Chapter 5. Understanding the Patient with Chronic Pain

“It is not suffering that diminishes man, but suffering without meaning.”

Victor Frankl

Asked to describe their pain, especially chronic pain, patients often appear perplexed, stating, “I don’t know. It just hurts.” Pain is a subject of deceptive complexity. It means different things to different people. Algology is the study of pain, and this chapter discusses a number of important points relevant to its clinical application, pain medicine.

Before we focus on the patient with chronic pain and a general approach to pain management, basic nosology and terminology need clarification.

There are a number of ways to classify pain. Some pain specialists separate it into malignant (cancer) and nonmalignant pain. Others divide it into acute, recurrent acute, and chronic pain. Acute pain is short-lived and follows injury or near injury to tissue. Recurrent acute pain is similar in duration but tends to recur. It need not involve injury. Examples are migraine headache and sickle cell vasoocclusive episodes. Depending on the injury, chronic pain is variably defined as that persisting 1 to 6 months after the tissue has healed. One example of chronic pain is postherpetic neuralgia.

Pain can also be classified in terms of mechanism. Nociceptive pain denotes pain arising from tissue injury, and the degree of pain is usually somewhat proportional to the degree of injury. Nociceptive pain itself may be subcategorized into visceral pain, a dull, crampy, and poorly localizable discomfort—as might be experienced in gastroenteritis—or somatic pain, a sharper and more localizable sensation of the body wall, as might be felt after a laceration. Each type of pain may be mild or intense.

Neuropathic pain is not nociceptive, and the degree of pain is not proportional to the degree of injury; it is caused by disordered sensory processing of the nervous system and is a pathologic persistence of a normal sensitizing mechanism that can be useful in the setting of acute pain. Neuropathic pain can be subcategorized into central neuropathic pain, which can originate at any level of the central nervous system, and peripheral neuropathic pain, which is generated at the level of a nerve or nerve root. The most famous example of central pain is poststroke thalamic pain; common examples of peripheral neuropathic pain are neuromas, diabetic neuropathy, and complex regional pain syndrome, types 1 and 2 (previously known as reflex sympathetic dystrophy and causalgia). As with central pain, a number of different mechanisms may be involved. Even when the damage occurs in the periphery, such as injury to a nerve, the constant bombardment of sensory neurons in the spinal cord with pain signals from the periphery renders the neurons hypersensitive to all input, even to non-noxious stimuli. Neurons then almost continuously “fire up” the pain pathway. Although this is a normal sequence of events in acute injury (i.e., sensitizing injured areas so that they may be protected from further harm), when it fails to abate with healing, it becomes pathologic. This process is called central sensitization of pain and is related to the concept of windup.

Other relevant terminology includes:

• Hyperpathia, an elevated sensory threshold above which is generated an abnormally intense and prolonged response to pain
• Hyperalgesia, which is secondary to a lowered threshold to pain
• Allodynia, a painful response to a nonpainful stimulus
• Hyperesthesia, caused by a lowered threshold to any stimuli
• Hypoesthesia, the opposite of hyperesthesia
• Analgesia, without pain
• Anesthesia, without sensation

Incident pain is generated by mechanical factors characteristic of movement and position. Incident pain commonly occurs in cancer patients in whom, for example, metastatic spread of the cancer involves the skeleton. Such pain may be neuropathic or nociceptive, depending on the structures involved. For example, a pathologic or metastatic rib fracture results in nociceptive bone pain and neuropathic pain in the distribution of the rib’s intercostal nerve.

Infants and Children

Patients within certain age groups are often subjected to unnecessary pain and suffering, which may have long-term consequences. Children are still relatively undermedicated compared with adults, and although the situation is improving, there continues to be room for improvement. Surgeons were operating on infants who were only partially anesthetized as late as the early 1980s.

