Chronic Pain
Maureen F. Cooney
This chapter provides a brief overview of chronic pain assessment and management with an emphasis on the role of the neuroscience nurse as a member of an interdisciplinary team providing medical and surgical management to people with chronic pain.
Pain is the most universal of all afflictions. It can be described in terms of sensory, emotional, and cognitive components that reflect the transmission and modulation of painful stimuli.1 Pain can be classified by a biologic mechanism that includes neuropathic, muscular, inflammatory, mechanical/compression, or malignancy or by an acute or chronic designation.2 Acute pain is a response to tissue injury or inflammation and results from the activation of peripheral pain receptors (nociceptors) and their specific sensory nerve fibers (A delta fibers and C fibers). It is a complex constellation of unpleasant sensory, perceptual, and emotional experiences and certain associated autonomic, psychological, emotional, and behavioral responses.3 Acute pain is often associated with an identifiable injury or trauma and resolves as the injury heals.
By comparison, chronic pain or persistent pain, is continuous or recurrent in nature, and of sufficient duration and intensity to adversely affect a patient’s well-being, level of function, and quality of life.2 Although a strict time frame is not applied, pain that continues after a reasonable time for healing (more than 3 to 6 months) suggests the need to assess the patient for presence of chronic pain. The causes of chronic pain are not well understood, but may be related to continual tissue injury caused by ongoing activation of A delta and C fibers as well as other sensitized pathways. Chronic pain is a complex multidimensional phenomenon with unclear pathogenesis, continuation of pain after resolution of the initial injury, and an unpredictable course of recovery.1 It is thought to be a biopsychosocial phenomena which is influenced by factors such as acute pain intensity, depressive symptoms, and past trauma or stressful life events.4 Chronic pain can be considered maladaptive because it has no useful function; it occurs without the presence of ongoing noxious stimuli and has no role in promotion of healing or repair. It is poorly responsive to conventional pain medications and it may be viewed as a disease process onto itself.5
Clinical Pearl: Pain is a subjective and personal experience; its reality is whatever the patient says it is in terms of description, intensity, and meaning. Pain intensity ratings can only be obtained by patient self-report.
Chronic pain is a significant problem faced by millions of Americans. The economic impact from traditional and nontraditional treatment, over-the-counter drugs, and loss of productivity is estimated at millions of dollars annually. Managing people with chronic pain is one of the greatest challenges in health care today.
Neuropathic pain is a subtype of chronic pain, which is caused by injury or dysfunction of the peripheral nervous system (PNS) or central nervous system (CNS).6 This includes injury or dysfunction of nerves, the spinal cord, or the brain. Chronic pain can be caused by nociceptive, neuropathic, or a combination of both as a result of injury and other conditions Box 26-1). Headache is discussed in Chapter 27, peripheral neuropathies in Chapter 35, and cranial nerve diseases in Chapter 36.
DEFINITION OF TERMS
The following are definitions of frequently used terms related to pain.7
Allodynia: abnormal perception of pain from a normally nonpainful mechanical or thermal stimulus
BOX 26-1 COMMON CAUSES OF CHRONIC NEUROGENIC PAIN
Spinal cord tumors
Traumatic spinal injuries
Intervertebral disc disease/sciatica
Spinal stenosis with root compression
Compression of nerve plexuses
Thalamic pain syndrome
Metastatic bone pain (e.g., vertebra)
Cauda equina disease
Trigeminal neuralgia
Postherpetic neuralgia
Peripheral nerve diseases/entrapment syndromes
Neuropathics: mononeurotherapy, polyneuropathy, diabetic neuropathy
Complex regional pain syndromes I and II
Crushing nerve injuries
Phantom pain
Anesthesia dolorosa: pain in an area or region that is anesthetic
Central pain: pain associated with a primary lesion or dysfunction in the CNS
Complex regional pain syndrome type 1 (CRPS-I), previously called reflex sympathetic dystrophy: a syndrome of varying patterns that include pain that is out of proportion to injury (if it can even be identified), sensory abnormalities (burning pain and hyperpathia), focal autonomic abnormalities, motor abnormalities, and trophic changes; follows soft tissue or bone injury most often to the limbs, but without discernible nerve injury (Box 26-2)8, 9
CRPS-II, previously called causalgia: has a similar clinical presentation to CRPS-I, but there is related nerve injury
Deafferentation pain: pain due to loss of sensory input into the CNS, such as occurs with avulsion of the brachial plexus or other types of lesions of peripheral nerves or due to pathology of the CNS. Phantom limb pain is an extreme example of deafferentation pain.
