Spotlight on hyperhidrosis in older patients

Hyperhidrosis is sweating in excess of that required for normal thermoregulation. It is a condition that usually begins in either childhood or adolescence and can affect any site on the body. However, the sites most commonly affected are the palms, soles, and axillae. Excessive sweating may be primary (idiopathic) or secondary to medication use, certain diseases, metabolic disorders, or febrile illnesses. Hyperhidrosis often causes great emotional distress and occupational disability for the patient, regardless of the form and the extent of the problem. Hyperhidrosis is difficult to treat effectively. With the newer treatment modalities now available, the patient has numerous options and is offered a better prognosis.

Types of hyperhidrosis

 Hyperhidrosis exists in three forms: emotionally induced hyperhidrosis- which affects palms, soles, and axillae, localized hyperhidrosis, and generalized hyperhidrosis ^1,2. Localized hyperhidrosis, unlike generalized hyperhidrosis, usually begins in childhood or adolescence. Localized unilateral or segmental hyperhidrosis is rare and of unknown origin. The condition usually presents on the forearm or forehead in otherwise healthy individuals, without evidence of the typical triggering factors found in essential hyperhidrosis. Unilateral hyperhidrosis with accompanying contra-lateral anhidrosis is also rare³. Palmar hyperhidrosis is a benign functional disorder that is a psychological and social handicap. Harlequin syndrome is characterized by unilateral hyperhidrosis and flushing, predominantly induced by heat or exercise⁴. The sympathetic deficits are usually limited to the face⁴. Night sweats among older people could be related to certain systemic conditions and clinical assessment is always required to rule out the presence of these causes, table 1.

Epidemiology

 People of all ages can be affected by hyperhidrosis. Primary hyperhidrosis affects men and women equally, and most commonly occurs among people aged 25–64 years. Some may have been affected since early childhood, and about 30–50% have another family member afflicted, implying a genetic predisposition⁵. Localized hyperhidrosis, unlike generalized hyperhidrosis, usually begins in childhood or adolescence. In a study of 850 patients with palmar, axillary, or facial hyperhidrosis, 62% of patients reported that sweating began since before they could remember; 33% since puberty; and 5% during adulthood⁶. In a cross-sectional primary care study among 795 older patients (older than 64 years), 10% reported being bothered by night sweats, 9% by day sweats, and 8% by hot flushes⁷.  All three symptoms were associated with reduced quality of life⁷.

 

Table 1. Common causes of night sweats among older patients

The Condition	Clinical Features
Menopause	Women would also experience hot flushes
Pulmonary tuberculosis (TB)	Usually associated with fatigue and anorexia. However, atypical presentation is not uncommon.
Diabetes mellitus	This type of hyperhidrosis could be a manifestation of autonomic dysfunction.
Medications*	Several medications may induce excessive sweating at night. In general, the following drugs can be associated with hyperhidrosis: Calcitonin,
Lymphoma	Nights sweats are a symptom of certain types of Hodgkin’s disease found in older patients
Parkinson’s disease	The condition can be associated with localized or generalized hyperhidrosis.
Mental Disorder/stress	Anxiety and depression may cause night sweats

* These include: Calcitonin, fentanyl, acyclovir, ceftriaxone, levothyroxine, levodopa and carbidopa, quetiapine, amlodipine, omeprazole, insulin, medroxyprogesterone, testosterone, prednisolone and tamoxifen.

Pathophysiology

The pathophysiology underlying hyperhidrosis is complex and not well understood. There are two distinct types of sweating: thermal sweating, which tends to occur on the trunk and is controlled by the hypothalamus via the thermo-sensitive preoptic sweat centre, and emotional sweating, which is predominately on the palms and soles and is regulated by the cerebral cortex. Thermoregulation and sweat production are mainly controlled by the cerebral cortex, anterior hypothalamus and the sympathetic nervous system. In addition, there are three types of sweat glands: eccrine, apocrine and apoeccrine. The eccrine type is the most numerous type, predominantly occurring on the soles of the feet, palms, axilla and face, and this type is innervated by the sympathetic nervous system, with acetylcholine as the principle neurotransmitter⁸.

Apocrine glands are androgen-dependent, less numerous and are found in the axilla and genital regions. The apoeccrine glands are found only in the adult axilla. The eccrine type is the one mainly involved in hyperhidrosis. Hyperhidrosis is usually stimulated by emotion and stress, so it does not occur during sleep or sedation. While 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 ⁸.

