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Daniel Novakovic and Andrew Blitzer

Hyperhidrosis is a common condition characterized by perspiration in excess of that required to regulate body temperature. It may be divided into primary and secondary forms. Primary (idiopathic or essential) hyperhidrosis is a focal disorder usually involving the palms, soles of feet, axillae, or face.1,2 The onset of primary hyperhidrosis is usually during adolescence, and 30 to 50% of affected individuals report a positive family history, which suggests a genetic component. The genetic locus in primary palmar hyperhidrosis has been localized to chromosome 14.³ Sweating episodes may be triggered by various factors including spicy foods, emotional stressors, and mental or physical activity, but do not occur during sleep. These episodes can cause significant social and occupational dysfunction, as well as psychological stress. Secondary hyperhidrosis is characterized by generalized perspiration and is usually related to excess adrenergic stimulation due to an underlying disease such as endocrine dysfunction, neoplasia, or chronic infection.⁴ Autonomic dysfunction associated with neurologic disorders and medication side effects are less common causes. Gustatory hyperhidrosis (Frey’s syndrome) is a secondary focal variant most commonly seen after parotid gland surgery. It is discussed in Chapter 17.

Topical medical therapies for hyperhidrosis are available, but the results are often unsatisfactory. Topical aluminum salts in a concentration of 20 to 25% are an effective first-line treatment, but localized burning, stinging, and irritation may limit their use.⁵ Iontophoresis is a second-line therapy that involves delivering ions through the skin using electrical current. Local irritation and the fact that it is time-consuming limit the use of this modality.

Systemic drugs are primarily indicated in the treatment of secondary hyperhidrosis. Anticholinergic medications, including glycopyrrolate, oxybutynin, propantheline bromide, and benztropine, have been used with some success. Unfortunately, due to the relatively large doses that are required, a significant side-effect profile exists. Common side effects, including dry mouth, blurred vision, tachycardia, and urinary retention, limit the clinical efficacy of oral anticholinergic medication.6

Surgical treatments can be effective, but involve considerable risk. Endoscopic thoracic sympathectomy involves resection or ablation of the sympathetic ganglia. Reported response rates are high, with up to 86% of patients noting improvement in their quality of life.⁷ The response appears to be lower in plantar hyperhidrosis. The usefulness of surgery is limited by a high incidence of compensatory hyperhidrosis usually on the torso and lower limbs in up to 86% of patients.⁶ In addition, there is the risk of other more serious complications including Horner’s syndrome and neuralgia.⁵ Other surgical therapies exist, such as removal of axillary glandular tissue, but are not appropriate in the craniofacial region.

Botulinum neurotoxin (BoNT) irreversibly blocks presynaptic acetylcholine release at the neuromuscular junction, thus exerting its muscular paralysis effects. Because acetylcholine is also the primary neurotransmitter responsible for transmission at the cholinergic neurosecretory junction, BoNT has also been shown to be a safe and highly effective method of abolishing focal sweating in idiopathic hyperhidrosis. BoNT exerts its effects in a similar way by cleaving pre-synaptic SNARE proteins at two different sites. All of the A toxins cleave SNAP-25, and the B toxin cleaves VAMP. In comparison to effects on muscle, BoNT has a longer duration of action in inhibiting glandular secretion, a phenomenon that is poorly understood, but is likely due to glandular atrophy.⁸ OnabotulinumtoxinA (Botox) was initially described for palmar hyperhidrosis but is also used commonly for axillary hyperhidrosis and is the only BoNT approved by the Food and Drug Administration (FDA) for treatment of hyperhidrosis.^9–13 However, incobotulinumtoxinA (Xeomin), abobotulinumtoxinA (Dysport), and other type A toxins currently in trials will likely show similar activity.

Böger et al¹⁴

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