Central sensitization in endometriosis-associated deep dyspareunia

Endometriosis affects 10% of reproductive-aged women and is the presence of ectopic endometrial glands and stroma. It is associated with different types of pain, such as dysmenorrhea, dyschezia, and deep dyspareunia. Deep dyspareunia affects approximately 50% of women with endometriosis. Previous research has suggested that, in addition to disease-specific factors (e.g., Stage), other factors such as comorbid conditions or central sensitization may also play a role in the etiology of deep dyspareunia. The thesis objective is to provide evidence for the role of these other factors in the etiology of deep dyspareunia in endometriosis. I propose that bladder/pelvic floor tenderness and painful bladder syndrome (PBS) are associated with an increased severity of deep dyspareunia in women with endometriosis, and that these factors may be related to central sensitization. In Aim 1, using data from a prospective registry, I found that bladder/pelvic floor tenderness (assess by physical exam) and PBS (diagnosed using established criteria) were independently associated with severity of deep dyspareunia in women with both Stage I/II endometriosis (AOR=1.94, 95% CI 1.11-3.38, p=0.019; AOR=1.99, 95% CI 1.15-3.44, p=0.013; respectively) and Stage III/IV (AOR=2.51, 95% CI 1.25-5.02, p=0.01; AOR=1.90, 95% CI 1.01-3.57, p=0.048; respectively). In Aim 2, by prospectively recruiting patients and measuring their pain-pressure thresholds (PPT), I determined that PPT at extra-pelvic sites were significantly associated with bladder/pelvic floor tenderness in women with endometriosis (t=2.9, p=0.007; t=2.3, p=0.029; respectively). In contrast, there was no association between PPT and PBS. In conclusion, I found that bladder/pelvic floor tenderness and PBS were associated with greater severity of deep dyspareunia, regardless of endometriosis stage. I also found evidence that bladder/pelvic floor tenderness is associated with lower PPT in women with endometriosis, which may indicate the presence of central sensitization. In contrast, PBS was not associated with changes in PPT, and thus may arise in endometriosis through mechanisms other than central sensitization. My findings point to a role for central sensitization, manifesting as bladder/pelvic floor tenderness, in some women with endometriosis-associated deep dyspareunia. Further research is needed to confirm these findings, and to incorporate measures of central sensitization into the clinical management of endometriosis.