A widely accepted notion is that one particular region of the “pain matrix”, the insula, plays a specific role in the perception of pain, and the activity recorded from this region is often considered as an objective signature of pain perception and its modulation. Taking advantage of the high spatio-temporal resolution of direct intracerebral recordings performed in patients undergoing pre-surgical evaluation of focal intractable epilepsy, we recently provided compelling evidence to the contrary. More specifically, we demonstrated that both nociceptive (laser) and non-nociceptive (vibrotactile, auditory, visual) stimuli perceived as equally intense elicit robust local field potentials (LFPs) in the anterior and posterior insula, with matching spatial distributions. These findings argue against the notion that LFPs recorded from the human insula reflect the brain activity through which pain emerges from nociception in the human brain.
Another finding that emerged from our intracerebral investigations is that nociceptive stimuli, but not tactile, auditory, and visual stimuli, elicit an early-latency burst of gamma-band oscillations (GBOs, 40-90 Hz) at several insular locations. Because perception has been proposed to emerge from temporal binding or synchronization of stimulus-evoked neural activity through GBOs, nociceptive GBOs generated in the insula could reflect cortical activity through which the perception of pain arises from nociceptive input in the human brain. These pain-related GBOs generated in the insula could also contribute to the generation of higher-order responses aiming at preserving the individual’s integrity.
Whereas insular LFPs appear to reflect multimodal activity unspecific for pain, the selective enhancement of insular GBOs elicited by nociceptive stimuli could reflect activity related to the processing of spinothalamic input, nociception, and/or the perception of pain.