Published: August 2010
The International Society for the Study of Pain defines pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”1 Chronic nonmalignant pain (CNMP) is defined variously as pain lasting 3 months or more, or as pain persisting beyond the time of expected healing. It can begin with trauma (e.g., back strain) or disease (e.g., pancreatitis) or can occur de novo (e.g., fibromyalgia, daily migraine).
One in 10 U.S. adults reports current pain that has lasted a year or more. Reviews have estimated the prevalence of severe chronic pain in the general adult population to be approximately 11%. It is our most common cause of disability.
Risk factors are biologic, sociologic, psychological, and environmental. It is more common in those with depression, anxiety, and substance-use disorders. Pain-associated disability is also more common in those from lower socioeconomic strata and in those who dislike their work or feel underpaid and unsupported at work. Risk is higher in certain vocations (e.g., truck driving), in survivors of overwhelming trauma (e.g., childhood abuse, natural disasters, combat), and in those genetically sensitive to noxious stimulation. Conditions commonly associated with CNMP include spine disease, headache disorders, fibromyalgia, neuropathies, and arthritis.
Some of the mystery surrounding chronic pain derives from concepts of nociceptive pain, which imply a strong relation between peripheral stimulation and pain perception. Pain is seen as an analogue representation of some event. Because of reliance on this acute pain model, when a patient complains of severe pain and no appropriate pathology is located, it is suspected that the complaints are not valid or that the workup missed something. In fact, excellent health does not preclude severe pain.
Pain is more a creation of the nervous system than a gauge of nociceptor activation.2, 3 Nociceptive afferent signals are subject to marked attenuation and amplification by descending tracts that have their action at the dorsal horn. Further, the presence of prolonged nociceptive stimulation, inflammation, or nerve injury can lead to sensitization of pain transmission fibers, death of inhibitory cells, loss of tonic inhibition, and structural neuroplastic changes. Activation of immune cells, including glia, previously believed to have only structural roles, produces exaggerated, widespread, and mirror image pains.
Pain facilitatory cells in the medulla fire in response to cortical processes, such as vigilance. In animals, simply anticipating a pain and expecting it to be important are sufficient to activate “on” cells, that initiate amplifiers before the pain stimulus has begun. Opioid withdrawal also activates these cells, explaining the associated muscle and bone pain.
Genetic factors modify pain perception and response to endogenous and exogenous opioids. Several single-nucleotide polymorphisms produce greater or lesser pain sensitivity. Imaging shows that persons reporting high or low pain in response to a standard stimulus demonstrate correspondingly high or low activation of the somatosensory cortex, anterior cingulate gyrus (a likely index of affective components of pain), and frontal cortex. The conclusion is that those who report unusual pain actually experience it, absent incentives for misrepresentation.
Patients with idiopathic chronic back pain, whiplash, and fibromyalgia, conditions often believed to be exaggerated or psychogenic, show evidence of central sensitization, again suggesting that their pain is genuine but not due to peripheral structural pathology.
Sensitization also leads to visceral hyperalgesia, which accounts for much obscure abdominal, pelvic, and chest pain. Interestingly, visceral hyperalgesia is easier to elicit in rats made anxious by genetic selection or by early maternal separation. These pain syndromes often respond to agents used for neuropathic pain, such as tricyclics or pregabalin.
Although psychological factors are rarely believed to cause pain, they dramatically modulate associated suffering and dysfunction. It has long been known that vigilance, expectation of pain, and reinforcement of pain behavior increase pain behavior, and it has now been demonstrated that these factors increase cortical activation associated with experimental pains. Conversely, distraction reduces pain.
Functional impairment that greatly exceeds pathology is not necessarily psychogenic (Box 1). Patients commonly interpret pain as a sign of fragility, leading to unwarranted self-protection and inactivity. The resulting deconditioning causes minor activities to become painful, creating a cycle of escalating pain and disability.
|Box 1 Toxic Cognitions in Pain|
Maladaptive cognitions play a central role in pain disorders. They tend to be automatic and thus not examined for validity, include such catastrophic interpretations as “the nerves are being crushed” or “these exercises must be tearing something loose,” which increase pain and disability.
