Annotation L: The pelvic floor

Click here for Key Points to Annotation

 

Introduction

The clinical importance of the muscles of the pelvic floor (PFM) far exceeds the clarity and accuracy of most descriptions of pelvic floor anatomy. Almost no other region of the body is so commonly described in unhelpful generalizations, confusing and overlapping terminology, and misleading metaphor resulting in real obstacles to understanding the pelvic organ support system and the role of the pelvic floor muscles within that system. The emergence of vulvodynia illuminated the need to understand the PFM; recent MRI studies have likewise cleared up much of the mystery.1

The pelvic floor is a complex structure of inter-related muscles that is one of the most intricate in the human body. It consists of 14 individual muscles and ligaments, intertwined with nerves and surrounded by connective tissue with multiple functions: support of pelvic organs and postural support, facilitation of urination and defecation while maintaining continence, sexual function, and formation of part of the birth canal. This unit of muscles, ligaments, and fascia has connections to the bony pelvis, to pelvic organs and to the extensive fibro-elastic network in the fat that contains anatomical spaces.2

Because the pelvic muscles relate to more than one organ system, their dysfunction can impact multiple systems at the same time, and each system can be a potential source of pain and symptoms.3

The bony pelvis is funnel shaped; for a long time the pelvic floor muscles were inaccurately believed to be bowl shaped to fit into the funnel. The pelvic floor is actually composed of striated muscles arranged in a dome-shaped sheet, often is described as a sling.

The levator ani and coccygeus muscles are the most important muscles specific to the deep pelvic floor. The levator ani is composed of 3 muscle bellies, including the iliococcygeus, pubococcygeus, and puborectalis. These muscles and their fascia support the bladder, uterus, and rectum. The levator ani act to lift up the pelvic organs and are active during defecation. The puborectalis muscles act together with the external anal and urethral sphincters to close the urinary and anal openings, contract the sphincters, and prevent urinary or fecal leakage.

 These are separate muscles that meet in the midline to form a muscular sheet, the pelvic diaphragm, across most of the floor of the pelvis. This diaphragm is perforated by an opening for the vagina and urethra (urogenital hiatus). The levator ani originate lateral to the pubic symphysis on the posterior surface of the superior ramus and inserts onto the inner surface of the spine of the ischium. It shares this site with the tendinous arch of the pelvic fascia and obturator fascia known as the arcus tendinous. The muscle fiber orientation of the levator ani is such that the fibers pass inferiorly and posteriorly to the center of the pelvis and attach to the coccyx and anus. The middle fibers insert into the rectum and then blend with the fibers of the sphincter muscles. The anterior muscle fibers insert into the sides of vagina in women. The perineal body, also termed the central tendon of the perineum, is located at the mid-portion of the perineum between the vagina and anus. It consists of fibrous tissue and muscle in the shape of a pyramid. 4

The constant muscle tone of the levator ani and coccygeus muscle prevents the ligaments from becoming over-stretched and damaged by constant tension.5 The muscle tone combined with the stability of the fascia results in a dome-shaped form of the pelvic floor (in the coronal plane) and closes the urogenital hiatus, a U-shaped defect in the muscles in the urogenital triangle that allows the passage of the urethra and vagina. During vaginal delivery, the levator ani muscle is substantially stretched and injury may occur, often near the pubic bone insertion.6

Normal anatomy of the pelvic floor

Review this excellent video for a clear understanding of the anatomy of the pelvic floor:

http://anatomyzone.com/tutorials/musculosketetal/pelvic-floor

Accurate diagnosis of pelvic floor disorders (PFM) requires comprehensive knowledge of the musculoskeletal (MSK) components of the pelvis and surrounding structures. Regarded often as only a single, muscular layer (the pelvic diaphragm or levator ani), the pelvic floor, in actuality, is composed of multiple layers. From superior to inferior, these are the endopelvic fascia, the muscular pelvic diaphragm (the levator ani), the perineal membrane (urogenital diaphragm), and a superficial layer of muscles (bulbospongiosus and ischiocavernosus). The nerve supply tothe pelvic floor and related organs is via branches of the sacral plexus: the pudendal nerve arises from the second, third and fourth sacral nerves and courses inferior to the pelvic floor, the levator ani nerve originates from the third sacral spinal nerve and courses superior to the pelvic floor, and the parasympathetic pelvic splanchnic nerves. The sympathetic supply is by the hypogastric nerve. Higher regulating levels of the central nervous system (e.g., pontine micturition center, cerebral cortex) are crucial for proper function of the pelvic floor.7

The levator ani muscles are the most important muscles in the pelvic floor with several muscle components: the pubococcygeus, puborectalis, and iliococcygeus. These are separate muscles that meet in the midline to form a muscular sheet, the pelvic diaphragm, across most of the floor of the pelvis. This diaphragm is perforated by an opening for the vagina and urethra (urogenital hiatus) and an opening for the rectum (anal hiatus).9 They attach to the tip of the coccyx at the anococcygeal body.10

 The tendinous arch of the levator anchors to the spine of the ischium posteriorly and to the pubic bone or the obturator membrane anteriorly. The arch attaches to the covering fascia of the obturator internus muscle so that the levator covers the lower portion of the obturator internus muscle and all of the obturator foramen. Although the obturator muscle is not considered a PFM per se, it has fascial connections to the PFMs, via the arcus tendineus fasciae pelvis, which create anatomic and functional synergy. It is important to understand that the obturator has a significant effect on pelvic floor function secondary to this direct connection. When the length of the obturator internus is altered because of overactivity, spasm, or tension, it can create tension on the levator ani, creating suboptimal functional ability of the levator ani. In addition, the obturator internus assists in hip external rotation and abduction. 11

 


]

 

The levator ani act to lift up the pelvic organs and are active during defecation. The puborectalis muscles act together with the external anal and urethral sphincters to close the urinary and anal openings, contract the sphincters, and prevent urinary or fecal leakage.

