(63) reviewed hormonal therapy in 217 patients: 68 in five observational studies, 59 in a cohort study, and 90 in a randomized controlled trial (63). The study compared aromatase inhibitor, vaginal danazol, GnRH agonist, intrauterine progestin, and two estrogen-progestin combinations, transvaginally or transdermally and an oral progestin. With the exception of an aromatase inhibitor used alone, the pain relief with medical therapies was satisfactory over the 6-to 12-month course of the treatment, with 60% to 90% of women reporting substantial decrease or complete relief from pain symptoms.
Chronic pelvic pain (CPP) is defined as pelvic pain that persists in the same location for greater than 6 months’ duration, causing functional disability or requiring treatment (64). CPP is an inclusive, general term that encompasses many more specific causes, ranging from reproductive, gastrointestinal, and urinary tract etiologies to myofascial pain and nerve entrapment syndromes. Chronic pelvic pain affects 12% to 20% of women in the United States. The differential diagnosis of CPP is outlined in Table 16.3. Nongynecologic causes of pain, such as irritable bowel syndrome, interstitial cystitis/bladder pain syndrome, abdominal wall or pelvic ﬂoor myofascial syndrome, or neuropathy, are frequently overlooked but common causes of chronic pelvic pain. This can in part explain why 60% to 80% of patients undergoing laparoscopy for chronic pelvic pain have no intraperitoneal pathology (2).
Patients with CPP are often anxious and depressed. Their marital, sexual, social, and occupational lives are disrupted. These patients frequently have poor treatment outcomes from traditionally effective gynecologic and medical therapy and may undergo multiple unsuccessful surgical procedures for pain. About 12% to 19% of hysterectomies are performed for pelvic pain, and 30% of patients who present to pain clinics have had a hysterectomy (65).
CPP states are characterized by up-regulation of central nervous system (CNS) responsiveness to peripheral stimuli. The relationship between the pain and pathology, such as endometriosis, adhesions, or venous congestion, is inconsistent and treatment is associated with pain recurrence. Recent investigations suggest that “plasticity” of the nervous system or alterations in signal processing may be involved in the maintenance of chronic pain states (2,6). Maladaptive changes within the peripheral and central nervous system predispose to allodynia (pain with usually nonpainful stimuli), hyperalgesia (excessive pain with a potentially painful stimulus), widening of the receptive field (pain experienced over a larger territory), and abnormal reﬂex responses in surrounding musculature (5–7).
The spinal cord is not a simple conduit between the periphery and the brain. It is an important site of “gating” mechanisms, such as excitation, inhibition, convergence, and summation of neural stimuli (66). With visceral tissue injury, a subset of nociceptive C-fibers that are usually dormant, called “silent” afferents, can become activated. The dorsal horn of the spinal cord is then ﬂooded with noxious chemical stimuli that, over time, can lead to up-regulation of the signaling in the dorsal horn and brain, and pain sensation can be persistent and amplified, even
Evaluation of Chronic Pelvic Pain after the peripheral pathology has resolved. The dorsal horn neurons demonstrate a number of electrophysiologic changes in this setting, such as the development of spontaneous activity, enlarged receptive fields, and lowered threshold for firing.