Chronic pelvic pain (CPP) is a highly prevalent pain condition, estimated to affect 15-20% of women in the United States. Endometriosis is often associated with CPP, however other factors, such as pre-existing or concomitant changes of the central pain system, might contribute to the development of chronic pain. We applied voxel-based morphometry to determine whether women with CPP with and without endometriosis display changes in brain morphology in regions known to be involved in pain processing.Four subgroups of women participated: 17 with endometriosis and CPP, 15 with endometriosis without CPP, 6 with CPP without endometriosis, as well as 23 healthy controls. All patients with endometriosis and/or CPP were surgically-confirmed. Relative to controls, women with endometriosis-associated CPP displayed decreased gray matter volume in brain regions involved in pain perception including the left thalamus, left cingulategyrus, right putamen, and right insula. Women with CPP without endometriosis also showed decreases in gray matter volume in the left thalamus. Such decreases were not observed in patients with endometriosis that had no CPP. We conclude thatCPP is associated with changes in regional gray matter volume within the central pain system. Although endometriosis may be an important risk factor for the development of CPP, acting as a cyclic source of peripheral nociceptive input, our data support the notion that changes in the central pain system also play an important role in the development of chronic pain, regardless of the presence of endometriosis.

OBJECTIVE To determine if women with chronic pelvic pain and variable degrees of endometriosis demonstrate altered pain sensitivity relative to pain-free healthy controls, and whether such differences are related to the presence or severity of endometriosis or comorbid pain syndromes. METHODS Four patient subgroups (endometriosis with chronic pelvic pain (n=42), endometriosis with dysmenorrhea (n=15), pain-free endometriosis (n=35), and chronic pelvic pain without endometriosis (n=22)) were each compared to 30 healthy controls in this cross-sectional study. All patients completed validated questionnaires regarding pain symptoms and underwent screening for comorbid pain disorders. Pain sensitivity was assessed by applying discrete pressure stimuli to the thumbnail using a previously validated protocol. RESULTS While adjusting for age and education, pain thresholds were lower in all subgroups of women with pelvic pain, relative to healthy controls (all p-values <0.01). There was no difference in pain thresholds when comparing endometriosis patients without pelvic pain to healthy controls (mean difference 0.02 kg/m2, 95% confidence interval -0.43, 0.47). The presence and severity of endometriosis and number of comorbid pain syndromes were not associated with a difference in pain thresholds. CONCLUSION Women with chronic pelvic pain demonstrate increased pain sensitivity at a nonpelvic site compared to healthy controls, which is independent of the presence or severity of endometriosis or comorbid pain syndromes. These findings support the notion that central pain amplification may play a role in the development of pelvic pain, and may explain why some women with pelvic pain do not respond to therapies aimed at eliminating endometriosis lesions.