Personal beliefs in self efficacy versus powerlessness are critical determinants of success in coping with chronic pain. Those who perceive events as a consequence of their own behavior tend to have better mood and function, whereas those who perceive events as due to other people or fate have more depression, anxiety, and dysfunction. The concept of learned helplessness also explains much impairment. A person who perceives himself or herself to be helpless is likely to stop trying entirely, leading to increased disability, depression, and ultimately pain.
Operant conditioning refers to the process by which forms of behavior increase when reinforced and extinguish when not reinforced. Plainly, animal life is contingent on a predisposition to selectively repeat behavior that leads to positive results. Reinforcement influences the extent of pain behavior and sick-role behavior. Although the sick role leads to multiple losses, including income, socialization, sexual function, and self esteem, it also can lead to care from others, a secure income, narcotics, and escape from a noxious work environment. Operant conditioning might explain the generally worse function and therapeutic outcomes seen in patients who are receiving pain-related disability income.
Reinforcers are time dependent, such that immediate weak reinforcers can overcome delayed stronger ones. This explains much maladaptive pain behavior: Actions that initially provided benefit persist after they have become liabilities. Neuroimaging suggests that reinforcing pain behavior can increase its actual perception.
Although prevalence of comorbidity (Box 2) varies with population, the most common psychiatric disorders in chronic pain are depression, anxiety disorders, substance-use disorders, and somatoform disorders.4 Conditions such as schizophrenia and mania are relatively uncommon.
|Box 2 Psychiatric Disorders Commonly Associated with Chronic Nonmalignant Pain|
Most patients disabled with chronic pain have substantial anxiety, and nearly 30% meet criteria for generalized anxiety disorder. Posttraumatic stress disorder and panic are also common. Anxiety sensitivity characterizes people who misinterpret the normal physiologic changes of anxiety as harbingers of medical catastrophe, such as a stroke. It is associated with chronic pain and with increased response to experimental pain.
The prevalence of depression in pain clinic patients is 30% to 84%. Mood strongly modulates pain, and simply reading sad stories or humorous ones alters pain threshold and tolerance, as does mood induction via hypnosis. In prospective studies, pain predicts the onset of depression, and depression predicts the onset of chronic pain, and they do so to approximately the same degree.
Identifying prescription drug addiction can be challenging, yet critical, because satisfactory management of chronic pain is unlikely in the addict (Box 3). Many hallmarks of addiction to recreational substances (driving citations, cirrhosis, work absenteeism, illegal behavior) are likely to be absent or attributed to pain. Official nomenclature relies heavily on the criteria of tolerance and physical dependence for diagnosing addiction. Although often appropriate for recreational substances, these criteria are not useful for prescribed analgesics. Structured interviews in a rehabilitation hospital identified 23% with active misuse or dependence and 9.4% in remission.
|Box 3 The 3 Cs of Addiction|
|Loss of Control|
|Craving or preoccupation|
|Use despite Consequences|
In pain disorder—classified as a somatoform disorder in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM IV-TR)—psychological factors are “judged to have important roles in the onset, severity, exacerbation, or maintenance of pain.”5 Other conditions involving physical symptoms or preoccupation with them that cannot be explained medically include somatization disorder, conversion disorder, and hypochondriasis. There is compelling evidence that major traumatic events, including childhood abuse, combat trauma, and natural disasters, often lead to a plethora of physical complaints, including pain, without identifiable medical pathology. Such traumas likely also augment the symptoms of pain that have a medical basis; this, however, is more difficult to establish.
Most studies of personality in CNMP lack pre-pain personality assessment data, and pain changes personality. Those trapped in the sick role often demonstrate inordinate regression and dependence not previously present. Nevertheless, personality disorder impedes coping with the stress of CNMP, thus leading to inordinate dysfunction. Additionally, traumas that damage personality also often lead to functional physical symptoms.