The anterior portion of the levators, the pubococcygeus, forms a sling around the anus, vagina, and urethra. It attaches along the dorsal surface of the pubic bone from the symphysis to the obturator canal. The two halves of the muscle meet in the midline, some fibers at the perineal body, most at the anococcygeal body.

The most anterior (medial ) fibers of the pubococcygeus that meet bilaterally at the perineal body superior to the anus, are called the pubovaginalis. These act as an important sphincter of the vagina. Vaginal closure is assisted by the bulbospongiosus and puborectalis muscles. these muscles aso activate the elevator and to facilitate vaginal ballooning. The most posterior fibers of the pubococcygeus (puborectalis) form a sling around the rectum. They attach to the tip of the coccyx at the anococcygeal body.

The posterior portion of the levators, the iliococcygeus muscle, anchors above the tendinous arch of the levator ani and to the spine of the ischium posteriorly. The tendinous arch of the levator anchors to the spine of the ischium posteriorly and to the pubic bone or the obturator membrane anteriorly. The arch attaches to the covering fascia of the obturatur internus muscle so that the levator covers the lower portion of the obturator internus muscle and all of the obturator foramen.

The shelf-like triangular coccygeus muscle forms the posterior part of the pelvic diaphragm. The coccygeus is not part of the levator ani, having a different function and origin. It originates at the ischial spine and courses along the posterior margin of the internal obturator muscle. The muscle inserts at the lateral side of the coccyx and the lowest part of the sacrum. The sacrospinous ligament is at the posterior edge of the coccygeus muscle and is fused with this muscle. The proportions of the muscular and ligamentous parts may vary. The coccygeus muscle is innervated by the third and fourth sacral spinal nerves on its superior surface.12

The constant muscle tone of the levator ani and coccygeus muscle prevents the ligaments from becoming over-stretched and damaged by constant tension.13 The muscle tone combined with the stability of the fascia results in a dome-shaped form of the pelvic floor (in the coronal plane) and closes the urogenital hiatus, a U-shaped defect in the muscles in the urogenital triangle that allows the passage of the urethra and vagina. During vaginal delivery, the levator ani muscle is substantially stretched and injury may occur, often near the pubic bone insertion.14

 

 


Pelvic Floor Dysfunction

Introduction

Pelvic floor muscle dysfunction generally refers to disorders of laxity (hypotonus), or overactivity (hypertonus). Hypotonus disorders are associated with muscle weakness and result in stress incontinence, fecal incontinence, and pelvic organ prolapse. However, it is the opposite condition that is most likely to lead to pain: the development of hypertonic dysfunctional muscles. Only recently, has the pelvic floor been recognized as a major contributor to pelvic and vulvar pain, vulvodynia, vaginismus, and dyspareunia. In a recent retrospective study of 238 patients with complaints of urination, defecation, and /or sexual problems, 77.2% had measurable pelvic floor dysfunction.15 But, pelvic floor hypertonic disorders are often not considered in the evaluation and management of patients with these problems.16

Neuropathology of myofascial pain

Muscles are made up of fibers that either overlap to contract (shorten) the muscle or pull apart to stretch (lengthen) the muscle. When muscles become too tight, and associated loose connective tissue thickens, blood flow becomes restricted, with less oxygen reaching the tissue. Anoxia causes pain. In addition, muscles that become too short because the fibers start to overlap too much (as with clenching) or too long because the fibers pull too far apart (with pushing during childbirth or constipation) become vulnerable to the development of trigger points, small, hyperirritable patches of painful, involuntarily contracted muscle fibers which refer pain to other areas.17 The intimate relationship between the pelvic organs and the soft tissue surrounding them is also a factor in pain. If any of the organs is inflamed, such as the bladder during a urinary tract infection, pain from the inflamed organ can be referred to the surrounding neuromuscular tissue- the pelvic floor muscles and nerves, the abdominal muscles, and even the skin of the vulva.With ongoing inflammation, near-by muscles tighten painfully. This impaired tissue can affect other nearby organs, such as the urethra, or rectum, creating further urinary symptoms of gastrointestinal distress, creating pain on pain.18 The mechanism of this pain is described below.

With trauma – such as overt injury, overuse or misuse- to a muscle fiber, a cascade of inflammatory mediators (bradykinin, serotonin, histamine, prostaglandins, adenosine triphosphate), released around the injured fiber sensitizes muscle nociceptors and reduces their mechanical threshold. This sensitivity results in a “hair-trigger” response of the muscle, resulting in muscle hyperalgesia (muscle pain) and mechanical allodynia (pain from muscle movement that should normally not cause pain). Normal muscle contraction is therefore perceived as painful. This process produces peripheral sensitization.19 (Annotation I: Pain and symptom mapping and the Q-tip test). Central sensitization in the brain and spinal cord can follow. Because of prolonged noxious stimuli, a series of neuroplastic changes occur in the central nervous system. Pain impulses are amplified because of biochemical and neuroinflammatory changes in the spinal cord. Generation of spontaneous pain impulses occurs, and there is expansion of the area of perceived pain. Non-noxious stimuli start to be perceived as painful.20Sensitization means that the whole pain process volume is turned up too high.

The up-regulation described above has received attention mainly in relation to neuropathic pain. Animal studies promote awareness that deep myofascial pain actually is more effective in the induction of central sensitization than is peripheral pain.21 22

Causes of pelvic floor dysfunction

Myofascial pain with hypertonic dysfunction can be a primary problem, or may be secondary to other pelvic and systemic disorders such as interstitial cystitis, irritable bowel syndrome, and endometriosis. Chronology of symptom onset is essential to make this distinction: for example,  voiding dysfunction since an early age, or life-long constipation would suggest a primary problem with the pelvic floor, whereas a recent diagnosis of endometriosis suggests that pelvic pain has resulted in hypertonicity of the pelvic floor.