Misconceptions about pain and the consequences of its treatment continue to impede patient care. For example, nurses concerned about the risk of addiction may read a physician’s “prn” order to mean “as little as possible” rather than “as needed.” Or they may rely too much on changes in vital signs, such as quickened heart rate or increased blood pressure, to decide if a child’s complaint of pain is “real” or not and may thus withhold “prn” medications inappropriately. We are aware of no evidence that appropriate opioid use in pediatric pain management leads to addiction in childhood or adulthood. And we now know that there is great variability in individual pain thresholds and ability to cope with pain, so that vital signs may not correlate as well with the level of pain as previously thought. In infants and children, fluctuating levels in vital signs may be a better indicator of pain than absolute levels. It is, therefore, wise to combine several methods of pain evaluation, no matter what the patient’s age. Verbal or visual analog pain scores (from 0 to 10), a developmentally sensitive analysis of general behavior and body language, and facial expression can provide valuable information for the assessment of pain.

Some practitioners believe that infants feel little pain because their nervous systems are immature. The anatomic, biochemical, and physiologic apparatus necessary for the perception of pain is present 2 to 3 months before term, but because the descending inhibitory modulating system is immature, and because of a higher than adult level of cutaneous pain receptor density, infants may, in fact, be hyperalgesic. They may have a lower average threshold to pain than adults. The main consequence of immature central and peripheral myelination is poorly coordinated nocifensive (defensive) behavior, which is reflexive but modified by experience. Newborns quickly learn to squirm and kick during a heelstick blood draw. Facial grimacing and fluctuating vital signs belie their experience of pain. There is even growing evidence that infants subjected to long and painful treatments without pain management in intensive care units are more likely to develop problems of somatization in school compared with those given intermittent or constant infusions of carefully adjusted opioid medications.1

Elderly Patients

Geriatric patients also suffer from caregivers who have been misinformed about pain management. Although those aged 70 or older may in general be more susceptible to medication side effects, it does not mean that they should be left untreated for pain.

Careful dose adjustment is key to good pain management, as is awareness of the various delivery systems that might minimize systemic side effects. Patients who experience intolerable side effects from high-dose oral narcotics for persistent malignant or nonmalignant pain may benefit from the implantation of an intrathecal opioid pump, through which relatively tiny amounts of medication are placed directly into the cerebrospinal fluid. It then enters the spinal cord and brain quickly and efficiently, minimizing spread to other systems. Similarly, a well-placed epidural catheter may provide better short-term postoperative analgesia with fewer side effects than intermittent nurse-given intravenous narcotics or boluses delivered by a patient-controlled analgesia (PCA) device. And even when dementia is of concern, one needs simply to titrate more carefully and to employ adjuvant medications and techniques that might prove opioid sparing. However, it must be remembered that in this group of patients, even normally well-tolerated medications may have adverse effects on mentation as well as on the gastrointestinal and cardiovascular systems.

It is a little appreciated but important concept that chronic pain is not merely a protracted form of acute pain, and it is often preventable. Chronic pain is not a symptom; it is a disease and should be treated as such. There is now a general consensus that an interdisciplinary or multidisciplinary approach to pain management is most effective. But prevention is still the key to avoiding the consequences of chronic pain. In addition to the effect that chronic pain has on the sufferer and his or her immediate family, it affects the greater community. The financial burden to society from lost productivity resulting from recurrent acute and chronic pain is staggering. Estimates range from $50 billion to $100 billion yearly for headache and low back pain alone. But the problem is wider and more serious than that. Failure to alleviate unnecessary suffering creates distrust between clinicians and patients, and this, in turn, diminishes the efficacy of our medical system. If patients feel forced to seek alternative and more caring treatments, they may fail to seek appropriate care for other serious conditions when it is needed. More people than ever before are seeking alternatives to allopathic medicine, but not necessarily always to their advantage. Missing the opportunity for early cancer detection, for example, may have tragic consequences.

The public’s trust must be regained. What causes this distrust? On both sides, much of it results from a feeling of lack of control. Patients become anxious and distraught as their pain persists and become frustrated with the inability of medical professionals to alleviate it. Clinicians become frustrated with their own lack of understanding of pain and their inability to control it. Sometimes these feelings of frustration and inadequacy are turned against the patient in the form of “there is nothing more that can be done” or “obviously something else is going on, so I’m sending you to a psychiatrist.” At such times, it may be more appropriate (and less destructive for the patient) to state that “there is little more that I am able to do,” or preferably, “your situation is quite complex and involves suffering beyond that of the physical pain alone, so we need to have it assessed more fully to formulate a better plan for pain management.” This last comment, of course, needs expansion and explanation because a common interpretation of this is that “the doctor thinks it is all in my head.” Trust takes considerable effort and risk on both sides. It requires empathy: the adage “to hear about pain is to have doubt, but to experience it is to have certainty” is true.