CNMP is not only a perception. CNMP is often associated with impairment in function that encompasses nearly all activities (Box 4). Patients not uncommonly spend upward of 20 hours per day reclining. Such a person reporting a back pain level of 7 of 10 is a far different clinical challenge than is a person whose pain is 7 of 10 but who maintains employment, socialization, and self care.
|Box 4 Signs and Symptoms in Chronic Nonmalignant Pain|
Sleep disruption is the rule in CNMP patients and is generally attributed to pain. However, counterintuitively, animal and human studies confirm that insomnia is more likely to exacerbate pain than pain is likely to exacerbate insomnia. Consequently, sleep disorder should be addressed specifically, with the expectation that its improvement can reduce pain.
Pain should be quantified (0 = no pain, 10 = the worst pain you can imagine) and characterized as to quality, timing, and relieving and exacerbating factors; however, this is not sufficient to characterize the symptoms. Function must also be assessed, along with emotional status and sleep.
These factors are most economically assessed and monitored over time by a simple self-report scale such as the Pain Disability Index or a similar scale of the clinician’s own devising (Fig. 1).
Diagnostic signs and symptoms of the conditions that underlie CNMP are addressed in their respective chapters. The Institute for Clinical Systems Improvement has prepared guidelines for CNMP assessment and management,6 a summary of which is available online.7
Several characteristics of the diagnostic workup in CNMP are noteworthy. First, it is to be expected that complaints often outweigh physical (and imaging) findings. Laboratory studies are often completely normal. This is because much of the discomfort of CNMP is due to neural sensitization and not peripheral pathology. Thus, after several episodes of pancreatitis, it is common to have persistent pain without laboratory abnormalities. Those with sickle cell disease develop pain between crises. Sciatica persists after diskectomy. Joints hurt when synovitis has resolved and acute-phase reactants have normalized.
Psychogenic pain is often suspected on the basis of nonphysiologic findings, such as Waddell’s signs in back pain (Box 5); however, these can be present even when unambiguous pathology explains the complaints. Inconsistencies are of much greater diagnostic import. Symptoms and signs can be inconsistent with anatomy (a patient presses with the “paralyzed” leg but not with the normal one). They can vary over time or with audience (a patient’s limp is much worse in the presence of a spouse).
Somatization is also suggested by preoccupation with somatic or medical issues. Patients with chronic medical problems typically report their symptoms, after which they are easy to distract. The person who cannot be diverted from symptoms, tests, and treatments is likely to be somatizing.
|Box 5 Waddell’s Signs of Nonphysiologic Pain|
|Pain on simulated rotation|
|Distracted straight leg raise|
|Regional sensory change|
Functional impairment should be congruent with pathology. For example, the antalgic gait of a back patient might or might not be appropriate to the pain experienced, because this is unknowable; however, the same patient has no medical reason for the questionnaire to be in the spouse’s handwriting or for the spouse to answer questions regarding the quality of pain or for the spouse to telephone in for prescription refills. These actions suggest inordinate regression, which is a psychological process. Such findings do not rule out organic disease; a person whose limp is dramatically worse in the presence of a spouse might still have a radiculopathy.
In the absence of objective pathology, the organic nature of symptoms is suggested when they are generally congruent with recognized syndromes (postcholecystectomy pain, migraine, fibromyalgia). The more atypical the symptoms, the more likely are psychogenic components.
Lack of consistency in psychological signs can suggest exaggeration, such as a patient whose screening questionnaire suggests severe depression yet is seen animated and laughing with peers in the cafeteria.
Patients with CNMP must be screened for psychiatric illness. Self-administered questionnaires (such as Beck’s depression inventory) or a clinical psychiatric interview to elicit symptoms of depression, anxiety, and other psychiatric illness may be used. Suicidal ideation, plan, and intent must be elicited, because risk is elevated in CNMP.
Many patients with depression and anxiety present to their primary care physicians with physical rather than psychological complaints.
