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COMMENTS AND OPINIONS
Pathogenesis of Nonarteritic Anterior Ischemic Optic Neuropathy—Reply
Leonard A. Levin, MD, PhD;
Helen V. Danesh-Meyer, FRANZCO
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In reply
The premise of our hypothesis1 is that obstruction of venous outflow, rather than arterial hypoperfusion, is the causative mechanism of NAION. Vasodilating arteries secondarily block venous outflow in a tight compartment and thereby cause venous engorgement. In the anterior optic nerve head, the central retinal artery and vein share a common adventitial sheath. In a disc at risk, prolonged arterial dilation within the fibrous sheath would decrease optic nerve drainage to the central retinal vein via its tributaries, resulting in optic nerve head engorgement, hyperemia, and, ultimately, NAION.
Dr Hayreh asserts that because the optic nerve is different from the brain, having pial septa but not gray matter, it cannot have cytotoxic edema, vasogenic edema, or venous congestion. We agree that the optic nerve is different from the brain and does not contain neuronal cell bodies. But neither does . . . [Full Text of this Article]
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Hypothesis: A Venous Etiology for Nonarteritic Anterior Ischemic Optic Neuropathy
Leonard A. Levin and Helen V. Danesh-Meyer
Arch Ophthalmol. 2008;126(11):1582-1585.
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Pathogenesis of Nonarteritic Anterior Ischemic Optic Neuropathy
Sohan Singh Hayreh
Arch Ophthalmol. 2009;127(8):1082-1083.
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