Abstract
BACKGROUND: Non-arteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute optic neuropathy in patients over 50 years of age, and many affected individuals are left with permanent visual deficits. Despite the frequency of NAION and its often devastating effects on vision, no effective treatment has been established. Further understanding of the acute vascular effects in NAION, using advanced ophthalmic imaging techniques like the retinal function imager, may shed light on potential treatment targets. METHODS: Five patients with acute NAION underwent retinal functional imaging within 2 weeks of the onset of their visual symptoms, and at 1 month and 3 months after onset. Average arteriolar and venular blood flow velocities were calculated for each eye at each time point. The Wilcoxon rank sum test was used to compare blood flow velocity results with a normative database. RESULTS: The average arteriolar blood flow velocity in the normative group was 3.8 mm/s, and the average venular blood flow velocity was 3.0 mm/s, versus 4.1 mm/s and 2.7 mm/s, respectively, in the NAION-affected group at presentation. Average arteriolar blood flow increased slightly to 4.2 mm/s one month after the acute NAION event, then decreased to 3.8 mm/s three months after the event. Average venular blood flow velocity was 2.8 mm/s 1 month after the NAION event and 2.7 mm/s 3 months after the event. Differences in blood flow velocity between the NAION-affected and control groups were not statistically significant at any time point; however, there was a trend toward increasing blood flow velocity initially after an NAION, with a decrease over time. CONCLUSIONS: This study demonstrates the feasibility of retinal function imaging to quantify macular blood flow velocity in patients with acute NAION. There were no statistically significant differences in blood flow velocity detected between NAION-affected eyes and healthy controls at any of the time points examined; however, there was a trend toward an increase in both arteriolar and venular BFV subacutely, then a decrease in the chronic phase after NAION, which could be suggestive of a mechanism of attempted compensation in the setting of acute ischemia.