{"title":"缺血性视神经病变:疾病机制的模型。","authors":"S V Potarazu","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Anterior ischemic optic neuropathy (AION) is an entity which involves infarction of the optic disc head. Factors involved with the arteritic variety are well understood, but less is known about the more common nonarteritic variety. A better understanding of variations between blood pressure and intraocular pressure could provide more information about circulation to the optic nerve head itself. Furthermore, the role of autoregulation at the optic nerve head (or lack of) as well as the role of vascular endothelium-mediated factors could play a large role in the disease. At a cellular level, axonal damage from ischemia appears to be mediated by sudden ionic shifts. A significant messenger in this process is a sodium-mediated calcium transporter which facilitates the influx of calcium ions leading to activation of proteolytic enzymes and ultimately axonal death. Various treatment options thus exist by either blocking calcium channels or inhibiting the transporter in order to prevent further axonal damage.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 5","pages":"264-9"},"PeriodicalIF":0.0000,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ischemic optic neuropathy: models for mechanism of disease.\",\"authors\":\"S V Potarazu\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Anterior ischemic optic neuropathy (AION) is an entity which involves infarction of the optic disc head. Factors involved with the arteritic variety are well understood, but less is known about the more common nonarteritic variety. A better understanding of variations between blood pressure and intraocular pressure could provide more information about circulation to the optic nerve head itself. Furthermore, the role of autoregulation at the optic nerve head (or lack of) as well as the role of vascular endothelium-mediated factors could play a large role in the disease. At a cellular level, axonal damage from ischemia appears to be mediated by sudden ionic shifts. A significant messenger in this process is a sodium-mediated calcium transporter which facilitates the influx of calcium ions leading to activation of proteolytic enzymes and ultimately axonal death. Various treatment options thus exist by either blocking calcium channels or inhibiting the transporter in order to prevent further axonal damage.</p>\",\"PeriodicalId\":79395,\"journal\":{\"name\":\"Clinical neuroscience (New York, N.Y.)\",\"volume\":\"4 5\",\"pages\":\"264-9\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1997-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical neuroscience (New York, N.Y.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical neuroscience (New York, N.Y.)","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Ischemic optic neuropathy: models for mechanism of disease.
Anterior ischemic optic neuropathy (AION) is an entity which involves infarction of the optic disc head. Factors involved with the arteritic variety are well understood, but less is known about the more common nonarteritic variety. A better understanding of variations between blood pressure and intraocular pressure could provide more information about circulation to the optic nerve head itself. Furthermore, the role of autoregulation at the optic nerve head (or lack of) as well as the role of vascular endothelium-mediated factors could play a large role in the disease. At a cellular level, axonal damage from ischemia appears to be mediated by sudden ionic shifts. A significant messenger in this process is a sodium-mediated calcium transporter which facilitates the influx of calcium ions leading to activation of proteolytic enzymes and ultimately axonal death. Various treatment options thus exist by either blocking calcium channels or inhibiting the transporter in order to prevent further axonal damage.