Generalized hyperhidrosis may be the consequence of autonomic dysregulation, or it may develop secondary to a metabolic disorder, febrile illness, or malignancy. In its localized form, hyperhidrosis may result from a disruption followed by abnormal regeneration of sympathetic nerves or a localized abnormality in the number or distribution of the eccrine glands, or it may be associated with other -usually vascular- abnormalities. When caused by stress, hyperhidrosis may be generalized or limited to the palms, soles, and forehead⁸.

Aetiology of hyperhidrosis

Hyperhidrosis can be idiopathic or sometimes secondary to other diseases, metabolic disorders, febrile illnesses, or medication use. Use of medications may affect one or more components of human thermoregulation and induce hyperhidrosis. Hyperhidrosis beginning later in life should prompt a search for secondary causes such as systemic diseases, adverse effects of medication use, or metabolic disorders. Secondary causes may include endocrine diseases such as diabetes mellitus, hyperthyroidism, and hyperpituitarism⁸. In one series, one third of cases were neurologic in origin, including peripheral nerve injury, Parkinson disease, reflex sympathetic dystrophy, spinal injury, and Arnold-Chiari malformation⁹. Other secondary causes to be considered may include pheochromocytoma, respiratory disease, and psychiatric disease table 2. Asymmetric hyperhidrosis may suggest neurologic disease⁹. Primary hyperhidrosis usually starts during adolescence or even before and 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. Primary hyperhidrosis can be differentiated from secondary type by certain clinical criteria, table 3. These criteria discriminate well between the two types (sensitivity: 0.99; specificity: 0.82; positive predictive value: 0.99; negative predictive value: 0.852) and may facilitate optimal clinical management¹⁰. Essential hyperhidrosis is a dermatologic and neurologic disorder characterized by excessive sweating of the eccrine sweat glands¹¹.

It is a disorder of the eccrine sweat glands and is associated with sympathetic overactivity¹². Essential hyperhidrosis does not appear to be a generalized disorder involving vascular endothelium. Patients note excessive sweating in affected areas, which ultimately prompts them to seek medical attention. Palmoplantar hyperhidrosis, excessive sweating of the palms and soles, is observed in persons with chronic alcoholism and it could be inherited in an autosomal dominant manner^13,14.

 

 

Table 2. Secondary causes of hyperhidrosis

Generalized hyperhidrosis (an area >100 square cm) §  Affecting almost any skin area §  Starts at older age §  Symmetry is not very distinctive §  Could be related to secondary causes, including medications and systemic disorders

Localized hyperhidrosis (an area <100 square cm) §  Affects axillae more than hands §  Starts at early age(<25) and improve later(>50) §  Usually bilaterally symmetrical §  Tends to cease during sleep §  Mainly related to autonomic dysfunction.

1.     Neurologic or neoplastic diseases 2.     Spontaneous periodic hypothermia and hyperhidrosis 3.     Metabolic disorders or processes: –        Thyrotoxicosis, diabetes mellitus, hypoglycemia, gout, pheochromocytoma, –        Menopause 4.     Febrile illnesses 5.     Medications: –        Propranolol, physostigmine, pilocarpine, tricyclic antidepressants, and serotonin reuptake inhibitors. 6.     Chronic alcoholism 7.     Hodgkin disease or tuberculosis (causing nocturnal hyperhidrosis)

1)    Gustatory stimuli: §  Seen in Frey syndrome, encephalitis, syringomyelia, diabetic neuropathies, herpes zoster parotitis, and parotid abscess 2)    Eccrine nevus & Blue rubber-bleb nevus 3)    Eccrine angiomatous hamartoma* 4)    Glomus tumor 5)    POEMS syndrome: Peripheral neuropathy, organomegaly, endocrinopathy, monoclonal plasma-proliferative disorder, and skin changes. 6)    Burning feet syndrome 7)    Pachydermoperiostosis 8)    Pre-tibial myxoedema

* A rare benign malformation characterized by both eccrine and vascular components, usually first evident at birth or during early infancy as a nodule/plaque, usually solitary, involving acral skin and although it is often asymptomatic, it may be associated with focal hyperhidrosis, hypertrichosis, and pain.

