hyperhidrosis

ijd3880609

Review

Hyperhidrosis

Alexander K.C. Leung, MBBS, FRCP(Lond), Paul Y.H. Chan, MD, andMatthew C.K. Choi, MD

From the Department of Pediatrics, University of Calgary, AlbertaChildren’s Hospital, and Asian Medical Centre (affiliated with theUniversity of Calgary Medical Clinic), Calgary, Alberta, Canada

CorrespondenceAlexander K.C. Leung, MBBS, FRCP, Alberta Children’s Hospital, 1820Richmond Road SW, Calgary, Alberta, Canada T2T 5C7

Hyperhidrosis denotes increased eccrine sweating. Excess-

ive sweating is a common complaint. In most patients, the

cause is benign. Occasionally, it may be due to a systemic

illness. Hyperhidrosis can lead to embarrassment, frustra-

tion, social withdrawal, low self-esteem, and even medical

illness. There is relatively little information in the literature

on hyperhidrosis. This article reviews the anatomy and

physiology of sweating, as well as the etiology of hyper-

hidrosis, and suggests an approach to the management of

this problem.

Anatomy and physiology of sweating

There are two types of sweat glands, eccrine and apocrine.

The human skin contains approximately 2 million eccrine

sweat glands.1 The eccrine glands are present over the

entire body surface, but are most numerous on the palms,

soles, face, axillae, and, to a lesser extent, the back and

chest.2 The eccrine glands are simple coiled tubular glands

that open directly onto the skin surface through sweat

pores. The deep coiled portion is located mostly in the

dermis and the duct passes to the surface of the skin.

Surrounding the secreting cells are myoepithelial cells,

whose contraction aids in the expulsion of sweat.3 The

secretory cells produce a plasma-like fluid. As the fluid

moves through the sweat duct, sodium is reabsorbed by

active transport.4 The sweat so produced is hypotonic and

contains approximately 0.3%–0.5% of sodium chloride.1

Potassium, lactic acid, and glucose are found in small

amounts, and the urea concentration is similar to that of

blood. Cyclic adenosine monophosphate (cAMP) plays an

important role in the sweating process. The sweat glands

have a rich blood supply and are innervated by cholinergic

nerve fibers arising from the sympathetic nervous system.5

As such, acetylcholine and other cholinergic agents accentu-

ate the sweating response, while atropine and anticholi-

© 1999 Blackwell Science Ltd International Journal of Dermatology 1999, 38, 561–567

561

nergic agents inhibit sweating. These glands can also be

stimulated by epinephrine or norepinephrine circulating in

the blood, even though the glands themselves do not have

adrenergic innervation.

The apocrine glands are confined to the axilla, the areola

of the nipple, the anogenital area, and the external auditory

meatus.5 These glands are simple coiled tubes, but are

about ten times larger than the eccrine glands.3 They are

situated in the lower dermis and the upper layer of the

subcutaneous fat. Originating from the pilosebaceous sys-

tem, the apocrine glands usually open onto hair follicles

superficial to the opening of the sebaceous glands. Apocrine

sweat is produced in small quantities and has very little, if

any, role to play in hyperhidrosis. The secretion results

from the decomposition of cuboidal cells lining the apocrine

gland.6 The secretion is milky and contains fat and choles-

terin. Bacterial breakdown of these products produces a

characteristic offensive odor. Unlike eccrine sweat glands,

which begin to function at birth, apocrine sweat glands

start to function at puberty. The apocrine secretion plays

an important role in sexual activity and bromohidrosis.

Apocrine glands have no direct secretory innervation,

although local stimulation with epinephrine will result in

sweat production.

