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Both primary somatosensory cortex (S1) and secondary somatosensory cortex (S2) are commonly activated in heat pain studies. Evidence suggests that the nociceptive input into these regions at least partially underlies the perception of sensory fea- tures of pain (Coghill et al., 1999; Peyron et al., 1999; Bushnell et al., 1999; Chen et al., 2002). Anterior cingu- late (ACC) and insular (IC) cortices, both components of the limbic system, are activated during the majority of PET or fMRI studies of heat pain, and these regions have been implicated in the affective processing of pain (Rainville et al., 1997; Tolle et al., 1999; Fulbright et al., 2001). Prefrontal cortical areas, as well as parietal association areas, are also sometimes activated by heat pain and may be related to cognitive variables, such as memory or stimulus evaluation (Coghill et al., 1999; Strigo et al., 2003). Motor and pre-motor cortical areas are on occasion activated by heat pain, but these activa- tions are less reliable, suggesting they may be related to pain epiphenomena, such as suppression of movement or actual pain-evoked movements themselves.
Subcortical activations are also observed, most notably in thalamus (Th), basal ganglia, and cerebellum (eTable 1). Fig. 1 illustrates the brain regions most com- monly reported activated in pain studies.
Utilizing similar methodology, rCBF responses to a l-opioid agonist, remifentanil, were com- pared to that elicited by a placebo (Petrovic et al., 2002a). The two effects overlapped in terms of rCBF increases in dorsal ACC, suggesting that this brain region may be in- volved in placebo effects. Perhaps more notably, placebo responders showed responses to remifentanil that were more prominent than non-responders. These data suggest that the placebo effect on pain responses may be mediated by inter-individual variations in the ability to activate this neurotransmitter system, as hypothesized by others (Amanzio and Benedetti, 1999).
Another recent study demonstrated that thermal stimulation in com- plex regional pain syndrome (CRPS) patients gives rise to activity that closely matches that observed in normal subjects. However, this pattern changes dramatically when the ongoing pain of CRPS is isolated, by com- paring brain activity before and after sympathetic blocks that reduce the ongoing CRPS pain but do not change the thermal stimulus pain (Apkarian et al., 2001). Thus, there is no compelling evidence that examining brain responses to experimental painful stimuli can predict the pattern of brain responses in chronic clinical pain states.
Thus, we can assert that brain activity for pain in chronic clinical conditions is different from brain activity for acute painful stimuli in normal subjects. We add the caution that this does not imply that all clinical pain conditions have a homo- geneous underlying brain activity pattern. On the con- trary, most likely the patterns involving different clinical conditions are unique but with the current avail- able data we cannot test this at a meta-analysis level.
The brain imaging studies reviewed here indicate the cortical and sub-cortical substrate that underlies pain perception. Instead of locating a singular ‘‘pain center’’ in the brain, neuroimaging studies identify a network of somatosensory (S1, S2, IC), limbic (IC, ACC) and asso- ciative (PFC) structures receiving parallel inputs from multiple nociceptive pathways (Fig. 1). In contrast to touch, pain invokes an early activation of S2 and IC that may play a prominent role in sensory-discriminative functions of pain. The strong affective-motivational character of pain is exemplified by the participation of regions of the cingulate gyrus. The intensity and affec- tive quality of perceived pain is the net result of the interaction between ascending nociceptive inputs and antinociceptive controls. Dysregulations in the function of these networks may underlie vulnerability factors for the development of chronic pain and comorbid conditions.
Our analysis, in- stead, suggests that chronic pain conditions may be a reflection of decreased sensory processing and enhanced emotional/cognitive processing.