Disorders from childhood

Dysfunctional pelvic floor behaviors originating in childhood can persist into adulthood.23 Control of the pelvic floor begins with toilet training. Some children develop hyper-vigilance, holding of urine, and inability to relax to void. Recurrent urinary tract infection, urinary retention, and vesicoureteral reflux with high tone pelvic floor dysfunction can follow. Similarly, constipation and incomplete emptying of the bowel also influence pelvic floor hypertonicity.24

Adult dysfunctional disorders

Urinary holding patterns related to job demands that preclude regular voiding in adults may lead to dysfunction of the pelvic floor. Abnormal postural positions, or postural abnormalities such as differential in leg length, gait abnormality, or pelvic girdle abnormality, may also lead to hypertonicity and pain. It is often the passage of time, or a trigger such as the demands of pregnancy and delivery, that lead to  symptom development. Prolonged lack of motion such as long car rides is another source of possible pelvic floor disability. Severe anxiety disorders and a history of sexual abuse can also contribute to such disorders.25

If these childhood or adult dysfunctions are not considered in the evaluation of dyspareunia, vulvovaginal symptoms and pelvic pain, the hypertonic pelvic floor may not be addressed, and the problems will persist.

Neuromuscular injury of the pelvic floor

Traumatic vaginal delivery by forceps or vacuum extraction can be a source of pelvic floor dysfunction and pain.26 Injury to the levators, widely regarded as a source of stress urinary incontinence or pelvic organ prolapse, may lead to persistent pain, urinary frequency and ongoing dysfunctional voiding after delivery.27 Vaginal surgery such as sacrospinous vault suspension or transvaginal tape placement, may affect the pudendal nerve and the levators, leading to post-operative voiding dysfunction, urinary frequency, urgency, and pain.

Overuse injury

In a woman tight pelvic floor muscles from an any source,  e.g., an anatomical/biomechanical abnormality such as a leg length discrepancy, overuse (any activity that exceeds the capacity of the muscle) of the tight muscles can lead to the development of pain. This could be a new activity – a high intensity work-out, or extended biking – or an activity of years’ duration, such as running or yoga.

Scar tissue

Scar tissue is a common source of pelvic floor dysfunction. It consists of fibrous tissue that replaces normal tissue after some type of injury- such as pelvic surgery, childbirth, an injury, or repeated abscess in the Bartholin gland. Lichen sclerosus is another source of scarring on the vulva. Scar tissue can adhere to skin, connective tissue, or muscle, pulling on neighboring tissue and making the area tight with restricted blood flow leading to pain. Nearby nerve tissue can also be affected, resulting in pain in that area or pain referred to a more distant site. Scar tissue also cause functional loss in the affected tissue such as the anal sphincter. The sphincter loses some of its ability to contract, leading to loss of control over bowel function.

Other pelvic pain (visceral) disorders

Prolonged pelvic pain disorders- interstitial cystitis/bladder pain syndrome, irritable bowel syndrome, endometriosis, and vulvodynia are the most common cause of secondary pelvic floor hypertonicity and pain.28 The noxious stimuli released by a pelvic pain disorder can up-regulate and centrally sensitize the dorsal horn neurons. The sensitization can lead to two different neural reflexes yielding pain. One is viscerovisceral hyperalgesia known as pelvic organ cross talk.29 Pain in the bladder, for example, can lead to bowel symptoms. The second reflex of visceromuscular pain, manifested as pelvic floor muscle hypertonicity, promotes self-perpetuation of the pain.30

The association between vulvodynia and interstitial cystitis/bladder pain syndrome (IC/BPS) may involve sex hormone-dependent mechanisms regulating vulvo-vaginal health. A significant positive effect of local estrogen therapy (three-times/week estriol 0.5 mg cream) after 12 weeks was evident on urinary and sexual function. The association between vulvar pain and bladder pain could be related to a vaginal environment carrying signs of hypoestrogenism. 31

Pelvic floor dysfunction/vaginismus

Pelvic Floor Dysfunction/Vaginismus is covered under Pain conditions: Pelvic Floor Dysfunction/Vaginismus

Vulvodynia and dyspareunia

We lack information regarding whether pain is a cause or a consequence of muscle dysfunction. However, in 1995 the first link between pelvic floor hypertonicity and dyspareunia was made in Howard Glazer’s treatment study using vaginal surface electromyography (sEMG) to treat women with provoked vestibulodynia (called vulvar vestibulitis syndrome [VVS] at the time).32 The electromyograph detects the electrical potential generated by muscle cells when active and at rest, to evaluate and record the activation signals of the muscles.

In two subsequent uncontrolled consecutive patient outcome studies using vaginal sEMG feedback, Glazer reported significant pain reduction with return to comfortable intercourse for women with VVS and vulvodynia.33 34 35 Another study utilizing the Glazer vaginal sEMG protocol and structured physical therapist palpation confirmed differences in muscle strength but not in muscle tone of VVS patients and matched controls. But from the data based on physical therapist palpation, the authors showed both increased pelvic floor tonicity and lowered muscle strength in women with VVS compared with the normal controls.36 37

The Glazer vaginal sEMG protocol was compared with cognitive-behavioral group pain management and vestibulectomy in a prospective, randomized controlled treatment outcome study. The Glazer protocol resulted in significant clinical improvement compared with baseline, and a reduction in pain of 40%. The same authors also conducted an uncontrolled retrospective consecutive case investigation on the usefulness of pelvic floor physical therapy including, but not limited to biofeedback, in the treatment of VVS. Fifty percent of the women reported complete to great improvement; another 20% reported moderate gains.38

Increased pelvic floor muscle tension or hypertonicity has been traditionally associated with vaginismus and more recently with dyspareunia, in particular with provoked vestibulodynia.39 Pelvic floor performance is significantly lower in affected patients in terms of contractile strength and resting ability and stability and efficiency of contraction. In our clinical experience, we are repeatedly able to palpate pelvic floor muscle tightness and hypertonicity on office examination, and in a majority of our patients, we receive from our physical therapists reports of elevated resting tone measured by biofeedback.

