Biology Reference
In-Depth Information
eye, that is, the mechanism by which changes in IOP could affect the retinal
ganglion cell axons, glia, and vasculature at the optic nerve head. This area
has become a leading subject of investigation in the field because it ties
together IOP with the mechanism leading to axon loss in glaucoma
(
Burgoyne & Downs, 2008; Sigal, Flanagan, Tertinegg, & Ethier, 2009a,
2009b
).
Although it has been suggested that the pathophysiology of glaucoma
could be due to primary retinal ganglion cell (soma) disease, it has been in-
creasingly recognized that the disease involves axon injury and glial changes
at the optic nerve head itself. This evidence includes the morphology of the
progressive visual field defects (
Boden et al., 2002; Levin, 2001
),
pathological study of human eyes and optic nerves, and a variety of
experimental assays in animal models of glaucoma (
Howell et al., 2007;
Soto et al., 2008
). The pathophysiology of retinal ganglion cell axon and
cell body degeneration in glaucoma has recently been comprehensively
reviewed (
Almasieh, Wilson, Morquette, Cueva Vargas, & Di Polo,
2012
) and will not be discussed further.
2.2. Ischemic optic neuropathy
Ischemic optic neuropathy is the optic nerve equivalent of a stroke, in that it
shares the rapidonset, poor recoveryof function, andpathological evidence of
infarction. However, in the same way that there are different types of strokes,
for example, embolic, hypoxic, hemorrhagic, etc., there are different types of
ischemic optic neuropathy, each with different pathogenic mechanisms.
Nonarteritic anterior ischemic optic neuropathy
(
NAION
) is the most common
ischemic optic neuropathy. The term “nonarteritic” is to distinguish it from
the less common arteritic ischemic optic neuropathies (see below). The term
“anterior” is used because it occurs at the most anterior part of the optic
nerve and is manifested acutely by an edematous optic nerve head. NAION
is almost always seen in individuals 50 years of age or older, unless there is
another risk factor such as diabetes, disc drusen (calcific deposits in the optic
nerve head), or systemic hypotension.
Curiously, NAION is dissimilar to stroke in that there are no signs of
emboli, thrombosis, or other vascular occlusive disease. Instead, the disease
resembles a compartment syndrome, where there is a relentless cycle of
infarction, edema, and consequent closure of small vessels within the confines
of the scleral canal (
Tesser, Niendorf, & Levin, 2003
). We have proposed
that NAION may be more similar to a venous infarction than to an arterial
