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!]

Treatment of hyperhidrosis
From Journal of Drugs in Dermatology, 10/1/03 by Lewis P Stolman


Hyperhidrosis, or excessive sweating, is a disorder that may cause social isolation or occupational disability. It may be generalized or localized, and although frequently idiopathic it may be a manifestation of a number of important systemic diseases. Drugs, surgical procedures, and electrical devices may all be employed by the physician as therapeutic weapons to treat hyperhidrosis.


The primary function of the eccrine sweat glands is to assist in the maintenance of body temperature in response to heat exposure or exercise. Hyperhidrosis may be defined as sweating beyond what is necessary to maintain thermal regulation. It may be primary (idiopathic, essential) or secondary to a number of diseases and prescribed drugs. It may be localized, regionalized, or generalized (1). Regardless of the type or the cause of the hyperhidrosis, it is frequently socially embarrassing and occupationally disabling. Excess sweat on the hands may soil paper and art work and make it virtually impossible to play many musical instruments. Careers in fields that require contact with paper, metal, or electrical components become unrealizable. Axillary and plantar hyperhidrosis may result in stains and damage to clothing and shoes. Generalized or regionalized hyperhidrosis may leave affected individuals with wet clothing that may have to be changed a number of times each day.

Physiologically, sweating is a function of the sympathetic nervous system. A sweat control center located in the preoptic area and anterior hypothalamus contains neurons that are sensitive to changes in internal temperature and also cerebral cortical events. Sweat glands are innervated by sympathetic postganglionic fibers but, unlike ordinary sympathetic innervation, the chemical mediator is acetylcholine. Sweating in response to thermal stimuli is generally acceptable and rarely a cause for complaint. Emotionally-induced sweating tends to be localized to the palms, soles, and sometimes the forehead. Axillary sweating may be the result of both emotional and thermal stimuli.

The causes for generalized hyperhidrosis (Table 1) include a number of febrile illnesses, neoplastic and neurologic diseases, metabolic disorders, and drugs. The causes and conditions associated with localized hyperhidrosis (Table 2) include primary or focal hyperhidrosis, unilateral circumscribed hyperhidrosis, hyperhidrosis associated with intrathoracic neoplasms, olfactory hyperhidrosis, gustatory hyperhidrosis, spinal cord injuries, and Frey's syndrome. Although primary or focal hyperhidrosis is the most common cause of palmoplantar hyperhidrosis, it may also occur in some patients with Raynaud's disease, rheumatoid arthritis, erythromelalgia, nail patella syndrome, keratosis palmaris et plantaris with clinodactyly, atrioventricular fistula, and cold injury. Whenever possible the cause for hyperhidrosis should be identified and if possible treated.

Primary or focal hyperhidrosis is a disorder in which there is excess sweating of the hands, feet, face, and axillae. A recent national survey estimated that 1.4% of the U.S. population (4.0 million individuals) suffers from axillary hyperhidrosis (2). One-third of these sufferers (1.3 million individuals) describe their sweating as barely tolerable or intolerable, and that it frequently or always interferes with their daily life. Primary hyperhidrosis may be inherited and in contrast to generalized hyperhidrosis usually has its time of onset in childhood or adolescence (3). Palmar hyperhidrosis usually commences in childhood and axillary hyperhidrosis in adolescence. Characteristically, focal hyperhidrosis does not occur while sleeping. Primary hyperhidrosis is aggravated by heat and emotional stimuli; however, it is important to note that although emotional stimuli are necessary for primary hyperhidrosis to occur in affected individuals, it is not a psychological disease but rather a physiological disorder. It seems that in patients with primary hyperhidrosis, the hypothalamic sweat centers are more sensitive to emotional stimuli of cerebral origin than those in ordinary people. The occasional onset of primary hyperhidrosis in the neonatal period is evidence that this is far more than an emotional disorder!

A number of medical and surgical remedies are available for the treatment of hyperhidrosis (Table 3).

