Commentary on central sensitization in chronic pelvic pain

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This commentary reviews the role of central sensitization in the pathophysiology of chronic pelvic pain, highlighting its impact on pain perception and treatment strategies.

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This commentary critiques a study by Alawadi et al. regarding central sensitization in women with chronic pelvic pain resistant to hormonal therapy, highlighting significant methodological limitations. The authors argue that relying on the non-gold-standard Convergences PP Score and the off-label use of the DN4 questionnaire likely introduced misclassification and measurement bias into the prevalence estimates. Additionally, the critique notes that the lack of surgical confirmation for endometriosis status created diagnostic heterogeneity, while the absence of psychological covariates and the use of analgesic consumption as a severity surrogate further confounded the results. Relevance to endometriosis: The paper explicitly discusses the challenge of confirming endometriosis status in chronic pelvic pain cohorts, noting that without laparoscopic verification, populations remain clinically heterogeneous and difficult to interpret.

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Author

All the authors meet the ICMJE authorship criteria and have made significant and equal contributions to this manuscript. All authors approved the final version and agree to be accountable for all aspects of the work, ensuring the accuracy and integrity of the data and interpretation.

Funding

The authors have nothing to report.

Coi Statement

The authors declare no conflict of interest.

Opening Section

We read with interest the article by Alawadi et al. 1 examining the prevalence and clinical correlates of central sensitization in women with chronic pelvic pain (CPP) resistant to hormonal therapy. The authors are commended for highlighting the multidimensional nature of CPP and reinforcing the need for trauma‐informed, multidisciplinary care. However, several methodological considerations warrant discussion, as they may affect the interpretation and generalizability of the findings. First, there is a use of a non‐gold‐standard instrument (Convergences PP Score) as the sole definition of central sensitization. PPCS was defined exclusively using the Convergences PP Score ≥5; however, central sensitization is a complex neurophysiological phenomenon ideally assessed through multiple modalities, including quantitative sensory testing, pressure pain thresholds, and validated inventories. Reliance on a single non‐gold‐standard instrument may have introduced misclassification bias, potentially rendering the reported prevalence of 54.4% an over‐ or underestimate. As Arendt‐Nielsen et al. 2 emphasized, symptom questionnaires alone are insufficient to fully characterize central sensitization without complementary psychophysical testing. Second, the DN4 questionnaire, which was originally validated for somatic neuropathic pain, was applied here to pelvic pain, a setting beyond its original validation scope. This off‐label use introduces measurement bias, potentially distorting the reported prevalence of neuropathic‐like features and may partly explain why neuropathic‐like pain correlated with quality of life but not analgesic use. Notably, the authors did not explicitly list this as a study limitation. Bouhassira et al. 3 developed DN4 specifically for neuropathic pain associated with nervous system lesions. Third, there is a lack of objective confirmation of endometriosis status. The cohort included women with or without endometriosis, with diagnoses based primarily on imaging and clinical assessment rather than surgical or histological confirmation. This may have introduced diagnostic heterogeneity. Consequently, the reported prevalence of pelvic and perineal pain central sensitization (PPCS) may not be attributable solely to endometriosis‐like pelvic pain, limiting the interpretability and comparability of the findings across studies. Howard FM et al. 4 emphasized that without laparoscopic confirmation, CPP populations become clinically heterogeneous and difficult to compare. Fourth, there is an absence of psychological and psychiatric covariates. Although violence history was assessed, the absence of systematic evaluation of depression, anxiety, catastrophizing, PTSD, and somatization introduces residual confounding, as observed associations between PPCS and quality of life may partly reflect psychological distress rather than sensitization per se, potentially exaggerating PPCS's independent effect, consistent with As‐Sanie et al.'s 5 demonstration of strong associations between psychological distress and CPP severity. Fifth, analgesic consumption was used as a surrogate marker of disease severity. The use of step 2/3 analgesic consumption as a surrogate for disease severity is subject to confounding by indication, as prescribing patterns are influenced by physician preference, access to pain specialists, socioeconomic status, patient beliefs, and healthcare utilization. Consequently, higher analgesic use may not reliably reflect greater central sensitization severity, limiting the validity of this proxy measure. Chiuve et al. 6 emphasized that chronic opioid prescribing in endometriosis is influenced by multiple healthcare‐related factors beyond pain intensity. Future studies should combine the Convergences PP Score with QST, validated sensitization inventories, and pelvic pain‐specific neuropathic tools, while stratifying patients by confirmed endometriosis status, adjusting for psychological confounders, and quantifying pain burden longitudinally using morphine‐equivalent doses. In conclusion, while this study valuably highlights central sensitization in hormonal therapy‐resistant CPP, the reliance on symptom‐based screening, diagnostic heterogeneity, absence of psychological covariates, and use of analgesic consumption as a surrogate outcome may have influenced the reported associations. Future prospective studies addressing these limitations will strengthen the evidence base and clarify the role of central sensitization in CPP management.

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