Find information on thousands of medical conditions and prescription drugs.


Primary hyperhidrosis is the condition characterized by abnormally increased perspiration, in excess of that required for regulation of body temperature. Some patients afflicted with the condition experience a distinct reduction in the quality of life. Sufferers feel at a loss of control because perspiration takes place independent of temperature and emotional state. more...

Hairy cell leukemia
Hallermann Streiff syndrome
Hallux valgus
Hantavirus pulmonary...
HARD syndrome
Harlequin type ichthyosis
Hartnup disease
Hashimoto's thyroiditis
Hearing impairment
Hearing loss
Heart block
Heavy metal poisoning
HELLP syndrome
Hemifacial microsomia
Hemolytic-uremic syndrome
Hemophilia A
Hemorrhagic fever
Hepatic encephalopathy
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatocellular carcinoma
Hepatorenal syndrome
Hereditary amyloidosis
Hereditary angioedema
Hereditary ataxia
Hereditary ceroid...
Hereditary coproporphyria
Hereditary elliptocytosis
Hereditary fructose...
Hereditary hemochromatosis
Hereditary hemorrhagic...
Hereditary spastic...
Hereditary spherocytosis
Hermansky-Pudlak syndrome
Herpes zoster
Herpes zoster oticus
Hidradenitis suppurativa
Hip dysplasia
Hirschsprung's disease
Hodgkin lymphoma
Hodgkin's disease
Horner's syndrome
Horseshoe kidney
Howell-Evans syndrome
Human parvovirus B19...
Hunter syndrome
Huntington's disease
Hurler syndrome
Hutchinson Gilford...
Hutchinson-Gilford syndrome
Hydatidiform mole
Hydrops fetalis
Hypereosinophilic syndrome
Hyperimmunoglobinemia D...
Hyperkalemic periodic...
Hyperlipoproteinemia type I
Hyperlipoproteinemia type II
Hyperlipoproteinemia type...
Hyperlipoproteinemia type IV
Hyperlipoproteinemia type V
Hypertensive retinopathy
Hypertrophic cardiomyopathy
Hypokalemic periodic...
Hypoplastic left heart...
Hypothalamic dysfunction

However, anxiety can exacerbate the situation for many sufferers. A common complaint of patients is that they get nervous because they sweat, then sweat more because they are nervous. Other factors can play a role; certain foods & drinks, nicotine, caffeine, and smells can trigger a response (see also diaphoresis).

There is controversy regarding the definition of hyperhidrosis, because any sweat that drips off of the body is in excess of that required for thermoregulation. Almost all people will drip sweat off of the body during heavy exercise.

Hyperhidrosis can either be generalized or localized to specific parts of the body. Hands, feet, axillae, and the groin area are among the most active regions of perspiration due to the relatively high concentration of sweat glands; however, any part of body may be affected. Primary hyperhidrosis is found to start during adolescence or even before, and interestingly, seems to be inherited as an autosomal dominant genetic trait.

Primary hyperhidrosis must be distinguished from secondary hyperhidrosis, which can start at any point in life. The latter form may be due to a disorder of the thyroid or pituitary gland, diabetes mellitus, tumors, gout, menopause or certain drugs.

Primary hyperhidrosis is estimated at around 1% of the population, afflicting men and women equally.


It is not known what causes primary hyperhidrosis. One theory is that hyperhidrosis results from an over-active sympathetic nervous system, but this hyperactivity may in turn be caused by abnormal brain function.


Hyperhidrosis can usually be treated, but there is no cure.

