The Journal of Neuroscience, November 4, 2009, 29(44):13746-13750; doi:10.1523/JNEUROSCI.3687-09.2009
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Brief Communications
Brain Gray Matter Decrease in Chronic Pain Is the Consequence and Not the Cause of Pain
Rea Rodriguez-Raecke,1
Andreas Niemeier,2
Kristin Ihle,1
Wolfgang Ruether,1 and
Arne May1
Departments of 1Systems Neuroscience and 2Orthopaedics, University Medical Center Hamburg Eppendorf, D-20246 Hamburg, Germany
Correspondence should be addressed to Dr. Arne May, Assistant Professor of Neurology, Department of Systems Neuroscience, University of Hamburg Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany. Email: a.may{at}uke.uni-hamburg.de
Recently, local morphologic alterations of the brain in areas ascribable to the transmission of pain were reported in patients suffering from chronic 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. We investigated 32 patients with chronic pain due to primary hip osteoarthritis and found a characteristic gray matter decrease in patients compared with controls in the anterior cingulate cortex (ACC), right insular cortex and operculum, dorsolateral prefrontal cortex (DLPFC), amygdala, and brainstem. We then investigated a subgroup of these patients (n = 10) 6 weeks and 4 months after total hip replacement surgery, monitoring whole brain structure. After surgery, all 10 patients were completely pain free and we observed 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, we suggest that the gray matter abnormalities found in chronic pain do not reflect brain damage but rather are a reversible consequence of chronic nociceptive transmission, which normalizes when the pain is adequately treated.
Received July 30, 2009;
revised Sept. 8, 2009;
accepted Sept. 10, 2009.
Correspondence should be addressed to Dr. Arne May, Assistant Professor of Neurology, Department of Systems Neuroscience, University of Hamburg Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany. Email: a.may{at}uke.uni-hamburg.de
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