The physician, having made a diagnosis, has a difficult task in explaining the condition to the CNMP patient and needs to convey five important messages whose goals are to create hope and clarify the patient’s expectations (Box 6).
|Box 6 Five-Point Message to the Patient With Chronic Nonmalignant Pain|
Because CNMP is rarely curable, much of its successful management is contingent on the behavior of the patient who suffers from it.
Perhaps the most important coping strategy for CNMP is to maintain fitness. This improves many causes of chronic pain (e.g., lumbago, fibromyalgia, migraine), reduces anxiety and depression, and helps protect the patient from losing access to formerly pleasurable activities. Patients require education as to what is safe, and as to what is harmful versus painful.
Obesity is a risk factor for CNMP and patients with CNMP often gain weight, which worsens many musculoskeletal pains and impedes rehabilitation. Weight loss programs and Overeaters Anonymous should be recommended, but results are often disappointing. Bariatric surgery may be an option.
Smoking is associated with CNMP and impedes rehabilitation. Various nicotine replacement products as well as nicotine receptor agonist therapy are helpful in ending tobacco use, but this often requires education and brief counseling as well.
A useful sound bite for CNMP patients is, “If your life is empty, pain will fill it up.” Distraction reduces pain perception, and even when it does not, a pain of 6 while attending an exciting event is more tolerable than a pain of 6 alone while bored at home. It is appropriate with acute pain and illness to put life on hold while awaiting recovery. This strategy can be devastating in CNMP, so it is critical that patients maintain recreation, hobbies, and social involvement.
Regular practice of such activities as yoga, progressive muscular relaxation, meditation, and even self-hypnosis can reduce pain, stress, and tension, while giving the patient a sense of being back in control.
Medications are a mainstay of pain treatment. They are divided into the true analgesics, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids, and those referred to as adjuvants or antihyperalgesics, such as antidepressants and antiepileptic drugs (Box 7).8 The adjuvants are generally ineffective for acute pain. Generally, opioids and NSAIDs are used in nociceptive pain and antiepileptics and antidepressants are more useful in the treatment of neuropathic pain and hyperalgesic states, although opioids can play a role in these as well.
|Box 7 Categories of Analgesics|
|Calcium channel blockers|
|Calcium channel α2δ1 subunit modulators|
|Lidocaine 5% patch|
|NMDA receptor antagonists|
GABA, gamma-aminobutyric acid; NMDA, N-methyl-d-aspartate; NSAIDs, nonsteroidal anti-inflammatory drugs; SNRIs, serotonin-noradrenergic reuptake inhibitors; TCAs, tricyclic antidepressants.
NSAIDs are useful for mild to moderate pain, especially bone and dental pain. They have opioid-sparing effects. Advantages of NSAIDs include absence of tolerance and psychic dependence. They are relatively safe in short-term use and are therefore often chosen as first-line drugs. Prolonged and high-dose use is more hazardous. Gastrointestinal (GI) complications of NSAIDs are the most prevalent category of adverse drug reactions and approximately 16,500 deaths result from ulcer-related complications in the United States each year.
Opioids are appropriate for moderate to severe pain that is unresponsive to nonopioids alone. They are the gold standard for analgesia, and nothing short of conduction block is more effective. They reduce nociceptive and neuropathic pain, although the dose-response curve is shifted to the right in the latter. Opioids are the primary treatment for acute and cancer pain, including recurrent acute pains in sickle cell disease and recurrent pancreatitis.
The appropriateness of opioids for CNMP has been disputed, and its role seemed to evolve from forbidden in the 1970s to mandatory in the 2000s. Currently, opinion is becoming more conservative. Historically it was believed that opioid analgesia for CNMP would diminish due to tolerance, leading to a cycle of ever-increasing doses without sustained relief and with ever-increasing risks of toxicity and addiction. These beliefs were based more on theory than on evidence.
In the late 1980s, the tide began to turn. In a seminal article, Melzack9 held that people suffer not because their discomfort is untreatable but because physicians are reluctant to prescribe morphine. Afraid of turning patients into addicts, physicians deliver amounts that are too small and too infrequent. When patients take morphine for pain, however, addiction is rare. Addiction seems to arise only in those who take it for psychological effects, such as to experience euphoria or to relieve tension. Patients who take morphine for pain do not develop the rapid tolerance that is often a sign of addiction.
