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Too Sweet to Eat: Delusional Hypergeusia
- S. Kalita, D. Birwatkar, A. Sundar, A.R Hirsch
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- Journal:
- CNS Spectrums / Volume 28 / Issue 2 / April 2023
- Published online by Cambridge University Press:
- 14 April 2023, pp. 225-226
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- Article
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Introduction
Delusional hypergeusia has not heretofore been reported.
Methods: Case reportA 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.
ResultsAbnormalities 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).
DiscussionPerhaps 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.
FundingNo Funding
Careful, Women! Is Orgasm Worth the Cost of Your Cerebellum? Flibanserin-Induced Cerebellar Dysfunction
- D. Birwatkar, S. Kalita, A.R Hirsch
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- Journal:
- CNS Spectrums / Volume 28 / Issue 2 / April 2023
- Published online by Cambridge University Press:
- 14 April 2023, p. 225
-
- Article
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- You have access Access
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Introduction
Flibanserin, a serotonin antagonist currently indicated for treatment of female sexual dysfunction disorder, has not heretofore been described to worsen cerebellar function. Such a case is presented.
MethodsA 60-year-old woman, 8 months prior to presentation, had an acute onset of fainting and hitting her head into a wall without loss of consciousness. She could not stand up, had left-sided weakness, and vomiting, with garbled, slow speech and severe headache. Findings in the emergency room showed a left cerebellar parenchymal hemorrhage of 3.2 x 3.1 x 2 cm with the epicenter at the dentate nucleus, extending medially towards midline into the cerebellar vermis, with surrounding perilesional edema extending into the middle cerebellar peduncle. Also, 5.2 cm of the hemorrhage extended from the petrous of the tentorium to the cerebellar vermis. Moreover, a ventral left thalamic hemorrhage with subependymal clot at the foramen of Monroe extended into the dependent portion of lateral ventricles without midline shift. Post one month of physical therapy, speech, walking, and coordination improved but she continued to have delayed speech and trouble getting up, with a wide stance.
ResultsNeurologic Examination: Cranial Nerve (CN) Examination: CN XI: Sternocleidomastoid hypertrophy, horizontal titubation. Motor examination: Drift test: L pronator drift with L abductor digiti mini sign. Gait examination: heel walking, dystonic posture of L hand. Tandem gait: unstable, wide based. Cerebellar examination: Both (B) finger-to-nose dysmetria, Left > Right. Slow rapid alternating movements (RAM) L Upper Extremity (UE). Due to absent sexual desire she started 100 mg of flibanserin nightly. Maintaining this for 5 weeks, her coordination markedly worsened with poor balance and a need for a cane to ambulate. She would stumble, with a wider gait, and found climbing stairs challenging. Physical examination displayed worse cerebellar function: prominent horizontal titubation. Finger-to-nose—dysmetria L>R. Decreased RAM, L UE. Markedly positive Holmes Rebound phenomenon, Bilateral UE. Tandem gait: unstable. A week post stopping flibanserin, gait and cerebellar examination returned to baseline.
DiscussionThe temporal correlation between the use of flibanserin and transient worsening of cerebellar function strongly suggests that this is the causative agent. Since serotonin is essential in cerebellar function, including its action on the cerebellar cortex and deep cerebellar nuclei, it strongly suggests that its action as a serotonin antagonist is the mechanism whereby flibanserin is causing cerebellar symptoms. In those on flibanserin, investigation to detect the presence of cerebellar dysfunction is warranted. Assessment for the presence of cerebellar dysfunction in those who are on anti-serotonin drugs, such as cyproheptadine and methysergide, may be worthwhile.
FundingNo Funding