  • Surgery (Endoscopic thoracic sympathectomy or ETS): Select sympathetic nerves or nerve ganglia in the chest are either cut or burned (completely destroying their ability to transmit impulses), or clamped (theoretically allowing for the reversal of the procedure). The procedure often causes anhidrosis from the mid-chest upwards, a disturbing condition. Major drawbacks to the procedure include thermoregulatory dysfuction (Goldstien, 2005), lowered fear and alertness (Teleranta, Pohjavaara, et al 2003, 2004) and the overwhelming incidence of compensatory hyperhidrosis. Some people find this sweating to be tolerable while others find the compensatory hyperhidrosis to be worse than the initial condition. It has also been established that there is a low (less than 1%) chance of Horner's syndrome. Other risks common to minimally-invasive chest surgery, though rare, do exist. Patients have also been shown to experience a cardiac sympathetic denervation, which results in a 10% lowered heartbeat during both rest and exercise.
  • Aluminum chloride (hexahydrate) solution: The most common brands are Drysol®, Maxim® and Odaban®. Aluminum chloride is used in regular antiperspirants, but hyperhidrosis sufferers need a much higher concentration. A 15% aluminum chloride solution or higher usually takes about a week of nightly use to stop the sweating, with one or two nightly applications per week to maintain the results. An aluminum chloride solution can be very effective; some people, however, cannot tolerate the irritation that it can cause. Also, the solution is usually not effective for palmar (hand) and plantar (foot) hyperhidrosis.
  • Botulinum toxin type A (trademarked as Botox®): Injections of the botulinum toxin are used to disable the sweat glands. The effects can last from 4-9 months depending on the site of injections. With proper anesthesia the hand and foot injections are almost painless. The procedure when used for underarm sweating has been approved by the US FDA, and now some insurance companies pay partially for the treatments.
  • Iontophoresis: The affected area is placed in a device that has two pails of water with a conductor in each one. The hand or foot acts like a conductor between the positively- and negatively-charged pails. As the low current passes through the area, the minerals in the water clog the sweat glands, limiting the amount of sweat released. A common brand of tap water iontophoresis device is the Drionic®, Idrostar or MD1 Fischer. Some people have seen great results while others see no effect. However, since the device can be painful to some and a great deal of time is required, no cessation of sweating in some people may be the result of not using the device as required. The device is usually used for the hands and feet, but there has been a device created for the axillae (armpit) area and for the stump region of amputees.
  • Oral medication: There are several drugs available with varying degrees of success. A class of anticholinergic drugs are available that have shown to reduce hyperhidrosis. Ditropan® (generic name: oxybutynin) is one that has been the most promising. For some people, however, the drowsiness and dry-mouth associated with the drug cannot be tolerated. A time release version of the drug is also available, called Ditropan XL®, with purportedly reduced effectiveness. Robinul® (generic name: glycopyrrolate) is another drug used on an off-label basis. The drug seems to be almost as effective as oxybutynin, with similar side-effects. Other less effective anticholinergic agents that have been tried include propantheline bromide (Probanthine®) and benztropine (Cogentin®). A different class of drugs known as beta-blockers has also been tried, but don't seem to be nearly as effective.

A potential for the temporary treatment of hyperhidrosis is dricor. It is primarily an odorless deodorant that is applied at night. Many find it irritating but the results could be apparent depending on the individual.


[List your site here Free!]

Palmoplantar hyperhidrosis: a therapeutic challenge
From American Family Physician, 3/1/04 by Isabelle Thomas

Palmoplantar hyperhidrosis is a common condition in which the eccrine (sweat) glands of the palms and soles secrete inappropriately large quantities of sweat. The condition may become socially and professionally debilitating. Idiopathic palmoplantar hyperhidrosis begins in childhood and frequently runs in families. (1)

Eccrine glands are distributed over almost all of the body surface but are most dense in the palms and soles. These glands are morphologically and functionally normal in patients with palmoplantar hyperhidrosis. (2,3) Because the hyperhidrosis is stimulated by emotion and stress, it does not occur during sleep or sedation. Conversely, normal sweating is controlled primarily by thermoregulation and, thus, occurs independently of level of consciousness. The primary defect in patients with hyperhidrosis may be hypothalamic hypersensitivity to emotional stimuli from the cerebral cortex. (2,3)

The clinical diagnosis of palmoplantar hyperhidrosis is obvious because the excess sweating may be readily observed. Various treatment options are available. Some work by interrupting the innervation of sweat glands by sympathetic nerves with acetylcholine as the neurotransmitter, but all have limitations or associated complications. Thus, treatment of palmoplantar hyperhidrosis remains a challenge, and a logical approach must be taken to individualize therapy based on the degree of functional impairment.

Topical Therapy

The most effective topical treatment for palmoplantar hyperhidrosis is 20 percent aluminum chloride hexahydrate in absolute anhydrous ethyl alcohol (Drysol). (3) Less satisfactory results have been achieved with other topical agents, including boric acid, anticholinergic drugs, resorcinol, tannic acid (2 to 5 percent solutions), potassium permanganate, formaldehyde, methenamine, and glutaraldehyde.

Aluminum chloride is thought to obstruct sweat pores and induce atrophy of secretory cells within the sweat glands. The only contraindication to this treatment is documented hypersensitivity, and aluminum chloride should not be used on irritated, broken, or recently shaven skin.

Patients should apply the agent to dry skin nightly until clinical relief is achieved, at which point maintenance therapy is instituted and frequency of applications can be spread out over time in some patients. The morning after an overnight treatment, patients should wash away residual aluminum chloride and apply topical baking soda to limit skin irritation.

