Studies on the pathogenesis of anterior ischemic optic neuropathy

Abstract

The pathogenesis of nonarteritic anterior ischemic optic neuropathy (AION) was investigated, on the basis of clinical findings from a patient with nonarteritic AION and experimental study of the vascular architecture of the human optic nerve head. The patient's visual field examination revealed a wide Bjerrum scotoma. This visual field defect suggests that the mechanism of the onset of nonarteritic AION might be similar to that of glaucoma. Fluorescein fundus angiography (FFA) findings suggest that the peripapillary choroidal circulation might recover more easily from perfusion disturbance than the rest. Further, experimental study of the human optic nerve heads revealed that the circle of Zinn forms a complete vascular circle and that small branches from this circle extend to the peripapillary choroid or the optic nerve head, and that the intraneural vascular meshwork is less dense than that in the retrolaminar portion. Based upon the above clinical findings and experimental results, the pathogenesis of nonarteritic AION is postulated as follows: (1) The blood flow in the circle of Zinn is decreased by stenosis of the posterior ciliary artery (PCA). (2) Hypoperfusion is produced in the whole optic nerve head. (3) As in glaucoma, arcuate nerve fibers are first affected, resulting in the onset of nonarteritic AION with arcuate visual field defect or altitudinal defect.

Key Words:

• anterior ischemic optic neuropathy
• pathogenesis