There are certain concepts that need emphasis to answer this question. The first of these is that pain and suffering are not synonymous. Although pain has been described as an unpleasant sensory and emotional experience arising from actual or potential damage to tissue, only when the consequences of pain—usually prolonged—begin to interfere negatively with the physical and emotional experience of life is suffering said to occur. In this way, pain may be likened to stress. A little pain is not necessarily a terrible thing. It may serve to focus attention on a stimulus and foster an appropriate reaction to it, but too much pain may prove overwhelming, exhausting, and demoralizing. It may lead to depression, which may intensify the experience. And depression is not benign. With little warning, it may lead to suicide. Saying that “there is nothing more that can be done” may take away the only hope that keeps the patient going.

Continuing the analogy to stress, pain is difficult to study. It is not easily monitored or objectively assessed, nor are its effects predictable from one individual to another. Indeed, pain thresholds may vary, not only between people, but also within the individual person over time according to mood, previous experience, and expectations. This complexity, fortunately, provides multiple levels or points at which pain management may prove successful. Appropriate interventions may be pharmacologic, invasive (i.e., surgery or nerve block), behavioral, or a combination of all three.

What, then, is the difference between pain and suffering? To answer this question, it must be understood that pain may affect a person’s life in different ways according to their general state of well-being. Someone who is tired, hungry, anxious, or depressed reacts to an unpleasant sensation differently from someone who is well rested, in excellent shape, and in high spirits. When pain persists and overwhelms a person’s coping mechanisms, it is likely to be seen as insurmountable and may take on a life of its own. Eventually, the tail wags the dog, as the saying goes. With this loss of control and autonomy and a growing feeling of helplessness, the person begins to experience a downward spiraling of emotional and physical well-being, in which severe deconditioning threatens normal functioning at home, work, and play. The consequence is a state of suffering of which only a portion is physical pain. This is why pain management clinicians do not advocate simply prescribing the strongest medication possible when the patient states, “if you just give me something to kill the pain, I will go back to work and everything will be OK.” If only it were so simple! The wise practitioner tries to convince the patient that going back to work first—in graded increments—may offer a useful distraction from the pain and explains why a concurrent and multifaceted approach to pain management is needed. Although no single physician is capable of all aspects of care, in a multidisciplinary setting, there needs to be one clinician in overall charge of each patient’s regimen to avoid processing patients “by committee.”

Clinical Example: The Downward Spiral That Turns Pain into Suffering

To illustrate how a fairly minor event may lead to catastrophic results if early warning signs of chronic pain are not recognized and responded to appropriately, one may use the common scenario of a 50-year-old citizen sitting in a stationary car, hit from behind. There is no apparent injury at the time. Over the next few days, the patient experiences tightening up of muscles and low back pain, described as “spasms.” These get worse over time. The patient is reassured by the family’s practitioner that it is only a muscular problem. Although the patient is willing to accept this for a while, a friend suggests initiating a lawsuit just in case something is more seriously wrong. This philosophy is reinforced by an attorney who states that he has seen many patients settle a case too early only to find out later that they have a lifelong disability for which they have no financial coverage.

The driver now sues and becomes hypervigilant about symptoms, becoming anxious every time pain is felt. The family physician reasserts that there is no neurologic dysfunction and states that x-ray studies fail to show any skeletal injury. The patient disagrees. The pain is prolonged and is seemingly becoming intensified. He or she seeks a second opinion and, not satisfied with it, seeks a third, fourth, and so on until somebody is found who echoes his or her concerns and who is willing to order a magnetic resonance imaging (MRI) scan. MRI then reveals degenerative changes not apparent on x-ray films, but probably consistent with age, such as “bulging discs” that do not clearly impinge a nerve root or the spinal cord but nonetheless are read correctly as just “touching” a nerve root. The consulting surgeon, wanting to help the patient, offers to operate and see if he or she can remove the tissue that “might” be touching a nerve and setting off the pain. The patient agrees, giving consent, but doesn’t hear the qualification “might.”

