The Place of Botulinum Toxin Type A in the Treatment of Focal Hyperhidrosis

N. Lowe; A. Campanati; I. Bodokh; S. Cliff; P. Jaen; O. Kreyden; M. Naumann; A. Offidani; J. Vadoud; H. Hamm


The British Journal of Dermatology. 2004;151(6) 

In This Article


The eccrine sweat glands are concentrated in the palms, soles and axillary areas of the body and it is estimated that each person has around 2–4 million of such glands.[1] The eccrine gland consists of a layer of single cells arranged in a coil, with this coil of cells surrounded by myoepithelial cells that contract on stimulation from sympathetic nerves. These nerves use acetylcholine as their neurotransmitter.[1,2] Thus, sweating is under the control of both circulating catecholamines and sympathetic innervation, although studies at the cellular level have also shown the involvement of cyclic adenosine monophosphate (cAMP) in sweating.[3] In the majority of hyperhidrotic patients the sweat glands are morphologically normal, but what is abnormal is the neurological response to stimuli in the hypothalamic sweat centres.[1] However, in some patients (both with and without hyperhidrosis) an unusual hybrid sweat gland has been described that has both eccrine and apocrine elements and has been found to be capable of a secretory rate 10 times higher than a normal eccrine gland.[4]

Hyperhidrosis may be defined as excessive sweating beyond what is required to return elevated body temperature to normal.[5] It may be primary (idiopathic, essential) or secondary to a number of medical conditions or prescribed drugs.[2] Hyperhidrosis can be local or generalized, and commonly affects the underarms (axillary hyperhidrosis), palms of the hands (palmar hyperhidrosis), the soles of the feet (plantar hyperhidrosis) and the face (facial hyperhidrosis).[6] Causes of hyperhidrosis include genetic, metabolic, hormonal or idiopathic pathology, with the main causes being shown in Table 1 . There seems to be a genetic predisposition to primary hyperhidrosis and it often manifests itself in childhood or puberty. Essential or focal hyperhidrosis characteristically does not occur during sleep, but is made worse by heat and emotional situations, since it is thought that the hypothalamic sweat centres are more sensitive to emotional stimuli than in nonhyperhidrotic subjects.[7]

Sweat rates are highly variable between individuals and are thought to be a factor of acclimatization, sex, age and possibly diet.[8] However, it is estimated that 0·6–1·0% of the population suffers from primary or essential hyperhidrosis[7] and in many it can become chronic and can lead to significant disruption in both social and professional life, leading to a marked impact on the patient's quality of life (QOL). Patients find the symptoms embarrassing and often complain that the anticipation of sweating leads to avoidance of certain activities.[3] In particular, axillary sweating causes social embarrassment and can cause staining and rotting of clothes. In addition, the profuse sweating can also result in odour production,[9] and in severe cases can lead to painful skin maceration, which can, in turn, lead to secondary infection, such as tinea pedis, viral warts and dermatitis.[10]

It is imperative to strive continually to improve the quality of clinical trials and the subsequent standards of care provided to patients. In this respect, a guide is provided for assessing the evidence base for each of the clinical studies under review using a scale for the quality of evidence comprising categories Ia–IV (see Table 2 ).