Pelvic Floor Dysfunction A Treatment Update
The pelvic floor is comprised of muscles and fascia and has three functions: support of the pelvic organs, contraction, and relaxation. Their function is critical to proper micturition, defecation, and sexual intercourse. In the past, pelvic floor dysfunction (PFD) has been variously termed spastic pelvic floor syndrome, levator ani syndrome, proctalgia fugax, vaginismus, male chronic pelvic pain syndrome, non-neurogenic neurogenic bladder, and coccydynia — all terms based upon the varied presenting features of the same phenomenon. Pelvic floor dysfunction may be defined as spasm or discoordination of the pelvic floor musculature. Spasm of these muscles commonly manifests with urological symptoms including poor urine stream, pelvic pain or pressure, urinary frequency and urgency, urge incontinence, and ejaculatory pain. These are the same complaints seen in patients with chronic pelvic pain (CPP) syndromes including interstitial cystitis (IC) and chronic prostatitis (CP). Other frequent co-existent symptoms include chronic constipation, lower back pain, penile, vaginal, peri-rectal pain, vulvodynia, dyspareunia, or generalized pain. Treatment of PFD, when present in IC or CP, is strongly recommended, along with bladder or bowel-directed therapy to achieve the optimal relief of symptoms. This article will review pelvic neuroanatomy, pathophysiology, PFD diagnosis, and treatment.
The pelvic floor muscles (PFM) include the levator ani (pubococcygeus, ileococcygeous, puborectalis), coccygeus, pyriformis, obturator and perineal muscles (see Figure 1). The levators derive circulation from the parietal branches of the internal iliac artery and innervation from sacral nerves S3 and S4, via the pudendal nerve. At rest, the PFM support the bladder and urethra in the anterior vaginal compartment, the anus and rectum in the posterior compartment, and the cervix and uterus in the middle compartment. Like all skeletal muscles, resting tone is maintained by slow-twitch (type 1) efferent fibers, which contribute to the integrity of the proper anatomic positions of the pelvic organs, in addition to supportive fascia. These vary with hormone status, parity and body habitus.
Voluntary contraction of the pelvic floor arises from a conscious impulse, while reflex contractions occur to close the urethra, anus and vagina, to prevent urine and stool loss, and as a vaginal protective mechanism. Phasic recruitment of large motor units propagated by fast twitch (type 2) fibers occurs in response to abdominal pressure increases such as coughing. Feedback inhibition (“guarding reflex") of the detrusor muscle will result in diminution of detrusor pressure, preventing bladder contraction. For an efficient contraction, the PFMs must have strength (via recruitment) and endurance (over time). In addition, during sexual arousal and orgasm, pelvic floor muscle contraction facilitates vasocongestion and contract involuntarily, respectively.
Coordinated floor relaxation must occur before, or in conjunction with, bladder or bowel contraction and is a result of inhibition of tonically active motor units, and is needed for proper micturition, defecation, and intercourse.
Overall, PFD and chronic pelvic pain are poorly managed because they are poorly understood. They can include bladder, bowel and sexual dysfunction, as well as be associated with depression, anxiety, and drug addiction. The prevalence of PFD is not well known, yet CPP affects 1 in 7 women1 and accounts for 10% of all outpatient visits to gynecologists,2 while CP accounts for 8% of all visits to urologists.3 CPP is most common among reproductive age women and men between 18-50 years. It is defined as non-menstrual pain for three months or longer, that localizes to the anatomic pelvis and is severe enough to result in disability requiring medical or surgical treatment.
Pelvic Floor Dysfunction
PFD is secondary to muscle overactivity or underactivity. Underactive PFMs contract poorly, resulting in incontinence of urine and stool, and is commonly attributed to birth trauma. Overactive PFMs can result from a variety of causes, and develops over time. They can be urologic, gynecologic, gastrointestinal, musculoskeletal, neurologic, or psychologic in nature (see Table 1). Overactive PFMs do not relax appropriately when they should, resulting in increased outlet resistance. This leads to strained voiding and incomplete emptying with poor flow, constipation, and dyspareunia. Postponing voiding or defecation is done by PFMs contraction, however chronic postponement or “rushed voiding" heightens PFMs activity. When voiding is attempted, often detrusor contraction is poor and, when abdominal straining is used to assist elimination, the guarding reflex results in PFM contraction.4 A muscle that is constantly contracting or in spasm will generate pain. Any nerve or vessel that travels through such muscle may be compressed,5 and may, in turn, lead to pain. Constant afferent pain signals to the sacral cord, pons and cerebral cortex can result in efferent activity that can aggravate the pain even further.6