 

Table 3. Criteria for the clinical diagnosis of primary (idiopathic)  hyperhidrosis

Diagnostic criteria favouring primary hyperhidrosis:   Excessive sweating of 6 months or more in duration,                                               with 4 or more of the following:   Primarily involving eccrine-dense (axillae/palms/soles/craniofacial) sites Bilateral and relatively symmetric sweating Cessation of sweating during sleep (absent nocturnally) At least one episode per week Onset at 25 years of age or younger. Family history of idiopathic hyperhidrosis(positive family history) Impairing daily activities.

 

Clinical assessment of hyperhidrosis

Diagnosis of this potentially embarrassing and socially disabling condition is based on the patient’s history and visible signs of sweating. Clinical examination may be normal, but will often reveal obvious areas of focal sweating or skin maceration. The primary objective of clinical examination is to reveal any evidence of underlying chronic illness suggestive of a secondary cause, for example lymphadenopathy. The main aims of clinical assessment should be:

1. Identifying anatomical sites with excessive sweating
2. Ensure the absence of physical findings suggestive of secondary hyperhidrosis

Investigation

Laboratory tests are not required to make a diagnosis of primary hyperhidrosis, but they only serve to rule out and work-up potential secondary causes of excessive sweating. A number of specialized tests have been developed that quantify both sweat production and the impact on quality of life, such as starch iodine test. However, they are not required, nor are they particularly useful in the clinical setting. The work-up for generalized sweating or secondary hyperhidrosis can be complicated, and often includes a number of investigations.

Laboratory Studies

Important laboratory studies in the hyperhidrosis workup may include the following:

1. Thyroid function tests may reveal underlying hyperthyroidism or thyrotoxicosis.
2. Blood glucose levels may reveal diabetes mellitus or hypoglycemia.

• Urinary catecholamines may reveal a possible pheochromocytoma.

1. Uric acid levels may reveal gout.
2. Screening test for tuberculosis, such as purified protein derivative (PPD) test.

Imaging Studies

Chest radiography may be used to rule out tuberculosis or a neoplastic cause of the hyperhidrosis.

Management of hyperhidrosis

Therapy for hyperhidrosis can be challenging for both the patient and the physician. Both topical and systemic medications have been used in the treatment of hyperhidrosis. Other treatment options for hyperhidrosis include iontophoresis and botulinum toxin injections. In addition to pharmacological therapy, other treatments include surgical sympathectomy, surgical excision of the affected areas, and subcutaneous liposuction. Each modality could be used effectively. In general, management of hyperhidrosis should follow a gradational step-wise approach, beginning first with the least invasive therapies and transitioning to progressively more invasive treatments for those patients who fail. The appropriate treatment will differ for each patient, and will depend on the location of focal hyperhidrosis, the severity and patient tolerance, table 4.

Pharmacological therapy

Topical Medications

Topical agents for hyperhidrosis therapy include topical anticholinergics, boric acid, 2-5% tannic acid solutions, resorcinol, potassium permanganate, formaldehyde, glutaraldehyde, and methenamine¹⁵. All of these agents are limited by staining, contact sensitization, irritancy, or limited effectiveness. Because of the limitations of other agents, Drysol, a 20% aluminum chloride hexahydrate in absolute anhydrous ethyl alcohol, is more commonly used as the first-line topical agent¹⁶. Drysol should be applied nightly on dry skin until a positive result is obtained, after which the intervals between applications may be lengthened. To minimize irritation, the remainder of the medication should be washed off when the patient awakes, and the area may be neutralized with the topical application of baking soda¹⁶. Aluminum chloride (frequently used in antiperspirants) 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. In addition, axillary hyperhidrosis may be treated with aluminium chloride gel, although the gel may cause mild cutaneous irritation¹⁷.

Systemic Medications

Systemic agents used to treat hyperhidrosis include anticholinergic medications, such as propantheline bromide, glycopyrrolate, oxybutynin, and benztropine. These agents are effective because the preglandular neurotransmitter for sweat secretion is acetylcholine; although the sympathetic nervous system innervates the eccrine sweat glands^18,19. However, the use of anticholinergics is limited because their adverse effect profile may include mydriasis, blurring of vision, dry mouth and eyes, difficulty with micturition, and constipation. However, other systemic medications, such as sedatives and tranquilizers, indomethacin, and calcium channel blockers, may be beneficial in the treatment of palmo-plantar hyperhidrosis.