Dysesthesia: an unpleasant abnormal sensation, whether spontaneous or evoked
Hyperpathia: abnormally painful reaction to a stimulus, especially a repetitive stimulus; pain is often explosive in nature
Hyperesthesia: an increased sensitivity to stimulation, excluding special senses
Hypoesthesia: a diminished sensitivity to stimulation, excluding special senses
Neuralgia: pain in distribution of a nerve or nerves
Neuritis: inflammation of a nerve or nerves
Neuropathy: a disturbance of function or pathological change in a nerve
Nociceptive neuron: a central or peripheral neuron of the somatosensory nervous system that is capable of encoding noxious stimuli
Nociceptive pain: pain that arises from actual or threatened damage to nonneural tissue and is due to activation of nociceptors.
Opioid-induced hyperalgesia (OIH): a state of nociceptive sensitization caused by opioid exposure. OIH is manifested by a paradoxical response in which opioids, administered for the treatment of pain, are capable of enhancing pain, sensitivity, and loss of analgesic efficacy. Although the precise mechanism of OIH is not understood, it is thought to result from neuroplastic changes in the peripheral and CNS that lead to sensitization of pronociceptive pathways. The N-methyl-D-aspartate (NMDA) receptor has been implicated in the pathophysiology of OIH.10
BOX 26-2 COMPLEX REGIONAL
Pain Syndrome Type I
Description: severe, deep, burning, or lancinating pain that is out of proportion to the injury present and wide variability of symptoms; pathophysiology and treatment are unclear; diagnosis is based on clinical presentation.
Diagnostic criteria: from the International Association for the Study of Pain:
Follows a traumatic event to soft tissue or bone without an apparent nerve lesion (in 10% of patients, no source of trauma can be identified)
Spontaneous pain (hyperalgesia and allodynia) disproportionate to the precipitating event
From onset of precipitating event there is edema, skin, temperature changes (usually cool), and color changes in distal aspect of affected limb
No other explanation for the degree of pain and dysfunction
In the latter stages look for hair loss, brittle nails, and skin atrophy in affected limb and impaired motor function, including weakness, tremor, and ankylosis.
Treatment: physical therapy, drug therapy, or spinal cord stimulator (transcutaneous electrical nerve stimulation) or sympathectomy (sympathetic block) in patients who do not respond to physical therapy and drugs used for neuropathic pain. Drug therapy includes tricyclic antidepressants, anticonvulsants, corticosteroids, lidocaine, nonopioids, opioids, adjuvant analgesics, and alendronate.
Pain: an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
Pain tolerance level: the maximum amount of pain that an individual is willing to accept in a given situation
Pain threshold: the minimum intensity of a stimulus that is perceived as painful
Paresthesia: an abnormal sensation, whether spontaneous or evoked
Peripheral neurogenic pain: pain caused by a primary lesion or dysfunction in the PNS
Sensitization: increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold inputs. (central sensitization if occurs in CNS nociceptive neurons; peripheral sensitization if occurs in peripheral nociceptive neurons)
Trigger point: a hyperirritable area or site in muscle or connective tissue, tender when compressed, usually associated with myofascial pain syndromes.11
PAIN THEORIES
Humans have struggled to understand and explain pain since the beginning of time. Some of the earliest pain theories, such as those from ancient Egypt and India, proposed that the heart was the
center of all sensation and that pain was associated with demons and gods. It was not until the 17th century that Descartes described some of the beginning concepts of pain pathways. According to Descartes, when the foot comes near a fire, the sensation enters the body and travels up threads to the brain (Fig. 26-1).
center of all sensation and that pain was associated with demons and gods. It was not until the 17th century that Descartes described some of the beginning concepts of pain pathways. According to Descartes, when the foot comes near a fire, the sensation enters the body and travels up threads to the brain (Fig. 26-1).
