Improvement in hypergeusia in response to alpha lipoic acid treatment has not heretofore been described. Such a case is presented.

Case Study: A 64 year old right handed nasute female noted the sudden onset of salty hypergeusia, about 200% saltier than foods should be. Concurrently she experienced a constant phantogeusia of salt involving the front half of her tongue, lips, and inside her mouth. She denied any smell problems, cacogeusia, or palinageusia. This persisted for five months until treatment with 1800mg/day of alpha lipoic acid, whereupon, over a one month duration, the salty hypergeusia gradually resolved. Suppression of the salty hypergeusia continued until she developed an upper respiratory infection, whereupon, despite the continuation of alpha lipoic acid, the salty hypergeusia returned to 250% of normal. During the cold, her ability to taste dropped down from 100% to 80%, and ability to smell dropped from 100% to 50% and upon resolution of the cold, the senses returned to normal and the salty hypergeusia remitted.

Abnormalities in Neurologic Examination: Reflexes: 3+ bilateral quadriceps femoris and pendular. Chemosensory testing: Olfaction: Alcohol Sniff Test: 12 (hyposmia), Phenylethyl Alcohol Threshold: greater than –2 (anosmia). Suprathreshold Amyl Acetate Odor Intensity Testing: parallel pattern (normosmia). Pocket Smell Test: 4(normosmia). Retronasal Olfactory Testing: Retronasal Smell Index: 8(normosmia). Gustatory testing: Propylthiouracil Disc Taste Test: 5(normogeusia). Taste Super threshold Testing: normogeusia to sodium chloride, sucrose, and phenylthiocarbamol: hypogeusia(10–30%) to urea; ageusia(0%) to hydrochloric acid. Taste Quadrant Testing: taste weakness to sodium chloride for the entire mouth.

The alpha lipoic acid may have acted to improve smell and associated enhanced retro nasal smell, inhibiting savory gustatory discharge, and thus, effectively reducing salt perception. Such a mechanism would also explain the recurrence of hypergeusia with the upper respiratory infection; the infection presumably transiently reducing the olfactory ability, overcoming any olfactory enhancing effects of alpha lipoic acid. On the other hand, this agent could have acted to improve smell as well as taste. With such enhanced chemosensory capacity, the normal olfactory and gustatory components of food would have inhibited competing pathologically discharging gustatory receptors for salt, reducing dysgeusia and hypergeusia. Moreover, the alpha lipoic acidmay have acted to focus the patient’s attention on the gustatory stimulation which may have caused her to perceive not just the predominant salt sensation but enhanced perception of the other gustatory sensations which acted to competitively inhibit the perception of salt. Further investigation of alpha lipoic acid in the management of dysgeusia and hypergeusia is warranted.