Survival of Retinal Ganglion Cells After Damage to the Occipital Lobe in Humans is Activity-Dependent
This dataset accompanies the following published paper:
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 that activity explains variability in retinal ganglion cell degeneration over and above visual ability. We prospectively studied 15 patients (4 females, mean age = 63.7 years) with homonymous visual field defects secondary to stroke, 10 of whom were tested within the first 2 months after stroke. Each patient completed automated Humphrey visual field testing, retinotopic mapping with functional magnetic resonance imaging, and spectral-domain optical coherence tomography of the macula. 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 for stimuli presented in the blind field soon after the stroke 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.