Delusional hypergeusia has not heretofore been reported.

A 62-year-old right-handed woman described a plethora of complaints after exposure to a solvent aroma, including headaches, diffuse weakness, fatigue, hallucinated smells and tastes, burning mouth syndrome, and panic attacks. The apogee of her symptoms was that salty taste was 800% of normal, making food taste disgustingly salty. She was unable to tolerate potato chips, pizza, spaghetti sauce, Coca Cola, root beer, Sprite, 7 Up, and even bottled water. Sugar was also too sweet, 600% of normal. Foods which were unbearably sweet included cookies, sugar, and breakfast cereals. Sour and bitter were normal.

Abnormalities in Neurological Examination: Mental Status Examination: hyperverbal, loud, overly inclusive, irritable with pressured speech; disheveled, racing thoughts, and tangential. Motor Examination: Drift Test: right pronator drift with right abductor digiti mini sign. Gait Examination: heel walking with bilateral decreased arm swing. Reflexes: bilateral quadriceps femoris 3+, positive left (L) Hoffman’s reflex. Chemosensory Testing: Olfaction: Brief Smell Identification Test: 12 (normosmia). Retronasal Olfactory Testing: Retronasal Smell Index: 1 (Anosmia). Gustatory Testing: Propylthiouracil Disc Taste Test: 10 (normogeusia). Waterless Empirical Taste Test: sweet: 4, sour: 3, salty: 7, bitter: 5, brothy: 0, total: 30 (ageusia to umami, otherwise normogeusia). Neuropsychiatric Testing: Go-No-Go Test: 2/6 (abnormal).

Perhaps hypergeusia may not have been true hypergeusia but a misperception of retronasal smell associated hyperosmia with physiologic synesthesia manifested as taste. Peradventure, the perceived hypergeusia, is just one component of a generalized delusional paradigm, where many sensory perceptions are intensified. The perceived delusional hyperosmia may be intensification of the sensory misperception due to an underlying dysgeusia. This may represent a variant of the two-factor hypothesis of delusions whereby a distorted sensory perception is then misrepresented in a delusion. Dysfunction of the right hemisphere, which normally acts to censor the left, allows the delusion to manifest. While two different anatomical abnormalities (one left and one right hemisphere) have been postulated to be the foundation of such delusions, it is distinctly possible that a single lesion of the inferior parietal lobule may be sufficient for both sensory distortions to be produced as well as loss of inhibition of delusional interpretation of distorted sensation of the frontal lobe by the right parietal lobe, yclept the sensorialist hypothesis. In those who present with hypergeusia, search for delusional origin is warranted and in those who present with delusions, query as to perceived hypergeusia may be revealing.

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