Do areas of retinal ganglion cell degeneration coincide with areas of decreased representation in V1 following stroke?

Abstract

Stroke in the territory of the posterior cerebral artery leads to cortical blindness in a hemifield or quadrant of the contralesional visual field. While about 50% of patients experience some degree of visual recovery within the first 6 months post-stroke, only 12.5% experience complete recovery (Tiel K., Kolmel, 1990). One limiting factor that may prevent further visual recovery is trans-synaptic retrograde degeneration of retinal ganglion cells, which has been observed in stroke patients starting as early as 3 months after stroke (Jindahra, Petrie, & Plant, 2009, 2012; Park, Park, Cho, & Park, 2013; Tanito & Ohira, 2013; Yamahachi, Marik, McManus, Denk, & Gilbert, 2009). Retinal ganglion cell thickness is easily measured in the clinic with optical coherence tomography, a technique that generates a 3-D image of the retina from which the thickness of the retinal ganglion cell complex can be measured. The visual cortex is organized in a retinotopic manner that can be measured with fMRI by presenting visual stimuli in various locations in the participant's visual field and then determining the stimulus location for which each voxel maximally responds (Sereno et al., 1995). Here we test the hypothesis that chronic stroke patients exhibit a homonymous decrease in retinal ganglion cell thickness specifically for visual locations with poor representation in V1. This research has implications for timely rehabilitative treatment because once the retina degenerates, visual recovery in that retinotopic location is impossible. Furthermore, this research may highlight the need for novel treatment strategies that prevent retinal ganglion cell degeneration in order to prolong the window of effective rehabilitation.