The successful treatment of women with vestibulodynia and its associated chronic pelvic floor dysfunctions requires interventions that address a broad field of possible pain contributors. Pelvic floor muscle hypertonicity was implicated in the mid-1990s as a trigger of major chronic vulvar pain. Painful bladder syndrome, irritable bowel syndrome, fibromyalgia, and temporomandibular jaw disorder are known common comorbidities that can cause a host of associated muscular, visceral, bony, and fascial dysfunctions. It appears that normalizing all of those disorders plays a pivotal role in reducing complaints of chronic vulvar pain and sexual dysfunction. Though the studies have yet to prove a specific protocol, physical therapists trained in pelvic dysfunction are reporting success with restoring tissue normalcy and reducing vulvar and sexual pain. A review of pelvic anatomy and common findings are presented along with suggested physical therapy management.
Introduction
Chronic pelvic pain (CPP), pelvic floor dysfunction (PFD), and sexual pain are among the most common yet challenging medical conditions that physicians and allied health-care providers face in clinical practice. Provoked vestibulodynia (PVD), a chronic vulvar pain disorder, straddles them all – it is often considered a symptom of CPP (though not related to pelvic organ pathology), it has been correlated with chronic pelvic floor muscle dysfunction (PFMD) , and it occurs (but not solely) with sexual contact . The prevalence of female sexual dysfunction resulting from concomitant chronic pelvic and sexual pain was estimated in 2006 to be 26% (range 7–58%) .
Unfortunately, many clinicians are not well equipped to assess and diagnose women plagued by the comorbid disorders . Vulvologists, looking primarily at the vulva, work to accurately diagnose and treat PVD, which, by definition according to the International Society for the Study of Vulvovaginal Diseases, has no definable disease or diagnosable cause associated with it . Physicians have historically been taught to investigate the pelvic viscera (e.g., bladder, urethra, uterus, ovaries, and bowel) as pain generators when attempting to identify the possible causation of pain , yet 28–55% of exploratory laparoscopic surgeries report negative findings . When treating women with chronic pain, physicians and other health-care providers (those outside of the psychosexual counseling realm) have struggled to deal with their patients’ comorbid sexual dysfunction, with 38% of patients thinking that the problem “will just go away .”
Pelvic floor muscle (PFM) disorders are major contributors to a multitude of dysfunctions, with one recent study suggesting that the increase in the demand for care of PFMD (inclusive of all disorders, including incontinence) is predicted to increase by 35% in the next 17 years, with >1.6 million patient visits predicted for the year 2030 . Beginning in the mid-1990s, PFMD was identified as a contributing factor to the pain of vulvodynia and PVD. Hypertonic PFMs were identified and successfully treated using surface electromyography or biofeedback, and complaints of vulvar pain and sexual dysfunction were decreased .
Physical therapists, by nature of their training, bring a much broader approach to the management of chronic vulvar and pelvic pain. As specialists, women’s health physical therapists (WHPTs) have received extensive education in the treatment of chronic pelvic dysfunction. They have utilized a variety of manual therapy techniques to treat comorbid conditions of PFD, including biofeedback. WHPTs utilize interventions that restore normal function to all systems (musculoskeletal, fascial, and visceral) throughout the body. They have played an integral role in the multidisciplinary team working to decrease pain associated with CPP, PFD, and PVD .
A recent multisite, randomized, and blinded trial compared a specific PFM myofascial therapy treatment protocol to nonspecific therapeutic massage in 81 women with interstitial cystitis/painful bladder syndrome (IC/PBS). The results suggested that, of the 78 who completed the 3-month, 10-treatment trial, 59% of those who received myofascial treatment reported improvement (moderate or marked) versus 26% of the massage-only group . Though there is some thought that IC/PBS and PVD may coexist more than reported – though there was no mention of the vulvar pain in the previous study – it may be surmised that the therapy provided might also benefit those with PVD.
Gentilcore-Saulnier et al. compared PFM behavior in women with and without PVD and how those with PVD responded to a physical therapy treatment. The study included eight patient visits with a protocol that included patient education, intervaginal manual therapy, biofeedback, electrical stimulation, use of vaginal dilators, and instruction in a home exercise program that prescribed the use of daily PFM exercises. Their prospective, cross-sectional study suggested that the presence of PVD alters PFM responsiveness to pain, with increased muscle activity (greater in the superficial PFMs than in the deep PFMs) following painful stimuli at the posterior vulvar vestibule. Pelvic floor (PF) physical therapy normalized the overall PFM tone, flexibility, strength, and ability to relax following active contraction. Following WHPT, there was decreased pain responsiveness in the PFM, reduced pressure sensitivity at the vaginal opening with reduced pain at the vulva, and improved tolerance to vaginal penetration .