A recent study explored the relative contribution of mucosal versus muscle pain sensitivity on pain report from intercourse among some with provoked vestibulodynia. The lower vestibule’s mucosa was significantly more sensitive than the upper vestibule on exam. However, mucosal sensitivity was not associated with intercourse pain, while muscle sensitivity was moderately associated with both average and highest intensity of intercourse pain. This preliminary study suggests that mucosal measures alone may not sufficiently capture the spectrum of clinical pain report in women with provoked vestibulodynia, which is consistent with the empirical success of physical therapy in this population.40


Symptoms of pelvic floor dysfunction typically involve the pelvic organs that are controlled by the pelvic floor. Bladder symptoms may exist, such as voiding dysfunction, post void pain, urethral pain, hesitancy or the constant or exaggerated urge to void. Colorectal symptoms may be present including constipation, obstructed defecation, painful defecation, or sharp rectal pain (proctalgia fugax). Vulvovaginal pain, burning, stinging, pain on touch in the vestibule with dyspareunia, and vaginismus may be complaints. Or, intercourse may not be painful at the time, but may lead to post-coital pain for 12 to 48 hours after intercourse. This is a common complaint with pelvic floor hypertonic dysfunction, as are clitoral pain and pain with orgasm.

The pain symptoms are often vague and poorly localized. Pain may be described as burning, aching, or throbbing, and as having a pressure or heaviness quality to it. Prolapse may come to mind, but the leading edge of prolapse must be at the level of the introitus to produce any symptoms.41

Women may describe the pain as vaginal, rectal, suprapubic, or in either or both lower quadrants, wondering if this is pain from an ovarian cyst. They are often treated repeatedly for urinary tract infection with negative cultures. They also report radiation into the hip and back. Almost all women say that the pain is worse as the day progresses and is typically exacerbated by pelvic floor muscle activities such as sitting, walking, exercise, intercourse, voiding, or bowel movement. Pain arising from a trigger point can be very misleading  since the knot of taut muscles refers pain elsewhere. Table L-1 describes the location of referred pelvic floor muscle pain.

Table L-1 Myofascial Trigger Point Referral Patterns42

Muscle Referral Pattern
Rectus abdominis Mid and low back and viscerosomatic symptoms
Iliopsoas Paravertebral and anterior thigh
Quadratus lumborum Iliac crest, outer thigh, buttock
Gluteus maximus Sacrum, coccyx, buttock
Gluteus medius Low back, sacrum, buttock, lateral hip/thigh
Adductors Groin and inner thigh
Hamstrings Gluteal fold, posterior thigh, popliteal fossa
Piriformis Low back, buttock, posterior thigh
Obturator internus Coccyx and posterior thigh, fullness in rectum or vaginal pain
Coccygeus Coccyx, sacrum, rectum
Pubococcygeus Coccyx, sacrum, rectum
Iliococcygeus Coccyx, sacrum, rectum
Ischiocavernosus Perineal aching
Bulbospongiosus Dyspareunia, perineal pain with sitting
Transverse perineum Dyspareunia
External anal sphincter Diffuse ache, pain with bowel movements, constipation
Urinary sphincter Urinary retention, perineal urge, frequency

Chronic urogenital pain is difficult to understand because it exists where there is no visible pathology, continues long after tissue irritation or damage, and persists well beyond the expected time of healing.43


The practicing clinician in an exam room wants to know if the pelvic muscles are contributing to the complexity of a woman’s genital pain syndrome. It is a given that the examiner is, at all moments, searching for evidence of disease. Pelvic floor muscle problems can occur in women who have discernible disease states, as well as in those who have no observable disease. After the Q- tip test is completed, (Annotation I: Pain and symptom mapping and the Q-tip test) it is our practice to obtain the vaginal pH by inserting the same Q-tip (moistened by resting at the hymenal ring for a few seconds ) gently into the lower vagina to the side wall, gently removing and applying the Q-tip to a pH strip. (Water, saline and lubricant all alter the pH). (Annotation P: Vaginal secretions, pH, microscopy, and cultures). Pelvic floor muscle evaluation is next done prior to inserting the speculum or doing a bimanual examination, both of which may trigger hypertonicity. Evaluation of the hymenal ring is done with careful inspection and gentle touch as part of the Q-tip test and is evaluated on physical exam during the bimanual exam. (Annotation Q: The hymenal ring and bimanual exam).

The first step in evaluating the status of the pelvic floor is, with permission, to insert a single lubricated digit just inside the vaginal introitus and to palpate for pelvic floor muscle activity. Note tightness, tension, or spontaneous muscle fasiculation; these subtle twitches palpated in the vaginal walls or deeper in the muscle are known as trigger points. Next, ask her to contract her vaginal muscles with the examiner’s digit still in place at the entrance of the introitus. A clear way to explain what is expected is to ask the woman to “squeeze inside as if preventing the passage of gas or urine.” This tightening is known to most women as a Kegel exercise, where the emphasis is on muscle contraction for the purpose of urinary continence or to improve tonicity after childbirth. The examiner can feel the tightening around the digit. A woman with pelvic floor hypertonicity may have so much muscle tension (leading to muscle weakness) that she is unable to contract her muscles well and produces only a feeble squeeze.

The more important consideration is whether a woman can relax the same pelvic floor muscles. After the “squeeze,” the woman is asked to relax her muscles. (All this is done without any use of the abdominal muscles in a technique described in Annotation D as “pelvic floor drop.”) (Pelvic floor drop in Anno D) The degree of relaxation (or lack thereof) may be surprising to the examiner. The person who does not have a problem with high tone in the muscles can almost double the size of the vaginal opening with the relaxation part of the maneuver. A further step is to ask the woman to (now using the abdominal muscles very gently) bear down slightly, at which point, the vestibule will gape slightly.

In a patient who is unable to relax the muscles, there is a continuum ranging from mild tightening to severe hypertonicity precluding digital entry; in a worst case scenario, the examiner will not even be able to slide a Q-tip past the tight vaginal muscles at the introitus. In some cases, there may be an absence of hypertonicity on office examination, but the woman is subject to situational tightening with fear, the sense of being rushed, and other performance pressures in the bedroom. Physical therapy to the pelvic floor is therapeutic for all the varying types.

