Nociceptive Processing in the Cerebral Cortex

The study of nociceptive processing in the cerebral cortex has come a long way. In addition to the primary and secondary somatosensory cortex, limbic areas such as the anterior and mid-cingulate cortex and the insula have also been recognized as part of the nociceptive network, and more recently also cognitive areas in the prefrontal cortex. Limbic areas are usually considered to mediate emotional processes, but they are also involved in autonomic and motor functions. In this way, the cortical nociceptive network mirrors the subcortical networks, which also include many connections to autonomic and motor nuclei. Images of brain activation by painful stimuli leave the impression that at least half of the brain participates in processing nociceptive information. At other times, many of the same areas participate in visual, motor, emotional, cognitive, or other signal processing. In that sense, our current understanding of the nociceptive network in the brain is consistent with our current understanding of how the brain uses distributed processing for its many functions. It is not clear, however, to what extent any part of the cerebral cortex is specific for nociception. The best candidate region for such a function lies in the parasylvian cortex, in the vicinity of the secondary somatosensory cortex and the dorsal insula. Cortical activity possesses properties necessary for involvement in pain perception, like somatotopic representation of painful stimuli, correlation with stimulus intensity, modulation with attention, modulation with expectation and other psychological variables, and distinct brain regions showing differential activity for sensory and affective dimensions of pain, as well as attenuation of responses with analgesic drugs. Thus, human brain imaging studies have asserted the role of the cortex in acute pain. However, perception of pain automatically directs attention to the source of pain, results in autonomic responses, motor reflexes to escape from the pain, and other emotional and cognitive responses. Therefore, the extent to which cortical activity in acute pain reflects secondary processes remains to be determined. In chronic pain, the clinical brain imaging studies indicate reduced information transmission through the thalamus to the cortex, and increased activity in prefrontal cortex (PFC), mostly in medial PFC coupled with atrophy in dorsolateral PFC. The observations regarding cortical and thalamic activity changes in chronic pain are consistent with the notion that chronic pain conditions preferentially engage brain areas involved in cognition/emotion and decrease activity in regions involved in sensory evaluation of nociceptive inputs.