Subsequently, controlled studies have compellingly demonstrated the efficacy of opioids in most noncancer chronic pain; however, these studies are almost all short term. Longer-term studies show high drop-out rates and modest (around 30%) pain reduction.10 Cross-sectional studies demonstrate that patients chronically taking opioids have more pain and less function than those not so treated, but they do not permit conclusions about cause.
Research has helped clarify the question of iatrogenic addiction, and a short term (6 months) trial appears to be very low risk. The risk is higher for inducing relapse of a prior addictive disorder, which is equally disastrous, but essentially unstudied. The key to a trial of chronic opioid analgesia is meticulous monitoring and documentation of drug response and behavior. Passik and Weinreb11 have proposed four As to identify successful chronic opioid analgesia (Box 8).
|Box 8 The 4 As of Chronic Opioid Analgesia|
When patients are doing well according to these criteria (perhaps with the addition of “affect”), it is likely that opioids are an asset to them. Physicians and patients are at risk when opioids are continued beyond the time of a failed trial. Patients doing poorly on chronic opioids often have improved pain and function when opioids are eliminated.
Many opioid formulations and routes of administration are available. Oral administration is generally as effective as parenteral and is much cheaper. Most opioids are absorbed transmucosally and can be used sublingually, rectally, or vaginally when there are impediments to swallowing or impaired GI absorption. Intrathecal administration might permit more analgesia with some reductions in GI and central nervous system (CNS) side effects; however, after several years, there is likely to be marked dose escalation, diminution of analgesia, and minimal functional improvement, all at considerable cost and risk.
It is generally held, although not conclusively shown, that chronic pain is best treated with agents that maintain a relatively constant blood level, avoiding the peaks and troughs of short-acting agents. Some molecules are intrinsically longer acting (buprenorphine, methadone, levorphanol), and others are made so through transdermal or sustained-release preparations.
The Veterans Health Administration has prepared guidelines for opioid therapy of CNMP.12
Antiepileptic drugs (Table 1) are especially useful in neuropathic pain, migraine, and chronic hyperalgesic states. They reduce pain by a number of mechanisms, but the modulators of the α2δ1 subunit of the calcium channel have the greatest use, fewest drug interactions, and lowest toxicity.
|Drug||FDA Approved||Evidence for Efficacy (RCTs)|
|Neuropathic Cancer Pain|
|Spinal Cord Injury|
|Lamotrigine (incomplete injury)||×|
|Lamotrigine (add-on refractory)||×|
FDA, United States Food and Drug Administration; RCTs, randomized, controlled trials.
Antiepileptics are approved for a number of conditions, and randomized controlled trials demonstrate efficacy in several others. They are therefore widely used off-label.
Antidepressants have shown efficacy in a number of types of chronic pain (Box 9). The analgesic and antidepressant actions are independent of each other. Efficacy is primarily shown with agents that inhibit the uptake of serotonin and norepinephrine in the CNS, which potentiates descending spinal inhibitory pathways. Studies typically find little or no analgesic effect of selective serotonin reuptake inhibitors except for (generally weak) benefit from those with some norepinephrine reuptake inhibition as well.13
|Box 9 Antidepressant-Responsive Pains|
|Central post-stroke pain|
|Chronic regional pain syndrome|
|Irritable bowel syndrome|
|Low back pain|
|Temporomandibular joint syndrome|
Numerous randomized controlled trials have shown effectiveness in fibromyalgia, functional GI disorders, and headache. Studies in spine pain have largely failed to exclude subjects with depression or sciatica; however, there is some evidence of efficacy of several tricyclics and maprotiline.
Tricyclics have been the most used antidepressants in pain; however, none is approved for such use. The serotonin-norepinephrine reuptake inhibitors (SNRIs), duloxetine and venlafaxine, are efficacious in some conditions and duloxetine has received FDA approval for treatment of pain of diabetic peripheral neuropathy.