Epidemiology

Although the exact incidence is not known, almost every-

body has experienced hyperhidrosis at some point in his

or her lifetime. Excessive sweating beyond that which is

required to cool the body affects between 0.6% and 1%

of the general population.7 The incidence is higher among

infants, teenagers, and young adults.8 Hyperhidrosis affects

both sexes equally, although females may find the condition

less acceptable and present more frequently for treatment

than males.6

562 Review Hyperhidrosis Leung, Chan, and Choi

Table 1 Causes of hyperhidrosis

1 Idiopathic2 Physiologic

Emotional factorsHot environmentOver-clothingExercise

3 Febrile illnesses4 Endocrine and metabolic disorders

ThyrotoxicosisDiabetes mellitusHypoglycemiaGigantism and acromegalyPheochromocytoma

5 Drugs, toxins and substance abuse6 Cardiovascular disorders7 Respiratory failure8 Hodgkin’s disease9 Intrathoracic neoplasms or lesions

10 Carcinoid tumor11 Gustatory hyperhidrosis12 Olfactory hyperhidrosis13 Spinal cord injuries14 Compensatory hyperhidrosis15 Familial dysautonomia (Riley–Day syndrome)16 Cold-induced hyperhidrosis17 Hypothalamic lesions18 Nail–patella syndrome19 Cutaneous diseases

Etiology

The causes of hyperhidrosis are listed in Table 1.

IdiopathicExcessive sweating is often a notable feature in normal

children.9 Some infants and children sweat profusely

around the head while asleep.10 In the majority of cases,

the cause of hyperhidrosis is unknown and is of no clinical

significance. The sweat glands in the involved areas are

normal in histologic appearance and in number.3 The

sympathetic nervous supply to these areas is also normal.

Physiologic

Emotional factors

Emotional sweating is confined mainly to the palms, soles,

and axillae, and, to a lesser extent, the forehead. In general,

the eccrine sweat glands in the palms and soles respond

well to emotional stimuli, those in the axillae and forehead

respond to both thermal and emotional stimuli, while those

in the rest of the body respond almost entirely to thermal

stimuli. It has been speculated that the hypothalamic sweat

center controlling the palms and soles (and the axillae in

some patients) is distinct from the rest of the hypothalamic

sweat centers and is under the exclusive control of the

International Journal of Dermatology 1999, 38, 561–567 © 1999 Blackwell Science Ltd

cerebral cortex without input from the thermosensitive

elements.11 Thus, sweating on the palms and soles rarely,

if ever, occurs during sleep or sedation, nor is it augmented

in a warm environment.11 Emotional sweating can be

induced by anxiety, embarrassment, fear, anger, excitement,

or mental stress.3 A special form of cortical and emotional

sweating has been described after sexual stimulation, occur-

ring post-orgasmically.12

Hot environment

Sweating is a protective physiologic response to heat that

provides evaporative cooling of the skin surface. Sweating

is generally more pronounced in a hot and humid environ-

ment, where the sweat glands are conditioned to secrete

more easily and where evaporation of sweat is minimized.

Thermal sweating is under the control of the heat regulatory

center situated in the hypothalamus. As ambient temper-

ature rises, heat loss from the body is increased by vasodilat-

ation of the cutaneous blood vessels and augmentation of

sweat production. Local heating potentiates the local sweat

gland response to reflex stimulation or acetylcholine, but

intense local heating can elicit sweating directly, even in

sympathectomized skin.13

Over-clothing

In children, over-clothing is an important cause of hyper-

hidrosis. Over-clothing has the same effect on the skin as

a hot environment.

Exercise

Exercise increases heat production, causing an increase in

core temperature, which in turn elicits the sweating

response. An additional 1 °C increase in body temperature

causes enough sweating to remove 10 times the basal rate

of body heat production.14 In addition, the release of

epinephrine during exertion may exacerbate the sweating

response.

Febrile illnessesFever of any cause may lead to excessive sweating. Pyrogens

released from bacterial cell membranes or breakdown

products of protein from degenerating tissues of the body

elevate the set-point of the hypothalamic temperature

regulatory center to a higher level. The hypothalamic

temperature regulatory center responds as if the core

temperature were too low. All the mechanisms for raising

the body temperature are brought into play, including

heat conservation through cutaneous vasoconstriction and

increased heat production through shivering.14 This may

account for the feeling of chill that precedes and accompan-

ies fever. When the body core temperature rises to the

higher set-point, a new equilibrium of heat production and

heat loss is achieved, but at a higher body temperature.15

Leung, Chan, and Choi Hyperhidrosis Review 563

When the fever breaks, the set-point returns to normal. The

hypothalamic temperature regulatory center then causes

sweating and cutaneous vasodilatation, leading to a fall in

body temperature to the new set-point. The sweating

seen in brucellosis and tuberculosis is characteristically

nocturnal, and may be due to an alteration in hypothal-

amic activity.