In two retrospective reviews of physical therapy treatment of women with vulvodynia, Bergeron et al. reported a 71% success rate of moderate or great improvement in vulvar pain, as well as decreased pain with intercourse and gynecological exam, and increased intercourse frequency, desire, and arousal . Hartmann reported that 71% of those receiving physical therapy for vulvar pain reported decreased vulvar pain symptoms and 62% reported improved sexual function . Bergeron’s protocol included patient education on PFM response to vulvar pain and the importance of muscle control (e.g., relaxation during vaginal insertion), internal and external manual therapy (including myofascial release, trigger-point pressures, and massage), biofeedback, electrical stimulation, and home exercises including use of vaginal dilators, manual stretching of the vaginal tissue, and PFM exercises . Hartmann’s protocol included internal and external manual therapy (soft tissue mobilization, myofascial release, and visceral manipulation), internal and external therapeutic exercise, electrical stimulation, biofeedback, and a home exercise program including twice-daily PFM exercises . In a 10-year follow-up survey, Hartmann found 13 of the original 24 women and asked about their current symptoms. Ninety-two percent suggested mild to no current or intermittent symptoms, and 85% reported vulvar pain symptoms completely or greatly resolved with no further physical therapy intervention. When comparing symptomology in 2007 to 1997, continued symptom reduction had occurred in 89% versus 71% of those responding 10 years earlier, quality-of-life issues improved in 79% versus 50%, and improved sexual function improved in 75% versus 62%. Sixty-seven percent reported continued daily PFM exercises as prescribed during their treatment 10 years previously .
The purpose of this article is to describe and review the normal and abnormal functional anatomy of the pelvis, to discuss common problems caused by PFD, and to summarize suggested assessment and intervention modalities that might be utilized by WHPTs when dealing with patients with chronic PFD. No specific treatment protocols for women with PVD have been studied and/or validated. Some portions of the material presented in this article are solely the views of the individual authors as a result of their independent years of clinical experience.
Functional anatomy of the pelvis
To understand the functional anatomy of the pelvis, it is essential to appreciate the integration of the static support provided by the bony pelvis along with several additional anatomical systems – the musculoskeletal, the fascial, and the visceral systems. To better define pelvic function, Wei and Delancey suggest that the descriptor “pelvic floor” (PF) should be used to refer to all the structures of support within the pelvic cavity, including the musculature. PF support begins with the abdominal peritoneum cranially and continues inferiorly through the viscera (bladder, urethra, uterus, and rectum), the endopelvic fascia, the deep PFMs, and the perineal membrane before ending caudally in the superficial portion of the PFMs ( Fig. 1 ). Together, the levator ani (pubococcygeus, puborectalis, and iliococcygeus muscles) and coccygeus form the PFMs. The total sum of the muscular attachments of the PFMs, the fascial attachments of the viscera (e.g., pubocervical and uterosacral ligaments), and the static support of bony pelvis combines to form the functional and structural support for the pelvic contents.
The normal function of the PFMs (i.e., the ability to actively and fully contract and relax) contributes to the most inferior support of the pelvic viscera, control of continence via input to the urethral and anal sphincters, maintenance of normal sexual function and orgasmic activity, and core stability at the base of the trunk. The quality of the pelvic support can be altered by abnormalities in any of the supportive systems, be it in the PFMs (e.g., PFM spasm or laxity), the fascia (e.g., uterine or bladder prolapse), or the viscera (e.g., urethral or rectal spasm).
From an anatomical perspective, the sling-like support of the PFMs attaches anteriorly at the inferior pubic rim and travels posteriorly to attach at the coccyx and sacrum. Normal contraction of the PFMs shortens the length of the muscles, creating a lift to the perineal body, pulling it up and in toward the pelvic cavity. Normal relaxation returns the muscles to their original length, allowing the perineal body to drop to its original position. In supine and with normal PFM function, the position of the perineal body should be above the plane of the ischial tuberosities. Hypotonic (i.e., laxity or decreased tone) PFMs allow the perineal body to drop below the plane of the tuberosities whereas hypertonic (i.e., elevated tension or spasm) PFMs cause a pull upward of the perineal body, keeping it more superior to the ischial tuberosities than in normal function. When hypertonicity is present, the resting position of the perineal body is further upward into the pelvis, similar to where it would be at the end of a full, voluntary contraction of normal functioning PFMs. The presence of chronic hypertonicity leaves the PFMs unable to release and return the perineal body to a normal position. This chronic hypertonicity can be visualized easily during an external clinical exam of the perineum.