 

Other Therapies

 

Iontophoresis: Iontophoresis consists of passing a direct current across the skin²⁰. The exact mechanism of action remains under debate^21,22. In palmo-plantar hyperhidrosis, the daily treatment of each palm or sole for 30 minutes at 15-20 mA with tap water iontophoresis is effective²³. Intact skin can endure 0.2-mA/cm2 galvanic current without negative consequences, and as much as 20-25 mA per palm may be tolerated²³. Numerous agents have been used in iontophoresis to induce hypohidrosis, including tap water and anticholinergics; however, treatment with anticholinergic iontophoresis is more effective than tap water iontophoresis²⁴.

 

Botulinum toxin: Botulinum toxin injections are effective because of their anticholinergic effects at the neuromuscular junction and in the postganglionic sympathetic cholinergic nerves in the sweat glands^25,26,27. Adverse effects of intradermal injections of botulinum A toxin may result from diffusion into underlying muscles^28,29. Treatment of axillary hyperhidrosis with botulinum toxin type A reconstituted in lidocaine was associated with less pain (from the injection) when compared with the one reconstituted in normal saline³⁰. The results were the same in the two groups, thus, lidocaine-reconstituted botulinum toxin A may be preferable for treating axillary hyperhidrosis. In cases with palmar hyperhidrosis, multiple (50) subepidermal injections result in anhydrosis lasting 4-12 months, and each injection produces an area of anhydrosis approximately 1.2 cm in diameter³¹. The only adverse effect is mild transient thumb weakness that resolves within 3 weeks.

Surgical treatment

Sympathectomy

 Sympathectomy has been used as a permanent effective treatment for almost 90 years. It is usually reserved for the final treatment option³². Sympathectomy involves the surgical destruction of the ganglia responsible for hyperhidrosis, T2 and T3 thoracic ganglia in palmar hyperhidrosis, T4 thoracic ganglia in axillary hyperhidrosis, and T1 thoracic ganglia in facial hyperhidrosis^33,34,35. Two surgical approaches are available: an open approach and a newer endoscopic approach, such as endoscopic thoracic sympathectomy (ETS). The endoscopic approach has become favored because of its improvements in terms of complications, surgical scars, and surgical times.  In palmar hyperhidrosis, a survey showed thoracoscopic sympathectomy to be minimally invasive and to improve the patient’s quality of life, even if compensatory hyperhidrosis occurs³⁶. Numerous complications are associated with the endoscopic treatment option; including compensatory sweating (induction of sweating in previously unaffected areas of the body), gustatory sweating, pneumothorax, intercostal neuralgia, Horner syndrome, recurrence of hyperhidrosis, and the sequelae of using general anesthetic. Topical glycopyrrolate application may be effective and safe for the treatment of excessive facial sweating in primary craniofacial and secondary gustatory hyperhidrosis following sympathectomy³⁷. Lumbar sympathectomy is a relatively new procedure aimed at those patients for whom ETS has not relieved excessive plantar sweating. The success rate is about 90% and the operation should be carried out only if patients first have tried other conservative measures³⁸.

Other Surgical Techniques

Surgical excision of the affected area identified using iodine starch testing, removes the appropriate sweat glands, thereby eliminating sweating. This technique is particularly useful in axillary hyperhidrosis.

Subcutaneous liposuction is another means of removing the eccrine sweat glands responsible for axillary hyperhidrosis. Compared with classic surgical excision, this modality results in less disruption to the overlying skin, resulting in smaller surgical scars and a diminished area of hair loss³⁹.

Laser treatment of axillary hyperhidrosis using the 1064-nm Nd-YAG laser was found to be effective and safe as well⁴⁰.

 

Table 4. Therapy options for hyperhidrosis (starting with the least invasive)

 

	Treatment Options
Affected  Area	Topical therapy	Systemic therapy	Ionto-phoresis	Focal Botulinum injections	Surgery (ETS& others)	Subcutaneous liposuction & Laser therapy
Axillae	√			√	√	√
Face/head	√	√		√	√
Palms/ hands	√		√		√
Feet/ soles	√	√	√
Groin	√
Generalized		√

 

Conclusion

Hyperhidrosis is a condition in which excess sweating affects various parts or the whole body. The condition usually is idiopathic and can be secondary to various disorders or medications use. Hyperhidrosis beginning later in life should prompt a search for secondary causes, including systemic diseases and adverse effects of certain medications. Treatment options for hyperhidrosis include topical agents, iontophoresis and botulinum toxin injections. In addition to pharmacologic therapy, endoscopic sympathectomy and surgical excision of the affected areas have been used. However, the condition is difficult to treat effectively and a logical approach must be taken to individualize therapy based on the degree of functional impairment.

