Comment on: Optical coherence tomography angiography in acute unilateral nonarteritic anterior ischemic optic neuropathy: A comparison with the fellow eye and with eyes with papilledema.

Sir,

I was interested to read the article by Gandhi et al.,[1] who reported the presence of peripapillary choroidal filling defect in acute nonarteritic anterior ischemic optic neuropathy (NA-AION) seen on optical coherence tomography angiography. In 1974, I described, for the first time, the clinical entity of “anterior ischemic optic neuropathy.”[2] Since then, I have exhaustively investigated, both experimentally and clinically, the pathogenesis and various aspect of NA-AION, including doing fluorescein fundus angiographic (FFA) studies in over a thousand patients with acute NA-AION. I have described my findings extensively in numerous of publications for more than 40 years and recently summarized those in my book entitled “Ischemic Optic Neuropathies.”[3] In the light of those studies, I have the following comments about the article by Gandhi et al.[1]

The authors have cited publications from the literature in support of their belief. It is well known that, unfortunately, misleading information gets published for a variety of reasons and that then gets perpetuated as established fact (as I discussed elsewhere[4]). The article by Gandhi et al.[1] has some examples of that.

They stated that “FFA studies performed earlier have shown the peripapillary choroidal circulation to be largely intact in these patients.” This is not true. Since 1985,[5] based on my FFA studies in NA-AION, I have published many articles showing the presence of distinct filling defects in the peripapillary choroid as well as in the choroidal watershed zones passing through the peripapillary choroid [Fig. 1]. Gandhi et al.[1] seem erroneously to imply that their study is the first to show that. They seem to reinvent the wheel. For evaluation of the peripapillary and the rest of the choroid, FFA provides superior information, because it covers a much bigger field than optical coherence tomography angiography. For example, had they done FFA, the authors would have found that in their Figure 4, the superior peripapillary defect was in fact a superior choroidal watershed zone filling defect [Fig. 1a].

Figure 1

(a) Fluorescein fundus angiogram of right eye with nonarteritic anterior ischemic optic neuropathy showing nonfilling of temporal part of the peripapillary choroid (vertical arrow) and adjacent optic disk and of upper half of the choroidal watershed zone (horizontal arrow). (b) Fluorescein fundus angiogram of right eye with nonarteritic anterior ischemic optic neuropathy showing nonfilling of the choroidal watershed zone (WSZ, arrows) between the lateral and medial posterior ciliary arteries and of the temporal part of optic disk

I am afraid that these authors are perpetuating invalid concepts prevalent in the literature, unsupported by scientific facts. Following are two examples of that.

They stated that the pathogenesis of NA-AION “is thought to be a result of the occlusion of the short posterior ciliary arteries.” Based on my studies on the pathogenesis of NA-AION, I have stressed time and time again that it is extremely important to remember that in NA-AION, there is no occlusion of the posterior ciliary artery. Occlusion of the posterior ciliary artery is responsible for the development of arteritic AION only and not of NA-AION – this is a crucial difference. In view of this, the common assertion in the literature that posterior ciliary artery occlusion causes NA-AION is simply not correct. My FFA studies in over a thousand patients with acute NA-AION over the years have shown that it is caused by transient hypoperfusion or nonperfusion of the optic nerve head vascular bed, due to transient fall of perfusion pressure. I have discussed at length the basis of that in my various publications[3]

Based on the use of automated static threshold perimetry, a serious misconception has emerged that inferior altitudinal visual field defect is the classical visual field defects in NA-AION. I investigated that subject in 312 consecutive eyes with NA-AION.[6] I showed that an absolute inferior nasal visual field defect is much more common than an absolute inferior altitudinal visual field defect in NA-AION and could be considered the most characteristic single field defect in NA-AION. The misconception that an altitudinal visual field defect is characteristic in NA-AION has emerged from the use of automated static threshold perimetry rather than manual kinetic perimetry performed with a Goldmann perimeter. This is because automated perimetry has the serious limitation of not providing information beyond the central 30° or less of the field, whereas kinetic perimetry covers the peripheral visual field up to 90°. It is most unfortunate that now kinetic perimetry is not used, resulting in misinformation about the true nature of the visual field defect and visual functional disability in NA-AION.[6]

Gandhi et al.[1] have used confusing terminology in their article. The peripapillary region has two vascular beds: anteriorly, the retinal vascular bed, and posteriorly, the choroidal vascular bed. When they mention “microvasculature cuff,” “peripapillary vascular zone,” and “loss of vasculature,” it is not at all clear which of these two vascular beds they are referring to. They have to be precise in their description. They mention “capillary dropout at the choroidal level,” but the choroidal vascular bed has “choriocapillaris,” not “capillaries.” I have pointed out repeatedly since 1964[7] that the term “papilloedema” scientifically is not correct; it arose because Briggs in 1676,[8] under a completely erroneous impression, called the optic disk a “papilla.” It has long been well established that the normal optic disk is not only a flat structure but also usually has a central cup – the opposite of a papilla. The correct term should be “optic disk edema.”

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