Gustatory sweating was first linked to diabetes mellitus by Watkins (75), and is now known to occur quite commonly in patients with either diabetic nephropathy or neuropathy (76). The syndrome consists of localized hyperhidrosis of the face during meals. The mechanism of gustatory sweating is not proven, but is considered to be because of sympathetic postganglionic denervation followed by aberrant reinnervation by parasympathetic fibers. It is suggested that sympathetic cholinergic fibers to eccrine sweat gland are lesioned. These denervated sweat glands are thought to become rein-nervated by misdirected cholinergic parasympathetic fibers. Evidence cited usually emanate from surgical lesions (77). In diabetic autonomic neuropathy, the sympathetic denervation that occurs in sweat glands might be compensated by reinnervation of aberrant parasympathetic fibers stemming from the minor petrous nerve, and normally innervating the parotid gland through the auriculotemporal and facial nerve, after being relayed in the otic ganglion (78). Thus, sweating occurs in the reinnervated area when salivation is induced on cholinergic stimulation (food ingestion).
The symptom can be troublesome and embarrassing. Occasionally it affects food intake to the degree that it could make glycemic control difficult. As sweating is controlled by sympathetic cholinergic pathways, treatment has traditionally involved oral anticholinergic drugs, but the acceptability of these to patients is low because of systemic side effects. Topical antimuscarinic agents, such as glycopyrrolate, have been demonstrated to be effective in controlling gustatory sweating caused by parotid surgery and in diabetic gustatory sweating (79,80). Gustatory sweating and flushing within and surrounding the cutaneous distribution of the auriculotemporal nerve (Frey's syndrome), can develop after surgery or trauma to parotid gland. Surgery as resection of the glos-sopharyngeal nerve (which supplies the otic ganglion and hence the auriculotemporal and buccal nerves with parasympathetic fibers) abolishes the syndrome (81,82). A better approach is the injection of botulinum toxin into the symptomatic skin to treat pathological gustatory sweating (83,84). This obviously is a major advance in treatment because it is far simpler and less invasive than sectioning parasympathetic nerves intracranially (85). Botulinum toxin enters cholinergic neuron terminals and prevents the exocytotic release of acetylcholine. As parasympathetic secretomotor fibers use acetylcholine as a neurotransmitter, and sweat glands have cholinergic muscarinic receptors, botulinum toxin abolishes the cholinergic activation of sympathetically-denervated sweat glands during salivation.
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