Gustatory sweating revisited: the unitary hypothesis for its pathogenesis

Abstract

We made a review on the nature of physiological gustatory sweating in the 1st part of this article. The 2nd part is focussed to the pathogenesis of pathological gustatory sweating. Pathological gustatory sweating includes auriculo-temporal syndrome (Frey syndrome), post-sympathectomy gustatory sweating, diabetic gustatory sweating, etc. Auriculo-temporal syndrome is gustatory sweating and flushing in the distribution of the auriculo-temporal nerve following injury, operation, or inflammation of the parotid gland. Thermoregulatory sweating seems to be preserved in most cases. Glaister et al. (1958) reported that gustatory sweating in auriculo-temporal syndrome was abolished by blocking the otic ganglion, but unaffected by cervical sympathectomy, confirming that gustatory sweating was mediated by the parasympathetic fibers. It is widely accepted that auriculo-temporal syndrome is resulted from misdirection of the regenerating parasympathetic fibers to sweat glands. Post-sympathectomy gustatory swating is coexistent with decrease in thermoregulatory sweating in the same side, and lacking facial flushing. Although recent articles describe that the pathogenesis of post-sympathectomy gustatory sweating is uncertain, Guttmann (1931) had postulated that sweat glands received dual innervation from the sympathetic and the parasympathetic nerves, and that loss of the sympathetic innervation enhanced parasympathetic sweating. We assume that all variants of pathological gustatory sweating develop by disinhibition of gustatory-sudorific reflex, the efferent pathway of which comprises both sympathetic and parasympathetic fibers (see the 1st part). While parasympathetic sweating is suppressed by the sympathetic activity in the physiological condition, it may be manifested by loss of the sympathetic innervation.