Topical Treatments

Aluminum chloride and tanning agents are sometimes effective in the control of localized hyperhidrosis (4). Aluminum chloride may decrease sweating by mechanically obstructing eccrine sweat gland pores, although this mechanism has been disputed. The atrophy of the secretory cells seen in eccrine sweat glands exposed to aluminum chloride may account for the reduced sweating that most people enjoy with the use of products containing aluminum chloride. For most people with axillary hyperhidrosis, over-the-counter products are sufficient. For more severe sweating, Drysol[R] (20% aluminum chloride hexahydrate dissolved in anhydrous ethyl alcohol; Person & Covey, Inc., Glendale, CA) is frequently useful. The skin should be dry before application, since if moisture is present then irritating hydrochloric acid may form. Washing just before application should be avoided. The optimum way to use the product seems to be to apply it at bedtime to take advantage of the relative inactivity of sweat glands through the night and wash the product off first thing in the morning. Minor irritation can be relieved with the use of hydrocortisone creams. The product should be used nightly until an effect occurs and then the interval between applications can be lengthened. Although occlusion with plastic wrap can be attempted if direct application is not effective, this method is not only inconvenient but often results in increased irritation.

Glutaraldehyde, tannic acid, and formaldehyde may be useful to treat palmar and plantar hyperhidrosis, but their tendency to stain the skin (and the sensitizing potential of formaldehyde solution) limit their usefulness (5).

Systemic Treatments

For those patients whose hyperhidrosis is related to specific anxiety-producing events such as a speaking engagement, school dance etc., the use of a drug such as Valium[R] (diazepam) may have an ameliorating affect. If hyperhidrosis is a part of a social anxiety disorder, Prozac[R] (flouxatine) may be a very useful therapeutic agent along with appropriate psychiatric care. Systemic anticholinergics may be helpful, but unfortunately the dosages required to achieve reduced sweating also result in side effects including xerostomia, mydriasis, cycloplegia, and bowel and bladder dysfunction. Most patients with localized or generalized hyperhidrosis can not tolerate them for long. However, the anticholinergic Ditropan[R] (oxybutynin) has been found to be useful in the relatively rare syndrome of episodic hyperhidrosis with hypothermia (6). A second anticholinergic, Cogentin[R] (benztropine) was successfully used to treat hyperhidrosis in a patient with venlafaxine-induced excess sweating (7). Effexor[R] (venlafaxine) is an antidepressant that inhibits the reuptake of serotonin and norepinephrine. Sweating is said to occur in as many as 12% of all patients exposed to venlafaxine and other serotonin selective reuptake inhibitors (SSRIs). The non-steroidal anti-inflammatory agent indomethacin in a dose of 25 mg t.i.d, was prescribed for a patient with arthritis who coincidentally had lifelong idiopathic generalized hyperhidrosis (8). Quite unexpectedly, she enjoyed a resolution of her lifelong hyperhidrosis. Although the mechanism for this beneficial effect is not clear, the fact that prostaglandin E is found in increased amounts in the sweat of some patients with hyperhidrosis may offer an explanation (9). Influx of calcium from the extracellular to the intracellular space is necessary for the active secretion of sweat by eccrine sweat glands. This likely accounted for the improvement in palmar and plantar hyperhidrosis observed when a calcium channel blocker, diltiazem, was used to treat a family with palmar and plantar hyperhidrosis (10). Tricyclic antidepressants may cause excess sweating, and yet one would expect the anticholinergic action of tricyclics should block sweating, not induce it. Catapres[R] (clonidine), a centrally active [alpha.sub.2]-adrenergic autoreceptor stimulant, has been found to be useful in the treatment of hyperhidrosis due to tricyclics as well as menopausen (11). Darvon[R] (propoxyphene hydrochloride), a narcotic and weak ganglionic blocking agent, may have an ameliorating effect on hyperhidrosis in patients with autonomic dysreflexia (12). Autonomic dysreflexia is a syndrome of sympathetic hyperactivity due to bladder or bowel distension seen in some patients with spinal cord lesions at or above the sixth thoracic level (T6). Fludrocortisone acetate 0.3 mg daily may control sweating in quadriplegics in whom orthostatic hypotension precipitates a sympathetic discharge (13). The reader is cautioned that many of these reports of therapeutic efficacy are anecdotal, and all of these systemic agents carry with them the risk of side effects.

