Patients with chronic pain exhibit individually unique cortical signatures of pain encoding

Abstract

Chronic pain is characterised by an ongoing and fluctuating intensity over time. Here, we investigated how the trajectory of the patients' endogenous pain is encoded in the brain. In repeated functional MRI (fMRI) sessions, 20 patients with chronic back pain and 20 patients with chronic migraine were asked to continuously rate the intensity of their endogenous pain. Linear mixed effects models were used to disentangle cortical processes related to pain intensity and to pain intensity changes. At group level, we found that the intensity of pain in patients with chronic back pain is encoded in the anterior insular cortex, the frontal operculum, and the pons; the change of pain in chronic back pain and chronic migraine patients is mainly encoded in the anterior insular cortex. At the individual level, we identified a more complex picture where each patient exhibited their own signature of endogenous pain encoding. The diversity of the individual cortical signatures of chronic pain encoding results bridge between clinical observations and neuroimaging; they add to the understanding of chronic pain as a complex and multifaceted disease.

Keywords: BOLD; chronic pain; endogenous pain; fMRI; insular cortex.

FIGURE 1

Schematic illustration of a 5 min fluctuating time course of pain rating

FIGURE 2

Cortical processing of chronic pain in chronic back pain (CBP). (a) The upper row shows the cortical encoding of the endogenous pain intensity (amplitude—AMP): the activities in the bilateral anterior insular cortex (AIC), the pons, and the frontal cortex were positively related to pain intensity. We found negative relationships between brain activity and pain intensity in the precuneus and the pregenual anterior cingulate cortex (pACC). (b) The processing of changes of pain intensity (slope—SLP) was mainly localised in the bilateral AIC. (c) The movement process, which prerequisites motor activity and decision‐making (absolute slope—aSLP), shows a vast network of activity in the thalamus, the cingulate cortex, the entire insula and the cerebellum. The graphs on the right show the temporal dynamics of the haemodynamic delay for several regions in relation to the current pain rating (at time point 0 s)

FIGURE 3

Cortical processing of chronic pain in chronic migraine (CM). (a) The upper row shows no major region that encodes the intensity of endogenous pain (amplitude—AMP). We found negative relationships between brain activity and pain intensity in the posterior cingulate cortex (PCC) and the pregenual anterior cingulate cortex (pACC). (b) The processing of changes of pain intensity (slope—SLP) was mainly localised in the left anterior insular cortex (AIC). Negative relationships were found in frontal and motor areas as well as in the precuneus. (c) The movement process, which prerequisites motor activity and decision‐making (absolute slope—aSLP), shows a vast network of activity in the thalamus, the cingulate cortex, the entire insula, and the cerebellum. The graphs on the right show the temporal dynamics of the haemodynamic delay for several regions in relation to the current pain rating (at time point 0 s)

FIGURE 4

Cortical processing of single chronic back pain (CBP) patients. Each triplet of maps belongs to one patient (20 in total) and shows the cortical encoding of pain (AMP) across all sessions of the patient. The numbers indicate the spatial correlation of the individual map with the group map

FIGURE 5

Cortical processing of single chronic migraine (CM) patients. Each triplet of maps belongs to one patient (20 in total) and shows the cortical encoding of pain (AMP) across all sessions of the patient. The numbers indicate the spatial correlation of the individual map with the group map