Obstetrician/gynecologists often are the initial management clinicians for pelvic neuropathic pain. Although treatment may require comprehensive team management and consultation with other specialists, there are a few critical and basic steps that can be performed during an office visit that offer the opportunity to improve quality of life significantly in this patient population. A key first step is a thorough clinical examination to map the pain site physically and to identify potentially involved nerves. Only limited evidence exists about how best to manage neuropathic pain; generally, a combination of surgical, manipulative, or pharmacologic methods should be considered. Experimental methods to characterize more precisely the nature of the nerve dysfunction exist to diagnose and treat neuropathic pain; however, additional scientific evidence is needed to recommend these options unanimously. In the meantime, an approach that was adopted from guidelines of the International Association for the Study of Pain has been tailored for gynecologic pain.
Modern obstetrics care obviously has progressed, with the addition of pain medicine to the management of labor, but application to gynecologic pain receives less attention. Neuropathic pain is defined as a pain arising as a direct consequence of a lesion or disease that affects the sensory component of the nervous system, according to the Neuropathic Pain Special Interest Group of the International Association for the Study of Pain definition. Although there are no uniform definitions on magnitude and duration, this type of pain is severe (>5 on a 0-10 scale, with 10 being worst possible) and persists longer than superficial wounds (weeks to decades). Words used to describe the perception of neuropathic pain include “electric shock,” “dull,” “itching,” and “burning.” The challenge of exclusively confirming that pain is of neuropathic origin has led to the clinical guideline that it be graded as “definite,” “probable,” or “possible” neuropathic pain. Cardinal symptoms of neuropathic pain include hyperalgesia (increased sensitivity to pain) and allodynia (increased sensitivity to touch), although these are nonspecific. Although injured tissue is expected to recover after the resolution of the initial acute trauma, persistent changes in sensory processing (ie, spinal neuron responsiveness) can maintain a state of severe pain. Women, unfortunately, face many abdominal/pelvic insults that can cause probable neuropathic pain. Estimates of chronic pain after cesarean or vaginal delivery range from 10–20%; gynecologic procedures may be associated with a 5–32% risk. Plausibly, sex-dependent physiologic processes and neuroanatomic differences between women and men underlie the high risk of chronic pain after pelvic surgery; between-gender comparisons after surgical procedures generally suggest that women experience higher levels of perioperative pain, which likely reflects some component of neuropathic pain.
The study of pelvic neuropathic pain likely has been hampered by the wide and confusing differential diagnosis to consider abdominopelvic pain. Consequently, we will make recommendations for clinical practice that are based on more clear-cut disorders, such as diabetic neuropathy. One unique pelvic neuropathy is pudendal nerve dysfunction, which appears to result from the convergence of myofascial dysfunction and anatomic nerve compression between the sacrospinous and sacrotuberous ligaments. However, it too remains a challenge to characterize, because pudendal neuropathy is still not a discrete entity, but one that appears to be seen often with concomitant pelvic floor spasm.
The most important characteristic to recognize is that “neuropathic pain can be reliably detected using psychophysical clinical examination” rather than using other “diagnostic modalities (electrical, magnetic resonance, x-ray, etc) beyond the exam.” At the most peripheral edge, mechanical and chemical receptors on sensory fibers, termed nociceptors , convey electrical signals to the spinal cord that indicate the presence of a painful stimulus. Tissue is innervated differentially by multiple sensory fibers of varying sizes and properties, and different kinds of painful stimuli are processed by discrete sensory fiber types. Indeed, different kinds of trauma can produce damage to specific fiber types. Although deficits can be identified roughly by description, more precise characterization can be accomplished through quantitative sensory testing, which evaluates a patient’s pain response to pressure, electrical stimulation, or heat-/cold-evoked stimulation. We and others have applied these measures to characterize a limited subset of pelvic pain conditions that may have neuropathic components. Consistent with this idea, localization of the damaged nerve, combined with psychophysiologic characterization, represents a standard component of the diagnostic work-up for neuropathic pain, as will be described later.
The second most important principle in diagnosing neuropathic pain “is recognizing it often involves changes in central nervous system processing, not just peripheral tissues.” With central aberrations in pain modulation and processing, symptoms can be out of proportion to the degree of tissue insult and may not correspond to tight dermatomal distributions. In animal models, multiple studies show that a completely peripheral neuropathy (such as sciatic nerve ligation) is maintained by changes in supraspinal neurons. Stimulation of specific brain sites can provide profound analgesia and has spurred the development of brain-stimulation strategies for the alleviation of pain in patients with the most severe forms of pain. Corollary to this principle is that neuropathic pain affects sleep and disposition; therefore, therapies that improve quality of life from neuropathic pain must rectify brain-wide problems. Patients who exhibit evidence of central sensitization may need treatment with centrally acting neuromodulatory medications that are labeled for use as antidepressants, anticonvulsants, and sedative-hypnotics, despite the appearance of a peripheral problem. With these principles in mind, we describe the approach to the diagnosis and treatment of a few common pelvic neuropathic conditions.
Diagnosis
History
In practice, diagnosis of many cases of abdominopelvic neuropathic pain occurs predominantly after a recent surgical procedure. Inadvertent suture ligation, anatomic compression (even from benign sources, such as pants or girdles), and alterations in the perineural environment that are the result of metabolic changes (such as diabetes mellitus) have all been described in cases in which treatment of the presumed underlying issue resolved the patient’s symptoms. Outside of the perioperative period, gynecologists mainly will confront probable neuropathic pain in rare circumstances: when it appears to be endometriosis invading into pelvic nerves or spontaneous pain that involves compression of pelvic nerves (such as branches of the obturator, pudendal, or lateral femoral cutaneous nerves). In contrast, women with the more common fascial or distal extremity neuropathies should be referred to a neurologist for treatment. Superficial perineal pain (vulvodynia and pudendal neuralgia) has been suggested to be a neuropathic pain conditions as well; however, the research on nerve involvement is limited, and the exact mechanisms may be a combination of chronic mucosal inflammation and hormone or infection-mediated peripheral sensitization, rather than overt nerve disease.
If the pain occurs after a recent gynecologic procedure, the clinician should take a thorough surgical history, focusing particularly on previous transverse abdominal incisions (hysterectomies, inguinal herniorrhaphy, and appendectomies) that place the iliohypogastric, ilioinguinal, and genitofemoral nerves at risk. For perineal and deep pelvic/vaginal pain, both natural and operative vaginal delivery and vaginal prolapse and antiincontinence procedures (cystocele or rectocele repair, vaginal vault suspension, midurethral slings) are associated specifically with neuropathic pain in the pudendal nerve distribution. Widely used and validated questionnaires exist to screen for neuropathic pain conditions (such as the Leeds assessment of neuropathic symptoms and signs); however, the results should be paired with results from the clinical examination. Other questionnaires (such as the McGill Pain Inventory) can monitor progress and regression quantitatively. Inquiry about comorbid psychologic disturbances (mood, anxiety) should be performed in concert with a diagnosis of neuropathic pain, because it is well-established that neuropathic pain with disability is correlated with catastrophization.
Beyond sensory input, many of the pelvic nerves contain motor branches, and damage can impair certain functions. Assessment of bowel and bladder function, that includes incontinence, may reveal potential pudendal nerve dysfunction. Pain after defecation (several minutes to 1 hour) is a positive sign for pudendal neuralgia, according to the Nantes criteria ( Table 1 ).
