Chronic pelvic pain can be a difficult condition to diagnose and manage. It encompasses a diverse group of medical conditions including vulvodynia, prostatitis, cystitis, endometriosis, and dyspareunia among others. Chronic pelvic pain can originate from gynecological, psychological, myofascial, urological, or gastrointestinal causes [1]. It is defined by The American College of Obstetricians and Gynecologists as pain of six or more months in duration that is located in the abdomen, groin, or low back. The prevalence of chronic pelvic pain is approximately up to 15 % in women and 2–10 % in men [2, 3]. In addition, chronic pelvic pain accounts for 40 % of gynecological laparoscopic procedures [4].

Myofascial pelvic pain, or myofascial pain syndrome (MPS) of the pelvis, refers to the pain originating from the pelvic floor musculatures and the associated connecting fascia and connective tissues. This pain syndrome often arises from preexisting urological, gynecological, or colorectal medical conditions or it can exist alone with no concomitant pathologies. Musculoskeletal/myofascial causes of pelvic pain is often overlooked because it is hard to diagnose. There is lack of highly sensitive and specific noninvasive diagnostic modalities, and the etiology of the pelvic floor muscle pain is not fully understood with several different existing theories. Also, the physical exam of pelvic floor muscle requires entry into the vaginal vault or rectum, which can be uncomfortable for patients. Furthermore, many providers are simply not adequately trained in this technique resulting in low numbers of proper digital palpation of the pelvic floor muscle during gynecological, urological, and colorectal examinations [5]. In this chapter, the overview of MPS, anatomy of the pelvic floor, the epidemiology/etiology, diagnosis, and treatment of myofascial pelvic pain will be discussed.

MPS is defined as the musculoskeletal pain characterized by sensory, motor, and autonomic dysfunction due to myofascial trigger points (MTrPs) in the muscle, fascia, or tendinous insertions. A trigger point (TrP) is a tiny discrete area or nodule approximately 5–10 mm in diameter that is hyperirritable/tender in a taut band of skeletal muscle. Reproducible pain upon palpation is required for the clinical diagnosis of MPS [6].

Two types of TrPs exist [6] as follows:

In contrast with the TrPs are the tender points, which are used for the diagnosis of fibromyalgia. TrPs produce a specific referred pain pattern to a distant site while tender points only produce a local response in their immediate surroundings. Many features of MPS and fibromyalgia overlap but they are two separate entities.

Myofascial pain is very common; however, in terms of the MPS diagnosis, the exact prevalence has not been obtained. The more broad diagnosis of chronic musculoskeletal pain is estimated to affect between 10 and 20 % of the population. One study reported about 85 % of patients seeking care at pain clinic to have MPS, but there has not been a study looking at the myofascial pain of the pelvic floor muscles specifically [7]. Overall, MPS is equally distributed between men and women, but for pelvic/urogenital myofascial pain, it is more common in women than in men. Difference in the incidence of MPS among races has not been reported in literature. However, the likelihood of developing active TrP increases with age and with a sedentary lifestyle [7].

There are several theories that have been proposed to correctly identify the etiology/pathophysiology of the MPS. A modern understanding of myofascial pain can be derived from the work of Dr. Janet Travell and Dr. David Simons. Their book, Myofascial Pain and Dysfunction: The Trigger Point Manual, is instrumental in defining the diagnosis and treatment of MPS. Simons postulated the integrated TrP hypothesis, which is one of the most accepted theories for myofascial pain, and it served as the groundwork for researchers after him.

Before discussing the integrated TrP hypothesis, the basic mechanism of muscle contraction and relaxation is reviewed: an action potential travels down a nerve axon causing acetylcholine (ACh) release into the neuromuscular junction [6]. ACh travels across the junction and binds to ACh receptors initiating an end-plate potential, which propagates along the sarcoplasmic reticulum down the T-tubule and triggers a downstream release of calcium. Calcium binds with troponin allowing actin–myosin crossbridge formation and subsequent muscle contraction. In order for the muscle to relax, adenosine triphosphate (ATP) is required for the release of actin–myosin crossbridge and the detachment of calcium from the troponin. In addition, ATP is required to actively pump calcium back into the sarcoplasmic reticulum. As hypothesized by Dr. David Simons, there is an abnormally excessive release of ACh resulting in increase of end-plate potential and subsequently causing overall increased muscle contraction/tension, which manifest as the taut band found in a MTrP. The taut band causes a state of energy crisis via reduced blood flow resulting in local hypoxia, increased metabolic demand, and ultimately overall decreased level of ATP. During this state of metabolic imbalance/energy crisis, noxious substances are released such as substance P, bradykinin, calcitonin gene-related peptide (CGRP), prostaglandins, and inflammatory cytokines. These noxious chemicals may account for the sensitization of the peripheral nociceptors and contribute to the pain associated with the active TrP [8–10].

