To evaluate retinal structural and functional abnormalities in a patient with acute macular neuroretinopathy.
An adaptive optics scanning light ophthalmoscope was used to image the photoreceptor mosaic and assess rod and cone structure. Spectral-domain optical coherence tomography was used to examine retinal lamination. Microperimetry was used to assess function across the macula.
Microperimetry showed reduced function of localized areas within retinal lesions corresponding to subjective scotomas. Spectral-domain optical coherence tomography imaging revealed attenuation of two outer retinal bands typically thought to reflect photoreceptor structure. Adaptive optics scanning light ophthalmoscope images of the photoreceptor mosaic revealed a heterogeneous presentation within these lesions. There were areas containing non-waveguiding cones and other areas of decreased cone density where the remaining rods had expanded to fill in the vacant space. Within these lesions, cone densities were shown to be significantly lower than eccentricity-matched areas of normal retina, as well as accepted histologic measurements. A 6-month follow-up revealed no change in rod or cone structure.
Imaging of acute macular neuroretinopathy using an adaptive optics scanning light ophthalmoscope shows a preferential disruption of cone photoreceptor structure within the region of decreased retinal sensitivity (as measured by microperimetry). Adaptive optics–based imaging tools provide a noninvasive way to assess photoreceptor structure at a level of detail that is not resolved by use of conventional spectral-domain optical coherence tomography or other clinical measures.
Adaptive optics imaging of acute macular neuroretinopathy shows a preferential injury to cone photoreceptors within characteristic parafoveal lesions. Adaptive optics imaging provides a noninvasive assessment of photoreceptor structure undetectable with current clinical imaging modalities.
*Department of Ophthalmology, Medical College of Wisconsin, Milwaukee, Wisconsin;
†Department of Biomedical Engineering, Marquette University, Milwaukee, Wisconsin; and
Departments of ‡Biophysics, and
§Cell Biology, Neurobiology, & Anatomy, Medical College of Wisconsin, Milwaukee, Wisconsin.
Reprint requests: David V. Weinberg, MD, 925 North 87th Street, Milwaukee, WI 53226; e-mail: firstname.lastname@example.org
Supported by NIH Grants P30EY001931 and R01EY017607, The E. Matilda Ziegler Foundation for the Blind, Thomas M. Aaberg, Sr., Retina Research Fund, Foundation Fighting Blindness, RD and Linda Peters Foundation, and an unrestricted departmental grant from Research to Prevent Blindness, Inc, New York, NY. This investigation was conducted in a facility constructed with support from Research Facilities Improvement Program, Grant Number C06 RR016511, from the National Center for Research Resources, National Institutes of Health. The sponsors or funding organizations had no role in the design or conduct of this research. A. Dubra holds a Career Award at the Scientific Interface from the Burroughs Wellcome Fund.
The authors declare no conflict of interest.