Based on histopathology, electron microscopic corrosion cast studies, optic nerve blood flow studies, and clinical data, the pathogenesis of idiopathic nonarteritic ischemic optic neuropathy includes the following features: (1) structurally crowded optic discs are predisposed; (2) laminar and retrolaminar regions are the most common locations for infarction; (3) there is flow impairment in the prelaminar optic disc during the acute phase; (4) lack of consistent choroidal flow impairment and the retrolaminar location of infarcts suggest vasculopathy within or distal to the paraoptic branches of the posterior choroidal arteries; (5) diabetes is the most consistently identified vasculopathic risk factor; (6) impaired autoregulation of the disc circulation by atherosclerosis, with a possible contribution from serotonin and endothelin-mediated vasospasm, may play a role; and (7) progression may be caused by secondary cell death after the initial ischemic insult or compression from cavernous degeneration and mechanical axonal distortion.
