Pain in the brain
Pain is one of the most prominent examples of the problem of consciousness: from a subjective point of view we know the experience of pain all too well. Seen from the objective side of pain, the neural processes related to pain are becoming unravelled. But the essential relationship between neural processes going on from the […]
Pain is one of the most prominent examples of the problem of consciousness: from a subjective point of view we know the experience of pain all too well. Seen from the objective side of pain, the neural processes related to pain are becoming unravelled. But the essential relationship between neural processes going on from the sensation to the experience are much less known.
In a study by Christmann and colleagues, a combination of EEG and fMRI demonstrates how regional brain areas make different contributions — and at different times — to the experience of pain.
Together with a detailed behavioral analysis, simultaneous measurement of functional magnetic resonance imaging (fMRI) and electroencephalography (EEG) permits a better elucidation of cortical pain processing. We applied painful electrical stimulation to 6 healthy subjects and acquired fMRI simultaneously with an EEG measurement. The subjects rated various stimulus properties and the individual affective state. Stimulus-correlated BOLD effects were found in the primary and secondary somatosensory areas (SI and SII), the operculum, the insula, the supplementary motor area (SMA proper), the cerebellum, and posterior parts of the anterior cingulate gyrus (ACC). Perceived pain intensity was positively correlated with activation in these areas. Higher unpleasantness rating was associated with suppression of activity in areas known to be involved in stimulus categorization and representation (ventral premotor cortex, PCC, parietal operculum, insula) and enhanced activation in areas initiating, propagating, and executing motor reactions (ACC, SMA proper, cerebellum, primary motor cortex). Concordant dipole localizations in SI and ACC were modeled. Using the dipole strength in SI, the network was restricted to SI. The BOLD signal change in ACC was positively correlated to the individual dipole strength of the source in ACC thus revealing a close relationship of BOLD signal and possibly underlying neuronal electrical activity in SI and the ACC. The BOLD signal change decreased in SI over time. Dipole strength of the ACC source decreased over the experiment and increased during the stimulation block suggesting sensitization and habituation effects in these areas.
We have had evidence for some time that humans can become habituated to pain, and that pain itself can be 100% moderated by environmental cues.
This study is an important one in relation to the mechanisms of acute pain, but it should be realised that chronic pain has different brain patterning and is almost indistinguishable from patterns associated with emotional distresss.
Whilst there is an overlap in our growing understanding of both acute pain and chronic pain, there are vast differences in the mechanisms, and very considerable differences in the way these two are treated.
We mustn’t assume that findings in relation to acute pain will necessarily hold for chronic pain.