Corresponding Ganglion Cell Atrophy in Patients With Postgeniculate Homonymous Visual Field Loss Jamie R. Mitchell, MD, Cristiano Oliveira, MD, Apostolos J. Tsiouris, MD, Marc J. Dinkin, MD Background: The goal of our study was to look for the presence of homonymous ganglion cell layer–inner plex- iform layer complex (GCL-IPL) thinning using spectral- domain optical coherence tomography (SD-OCT) in patients with a history of adult-onset injury to the post- geniculate pathways with rigorous radiological exclusion of geniculate and pregeniculate pathology. Methods: We performed a retrospective review of twenty- two patients (ages 24–75 y, 6 men, 16 women) with homonymous visual field (VF) defects secondary to postgeniculate injury examining the GCL-IPL with SD-OCT. An additional fifteen patients (ages 28–85 y, 5 men, 10 women) with no visual pathway pathology served as controls. Using segmentation analysis software applied to the macular scan, a normalized asymmetry score was calculated for each eye comparing GCL-IPL thickness ipsilateral vs contralateral to the pa- tient’s brain lesions. Results: We found that 15 of the twenty-two subjects had a relative thinning of the GCL-IPL ipsilateral to the post- geniculate lesion in both eyes (represented by a positive normalized asymmetry score in both eyes), whereas a similar pattern of right/left asymmetry was found in 4 controls (P = 0.0498). The magnitude of asymmetry was much greater in subjects compared with controls (P = 0.0004). There was no association between the degree of GCL-IPL thinning and the mean deviation on automated VF testing. A moderate correlation (R = 0.782, P = 0.004) between the magnitude of thinning and latency from onset of retrogeniculate injury was observed only after excluding patients beyond a cutoff point of 150 months. Conclusions: This data provides compelling new evidence of retrograde transsynaptic degeneration causing retinal ganglion cell loss after postgeniculate visual pathway injury. Journal of Neuro-Ophthalmology 2015;35:353–359 doi: 10.1097/WNO.0000000000000268 © 2015 by North American Neuro-Ophthalmology Society C ircumpapillary retinal nerve fiber layer (RNFL) atro- phy, as measured by time domain optical coherence tomography (TD-OCT) and spectral domain OCT (SD- OCT) is known to occur following pregeniculate optic tract lesions in humans (1). Athough retrograde transsynaptic degeneration (RTSD) within parts of the central nervous system has been demonstrated in animal models (2) and humans (3,4), its occurrence in the visual pathways has been controversial. RTSD has been documented in non- human primates after lesions to the primary visual cortex (5–7), and clinical atrophy of the optic nerve and retinal nerve fibers on funduscopy has been reported in cases of injury to the postgeniculate visual pathways occurring either congenitally or at a very early age (8,9). RTSD of the visual system has been shown histologically in a patient with a con- genital occipital malformation status post occipital lobec- tomy more than 40 years before (10) and is the likely cause of bilateral optic nerve cupping in patients with peri- ventricular leukomalacia as a result of ischemic degeneration of the occipital radiations in children with perinatal hypoxic injury (11). Decreased signal responses of the parvocellular retinal ganglion cells using pattern electroretinography (PERG) have been recorded in patients with postgeniculate hom- onymous hemianopia suggestive of RTSD (12). But a follow-up PERG study using different temporal and spatial frequencies found no significant difference between the ganglion cell response to hemifield visual stimuli on the blind or intact side (13). Magnetic resonance imaging stud- ies showing T2 hyperintensity within the lateral geniculate Departments of Ophthalmology (JM, CO, MD), Radiology (AJT), and Neurology (MD), Weill Cornell Medical College, New York, New York. The authors report no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the full text and PDF versions of this article on the journal’s Web site (www. jneuro-ophthalmology.com). Address correspondence to Marc J. Dinkin, MD, Department of Oph- thalmology, Weill Cornell Medical College, 1305 York Avenue, 11th Floor, New York, NY 10021. E-mail: mjd2004@med.cornell.edu Mitchell et al: J Neuro-Ophthalmol 2015; 35: 353-359 353 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.