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L. A. Levin, H. V. Danesh-Meyer; Focal Venous Congestion: A Mechanism for the Pathogenesis of Non-Arteritic Anterior Ischemic Optic Neuropathy. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4411.
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Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common acute optic neuropathy in those over age 50. In most cases its etiology and pathogenesis are unknown, and there is no effective treatment. The most commonly accepted risk factor is a small cup-to-disk ratio in the optic nerve head. It is generally assumed that NAION occurs as a result of microvascular arterial ischemia. We propose a venous congestion mechanism for NAION that better explains its idiosyncratic features.
Known risk factors (small cup:disk ratio, age, diabetes, hypotension, spine surgery, PDE5 inhibitor use) and unusual clinical features (primarily inferior visual field involvement, low prevalence of recurrence) for NAION were catalogued, and common features analyzed. These were then correlated with optic nerve arterial and venous anatomy to produce a unifying mechanism that accords with epidemiological, clinical, and histological features of the disease.
We propose that focal venous congestion is the initiating step in NAION, resulting from either downstream venous hypertension (e.g. prolonged head-down position, sleep apnea), arterial vasodilation (PDE5 inhibitors, hypotension), or venous obstruction as the central retinal vein exits the nerve (sleep-associated doll’s eye reflex). The venous congestion creates a compartment syndrome in an optic nerve that is anatomically predisposed (small cup:disk ratio), leading to secondary venous occlusive disease. The commonly observed superior optic nerve loss results from the anatomical relation of the CRA and CRV within its shared sheath.
NAION has more in common with venous occlusive disease than arterial occlusive disease. If validated, this mechanism may suggest novel strategies for treating NAION.
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