Endocrine and metabolic disorders

Thyrotoxicosis

Increased sweating in thyrotoxicosis is partly due to an

increase in body metabolism secondary to excessive

amounts of circulating thyroid hormone,5 and partly due

to an increase in sensitivity of the autonomic nerve fibers

to circulating epinephrine.2

Diabetes mellitus

Patients with diabetes mellitus may experience excessive

sweating during attacks of hypoglycemia. Diabetic patients

may show a gustatory hyperhidrosis (vide infra), principally

of the face and neck, as a symptom of diabetic autonomic

neuropathy.16

Hypoglycemia

The hyperhidrosis seen in hypoglycemia is due to activation

of the autonomic nervous system and epinephrine release,

usually associated with a rapid decline in blood glucose.

Gigantism and acromegaly

The hyperhidrosis occasionally seen in pituitary gigantism

and acromegaly is probably secondary to hypermetabolism.

Pheochromocytoma

Paroxysms of sweating are characteristic of pheochromocy-

toma and these may result from excessive secretion of

epinephrine and norepinephrine.12

Drugs, toxins, and substance abuseHyperhidrosis has been reported as a side-effect of acetami-

nophen, aspirin, insulin, antiemetics, morphine,

bethanechol, pilocarpine, physostigmine, neostigmine,

cyclobenzaprine, and fluoxetine.5,11 Excessive sweating has

also been reported in mercury poisoning.11 Hyperhidrosis

has been noted in patients experiencing narcotic with-

drawal.

Cardiovascular disordersExcessive sweating is a cardinal feature in congestive heart

failure, and is probably due to an increased sympathetic

activity in response to myocardial ineffectiveness. Sweating

is most common around the head and neck. Hyperhidrosis


is a common feature of myocardial ischemia, occurring in

60% of patients with myocardial infarction in one series.17

Respiratory failureHyperhidrosis is a notable feature in respiratory failure.

The increase in sweating is presumed to be due to autonomic

nervous system stimulation.

Hodgkin’s diseaseNocturnal sweating occurs in patients with Hodgkin’s

disease. Patients with Hodgkin’s disease are often affected

by an instability of the hypothalamic temperature regu-

latory center.18 Affected patients have slight unperceived

febrile pulses that precede sweating, but the slight rise in

temperature may not be perceived by a sleeping patient,

who is more likely to be awakened by the discomfort of

the resulting sweating.18

Intrathoracic neoplasms or lesionsIntrathoracic neoplasms (e.g. mesothelioma) or lesions

(e.g. cervical rib) can cause ipsilateral hyperhidrosis.19 The

hyperhidrosis is due to an increase in sympathetic activity as

a result of the pressure exerted on the thoracic sympathetic

trunk or postganglionic fibers.20

Carcinoid tumorA carcinoid tumor is a slowly growing neoplasm of entero-

chromaffin cells. The associated cutaneous flushes, frequent

watery stools, and bronchial spasms are mediated by the

release of one or more biologically active agents by the

tumor. These biologically active agents include serotonin,

histamine, prostaglandins, and bradykinin. The hyper-

hidrosis seen in patients with carcinoid tumors can be

attributed to cutaneous vasodilatation with a resultant

increase in cutaneous blood flow and activation of the

thermoregulatory effect of the sweating mechanism.5

Gustatory hyperhidrosisSweating around the lips, perioral region, and forehead is

a physiologic response to eating certain hot or spicy

foods. Such sweating is usually relatively mild and occurs

symmetrically.20 Pathologic gustatory hyperhidrosis may

be due to diabetic neuropathy,16 herpes zoster of the

preauricular area,21 invasion of the cervical sympathetic

trunk by a tumor, or injury to the parotid gland such as

that experienced in Frey’s (auriculotemporal) syndrome.20

Frey’s syndrome develops following surgery, trauma, infec-

tion, or other disease of the parotid gland that disrupts

the postganglionic sympathetic and parasympathetic nerve

fibers in the area.22 Misdirected regrowth of the parotid

secretomotor (parasympathetic) fibers into sudomotor

(sympathetic) fibers supplying the affected skin is thought


to be the basis of sweating over the cutaneous distribution of

the auriculotemporal nerve in response to salivary stimuli.