As often happens, the surgery does not ameliorate the pain, and within a few months, a new pain begins. Subsequent MRI reveals evidence of scarring about the nerve root, one of the possible complications of invasive surgery. As the scar contracts, it pulls and irritates the nerve root, causing radicular pain in the dermatomal distribution of the corresponding peripheral nerve. The patient becomes frustrated, despondent, and depressed. The family physician then prescribes antidepressants for pain, but they seem to negatively affect the patient’s ability to think clearly at work. The patient now no longer trusts the family physician’s judgment (or prescriptions) and begins to take multiple over-the-counter drugs or uses “alternative” therapy that may be expensive and of dubious value. The pain persists.

Eventually, the family physician is forced to prescribe a mild narcotic for ongoing and worsening pain. This is taken over the next few months, with escalating dose requirements because the patient has developed tolerance to the drug, leading to stronger medications, a pattern to which the clinician responds with concern, stating that he or she is not going to prescribe these medicines any more “because you are becoming addicted to them.” They argue, and the patient is forced to seek care elsewhere. By now, having missed work so often and failing as well in personal relationships, the patient is fired at work and unhappy at home. The patient becomes more depressed and cannot sleep well, escalating the pain.

Having been physically inactive now for several months, the patient is physically deconditioned and the ensuing poor posture and ill-functioning musculature (some muscles are chronically contracted to minimize painful movements; others are weak and flaccid from disuse) induces myofascial (soft-tissue) pain, worsening the situation. The patient is no longer able to go out with friends or to visit family because of neck and back pain that prohibit driving. Sitting or standing in any one place for too long brings on the pain. The family withdraws, unable to console the patient and feeling inadequate. The patient ends up at a multidisciplinary pain management clinic, diagnosed with failed back surgery syndrome complicated by depression and severe deconditioning. A fairly long and expensive treatment program is now required to help the patient pick up the pieces. The pain has become a state of suffering.

Without analyzing this scenario step-by-step, it is clear that a fairly innocuous event initiated a domino effect, resulting in biologic, psychological, and social disruption of the patient’s life. This is why a biopsychosocial approach to pain management is necessary. Early recognition of this downward spiral might have helped the patient if a brief period of pain management–oriented counseling or relaxation-based cognitive therapy was initiated to help the patient look at the pain from a different perspective. Furthermore, the likelihood of successful pain management might have been increased by incorporating physical therapy early to prevent a deconditioning process. Short-term use of nonsteroid antiinflammatory drugs (NSAIDs), tricyclic antidepressants, or muscle relaxants might have decreased pain and improved sleep, minimizing the potential for depression.

Close communication between the clinician and patient is needed to develop mutual trust. Limits need to be specified with regard to medication refill requests and self-adjustments of dose to avoid misunderstandings that might lead to suspicion of addictive behavior. Prescribing medications without adequate thought and discussion and then abruptly stopping them simply generates patient frustration, bewilderment, and resentment. Setting limits early and paying firm attention to them fosters the patient’s respect and trust. With the rules established at the outset, perhaps in the form of a signed agreement, the chance for misunderstanding is minimized. Such an agreement amounts to informed consent.

A common misconception is that chronic pain is the result of psychiatric disease. No doubt the two often coexist, but psychiatric illness is more often a reaction to the pain. The prevalence and incidence of psychiatric comorbidity in patients with chronic pain is probably no greater than that seen in other patients with chronic medical disorders (e.g., epilepsy). A history of sexual, physical, or emotional abuse, with the resultant psychological ramifications, is astonishingly prevalent in a wide range of clinical settings, if one takes the time to look. These issues may have special relevance to patients for whom invasive treatments are being contemplated, and this is one of the reasons that such histories are pursued (and found to exist) in the pain clinic.

