Abstract
Purpose :
The Blood-oxygenation-level dependent (BOLD) contrast measured by Functional Magnetic Resonance Imaging (fMRI) in the primary visual cortex (V1) represents neuronal activity as a reaction to the stimulation of the central retinal regions (“population receptive fields” (pRF)). With appropriate stimuli this allowed us to acquire a retinotopic map. Patients with inherited retinal dystrophies develop an absolute functional deficit at the level of retina as a result of photoreceptors’ death. The consequences of such retinal dysfunction at the cortical level in such patients are not fully determined. Here, we link microperimetry and fMRI results to investigate the influence of retinal dystrophies on cortical activity.
Methods :
We used BOLD fMRI (3T Siemens Trio; TE/TR=30/1500ms, voxel size 1x1x1mm, CMRR multiband sequence with 28 slices) in 5 patients with Morbus Stargardt and 5 patients with Retinitis Pigmentosa (RP). Functional loss in all patients was determined using microperimetry MP1 (Nidek, Italy). Visual stimulus for fMRI was a moving, flickering checkerboard bar crossing the screen in eight different directions and covering the central 20° visual angle. BOLD response was modelled for each voxel using a 2D Gaussian pRF model as implemented in mrVista (Stanford University, Stanford, CA).
Results :
Eccentricity parameters of the pRF model showed the expected mapping, but no significant BOLD response was obtained near the posterior pole of the occipital visual cortex for patients with M. Stargardt and anterior parts of occipital visual cortex for RP patients, implying a lack of stimulus-related cortical activity. The regions where the pRF model explained more than 10% BOLD signal variance threshold corresponded to a large extend to preserved retinal function as measured by microperimetry (See Fig. 1 for M. Stargardt and Fig. 2 for RP).
Conclusions :
We demonstrated that retinotopic maps for M.Stargardt showed central scotomas, while activation corresponding to preserved central retina function was found in RP patients. We did not detect any stimulus-related activity in V1 regions corresponding to central or peripheral retinal dysfunction. This suggests that visual cortex is not reorganised in response to retinal disease in adult humans.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.