*3.3. Electrophysiological Results*

Results showed no significant amplitude or latency differences between groups for P1 (*F*(2,55) = 1.737, *p* = 0.186; *F*(2,55) = 0.679, *p* = 0.52) and N1 components (*F*(2,55) = 0.232, *p* = 0.79; *F*(2,55) = 0.605, *p* = 0.55). Although it did not reach the significance level, there was a tendency toward a larger P2 amplitude in controls (*F*(2,55) = 2.783, *p* = 0.07). The were no significant latency differences for the P2 component (*F*(2,55) = 2.312, *p* = 0.11) (see Figure 2).

**Figure 2.** Grand average waveforms at Oz showing the visual P1, N1, and P2 components, and corresponding topographical maps, for controls (plain line), subacute mTBI (dashed line), and chronic mTBI (dotted line) participants. There is a tendency towards a larger P2 amplitude in controls.

N2pc results show that there were no significant differences between groups for the amplitude of the N2pc (*F*(2,55) = 0.960, *p* = 0.39), nor for its latency (*F*(2,55) = 1.368, *p* = 0.26) (see Figure 3). The same was found for the amplitude of the Ptc component (*F*(2,55) = 1.07, *p* = 0.35), and its latency (*F*(2,55) = 2.616, *p* = 0.08). When comparing peak-to-peak amplitude shifts from the N2pc to the next-positive peak, the Ptc, the result was significant (*F*(2,55) = 4.25, *p* = 0.02, η2 = 0.13), with a smaller amplitude shift between these components for subacute mTBI participants compared to controls (*p* < 0.05). Figure 3 also depicts averaged SPCN waveforms obtained on pooled electrodes PO7-PO8. There were no significant between-group differences for SPCN amplitude (*F*(2,55) = 0.7, *p* = 0.5).

There were significant differences between groups for the amplitude of the P3a (*F*(2,55) = 5.571, *p* = 0.01, η2 = 0.17). Post hoc analysis showed that P3a was significantly larger for mTBI groups (subacute and chronic compared to controls: *p* < 0.05). There were no significant differences between groups for P3a latency (*F*(2,55) = 1.483, *p* = 0.24) (see Figure 4).

**Figure 3.** Grand average N2pc, Ptc, and SPCN components, evoked by lateralized stimuli, recorded at P07-P08 for controls (plain line), subacute mTBI (dashed line), and chronic mTBI (dotted line) groups. The N2pc-Ptc peak-to-peak amplitude shift is significantly smaller in the subacute mTBI group than in controls.

**Figure 4.** Average P3a components, obtained after the subtraction of activity evoked by same colour target and frequent colour standard stimuli, recorded at Fz, and corresponding topographical maps. The amplitude of the P3a component is significantly enhanced for subacute mTBI (dashed line) and chronic mTBI (dotted line) participants, in comparison with controls (plain line).

P3b results are shown in Figure 5. P3b amplitude was significantly smaller in both groups of mTBI participants (*p* < 0.05) relative to control participants (*F*(2,55) = 7.214, *p* < 0.002, η2 = 0.21). The latency of the P3b was also significantly delayed in the mTBI groups (*p* < 0.05) compared to controls (*F*(2,55) = 7.839, *p* < 0.001, η2 = 0.22).

**Figure 5.** Grand average P3b components, obtained after the subtraction of activity evoked by infrequent position target stimuli and frequent position standard stimuli, recorded at Pz, and corresponding topographical maps. The P3b is significantly reduced and delayed in the subacute mTBI group (dashed line) and reduced in the chronic mTBI group (dotted line) in comparison with controls (plain line).