Poor coping skills and mood disorders may affect the experience of pain, but the decision that depression, for example, is causing a person’s pain should be made with the help of a trained mental health professional. Even somatoform pain is real pain; it is simply treated from a more behavioral perspective. Assuming somatization without the assistance of a mental health professional may prove incorrect and result in invalidation of the patient’s complaint. Worse, somatization may be confused with malingering and may unjustly and significantly influence legal and disability compensation issues. Thus, one must be careful in using terms such as “psychogenic” or “somatoform pain.”2 According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), the former term is no longer acceptable and the latter is relatively uncommon. The current terminology is “pain disorder associated with psychological factors.” When a medical condition also affects the patient’s experience of pain, it is termed “pain disorder associated with both psychological factors and a general medical condition.”

Evaluating pain as physical (“real”) or psychological (“unreal”) is a simplistic and a limited approach that serves no useful purpose: “absence of evidence is not evidence of absence.” For example, when MRI and a nerve conduction test fail to reveal a cause of a person’s chronic low back pain, it is often assumed that there is no observable lesion. The problem is then usually treated with physical therapy and often with psychotherapy. Recent work has demonstrated that focal pathology may, in fact, exist but be out of the reach of the technology used to find it. For example, although MRI of a disk may appear normal, this technology cannot evaluate the inside of the disk: it will not reveal internal disk disruption, a painful tear. Thus, some specialists inject disks with a contrast agent (provocative diskography), pressurizing it to determine if the pain induced is concordant with the clinical complaint. A normal disk is not painful during this procedure; however, whereas this is true of the lumbar region, it is controversial in the cervical spine. Specially guided computed tomographic (CT) scans of these contrast-injected disks may then reveal fissures within the disk, some grades of which correlate well with the pain, and may prove predictive of success with further intervention. Elimination of the pain might be achieved (rarely) by corticosteroid injection into the disk; ablation of the sensory nerves subserving the disk; stiffening the disk by intradiskal electrothermal therapy (IDET), sometimes referred to as intradiskal electrothermal annuloplasty (IDEA); or disk removal with fusion of the vertebrae. IDET was approved by the Food and Drug Administration (FDA) in 1998 and was found useful in worker’s compensation and non–worker’s compensation patients in a controlled study.3 Similarly, facet joint–mediated spine pain may be missed without precision spine injections, because there is a relatively poor correlation between the reported symptoms, physical examination, and electrodiagnostic and imaging test results. Currently, there is renewed interest in this controversial approach to the diagnosis and treatment of spine pain, because improvements in patient selection and procedure technique have begun to help a significant number of those with “whiplash” and other so-called minor strain injuries.4,5

To summarize, one need not attribute a patient’s pain to organic pathology in order to validate it as real. Pain is what the patient says it is. And if psychological factors are found to be important in a patient’s experience of pain, their importance should not be underestimated. Depression kills. Conversely, unless the diagnostic workup is well thought out, important physical pain generators may be missed; centralization of pain, however, may still prove problematic. Therefore the question should not be, “Is this person’s pain real (physical) or unreal (psychological)?” but, “Will this person’s pain most likely respond to medical, invasive, or psychological intervention?”

The systematic use of placebo control is important in clinical research, but it is controversial in diagnostic medicine. This is another deceptively complex topic, fraught with misunderstanding. The placebo response has no bearing on whether pain is real or unreal, it merely defines the sufferer as a placebo responder or nonresponder. It neither confirms a psychogenic cause nor rules out physical pathology. And there is no clear correlation of personality type with the likelihood of placebo response. A person may respond to placebo on one occasion but not on another. There may even be a spectrum of responses. And contrary to popular belief, the placebo response does not predictably occur one third of the time or in one third of the subjects. This notion stems from a paper in the Journal of the American Medical Association in which the author averaged the results of 11 studies to come up with 35.2%.6 More recent studies estimate the rate to vary between 0% and 100%.7 Placebo response varies widely between and within groups according to the expectations of both examiners and examinees. Its mechanism is controversial and incompletely understood, although it may, in part, result from the release of endorphins. The use of placebo may, under some circumstances, prove damaging. When used without consent, it may be seen by the patient as trickery. It can undermine the patient-clinician relationship, resulting in loss of trust. We have already established that trust is necessary for a good therapeutic outcome. Using a placebo may even violate the spirit of informed consent, if the placebo-controlled part of a procedure is not disclosed. Disclosure will not necessarily interfere with the placebo’s usefulness. One simply explains to the patient that response to treatment is complicated and may be influenced by patient expectation. The patient should be reassured that the medicine will be given, but in a manner and timing of which the patient will be unaware. The reassurance that they will receive the medication (not just placebo) is important. And as Patrick Wall has noted, the power of suggestion is a tool that may be employed benevolently and appropriately: “Mummy will kiss it better” is a wonderfully effective remedy.8

