Conflict of interest
Optic neuritis/multiple sclerosis
Ischemic optic neuropathy
Morphological changes comprise severe swelling after onset of AION, which rapidly turns into atrophy. Contreras et al. reported that prostaglandin receptor mean OCT-measured RNFL thickness increased to 96.4% in the affected eye compared with the fellow eye at the onset of nonarteritic AION (NAION). Already after 2months, more than 80% of the patients showed a RNFL thinning. Progressive RNFL thinning between month 2 and month 4 suggests ongoing atrophy, whereas a stable morphologic end point is reached after month 6.
In the acute phase of AION, optic disk and axonal swelling prevents by RNFL thickening to detect axonal damage. As previously commented in anterior ON, a useful alternative approach is to analyze GCL. Kupersmith demonstrated that at 1month, only 10% eyes with NAION had RNFL loss, while 76% had GCIPL thinning. Therefore GCL thinning can be detected prior to RNFL loss, and could be a biomarker of early structural loss in AION (Fig. 6).
A cupping enlargement is a well-known characteristic of AION caused by giant cell arteritis. Although milder, OCT has also demonstrated an enlargement of cupping after NAION (around 50% of eyes had a cup to disk ratio that differed from that in the fellow eye by more than 0.1).
It has been hypothesized that most of the VA loss after a NAION episode depends on the severity of the damage to the papillo-macular bundle (PMB). In fact, in eyes with significantly lower VA, the RNFL thickness of the temporal quadrant by Stratus-OCT was almost 40% lower than that of the fellow eye. Moreover there is a significant correlation between nasal macular thickness by Stratus-OCT and VA in patients with AION.
OCT can identify different patterns of RNFL involvement specific to different classic visual field (VF) defects in eyes with NAION. Bellusci et al. reported that eyes with VF defect confined to the inferior hemifield had RNFL involvement limited to the temporal, superior and nasal optic disk quadrants. Diffuse RNFL damage involving all quadrants around the disk was observed in eyes with diffuse VF loss and eyes with central or centro-cecal scotoma revealed RNFL atrophy limited to the superior and temporal sectors of the disk.
Macula and GCL are also thinner in NAION eyes and show stronger correlation with VF than RNFL parameters. With newer automated segmentation software thinning of individual macula layers including RNFL, inner plexiform and GCL can be detected (ongoing study).
Macular analysis by OCT can demonstrate subretinal fluid in around 12% patients with NAION that may contribute to some of the visual loss associated with this condition and could account for some of the visual improvement that can follow after its resolution (Fig. 7).
Controversy exists regarding the optic disk size in NAION. Although subjects suffering NAION have lower cup to disk ratios than does the normal population, nerve fiber crowding does not mean necessarily a small optic disk. In fact, Contreras et al. did not show any significant difference in optic disk size between patients with NAION and control subjects. New Bruch’s membrane opening (BMO) disk size analysis could be useful in the future to assist in addressing this unanswered question.
OCT technology is a reliable and objective tool to assess new therapies arising in the future for this devastating disorder.
OCT provides reliable and quantitative information on optic disk edema and structural changes during the resolution of optic nerve head swelling. For lower grades of papilledema, pRNFL analysis is very useful as an adjunct method to confirm and quantify the severity of disk swelling. However, in moderate to severe papilledema (Frisén grade 3 or above), substantial thickening of the pRNFL (average RNFL >200μm) causes the software algorithm to fail in over a third of the cases, yielding inaccurate values of RNFL thickness.