Olfactory hyperhidrosisHyperhidrosis may result from olfactory stimuli. A 42-year-

old woman was reported to have profuse facial sweating

precipitated by the smell of perfume.23 Her olfactory facial

sweating was successfully treated with amitriptyline.

Spinal cord injuriesInjuries to the spinal cord usually result in anhidrosis below

the level of the lesion. Some patients with spinal cord

injuries, however, experience episodic hyperhidrosis which

may be due to autonomic dysreflexia,20,24 orthostatic hypo-

tension,25 or post-traumatic syringomyelia.26

Compensatory hyperhidrosisLocalized hyperhidrosis may occur in response to thermal

stimuli when other areas of the body are anhidrotic. Causes

of localized anhidrosis which may result in compensatory

hyperhidrosis include injury to the sympathetic trunk

(e.g. thoracic sympathectomy), lesion in the spinal cord or

sympathetic trunk, diabetic autonomic neuropathy,16 and

widespread poral occlusion in atopic dermatitis or in

extensive miliaria.11

Familial dysautonomia (Riley–Day syndrome)Familial dysautonomia (Riley–Day syndrome) is character-

ized by a congenital decrease in the number of small

unmyelinated autonomic and peripheral fibers that carry

pain, temperature, and taste sensations.5 The syndrome is

manifested by episodic hyperhidrosis, increased salivation,

absence of fungiform papillae on the tongue, vasomotor

instability, diminished deep tendon reflexes, relative indif-

ference to pain, impaired neuromuscular coordination,

decreased lacrimation, corneal hyperesthesia, failure to

thrive, and mild mental retardation.27 The hyperhidrosis

is probably due to an increase in excitability of the sweat

center.27 Familial dysautonomia is inherited as an

autosomal recessive trait and occurs mainly in children of

Ashkenazic Jewish descent.

Cold-induced hyperhidrosisHyperhidrosis may be induced by cold weather.28 Two

sisters, whose parents shared a grandfather, with cold-

induced sweating, were reported.28 Since childhood, the

two sisters had sweated profusely from the chest and back

when exposed to an environmental temperature of 18 to

7 °C. In normal people, thermal sweating occurs at rest

only at external temperatures above 24 °C. At temperatures

less than 18 °C, there is virtually no sweating.28 The exact

etiology in this family is not known. The condition seems

to be transmitted by an autosomal recessive gene.


Hypothalamic lesionsEpisodic hypothermia and hyperhidrosis have been

reported in patients with lesions in or adjacent to the

hypothalamus.29 Hyperhidrosis is most likely due to an

episodic decrease of the hypothalamic temperature set-

point.

Nail–patella syndromeIn one study, 33 of 68 members of an extended family

involving six generations were affected with nail–patella

syndrome.30 Nine of the 33 affected members also had

palmar–plantar hyperhidrosis. The pedigree supported the

previously known autosomal dominant mode of inheritance

for nail–patella syndrome. The occurrence of palmar–

plantar hyperhidrosis only in members affected with nail-

patella syndrome suggests that palmar-plantar hyper-

hidrosis may be inherited as an autosomal dominant trait

closely linked to the nail–patella syndrome, or that palmar–

plantar hyperhidrosis represents a previously unrecognized

association.

Cutaneous diseasesLocalized hyperhidrosis has been reported to occur in the

skin over blue rubber bleb nevus, sudoriparous angioma,

glomus tumor, and nevus sudoriferous.31 The hyperhidrosis

may be related to a change in the blood flow through the

affected skin, or may be due to an axon reflex.20 There

is also the possibility that the association may just be

coincidental.20 Hyperhidrosis has also been reported to

occur in pretibial myxedema.32 The hyperhidrosis in preti-

bial myxedema has been ascribed to eccrine glandular

hypertrophy.32

Clinical evaluation

A thorough history and physical examination are important

in the evaluation of hyperhidrosis.

