Case Reports

Oxybutynin Treatment for Hyperhidrosis in Spinal Cord Injury Patients

Fed Pract. 2017 March;34(3):24-26

References

1. Strutton DR, Kowalski JW, Glaser DA, Stang PE. US prevalence of hyperhidrosis and impact on individuals with axillary hyperhidrosis: results from a national survey. J Am Acad Dermatol. 2004;51(2):241-248.

2. Walling HW. Clinical differentiation of primary from secondary hyperhidrosis. J Am Acad Dermatol. 2011;64(4):690-695.

3. Andersen LS, Biering-Sørensen F, Müller PG, Jensen IL, Aggerbeck B. The prevalence of hyperhidrosis in patients with spinal cord injuries and an evaluation of the effect of dextropropoxyphene hydrochloride in therapy. Paraplegia. 1992;(30):184-191.

4. 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(5, pt 1):713-726.

5. Kewalramani LS. Autonomic dysreflexia in traumatic myelopathy. Am J Phys Med. 1980;59(1):1-21.

6. Low PA, Engstrom JW. Disorders of the autonomic nervous system. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York, NY: McGraw-Hill; 2015.

7. Milhort TH. Classification of syringomyelia. Neurosurg Focus. 2000;8(3):E1.

8. National Institute of Neurological Disorders and Stroke. Syringomyelia fact sheet. https://www.ninds .nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Syringomyelia-Fact-Sheet. Accessed February 13, 2017.

9. Meschner AL. Junqueira’s Basic Histology. 14th ed. New York, NY: McGraw-Hill; 2016:371-392.

10. Mauro TM. Biology of eccrine and apocrine glands. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. eds. Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York, NY: McGraw-Hill; 2012.

11. Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of Medical Physiology. 25th ed. New York, NY: McGraw-Hill; 2016:261-272.

12. Kellogg DL Jr. Thermoregulation. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, eds. Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York, NY: McGraw-Hill; 2012.

13. Rovner ES, Wyman J, Lam S. Urinary Incontinence. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. eds. Pharmacotherapy: A Pathophysiologic Approach. 9th ed. New York, NY: McGraw-Hill; 2014:1377-1396.

14. Teivelis MP, Wolosker N, Krutman M, Kauffman P, Campos JR, Puech-Leão P. Treatment of uncommon sites of focal primary hyperhidrosis: experience with pharmacological therapy using oxybutynin. Clinics (Sao Paulo). 2014;69(9):608-614.

15. Wolosker N, de Campos JR, Kauffman P, Puech-Leão P. A randomized-placebo-controlled trial of oxybutynin for the initial treatment of palmar and axillary hyperhidrosis. J Vasc Surg. 2012;55(6):1696-1700.

16. Schollhammer M, Brenaut E, Menard-Andivot N, et al. Oxybutynin as a treatment for generalized hyperhidrosis. Br J Dermatol. 2015;173(5):1163-1168.

17. Gonzalez F, Chang JY, Banovac K, Messina D, Martinez-Arizala A, Kelley RE. Autoregulation of cerebral blood flow in patients with orthostatic hypotension after spinal cord injury. Paraplegia. 1991;29(1):1-7.

18. Fealey RD, Hebert AA. Disorders of the eccrine sweat glands and sweating. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, eds. Fitzpatrick’s Dermatology in General Medicine. New York, NY: McGraw-Hill; 2012:chap 84.

Discussion

Sweating is a physiological process that involves the active secretion of water by specialized sweat glands in the skin.^9-11 There are 2 types of sweat glands in the skin; apocrine and eccrine.⁹ Collectively the 3 million eccrine sweat glands of the average person approximately equal the mass of a kidney and exceed the secretory rate of exocrine glands.⁹ They function in evaporative cooling in response to thermal or physiologic stimuli and are widely distributed over the body, especially on the forehead, back, palms, and soles.¹⁰

Sympathetic cholinergic nerves are mainly responsible for sweat secretion by the release of acetylcholine to activate muscarinic receptors on the gland.¹¹ Postganglionic fibers from sympathetic nerve cells innervate sweat glands that release cholinergics.⁶ Postganglionic cholinergic receptors that are activated by muscarinic drugs are termed muscarinic receptors and are readily accessible to antimuscarinic drugs.^6,12 Anticholinergic/antimuscarinic agents antagonize muscarinic receptors and suppress premature detrusor contractions to enhance bladder storage.¹³ They include oxybutynin, tolterodine, trospium, solifenacin, darifenacin, and fesoterodine.¹³Oxybutynin was used in both cases because it is on VA formulary. It was effective in treating HH, although the etiology is unclear and the presentations were different.

One retrospective study that analyzed 20 patients who received oxybutynin for primary HH at uncommon sites, such as the back and groin, found that QOL improved in 85% of the subjects after 6 weeks.¹⁴ Randomized placebo-controlled trials also have found oxybutynin effective for treatment of palmar and axillary HH and generalized HH.^15,16

Syringomyelia was ruled out in both cases based on history and radiologic studies, specifically magnetic resonance imaging. Autonomic dysreflexia was ruled out as the HH was not an acute finding and BP was within normal limits. Orthostatic hypotension is a common finding in SCI, mainly in tetraplegic patients, and could be suspected in both cases. Sweating was usually worse in the mornings in both cases and during transfers, as noted in the first case.¹⁷ However, chronic autoregulation allows for chronic adaption to tissue hypoperfusion over time.¹⁶

Hyperhidrosis or other disorders of eccrine sweating can occur for various reasons, including changes in the spinal sympathetic preganglionic, ganglionic, or postganglionic neurons; dysfunction of the thermoregulatory centers in the brain’s central autonomic network; or changes in the muscarinic cholinergic synapse on sweat glands.¹⁸

Conclusion

Patients with SCI may have an acute or chronic presentation of HH. Removal of the inciting cause in the case of autonomic dysreflexia and/or the administration of a pharmaceutical agent is the usual treatment.

Regardless of the etiology of HH that persists, effective treatment should be a goal, especially in those patients whose QOL is affected by this condition. The outcome of treatment with oxybutynin in these case reports is consistent with the findings of the limited retrospective study and randomized placebo-controlled studies that show oxybutynin is effective for treating bothersome HH.^14-16

The results of these case reports are not generalizable to patients with SCI and HH, nor are the results of the limited retrospective study and randomized placebo-controlled studies, as their sample sizes were small.^14,16,17 However, information on the use of oxybutynin for the effective treatment of HH in the SCI population is promising. Research studies on the prevalence of HH and randomized placebo-controlled trials with a larger SCI population are considerations for future studies.

References

2. Walling HW. Clinical differentiation of primary from secondary hyperhidrosis. J Am Acad Dermatol. 2011;64(4):690-695.

4. 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(5, pt 1):713-726.

5. Kewalramani LS. Autonomic dysreflexia in traumatic myelopathy. Am J Phys Med. 1980;59(1):1-21.

7. Milhort TH. Classification of syringomyelia. Neurosurg Focus. 2000;8(3):E1.

9. Meschner AL. Junqueira’s Basic Histology. 14th ed. New York, NY: McGraw-Hill; 2016:371-392.

11. Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong’s Review of Medical Physiology. 25th ed. New York, NY: McGraw-Hill; 2016:261-272.

16. Schollhammer M, Brenaut E, Menard-Andivot N, et al. Oxybutynin as a treatment for generalized hyperhidrosis. Br J Dermatol. 2015;173(5):1163-1168.

Oxybutynin Treatment for Hyperhidrosis in Spinal Cord Injury Patients

References

Discussion

Conclusion

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