To determine whether women with chronic pelvic pain and variable degrees of endometriosis demonstrate altered pain sensitivity relative to pain-free healthy women in a control group and whether such differences are related to the presence or severity of endometriosis or comorbid pain syndromes.
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 with 30 healthy women in a control group 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.
While adjusting for age and education, pain thresholds were lower in all subgroups of women with pelvic pain relative to healthy women in the control group (all P values <.01). There was no difference in pain thresholds when comparing patients with endometriosis without pelvic pain with healthy women in the control group (mean difference 0.02 kg/m2, 95% confidence interval −0.43 to 0.47). The presence and severity of endometriosis and number of comorbid pain syndromes were not associated with a difference in pain thresholds.
Women with chronic pelvic pain demonstrate increased pain sensitivity at a nonpelvic site compared with healthy women in a control group, 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.
Pelvic pain is associated with increased pain sensitivity, which is unrelated to the presence or severity of endometriosis or comorbid pain syndromes.
Departments of Obstetrics and Gynecology, Anesthesiology, and Internal Medicine (Rheumatology), University of Michigan Health Center, Ann Arbor, Michigan; and the Department of Obstetrics and Gynecology, Northshore University Health System, Chicago, Illinois.
Corresponding author: Sawsan As-Sanie, MD, MPH, Department of Obstetrics and Gynecology, University of Michigan Health System, L4100 Women's Hospital, 1500 East Medical Center Drive, Ann Arbor, MI 48109; e-mail: firstname.lastname@example.org.
Supported in part by National Institutes of Health (NIH) K12HD001438, NIH UL1RR024986, and the Bayer Droegemueller Award in Clinical Research.
Presented in part at the Society for Gynecologic Investigation annual scientific meeting, March 17–21, 2009, Glasgow, United Kingdom.
Financial Disclosure Dr. Tu receives research funding from AbbVie. The other authors did not report any potential conflicts of interest.