After trying the pelvic floor drop technique, the clinician inserts the examining digit with a slight downward curve, posterior to the hymenal ring, to gently press on the bulbocavernosus muscle. The examiner’s fingers are moved laterally from the posterior midline to the lateral pelvic side walls, palpating along the iliococcygeus muscle inferiorly. At the attachment of the pelvic floor to the side wall of the pelvis one can palpate the taut, string-like presence of the arcus tendinous as it runs from the ischial spine anteriorly to the pubic bone. Pubovaginalis and puborectalis can be palpated by withdrawing the examining fingers over the muscle belly to the vaginal opening. Then, as the fingers are directed posteriorly towards the posterior bony pelvis, the small coccyges and pirformis muscles are contacted. The obturator internus is localized laterally and superior to the iliococcygeus by asking the patient to abduct the knee against resistance, with the hip in flexion. Follow the obturator interns muscle belly posteriorly until it is no longer palpable and the examining finger is at the ischial spine. Moving the examining finger anteroinferiorly enables palpation over the course of the pudendal nerve in Alcock’s canal, inferior to the arcus tendinous fascia.44

Further evaluation can be performed on removal of the digit from inside the vagina. If the pelvic floor drop technique is requested again, the examining digit placed against the perineum and lower part of the introitus can discern lengthening and softening of the muscles if there is good relaxation.

Some women cannot completely or continuously relax their muscles and others show a step-like relaxation. They may show rebound hypertonicity, with brief relaxation followed immediately by marked tension.  There are many measuring techniques to quantify the amount of relaxation. But what a clinician needs to know is whether the patient has any control over her pelvic floor muscles at all; she should be rated as having absent, weak or strong control. Often women cannot relax completely or in a continuous manner; the vulva and perineum never bulge and nothing moves although she may be wiggling thighs and buttocks in an effort to be compliant. Repeat your instructions to her: “Keep your back flat on the table, knees bent. Squeeze the muscles inside as if trying to avoid passing wind, then relax them, and add a little abdominal pressure to push the anus out.” (Pelvic Floor Drop in Annotation D: Patient tolerance to exam). The woman who is unable to relax the pelvic floor will greatly benefit from pelvic floor physiotherapy.

When a woman tells us that she has made little progress with physical therapy to the pelvic floor or that it “is not working” we always test relaxation ability. “Show me what you have learned in therapy.” A woman who is not able to relax the pelvic floor muscles has either not had proper physical therapy instruction or is still being controlled by her anxiety. She may need a different therapist or benefit from behavioral health intervention. We encourage the latter by explaining to the woman that it is not just one modality that makes her better. Evaluation for pain is ongoing.

After completion of the pelvic floor assessment, a little work with relaxation and internal muscle massage when muscle control seems weak or absent can demonstrate to the patient just how important these factors are in her total plan of care. Besides learning that pelvic floor drop gives more room, the woman responds to gentle massage from the sweep of the inserted digit from left to right with the realization that this is a muscle group over which she can have cognitive control. She will then, hopefully, be convinced of the value of pelvic floor work. She also needs to realize that pelvic floor work is an adjunct to control of her pain, which is achieved through a combination of therapies.


Physical therapy to the pelvic floor

The goals of physical therapy treatment include:45

  • increased awareness and proprioception of the pelvic floor muscles
  • improved muscle discrimination and muscle relaxation
  • normal muscle tone
  • increased elasticity at the introitus and desensitization of painful areas
  • decreased fear of vaginal penetration
Pelvic floor muscle exercises

Interventions most commonly prescribed for myofascial pelvic pain are designed to address pain and range of motion loss of the local and regional tissues (muscle/fascia, nerve and joints). There is moderate evidence to support the use of manual techniques, when combined with other physical therapy techniques such as exercise, biofeedback and electrical stimulation to improve pain severity, bowel, bladder, and sexual function in both adult men and women with myofascial pelvic pain.46The sine qua non of pelvic floor rehabilitation consists of pelvic floor muscle exercises prescribed to improve muscle control and relaxation, since pain is believed to be associated with a pelvic floor that is both hypertonic and hyperactive.47 No standardized protocol exists for pelvic floor muscle exercises to treat pain and they have not been investigated as a single treatment,48 but comprehensive pelvic floor rehabilitation, including pelvic floor muscle exercises, has demonstrated effectiveness.49 50 51 Multidisciplinary approaches including pelvic floor exercises for provoked vestibulodynia have also been successful.52 53

Specifically, manual manipulations of the tissues include trigger point release (internal or external digital pressure applied to trigger points in the pelvic floor/levator ani muscles), massage, and stretching, and are applied directly to the pelvic floor musculature. In addition to manual techniques, therapists employ biofeedback, electrical stimulation, dilator usage, exercise/stretching, and dry needling. Corrective exercises aid in retraining movement and reduce mechanical stress on the tissues potentially affecting both the peripheral and central adaptations that perpetuate chronic pain. Inclusion of psychological services for cognitive behavioral interventions including instruction on relaxation techniques are also useful for women.

Manual therapy techniques

Equally important are manual therapy techniques – massage, myofascial release, trigger point release and stretching- to treat abnormal pelvic muscles and connective tissues as well as restrictions from scarring or fibrosis. Normal pelvic muscle function is dependent on structural integrity throughout the body; hence, manual techniques may be used for the thighs, hips, pelvis, abdomen and low back. Effectiveness is reported from uncontrolled studies.54

Dilators

Desensitization with vaginal dilators (trainers) is discussed in (Annotation D: Patient tolerance for genital exam.)

Biofeedback

Biofeedback is an evaluative and therapeutic technique (Vulvar pain and provoked and unprovoked vulvodynia) in which information about a normal physiological process is presented to the patient via subconscious methods and/or via a therapist (or machine) who offers a visual, auditory, or tactile cue.55 In the case of pelvic floor disorders causing pain or disability, muscle activity is measured by means of the electromyograph (EMG), which detects the electrical potential generated by muscle cells when active or at rest, recording their signals. Surface electrodes on a small probe inserted into the vagina or the anus detect the activity of the pelvic floor muscles and display the EMG on a computer monitor screen. A woman who is able to visualize the activity of her pelvic floor muscles may be aided in improving control and recovery following contraction and normalize muscle activity. Thus biofeedback has been widely used in treatment of pelvic floor dysfunctions, mainly by promoting patient learning about muscle contraction. When asked to tighten her muscles, she can see a measurement of how well she is doing. When asked to release her muscles, she watches as the EMG activity lessens.

