Ophthalmology
Volume 110, Issue 10
,
October 2003,
Pages 2031-2035
doi:10.1016/S0161-6420(03)00804-2 
Copyright © 2003 American Academy of Ophthalmology. Published by Elsevier Science Inc.
Case report
The morphology of an infarct in nonarteritic anterior ischemic optic neuropathy*1
Presented in part at the Association for Research in Vision and Ophthalmology annual meeting, Fort Lauderdale, Florida, May 2, 2001.
Rachel A. Tesser MD1, Eric R. Niendorf MD1 and Leonard A. Levin MD, PhD
, 1
1 Department of Ophthalmology and Visual Sciences, University of Wisconsin Medical School, Madison, Wisconsin, USA
Received 19 June 2002; accepted 11 April 2003. ; Available online 15 October 2003.
Abstract
Objective
The mechanism by which nonarteritic anterior ischemic optic neuropathy (NAION) causes an infarct in the optic nerve is controversial. We studied the three-dimensional anatomic configuration of a NAION infarct to better elucidate its pathophysiology.
Design
Case report with clinicopathologic correlation.
Methods
Serial sections of the optic nerve from a previously reported patient diagnosed with NAION 20 days before death were studied. Every fourth slide was stained with hematoxylin–eosin, photographed, and digitized. NIH Image
1.62 was used to reconstruct the nerve in all three dimensions, and the infarct morphology was analyzed.
Main outcome measures
Morphology of the reconstructed optic nerve infarct.
Results
The area of axonal loss within each section of the optic nerve was identified and reconstructed. The loss was in the superior part of the nerve, encircling the central 
retinal artery at its greatest extent. Remaining areas of the nerve appeared healthy, and, notably, the periphery of the uninvolved inferior portion of the nerve was normal. Three-dimensional analysis revealed two distinct areas of infarct at the posterior extent of the lesion which coalesced toward the center of the lesion and finally tapered as the infarct reached the optic nerve head. Sagittal reconstructions gave the appearance of a two-pronged fork posteriorly connecting to a single “handle” anteriorly. There was no obvious correlation between the configuration of the infarct and any single vascular territory. The total length of the nerve involved by the infarct was approximately 1.5 mm.
Conclusions
The morphology of this NAION infarct is not consistent with disease of large or small vessels and, more likely, represents a form of compartment syndrome that causes tissue ischemia.
Corresponding author. Reprint requests to Leonard A. Levin, MD, PhD, University of Wisconsin Medical School, 600 Highland Avenue, , Madison, WI, , USA 53792.
*1 Manuscript no. 220419.
Supported by National Institutes of Health grant no. R01 EY12492 and an unrestricted departmental grant from Research to Prevent Blindness, Inc. LAL is a Research to Prevent Blindness Dolly Green Scholar.