Of all the types of hyperhidrosis, focal hyperhidrosis, which may involve the axillae, palms, sole and face, is the most common. Two therapeutic interventions, one old (iontophoresis) and one relatively new (botulinum toxin), are particularly valuable in the treatment of primary or focal hyperhidrosis.


One of the simplest, safest, and most cost-effective treatments for palmar and/or plantar hyperhidrosis is that of iontophoresis, which is defined as the introduction of an ionized substance through intact skin by the application of a direct current. In 1936, Ichihashi used various solutions of atropine, histamine, and formaldehyde and demonstrated that sweating of the palms could be reduced by iontophoresis (14). His work went relatively unnoticed until 1952, when Bouman and Gruenwald

Lentzer published a report clearly demonstrating the efficacy of iontophoresis for the treatment of palmar and plantar hyperhidrosis in 113 patients (15). They demonstrated that the addition of an ionizable substance to the water was not necessary to obtain a therapeutic effect. Levit demonstrated a simple galvanic device that could be employed to relieve hyperhidrosis in 85% of affected patients (16,17).

Although the exact mechanism by which iontophoresis relieves palmar or plantar hyperhidrosis is not known it is thought to be due to poral plugging, since the effect is reversed by cellophane tapestripping of the skin overlying eccrine sweat glands rendered euhidrotic by iontophoresis (18,19). For those patients who fail to respond to simple tap-water iontophoresis, the addition of an anticholinergic directly to the tap water-filled treatment trays is frequently helpful.

Although a number of devices are available for the administration of iontophoresis, this author prefers the Fischer MD1a Galvanic unit, and the technique employed is described in Tables 4 and 5. Side effects from iontophoresis are few. Occasionally the palms become too dry and may become cracked or fissured. This may be relieved with the use of moisturizers and/or a reduction in the frequency of treatments. Erythema--and less frequently vesiculation of the skin--may follow treatments and can be treated if necessary with simple 1% hydrocortisone cream. Compensatory hyperhidrosis does not occur. Iontophoresis is difficult to administer to the axillae and seems to cause more irritation than when administered to the palms and soles; thus it not as useful for the treatment of axillary hyperhidrosis.

Botulinum Toxin

Justinus Kerner, a German physician and poet, published the first comprehensive description of the symptoms of botulism between 1817 and 1822. He also proposed the possible therapeutic use of botulinum toxin, which he called "sausage poison." Kerner's monograph (20) describes the following illness from ingesting inadequately cooked smoked bloodsausages:

Kerner went on to describe further effects in humans and animals: vomiting, intestinal spasms, mydriasis, ptosis, dysphagia, and in the end, respiratory failure. His reputation as an expert on "sausage poisoning" earned him the nickname "Sausage Kerner." Subsequently sausage poisoning was named botulism from the Latin word for sausage, botulus. Years later, in 1895, the bacterium responsible for botulism was identified by Emil-Pierre van Ermengem.

Today botulinum toxin is a useful therapeutic agent for the treatment of a number of diseases related to muscular dystonia. This potent toxin has proven to be a highly effective remedy for the treatment of conditions previously recalcitrant in the fields of ophthalmology, otorhinolaryngology, pediatrics, gastroenterology, and urology. The cosmetic denervation of muscles of facial expression using botulinum toxin have given dermatologists and plastic surgeons a new weapon against facial expression-induced wrinkles and lines. In recent years certain types of hyperhidrosis have been successfully treated with botulinum toxin. Side effects reported following the local injection of botulinum toxin have been few and are usually related to undesired weakness in muscles adjacent to the treatment sites.

