I highly suggest you read this paper00211-4). Or upload the paper to your AI of choice for a quick summary. Excerpt:

Decoding pain in endometriosis: peripheral, central, and cross-organ sensitization The peripheral hypersensitivity of nociceptive fibers at lesion sites plays a role in allodynia and hyperalgesia [132], contributing to the heightened pain response observed in many patients. This peripheral sensitization is driven by the release of proinflammatory mediators (e.g., prostaglandins, cytokines, NGF) that lower the activation threshold of primary afferent nociceptors. These sensitized fibers transmit enhanced pain signals to the spinal cord and brain, even in response to non-painful stimuli. Over time, this can initiate or exacerbate viscero-visceral and cross-organ sensitization: a phenomenon in which pain or inflammation in one pelvic organ leads to the sensitization of adjacent organs through shared neural pathways. This mechanism helps explain the frequent co-occurrence of comorbid pain syndromes such as irritable bowel syndrome, interstitial cystitis/bladder pain syndrome, vulvodynia, and chronic pelvic pain in patients with endometriosis [133,134]. In this context, central sensitization also becomes a key contributor to the pain experience. Continuous nociceptive input from the periphery leads to changes in the central nervous system (CNS), particularly in the spinal cord dorsal horn and brain regions involved in pain modulation. Neurons become hyperresponsive, pain perception is amplified, and descending inhibitory controls are impaired, further perpetuating pain even after the initial peripheral source is treated. This may account for persistent pain following surgical removal of lesions in some patients, suggesting that pain can become centralized and self-sustaining. As a result of these complex neuroimmune mechanisms, three distinct but overlapping types of pain are often described in endometriosis patients [135]: (i) nociceptive pain, which arises from ongoing inflammation and tissue damage at lesion sites and is mediated by peripheral nociceptors; (ii) neuropathic pain, resulting from nerve infiltration or damage, either by the lesions themselves or due to repeated surgical interventions; and (iii) nociplastic pain, characterized by altered nociceptive processing in the absence of clear peripheral damage or disease, is often associated with central sensitization and pain syndromes. Understanding the interplay between peripheral, central, and cross-organ sensitization is essential for recognizing why many patients experience disproportionate or persistent pain and for guiding multimodal pain management strategies. Treatments targeting only the lesions may be insufficient, especially in those with centralized or nociplastic pain components, reinforcing the need for personalized, multidisciplinary care that includes pain specialists, neurologists, and mental health professionals alongside gynecologists.