Nonarteritic anterior ischemic optic neuropathy (NAION): A misnomer. A non‐ischemic papillopathy caused by vitreous separation

Abstract

PurposeVascular abnormalities such as disc hemorrhages and swelling present at the time of visual loss in NAION, followed by peripapillary vascular narrowing and ensuing disc pallor is enticing, but not etiologically conclusive for ischemia. Optic disc as well as retinal findings of whiteness with disc swelling is indicative of axoplasmic stasis that may also occur simply from anatomic distortion of axons rather than occlusion of vessels. It may also occur from mechanical stretching with fracture of the axonal cytoskeleton.MethodsReview of the literature regarding (1) vitreous attachments and effects of separation from the optic disc, (2) dynamic shear force stretch injury to axons.ResultsWithin the normal population and in the age‐goup in which NAION occurs, 10% have complete PVD, 70% partial PVD, and 20% no PVD. In those with acute NAION, however, either total vitreous separation from the disc, or complete parapapillary detachment, is always present. Any teleangectatic vessels on the disc surface correspond to areas of visual field sparing and encompass areas of unseparated vitreous still under tension.ConclusionsWhere internal limiting membrane is absent over the disc and peripapillary retina, most notably in cupless discs where epipapillary membrane adhesions are strongest, vitreous separation may momentarily stretch and elongate axons, breaking the cytoskeleton in more aged and less distensible axons, leading to immediate axoplasmic accumulation and atrophy in the prelaminar sites of separation. Vitreous synchysis occurs more precociously in diabetics. Ischemic pathophysiology need not be invoked in so‐called NAION, better termed papillary vitreous detachment, or PVD‐N. In those at risk, the timely and controlled release of vitreous connections to the optic disc may prevent such optic disc injury.