Relating Chronic Pelvic Pain and Endometriosis to Signs of Sensitization and Myofascial Pain and Dysfunction

Abstract

Chronic pelvic pain is a frustrating symptom for patients with endometriosis and is frequently refractory to hormonal and surgical management. While these therapies target ectopic endometrial lesions, they do not directly address pain due to central sensitization of the nervous system and myofascial dysfunction, which can continue to generate pain from myofascial trigger points even after traditional treatments are optimized. This article provides a background for understanding how endometriosis facilitates remodeling of neural networks, contributing to sensitization and generation of myofascial trigger points. A framework for evaluating such sensitization and myofascial trigger points in a clinical setting is presented. Treatments that specifically address myofascial pain secondary to spontaneously painful myofascial trigger points and their putative mechanisms of action are also reviewed, including physical therapy, dry needling, anesthetic injections, and botulinum toxin injections.

Fig. 1

Nervous system engagement by endometrial lesions gives rise to different types of pain. (a) This figure illustrates how endometrial lesions can engage the nervous system to give rise to different types of pain associated with endometriosis and comorbid conditions. (1) Typical laparoscopic view of pelvic organs from the umbilicus. Inset demonstrates a deeply infiltrating lesion on the left uterosacral ligament. Both peptidergic sensory (blue) and sympathetic nerve fibers (green) sprout axon branches (red dashed lines) toward this lesion. Estradiol and sympathetic-sensory coupling drive peripheral sensitization (red asterisk) of new sensory fibers within the lesion. (2) Central sensitization (red asterisk) is propagated at synapses between sensitized peripheral nerve fibers and neurons in the sacral spine. This central sensitization is modulated differently from and can eventually become independent of peripherally sensitizing signals. (3) Although input from pelvic peripheral afferent fibers typically synapse with dorsal root ganglia in the sacral spine, branches of the fibers extend to other segments (blue dashed lines), and can propagate sensitization at distant spinal cord segments (red dashed lines). (4) Normally, multiple intersegmental spinal synaptic connections exist to coordinate bodily functions (double-arrowed black lines). In pathological pain conditions, this communication can alter processing of nociceptive and non-nociceptive sensory information in remote segments (“remote central sensitization, red asterisks). Via (3) and (4), increased nociception propagates into distant spinal segments. (5) Multiple afferent (blue) and efferent (green) pathways exist between the CNS and PNS with terminal connections in the brain. Input from sensitized spinal neurons can affect activity throughout the neuroaxis (red asterisks), altering normal processing of nociceptive and non-nociceptive information. Alterations in processing can occur on the medial cortical surface; the lateral prefrontal, frontal, and parietal lobes; and within the temporal lobe (dotted black ellipses). These influences can propagate signals independent of peripheral sensitization associated with lesions. (b) Muscles of the pelvic floor feed into sensitization pathways in the same manner as endometrial lesions. All mechanisms outlined can cause endometriosis-associated pain in the pelvis and at distant sites. (Reprinted with permission from Stratton and Berkley.)