LAUSR

T he advent of spectral domain and swept-source optical coherence tomography (SD-OCT and SSOCT, respectively) along with enhanced depth imaging (EDI), postprocessing shadow removal, and light attenuation compensation algorithms have improved the visualization of the deep structures in the optic nerve head including the anterior surface structure of the lamina cribrosa and sclera (1). These techniques have afforded the opportunity to visualize and quantify the in vivo morphology of the underlying load-bearing connective tissues of the optic nerve head (i.e., the peripapillary sclera and lamina cribrosa), the overlying neurovascular tissues lying within the rim and cup, and the surrounding peripapillary choroid. The ability to visualize these components of the optic nerve head provide an unprecedented opportunity to explore the differential effects of aging and disease on these regions of the optic nerve in the living eye. This is fueling the development of new biomarkers for glaucoma and, possibly, other optic neuropathies that have mechanistic relevance and may further serve to differentiate different types of optic neuropathies based on the differential effects within these tissues. The article in this issue of the Journal of Neuro-ophthalmology by Pérez-Sarriegui et al (2) is the first report of choroidal thickness in the macula and surrounding the optic nerve head in nonarteritic anterior ischemic optic neuropathy (NAION) using SS-OCT. Their findings are additive to a body of literature exploring the in vivo structural findings provided by SD-OCT and SS-OCT in NAION. Previous studies have suggested that the classic interpretation of the “disc-at-risk” may be inaccurate, namely that the optic nerve head may be “small” or “crowded” (3). Several SD-OCT studies have now shown that Bruch membrane opening (BMO), the anterior opening of the neural canal, is actually not smaller in patients with NAION than in age-matched controls (4–6). SD-OCT also has demonstrated that ophthalmoscopic identification by the clinician of the optic disc boundary often does not correspond to the location of BMO or the anterior scleral canal opening (7). This adds to the variability in the estimation of optic disc size, a critical factor in the diagnosis of glaucoma, and may explain these discrepancies seen with imaging based disc area. Interestingly, Pérez-Sarriegui et al found that both the involved and fellow eyes of patients with NAION had much thicker peripapillary choroid than control eyes. Their study confirms results from our group (8) and Fard et al (9) in finding a bilaterally thicker choroid in patients with NAION. By contrast, 1 previous study found a thinner peripapillary choroid in eyes with NAION and their fellow eyes when compared with control eyes (10). That study quantified choroidal thickness using only single horizontal and vertical b-scans centered on the optic nerve head with EDI SD-OCT and not a 3dimensional quantification of the entire surface. Moreover, there was no compensation algorithm used, which may have limited the visualization of the anterior sclera. Most importantly, the control group was significantly more hyperopic than the patients studied and this may have accounted for a thicker choroid found in the control group. Indeed, the control group had a choroidal thickness of over 180 mm, much thicker than that reported in any of the other studies. Table E5 found in the article by Pérez-Sarriegui et al, provides a helpful summary of this literature.