Taste Damage: Previously Unsuspected Consequences

Abstract

Studies using anesthesia provide insights into oral phantoms. The chorda tympani nerve is accessible for anesthesia at two sites. First, the chorda tympani leaves the tongue with the lingual nerve (CN V) and the two travel through the pterygomandibular space. The inferior alveolar nerve, which conveys pain from the lower teeth, passes through the same space; thus dental anesthesia abolishes taste and touch as well as pain. Secondly, the chorda tympani passes through the middle ear after separating from the lingual nerve, so injection of an anesthetic just under the skin near the ear drum anesthetizes taste but not touch. Using both procedures, we showed that anesthesia of the chorda tympani intensifies tastes evoked from the contralateral rear of the tongue, the area innervated by the glossopharyngeal nerve (Lehman et al., 1995; Yanagisawa et al., 1998). This finding supports the earlier evidence of Halpern and Nelson (1965) for central inhibitory connections between the chorda tympani and glossopharyngeal nerves. This inhibition acts as a constancy mechanism: when one nerve is damaged, its input to the central nervous system (CNS) is reduced, releasing inhibition on other taste structures and thus compensating for the loss of input from the damage. During our anesthesia experiments, about half of the subjects developed taste phantoms typically localized to the contralateral rear of the tongue (Yanagisawa et al., 1998). This suggested that clinical taste phantoms (i.e. dysgeusia) might be the result of localized taste damage. Indeed, we have found taste damage in patients reporting taste phantoms (Bartoshuk et al., 2002).