Around the same time the integrated TrP hypothesis came out, Hagg et al. postulated the Cinderella hypothesis. Many of the tenets overlap with integrated TrP hypothesis. The Cinderella hypothesis theorized the state of sustained, low level, and repetitive muscle contractions results in hypoxia, ischemia, and reduced ATP production and is responsible for reduced pH, increased acidity, calcium accumulation, and ultimately sarcomere contraction. Constant muscle contraction leads to the release of several sensitizing substances causing peripheral sensitization similar to the integrated TrP hypothesis [10].

Many researchers including Gerwin and his colleagues further expand on Simons’ integrated TrP hypothesis. The inciting event is that the muscles are being stressed beyond normally tolerated level causing muscle injury and capillary constriction. Muscle injury triggers the release of noxious chemicals that activate the nociceptors causing pain, which then further cause the sympathetic activation leading to more capillary constriction and decreased blood perfusion. The pH becomes acidic, inhibiting acetylcholinesterase (AChE) causing more ACh reaching the motor end plate. One of the noxious chemicals released from the injured muscle includes CGRP, and CGRP causes further inhibition of AChE and facilitate more ACh release and upregulate the ACh receptors at the motor end plate. The end result is the altered activity at the motor end plate triggering more end-plate potential, muscle contraction, and increased muscle activity forming the taut band of the TrP [11].

The theories discussed above involve the sensitization of the peripheral nociceptors. Researchers now have shown that there is modification of the central nervous system and this further complicates the muscle pain associated with MTrP. With the nociceptors activation/peripheral sensitization, the signal also travels via the afferent fiber to the dorsal root ganglion and triggers the release of substance P and CGRP from the dorsal root ganglion to the peripheral tissues. The release of these chemicals into the periphery causes further noxious chemical release leading to more local hyperalgesia and exacerbates local tissue tenderness. Overtime, the continuous and repetitive activation of these primary afferent activities results in the modulation of the dorsal root ganglion and dorsal horn neurons, a process known as central sensitization. The overall effect of central sensitization is increased pain and making the active TrP even more painful and tender [8–10].

As explained earlier, MTrP is the underlying cause of MPS. In the pelvis, there is an extensive network of muscles, fascia, and connective tissue where TrPs can be found. These active and/or latent TrPs of the pelvic muscles, or any muscle in the body, can develop due to mechanical, physical, organ system, and psychological stressors. Examples of mechanical stressors include improper posture, leg length discrepancy, overuse of muscles, prolonged mobility/immobility, and dysfunctional gait among others. Events such as pelvic surgeries, colonoscopy, vagina ultrasound, pelvic/rectal exam, and childbirth are examples of physical stressor that can produce localized trauma and ultimately the development of TrPs. Emotional or psychological stressors such as prior history of sexual abuse, depression, lack of sleep, or general stress/anxiety in life can often cause dysfunction to the pelvic muscles resulting in TrPs and myofascial pain in the area. Lastly, pathologies in the pelvic region such as prostatitis, endometriosis, chronic cystitis, colitis, or hemorrhoids can cause TrPs to the pelvic floor muscles via a viscerosomatic reflex [2, 6, 12].

In addition, researchers have also looked into the role of nutritional deficiencies of water-soluble vitamins, folic acid, vitamin C, calcium, iron, and potassium in the development of MTrPs. Vitamin C in particular is an important cofactor for norepinephrine and serotonin production, and these chemicals are involved with the modulation of pain transmission. Vitamin C is also involved in collagen synthesis, which is important for muscle, ligament, bone, and joint health [13, 14].

Myofascial pelvic pain or pelvic MPS can be explained by three general tenets with the understanding of the pathophysiology of the MTrP discussed earlier: (1) viscerosomatic reflex, (2) somatovisceral reflex, and (3) central sensitization.