History

Age of onset

The younger the patient, the more likely that an organic

or congenital cause will be found.

Severity

Severe hyperhidrosis can lead to social embarrassment, and

limitation in certain tasks or occupations.

Location

Hyperhidrosis restricted to one anatomic area usually

points to a specific local cause. Generalized hyperhidrosis

is usually due to a systemic cause.


Time of occurrence

Nocturnal hyperhidrosis suggests tuberculosis, brucellosis,

or lymphoma.

Precipitating factors

Any precipitating factors, such as environmental heat, over-

clothing, exercise, fever, or ingestion of spicy foods, should

be noted. A unilateral facial flush that is associated with

food intake suggests Frey’s syndrome.

Associated symptoms

Polyuria, polydipsia, and weight loss suggest diabetes mel-

litus. Palpitation, tremulousness, and headache in a diabetic

patient suggest hypoglycemia. Nervousness, restlessness,

weight loss in spite of an increased appetite, and heat

intolerance point to thyrotoxicosis. Chronic cough suggests

a respiratory disorder or congestive heart failure. Headache,

palpitation, flushing, nausea, vomiting, and abdominal pain

point to pheochromocytoma. Sudden flushing of the skin,

frequent watery stools, and asthmatic attacks are suggestive

of carcinoid tumor.

Drug use

A detailed drug history is important as the use of medica-

tion, such as acetaminophen or aspirin, may lead to

hyperhidrosis.

Psychosocial history

Any psychosocial or emotional stress should be noted as a

potential cause of hyperhidrosis.

Past health

Significant illness, such as pheochromocytoma, cardiovas-

cular disorder, spinal cord injury, sympathectomy, and

surgery of the parotid gland, should be noted.

Family history

A family history of thyrotoxicosis or familial dysautonomia

suggests the corresponding disorder.

Physical examination

General

The weight and height of the patient should be noted. Poor

growth may indicate a chronic disorder, such as diabetes

mellitus or cardiovascular disorder. Excessive growth sug-

gests gigantism. Vital signs, such as temperature, respiratory

rate, heart rate, and blood pressure, should also be noted.

If the patient has a fever, it may indicate an underlying

infection. Tachycardia in the absence of fever, anxiety,

or exercise suggests thyrotoxicosis. Tachypnea suggests

pulmonary infection, respiratory failure, or congestive heart

failure. Episodic hypertension is suggestive of pheochromo-


cytoma, whereas postural hypotension is suggestive of

familial dysautonomia. The degree of hyperhidrosis and its

location should be noted. Sweating as an emotional reaction

occurs primarily on the palms and soles and in the axillae.

Thermal sweating occurs primarily on the trunk and face.

The skin should also be examined for any local pathology.

As hyperhidrosis may be compensatory, a search for anhid-

rotic areas should be made. The clothes and socks should

be inspected for evidence of discoloration or staining. It is

also important to determine whether the patient is wearing

excessive clothing.

Associated signs

Physical signs may give clues to the cause of hyperhidrosis.

Cyanosis suggests an underlying respiratory or cardiac

disorder. The presence of a heart murmur or arrhythmia

is suggestive of a cardiac disorder. Dilated pupils, tremor

of the hands, tachycardia, and altered mental status point to

alcohol or narcotic withdrawal. The absence of fungiform

papillae on the tongue, increased salivation, blotchy skin,

and hyporeflexia point to familial dysautonomia. The

presence of goiter, hand tremor, and exophthalmos suggests

thyrotoxicosis. Lymphadenopathy suggests a chronic infec-

tion or Hodgkin’s disease. Increased peripheral reflexes and

a positive Babinski’s sign suggest an upper motor neuron

lesionwhichmay result from a spinal cord injury.Hypoplas-

tic nails and hypoplastic or absent patella are characteristic

of nail–patella syndrome.