Other major components within the anterior compartment are the paired obturator internus muscles. They are fan-shaped and originate from a broad section of the anterolateral wall of the pelvis at the inner surface of the obturator foramen, the ischiopubic ramus, and the inner surface of the femur. Their fibers narrow and become band-like as they traverse inferior, running posterior to the ischial tuberosities where they make a 120° turn upward to insert at the greater trochanters of each femur ( Figs. 2 and 3 ). Their function is to externally or laterally rotate the hip with extension (i.e., to turn the toes and knee outward in standing) and to abduct the hip when flexed (i.e., drop the knee out to the side when the knees and hips are flexed while in the supine position).
Functional anatomy of the pelvis
To understand the functional anatomy of the pelvis, it is essential to appreciate the integration of the static support provided by the bony pelvis along with several additional anatomical systems – the musculoskeletal, the fascial, and the visceral systems. To better define pelvic function, Wei and Delancey suggest that the descriptor “pelvic floor” (PF) should be used to refer to all the structures of support within the pelvic cavity, including the musculature. PF support begins with the abdominal peritoneum cranially and continues inferiorly through the viscera (bladder, urethra, uterus, and rectum), the endopelvic fascia, the deep PFMs, and the perineal membrane before ending caudally in the superficial portion of the PFMs ( Fig. 1 ). Together, the levator ani (pubococcygeus, puborectalis, and iliococcygeus muscles) and coccygeus form the PFMs. The total sum of the muscular attachments of the PFMs, the fascial attachments of the viscera (e.g., pubocervical and uterosacral ligaments), and the static support of bony pelvis combines to form the functional and structural support for the pelvic contents.
The normal function of the PFMs (i.e., the ability to actively and fully contract and relax) contributes to the most inferior support of the pelvic viscera, control of continence via input to the urethral and anal sphincters, maintenance of normal sexual function and orgasmic activity, and core stability at the base of the trunk. The quality of the pelvic support can be altered by abnormalities in any of the supportive systems, be it in the PFMs (e.g., PFM spasm or laxity), the fascia (e.g., uterine or bladder prolapse), or the viscera (e.g., urethral or rectal spasm).
From an anatomical perspective, the sling-like support of the PFMs attaches anteriorly at the inferior pubic rim and travels posteriorly to attach at the coccyx and sacrum. Normal contraction of the PFMs shortens the length of the muscles, creating a lift to the perineal body, pulling it up and in toward the pelvic cavity. Normal relaxation returns the muscles to their original length, allowing the perineal body to drop to its original position. In supine and with normal PFM function, the position of the perineal body should be above the plane of the ischial tuberosities. Hypotonic (i.e., laxity or decreased tone) PFMs allow the perineal body to drop below the plane of the tuberosities whereas hypertonic (i.e., elevated tension or spasm) PFMs cause a pull upward of the perineal body, keeping it more superior to the ischial tuberosities than in normal function. When hypertonicity is present, the resting position of the perineal body is further upward into the pelvis, similar to where it would be at the end of a full, voluntary contraction of normal functioning PFMs. The presence of chronic hypertonicity leaves the PFMs unable to release and return the perineal body to a normal position. This chronic hypertonicity can be visualized easily during an external clinical exam of the perineum.
Other major components within the anterior compartment are the paired obturator internus muscles. They are fan-shaped and originate from a broad section of the anterolateral wall of the pelvis at the inner surface of the obturator foramen, the ischiopubic ramus, and the inner surface of the femur. Their fibers narrow and become band-like as they traverse inferior, running posterior to the ischial tuberosities where they make a 120° turn upward to insert at the greater trochanters of each femur ( Figs. 2 and 3 ). Their function is to externally or laterally rotate the hip with extension (i.e., to turn the toes and knee outward in standing) and to abduct the hip when flexed (i.e., drop the knee out to the side when the knees and hips are flexed while in the supine position).
Pelvic floor dysfunction
Chronic PFD, CPP, PFMD, and PVD usually, but not always, coexist. There are rare clinical cases who present with no physical findings; however, those cases are, by far, not the norm. The 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 . Visceral disorders within the pelvis that are known to contribute to pain include 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 . Fascial laxity and resulting organ prolapse may contribute to the pain puzzle as can bony irregularities (e.g., sacroiliac joint dysfunction and hip pain).
Pelvic floor muscle dysfunction
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 . 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 urinary tract infections), free calcium is released, disturbing the sarcoplasmic reticulum and causing hypertonicity 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 .
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 . An example of this phenomenon can be seen when bladder and urethral function are impacted by PFMD. Once PFM hypertonicity 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 . Patients will involuntarily contract their PFMs for extended periods in response to the 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 1 ).
| Faulty biomechanics |
|
| Postural and structural dysfunction |
|
| Injury to the pelvic floor muscles |
|
| Faulty cumulative behaviors of the pelvic floor muscles |
|
| Inflammatory pain disorders involving pelvic viscera |
|
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