Local anesthetics applied topically lack systemic effects. Lidocaine 5% patch is indicated for pain from post-herpetic neuralgia and is effective for carpal tunnel syndrome. Open studies suggest possible usefulness in low back pain.
Capsaicin treats pain of post-herpetic neuralgia. It causes persistent activation of the vanilloid receptor, TRPV1, permitting high levels of calcium to enter nociceptors, thereby impairing their function. It is typically not well tolerated, because it produces a burning sensation on initial application that can be painful to regions that are already hyperalgesic. If hand washing is incomplete, capsaicin can later produce considerable pain on contact with mucous membranes and eyes and with other people.
Counterirritants stimulate dermal receptors to produce feelings of heat or cold. They commonly contain such substances as menthol, eucalyptus oil, or salicylates.
A number of other agents have been used topically, including NSAIDs and tricyclic antidepressants. Benefit is generally modest and not well demonstrated.
Because psychiatric comorbidity is common in CNMP, many patients receive combinations of psychotropics and analgesics or antihyperalgesics, leading to problems of cost, compliance, drug interactions, and toxicity. Choosing drugs with both psychotropic and analgesic effects helps maximize therapeutic impact and minimize drug burden. For example, several analgesic antiepileptic drugs are also anxiolytic. Evidence supports the use of pregabalin for social phobia and generalized anxiety disorder, gabapentin for social phobia, lamotrigine for posttraumatic stress disorder, and valproic acid for panic disorder.14 Sedative effects of these drugs can also be used to advantage.
Similarly, tricyclic antidepressants and SNRIs help not only chronic pain and mood but also anxiety. Several have anxiolytic effects comparable with those of diazepam and are effective for sleep.
The profound impact of psychological variables on CNMP requires that these issues be considered in its treatment.15
Because misunderstandings and uncertainty exacerbate pain and functional impairment, it is essential to educate patients about their pain, underlying medical conditions, appropriate management strategies, and the critical role of their own actions for pain moderation and successful rehabilitation.
Biofeedback training is based on the fact that control of normally involuntary physiologic functions can be learned if the person (or animal) receives feedback. For example, thermistors provide feedback as to whether a body part (e.g., a finger) is warming or cooling. Most patients rapidly learn to regulate skin temperature, sweating, and superficial muscle tension. Biofeedback is effective in migraine, musculoskeletal pain, and GI pain. It is often combined with such techniques as autogenic training, hypnosis, transcendental meditation, yoga, progressive muscular relaxation, and guided imagery. These have been shown to be beneficial, but there are few studies demonstrating the superiority of any one. They all teach patients to control body responses that they had considered beyond their control, reduce anxiety without the need for drugs, and improve their ability to discriminate the effects of stress on physical function.
Rehabilitation is facilitated when others consistently reinforce wellness behavior, such as physical activity and healthy interactions with others, and avoid reinforcing pain behavior and sick role activities. Yet experience with acute illness leads us to attend to CNMP patients when they seem ill and perhaps to leave them alone when they’re doing better. Families who learn to reverse these contingencies can help move the patient toward an improved quality of life.
Both individual and family therapy may be needed to resolve issues that increase pain, stress, or disability. The best-studied therapies in CNMP pain are cognitive-behavioral therapies, which typically focus on monitoring and correcting automatic negative thoughts, internalization of locus of control, elimination of catastrophizing, and acceptance of pain as an unfortunate problem that needn’t control one’s life. Numerous studies confirm that cognitive-behavioral therapies improve function and decrease pain in CNMP.
|Box 10 Pain Interventions|
|Diagnostic nerve blocks|
|Intraspinal drug delivery|
Diagnostic blocks may help identify a myofascial or visceral pain component, indicate sympathetically mediated pain, or locate a central pain generator, thereby guiding treatment.