Topical therapy has some drawbacks. Compliance may become an issue because the daily applications necessary for efficacy may be considered too time-consuming for patients. (3,4) Topical therapy also may fail to adequately control hyperhidrosis.

Systemic Therapy

In the past, systemic anticholinergic drugs have been somewhat successful in the treatment of palmoplantar hyperhidrosis, based on the action of acetylcholine as the periglandular neurotransmitter within the sympathetic innervation of sweat glands. Despite their potential, systemic anticholinergic drugs are impractical treatments for this condition. Long-term therapy is required, and the drugs have numerous side effects, including dry mouth, dry eyes, constipation, blurry vision, mydriasis, and difficulty with urination. (5)

Benzodiazepines can reduce anxiety levels, thereby decreasing the emotional stimuli that trigger hyperhidrosis. However, these agents generally are not used because they may cause dependency and side effects such as lethargy and drowsiness. (6)


Iontophoresis, the passage of a direct electrical current onto the skin, is a long-established therapy for hyperhidrosis. (7) Since its introduction in 1952, iontophoresis has proved to be a safe, effective, and relatively inexpensive treatment that is suitable for patients to use at home. (8-10) Side effects usually are minor and related to individual susceptibility, higher amperage, and the length of time that a patient repeatedly uses the treatment. Skin irritation may occur, sometimes with erythema, vesicle formation, slight pain, or paresthesia in the treated areas; in addition, minor burns can occur in previously injured skin. (11)

The underlying mechanism of iontophoresis is not fully understood. (12) According to one hypothesis, iontophoresis may induce hyperkeratosis of the sweat pores and obstruct sweat flow and secretion (although no plugging of the pores has been found). (12) Other proposed mechanisms include impairment of the electrochemical gradient of sweat secretion and a biofeedback mechanism.

Various agents have been used in conjunction with iontophoresis, including tap water, salt water, and anticholinergic drugs. (13) Iontophoresis with saline is less effective than tap-water iontophoresis. A galvanic current of 0.2 milliamperes (mA) per [cm.sup.2] on intact skin has no adverse side effects, and a rate of up to 20 to 25 mA per surface generally is tolerable. (14)

Successful induction of hypohidrosis by tap-water iontophoresis requires the application of 15 to 20 mA to each palm or sole for 30 minutes per session for 10 consecutive days, followed by one or two maintenance sessions per week. Initially, many patients experience an aggravation of their symptoms, but this problem resolves after three to five treatments. Without maintenance therapy, symptoms recur in one to two weeks. (11) No side effects have been reported from the use of 20-mA iontophoresis in pregnant women or patients with pacemakers.

Use of the anticholinergic drug atropine during tap-water iontophoresis sometimes is helpful, but extreme caution is necessary to avoid toxicity from atropine overdose. No more than 1 mg of atropine should be added to 30 mL of tap water. The solution is poured over thin gauze placed on a stainless steel anodal plate. Atropine--tap-water iontophoresis should be used only by physicians well trained in this method.

Use of combined aluminum chloride, an anticholinergic drug, and tap-water iontophoresis for one hour each day resulted in the remission of symptoms for 20 days, compared with 3.5 days for the use of iontophoresis alone; this combination also was more effective in reducing the severity of symptoms. (15) Employing a device for home use makes this treatment relatively affordable and accessible.

Botulinum Toxin Type A

Injections of botulinum toxin type A (Botox) are safe and effective, and often improve quality of life in patients with hyperhidrosis. (16) The toxin inhibits the release of acetylcholine at the neuromuscular junction and affects the postganglionic sympathetic innervation of the sweat glands. (17)

An area about 1.2 cm in diameter is made anhidrotic around each injection site; therefore, multiple injections spaced 1 to 2.5 cm apart are necessary over the hyperhidrotic areas. Efficacy can be observed within one week. Anhidrosis induced by botulinum toxin injections persists for four to 13 months. (18,19) For successful long-term therapy, injections must be repeated regularly.

Intracutaneous injections are recommended rather than subepidermal injections, which are too close to nerve endings. (20) Botulinum toxin injections are painful and require the use of an anesthetic. Ulnar and median nerve blocks or intravenous regional anesthesia is more effective in preventing pain than is topical application of a local anesthetic. (21)

Potential side effects of botulinum toxin injections include transient, slight weakness in the muscles of the hand and the formation of small hematomas at the injection sites. (22) Cost also should be considered. It may take 100 units (acquisition cost: approximately $426) for each hand. Many physicians charge $1,400 to $1,600 for both palms, and the injections have to be repeated every four to six months.

