Persistent or Chronic Pelvic Pain
Matthew T. Siedhoff
DEFINITIONS
Allodynia—Pain resulting from a nonnoxious stimulus.
Hyperalgesia—Painful sensation of abnormal severity following noxious stimulation.
Neuropathic pain—Pain persisting after healing of disease or trauma-induced tissue damage.
Neuroplasticity—The malleability of central pain perception mechanisms in response to chronic pain states.
Nociceptor—A nerve receptor for pain.
There is not universal agreement on a single definition of chronic pelvic pain (CPP), but most practitioners accept the proposal of the American Congress of Obstetricians and Gynecologists: noncyclic pain of 6 or more months’ duration that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, or the lumbosacral back or the buttocks and is of sufficient severity to cause functional disability or lead to medical care. We are in need of deeper and updated investigation into the epidemiology of pelvic pain, but likely, at least 15% of women are affected by pelvic pain, most commonly during reproductive-age years. When last tabulated in 1996, it was estimated nearly $3 billion was spent annually in physician costs and out-of-pocket expenses. CPP accounts for at least 10% of outpatient visits to a gynecologist and is the indication for 40% of gynecologic laparoscopies.
Endometriosis and adhesions are some of the most common conditions assigned as an etiology of pelvic pain, but the connection between these problems and pain symptoms is actually more tenuous than has been traditionally taught. More and more data confirming the coexistence of multiple chronic pain disorders in patients—conditions such as interstitial cystitis (IC), painful bladder syndrome, irritable bowel syndrome (IBS), temporomandibular joint disorder, migraine headaches, vulvodynia, and fibromyalgia—suggest that perhaps we ought to be treating pelvic pain under an updated paradigm where the disease is pain itself rather than pain a manifestation of a specific etiology. In this chapter, we will apply the concept of central sensitization to CPP and point out common peripheral pain generators—nociceptive stimuli—than can be modulated by gynecologic interventions. We will review important elements in evaluation and describe the criteria for a chronic pain syndrome (CPS), offering a theoretical model to explain the evolution of chronic pain over.
HISTORY
Over the past 60 years, the study of CPP has gone through significant changes in approach. Investigations undertaken before the development of laparoscopy focused on correlations between pelvic pain and psychological distress. In the absence of palpable pathology, the gynecologist of the 1950s and 1960s was understandably reluctant to subject a patient to laparotomy to investigate pain. During this era, the prevailing cartesian theory of pain perception suggested that pain should be somewhat proportional to the degree of tissue damage found. Hence, if the pathology was not big enough to palpate, it was seldom operated on. Although this model was sufficient to address most causes of acute pain, it fails to elucidate the majority of chronic pain disorders, in gynecology as well as other areas of medicine. The gate control theory, promulgated by Melzack and Wall in 1965, allowed integration of physical and psychological parameters and explained how chronic pain can be quite different from acute pain. The model also suggests that information flows in two directions regarding pain: (a) nociceptive signals from peripheral tissue ascend through the spinal cord to higher centers, and (b) central centers can modulate, via descending signals altering spinal cord neurotransmitter and interneuron activity, the transmission of these nociceptive signals from the periphery. Deterioration of these regulatory processes was thought to potentially account for development of chronic pain states by allowing too many peripheral signals to pass through the spinal cord “gates.” Variation in patients’ relative degree of gate opening could thus explain why similar amounts of physical tissue damage result in different degrees of pain perception. The concept is similar to the way we view differences in depth of sleep—for some, the brain can easily filter out stimuli; for others, it takes very little exposure (e.g., light, sound) to overcome unconsciousness and bring about wakefulness.
TABLE 29.1 Contributors to Pelvic Pain in Laparoscopy-Negative Patients | ||||||||||||||||||||||||||||||||||||||||
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While these theory changes were stimulating the field of pain research, gynecologists were busy developing laparoscopy. Previously cherished myths soon fell by the wayside: for example, the incorrect assumption that endometriosis is seldom found in adolescents or women of African descent. With these observations came the hope that laparoscopic and medical treatment of encountered pathology would fix CPP. Reports of CPP from that era focused on “laparoscopy-negative” patients; indeed, some pelvic pain clinics required a negative laparoscopy as an entry criterion, implying that if some pathology were found, it must be a “real” cause for pain. Subsequent experience has shown that even though treatment
of laparoscopically diagnosed pathology is often helpful, the clinical reality is more complex:
of laparoscopically diagnosed pathology is often helpful, the clinical reality is more complex:
In many instances, the organic pathology found at laparoscopy may be incidental and not related to the pain.