Diagnostic studies

The iodine–starch technique and the quinizarin powder

dusting technique can be used to delineate the precise

pattern and quantitative level of sweating.33 Both tech-

niques produce calorimetric changes induced by contact

with water (sweat).

Laboratory tests are usually not necessary in the majority

of patients with hyperhidrosis; they should be ordered only

when indicated by history or physical examination.

A complete blood count is helpful if an infection is

suspected. A serum glucose is useful if diabetes mellitus or

hypoglycemia is suspected. A serum thyroxine level should

be ordered if thyrotoxicosis is suspected. A serum growth

hormone, skull roentgenogram, and cranial computerized

axial tomogram (CAT) should be considered if gigantism

or acromegaly is suspected. A chest roentgenogram is

indicated when pulmonary or cardiac disease is suspected.

An electrocardiogram is indicated if arrhythmia or signific-

ant heart murmur is present, or when structural heart

disease or myocardial ischemia is suspected. An echocardio-

gram helps to diagnose structural heart disease. A 24-h

urine collection for vanilly mandelic acid, metanephrines,

and catecholamines should be considered if pheochromocy-


toma is suspected. Likewise, a 24-h urine collection for 5-

hydroxyindoleacetic acid should be considered if carcinoid

tumor is suspected.

Complications

Patients with hyperhidrosis tend to avoid shaking hands.

As such, they may become socially withdrawn and have

low self-esteem. Affected individuals may be unable to

grasp certain objects: the papers they hold may become

wet and metals they hold may become rusted. This may

impose restrictions on the kinds of tasks that they may be

able to do.

Hyperhidrosis may aggravate eczematous dermatitis.

Patients with hyperhidrosis are at risk for contact dermatitis

and miliaria. Hyperhidrosis may lead to maceration of the

skin and predisposition to various bacterial and fungal

infections. If hyperhidrosis is excessive and prolonged, and

no replacement is made for the loss of fluid and electrolytes,

heat stroke may occur.

Management

Treatment should be directed at the underlying cause

whenever possible. Light clothing should be worn. The

environment should be kept cool. The water and salt that

have been lost through sweating should be replenished.

For symptomatic treatment, many commercial topical

applications are available. Most of them contain aluminum

chloride or aluminum chlorhydroxide. The most effective is

a 20% alcohol solution of aluminum chloride hexahydrate

(Drysol).34 The medication acts by blocking the openings

of the sweat ducts. The area to be treated should be dried

first. The solution should ideally be applied at night and

washed off the following morning. Occlusion with plastic

wrap increases its effectiveness. The medication can be

applied, daily to weekly or as required, according to the

degree of hyperhidrosis. Skin irritation resulting from

the treatment can be treated with a mild hydrocortisone

cream.35 Tanning agents, such as glutaraldehyde and tannic

acid, are usually effective in the treatment of hyperhidrosis,

but are associated with undesirable side-effects, such as

contact dermatitis and brownish discoloration of the skin,

that preclude their use in most instances.35

Iontophoresis is the introduction by means of an electric

current of ions of soluble salts through the skin.36 It is an

effective alternative treatment for palmar, plantar, and

axillary hyperhidrosis. Iontophoresis causes blockage of

the sweat duct at the level of the stratum corneum by

directing a mild electrical current through the skin.37 With

iontophoresis, the anode is connected to the area to be

treated in a shallow water bath, while the cathode is

attached similarly to the contralateral area. Tingling and


burning can be a problem if the skin is broken. It is

therefore essential to cover any raw area with an ointment

so that the current cannot reach that area.36 Although

iontophoresis with plain tap water is relatively free of side-

effects, the necessity for repetitive frequent treatments is a

drawback. Treatment can be made more effective by the

addition of anticholinergic agents, such as poldine methyl-

sulfate and glycopyrronium bromide.38

Systemic anticholinergics, such as propantheline bromide

(Probanthine), glycopyrrolate (Robinul), and oxyphencycli-

mine (Daricon), have been used with transient effect in

some patients with hyperhidrosis. Unpleasant side-effects,

such as blurring of vision, dryness of mouth, constipation,

and urinary retention, preclude their long-term use.

