Few studies have explored the effect of acute pain on attentional networks and on the default mode network. Moreover, these studies convey conflicting results, seemingly caused by design. To reassess this issue, we studied 20 healthy subjects with functional magnetic resonance imaging while delivering painful electric shocks. The design was purposely constructed to separate rest, anticipation, and pain perception. We found that default mode network activity in response to pain was biphasic. It deactivated during anticipation when the dorsal attentional network was activated. During pain perception, the default mode network was activated, as were attentional networks. The left posterior fusiform gyrus showed the same dynamics as the default mode network, and its activity was negatively correlated to the subject's pain intensity rating. The associative pregenual anterior cingulate cortex seemed to play a key role in these coactivations. These results concur with data from the literature showing that enhanced pain perception results in greater default mode network activity and that the anticorrelation between the default mode network and the dorsal attentional network disappears in chronic pain patients.

EEGs are known to provide biomarkers for consciousness. Although EEG correlates of loss of consciousness (LOC) are often ascribed to changes in neural synchrony, mounting evidence suggests that some changes result from asynchronous neural activity. By combining EEG recordings of humans undergoing propofol administration with biophysical modelling, we present here a principled decomposition of EEG changes during LOC into synchronous and asynchronous sources. Our results reveal that IPSP decay rate and mean spike rate shape aperiodic EEG features, and that propofol's effects on these parameters largely explain the changes in EEG spectra following propofol infusion. We further show that traditional spectral EEG analysis likely conflates these effects with changes in rhythmic activity, thereby masking the true dynamics of neural synchrony. We conclude that the well-documented propofol-induced alpha rhythm in fact appears before LOC, and that the moment of LOC is uniquely correlated with the sudden appearance of a delta rhythm.