Management Strategies for Chronic Pain


Introduction

The prevalence of chronic pain in the United States is variable; however, the burden is substantial and continues to grow. Chronic pain is defined as pain that lasts longer than 3 months or past the time of normal tissue healing. Most recently, analysis of data from the 2012 National Health Interview Study showed that 11.2% of adults report having daily pain ( ). Pain is among the most common reason people seek medical attention and is reported by 20%–50% of patients seen by primary care physicians ( ). Pain is a leading cause of disability and major contributor to healthcare expenditures in the United States. It contributes to societal loss of productivity and employment and decreased quality of life (QOL) ( ).

Although there are many etiologies of chronic pain, chronic low-back pain (CLBP) and failed back surgery syndrome (FBSS), also known as postlaminectomy pain syndrome, account for a large proportion of disability ( ). According to the United States Burden of Disease Collaborators, CLBP consistently accounted for the largest number of years lived with disability in the United States population in 1990 and also in 2010 ( ). Healthcare costs for adults with CLBP increased to an estimated $6000 per person in 2005, with a total cost of $102 billion annually ( ).

Postlaminectomy pain syndrome occurs subsequent to surgery of the lumbar spine, and is characterized by intractable pain of the back and/or legs and varying degrees of functional incapacitation after spine surgery ( ). The rates of operations on the lumbar spine have increased substantially, with an estimation of more than 250,000 new laminectomies being performed each year in the United States ( ). In 1990 122,000 lumbar fusions were performed, while 500,000 were performed in 2006 ( ). Despite the increase in surgery rates, about 30,000–40,000 laminectomy patients per year do not have relief of pain symptoms or have recurrence of pain ( ).

Back pain is just one of many conditions that contribute to the widespread prevalence of chronic pain in our modern society. To manage these varied conditions and provide patients with appropriate treatment options, it is important to understand the pathophysiologic mechanisms involved in a patient’s pain. These mechanisms include chronic nociceptive pain, chronic neuropathic pain, central pain, and mixed etiology.

Chronic nociceptive pain is caused by remnants of tissue damage or a disease process, often autoimmune, that periodically or persistently activate tissue nociceptors through an inflammatory process or trauma, leading to peripheral and central sensitization ( ). Familiar and common examples include arthritis caused by disease (rheumatoid arthritis or osteoarthritis—OA) and persistent or recurrent trauma (gait changes from a knee injury or arthritis, regular occupational heavy lifting and twisting, and fusion hardware causing stress on facet joints and discs in the lumbar spine).

Chronic neuropathic pain involves damage to the peripheral pain sensory system by disease, such as diabetic neuropathy, or trauma such as crush injury, surgery, or amputation ( ). Such injury may lead to atrophy of sensory neurons that modulate pain sensation or to a persistent firing of damaged pain sensory fibers activating ascending pathways in the central nervous system (CNS), thereby transmitting the signal of the sensation of pain to the rostral neural networks governing the experience of pain perception. Persistence of this peripheral signal can cause changes in the CNS at both the molecular and structural levels, altering the actual neuronal–glial networks of the CNS through a process broadly termed neuroplasticity. These processes of central sensitization may result in a state whereby pain can be activated or worsened by normally nonpainful stimuli, including emotional arousal (e.g., anger, anxiety), movement, loud noise, bright lights, cold temperature, or light touch such as allodynia ( ). The pathophysiology of these systems extends rostrally to the brain, where centers involved in the perception of pain undergo neuroplastic changes such as the enlargement of receptive fields, and in turn these sensitized neural networks augment pain perception ( ).

Central pain is defined by anatomic damage to parts of the central nervous system (CNS) governing pain signal transmission, perception, or modulation caused by diseases such as multiple sclerosis, thalamic stroke, tumor, and Parkinson’s disease, or trauma such as spinal cord injury or compression, brain tumor, or brain surgery ( ).