Treatment of Axillary Hyperhidrosis

Patients with quality-of-life-impairing axillary hyperhidrosis should be offered treatment with either botulinum toxin or surgical ablation of the axillary sweat glands. Since botulinum toxin not only inhibits the release of acetylcholine at neuromuscular junctions but also in postganglionic sympathetic fibers to sweat glands, it has been found to be useful to treat axillary hyperhidrosis (21-27). In the treatment of axillary hyperhidrosis as little as 50 units injected and distributed intradermally to each axilla can produce euhidrosis lasting as long as 6 months. With larger doses responses have been as long as 15 months. Many clinicians perform a starch iodine test prior to treatment to document the extent of the hyperhidrosis and to identify any so called "hot spots," which are areas that produce greater amounts of sweat. This author uses a simple facial tissue and a gentian violet marker to identify such areas. The hyperhidrosis generally occurs in the hair-bearing part of the axillae and so it is in these areas that the toxin should be placed. Discomfort is minimal and simple ice-packs applied to the axillae prior to injection are sufficient for anesthesia.

Patients with axillary hyperhidrosis who are unresponsive to topical therapy do not want botulinum toxin or in whom it is contraindicated or simply want a more long-lasting remedy may be offered a variety of surgical techniques designed to ablate the axillary sweat glands. The areas of greatest sweat production may be identified by draping a piece of facial tissue paper over the axilla or a starch iodine test. Sometimes this area is quite small and a simple excision with closure is sufficient to remedy the problem (28). Patients with moderate to severe hyperhidrosis may require a more extensive procedure with undermining and resection of all exposed sweat glands (29). In order to obtain good closure and avoid limitation of movement due to cicatricial contracture, Z-plasty and bat-shaped excisions and repairs can be employed (30). Alternative treatments for axillary hyperhidrosis include subcutaneous liposuction and subcutaneous curettage (31,32).

Treatment of Palmar/Plantar Hyperhidrosis

Patients with palmar or plantar hyperhidrosis should be given a trial of a prescription-strength antiperspirant such as Drysol[R] prior to botulinum toxin or iontophoresis treatments(32). Botulinum injections are very effective for the treatment of palmar hyperhidrosis (33-35). The doses used are generally higher than those used for axillary hyperhidrosis, ranging from 100 to 200 units of Botox[R] per hand. Euhidrosis following such treatment may last for as long as a year. Although effective, the clinical usefulness of this treatment is limited by the need for repetitive relatively painful injections, the cost of the botulinum toxin, and reports of weakness of the small muscles of the hands (33).

Anesthesia is mandatory for the administration of botulinum toxin to the hand or feet. Although topical anesthesia in the form of Elamax[R] under occlusion for an hour followed by ice packs seems satisfactory for some, most practitioners have found the need for a either a Bier block or a block of the median, ulnar, and radial nerves (36). The Bier block, once learned, is not only safe and effective but also carries with it the advantage over nerve blocks of not affecting motor function. As a result, patients can still use their hands immediately after the treatment.

Iontophoresis still remains a useful therapy since botulinum toxin injections for the treatment of palmar and plantar hyperhidrosis are not suitable for all patients (32). Specifically, musicians, surgeons, and others who depend on fine motor dexterity in their hands may not be able to accept the risks of diminished strength of their thumbs that may accompany botulinum toxin injections. Young children may not accept the discomfort involved in either regional nerve blocks or a Bier block for the anesthesia for botulinum injections into the hands. Finally, iontophoresis is far less costly than botulinum treatments for palmar and plantar hyperhidrosis, keeping in mind that from 100 to 200 units of botulinum toxin are used per hand and that anesthetic/administration fees would be involved.

Treatment of Craniofacial Hyperhidrosis

Craniofacial hyperhidrosis may respond to topical antiperspirants such as Drysol[R] or topical glycopyrrolate. Topical glycopyrrolate has been found to be useful to treat gustatory craniofacial hyperhidrosis in diabetics (37). Botulinum toxin is very effective for craniofacial hyperhidrosis and is considered the treatment of choice for patients with Frey's syndrome. Frey's syndrome is characterized by unilateral gustatory hyperhidrosis that occurs in as many as 50% of patients who have a parotidectomy (38). The most likely explanation is recurrence of parasympathetic nerve fibers that have lost their "target organ." When botulinum toxin is used to treat craniofacial hyperhidrosis the technique differs from that to treat the facial musculature in that the injections are more superficial (i.e., intradermal) and evenly distributed over the hyperhidrotic area. The area may be identified by either the starch iodine technique or a facial tissue held against the skin. The botulinum toxin, 50 to 100 units of Botox[R], should be administered at least one and half centimeters above the supraorbital bridge in order to avoid a brow drop.