In those with pathology that does contribute to nociception, the pain experienced by the patient may differ from another patient with anatomically similar pathology.
Pain from a laparoscopic finding may be the sum of that contribution plus signals from some or all of the disorders listed in Table 29.1.
Consider the research of the 1980s that documented a distressingly high prevalence of physical and sexual abuse. Epidemiologic surveys of community samples revealed that as many as 25% to 30% of adult women reported having experienced sexual abuse during childhood. Studies of women attending pelvic pain clinics, especially those based in psychiatric settings, showed that up to 60% of these women had been abused. These observations led to the speculation that the experience of abuse may make a person more vulnerable to the development of CPP or perhaps be a specific cause for pain. Studies using positron emission tomography and functional magnetic resonance imaging suggest that the experience of abuse may indeed leave its neurophysiologic footprints: stressful stimuli produce different central response patterns in abused versus nonabused subjects. In relation to pain, abuse, particularly that which occurs in formative years, may serve to alter response to nociception and central pain processing. That said, not all abused patients go on to have chronic pain nor do all patients with pain have a history of abuse, so it might be the response to trauma that plays a key role in development of chronic pain. Health care providers need to take into account the presence of abuse in a patient’s history when detected, but be careful to avoid necessarily concluding a causal relationship in that patient’s pain.
Melzack neuromatrix theory is an expansion of his original work that includes the notion of neuroplasticity, among other elements. The concept of neuroplasticity suggests that experience can change the neurophysiologic behavior of the central nervous system in a manner that influences the subsequent processing of nociceptive stimuli. It may explain the apparent development of pain responses to stimuli usually thought of as nonpainful (allodynia), as well as exaggerated responses to painful stimuli (hyperalgesia). Every practicing gynecologist has seen patients whose pain responses seem out of proportion to the pathology found. This may reflect the emotional meaning of the problem for the patient, as well as past or present trauma, but it may also be the result of nociceptive mechanisms not yet fully understood (e.g., the exact mechanism of pain from endometriosis) or the result of sensitization of spinal cord interneurons that have become pain amplifiers as a result of being on the receiving end of peripheral nociceptive stimuli for prolonged periods. When nociception has been emanating from one organ system for a period of time, adjacent organs may join the chorus. This concept may help explain the common finding of coexistent somatosensory disorders in the same patient, an observation that has led some investigators to pursue potential genetic variations in central neurotransmitter networks that might predispose to the development of multiple such disorders. The above is the negative side of neuroplasticity. The positive side of the neuroplasticity concept is that, perhaps, given enough time and the right treatment, even seemingly intractable chronic pain problems may ameliorate to the point of allowing substantially improved function.
The concept of central sensitization adds another layer to theoretical understanding of chronic pain. This idea emphasizes the ramping up of pain signaling with repeated stimuli over time. The centralized pain hypersensitivity helps us understand how multiple organ systems can be recruited into the syndrome, incorporating genetic and social factors in pain amplification.
CONTRIBUTIONS OF PERIPHERAL PAIN GENERATORS
This section deserves an important caveat. Though we believe that types of tissue damage or other nociceptive input can generate pain, they cannot be viewed in isolation of the patient’s individual central pain processing. Management strategies will be discussed in more detail, but, in general, the goal of the treating provider involves trying to dampen overall pain signaling sensitivity—“turning down the master volume”— and looking for areas in the periphery that can be “tuned up” toward better functioning. The following peripheral generators represent areas where we can intervene but should not be described to patients with CPP as the cause of their pain. These conditions can be completely asymptomatic in many patients, and thus the host where the disease manifests is much more important than the disease itself.
