The Pathogenesis of Nonarteritic Anterior Ischemic Optic Neuropathy

Although nonarteritic anterior ischemic optic neuropathy (NAION) is known to occur as a result of ischemic insult to the anterior portion of the optic nerve, its etiology and pathogenesis remain elusive. Because NAION is a nonfatal condition, acute, postmortem histopathologic analysis has never been undertaken. Animal models of NAION have been created with the use of an iodinated derivative of fluorescein, rose bengal. When rose bengal is stimulated with the use of a frequency-doubled neodymium-Yttrium aluminium garnet (YAG) laser diode, vascular endothelial damage may be induced in a precise and focal manner, within the anterior optic nerve. Primate and nonprimate animal models of NAION differ from the human pattern of NAION in the duration of the disease course, as well as the anatomy. The rat lamina cribrosa contains a differing connective tissue structure, which may result in a differing pathogenesis of ischemic insult. Optic disk swelling resolves within 5 days in rats and 14 days in primates; in humans, it is known to persist for up to 6 weeks. Animal models have nonetheless enabled a deeper understanding of the underlying patho-logic processes in NAION.