The use of opioid medications in the management of nonmalignant pain remains controversial, despite more than a decade of active debate. Here, too, there is much prejudice and misunderstanding. Contrary to popular belief, narcotic medications have a lower risk for addiction than previously thought, if used appropriately in the management of pain. This is especially true in patients without a history of substance abuse and applies to infants, children, and adults.

Tolerance is defined as an increasing dose requirement to maintain the same therapeutic effect. This may or may not occur in an individual on opioid therapy, but when it does, it does not necessarily equate with addiction. Physical dependence is another confusing term that is often misapplied as a synonym for addiction. It merely describes the potential for developing a physical state of withdrawal if the medication is weaned too quickly. Patients can usually be weaned successfully from drug therapy without inducing symptoms of withdrawal. Furthermore, tolerance and physical dependence together do not make for addiction. Psychological dependence, however, is equivalent to addiction. It may be present long after the weaning process and, therefore, long after tolerance and physical dependence abate.

Psychological dependence is defined as a psychological fixation on a drug; the behavioral manifestation is continued use of it, despite potential harm to the patient. This problem is estimated to occur less than one tenth of 1% of the time in short-term treatment with strong narcotics (when there is no history of substance abuse). Even in long-term treatment, the addiction rate is probably between 3% and 16%; the vast majority of those addicted have a history of substance abuse.9,10 This means that there is unlikely to be a problem with addiction 84% to 97% of the time. The role of cigarette smoking is unknown, but it is not generally considered to be an indicator of potential medication abuse problems. A history of addiction does not mean that patients in pain should go untreated or be denied opioids. The clinician must simply monitor the patient more closely than usual for signs of addictive behavior. In general, it is good advice to have the patient sign a contract or an agreement that outlines the parameters within which the relationship of prescriber to prescribee may operate smoothly. Breaking this agreement is grounds for dissolution of the relationship. If this happens, there is an ethical obligation on the part of the physician to reasonably help the patient find care elsewhere.

Drug-seeking behavior is not synonymous with pain avoidance behavior (otherwise known as pseudoaddiction). The main difference between the two is that a person who is initially undermedicated and protests such treatment as though he or she is drug-seeking will likely stop such demands once the pain is controlled. His or her protests and pain behaviors are rational. The psychologically dependent (addicted) person may never seem to be appeased. When there is concern over patient behavior, it is appropriate to ask for help from a pain specialist or an addictionologist to evaluate and interpret the situation.

Pharmacotherapy is one of the mainstays of treatment of pain. Only brief mention of it is made here. The reader is directed to Fields and Liebeskind11 for a detailed overview. In addition to the antiinflammatory agents and narcotics, certain antidepressant and antiepilepsy medications may prove useful for a variety of painful conditions. Those agents that elevate serotonin and norepinephrine in the brain, primarily the tricyclic and several atypical antidepressants, may activate a descending pain modulatory system, thereby diminishing some forms of pain. Antidepressants may also diminish anxiety and improve sleep, reducing irritability and the negative affective ramifications of chronic pain. Pain relief with antidepressants usually occurs independent of the drug’s effect on mood; antidepressants attenuate pain more quickly and at lower doses than is commonly needed for depression. Of the selective serotonin reuptake inhibitors (SSRIs), only paroxetine hydrochloride (Paxil), venlafaxine hydrochloride (Effexor), and citalopram hydrobromide (Celexa) have clinically demonstrable effects on neuropathic pain. It is not clear why the effects should differ from those of fluoxetine hydrochloride (Prozac) or sertraline hydrochloride (Zoloft).