Endometriosis
A review summarized laparoscopic findings from 2,615 patients in 15 studies (nine retrospective, six prospective). Endometriosis was found in 2% to 51% of patients, suggesting that referral biases lead to very skewed samples. Clearly, not every woman with pain has endometriosis, nor does every woman with endometriosis have pain, although women with the disease had pain more often than those without it. A number of previous studies of CPP described only either patients without visible laparoscopic findings or stratified patients according to the presence or absence of such findings. The description of atypical (nonpigmented) endometriosis by Jansen and Russell in 1986 calls these classifications into question. Laparoscopy studies published before that time reported that 11% of women with CPP had endometriosis, whereas three similarly conducted studies published since 1986 reported a 41% prevalence of endometriosis in women undergoing laparoscopy for CPP. The pre-1986 literature on pelvic pain must be reevaluated with this information in mind. Many studies may have included women with endometriosis in the anatomically normal group, thus generating erroneous conclusions about the entirely psychogenic nature of their pain.
There are a variety of proposed mechanisms explaining pain associated with endometriosis, including inflammatory, nociceptive, and neuropathic. There is no pathognomonic symptom associated with endometriosis. Laparoscopic treatment of endometriosis improves pain symptoms more than diagnostic surgery alone, but many of the symptoms often assigned to the disease (e.g., dyspareunia, dysmenorrhea, abnormal bowel or bladder function) are commonly found in functional disorders such as IBS, making it difficult to understand the relevant contribution of endometriosis to CPP. The severity of the pain correlates poorly with the amount of superficial peritoneal disease, and such implants do not localize to the site of patients’ symptoms. Deeply infiltrating endometriosis (DIE)—fibrotic, vascular, desmoplastic tissue destruction—is an exception to this rule. Nodular disease of the colon is associated with dyschezia and hematochezia; urologic tract disease with hematuria, dysuria, and obstruction; and cul-de-sac disease (uterosacral ligaments, rectovaginal septum, ovarian endometriomas) with deep dyspareunia. Fear of worsened pain, impaired fertility, or recurrent disease after treatment may increase pain levels. Of the women for whom we repeat laparoscopy for recurrent pain following complete hysterectomy and adnexectomy for endometriosis, only a small minority (3% to 5%) prove to
have recurrent disease. Most cases of continued postoperative pain are interpreted in the context of the patient’s overall sensitivity to pain and other peripheral stimuli functioning under that same sensitivity, such as pelvic floor tension myalgia, painful bladder, or functional gastrointestinal disease.
have recurrent disease. Most cases of continued postoperative pain are interpreted in the context of the patient’s overall sensitivity to pain and other peripheral stimuli functioning under that same sensitivity, such as pelvic floor tension myalgia, painful bladder, or functional gastrointestinal disease.
Those experienced in treating the disease can often detect DIE with clinical exam and imaging. When endometriosis is strongly suspected otherwise, and initial treatment with oral contraceptives (OCs) has failed, diagnostic laparoscopy should be the next step. One widely discussed study by Ling et al. concluded that a careful clinical history and physical examination can predict the presence of endometriosis in approximately 80% of cases. However, this was done in the setting of a strict research protocol; the diagnostic sensitivity of this approach in general clinical practice is likely much lower. Unfortunately, the study is often misinterpreted as implying that pain relief following gonadotropin-releasing hormone (GnRH) agonist treatment is not only a sensitive detector of endometriosis but is also specific—that is, it makes the diagnosis of endometriosis. Careful reading of the data reveals that this is not the case: the frequency of relief following GnRH treatment was the same in women with and without endometriosis. In addition, pain sensitivity is known to increase perimenstrually even in women without CPP. This may mean that nociception from pain disorders outside the reproductive tract may also improve when menstrual cyclicity is eliminated. For example, IBS symptoms also decline in women taking GnRH agonists. Hence, although failure to relieve pain with a GnRH agonist supports the notion that the reproductive organs are not involved, relief of pain with these medications does not prove that they are to blame.
Pelvic Adhesions
Early reviews supported the role of adhesions as a significant peripheral pain generator in CPP. In one, 6% to 55% of the 2,615 patients who underwent laparoscopy for pelvic pain had pelvic adhesions. In more recent investigation, Latthe et al. demonstrated a relatively weak correlation between adhesions and CPP, much less than factors such as psychosomatic symptoms and substance abuse. Correlation, of course, does not imply causality, and few, if any, well-designed studies demonstrate effective treatment of CPP with adhesiolysis. Unfortunately, in an effort to provide some explanation for complex pain disorders, providers often still posit adhesions as an etiology, even when a patient’s surgical history includes only laparoscopy with findings of minimal or no endometriosis, pelvic inflammatory disease, or other conditions associated with meaningful adhesions. This explanation can happen even when the patient’s pain escalation is remote from the last surgery. Adhesions may play some role in pain conditions in some women, but the relative contribution is probably small. Also, the putative treatment—repeat surgical intervention—can add new contributions to pain syndromes, such as the impact of surgical trauma, disappointment from lack of pain relief, feeding the psychological need of being “ill” with more surgery, and, in the worst case, generating a complication such as enterotomy.