 Figure 26-1 ▪ Descartes’ (1664) concept of the pain pathway. He writes: “If for example fire (A) comes near the foot (B), the minute particles of this fire, which as you know move with great velocity, have the power to set in motion this spot of the skin of the foot which they touch, and by this means pulling upon the delicate thread (c.c.) which is attached to the spot of the skin, they open up at the same instant the pore (d.e.) against which the delicate thread ends, just as by pulling at one end of a rope makes to strike at the same instant a bell which hangs at the other end.” (From: Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new theory. Science, 150, 971-979.) |
The 19th century heralded the study of pain physiology, which led to the discovery that the dorsal root of the spinal cord was involved with sensory function and the ventral root with motor function. In 1840, Muller reported that the brain could only receive information about the external environment by way of the sensory nerves. This information, plus discoveries in pain management with morphine, codeine, and regional anesthesia, paved the way for several physiologic pain theories. The specificity theory noted that there were different afferent sensory neurons for pain and touch, while the intensive theory supported the idea that any sensory stimulus could become painful if it becomes intense enough.
Debate about these theories and development of several new theories continued into the 20th century. One of the most widely accepted theories is the gate control theory proposed by Melzack and Wall, which states that the CNS is surrounded by a barrier that can only be entered by a gate (Fig. 26-2).12 Pain enters through the gate, and increasing noxious stimulation, as well as anxiety and depression, opens the gate wider. The gate can be pulled closed from the outside (peripheral) or pushed closed from the inside (centrally by the brain and spinal cord). This theory takes into account the effect of the person’s motivational, cognitive, and affective state during the pain experience in that the gate can be pushed closed by higher centers of the brain through distraction, relaxation, meditation, high levels of endorphins, and enkephalins. Activities such as transcutaneous nerve stimulation and massage can pull the gate closed from the periphery.
 Figure 26-2 ▪ Gate control theory. This shows how thin (tissue damage responding) fibers force open the “gate” into the central nervous system, bringing pain to consciousness. The gate can be pulled shut from the outside, reducing pain, by the activation of large A-beta fibers, rubbing/massage, transcutaneous electrical nerve stimulation, or vibration. The gate can also be pushed shut from inside the central nervous system by various inhibitory systems descending from the brain; some of these inhibitory systems are activated by acupuncture, others by drugs. (From: Carol R. Taylor, Carol Lillis, R. N., LeMone, P., & Lynn, P. (2008). Fundamentals of nursing: The art and science of nursing care, 6th ed. Philadelphia: Lippincott Williams & Wilkins.) |
Research. There is an evolving body of evidence pointing to the role of genetics in the development of chronic pain. Chronic pain is identified as a classic example of the gene and environment interaction. Injuries resulting in inflammatory processes as well as nerve damage result in acute pain, but only a subset of these individuals go on to develop chronic pain. Pain severity, as well as response to pharmacologic agents is also variable among individuals, and it is thought that genetics may play a significant role contributing to these varied responses.13 Pharmacogenetic research is contributing to a greater understanding of individual responses to analgesia. For example, research has demonstrated that genetic variation may significantly affect opiate absorption, distribution, metabolism, excretion, and toxicity. It is thought that as this body of evidence grows, it will become possible to personalize pain management strategies, based on genetics, to provide the most effective treatment with the lowest side effect profile.14 In other studies, the role of genetics in the pain experience has been demonstrated by results which have shown that red hair is the phenotype for mutations of the melanocortin-1 receptor. Redheads have been found to be more sensitive to thermal pain than nonredheads and are resistant to the analgesic effects of subcutaneous lidocaine.15
 Figure 26-3 ▪ Schematic representation of primary pain pathways and connections. (From: Premkumar K. (2004). The massage connection: anatomy and physiology. Baltimore: Lippincott Williams & Wilkins.) |
ANATOMY AND PHYSIOLOGY OF PAIN
Nociception is the process by which information about tissue damage is conveyed to the CNS. It typically involves four processes: transduction, transmission, perception, and modulation. The PNS has specialized nerve fibers with terminal branches in the skin, blood vessels, viscera, and musculoskeletal structures that recognize tissue damage called nociceptors. In transduction, the nociceptors convert energy from the noxious stimuli into electrical energy (nerve impulses). Transmission involves the movement from the nociceptors through the cell bodies, which lie in the dorsal root ganglia, and synapse with a secondary neuron in the dorsal horn of the spinal cord, thus entering the CNS (Fig. 26-3). Different types of primary afferent fibers transmit impulses from the PNS to the CNS. The larger (6 to 12 µm diameter) A-beta fibers are myelinated fibers that conduct at higher speed (30 to 70 milliseconds); they transmit impulses for touch, pressure, and vibration. A-delta fibers are also myelinated, but smaller (1 to 6 µm diameter), and conduct impulses at a slower speed (5 to 30 milliseconds). They are associated with mechanical or heat nociceptors and are responsible for pinprick pain. C fibers are the smallest fibers (<1.5 µm diameter) and conduct at the slowest rate of speed (0.5 to 2 milliseconds). They are polymodal unmyelinated fibers that transmit burning sensation and poorly localized aching-type pain (Fig. 26-4).
