Abstract
In the past decade of pain research, a network of pain transmitting areas within the CNS has been established, based on both animal studies and findings from functional imaging studies in humans. Consequently, the neurobiology of pain is increasingly understood as an integration of activity in distinct neuronal structures. Evidence of altered local brain chemistry and functional reorganization in chronic back pain patients supports the idea that chronic pain could be understood not only as an altered functional state, but also as a consequence of central plasticity. Recently, local morphologic alterations of the brain in areas ascribable to the transmission of pain were detected in patients suffering from phantom pain, chronic back pain, irritable bowl syndrome, fibromyalgia and two types of frequent headaches. These alterations were different for each pain syndrome, but overlapped in the cingulate cortex, the orbito-frontal cortex, the insula and dorsal pons. These regions function as multi-integrative structures during the experience and the anticipation of pain. Although some authors discussed these findings as damage or loss of brain gray matter, one of the key questions is whether these structural alterations in the cerebral pain transmitting network precede or succeed the chronicity of pain. A very recent paper investigated patients with chronic pain due to primary hip osteoarthritis and found a characteristic gray matter decrease in patients compared to controls in the anterior cingulate cortex (ACC), right insular cortex and operculum, DLPFC, amygdala and brainstem. Following total hip replacement a subgroup of these patients were completely pain free and showed 6 weeks and 4 months after surgery, monitoring a gray matter increase in the DLPFC, ACC, amygdala and brainstem. As gray matter decrease is at least partly reversible when pain is successfully treated, the author suggests that the gray matter abnormalities found in chronic pain do not reflect brain damage, but are rather a reversible consequence of chronic nociceptive transmission, which normalizes when the pain is adequately treated.
Published Version
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