Abstract
Damage to the optic radiations or primary visual cortex leads to blindness in all or part of the contralesional visual field. Such damage disconnects the retina from its downstream targets and, over time, leads to trans-synaptic retrograde degeneration of retinal ganglion cells. To date, visual ability is the only predictor of retinal ganglion cell degeneration that has been investigated after geniculostriate damage. Given prior findings that some patients have preserved visual cortex activity for stimuli presented in their blind field, we tested whether this activity explains variability in retinal ganglion cell degeneration over and above visual field testing. We prospectively studied 15 chronic stroke patients (4 females, mean age = 63.67 years) with homonymous visual field defects secondary to stroke, 10 of whom were also tested within the first 2 months post-stroke. Each patient completed Humphrey visual field testing, retinotopic mapping with functional magnetic resonance imaging, and macular optical coherence tomography. There was a positive relation between ganglion cell complex thickness in the blind field and early visual cortex activity for stimuli presented in the blind field. Furthermore, residual visual cortex activity from blind field stimulation at the first time point predicted the degree of retinal ganglion cell complex thinning 6 months later. These findings indicate that retinal ganglion cell survival after ischemic damage to the geniculostriate pathway is activity-dependent.