Surgical Treatment

Sympathectomy has been performed since 1920 in patients with disabling, recalcitrant hyperhidrosis. Although the procedure is generally quite effective, it is permanent and therefore should be considered only after all other therapeutic options have been exhausted. Sympathectomy involves the surgical destruction of the second and third thoracic sympathetic ganglia for the palms. The risk of permanent sexual dysfunction limits the usefulness of lumbar sympathectomy for the treatment of plantar hyperhidrosis. (3)

In recent years, open surgery has been replaced by a minimally invasive endoscopic approach that has fewer complications, requires less operating time, and results in less scarring. There still can be complications, including recurrence of the hyperhidrosis, gustatory sweating, compensatory sweating in previously unaffected areas of the body (in up to 60 percent of patients), pneumothorax, Horner's syndrome, neuralgia, atelectasis, pneumonia, and hemothorax. (23,24) In some patients, compensatory sweating can be treated effectively with intradermal botulinum toxin injections. (25)

Cauterization and clamping methods for endoscopic thoracic sympathectomy have been compared in a study of 1,312 patients with hyperhidrosis. (26) All but one patient with palmar hyperhidrosis were cured. Within the two cauterization groups, the satisfaction rate was 94.3 percent for early treatment and 95.1 percent for late treatment; the satisfaction rate was 98 percent in the clamping group. Fewer than 6 percent of patients had severe compensatory hidrosis, and the recurrence rate was 3 percent. Clamping was shown to be at least as effective and safe as electrocautery and had the advantage of being potentially reversible.

Dorsal percutaneous stereotactic thermocoagulation in T2 ganglionectomy and sympathectomy is a newer alternative procedure. It involves the insertion of a thermocoagulation probe through the skin of the back after the application of a local anesthetic and the administration of a mild systemic analgesic. The procedure can be performed on an outpatient basis. One study of 1,688 patients with palmoplantar hyperhidrosis reported a 99.5 percent success rate after initial treatment, with a 7.8 percent relapse rate after an average of 39 months; all of the patients who relapsed were retreated successfully, resulting in a final success rate of 99.9 percent. (27) This study did not address compensatory hyperhidrosis but did report pneumothorax in 0.2 percent of patients and partial Horner's syndrome in 0.15 percent of patients.

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.


(1.) Tugnoli V, Eleopra R, De Grandis D. Hyperhidrosis and sympathetic skin response in chronic alcoholic patients. Clin Auton Res 1999; 9:17-22.

(2.) Wenzel FG, Horn TD. Nonneoplastic disorders of the eccrine glands. J Am Acad Dermatol 1998;38:1-17.

(3.) Stolman LP. Treatment of hyperhidrosis. Dermatol Clin 1998; 16:863-9.

(4.) Leung AK, Chan PY, Choi MC. Hyperhidrosis. Int J Dermatol 1999; 38:561-7.

(5.) Hashmonai M, Kopelman D, Assalia A. The treatment of primary palmar hyperhidrosis: a review. Surg Today 2000;30:211-8.

(6.) Atkins JL, Butler PE. Hyperhidrosis: a review of current management. Plast Reconstr Surg 2002;110:222-8.

(7.) Boumann HD, Grunewald-Lentzer EM. The treatment of hyperhidrosis of the hands and feet with a constant current. Am J Phys Med 1952;31:158-69.

(8.) Holzle E, Alberti N. Long-term efficacy and side effects of tap water iontophoresis of palmoplantar hyperhidrosis--the usefulness of home therapy. Dermatologica 1987;175:126-35.

(9.) Stolman LP. Treatment of excess sweating of the palms by iontophoresis. Arch Dermatol 1987;123:893-6.

(10.) Reinauer S, Neusser A, Schauf G, Holzle E. Iontophoresis with alternating current and direct current offset (AC/DC iontophoresis): a new approach for the treatment of hyperhidrosis. Br J Dermatol 1993;129:166-9.

(11.) Karakoc Y, Aydemir EH, Kalkan MT, Unal G. Safe control of palmoplantar hyperhidrosis with direct electrical current. Int J Dermatol 2002;41:602-5.

(12.) Hill AC, Baker GF, Jansen GT. Mechanism of action of iontophoresis in the treatment of palmar hyperhidrosis. Cutis 1981;28:69-70,72.