Sympathectomy or upper thoracic (T2) ganglionectomy is often offered to patients with severe palmar hyperhidrosis. Lumbar sympathectomy is not usually employed for plantar hyperhidrosis because of the risk of sexual dysfunction. Although the efficacy of this procedure in the treatment of palmar hyperhidrosis is not in doubt, with success rates of 9299%, the potential complications ate significant. Among the likely complications related (24% to 100% depending on the study) are compensatory hyperhidrosis (increased sweating in some other area of the body), gustatory sweating (sweating, usually of the face, related to the eating of foods), permanent Homers syndrome, wound infection, hemothorax, intercostal neuralgia, and recurrence of hyperhidrosis (39-48). The advent of endoscopic sympathectomy has reduced the incidence of many complications.

Compensatory hyperhidrosis is the most common complication and the major reason for patient dissatisfaction with the procedure. Compensatory hyperhidrosis following sympathectomy can be far more life-disrupting than palmar hyperhidrosis in that afflicted individuals may have to change sweat-soaked clothing two or three times per day. In a recent systematic literature review of sympathectomy for the treatment of hyperhidrosis the question was asked, "Are we paying a high price for surgical sympathectomy?" 135 articles are reviewed, reporting on 22,458 patients and 42,061 procedures. 84.3% of the reported patients had the surgery for hyperhidrosis. Compensatory hyperhidrosis occurred in 52.3% of the patients, gustatory sweating in 32.3%, phantom sweating in 38.6%, and Horner's syndrome in 2.4%. In all, neuropathic complications occurred in 11.9% but were less common in patients who had the procedure for hyperhidrosis (48).

Moran (45) states it quite succinctly: "Complications related to the surgical approach, such as Homer's syndrome, brachial plexus injuries, pneumothorax, and painful scars may occur, while following sympathectomy compensatory hyperhidrosis is usual and hyperhidrosis may recur."


The patient who complains of hyperhidrosis presents the physician with a diagnostic and therapeutic challenge. Patients who present with generalized hyperhidrosis are in general adults whose sweating occurs both during the waking and sleeping hours. Such patients require a search for a cause which may sometimes be as simple as a drug that they are taking for some medical disorder. Occasionally a systemic illness may account for the onset of hyperhidrosis and a thorough exam and appropriate testing may be necessary to identify the cause. Most patients with primary or focal hyperhidrosis present in childhood or adolescence and have a problem localized to their axillae, hands, and/or feet. They have a physiologic disorder, not a psychiatric or endocrinologic disease. A number of systemic, topical, surgical, and electrical remedies are available for the treatment of hyperhidrosis. Patients with hyperhidrosis of the palm or soles who fail to respond to topical agents deserve a trial of conservative therapy, botulinum toxin, or iontophoresis before aggressive surgical techniques that carry with them the risk of lifelong troublesome side effects are offered.


(1.) Stolman LP. Management of Hyperhidrosis. Dermatol Clinics 1998; 16(4):863-9.

(2.) Strutton DR et al. Impact of hyperhidrosis on daily activities for individuals in the U.S. with axillary hyperhidrosis: Results of a national survey. Poster #363, American Academy of Dermatology, March 21-6, 2003.

(3.) Ro KM et al. Palmar hyperhidrosis: Evidence of genetic transmission. J Vasc Surg 2002; 35:382-6.

(4.) Shelley WB, Laskas JJ, Satonove A. Effect of topical agents on plantar sweating. Arch of Derm and Syph 1954; 69:713-716,

(5.) Juhlin L, Hansson H. Topical glutaraldehyde for plantar hyperhidrosis. Brit J of Derm 1968; 97:327-30.

