No CrossRef data available.
Article contents
193 A New Syndrome: Phantogeusia-Induced Phantosmia
Published online by Cambridge University Press: 15 June 2018
Abstract
While phantosmia-induced phantogeusia has been described (Ahmed, 20173), the reverse, phantogeusia-induced phantosmia, has not heretofore been described. Such a case is presented.
Case Study: A 39-yr-old left-handed (pathological) male, six years prior to presentation, noted a sudden onset of phantogeusia of roast cooking, pizza, fruit, strawberries, or a sour taste, and shortly thereafter he would develop unpleasant phantosmias which would sometimes combine with the ambient aroma. These would occur 3-10 times per week and would last for the duration of the phantogeusia, for as long as 1-2 hours. Occasionally the phantosmia would occur first and then induce the phantogeusia of asour taste.
Abnormalities in Neurologic examination: Mental status examination: Immediate recall: Digit span: 6 digits forward and 3 digits backwards. CN XI, X: Decreased gag bilaterally. Motor Examination: Drift: left pronator drift with right abductor digiti minimi sign and right cerebellar spooning. Gait Examination: Tandem Gait: unstable. Cerebellar Examination: Holmes Rebound Phenomena: bilaterally positive, left greater than the right. Sensory Examination: Ipswich Touch Test: decreased in left lower extremity. Temperature: decreased in left lower extremity. Rydel-Seiffer Vibratory Test: bilateral upper extremities 5, bilateral lower extremities 3. Reflexes: upper extremities 1+, absent lower extremities. Neuropsychiatric Examination: Go-No-Go Test: 6/6 (normal). Animal Fluency Test: 15 (normal). Clock Drawing Test: 3 (abnormal). Center for Neurologic Study Lability Scale: 16 (Pseudobulbar affect).
Close connection of the tertiary smell and taste integration areas, where smell and taste converge, in the posterior orbitofrontal cortex, anterior to the insular taste cortex, and posterior to the granular orbitofrontal cortex may have allowed activation of memory engrams connecting these two (Rolls, 19944). Alternatively, electrical discharge from the primary taste area may have spread to involve the cortical representation of smell. Since the cortical area involved in the interpretation and hedonics of taste co-localize with the area involving olfactory hedonics, spread from one area to the other area may occur. As a result of electrical discharge (from an epileptiform focus) or as a result of well-connected and developed memory engrams with associated hedonics, phantom tastes may induce phantom smells. Alternatively, this may represent a distorted retronasal smell whereby the olfactory component of the gustatory hallucination causes a discharge of the olfactory epithelium (a pseudoretronasal smell).
Given the above, treatment of those with both phantosmia and phantogeusia may respond to treatment of phantogeusia alone. Under this construct, the phantosmia is the slave of the phantogeusia whereby management of the taste hallucination will thus eliminate the smell hallucination.
Smell and Taste Treatment and Research Foundation.
- Type
- Abstracts
- Information
- Copyright
- © Cambridge University Press 2018