Pelvic Support
Most women in pain clinics are in their third or fourth decade of life, while pelvic organ prolapse affects significantly older women, suggesting a very minimal role for support problems in CPP.
Pelvic relaxation usually leads to reports of heaviness, pressure, dropping sensations, or aching. In attempting to hold in prolapsing organs, the patient may tense the levator plate, leading to tenderness during daily activities and intercourse. Fear of (or actual) loss of urinary control during coitus can add to the discomfort by impairing physiologic sexual response.
Uterine retroversion is another potential etiology for CPP, particularly in the form of deep dyspareunia. Clearly for many women, retroversion is an innocent anatomic variant, but for those with pain, uncontrolled clinical series of uterine suspension procedures suggest changing the position of the uterus to an axial or anteverted position can improve dyspareunia by elevating a tender fundus out of the posterior cul-de-sac and allowing for better vaginal expansion as a natural part of the sexual response cycle.
Pelvic Congestion
Overfilling (congestion) of the pelvic venous system has been implicated as a cause of dull chronic aching pain that usually is unilateral and worse at the end of the day after prolonged standing, premenstrually, and postcoitally. Some studies suggest the condition is present in nearly one third of women with CPP, but there is no agreed-upon reference standard for diagnosis, despite individual technical regimens involving venography, MRI, and ultrasonography. Hormonal suppression, percutaneous embolotherapy, and surgery (vein ligation, hysterectomy, and salpingo-oophorectomy) represent available treatments, but study protocols involving these interventions are diverse, and few have been investigated in controlled trials.
Residual Ovary
When the uterus has been removed, with or without removal of one ovary, the remaining ovary or ovaries become symptomatic in 1% to 4% of women. Pain from the ovary can be increased by confinement within postoperative adhesions, rupture or leakage of a cyst prompting additional adhesion formation, or attachment of the ovary to the sigmoid colon or vaginal apex by postoperative adhesions. In the case of attachment to the vaginal apex, deep dyspareunia can result when the area is struck.
Ovarian Remnant
A more difficult situation can develop if a small fragment of ovarian tissue is left behind during attempted oophorectomy. In most instances, this happens when challenging dissection is required, such as cases of extensive pelvic adhesions and/or DIE. Within 1 to 3 years of the attempted oophorectomy, continued folliclestimulating hormone (FSH) stimulation will result in growth of the ovarian fragment, often producing an intermittently symptomatic pelvic mass located along the course of the ovarian vascular supply. A postulated mechanism for pain generation includes the cystic enlargement of the mass confined within fibrotic adhesions. If the remnant developed because endometriosis is made for difficult oophorectomy, that disease is often found in the remnant and probably also serves as a pain generator. Ovarian remnants are uncommon, but not rare, as implied by early case series. Classic symptoms include absence of vasomotor symptoms when bilateral oophorectomy was intended and presence of cyclic unilateral pain. As in the case of the residual ovary, the remnant can produce dyspareunia if it is located close to the vaginal apex. When performing oophorectomy, it is best to open the pararectal space and completely skeletonize the infundibulopelvic (IP) ligament, not only to avoid complications such as ureteral injury but also to prevent ovarian remnant syndrome. In difficult cases, dividing the IP at or above the pelvic brim, as in risk reduction prophylactic oophorectomy, is prudent.
Vaginal Apex Pain
Following hysterectomy, pain may persist or recur because of intrinsic sensitivity of the vaginal apex. Although the cuff may appear to have healed perfectly well, gentle examination with a cotton-tipped applicator may reveal focal sensitivity of
moderate-to-severe degree, many times located in one lateral fornix or the other and often replicating the reported pain of dyspareunia. When this is not done, the unaware examiner may then, noting pain upon traditional bimanual examination, mistakenly conclude that the source of nociception lies cephalad, for example, in a remaining ovary, pelvic scarring, or bowel adhesions.
moderate-to-severe degree, many times located in one lateral fornix or the other and often replicating the reported pain of dyspareunia. When this is not done, the unaware examiner may then, noting pain upon traditional bimanual examination, mistakenly conclude that the source of nociception lies cephalad, for example, in a remaining ovary, pelvic scarring, or bowel adhesions.
