- 著者
-
三輪 高喜
- 出版者
- The Society of Practical Otolaryngology
- 雑誌
- 耳鼻咽喉科臨床 (ISSN:00326313)
- 巻号頁・発行日
- vol.103, no.12, pp.1073-1081, 2010-12-01
- 被引用文献数
-
1
Remarkable progress has been made in basic research on the sense of smell during the last few decades. This progress has been accelerated by the discovery made by Axel and Buck of the genes that encode olfactory receptors. These rescarchers won the Nobel Prize in Physiology or Medicine in 2004. The detection and discrimination of odor molecules in humans is mediated by 388 olfactory receptors that are expressed on olfactory sensory neurons. A basic understanding of the mechanism of odor reception is crucial to an understanding of olfactory dysfunction. Olfactory disorders can be classified as quantitative or qualitative disorders. The former category includes the deterioration or total loss of olfactory sensation, while the latter category includes distortions of the sense of smell. Quantitative olfactory disorders can be classified by the area affected by the disease into four major groups: (1) sino-nasal, (2) olfactory mucosa, (3) olfactory fila, and (4) central pathway. Chronic rhinosinusitis, which is the most frequent cause of olfactory disorders, is caused by the conductive loss of odor molecules. The second most common cause is postviral olfactory disorders occurring after an upper respiratory tract infection. The prognosis for olfactory function in individuals affected by these causes is relatively good. However, olfactory loss caused by neural disorders, such as posttraumatic olfactory loss, has a poor prognosis. Dysosmia, or a distorted sense of smell, is mainly caused secondary to postviral or posttraumatic olfactory disorders. Dysosmia is classified as either parosmia or phantosmia. Parosomia occurs in patients who are unable to correctly identify odors, while phantosmia involves the smelling of odors that are not derived from any physical stimulus. The mechanism of dysosmia has been clarified by basic research on olfactory reception and conduction.<br>