Key Points

• Hyperhidrosis is excess sweating or perspiration which can either be generalized or localized to specific parts of the body, such as hands, feet, axillae.
• Hyperhidrosis may represent an autonomic nervous system response to physical or psychogenic stress or to a fever or high environmental temperature.
• Hyperhidrosis beginning later in life should prompt a search for secondary causes
• Night sweats among older people could be related to certain conditions which should be ruled out.
• The condition is difficult to treat effectively and its treatment can be challenging for both patients and physicians.
• Pharmacological treatment options include topical and systemic agents, iontophoresis and botulinum toxin injections.
• Endoscopic surgical sympathectomy and surgical excision of the affected areas could be considered in certain patients.

 

---

 Nabil Aly, Consultant physician, University Hospital Aintree, Liverpool

E-mail: [email protected]

---

References

1. Altman RS, Schwartz RA. Emotionally induced hyperhidrosis. Cutis. May 2002; 69(5):336-8.
2. Ruchinskas R. Hyperhidrosis and anxiety: chicken or egg?. Dermatology. 2007; 214(3):195-6.
3. Kocyigit P, Akay BN, Saral S, Akbostanci C, Bostanci S. Unilateral hyperhidrosis with accompanying contralateral anhidrosis. Clin Exp Dermatol. Dec 2009;34(8):e544-6.
4. Moon SY, Shin DI, Park SH, Kim JS. Harlequin syndrome with crossed sympathetic deficit of the face and arm. J Korean Med Sci. Apr 2005;20(2):329-30.
5. Haider, A and Solish N. Focal hyperhidrosis: diagnosis and management. Canadian Medical Association Journal- January 2005; 172 (1): 69–75.
6. Drott C, Gothberg G, Claes G. Endoscopic transthoracic sympathectomy: an efficient and safe method for the treatment of hyperhidrosis. J Am Acad Dermatol. Jul 1995;33(1):78-81.
7. Mold JW, Roberts M, Aboshady HM. Prevalence and predictors of night sweats, day sweats, and hot flashes in older primary care patients: an OKPRN study. Ann Fam Med. 2004 Sep-Oct;2(5):391-7.
8. Stolman LP. Treatment of hyperhidrosis. Dermatol Clin.  1998; 16:863–9.
9. Walling HW. Clinical differentiation of primary from secondary hyperhidrosis. J Am Acad Dermatol. 2011; 64(4):690-5.
10. Walling HW. Clinical differentiation of primary from secondary hyperhidrosis. J Am Acad Dermatol 2011 Apr;64(4):690-5.
11. Saglam M, Esen AM, Barutcu I, et al. Impaired left ventricular filling in patients with essential hyperhidrosis: an echo-Doppler study. Tohoku J Exp Med. Apr 2006;208(4):283-90.
12. Esen AM, Barutcu I, Karaca S, et al. Peripheral vascular endothelial function in essential hyperhidrosis. Circ J. Jun 2005;69(6):707-10.
13. Tugnoli V, Eleopra R, De Grandis D. Hyperhidrosis and sympathetic skin response in chronic alcoholic patients. Clin Auton Res. Feb 1999;9(1):17-22.
14. Yamashita N, Tamada Y, Kawada M, Mizutani K, Watanabe D, Matsumoto Y. Analysis of family history of palmoplantar hyperhidrosis in Japan. J Dermatol. Dec 2009;36(12):628-31.
15. Shelley WB, Laskas JJ, Satanove A. Effect of topical agents on planter sweating. AMA Arch Derm Syphilol. Jun 1954;69(6):713-6.
16. 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. May 1989;20(5 Pt 1):713-26.
17. Streker M, Reuther T, Verst S, Kerscher M. [Axillary hyperhidrosis–efficacy and tolerability of an aluminium chloride antiperspirant. Prospective evaluation on 20 patients with idiopathic axillary hyperhidrosis]. Hautarzt. Feb 2010;61(2):139-44.
18. Klaber M, Catterall M. Treating hyperhidrosis. Anticholinergic drugs were not mentioned. BMJ. Sep 16 2000;321(7262):703.
