage of patients develop temporary local muscle weakness. (See 'Botulinum toxin' above.) • Patients with palmar hyperhidrosis who fail topical therapies and iontophoresis, and who do not tolerate or get relief from BTX, can be treated effectively with endoscopic thoracic sympathectomy (ETS) Side effects, especially compensatory hyperhidrosis in other parts of the body, which may reduce long-term patient satisfaction with this procedure. Patients should be informed of the potential for this adverse effect. ETS can also be used for axillary hyperhidrosis, but the relapse rate is high. (See 'Surgery' above.) • While ETS has also been used for facial hyperhidrosis, rates of compensatory and gustatory hyperhidrosis after the procedure appear to be very high. (See 'Surgery' above.)

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