In Glazer’s previously cited study, after 16 weeks of sEMG biofeedback, 70% of women with provoked vestibulodynia who were abstaining from intercourse at the beginning of the study resumed activity; 52% reported pain free intercourse at six months follow-up.56 These results were supported by another study reporting that after four to six months of daily sEMG biofeedback exercises 83% of women with PVD reported negligible to mild pain with intercourse.57 In a randomized treatment study comparing sEMG biofeedback with topical lidocaine gel for treatment of provoked vestibulodynia, 78% of the women in the biofeedback group reported significant improvement at one year follow-up.58 Bergeron (previously cited) studied sEMG biofeedback compared with group cognitive behavioral therapy (GCBT) and vestibulectomy and found sEMG to be as effective as GCBT but less effective than vestibulectomy.59
35% of the biofeedback group reported ongoing success at six months and 2.5 years.60 A recent systematic review of biofeedback, however, has suggested that pelvic floor muscle training with biofeedback is not more effective than other conservative treatments for female pelvic floor muscle dysfunction.61

Combined pelvic floor and other rehabilitation therapies

The success of combining pelvic floor treatment components- exercises, manual therapy techniques, biofeedback and dilators- has been demonstrated in patients with vulvodynia (Ref 36, 37). Multiple studies have demonstrated excellent response to pelvic floor rehabilitation with improvement of vulvodynia as cited above, chronic pelvic pain,62 painful bladder syndrome/interstitial cystitis,63 64 sexual pain and dysfunction,65 and anal rectal pain disorders.66 67

Pelvic floor treatments have also been combined with other modalities. The effectiveness of pelvic floor rehabilitation combined with surgical, topical and/or psychological intervention reached 81% pain reduction post treatment in a retrospective study.68

The pelvic floor therapist experienced in pelvic floor disorders is a vitally important member of the multi-specialty team that women with vulvar pain syndromes need for improvement. Through every aspect of her work, she not only performs pelvic floor muscle evaluation and rehabilitation, but also provides sex education and promotes a woman’s comfort with her body. Identification of environmental factors such as job stress, constipation, or menstrual cycle triggers may provide targets for intervention such as modification of work related practices- bathroom breaks, a different chair or provision to stand at the computer, institution of a bowel regimen, or menstrual cycle suppression.

The American Physical Therapy Association Web site (http:// www.womenshealthapta.org) can assist in locating physical therapists that specialize in pelvic floor hypertonic dysfunctions.

Centrally Acting Medications

Because central sensitization and neuropathic up-regulation perpetuate pelvic floor hypertonic disorders, especially if pain is a component of the woman’s symptoms, down-regulation of the neuropathic changes is often necessary with drugs to assist in decreasing muscle spasticity, and the allodynia (pain present from a stimulus that normally does not produce pain, i.e., touch). Medications used for this are discussed in Annotation K Vulvar pain and provoked and unprovoked vulvodynia.

References

  1. Van Houten T. Anatomy of the pelvic floor and pelvic organ support system. In:Women’s Sexual Function and Dysfunction.Goldstein I, Meston C, Davis S. Traish A, Eds. Oxford, England. Taylor & Francis, 2006.
  2. Prendergast SA, Rummer EH.Pelvic Pain Explained. Rowman & Littlefield, Latham, MD 2016.
  3. Jantos M, Johns S, Torres A, Baszak-Radomanska E. Mapping chronic urogenital pain in women: review and rationale for a muscle assessment protocol- Part 1. Pelviperinology 2015; 34:21-17.
  4.  Prather H, Dugan S, Fitzgerald C, et al. Review of anatomy, evaluations and treatment of musculoskeletal pelvic floor pain in women. PM R 2009;1(4):346-358.
  5. Kearney R, Miller JM, Ashton-Miller JA, et al. Obstetric factors associated with levator ani muscle injury after vaginal birth. Obstet Gynecol 2006; 107. 144-149.
  6. Kearney R, Miller JM, Ashton-Miller JA, et al. Obstetric factors associated with levator ani muscle injury after vaginal birth. Obstet Gynecol 2006; 107. 144-149.
  7. Stoker J, Wallner C. The anatomy of the pelvic floor and sphincters. In: Stoker J, Taylor SA, DeLancey JOL, eds.Imaging pelvic floor disorders. 2nd revised ed. Berlin Heidelberg: Springer-Verlag, 2008. 1-29.
  9. Stoker J, Wallner C. The anatomy of the pelvic floor and sphincters. In: Stoker J, Taylor SA, DeLancey JOL, eds.In Imaging pelvic floor disorders, 2nd revised ed,Berlin Heidelberg: Springer-Verlag, 2008. 1-29]/efn_note]

    The most anterior (medial) fibers of the pubococcygeus that meet bilaterally at the perineal body superior to the anus, are called the pubovaginalis. These act as an important sphincter of the vagina. Vaginal closure is assisted by the bulbospongiosus and puborectalis muscles. these muscles also activate the elevator and to facilitate vaginal ballooning. The most posterior fibers of the pubococcygeus (puborectalis) form a sling around the rectum. 8 Lee D, Lee L-J, Vleeming A, et al. The Pelvic Girdle: An Integrations of Clinical Expertise and Research. 4th ed. Toronto, Ontario, Canada: Churchill Livingstone: 2011.