The diagnosis may be confirmed by noting elimination of the pain following injection of local anesthetic. The condition is generally considered neuropathic, by virtue of the character of the pain (burning, stinging, sharp), and that neuropathic treatments (overnight application of lidocaine, oral medications such as nortriptyline, amitriptyline, gabapentin, etc.) seem to benefit some patients. Laparoscopic revision of the vaginal cuff may give good initial relief in approximately two thirds of patients, but pain tends to recur to a degree over the subsequent 2 to 3 years.
Musculoskeletal Problems
Musculoskeletal changes can become involved with CPP, either as the primary problem or as a secondary reaction to the pelvic pain. Dysmenorrhea can be referred to the midline of the low back, especially when the uterus is retroverted. Pain can also be referred to the midline of the low back in the presence of cul-desac endometriosis. An ovary fixed to the pelvic sidewall can refer pain to the ipsilateral low back, lower quadrant, and upper thigh.
The muscular problem that most often produces pelvic pain is pelvic floor tension myalgia. Intermittent or constant painful contraction of the levator plate can be present as a primary psychophysiologic problem, but contraction is more often a reaction to some other source of pain. Even when the primary source of pain is successfully treated, the reactive muscle contraction can persist as a learned response, in much the same way that vaginal introital muscle spasm (vaginismus) can persist after transient but repeated painful vaginal events. Pelvic floor tension myalgia is often found in the setting of generalized somatic hypersensitivity, a condition whose worst case includes fibromyalgia.
Lumbar musculature can become tender as a primary problem or in reaction to subtle changes in posture and motion. Trigger points can be present in the low back and gluteal areas in the muscles best inspected by pelvic examination (e.g., levator plate, piriformis, obturator internus).
The piriformis and obturator muscles warrant additional mention because they are seldom appreciated as possible sources of pain. These muscles are external rotators of the leg, and rotation against resistance can allow detection of tender spasm of the muscles during the pelvic examination. The sciatic nerve can traverse the belly of the piriformis as a normal anatomic variant, producing symptoms similar to sciatica when the muscle is in spasm.
Myofascial Pain
Focal lower quadrant abdominal wall pain can be produced by entrapment of the genitofemoral and ilioinguinal nerves, as described by Applegate. Such entrapment appears most often after Pfannenstiel abdominal incisions. Reiter and Gambone reported that 14% of 122 laparoscopy-negative women had myofascial pain probably related to a previous surgical incision. Myofascial trigger points—palpable taut bands of tender skeletal muscle—may be a primary problem or a later reaction to the long duration of pain from some other source.
Medical Comorbidity
Peripheral pain generation in CPP often involves nongynecologic systems (Table 29.1). A careful history and close physical examination of gastrointestinal, urologic, musculoskeletal, and neurologic systems are needed to evaluate these additional contributions to CPP. Most of the available literature examines these problems of other systems independently of each other and without reference to their relevance to CPP or to the overall prevalence of these disorders in CPP.
The gastrointestinal system is perhaps the most common nongynecologic contributor to CPP. Constipation and IBS occur most frequently, although inflammatory bowel disease and diverticulitis can at times present with pain alone. Women are proportionately more affected by IBS, and some have hypothesized increased relaxin levels produced by a dysfunctional corpus luteum as one of many possible contributing factors. As previously mentioned, treatment with a GnRH agonist may reduce symptoms of IBS.
Urologic problems, which are less easily confused with gynecologic disorders, are perhaps second in terms of prevalence. The urethral syndrome (frequency, urgency, and dysuria in the absence of bacteriuria), IC, and bladder spasms are all accompanied by significant anxiety and depression symptoms. The symptoms of these three disorders are very similar to those in a population of gynecologic CPP patients. Structured questionnaires (e.g., the Pelvic Pain and Urgency/Frequency [PUF] scale) help detect symptoms possibly emanating from the bladder. In some patients, however, a “positive” score can be achieved on the basis of other components of pelvic pain alone—without specific bladder symptoms—making the measure perhaps too sensitive and hence insufficiently specific. A history (whether pain occurs during micturition, daily activities, or coitus) does not always reveal the involved system, but careful pelvic examination with stepwise gentle palpation of the urethra, bladder base, and bladder may help the physician identify the site of the pain the patient is experiencing.
