Pain- it’s complicated 

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Pain is a complex phenomenon, with multiple contributing factors. It is also one of the most prevalent symptoms of endometriosis. Pain can be a mix of several factors, such as inflammation, nerves, and myofascial components. Maddern et al. (2020) looked at the inflammatory and nerve component to pain with endometriosis. They report that the inflammation caused by the presence of endometriosis lesions activates sensory nerves and pain pathways. This activation of nerves then signals the body to incite more inflammation, which leads to more nerve activation. 

The longer this goes on then it creates a positive feedback loop where the nerves are primed for pain (which is part of the reason why earlier intervention is important). Maddern et al. (2020) note that in endometriosis lesions there are “increased density of small, unmyelinated nerve fibers.” They report that the “vast majority of these unmyelinated nerve fibers have been identified as C-fiber sensory afferents, unmyelinated nerves that typically function as nociceptors, implicating them strongly in the generation of CPP [chornic pelvic pain] in endometriosis” (Maddern et al., 2020). The authors report that the “early removal of lesions, before they established nerve fiber innervation” is important (Maddern et al., 2020).  

Maddern et al. (2020) also state that this activation of nerves in one area can cause cross activation of other nerve pathways in nearby organs (such as colon and bladder). Endometriosis lesions can promote the growth of more nerves and blood vessels called neuroangiogenesis. “Neuroangiogenesis aids irritation and invasion of existing nerves” and “the close proximity of endometrial adhesions and lesions to pelvic nerves can cause their encapsulation or compression, which contributes to CPP [chronic pelvic pain] associated with endometriosis” (Maddern et al., 2020). People with “endometriosis have a high comorbidity rate with other chronic pain syndromes associated with peripheral and central changes in pain processing, including, fibromyalgia, migraine headaches, IBS and painful bladder syndrome” (Maddern et al., 2020)  

Another contributing factor to this loop of pain is the affects on muscles and the fascia of the body. “Myofascial pain arises from dysfunction in the muscle and surrounding connective tissue” (Aredo et al., 2017). Aredo et al. (2017) reports that “ongoing visceral input can produce increased muscle tone and spasm” in addition to “‘guarding reflexes,’ which involve heightened sacral reflexes that are triggered by visceral pain and inflammation, could contribute to muscle tightening and result in pelvic floor dysfunction.” This myofascial pelvic pain can manifest as pain with penetration, defecation, and urination (Aredo et al., 2017). As Aredo et al. (2017) points out, “a myofascial component to pelvic pain adds another dimension to a patient’s disease and requires its own diagnosis and treatment.” This involvement of the myofasica can create what are called myofascial trigger points (MTrP). Aredo et al. (2017) states that:  

“Once formed, MTrPs can become a self-sustaining source of pain even after the visceral insult has resolved. Active MTrPs, in particular, serve as a source of ongoing nociception; they can reduce pain thresholds, enhance visceral and referred pain, and sensitize the nervous system. In regard to endometriosis, MTrPs that develop secondary to disease could sustain the pain and dysfunction despite lesion removal and hormonal management.” 

This is just the tip of the iceberg in the complicated process of pain with endometriosis. It is multifactorial and requires multidisciplinary care.  


Aredo, J. V., Heyrana, K. J., Karp, B. I., Shah, J. P., & Stratton, P. (2017, January). Relating chronic pelvic pain and endometriosis to signs of sensitization and myofascial pain and dysfunction. In Seminars in reproductive medicine (Vol. 35, No. 01, pp. 088-097). Thieme Medical Publishers. Retireved from  

Maddern, J., Grundy, L., Castro, J., & Brierley, S. M. (2020). Pain in endometriosis. Frontiers in Cellular Neuroscience14. Retreived from