Is it Time to Explore the Processing of Inflammatory Pain in the Human Brain

p ain arising from inflammatory disease is a major medical problem that is expanding in step with our aging population. Dr. Guilbaud's studies, using rat models of inflammation, have provided invaluable information about supraspinal processing of nociceptive information related to inflammatory pain. Her work has revealed changes in neuronal responsiveness in the ventrobasal (VB) thalamus and in somatosensory cortex (Sml) of rats that are consistent with inflammatory hyperalgesia and allodynia, suggesting that these regions could subserve such phenomena. Nevertheless, Dr. Guilbaud also points out that in addition to providing at least partial answers to questions about theneural basis of inflammatory pain, her data also raises new questions, including whether there exists a specific pathway devoted to joint pain and what function is served by the large imbalance between neuronal responsiveness to an inflamed joint and other somatic inputs. I would like to propose that a clear answer to these questions will most likely Come from studies in primates, and particularly in man. Recent data from monkeys and humans reveal a much more elaborate thalamocortical pain processing system than that identified in rats. Anatomical and physiological evidence shows that there are multiple thalamic and cortical sites that probably receive nociceptive input. The primate spinothalamic tract that transmits nociceptive information terminates in several thalamic regions, including the ventral