(13.) Timm D, Meletiou DS, Sato K. Mechanism of galvanic current-induced inhibition of palmar sweating in hyperhidrotic patients. Clin Res 1987;35:721A.

(14.) Sato K, Ohtsuyama M, Samman G. Eccrine sweat gland disorders. J Am Acad Dermatol 1991;24(6 pt 1):1010-4.

(15.) Shen JL, Lin GS, Li WM. A new strategy of iontophoresis for hyperhidrosis. J Am Acad Dermatol 1990;22(2 pt 1):239-41.

(16.) Tan SR, Solish N. Long-term efficacy and quality of life in the treatment of focal hyperhidrosis with botulinum toxin A. Dermatol Surg 2002;28:495-9.

(17.) Shelley WB, Talanin NY, Shelley ED. Botulinum toxin therapy for palmar hyperhidrosis. J Am Acad Dermatol 1998;38(2 pt 1):227-9.

(18.) Rusciani L, Severino E, Rusciani A. Type A botulinum toxin: a new treatment for axillary and palmar hyperhidrosis. J Drugs Dermatol 2002;1:147-51.

(19.) Vadoud-Seyedi J, Heenen M, Simonart T. Report of idiopathic palmar hyperhidrosis with botulinum toxin. Review of 23 cases and review of the literature. Dermatology 2001;203:318-21.

(20.) Wollina U, Karamfilov T. Botulinum toxin A for palmar hyperhidrosis. J Eur Acad Dermatol Venereol 2001;15:555-8.

(21.) Blaheta HJ, Vollert B, Zuder D, Rassner G. Intravenous regional anesthesia (Bier's block) for botulinum toxin therapy of palmar hyperhidrosis is safe and effective. Dermatol Surg 2002;28:666-71.

(22.) Schnider P, Binder M, Auff E, Kittler H, Berger T, Wolff K. Double-blind trial of botulinum A toxin for the treatment of focal hyperhidrosis of the palms. Br J Dermatol 1997;136:548-52.

(23.) Lin TS, Kuo SJ, Chou MC. Uniportal endoscopic thoracic sympathectomy for treatment of palmar and axillary hyperhidrosis: analysis of 2000 cases. Neurosurgery 2002;51(5 suppl):84-7.

(24.) Ng I, Yeo TT. Palmar hyperhidrosis: intraoperative monitoring with laser Doppler blood flow as a guide for success after endoscopic thoracic sympathectomy. Neurosurgery 2003;52:127-31.

(25.) Huh CH, Han KH, Seo KI, Eun HC. Botulinum toxin treatment for a compensatory hyperhidrosis subsequent to an upper thoracic sympathectomy. J Dermatolog Treat 2002;13:91-3.

(26.) Reisfeld R, Nguyen R, Pnini A. Endoscopic thoracic sympathectomy for hyperhidrosis: experience with both cauterization and clamping methods. Surg Laparosc Endosc Percutan Tech 2002;12:255-67.

(27.) Chuang KS, Liu JC. Long-term assessment of percutaneous stereotactic thermocoagulation of upper thoracic ganglionectomy and sympathectomy for palmar and craniofacial hyperhidrosis in 1742 cases. Neurosurgery 2002;51:963-70.

ISABELLE THOMAS, M.D., is associate professor of dermatology at the University of Medicine and Dentistry of New Jersey (UMDNJ)-New Jersey Medical School, Newark, and chief of dermatology at the East Orange Veterans Affairs Medical Center, N.J. She received her medical degree from the University of Paris School of Medicine. Dr. Thomas is board certified in dermatology in the United States and France.

JUSTIN BROWN, M.D., is a resident in dermatology at the UMDNJ-New Jersey Medical School, where he also received his medical degree.

JANET VAFAIE, M.D., is a special fellow in dermopathology at the UMDNJ-New Jersey Medical School. She received her medical degree from George Washington University School of Medicine, Washington, D.C.

ROBERT A. SCHWARTZ, M.D., M.P.H., is professor and head of dermatology at the UMDNJ-New Jersey Medical School. He received a master of public health degree in medical administration from the University of California at Berkeley School of Public Health, and a medical degree from New York Medical College, Valhalla. He serves on the Editorial Advisory Board of American Family Physician.

Address correspondence to Robert A. Schwartz, M.D., M.P.H., UMDNJ-New Jersey Medical School, 185 South Orange Ave., Newark, NJ 07103-2714 (e-mail: Reprints are not available from the authors.

COPYRIGHT 2004 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

Return to Hyperhidrosis
Home Contact Resources Exchange Links ebay