Therapeutic blocks may be temporary or permanent. Permanent is a relative term, because reinnervation occurs after a variable period of time. Even temporary blocks can have a lasting effect because they can facilitate resolution, for example, of radiculitis, or make it easier for patients to engage in rehabilitation exercises they could not otherwise tolerate.
Neuroaugmentation (or neuromodulation) refers to techniques based on stimulation of neural tissues. Spinal cord stimulation involves placement of an electrode, energized by a (usually) implanted programmable generator, against the posterior spinal cord. The most important indications are neuropathic pains. Peripheral nerve stimulators are also used for neuropathic pain and have been efficacious in complex regional pain syndrome. The role of motor cortex stimulation for chronic pain remains to be determined.
Surgical pain management is generally reserved for patients who have failed less aggressive treatments.
Physical therapies play an essential role in the rehabilitation of those with pain-related functional impairment. General reconditioning, focused on endurance, strength, and flexibility, can produce profound effects for a variety of reasons. A significant component of chronic pain is often the deconditioning that results from prolonged inactivity. This leads to weak, shortened muscles that are painful in response to trivial activities. Reconditioning reverses this. Physical reconditioning also markedly reduces patients’ sense of helplessness, their ideas that relief can only come from an expert, and their sense of fragility.
A variety of active and passive exercises are useful for specific conditions, such as mechanical low back pain (e.g., McKenzie exercises, Williams exercises), cervicogenic headache, shoulder impingement, piriformis pain, and others.
Massage or myofascial release may be useful for those with muscle pains and trigger points. Identification and treatment of pelvic floor myofascial pains can often produce major benefit for patients with obscure pelvic pain syndromes.
Interdisciplinary pain rehabilitation programs (IPRPs) provide an approach to management and rehabilitation of CNMP in which professionals with disparate training collaborate to treat patients.17 Treatment is typically intensive, for as little as 9 hours a week to as long as all day, 5 days a week, for a month or more.
The approach addresses multiple contributors and consequences of pain. Programs typically serve those unresponsive to multiple unimodal therapies, although early treatment is more effective than delayed treatment.
Programs differ in several particulars, but they share the perspectives that when chronic pain does not involve correctable pathology, an endless quest for such is deleterious, and because most chronic pain can be decreased but not eliminated, treatment must be directed toward producing the best possible quality of life despite some persistent pain. Program goals include physical rehabilitation, psychological rehabilitation, and symptom reduction. A number of services are combined to produce these outcomes (Box 11).
|Box 11 Interdisciplinary Pain Rehabilitation Program Components|
|Medications (pain, mood, sleep, anxiety)|
|Biofeedback, relaxation training|
|Chemical dependence treatment|
|Transcutaneous electrical nerve stimulation (TENS)|
|Detoxification or weaning|
|Treatment of psychiatric comorbidity|
Studies of IPRP outcomes generally demonstrate improvements in pain, mood, and function. Many patients return to work and decrease their use of health care. Benefits are stable over time. Deconditioning markedly improves, and there are dramatic increases in activity levels, with a substantial decrease in opioid use. From a financial perspective, reductions in surgeries and other use of health care and reduction of disability income demonstrate that IPRP treatment, albeit expensive, is a good investment.
Sanders and colleagues have prepared guidelines for interdisciplinary CNMP rehabilitation.18
Pain treatment is not evenly distributed in our society. Studies demonstrate that African Americans and Latin Americans are less likely to receive adequate analgesia (e.g., opioids following femoral fracture) than are persons of European descent. The elderly are also at special risk for undertreatment of pain, and those in nursing homes may be sedated when they actually need analgesia. Infants have been believed not to experience pain as do adults, leading to such practices as circumcision without analgesia. Fortunately, these latter misunderstandings have been largely corrected.
A search of the National Guideline Clearinghouse19 revealed 871 guidelines dealing with pain, of which 485 address chronic pain. Some are disease centric (low back pain, sickle cell disease, pelvic pain, osteoarthritis), others drug centric (opioids, NSAIDs), others intervention centric (facet denervation, discography, epidural steroid injections), and others population centric (geriatric, the cognitively impaired).