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.
