In both studies, principal components analysis showed that P1 amplitudes to frequent stimuli and to rare negative stimuli were larger than P1 amplitudes to rare positive stimuli.
We think the causal arrow points the other way: People like alerts, updates, and tweets precisely because the brain is built to pay more attention to short, frequent stimuli than to sustained input.
The interaction of stimulus by electrode by diagnosis was due to larger amplitudes associated with infrequent compared to frequent stimuli at Fz, Cz and Pz [p = 0.026, p < 0.001 and p < 0.001] for unexposed children but not for children with a history of PM [p = 0.479, p = 0.884 and p = 0.136 respectively].
The interaction of Stimulus by Site occurred due to longer N170 latency associated with the frequent stimuli compared to the infrequent stimuli at right hemisphere – T6 (frequent > infrequent, p = 0.012) but not left hemisphere – T5 (p = 0.054).
The interaction was due to significantly larger P3a amplitude associated with frequent stimuli compared to novel stimuli at fronto-central electrodes (Fz: frequent > novel, p < 0.001; FCz: frequent > novel, p < 0.001; Cz: frequent > novel, p < 0.001) but not at posterior sites (Pz: p = 0.447).
Figure 2a, e show the trial-averaged MEG sensor waveforms evoked by the frequent stimuli delivered to one representative healthy control subject's right median-nerve.
In 91 trials, an infrequent up or down arrow interrupted the frequent stimuli at an unpredictable offset (mean=323 ms, s.d.=122 ms).
This interaction occurred because the Nc component associated with the novel stimuli was larger than that associated with the frequent stimuli at fronto-central sites (Fz: novel > frequent, p < 0.001; FCz: novel > frequent, p < 0.001; Cz: novel > frequent, p < 0.001) but not at Pz (p = 0.933).
The frequent stimuli immediately prior to each infrequent stimulus were selected for averaging to provide similar signal-to-noise ratios.
