Brain activity in rectosigmoid pain: unravelling conditioning pain modulatory pathways

Conditioning Pain Modulation (CPM) represents the various descending inhibitory mechanisms induced by a heterotopic noxious stimulation (previously termed DNIC). CPM-induced modulations in brain activity have not previously been investigated to visceral pain. Hence the aims were to assess the role of CPM in terms of: (1) psychophysics, (2) alterations in topography and amplitudes of evoked brain potentials and (3) modelling the brain activity.

Fifteen healthy volunteers were stimulated electrically in the rectosigmoid, and 64-channel brain activity was recorded two times before (reproducibility), during and after induction of CPM by immersing the non-dominant hand into water at 2°C for 180 s (cold pressor).

During CPM pain scores were reduced in comparison to baseline (P ≤ 0.001), which corresponds to 30% pain attenuation. In comparison to baseline significant differences in bipolar EEG topography were seen during CPM, where N2 moved from central to frontal activity (P<0.001), and peak-to-peak amplitude of the central N2-P2 complex measured at the Fz-electrode was enhanced (P=0.04). Furthermore, dipolar source modelling showed an anterior shift of the mid-line cingulate dipole (P=0.004) and a caudo-posterior shift of the insular dipole (P=0.01) during CPM.

A visceral platform was established to reliably assess the role of CPM, which for the first time demonstrated dynamic changes in cortical processing of visceral pain before, during and after CPM induction.

The model provides a unique approach to study basic pain and pharmacological intervention in healthy volunteers as well as in patients with dysfunctional pain inhibition.