Altered cortical visual processing in individuals with a spreading photoparoxysmal EEG response.

Photosensitive individuals respond with epileptiform electroencephalography (EEG) discharges to intermittent photic stimulation. The pathogenetic mechanisms underlying this photoparoxysmal response (PPR) remain to be clarified. We investigated the involvement of magnocellular and parvocellular pathways in the processing of nonprovocative visual stimuli in healthy subjects with different phenotypic expressions of PPR (15 individuals with a local PPR, i.e. occipital discharges only, and 15 with a PPR propagating to anterior brain regions) and in 17 PPR-negative healthy controls using pattern-reversal visual evoked potentials (VEP). Checkerboard stimulation was performed at a low and a high spatial frequency to preferentially activate the magnocellular and parvocellular pathways. VEP habituation was also assessed over 15 blocks (each 100 trials) of recording. PPR-positive individuals with propagating PPR showed an increase in the N75-P100 and P100-N135 VEP components for both spatial frequencies, whereas individuals with a local PPR had normal VEP amplitudes. Individuals with propagating PPR also showed a stronger VEP habituation and reported more aversive sensations during continuous visual stimulation with the high spatial frequency checkerboard. The selective increase in VEP amplitudes in individuals with propagating PPR corroborates the notion that PPR with propagation is pathophysiologically distinct from local PPR. The increase in VEP amplitudes was independent of the spatial frequency of visual stimulation, indicating an increased neuronal excitability in both the parvocellular and magnocellular pathways. The stronger habituation in these individuals may reflect a compensatory mechanism to stabilize excitability in the visual system.