Evaluation of brain pain centers in endometriosis-associated chronic pelvic pain: Retrospective insights into central sensitization using a novel magnetic resonance imaging technique

IŞIN ERDOĞAN, Isin Erdogan, Barış Kaya, Serdar Arslan, Ahmet Oz, Koray Gök, Abdullah Tüten, Abdullah Tuten, Abdullah Serdar Açıkgöz
International Journal of Gynecology & Obstetrics · 2026 · doi:10.1002/ijgo.71039 · PMID:42033133 · W7155651572
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Women with endometriosis-associated chronic pelvic pain showed altered brain connectivity in pain processing networks, supporting central sensitization, unlike those with ovarian endometriomas without pain.

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This retrospective study used resting-state functional MRI and seed-to-voxel analyses (SPM12 and CONN toolbox) to compare brain pain-processing network connectivity among 10 women with deep infiltrating endometriosis and chronic pelvic pain, 10 women with ovarian endometriomas without pain, and 10 healthy controls. Compared with controls, the DIE-with-pain group showed FWE-corrected increased connectivity involving regions such as the amygdala, frontal pole, paracingulate gyrus, frontal operculum, and anterior cingulate gyrus, as well as increased posterior cingulate–precuneus connectivity, alongside decreased anterior cingulate–middle temporal connectivity. Women with ovarian endometriomas without pain had no significant connectivity differences versus controls. The authors conclude these neurofunctional alterations support central sensitization in endometriosis-associated chronic pelvic pain, while noting the limitations inherent to retrospective design and no data sharing. This paper is centrally about endometriosis—investigating brain pain-network connectivity differences in women with deep infiltrating endometriosis-associated chronic pelvic pain.

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Abstract

OBJECTIVE: To investigate alterations in brain pain-processing networks using resting-state functional magnetic resonance imaging (rs-fMRI) in women with endometriosis-associated chronic pelvic pain and to evaluate neurobiological evidence of central sensitization relevant to clinical management. METHODS: This retrospective study included 30 women aged 18-45 years: 10 with deep infiltrating endometriosis (DIE) and chronic pelvic pain, 10 with ovarian endometriomas without pain, and 10 healthy controls. rs-fMRI data were analyzed using the SPM12 and the CONN toolbox. Seed-to-voxel functional connectivity analyses focused on predefined pain-related brain regions. Between-group differences were assessed using two-sample t tests with family-wise error (FWE) correction. RESULTS: Compared with controls, women with DIE and chronic pelvic pain demonstrated significantly increased connectivity between the amygdala and the right frontal pole (FWE-corrected P = 0.012 and 0.044), left paracingulate gyrus (FWE-corrected P = 0.036), right frontal operculum cortex (FWE-corrected P = 0.040), and anterior cingulate gyrus (FWE-corrected P = 0.044). Increased con was also observed between the posterior cingulate gyrus and the precuneus cortex (FWE-corrected P = 0.002), whereas decreased connectivity was detected between the anterior cingulate gyrus and the posterior left middle temporal gyrus (FWE-corrected P = 0.002). No significant differences were found in patients with ovarian endometriomas without pain. CONCLUSION: Endometriosis-associated chronic pelvic pain is associated with altered connectivity within key pain modulation networks, supporting central sensitization. Persistent pelvic pain may therefore reflect maladaptive central pain processing in addition to peripheral pathology. Recognition of these neurofunctional alterations may improve understanding of treatment-resistant pain and support earlier multidisciplinary and individualized management strategies.
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Abstract

Objective To investigate alterations in brain pain-processing networks using resting-state functional magnetic resonance imaging (rs-fMRI) in women with endometriosis-associated chronic pelvic pain and to evaluate neurobiological evidence of central sensitization relevant to clinical management.

Methods

This retrospective study included 30 women aged 18–45 years: 10 with deep infiltrating endometriosis (DIE) and chronic pelvic pain, 10 with ovarian endometriomas without pain, and 10 healthy controls. rs-fMRI data were analyzed using the SPM12 and the CONN toolbox. Seed-to-voxel functional connectivity analyses focused on predefined pain-related brain regions. Between-group differences were assessed using two-sample t tests with family-wise error (FWE) correction.

Results

Compared with controls, women with DIE and chronic pelvic pain demonstrated significantly increased connectivity between the amygdala and the right frontal pole (FWE-corrected P = 0.012 and 0.044), left paracingulate gyrus (FWE-corrected P = 0.036), right frontal operculum cortex (FWE-corrected P = 0.040), and anterior cingulate gyrus (FWE-corrected P = 0.044). Increased con was also observed between the posterior cingulate gyrus and the precuneus cortex (FWE-corrected P = 0.002), whereas decreased connectivity was detected between the anterior cingulate gyrus and the posterior left middle temporal gyrus (FWE-corrected P = 0.002). No significant differences were found in patients with ovarian endometriomas without pain.

Conclusion

Endometriosis-associated chronic pelvic pain is associated with altered connectivity within key pain modulation networks, supporting central sensitization. Persistent pelvic pain may therefore reflect maladaptive central pain processing in addition to peripheral pathology. Recognition of these neurofunctional alterations may improve understanding of treatment-resistant pain and support earlier multidisciplinary and individualized management strategies. CONFLICT OF INTEREST STATEMENT The authors declare no conflicts of interest to disclose. DATA AVAILABILITY STATEMENT Research data are not shared.

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Condition tags

endometriosisdie_deep_infiltratingchronic_pelvic_pain

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (32)

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