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infarction, based on the congested appearance of the optic nerve head in the
acute phase and analysis of specific risk factors such as spine surgery, sleep
apnea, and use of phosphodiesterase-5 inhibitor drugs ( Levin & Danesh-
Meyer, 2008 ).
Until recently, the lack of an animal model for NAION made it difficult
to explore the disease in the laboratory, and particularly, to develop therapies
for what has long been an untreatable disease ( Arnold & Levin, 2002 ). The
development of a rat model of anterior ischemic optic neuropathy
( Bernstein, Guo, Kelman, Flower, & Johnson, 2003 ) was a significant
advance and was extended to mice and nonhuman primates ( Chen et al.,
2008; Goldenberg-Cohen et al., 2005 ). Although this model relied on
photosensitizer-dependent photic occlusion of small disc vessels, which is
somewhat different from what happens in the human disease, it shares
with NAION the critical features of ischemic axon injury at the optic
nerve head without secondary retinal infarction.
Arteritic anterior ischemic optic neuropathy ( AAION ) is an anterior ischemic
optic neuropathy where the etiology is an inflammatory occlusion of the
posterior ciliary arteries that supply the optic nerve head. The cause is almost
always giant cell arteritis, a vasculitis that is only seen in older individuals, and
involves a Th1- and Th17-dependent immune dysregulation that is aging
related ( Deng, Younge, Olshen, Goronzy, & Weyand, 2010; Mohan,
Liao, Kim, Goronzy, & Weyand, 2011 ). Unlike NAION, where the disc
is congested, in AAION, the disc appears not only swollen but also pale,
implying decreased arterial perfusion. This is the result of vasculitic
occlusion of the supplying vessels and is therefore somewhat akin to
other central nervous system strokes caused by vasculitis.
Both NAION and AAION are anterior optic nerve diseases and require
the presence of disc edema to be present in the acute phase. Much less com-
mon are the posterior ischemic optic neuropathies, where there is no disc
edema because the infarct is in the posterior optic nerve. Etiologies include
shock, spine surgery, giant cell arteritis (or other vasculitides), and radiation
in the distant past. Although the effects of ischemia on retinal ganglion cell
axons superficially appear the same whether the disease is in the anterior or
posterior optic nerve, the nonaxonal compartments are critically different
between these locations. The human optic nerve only becomes myelinated
posterior to the optic nerve head, in the retrolaminar region, and thus an-
terior ischemic optic neuropathies affect the unmyelinated portion (as well as
some myelinated axons). Thus, the energy demands of ischemic axons are
likewise different. Also, the glial compartment within the optic nerve head
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