  10. Prather H, Dugan S, Fitzgerald C, et al. Review of anatomy, evaluations and treatment of musculoskeletal pelvic floor pain in women. PM R 2009;1(4):346-358.
  11. Hodges PW, McLean L, Hodder I. Insight into the function of the obturator internus muscle in humans: observations with development and validation of an electromyography recording technique. Kinesiol J Electromyor 2014;2(4):489-496.
  12. Stoker J, Wallner C. The anatomy of the pelvic floor and sphincters. In: Stoker J, Taylor SA, DeLancey JOL, eds. Imaging pelvic floor disorders, 2nd revised ed, Berlin Heidelberg: Springer-Verlag, 2008. 1-29
  13. Kearney R, Miller JM, Ashton-Miller JA, et al. Obstetric factors associated with levator ani muscle injury after vaginal birth. Obstet Gynecol 2006; 107. 144-149.
  14. Kearney R, Miller JM, Ashton-Miller JA, et al. Obstetric factors associated with levator ani muscle injury after vaginal birth. Obstet Gynecol, 2006; 107:144-149.
  15. Voorham-van der Zalm PJ, Lycklama A, Nijeholt GA, Elzevier HW, Putter H, Pelger RC. “Diagnostic investigation of the pelvic floor”: a helpful tool in the approach in patients with complaints of micturition, defecation, and/or sexual dysfunction. J Sex Med 2008 Apr 5(4):864-871.
  16. Butrick CW. Pathophysiology of pelvic floor hypertonic disorders. Obstet Gynecol Clin N Am, 2009; 36: 699-705.
  17. Simons DG, Travell JG, et al. Myofascial Pain and Dysfunction: The Trigger Point Manual. Lippincott, Williams & Wilkins. Philadelphia, 1998
  18. Prendergast SA, Rummer EH. Pelvic Pain Explained. Rowman & Littlefield, Latham, MD 2016, p. 18
  19. Graven-Nielsen T, Mense S. The peripheral apparatus of muscle pain: evidence from animal and human studies. Clin J Pain, 2001;17(1):2–10.
  20. Butrick CW. Interstitial cystitis and chronic pelvic pain: new insights in neuropathology, diagnosis, and treatment. Clin Obstet Gynecol 2003;46(4):811–823.
  21. DeSantana JM, Sluka KA. Central mechanisms in the maintenance of chronic widespread noninflammatory muscle pain. Curr Pain Headache Rep, 2008; 12(5):338-343.
  22. Jensen R. Pathophysiological mechanisms of tension-type headache: a review of epidemiological and experimental studies. Cephalgia, 1999; 19(6):602-621.
  23. Minassian VA, Lovatsis D, Pascali D, et al. Effect of childhood dysfunctional voiding on urinary incontinence in adult women. Obstet Gynecol, 2006;107(6): 1247–1251.
  24. De Paepe H, Renson C, Van Laecke E, et al. Pelvic-floor therapy and toilet training in young children with dysfunctional voiding and obstipation. BJU Int, 2000; 85(7):889-893.
  25. Peters KM, Carrico DJ. Frequency, urgency, and pelvic pain: treating the pelvic floor versus the epithelium. Curr Urol Rep, 2006; 7(6):450–455.
  26. Dietz HP. Pelvic floor trauma following vaginal delivery. Curr Opin Obstet Gynecol, 2006; 18(5):528–537.
  27. Quinn M. Injuries to the levator ani in unexplained, chronic pelvic pain. J Obstet Gynaecol, 2007; 27(8):828–31.
  28. Butrick CW. Pathophysiology of pelvic floor hypertonic disorders. Obstet Gynecol Clin N Am 2009; 36:699-705.
  29. Ustinova EE, Fraser MO, Pezzone MA. Colonic irritation in the rat sensitizes urinary bladder afferents to mechanical and chemical stimuli: an afferent origin of pelvic organ cross-sensitization. Am J Physiol Renal Physiol, 2006;290(6): F1478–1487.
  30. Doggweiler-Wiygul R. Urologic myofascial pain syndromes. Curr Pain Headache Rep. 2004;8(6):445–451.
  31. Gardella B, Iacobone A, Musacchi V, et al. Effect of local estrogen therapy (LET) on urinary and sexual symptoms in premenopausal women with interstitial cystitis/bladder pain syndrome (IC/BPS). Gynecol Endocrinol. 2015 Aug 10:1-5. (Epub ahead of print)
  32. Glazer HI, Rodke G, Swencionis C, et al. Treatment of vulvar vestibulitis with electromyographic biofeedback of pelvic floor musculature. J Reprod Med, 1995; 40:283-290.
  33. Glazer HI, Jantos M, Hartmann EH, Swencionis C. electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med, 1998; 43:959-962.
  34. Glazer HI, Jantos M, Hartmann EH. Dysesthetic vulvodynia: Long-term follow-up after treatment with surface electromyography-assisted pelvic floor muscle rehabilitation. J Reprod Med, 2000; 45:798-802.
  35. White G, Jantos M, Glazer H. Establishing the diagnosis of vulvar vestibulitis. J Reprod Med, 1997; 42:157-160.
  36. Reissing ED, Binik YM, Khalife S, Cohen D, Amsel M. Vaginal spasm, pain and behavior: An empirical investigation of the diagnosis of vaginismus. Arch Sex Behav, 2004; 33:5-17.
  37. Bergeron S, Binik YM, Khalife S, Pagidas K, Glazer HI. A randomized comparison of group cognitive-behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis. Pain, 2001; 91:297-306.
  38. Bergeron S, Brown C, Lord MJ, Oala M, Binik YM, Khalife S. Physical therapy for vulvar vestibulitis syndrome:a retrospective study. J Sex Marital Ther, 2002; 28:183-192.
  39. Reissing ED, Brown C, Lord MJ, Binik YM, Khalife S. Pelvic floor muscle functioning in women with vulvar vestibulitis syndrome. J Psychosom Obstet Gynecol, 2005; 26(2):107-113.
  40. Witzeman K, Nguyen R, Eanes A, As-Sanie S, Zolnoun D. Mucosal versus muscle pain sensitivity in provoked vestibulodynia. J Pain Res . 2015 Aug 12;8:549-55.
