Patients with ONHD pose a challenging diagnostic dilemma and are often difficult to manage because of uninterpretable optic nerve head appearance. Patients may have visual field defects secondary to the presence of ONHD,8–10
and may be diagnosed with glaucoma. Conversely, other patients are not diagnosed with glaucoma because of the alteration in the optic nerve head appearance by ONHD, with diminution of the optic nerve cup. The extent of NFL thinning may not be realized in these cases. With OCT, it is possible to measure the thickness of the NFL directly. Optical coherence tomography allows in vivo visualization of cross-sectional images of the retina and NFL at histologic resolution. Schuman et al have shown that NFL thickness by OCT measurements correlate highly with visual function as measured by visual fields.2
Nerve fiber layer thinning has been shown to be the most sensitive indicator of glaucomatous damage, preceding both measurable visual function loss and detectable changes in optic nerve appearance.11–13
In our two patients with coincident ONHD and glaucoma, in which the optic nerve heads appeared full, we found OCT to be a useful tool in evaluating generalized NFL thinning, as well as specific, localized areas of NFL thinning. We were unable to obtain the same information with the traditional methods of glaucoma evaluation.
Case 1 demonstrated marked asymmetry of optic nerve appearance due to ONHD, in which the right optic nerve appeared to have advanced cupping from glaucomatous damage, although the left optic nerve appeared undamaged and full. By OCT measurements, significant NFL thinning was evident in the left eye, with measurable NFL remaining only in the inferior quadrant at 45 microns and the temporal quadrant at 48 microns. This was consistent with the superonasal sparing seen on visual field testing. However, this partial sparing of NFL was not evident by red-free photography, which revealed diffuse, generalized NFL loss, with no focal areas of NFL thinning seen.
In case 2, OCT measurements showed generalized NFL thinning in the left eye. In addition, the inferior quadrant in the left eye at 86 microns was much thinner than the corresponding inferior quadrant in the right eye at 152 microns. This was the quadrant in which the drusen in the left eye were most abundant clinically. Thus, although the optic nerve of the left eye appeared to have less cupping, the NFL by OCT was thinner in comparison to the right eye, particularly in the region in which the drusen were located. The presence of a small optic nerve head cup did not correspond necessarily with less NFL loss. At this level of NFL thinning, visual fields remained full, although a clear difference was seen in the NFL thickness by OCT and red-free photography between the two eyes.
Our conventional means of monitoring glaucoma using visual field testing and red-free photography were not as sensitive in the evaluation of our two patients with ONHD. Nerve fiber layer interpretation by red-free photography has been known to be difficult not only because of factors such as hypopigmented fundi, but also because of the lack of clarity in the photographs.14
These factors are not an issue with OCT evaluation of the NFL, and interpretation is not variable among different observers because OCT quantifies NFL thickness.
Optical coherence tomography provided a more accurate assessment of NFL than either visual field testing or red-free photography. Furthermore, we were able to quantify NFL thickness objectively, allowing early detection of NFL thinning and identification of specific areas of thinning. This allowed us to recognize eyes requiring closer attention and lower intraocular pressures than we may have assumed based on our traditional assessment with optic nerve appearance and visual field testing.