Non-arteritic anterior ischemic optic neuropathy versus cerebral ischemic stroke

Non-arteritic anterior ischemic optic neuropathy (NAAION) is a common, visually disabling disease. However, its pathogenesis and management have been highly controversial. There is a common belief that NA-AION and cerebral ischemic stroke are similar in nature pathogenetically and in management. For example, ophthalmologists and neurologists routinely tend to prescribe aspirin to NAAION patients with the rationale that NA-AION, like stroke, is a thromboembolic disorder and aspirin helps thromboembolic disorders. NA-AION patients who come to consult me usually tell me that their neuro-ophthalmologists and neurologists have stated that NA-AION and cerebral ischemic stroke are similar in nature. This concept has resulted in major controversy on the pathogenesis and management of NA-AION. The evidence shows, however, that NA-AION is pathogenetically a totally different clinical entity from cerebral ischemic stroke. It is well-established that cerebral ischemic stroke is a thromboembolic disorder in most cases. In a smaller number of cases, cerebral ischemic stroke can also be due to hypoperfusion and watershed infarcts when blood pressure drops to a critical level. My studies have shown that NA-AION, unlike most cases of cerebral ischemic stroke, is NOT a thromboembolic disorder, except very rarely [1–3]. Fluorescein fundus angiography provides the crucial information about this, as is evident from the following. The optic nerve head (ONH) is supplied by the posterior ciliary artery [4, 5]. First and foremost, if NA-AION were a thromboembolic disorder, fluorescein fundus angiography during the early stages of the onset of visual loss would invariably show evidence of complete occlusion of the posterior ciliary artery, with no filling of the ONH and the choroid. For example, in arteritic AION, due to giant cell arteritis, where there is complete occlusion of the posterior ciliary artery due to thrombosis [6–8], the ONH and choroid do not fill at all, as shown in Fig. 1. In sharp contrast to that, in my angiographic studies of more than 1,000 eyes with acute, classical NA-AION, no such occlusion was ever seen (except in a rare case when NA-AION was due to embolism to the posterior ciliary artery). Angiography soon after the onset of NA-AION may show only a transient hypoperfusion or non-perfusion of the peripapillary choroid and/or choroidal watershed zones, but these areas eventually fill with fluorescein during angiography, indicating no arterial occlusion and that NA-AION is not a thromboembolic occlusive disorder, as shown in Fig. 2. Fluorescein fundus angiography in Fig. 2 was performed during the day when the patient’s blood pressure was normal, yet it still revealed a transient filling defect in the peripapillary choroid and watershed zone. My 24-hour ambulatory blood pressure monitoring studies in more than 700 patients have shown that in all normal persons, daytime blood pressure is in the normal range, but nevertheless there is always a variable degree of fall in blood pressure during sleep (see Figs. 3, 4). In the eye in Fig. 2, it is hypothesized that prolonged nonfilling of the peripapillary choroid (main source of blood supply to the ONH) and the watershed zone surrounding the ONH during sleep, due to a fall of blood pressure, must have reduced blood flow to the ONH maximally, resulting in S. S. Hayreh Department of Ophthalmology and Visual Sciences, College of Medicine, University of Iowa, Iowa City, IA, USA