  41. Gutman RE, Ford RE, Quiroz LH, et al. Is there a pelvic organ prolapse threshold that predicts pelvic floor symptoms? Am J Obstet Gynecol, 2008;199(6):e1–e7.
  42. Prendergast SA, Rummer EH. Pelvic Pain Explained. Rowman & Littlefield, Latham, MD 2016, p. 40.
  43. Jantos M, Johns S, torres a, Baszak-Radomanska E. Mapping chronic urogenital pain in women: review and rationale for a muscle assessment protocol- Part 1. Pelviperinology 2015; 34:21-17.
  44. Fitzgerald MP, Kotyarinos R. Rehabilitation of the short pelvic floor. I:Background and patient evaluation. Int Urogynecol J 2003; 14:261-268
  45. Bergeron S, Brown C, Lord MJ, Oala M, Binik YM, Khalife S. Physical therapy for vulvar vestibulitis syndrome: a retrospective study. J Sex Marital Ther 2002; 28:183-192.
  46. Spitznagle T, Robinson C. Myofascial pelvic pain. Obstet Gynecol Clin N Am. 2014; 41:409-32.
  47. Strauhal MJ, Frahm J, Morrison P, Featherstone W, Hartman D, Florendo J, Parker S. Vulvar pain: a comprehensive review. J Womens Health Phys Therap, 2007; 31:7-25.
  48. Boyer SC, Goldfinger C, Thibault-Gagnon S, Pukall CF. Management of female sexual pain disorders. In: Balon R (ed). Sexual dysfunction: Beyond the Brain-Body Connection. Adv Psychosom Med, Basel, Karger 201, vol 31, 83-104.
  49. Gentilcore-Saulnier E, McLean L, Goldfinger C, Pukall CF, Chamberlain S. Pelvic floor muscle assessment outcomes in women with and without provoked vestibulodynia and the impact of a physical therapy program. J Sex Med, 2010; 7:1003-1022.
  50. Goldfinger C, Pukall Cf, Gentilcore-Saulnier E, McLean L, Chamberlain S. A prospective study of pelvic floor physical therapy: pan and psychosexual outcomes in provoked vestibulodynia. J Sex Med 2009; 6:1955-1968.
  51. Bergeron S, Brown C, Lord MJ, Oala M, Binik YM, Khalife S. Physical therapy for vulvar vestibulitis syndrome: a retrospective study. J Sex Marital Ther 2002; 28:183-192.
  52. Backman H, Widenbrant M, Bohm-Starke N, Dahlof L-G. Combined physical and psychosexual therapy for provoked vestibulodynia; an evaluation of a multidisciplinary treatment model. J Sex Res, 2008; 45:378-385.
  53. Spoelstra SK, Dijkstra JR, van Driel MF, Weijmar Schultz WC. Long-term results of an individualized, multifaceted, and multidisciplinary therapeutic approach to provoked vestibulodynia. J Sex Med, 2011; 8:489-496.
  54. deSouza Montenegro MLL, Mateus-Vasconcelos EC, Candido dos Reis FJ, Rosa e Silva JC, Nogueira AA, Poli Neto OB. Thiele massage as a therapeutic option for women with chronic pelvic pain caused by tenderness of the pelvic floor muscles. J Eval Clin Pract, 2010; 16:981-982.
  55. Abrams P, Cardozo L, Fall M, Griffiths D et al. The standardisation of terminology of lower urinary tract function: report from the Standarisation Sub-committee of the International Continence Society. Am J Obstet Gynecol, 2002; 187:116-126.
  56. Glazer HI, Rodke G, Swencionis C, et al. Treatment of vulvar vestibulitis with electromyographic biofeedback of pelvic floor musculature. J Reprod Med, 1995; 40:283-290.
  57. McKay E, Kaufman RH, Doctor U, Berkova Z, Glazer H, Redko V. treating vulvar vestibulitis with electromyographic biofeedback of pelvic floor musculature. J Reprod Med, 2001; 46:337-342.
  58. Danielsson I, Tortensson T, Brodda-Jasen G, Bohm-Starke N. EMG biofeedback versus topical lidocaine gel: a randomized study for the treatment of women with vulvar vestibulitis. Acta Obstet Gynecol Scand, 2006; 85:1360-1367.
  59. Bergeron S, Binik YM, Khalife S, Pagidas K, Glazer HI. A randomized comparison of group cognitive-behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis. Pain, 2001; 91:297-306.
  60. Bergeron S, Khalife S, Glazer HI, Binik YM. Surgical and behavioral treatments for vestibulodynia: two and one half year follow-up and predictors of outcome. Obstet Gynecol 2008; 111:159-166.
  61. Fita FF, Resende APM, Stupp L, Ferreira Sartori MG, et al. biofeedback for the treatment of female pelvic floor muscle dysfunction: a systematic review and meta-analysis. Int Urogynecol J 2012 Mar 17 e-pub prior to print.
  62. Montnegro ML, Vasconcelos ED, Candido Dos Reis FJ, et al. Physical therapy in the management of women with chronic pelvic pain. Int J Clin Pract 2008; 62(2):263-269
  63. Weiss JM. Pelvic floor myofascial trigger points: manual therapy for interstitial cystitis and the urgency-frequency syndrome. J Urol, 2001; 166(6):2226-2231.
  64. Oyama IA, Rejba A, Lukba JC, etal. Modified Thiele massage as therapeutic intervention for femal patients with interstitial cystitis and high-tone pelvic floor dysfunction. Urology, 2004; 64(5):862-865.
  65. Rosenbaum TY, Owens A. The role of pelvic floor physical therapy in the treatment of pelvic and genital pain-related sexual dysfunction. J Sex Med, 2008; 5(3):513-523.
  66. Markwell SJ. Physical therapy management of pelvic/perineal pain syndromes. World J Urol, 2001; 19(3):194-199.
  67. Bharucha AE, Trabuco E. Functional and chronic anorectal and pelvic pain disorders. Gastroenterol Clin North Am, 2008; 37(3):685-696.
  68. Spoelstra SK, Dijkstra JR, van Driel MF, Weijmar Schultz WE. Long term results of an individualized, mulifaceted, and multi-disciplinary therapeutic approach to provoked vulvodynia. J Sex Med, 2011; 8:489-496.