(6.) LeWitt P. Hyperhidrosis and hypothermia responsive to oxybutynin. Neurology 1988; 38:506-7

(7.) Garber A, Gregory R. Benztropine in the treatment of venlafaxine-induced sweating. J Clin Psychiatry 1997; 58:4176-7

(8.) Tkach JR. Indomethacin treatment of generalized hyperhidrosis. J Am Acad Derm 1982; 6:545.

(9.) Goldyne ME. Indomethacin and hyperhidrosis, J Am Acad Derm 1982; 7:801.

(10.) James WD, Schoomaker MC, Rodman MC. Emotional eccrine sweating. Arch Dermatol 1987; 123:925-29.

(11.) Feder R. Clonidine treatment of excessive sweating. J Clin Psychiatry 1995; 56:1,35

(12.) Tashjian EA, Richter KJ. The value of propoxyphene hydrochloride (Darvon) for the treatment of hyperhidrosis in the spinal cord injured patient: An anecdotal experience and case reports. Paraplegia 1985; 23:349-53.

(13.) Khurana RK. Orthostatic hypotension-induced autonomic dysreflexia. Neurology 1987; 37:1221-4.

(14.) Ichihashi T. Effect of drugs on the sweat glands by catophoresis, and an effective method for suppression of local sweating: Observation on the effect of diaphoretics and adiaphoretics. J Orient Med 1936; 25:101-2.

(15.) Bouman HD, Grunewald Lentzer EM. The treatment of hyperhidrosis of hands and feet with constant current. AmJ Phys Med 1952; 31:158 169,

(16.) Levit F. Simple device for the treatment of hyperhidrosis by iontophoresis. Arch Dermatol 1968; 98:505-7

(17.) Levit F. Treatment of hyperhidrosis by tap water iontophoresis. Cutis 1980; 26:192-4.

(18.) Gordon B, Maibach H. Eccrine anhidrosis due to glutaraldehyde, formaldehyde, and iontophoresis. J lnvest Dermatol 1969; 53:436-9.

(19.) Grice K. Sattar H, Baker H. Treatment of idiopathic hyperhidrosis with iontophoresis of tap water and poldine methosulphate. Br J Dermat 1972; 86:72-8.

(20.) Kerner J. New observations on the lethal poisoning occurring so frequently in Wurttemburg through the consumption of smoked sausages. 1815.

(21.) Bushara KO, Park DM,Jones JC, Schutta HS. Botulinum toxin: a possible new treatment for axillary hyperhidrosis. Clinical and Experimental Dermatology 1996; 21:276-8.

(22.) Heckmann M et al. Side-controlled intradermal injection of botulinum toxin A in recalcitrant axillary hyperhidrosis. J Am Acad Dermatol 1999; 41:987-90.

(23.) Heckmann M, Ceballos-Baumann AO, Plewig G. Botulinum toxin A for axillary hyperhidrosis, N Engl J Med 2001; 344:488-93.

(24.) Wollina U, Karamfilov T, Konrad H. High-dose botulinum type A therapy for axillary hyperhidrosis markedly prolongs the relapse interval. J Am Acad Dermatol 2002; 46:536-40.

(25.) Naumann M, Lowe NJ. Botulinum toxin type A in treatment of bilateral primary axillary hyperhidrosis: randomized, parallel group, double blind, placebo controlled trial, grit Med J 2001; 323; 596-99

(26.) Glogau RG. Botulinum: a neurotoxin for axiliary hyperhidrosis. Dermatol Surg 1998; 24:817-9.

(27.) Hurley HJ. Shelley WB. A simple surgical approach to the management of axillary hyperhidrosis. JAMA 1963; 186:109.

(28.) West JR. Management of hyperhidrosis & bromhidrosis. Cutaneous Surgery; WB Saunders. 1993; 699-707.

(29.) Stenquist B. Axillary hyperhidrosis: A simple surgical procedure. J Dermatol Surg Oncol 1985; 11(4):388-91.

