• Shumpei Ogawa, Hiromasa Takemura, Hiroshi Horiguchi, Masahiko Terao, Tomoki Haji, Franco Pestilli, Jason D Yeatman, Hiroshi Tsuneoka, Brian A Wandell, and Yoichiro Masuda.
• Department of Psychology, Stanford University, Stanford, California, United States Department of Ophthalmology, The Jikei University School of Medicine, Tokyo, Japan.
• Invest. Ophthalmol. Vis. Sci. 2014 Sep 25; 55 (10): 6976-86.

PurposePatients with Leber hereditary optic neuropathy (LHON) and cone-rod dystrophy (CRD) have central vision loss; but CRD damages the retinal photoreceptor layer, and LHON damages the retinal ganglion cell (RGC) layer. Using diffusion MRI, we measured how these two types of retinal damage affect the optic tract (ganglion cell axons) and optic radiation (geniculo-striate axons).MethodsAdult onset CRD (n = 5), LHON (n = 6), and healthy controls (n = 14) participated in the study. We used probabilistic fiber tractography to identify the optic tract and the optic radiation. We compared axial and radial diffusivity at many positions along the optic tract and the optic radiation.ResultsIn both types of patients, diffusion measures within the optic tract and the optic radiation differ from controls. The optic tract change is principally a decrease in axial diffusivity; the optic radiation change is principally an increase in radial diffusivity.ConclusionsBoth photoreceptor layer (CRD) and retinal ganglion cell (LHON) retinal disease causes substantial change in the visual white matter. These changes can be measured using diffusion MRI. The diffusion changes measured in the optic tract and the optic radiation differ, suggesting that they are caused by different biological mechanisms.Copyright 2014 The Association for Research in Vision and Ophthalmology, Inc.

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