Certain diseases or injuries may have mixed pathologies. Complex regional pain syndrome (CRPS1 or CRPS2) may involve nociceptive and neuropathic pathophysiology in the peripheral nervous system (PNS) and/or the CNS ( ). Degenerative disc disease of the lumbar spine may be associated with all three categories as well: strain on facet joints activating nociceptors and muscle spasm causing chronic pain of nociceptive origin; leaking intervertebral disc material or herniated disc irritating or compressing nerve roots, activating chronic pain of neuropathic origin (radiculopathy); and chronic activation of the perceptual system in the spinal cord and brain, leading to secondary changes in brain processing centers that govern the emotional aspects of pain, such as the cingulate gyrus, and in cognitive centers affecting executive functioning and coping skills (“Classification of chronic pain,” 1986). These changes may contribute to risk for secondary adverse outcomes such as accidents, depression, disability, and suicide ( ).

The choice of an appropriate therapeutic strategy for a patient’s pain depends on determination of the pathophysiologic mechanism and the type of chronic pain syndrome. By understanding the underlying nature of pain mechanisms, nociceptive versus neuropathic, the clinician is better able to choose mechanistic-specific therapies, thereby increasing the chance of therapeutic success.

For neuropathic pain, neuromodulation, particularly spinal cord stimulation (SCS), is a good option for pain control in the appropriate patient. SCS is effective, predominantly for neuropathic pain. The mechanism of action/s (MOA) of SCS has not been fully elucidated but is believed to be multifactorial and to depend on frequencies of stimulation and particular waveforms that are used. This topic of the MOAs is discussed elsewhere in this textbook (see Chapter 15 ). SCS has been shown to be effective for patients with FBSS, CLBP, and neuropathic pain conditions such as peripheral neuropathy and CRPS ( ).

Evaluation of the Patient With Chronic Pain

Obtaining an accurate history is the pivotal first step when evaluating a patient with chronic pain to help identify the etiology of pain and develop an appropriate individualized treatment plan. Typically, a thorough history can establish a working diagnosis in the practitioner’s mind and guide the physical examination (PE). The details of the patient’s history will depend on the clinician’s ability to elicit vital information that comes from an understanding of the patient’s presentation and pathophysiology of common chronic pain syndromes. Interpersonal communication skills and the ability to listen and direct the conversation play a key role in extracting pertinent information from the patient. Asking open-ended questions, such as “Tell me more about what brings you in today,” allows the patient to feel calm and makes history taking feel more like a conversation, and will help to establish long-term trust. While taking a thorough history, the clinician should simultaneously assess the patient’s mood, anxiety level, and overall demeanor. Common characteristics of different types of pain are detailed in Table 44.1 . These help in elucidating the nature of pain (neuropathic versus nociceptive or other).

Table 44.1
Common Types of Pain Encountered
Types of Pain Characteristics Examples
Nociceptive

  • Visceral

  • Somatic

Dull, aching, throbbing Inflammatory disease states (e.g., OA), pancreatitis, ischemic pain, myofascial pain syndromes
Neuropathic Burning, tingling, shooting, shock-like Lumbar radiculopathy, CRPS, diabetic neuropathy, postherpetic neuralgia, trigeminal neuralgia
Mixed
Central Constant and burning Poststroke pain syndrome, spinal cord injury, multiple sclerosis, Parkinson’s disease
Fibromyalgia Widespread musculoskeletal aches, pain and stiffness, soft tissue tenderness, associated with general fatigue and sleep disturbances

A basic pain history must include the following characteristics/features of the patient’s pain complaints.

  • 1.

    Onset/duration.

  • 2.

    Location.

  • 3.

    Intensity.

  • 4.

    Quality/character.

  • 5.

    Chronicity.

  • 6.

    Frequency.

  • 7.

    Associated symptoms.

  • 8.

    Precipitating factors.

  • 9.

    Relieving factors.

  • 10.

    Effect of pain → functional abilities/disabilities.

  • 11.

    Past treatments, including medications and nonpharmacologic modalities.

Additionally, the patient’s past medical history and family history are often as important as the current complaints. The first step to achieving successful outcomes with therapeutic interventions, whether using pharmacological, psychological, physical, or interventional strategies, begins with appropriate patient selection. Factors that influence successful outcomes include proper diagnosis, identifying properly motivated patients, managing psychopathologies, promoting cessation of smoking and drug use, controlling confounding comorbidities, such as diabetes mellitus and obesity, glycemic control, and properly managing immunosuppressant states and anticoagulation ( ). Surgical procedures and prior imaging studies should also be explored in adequate detail. Questions directed at ruling out “red flags” should also be asked ( Table 44.2 ), such as unexplained weight loss, unexplained fever, bowel or bladder incontinence, motor weakness, and progressive neurological deficits.

