Endometriosis: an investigation into persistent pelvic pain
Martel, Elena Patrice
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OBJECTIVES: This study aims to explore the relationship between central pain amplification and persistent pelvic pain. No previous studies have utilized bimanual pelvic examination findings, in addition to pressure-pain analysis, in an effort to investigate the mechanisms contributing to Chronic Pelvic Pain (CPP) in women with endometriosis. METHODS: Participants included 144 women aged 18-50 years old, diagnosed with CPP and/or surgically-confirmed endometriosis compared to healthy controls. Participants were categorized into four groups, including pain-free endometriosis (Endo Ø Pain), painful endometriosis (Endo + Pain), Chronic Pelvic Pain without endometriosis (CPP Ø Endo), and healthy controls. Pressure-pain Quantitative Sensory Testing (QST) was conducted on all participants to determine levels of pain thresholds. External systemic tenderpoints were assessed utilizing standardized fibromyalgia tenderpoint criteria. A pelvic examination was performed on participants in the gynecological sample in order to assess internal tenderness. One-way ANOVA, chi-square analyses were conducted to assess descriptive variables. Correlation calculations were performed to assess the relationship between pressure-pain thresholds and tenderpoints. Generalized Linear Models (GLM) were conducted to analyze the differences on pressure-pain thresholds and pelvic exam tenderpoints between groups, while controlling for age and number of comorbid chronic pain syndromes (CPS). RESULTS: Endo Ø Pain had a significantly higher stage of endometriosis and were significantly older than the Endo + Pain group. Healthy controls had less external systemic tenderpoints than all patient subgroups. CPP Ø Endo and Endo + Pain had more CPS than healthy controls and Endo Ø Pain. Pelvic exam tenderpoints (r= -0.31, p < 0.01) and systemic external tenderpoints (r = -0.35, p <0.01) were negatively correlated with low pressure-pain threshold. Systemic external tenderpoints were negatively correlated with the high pressure staircase (r= -0.41, p < 0.01), but pelvic exam tenderpoints were not. The GLMs conducted revealed that Endo Ø Pain had significantly higher low pressure-pain threshold compared to both Endo + Pain (difference = 0.57, p < 0.01, CI= 0.12, 1.02) and healthy controls (difference = 0.55, p < 0.05, CI= 0.08, 1.02). The CPP Ø Endo group had significantly lower high pressure-pain threshold scores compared to healthy controls (difference = 0.38, p < 0.05, CI= 0.05, 0.71). The Endo + Pain group also had significantly lower high-pain thresholds as compared to healthy controls (difference= 0.31, p < 0.05, CI= 0.04, 0.58). CPP Ø Endo group had significantly more pelvic tenderpoints compared to Endo Ø Pain (difference = 2.81, p < 0.001, CI = 1.36, 4.27); Endo + Pain group also had significantly more pelvic exam tenderpoints than the Endo Ø Pain (difference= 2.10, p < 0.001, CI = 0.96, 3.24). CONCLUSIONS: The findings of this study suggest that pain thresholds, as measured by QST pressure-pain testing, are associated with persistent pelvic pain. CPP Ø Endo and Endo + Pain experienced more systemic tenderness, and more CPS than the Endo Ø Pain group and healthy controls. This indicates that chronic pain, not endometrial lesions, are likely responsible for the development of centralized pain amplification. Although the etiology of endometriosis and CPP is poorly understood, the findings of this study contribute to the idea that central sensitization is associated with the shared underlying pain mechanism in chronic pain syndromes.
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