Surgical management is usually not indicated, but may be

considered for the rare patient with genuinely incapacitating

hyperhidrosis. Axillary hyperhidrosis can be treated by

elliptical excision of the most actively sweating portion of

the axillary skin, along with undercutting and subcutaneous

resection of the sweat glands for 1 to 2 cm on each

side of the excised skin.35 The area of maximum sweat

production roughly corresponds to the hair-bearing areas

of the axilla; accurate mapping of the area can be achieved

by using the iodine–starch technique. Complications of

surgical excision of the axillary skin include infection,

hidradenitis, and scarring.

Sympathectomy should be considered only for those

individuals with intractable palmar or plantar hyperhidrosis

resistant to conservative measures. Sympathectomy abol-

ishes eccrine sweating in all areas supplied by the postgangli-

onic fibers. Upper thoracic sympathectomy may be

performed for palmar hyperhidrosis. Various approaches,

including supraclavicular, transaxillary, transthoracic, and

dorsal thoracic, have been used for upper thoracic sympath-

ectomy.35 The endoscopic transthoracic approach has been

advocated in recent years because of adequate exposure,

ease of performing bilateral sympathectomy, and excellent

esthetic results.38,39 Complications of upper thoracic sym-

pathectomy include wound infection, hemorrhage, pneu-

mothorax, Horner’s syndrome, brachial plexus injuries,

recurrent laryngeal nerve palsy, post-sympathetic neuralgia,

gustatory sweating, and compensatory hyperhidrosis in

nondenervated areas.7,38 Lumbar sympathectomy is rarely

indicated for the treatment of plantar hyperhidrosis.

Acknowledgments

Mr Sulakhan Chopra of the University of Calgary Medical

Library and Ms Dianne Leung assisted in the preparation

of the manuscript.


References

1 Bisbal J, de Cacho C, Casalots J. Surgical treatment of

axillary hyperhidrosis. Ann Plast Surg 1987; 18:

429–436.

2 Cunliffe WJ, Tan SG. Hyperhidrosis and hypohidrosis.

Practitioner 1976; 216: 149–153.

3 Ellis H. Hyperhidrosis and its surgical management.

Postgrad Med 1975; 58: 191–196.

4 Grice K. Treating hyperhidrosis. Practitioner 1988; 232:

953–956.

5 Phillips DM. Hyperhidrosis. In: Taylor RB, ed. Difficult

Diagnosis. Philadelphia: WB Saunders, 1985: 252–261.

6 Tabet JCM, Bay JW, Magdinec M. Essential

hyperhidrosis: current therapy. Clev Clin Quart 1986;

53: 83–88.

7 Quraishy MS, Giddings AEB. Treating hyperhidrosis:

endoscopic transthoracic sympathectomy may be the

best treatment. Br Med J 1993; 306: 1221–1222.

8 Dohn DF, Zraik O. Essential hyperhidrosis—

pathogenesis and treatment. Clev Clin Quart 1969; 36:

79–83.

9 Fan WJW, Cohen NM. Excessive sweating in an

apparently normal teenager. Pediatrics 1979; 64: 698.

10 Illingworth R. The Skin and Umbilicus. Edinburgh:

Churchill Livingstone, 1987: 102–108.

11 Sato K. Eccrine sweat glands. In: Fitzpatrick TB, Eisen

AZ, Wolff K, et al., eds. Dermatology in General

Medicine. New York: McGraw-Hill, 1993: 742–746.

12 Hurley HJ. The eccrine sweat glands. In: Moschella SI,

Hurley HJ, eds. Dermatology. Philadelphia: WB

Saunders, 1985: 1341–1368.

13 Wenger CB. The regulation of body temperature. In:

Rhoades RA, Tanner GA, eds. Medical Physiology.

Boston: Little, Brown and Company, 1995: 587–613.

14 Guyton AC, Hall JE. Body temperature, temperature

regulation, and fever. In: Guyton AC, Hall JE, eds.

Textbook of Medical Physiology. Philadelphia: WB

Saunders, 1996: 911–922.

15 Schafer JA. Body temperature regulation. In: Johnson

LR, ed. Essential Medical Physiology. New York: Ravens

Press, 1992: 711–721.

