味觉错觉临床1例调查

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摘要

味觉亢进是一种味觉障碍,伴随着味觉感知的增加。妄想性癔症至今未见报道。病例报告:一名62岁的右撇子妇女在接触溶剂香气后描述了大量的抱怨,包括头痛,弥漫性虚弱,疲劳,幻觉气味和味道,灼口综合征和恐慌发作。她最严重的症状是咸的味道是正常的800%。糖也太甜了,是正常的600%。结果:运动检查:漂移试验:右旋前肌漂移伴右外展指最小征。步态检查:脚跟行走,双侧手臂摆动减少。反射:双侧股四头肌3+,左(L)霍夫曼反射阳性。复古鼻嗅觉测试:复古鼻嗅觉指数:1(嗅觉缺失)。无水经验性味觉测试:甜:4,酸:3,咸:7,苦:5,浓:0,共:30(老味子至Unami,否则为normogeusia)。神经精神测试:Go-No-Go测试:2/6(异常)。讨论:也许,嗜睡症可能不是真的,但对复古鼻气味的误解与嗜睡症的生理联觉表现为味觉。妄想性嗜睡可能会因潜在的阅读障碍而加剧感觉上的误解。这可能是错觉的双因素假说的一种变体,即扭曲的感官知觉在错觉中被歪曲。通常负责检查左脑的右半球功能紊乱,使错觉得以显现。虽然两种不同的解剖异常(一个左半球和一个右半球)被认为是这种错觉的基础,但很明显,顶叶下小叶的单一损伤可能足以产生感觉扭曲,以及右侧顶叶对额叶扭曲感觉的妄想解释的抑制丧失,这是感觉假说。对于那些表现出亢进的人来说,寻找妄想的起源是有保证的。结论:对于那些表现出重度焦虑症的患者,对妄想起源的搜索是有保证的,而对于那些表现出妄想的患者,对感知重度焦虑症的查询可能是有启示的
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Investigating a Clinical Case of Deluded Gustatory Perception
Introduction: Hypergeusia is a taste disturbance with an increased perception of taste. Delusional hypergeusia has not heretofore been reported. Case Report: 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 the salty taste was 800% normal. Sugar was also too sweet, 600% of normal. Results: Motor Examination: Drift Test: right pronator drift with right abductor digit minima sign. Gait Examination: heel walking with bilateral decreased arm swing. Reflexes: bilateral quadriceps femoris 3+, positive left (L) Hoffman’s reflex. Retro nasal Olfactory Testing: Retro nasal Smell Index: 1 (Anosmia). Waterless Empirical Taste Test: sweet: 4, sour: 3, salty: 7, bitter: 5, brothy: 0, total: 30 (ageusia to Unami, otherwise normogeusia). Neuropsychiatric Testing: Go-No-Go Test: 2/6 (abnormal). Discussion: Perhaps, hypergeusia may not have been true, but a misperception of retro nasal smell associated hypersomnia with physiologic synesthesia manifested as taste. The perceived delusional hypersomnia may intensify the sensory misperception due to 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 usually 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 sensorial hypothesis. A search for delusional origin is warranted for those who present with hypergeusia. Conclusion: In those who present with hypergeusia, a search for delusional origin is warranted, and for those who present with delusions, a query to perceive hypergeusia may be revealing
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