Many patients do not experience the problems described here in pure form, but rather in varying degrees of intensity, with varying contributions to an individual’s total discomfort. Indeed, we suspect that shared innervation of pelvic organs may often lead to subsyndromal symptoms in an organ system that neighbors one with different pathology. Such patients have a multifaceted somatosensory disorder, as opposed to being the unfortunate victim of multiple unrelated organ-specific disease processes. Close attention to such nuances of detail is warranted both in clinical management and in published reports.
PSYCHOLOGICAL FACTORS
Personality
The links between chronic pain and individual psychology and personality style have been sought after and discussed in the psychiatric literature for many years. Some early reports implied that women who reported CPP had a high prevalence of feminine identity problems related to conflicts about adult sexuality, psychiatric disturbance characterized by mixed character disorder with predominant schizoid features, high neuroticism, and unsatisfactory relationships. Although these initial studies were an important beginning, the high prevalence of psychopathology in some reported samples did not seem applicable to significant numbers of CPP patients seen in practice. The findings are difficult to interpret, partly because there is a lack of clarity concerning the operational definition of CPP that was used. Biases in patient selection and interviewer information, inadequate control groups, and the absence of diagnostic laparoscopy also contribute to the confusion. Despite these shortcomings, it seems apparent that disorders of personality, especially borderline personality, are overrepresented both in the general population of severe chronic pain patients and in the population of those with CPP.
In primary care, such patients usually are seen less often. In any case, a label of personality disorder should not be applied indiscriminately to every angry patient by her frustrated physician. People who have difficulties maintaining satisfactory relationships and function in life, even when these difficulties are caused in part by subsyndromal personality problems, can be more vulnerable to nociceptive signals from tissue damaged by endometriosis, infection, or surgery. Unmet dependency needs may lead them to seek external solutions such as medications and further surgery, rather than to rely on their own impaired coping skills.
In primary care, such patients usually are seen less often. In any case, a label of personality disorder should not be applied indiscriminately to every angry patient by her frustrated physician. People who have difficulties maintaining satisfactory relationships and function in life, even when these difficulties are caused in part by subsyndromal personality problems, can be more vulnerable to nociceptive signals from tissue damaged by endometriosis, infection, or surgery. Unmet dependency needs may lead them to seek external solutions such as medications and further surgery, rather than to rely on their own impaired coping skills.
Depression
Focusing specifically on a CPP sample that had been evaluated by diagnostic laparoscopy, Walker and associates found that women with CPP (with and without positive laparoscopic findings) met criteria for lifetime major depression, current major depression, lifetime substance abuse, adult sexual dysfunction, and somatization more often than did control subjects. Stout and Steege found that 59% of 294 women seeking evaluation at a pelvic pain clinic scored in the depressed range (>16) on the Center for Epidemiologic Studies Depression Scale at the time of their initial visit. Slocumb and colleagues reported that patients with an abdominal pelvic pain syndrome scored higher on scales of anxiety, depression, anger-hostility, and somatization on the Hopkins Symptom Checklist.
Because no study of CPP has assessed its association with depression over time, no statement can be made as to whether depressive symptoms are a predisposing factor leading to, or a reaction to, the pain condition. There seem to be two distinct groups of CPP patients: one in which pain and depression are common final presentations reached by a number of pathways and another in which depression develops in reaction to pain, as is the case with many other acute and chronic medical diseases.
History of Sexual Abuse
Women seeking treatment for CPP have a high prevalence of sexual trauma in their personal histories. In Reiter’s study of 106 women with CPP, 48% had a history of major psychosexual trauma (molestation, incest, or rape) compared with 6.5% of 92 pain-free control subjects presenting for annual routine gynecologic examination (P < 0.001). The high prevalence of reports of psychosexual trauma elicited from CPP patients supports the hypothesis that pelvic pain is specifically and psychodynamically related to sexual abuse. However, Rapkin and colleagues did not find a higher prevalence of childhood or adult sexual abuse in a group of women with CPP compared with women with chronic pain in other locations. These findings argue against a unique relation between sexual abuse and CPP and suggest that abusive experiences promote the chronicity of many different painful conditions.
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