“…The PCC activity observed here developed concomitantly, and peaked after the conscious detection of nociceptive stimuli by participants (i.e., later than their motor responses), and this was also the case in intracranial EEG studies (Bastuji et al, ), which is consistent with a possible contribution to stimulus awareness, or to its modulation and further cognitive processing such as memory encoding. Concordant with this view, subjective reports of touch in the absence of actual somatosensory stimulation were shown to result in activation of a network comprising the posterior cingulate and precuneus together with medial frontal cortex (Lloyd et al, ), while subliminal, imperceptible somatosensory stimulation resulted in decreased functional connectivity between somatosensory and PCC cortices as compared to rest (Nierhaus et al, ). However, PCC activation is absent from many neuroimaging studies of pain, and PCC deactivations (i.e., a decrease in BOLD signal) have been reported, for example, in response to painful punctate stimuli, in the context of hyperalgesia (Iannetti et al, ), or in the development of wind‐up pain (Perrotta et al, ).…”