Abstract
A visual evoked potential (VEP) stimulus battery was developed and applied in a pilot study of adults with age-related macular degeneration (AMD) and adults with intact retinal function to explore neural mechanisms and pathways in central visual function. Adults with and without AMD were recruited from an ophthalmology clinic. Some individuals in both groups were tested with dilated pupils following standard clinic protocol, while others were tested prior to dilation. Testing conditions (10° square field, ~50cd/m[sup]2[/sup]) were short (2-7s, condition dependent) and repeated ten times for statistical analyses. To elicit transient VEPs, a high-contrast 1Hz contrast-reversing 32x32 checkerboard was used. To elicit steady-state VEPs, the following conditions were used: high-contrast horizontal square-wave gratings contrast-reversed at 7.5Hz with spatial frequency swept in octave steps, isolated-checks (bright or dark) appearing/disappearing at 12.5Hz with contrast swept in octave steps, and radial partial-windmill and windmill-dartboard conditions with spatial elements contrast-reversed (32% contrast) at ~4Hz and surrounding regions set to a uniform field or static 32% contrast elements, respectively, for responses reflecting nonlinear short- and long-range lateral interactions. The electroencephalogram was recorded by a single channel with an active electrode over V1. Magnitude-squared coherence (MSC) was computed for response components extracted by Fourier analysis. Increased latencies and lower MSC values in transient VEPs were found in the AMD group, compared to controls. Spatial frequency functions demonstrated deficits at high spatial frequencies for the AMD group. Low contrast responses were not significant in many observers, possibly associated with pupil dilation. Short-range lateral interactions, presumably of GABAergic origin, were relatively intact in the AMD group, even when input signals to the cortex were weak. This stimulus battery, combined with objective response measures, yields sensitive indices of central visual function. Both magnocellular and parvocellular inputs to V1 appear compromised in AMD, while local intracortical inhibitory activity appears robust
Meeting abstract presented at VSS 2013