Conduction of the pain impulse is mediated by activation of voltage-gated sodium channels by excitatory current strong enough
to generate an action potential. Pain impulses enter the spinal cord through the dorsal root synapse in lamina I, II, or V and then cross the other side of the spinal cord through the gray matter to the spinothalamic tract. Next, the process of perception, which involves both cortical and limbic system structures occurs. The spinothalamic tract transmits pain impulses to the thalamus and then to the primary sensory cortex, where the discrimination of pain is perceived, and then to the limbic cortical areas for perception of the affective and emotional aspects of pain. The final process, modulation, occurs at multiple levels (e.g., peripheral, spinal, and supraspinal). Nerve fibers in the descending inhibitory pathways release inhibitory substances (endogenous opioids, serotonin, norepinephrine, GABA) at synapses with other neurons in the dorsal horn which block nociceptive transmission. The pain impulse also activates a reflex withdrawal from the painful stimulus in the spinal cord, and also increases the state of arousal and emotional, autonomic, and neurohumoral responses.1
to generate an action potential. Pain impulses enter the spinal cord through the dorsal root synapse in lamina I, II, or V and then cross the other side of the spinal cord through the gray matter to the spinothalamic tract. Next, the process of perception, which involves both cortical and limbic system structures occurs. The spinothalamic tract transmits pain impulses to the thalamus and then to the primary sensory cortex, where the discrimination of pain is perceived, and then to the limbic cortical areas for perception of the affective and emotional aspects of pain. The final process, modulation, occurs at multiple levels (e.g., peripheral, spinal, and supraspinal). Nerve fibers in the descending inhibitory pathways release inhibitory substances (endogenous opioids, serotonin, norepinephrine, GABA) at synapses with other neurons in the dorsal horn which block nociceptive transmission. The pain impulse also activates a reflex withdrawal from the painful stimulus in the spinal cord, and also increases the state of arousal and emotional, autonomic, and neurohumoral responses.1
 Figure 26-4 ▪ Primary afferent fibers from skin to spinal cord. The largest (Aβ) and most rapidly conducting myelinated fibers are activated by light touch (illustrated by a cotton bud); these are the fibers that are activated by transcutaneous electrical nerve stimulation and vibration. Smaller, more slowly conducting (Aδ) myelinated fibers are activated by pinprick and are involved in acupuncture stimulation. The smallest and slowest fibers (C) are unmyelinated and are excited by tissue damage, here illustrated by a lighted match; they are often called nociceptors. (From: Carroll, D., & Bowsher, D. (1993). Pain management and nursing care (p. 9). Boston: Butterworth & Heinemann.) |
Nociceptive pain is activated by essentially normal neural systems and involves the processes described above, but neuropathic pain, by contrast, is sustained by a set of mechanisms that is caused by damage to, or dysfunction of the peripheral or CNS.6 Nociceptive pain usually involves tissue damage or inflammation, but neuropathic pain can occur in the absence of either. Acute nociceptive pain serves a protective function, but neuropathic pain is not believed to serve any useful purpose. Sensitization is one of the processes that initiates and maintains neuropathic pain. Sensitization is the process by which the action potential threshold is shifted toward less intense stimuli and can be peripheral or central. Peripheral sensitization results from a variety of sources such as chemical mediators released as part of the inflammatory response, blood cells (e.g., macrophages, leukocytes, fibroblasts), and other neurons, which are only activated during inflammatory states. Chemical mediators included in the inflammatory response are serotonin, histamine, bradykinins, capsaicin, glutamate, prostaglandins (i.e., from cyclo-oxygenase induction), nitrous oxide, tumor necrosis factors, and substance P, which activate nociceptors and further contribute to the pain. Neurons can release calcitonin, peptides, somatostatin, neurotrophins, and other substances. Central sensitization is the result of increased primary afferent discharges into the spinal cord that maintains a state of excitation, PNS changes, and ongoing tissue damage or inflammation.16 The result of central sensitization is spontaneous discharges, decreased pain threshold, and an increase in the receptivity of the sensory neurons to less intense stimuli.1, 16 Simply stated, in central sensitization, repeated exposures to a painful stimulus may result in a stronger neural memory of the pain, thus changing the pain threshold and yielding a stronger pain response. The processes of peripheral and central sensitization are thought to be maintained by release of glutamate, an excitatory neurotransmitter, from activatied N-methyl-D-aspartate (NMDA) receptors. Clinically hyperalgesia, allodynia, and dysesthesias are common along with behavioral changes (e.g., hyperactivity, withdrawal, irritability, depression). Because of the “rewiring changes” that can occur in the PNS and CNS from ongoing acute pain, there is good rationale to treat acute pain well before it undergoes changes and becomes chronic pain triggered by a less painful stimulus and diffuse in nature.1
Clinical Pearl: The pathophysiology of chronic pain is not yet fully understood; it is important to treat acute pain early and effectively to reduce the risks for development of nervous system changes that may contribute to the development of chronic pain.
