To demonstrate the value of infrared scanning laser ophthalmoscopy (SLO) for determining structural retinal and choroidal changes in patients with Stargardt disease and its comparison to findings on short-wavelength fundus autofluorescence (SW-AF) imaging, spectral-domain optical coherence tomography, and microperimetry measurements.
Forty-four eyes of 22 patients with Stargardt disease were studied using infrared-SLO, spectral-domain optical coherence tomography, macular microperimetry, SW-AF, electroretinography, and fundus photography.
Although SW-AF imaging outlined the regions of retinal pigment epithelial (RPE) atrophy (hypofluorescence) and enhanced the visibility of more funduscopically apparent flecks (hyperfluorescence), infrared-SLO imaging outlined the regions of choroidal, and RPE, atrophic changes. Degenerative changes in photoreceptor and RPE cell layers, evident on spectral-domain optical coherence tomography imaging, were associated with either hyporeflective or hyperreflective images on infrared-SLO imaging, depending on whether both RPE and choroidal atrophy (hyperreflectance) or solely RPE atrophy (hyporeflectance) was present. Threshold elevations on microperimetry testing corresponded to both RPE and choroidal atrophy on infrared-SLO imaging and RPE atrophy on SW-AF.
Although SW-AF identifies regions of RPE atrophy, infrared-SLO also identifies the involvement of the choroid that has important implications for the potential improvement in visual function from treatment. Thus, infrared-SLO imaging offers an additional advantage beyond that obtained with SW-AF.
Although short-wavelength autofluorescence identifies regions of fundus flecks and retinal pigment epithelial atrophy, infrared scanning laser ophthalmoscopy additionally identifies the involvement of the choroid. Infrared laser imaging, used in conjunction with spectral-domain optical coherence tomography and microperimetry, provides a clinically useful correlation of structural retinal changes with functional loss in patients with Stargardt disease.
*Pangere Center for Inherited Retinal Disease, The Chicago Lighthouse For People Who Are Blind or Visually Impaired, Chicago, Illinois;
†Department of Ophthalmology, University of Illinois, Chicago, Illinois;
‡Howard Hughes Medical Institute, Chevy Chase, MD;
§Department of Ophthalmology and Visual Sciences, University of Iowa Carver College of Medicine, Iowa City, Iowa; and
¶Department of Ophthalmology, Columbia University, New York, New York.
Reprint requests: Gerald A. Fishman, MD, Pangere Center for Inherited Retinal Disease, The Chicago Lighthouse For People Who Are Blind or Visually Impaired, 1850 West Roosevelt Road, Chicago, IL 60608; e-mail: email@example.com
Supported by the Pangere Corporation, Grousbeck Family Foundation, Stanford, CA, Cless Family Foundation, Northbrook, IL, Wynn-Gund Foundations, and in part by the National Eye Institute/National Institutes of Health grants (EY021163, EY019861) and Foundation Fighting Blindness (Owings Mills, MD).
None of the authors have any financial/conflicting interests to disclose.