16 Stuart DD. Diabetic gustatory sweating. Ann Int Med

1978; 89: 223–224.

17 Pfeifer MP, Hardison JE. Profuse diaphoresis relieved by

coronary angioplasty. Am J Med 1989; 86: 338–339.

18 Gobbi PG, Pieresca C, Ricciardi L, et al. Night sweats in

Hodgkin’s disease: a manifestation of preceding minor

febrile pulses. Cancer 1990; 65: 2074–2077.

19 Pleet DL, Mandel S, Neilan B. Paroxysmal unilateral

hyperhidrosis and malignant mesothelioma. Arch Neurol

1983; 40: 256.

20 Sato K, Kang WH, Saga K, Sato KT. Biology of sweat

glands and their disorders. II. Disorders of sweat gland

function. J Am Acad Dermatol 1989; 20: 713–726.


21 Drummond PD, Boyce GM, Lance JW. Postherpetic

gustatory flushing and sweating. Ann Neurol 1987; 21:

559–563.

22 Harper KE, Spielvogel RL. Frey’s syndrome. Int J

Dermatol 1986; 25: 524–526.

23 Eedy DJ, Corbet JR. Olfactory facial hyperhidrosis

responding to amitriptyline. Clin Exp Dermatol 1987;

12: 298–299.

24 Jane MJ, Freehafer AA, Hazel C, et al. Autonomic

dysreflexia. A cause of morbidity and mortality in

orthopedic patients with spinal cord injury. Clin Orthop

1982; 169: 151–154.

25 Khurana RK. Orthostatic hypotension-induced

autonomic dysreflexia. Neurology 1987; 37: 1221–1224.

26 Stanworth PA. The significance of hyperhidrosis in

patients with post-traumatic syringomyelia. Paraplegia

1982; 20: 282–287.

27 Green M, Behrendt H. Sweat gland reactivity to local

thermal stimulation in dysautonomia. Am J Dis Child

1976; 130: 816–818.

28 Sohar E, Udassin R, Shoenfeld Y, et al. Cold-induced

profuse sweating on back and chest. A new genetic

entity? Lancet 1978; ii: 1073–1074.

29 LeWitt PA, Newman RP, Greenberg HS, et al. Episodic

hyperhidrosis, hypothermia, and agenesis of corpus

callosum. Neurology 1983; 33: 1122–1129.

30 Pechman KJ, Bergfeld WF. Palmar–plantar hyperhidrosis

occurring in a kindred with nail–patella syndrome. J Am

Acad Dermatol 1980; 3: 627–632.

31 Goldstein N. Ephidrosis (local hyperhidrosis): nevus

sudoriferous. Arch Dermatol 1967; 96: 67–68.

32 Gitter DG, Sato K. Localized hyperhidrosis in pretibial

myxedema. J Am Acad Dermatol 1990; 23: 250–254.

33 Hurley HJ. Disorders of the sweat glands. In: Orkin M,

Maibach HI, Dahl MV, eds. Dermatology. Norwalk:

Appleton & Lange, 1991: 344–348.

34 Shellow WV. Disturbances of skin hydration: dry skin

and excessive sweating. In: Goroll AH, May LA, Mulley

AG Jr, eds. Primary Care Medicine. Philadelphia: JB

Lippincott, 1995: 903–906.

35 White JW Jr. Treatment of primary hyperhidrosis. Mayo

Clin Proc 1986; 61: 951–956.

36 Elgart ML, Fuchs G. Tapwater iontophoresis in the

treatment of hyperhidrosis. Int J Dermatol 1987; 26:

194–197.

37 Shen JL, Lin GS, Li WM. A new strategy of

iontophoresis for hyperhidrosis. J Am Acad Dermatol

1990; 22: 239–241.

38 Moran KT, Brady MP. Surgical management of primary

hyperhidrosis. Br J Surg 1991; 78: 279–283.

39 Malone PS, Cameron AEP, Rennie JA. The surgical

treatment of upper limb hyperhidrosis. Br J Dermatol

1986; 115: 81–84.

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