Some antiepilepsy medications (and tricyclic antidepressants) act as membrane-stabilizing agents, elevating the threshold for neuronal firing. They, too, may help diminish neuropathic pain. Whether or not membrane stabilization is the mechanism for their analgesic effect is controversial (each drug may have multiple mechanisms of action). And, although it is often taught that tricyclic depressants are best for treatment of burning neuropathic pain and anticonvulsants are best for paroxysmal or shooting pain, either class can be used with some efficacy and should be selected on the basis of cost, effect and side-effect profile, and likelihood of compliance. Antidepressants are commonly tried first because of their potential effect on problems other than pain. The only clear indication for a specific medication for neuropathic pain is that for the antiepilepsy drug carbamazepine (Tegretol) to treat trigeminal neuralgia. In this case, there is well-documented evidence for its superiority over other agents. Likewise, the majority of the literature supports the use of tricyclic antidepressants over other agents for treatment of postherpetic neuralgia, although a number of viable options exist. These include opioids, gabapentin (Neurontin), and topical lidocaine (Lidoderm 5% patches).

There are many other medications for which anecdotal evidence for efficacy in pain control exists. The skillful practitioner should be able to use combinations of some of these agents to minimize pain and suffering in patients for whom single agents have proven ineffective. It also pays to be aware of different delivery systems available for these agents. Epidural and subarachnoid catheters, PCA devices, and the use of oral, rectal, sublingual, buccal, subcutaneous, intravenous, and intramuscular routes of administration all have their place in pain management.

Added to these modes of delivery is the neurosurgical approach to pain management. Under appropriate circumstances, pain pathways may be cut or neurostimulatory devices used with considerable efficacy at the level of the peripheral nerve, spinal cord, and subcortical and neocortical brain regions. Even ablation of the pituitary gland may significantly diminish the whole-body pain of metastatic cancer. Implanted intrathecal medication pumps and intraventricular catheters are useful modes of treatment in selected cases. Pain-oriented neurosurgery may prove valuable to multidisciplinary pain management teams. And, because some of the procedures are reversible (e.g., spinal cord stimulation), neurosurgical intervention is not necessarily a “last resort.” Use of it early in the course may preclude medication side effects and toxicity. Surgical treatment of pain is thoroughly addressed elsewhere.12

What we have discussed here is a multimodal and interdisciplinary approach to the patient with chronic pain. A biopsychosocial approach (however fuzzy that sounds) is useful to analyze and effectively manage the physical, emotional, and social aspects of patients’ pain and suffering. Reasonable goals should be set with respect to diminution of pain and improvement in function. At a minimum, a good interdisciplinary team should include (1) one or two physicians well-versed in pharmacologic and interventional procedures; (2) a counselor, psychologist, or psychiatrist to diagnose and treat psychiatric conditions that may result from, cause, or exacerbate the pain; (3) a physical therapist or rehabilitation specialist to assess physical conditioning requirements; and (4) nurses knowledgeable about how these approaches may be applied to the specific patient.

Nurses help move clinics along efficiently and allay patient anxiety by being able to return calls promptly and expertly. Their skill in patient triage and procedure and postprocedural evaluation may prove invaluable to successful pain management. From the patient’s perspective, the quality and responsiveness of the nursing staff may make the difference between an overall positive or negative clinical experience.13

Pain management teams that have frequent multidisciplinary meetings to discuss individual patients and their diagnoses and progress are more likely to be effective in carrying out a reasonable plan. But there are too many patients with chronic pain to expect pain specialists alone to care for them. Primary care physicians are also well suited to the task and can be highly successful if some of the principles discussed in this chapter are followed. Note, however, that success does not always mean cure. If an approach to pain management diminishes a person’s pain score by 1 point out of 10, then applying three or four approaches in concert may drop a person’s pain score from 8 to 4, making the difference between a state of suffering and one of simple pain. If this allows that person to return to school or to work with an improved level of function, then the pain management program may be called a success.

The authors wish to express their gratitude to Julie A. Brady, RN, whose experience and comments proved invaluable to the production of this manuscript.