Research. It is becoming increasingly recognized that spinal glia play a significant role in modulation of the neuronal network; Various experimental animal models of peripheral inflammation, spinal injury, or nerve injury demonstrate a crucial role of glia in central sensitization and pathological pain.17
Assessment and Management of Chronic Pain
This section examines assessment and management of chronic pain to provide the nurse with an evidence-based practice approach to patient care. There are many published guidelines on the management of chronic pain posted on the National Guideline Clearinghouse website (www.guideline.gov). One of the most comprehensive and current guidelines is from the Institute for Clinical Systems Improvement (ICSI).18 In this chapter, recommendations from ICSI guidelines as well as other guidelines and sources are included to present best practices for chronic pain management.
Comprehensive Assessment and Development of a Plan of Care
As of 2001, The Joint Commission required that every patient have his or her pain assessed and treated promptly and adequately.19 This requirement lends further support to the importance of recognizing and adequately treating pain.
Pain is a subjective and personal phenomenon, which is often challenging to assess. Millions of Americans suffer from chronic pain, most of whom are either self-managed or managed by their primary health care provider. A smaller number of patients with debilitating intractable pain seek care from pain management specialists or pain centers. Under ideal circumstances, patient with chronic pain are managed in centers offering Integrative Interdisciplinary Chronic Pain Management Programs (also referred to as Interdisciplinary Pain Rehabilitation Programs, Chronic Pain Programs, or Multidisciplinary Pain Management Programs). In these programs, interdisciplinary teams work in concert with each other to implement strategies which will aid the patient to overcome the challenges of persistent pain (Tables 26-1 and 26-2). Because of its complexity, multidimensionality, and resistance to treatment, chronic pain management is ideal for these interdisciplinary teams. In this chapter, chronic pain management is addressed from a center perspective to assist the reader in appreciating a comprehensive view of management.
Research. Since the 1980s, numerous methodologically robust studies have yielded results supporting the clinical efficacy as well as the cost effectiveness of interdisciplinary chronic pain management programs.4, 20, 21, 22 The goals of these intense, duration limited programs are to restore patients to greater levels of independence
and improve overall quality of life. Through medical management, graded physical exercise, and cognitive and behavioral pain and stress management techniques, the following outcomes have been reported: reductions in pain scores, reduced emotional distress, decreased opioid use, improved function, and reduced health care utilization.21 (Schatman in Bonica)
and improve overall quality of life. Through medical management, graded physical exercise, and cognitive and behavioral pain and stress management techniques, the following outcomes have been reported: reductions in pain scores, reduced emotional distress, decreased opioid use, improved function, and reduced health care utilization.21 (Schatman in Bonica)
TABLE 26-1 COMMON COMPONENTS OF AN INTEGRATED INTERDISCIPLINARY REHABILITATION PROGRAM | |
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TABLE 26-2 COMMON PSYCHOLOGICAL AND BEHAVIORAL TECHNIQUES USED TO TREAT CHRONIC NONCANCER PAIN | |
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A comprehensive pain assessment is the initial step in the management of chronic pain (see Box 26-3. outlines the components of a chronic pain assessment. In addition to a complete medical history and physical examination, a neurological assessment, pain history, and current pain management report are collected. A comprehensive initial pain assessment tool may be useful for new or difficult-to-control pain.23 A standardized tool such as the Brief Pain Inventory (BPI) (see Box 26-4) may be used during patient encounters to assess current and recent past pain intensity, quality, aggravating and alleviating factors, as well as functional impact. The following components are included in a pain history.
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