(30.) Shenaq SM, Spira M. Treatment of bilateral axillary hyperhidrosis by suction-assisted lipolysis technique. Annals of Plas Surg 1987; 19:548-51.

(31.) Proebstle TM, Schneiders V, Knop J. Gravimetrically controlled efficacy of subcorial curettage: A prospective study for treatment of axillary hyperhidrosis. Dermatol Surg 2002; 28(11)1022-26.

(32.) Stolman LP. The treatment of palmar hyperhidrosis by iontophoresis. Arch Derm 1987: 123:893-6.

(33.) Schnider P, Binder M, Auff E. Kittler H et al. Double-blind trial of botulinum A toxin for treatment of focal hyperhidrosis of the palms. Br J Dermatolog 1997; 136:548-52.

(34.) Solomon BA, and Hayman R. Botulinum toxin type A therapy for palmar and digital hyperhidrosis. J Am Acad Dermatol 2000; 42:1026-9.

(35.) Lowe NJ et al. Efficacy and safety of Botulinum toxin type A in the treatment of palmar hyperhidrosis: A double-blind, randomized, placebo-controlled study. Dermatol Surg 2002; 28:9 822-22

(36.) Fujita M et al. Use of nerve blocks for botulinum toxin treatment of palmar-plantar hyperhidrosis. J Am Acad Dermatol 2001; 45:587-9.

(37.) Shaw JE et al. A randomized controlled trial of topical glycopyrrolate, the first specific treatment for diabetic gustatory sweating. Diabetologia 1997; 40(3):299-301.

(38.) Laskawi et al, Up-to-date report of botulinum toxin type A treatment in patients with gustatory sweating (Frey's Syndrome). Laryngoscope 1998; 108:381-84.

(39.) Chen HJ, Shih DY, Fung ST. Transthoracic endoscopic sympathectomy in the treatment of palmer hyperhidrosis. Archives of Surgery 1994; 129 (6):630-3.

(40.) Edmondson RA, Banerjee AK, RennieJA. Endoscopic thoracic sympathectomy in the treatment of hyperhidrosis. Annals of Surgery 1992; 215(3):289-93.

(41.) Gordon A, Zecmeister K. CollinJ, The role of sympathectomy in surgical practice. Europ J of Vascul Surg 1994; 8(2):129-37.

(42.) Herbst F. Plas EG, Fugger R, Fritsch A. Endoscopic thoracic sympathectomy for primary hyperhidrosis of the upper limbs: A critical analysis and long-term results of 480 operations. Annals of Surgery 1994; 220(1):86-9.

(43.) Chu D, Shi P, Wu C. Transthoracic endoscopic sympathectomy for treatment of hyperhidrosis palmaris. Kaohsiung J Med Sci 1997; 13:162-8.

(44.) Drott C, Gothberg G, Claes G, Endoscopic transthoracic sympathectomy: an efficient and safe method for the treatment of hyperhidrosis. J Am Acad Derm 1995; 33(1):78-81.

(45.) Moran KT. Brady ME Surgical management of primary hyperhidrosis. Brit J of Surgery 1991; 78(3):279-83.

(46.) Pillay PK, Thomas J, Mack P. Thoracoscopic ganglionectomy for hyperhidrosis. Stereotactic & Functional & Neurosurgery 1994; 63(1-4): 198-202.

(47.) Welch E, Geary J. Current status of thoracic dorsal sympathectomy. J Vasc Surg 1984; 1:202-214

(48.) Furlan AD, Mailis A, Papagapiou M. Are we paying a high price for surgical sympathectomy? A systematic literature review of late complications. J of Pain 2000; 1(4):245-57.



Lewis P Stolman MD FACP FRCP(C)

Dermatology and Laser Center of Northern New Jersey

290 South Livingston Ave

Livingston, NJ 07039

T: (973) 740-0101

F: (973) 740-0103

COPYRIGHT 2003 Journal of Drugs in Dermatology
COPYRIGHT 2003 Gale Group

Return to Hyperhidrosis
Home Contact Resources Exchange Links ebay