Chronic pelvic and vulvar pain pelvic floor dysfunction ( PFD), and PFMD typically, but not always, coexist. There are rare clinical cases that present with no physical findings; however, those cases are, by far, not the norm. Such complexity is elucidated by the European Association of Urology in their “Guidelines on Chronic Pelvic Pain .” They list 15 definitions relating to female pelvic pain, implicating involvement of PFMs, bladder, urethra, uterus, vagina, vulva, clitoris, pudendal nerve, rectum, and perineum [5]. Visceral disorders within the pelvis that are known to contribute to pain include painful bladder syndrome/interstitial cystitis (PBS/IC), irritable bowel syndrome (IBS), dysmenorrhea, and endometriosis. Chronic, abnormal stimuli that are present with these visceral pain( disorders can slowly upregulate the spinal cord, disrupting sacral reflexes that regulate sensation and pain [6]. Fascial laxity and resulting organ prolapse may contribute to the pain puzzle, as can bony irregularities (e.g., sacroiliac joint dysfunction and hip pain).

Understanding pain related only to PFMD can be equally confusing as it has received multiple labels over time—coccydynia, levator (spasm) syndrome, tension myalgia of the PF, PF spasticity, urethral/anal sphincter dyssynergia, vaginismus, and shortened PF [7]. The progression of PFMD occurs in two stages: the first, neuromuscular, and the second, musculodystrophic. Following some injury or insult (e.g., coccygeal injury with a fall, chronic hip pain, or recurrent yeast or UTIs), free calcium is released, disturbing the sarcoplasmic reticulum and causing over activity within the muscle. In the presence of ATP, calcium ions stimulate the actin/myosin activity, increasing metabolic activity. The release of various neurotransmitters, including serotonin, histamine, kinins, and prostaglandins, stimulate muscle nociceptors and set up a neural circuit between the central nervous system, nociceptors, and motor units [8]. Over time, the hypertonic muscles enter the musculodystrophic phase while attempting to adjust to the overall increase in metabolic activity. When that adjustment fails, localized fibrosis begins and atrophied muscle tissue is replaced by less metabolically active and extensible connective tissue [9]. An example of this phenomenon can be seen when bladder and urethral function are impacted by PFMD. Once PFM over activity becomes chronic and full range of motion is reduced, the tension may obstruct voiding or make it impossible, with severe cases requiring intermittent self-catheterization. Not only will the PFMD cause restriction in the urethra but it can also inhibit the detrusor during bladder filling and emptying, resulting in urinary urgency, frequency, and hesitation [10]. Patients will involuntarily contract their PFMs for extended periods in response to urinary urgency, reflexively inhibiting bladder filling and emptying. With time, the PFMs lose their flexibility and are unable to normally relax. It then becomes impossible to separate the visceral from the muscular dysfunction as each drives the other: more muscular tension creates more urgency and increased urgency creates more PFM tension. The vicious cycle begins (Table 17.1).