Localized Unilateral Hyperhidrosis—a Clinical and Laboratory Study

Abstract

Summary.— Three case of unilateral idiopathic hyperhidrosis are described. Two of the lesions were congenital; the thrid occurred in later life. Quantitative sweat collections demonstrated that the sweat glands in the lesion were hyperresponsive to those stimuli, which normally evoked sweating in the skin sites where the lesions occurred. Hyper‐responsiveness of the sweat glands to cholinergic stimuli was also demonstrated, and histology revealed greatly enalrged glands. These results suggest that the hyperhidrosis is due to Increased glandular mass, although sweat gland hypersensitivity could notberuled out as an additional contributing factor to the hyperhidrosis. Local anticholinergic therapy was found to besuccessful in the treatment of all 3 patients.

Local Hyperhidrosis

“…It has been demonstrated that sweat glands of the hyperhidrotic area present increased sensitivity against both the muscarinic action of acetylcholine (direct sweat gland stimulation) and the nicotinic action (axon-reflex sweating). These findings are in agreement with the results of Cunliffe et al [1972], The immediate and abundant glandular response to the injected acetylcholine as well as to the nervous impulse eliciting the pheno menon presents similarities with acclimatization and the phenomenon of 'sweat gland training' described by Collins et al [1963]. The end of the hyperhidrotic crisis is attributed primarily to sweat gland fatigue and secondarily to mechanical obstruction of the sweal ducts, resulting from the hydration and swelling of stratum corneum during the crisis [Cunliffe et al, 1972], The mild erythema observed during the phenomenon is evidently due to release of kallikrein by the functioning sweat glands; kallikrein acting on globulins of the tissue fluids produces bradykinin with resultant vasodilation.…”

“…These findings are in agreement with the results of Cunliffe et al [1972], The immediate and abundant glandular response to the injected acetylcholine as well as to the nervous impulse eliciting the pheno menon presents similarities with acclimatization and the phenomenon of 'sweat gland training' described by Collins et al [1963]. The end of the hyperhidrotic crisis is attributed primarily to sweat gland fatigue and secondarily to mechanical obstruction of the sweal ducts, resulting from the hydration and swelling of stratum corneum during the crisis [Cunliffe et al, 1972], The mild erythema observed during the phenomenon is evidently due to release of kallikrein by the functioning sweat glands; kallikrein acting on globulins of the tissue fluids produces bradykinin with resultant vasodilation. This local vasodilator mechanism during the sweat gland activity is still debated [Guyton, 1977], The fact that the erythema was mild in comparison with the intense function of the sweat glands is an indication that this local vasodilator mechanism is of minor capacity and importance.…”

“…), as a result of surgical removal of the stellate ganglion [Gold stein, 1967;Cunliffe et al, 1972], or may be due to nerve pressure [Ellis, 1972]. It may be an atypical manifestation of gustatory sweating [Mellinkoff and Mellinkoff, 1950;Mellinkoff, 1951;Cunliffe et al, 1972] or it may finally be idiopathic [Lapiere, 1957;Goldstein, 1967;Cunliffe et al, 1972, Verbov, 1974, Few similar cases have been reported in the literature. Mainly thermal stimuli and also emotional stress have been accused as eliciting factors.…”

“…It has been proved that sweat glands of this region are more responsive to cholin ergic drugs. Cunliffe et al [1972] consider these conditions as 'functional naevi' and the detected enlargement of sweat glands [Lapiere, 1957] as secondary to the sweat gland hyperactivity.…”

Localized Unilateral Hyperhidrosis and Neurofibromatosis Type 1: Case Report of a New Association

“…Frey’s syndrome), associated with diabetes mellitus or parotid diseases [21, 22, 33]. Cutaneous diseases described in association with localized hyperhidrosis include palmoplantar keratodermas, glomus tumor, blue rubber bleb nevus, sudoriferous nevus, POEMS (polyneuropathy, organomegaly, endocrinopathy, M protein, skin changes) syndrome, speckled lentiginous nevus syndrome, Riley-Day syndrome, pachydermoperiostosis, Gopalan syndrome, causalgia, pretibial myxedema, Buerger disease and eccrine pilar angiomatous hamartoma, local injury and increased size of eccrine glands [5,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37]. LUH, without other cutaneous findings, may occur as a symptom of disease of the central nervous system or peripheral neuropathy, such as stroke, trauma, syringomyelia, tabes dorsalis or pressure on a nerve root caused by a benign or malignant condition such as cervical rib, vertebral osteoma, mesothelioma or pulmonary carcinoma [3, 4,6,7,8,9, 11, 33, 38].…”