THERAPEUTICS DOI 10.1111/J.1365-2133.2004.06255.X No compensatory sweating after botulinum toxin treatment of palmar hyperhidrosis A.L. Krogstad,* A. Skymne,* G. Pegenius,* M. Elam* and B.G. Wallin* Unit of Clinical Neurophysiology, *Institute of Clinical Neuroscience and  Department of Dermatology, Sahlgren University Hospital, S-413 45 Go¨teborg, Sweden Correspondence: Mikael Elam. E-mail: mikael.elam@neuro.gu.se Accepted for publication 19 May 2004 Key words: botulinum toxin, compensatory sweating, evaporimetry, hyperhidrosis, subjective evaluation of sweating Conflict of interest: None declared. Summary Background Primary focal hyperhidrosis is caused by excessive secretion by eccrine sweat glands, usually at the palms, soles and axillae. The underlying mechanism is unclear. In recent years botulinum toxin A has emerged as a useful treatment. Compensatory sweating, which is a major problem in many patients who have undergone transthoracic endoscopic sympathectomy for hyperhidrosis, has only rarely been reported after botulinum toxin. However, this potential side-effect of botulinum toxin treatment has not been systematically examined. Objectives To investigate if treatment with botulinum toxin A in hyperhidrotic hands may cause compensatory sweating at other skin locations. Methods In 17 patients with a history of palmar hyperhidrosis repeated measure- ments of evaporation were made before and up to 6 months after treatment of the hands with botulinum toxin A. Recordings were made at 16 skin areas and compared with subjective estimates of sweating. Results Following treatment, palmar evaporation decreased markedly and then returned slowly towards pretreatment values, but was still significantly reduced 6 months after treatment. No significant increase of sweating was found after treatment in any nontreated skin area. Conclusions Successful treatment of palmar hyperhidrosis with botulinum toxin does not evoke compensatory hyperhidrosis in nontreated skin territories. Primary focal hyperhidrosis most commonly affects palms, axillae and soles and may have a severe negative impact on quality of life. 1 The underlying mechanisms are unknown, but available evidence points to a regional increase of sympathetic sudomotor activity 2 rather than an exaggerated sweat gland function. No causal therapy is available. The treatment options involve a range of topical or systemic medications, psycho- therapy and surgical or nonsurgical invasive techniques. Trans- thoracic endoscopic sympathectomy has proved to be effective 3,4 against palmar hyperhidrosis but is not an ideal treatment, as other sympathetic functions may be permanently disturbed. In addition, many patients complain of so-called compensatory sweating, i.e. sweating in new skin areas, 5–7 after sympathectomy and occasionally patients consider this a worse suffering than the original symptoms. Recently, local injection of botulinum toxin A has emerged as a successful treatment for hyperhidrosis. In contrast to sym- pathectomy, which influences sweat gland function in a fairly large area, the effect of the botulinum toxin on sweat glands is limited to the treated skin. A large number of patients have been treated in this way and as only minor side-effects have been reported, the new therapy has become an important alternative to surgery. The aim of the present study was to evaluate if treatment with botulinum toxin A may induce compensatory sweating in nontreated glabrous or hairy skin. To this end, sweating was assessed by evaporimetry in 17 patients with palmar hyperhidrosis. Recordings were made bilaterally in eight dif- ferent skin locations, before and up to 6 months after treating the palms with botulinum toxin A. In conjunction with the measurements the patients made subjective estimates of the degree of sweating in hands and feet. Materials and methods Study population We studied 17 patients (10 females and seven males) with palmar hyperhidrosis, aged 17–42 years (26 ± 10 years, mean ± SD). The first symptoms of increased sweating appeared when the patients were 10 ± 5 (mean ± SD) years of age. In 59% of the cases a patient’s father or mother had Ó 2005 British Association of Dermatologists • British Journal of Dermatology 2005 152, pp329–333 329