Pathogenesis of Nonarteritic Anterior Ischemic Optic Neuropathy

Abstract

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.

Perioperative visual loss: what do we know, what can we do?

“…Specific mechanism and location of the vascular insult remain uncertain. 5 A rodent model for anterior ION (AION) has been described; its relevance to perioperative ION is not known. 9 Most knowledge is from individual case reports and case collections; the largest and best described single series is the ASA Postoperative Visual Loss Registry.…”

“…Mechanisms of injury with a crowded disc include axoplasmic flow mechanical obstruction or stasis, stiff cribriform plate, and decreased neurotrophic factor delivery to retinal ganglion cells after ischaemia. 5 Vasopressors Shapira and colleagues 88 showed an association between prolonged epinephrine infusions or long bypass time and ION in patients undergoing open-heart surgery. Lee and Lam 59 reported ION after lumbar spine fusion during which phenylephrine infusion maintained arterial pressure.…”

Nonarteritic anterior ischemic optic neuropathy with PDE-5 inhibitors for erectile dysfunction

“…21 A variety of other factors, such as vasospasm and impaired vascular autoregulation, might be important in the pathogenesis. 19 Consistently, however, the fellow (unaffected) eye has a small optic nerve head with a small or absent physiologic cup ( Figure 1a); this anatomic variant, which is associated with normal visual acuity and fields (Figure 1b), is well established as a marker for increased risk of NAION, although the exact means by which it influences pathogenesis is unclear. 19,22 The presence of this so-called 'disk at risk', which is usually a bilateral finding and more common in Caucasians, 23 could also partly explain the increased risk of NAION developing in the fellow eye.…”

“…19 In contrast with the arteritic form (AAION), where giant cell (temporal) arteritis causes inflammatory occlusion of the small vessels supplying the optic nerve head, the pathogenesis of the nonarteritic form (NAION) is not well understood. 19 As it is associated with diabetes and hypertension, it might occur as a result of atherosclerotic changes in these vessels, although the association with other atherosclerosis risk factors, such as smoking and dyslipidemia, is not as consistent. 18 As many patients with NAION wake with the visual loss, 20 it has been proposed that nocturnal hypotension could be an important etiologic factor.…”

Is There A Role for Intravitreal Pharmacotherapy in the Treatment of Acute Nonarteritic Ischemic Optic Neuropathy?

“…Inadequate perfusion of the optic nerve head deriving from the short posterior ciliary vessel plexus is the key mechanism in the development of acute NAİON [6] . However, a prevalent anatomic finding of a small or absent physiologic cup, which is common known as 'disc at risk', seems to play also an important role [6,7] .…”