19. Wozniacki L, Zubilewicz T. Primary hyperhidrosis controlled with oxybutynin after unsuccessful surgical treatment. Clin Exp Dermatol. Dec 2009;34(8):e990-1.
20. Bouman HD, Lentzer EM. The treatment of hyperhidrosis of hands and feet with constant current. Am J Phys Med. Jun 1952;31(3):158-69.
21. Karakoç Y, Aydemir EH, Kalkan MT, Unal G. Safe control of palmoplantar hyperhidrosis with direct electrical current. Int J Dermatol. Sep 2002;41(9):602-5.
22. Murphy R, Harrington CI. Treating hyperhidrosis. Iontophoresis should be tried before other treatments. BMJ. Sep 16 2000;321(7262):702-3.
23. Sato K, Ohtsuyama M, Samman G. Eccrine sweat gland disorders. J Am Acad Dermatol. Jun 1991;24(6 Pt 1):1010-4.
24. Abell E, Morgan K. The treatment of idiopathic hyperhidrosis by glycopyrronium bromide and tap water iontophoresis. Br J Dermatol. Jul 1974;91(1):87-91.
25. Fujita M, Mann T, Mann O, Berg D. Surgical pearl: use of nerve blocks for botulinum toxin treatment of palmar-plantar hyperhidrosis. J Am Acad Dermatol. Oct 2001;45(4):587-9.
26. Moraru E, Voller B, Auff E, Schnider P. Dose thresholds and local anhidrotic effect of botulinum A toxin injections (Dysport). Br J Dermatol. Aug 2001;145(2):368.
27. Naumann M. Evidence-based medicine: botulinum toxin in focal hyperhidrosis. J Neurol. Apr 2001;248 Suppl 1:31-3.
28. Naumann M, Lowe NJ. Botulinum toxin type A in treatment of bilateral primary axillary hyperhidrosis: randomised, parallel group, double blind, placebo controlled trial. BMJ. Sep 15 2001;323(7313):596-9.
29. Swartling C, Farnstrand C, Abt G, Stalberg E, Naver H. Side-effects of intradermal injections of botulinum A toxin in the treatment of palmar hyperhidrosis: a neurophysiological study. Eur J Neurol. Sep 2001;8(5):451-6.
30. Vadoud-Seyedi J, Simonart T. Treatment of axillary hyperhidrosis with botulinum toxin type A reconstituted in lidocaine or in normal saline: a randomized, side-by-side, double-blind study. Br J Dermatol. May 2007;156(5):986-9.
31. Shelley WB, Talanin NY, Shelley ED. Botulinum toxin therapy for palmar hyperhidrosis. J Am Acad Dermatol. Feb 1998; 38(2 Pt 1):227-9.
32. Kotzareff A. Resection partielle de trone sympathetique cervical droit pour hyperhidrose unilaterale. Rev Med Suisse Romande. 1920;40:111-3.
33. Chen HJ, Lu K, Liang CL. Transthoracic endoscopic T-2, 3 sympathectomy for facial hyperhidrosis. Auton Neurosci. Oct 8 2001; 93(1-2):91-4.
34. Hsu CP, Shia SE, Hsia JY, Chuang CY, Chen CY. Experiences in thoracoscopic sympathectomy for axillary hyperhidrosis and osmidrosis: focusing on the extent of sympathectomy. Arch Surg. Oct 2001;136(10):1115-7.
35. Kim BY, Oh BS, Park YK, Jang WC, Suh HJ, Im YH. Microinvasive video-assisted thoracoscopic sympathicotomy for primary palmar hyperhidrosis. Am J Surg. Jun 2001; 181(6):540-2.
36. Kumagai K, Kawase H, Kawanishi M. Health-related quality of life after thoracoscopic sympathectomy for palmar hyperhidrosis. Ann Thorac Surg. Aug 2005;80(2):461-6.
37. Kim WO, Kil HK, Yoon KB, Yoon DM. Topical glycopyrrolate for patients with facial hyperhidrosis. Br J Dermatol. May 2008;158(5):1094-7.
38. Rieger R, Pedevilla S (). Retroperitoneoscopic lumbar sympathectomy for the treatment of plantar hyperhidrosis: technique and preliminary findings”. Surg Endosc- January 2007; 21 (1): 129–35.
39. Lillis PJ, Coleman WP 3rd. Liposuction for treatment of axillary hyperhidrosis. Dermatol Clin. Jul 1990;8(3):479-82.
40. Na GY, Park BC, Lee WJ, Park DJ, Kim do W, Kim MN. Control of palmar hyperhidrosis with a new “dry-type” iontophoretic device. Dermatol Surg. Jan 2007;33(1):57-61.