Table 44.2
Red-Flag Presentations Requiring Magnetic Resonance Imaging (MRI)
Red Flags
MRI
  • Risk factors for spinal infection (new onset of CLBP with fever and history of intravenous drug use or recent infection)

  • Risk factors for or signs of cauda equina syndrome (new urinary retention, fecal incontinence, or saddle anesthesia)

  • Severe neurologic deficits (progressive motor weakness or motor deficits at multiple neurologic levels)

Clinicians should review the patient’s medications with a keen attention to controlled substances, and review their respective state’s prescription drug monitoring program data to verify controlled substance dosages and ensure there is no pattern of misuse, abuse, or diversion.

Assessment of a patient with chronic pain can be enhanced by use of the McGill Pain Questionnaire, which assesses three categories of word descriptors of pain qualities (sensory, affective, and evaluative) ( ). Research has demonstrated the importance of assessing overall health-related QOL and function in patients with chronic pain ( ; ). Assessment of functional disability using metric tools, e.g., the 36-Item Short-Form Health Survey (SF-36) or the Oswestry Disability Index which evaluates back pain, can objectively measure baseline functionality assessments and response to subsequent interventions ( ). The vital signs of temperature, heart rate, respiratory rate, blood pressure, and weight should be recorded. Measuring these standard health metric allows an overall assessment of health which will be factored in when designing treatment regimens and can help a clinician to support findings in a directed history and PE.

The PE objectifies the patient’s history. Components of the PE include a general examination, detailed neurological examination, and a detailed musculoskeletal examination with inspection, palpation, and provocative maneuvers, when appropriate. Common spinal radicular findings corresponding to dermatomal pain distribution, sensory findings, motor trophic changes, and reflex findings in the cervical region are summarized in ( Table 44.3 ), and changes corresponding to the lumbar region are summarized in ( Table 44.4 ). A thorough and complete understanding of the examination region allows the practitioner to integrate the findings of the history to generate a reasonable assessment of the diagnosis and implement a plan of care.

Table 44.3
Cervical Radicular Findings
Cervical Root Sensory Findings Motor Exam Weakness Reflex Findings
C5 Deltoid Deltoid and biceps Biceps reflex
C6 Thumb and index finger Wrist extensors, pollicis longus, biceps Brachioradialis reflex
C7 Index and middle finger, dorsum of hand triceps Triceps reflex

Table 44.4
Lumbar Radicular Findings
Lumbar Root Sensory Findings Motor Exam Weakness Reflex Changes
L4 Medial malleolus Dorsiflexion of the ankle Knee reflex
L5 First web space Extensor halluces longus
S1 Lateral aspect of the foot Gastrocnemius and soleus Ankle reflex

Findings of the history and PE are often complemented by radiological findings. With back pain having a 75% lifetime prevalence in the United States ( ), utilization of advanced imaging for Medicare recipient patients tripled from 1997 to 2006 ( ). A few exceptions notwithstanding, the role of spinal imaging is primarily to rule out systemic disease manifesting as CLBP. These nonmechanical spine conditions include infection, neoplasia, and inflammatory arthritis, and account for roughly 1% of causes of CLBP ( ); hence imaging may not be indicated in the absence of “red-flag” manifestations ( Table 44.4 ). Imaging findings often poorly correlate with patient clinical presentations, as there is a high prevalence of asymptomatic findings on advanced imaging ( Table 44.5 ). reviewed imaging findings in 3110 asymptomatic patients and found disk degeneration and signal loss in nearly 90% of patients over 60 years of age.

Table 44.5
Asymptomatic Findings in Advanced Imaging
Courtesy of Kanayama, M., Togawa, D., Takahashi, C., et al., 2009. Cross-sectional magnetic resonance imaging study of lumbar disk degeneration in 200 healthy individuals. J. Neurosurg. Spine 11, 501–507.
Lumbar Segment Disk Herniation (%) T2 Signal Loss (%) Modic Changes (%) High Intensity Zone (%)
L3 16.5 15.5 4 5.0
L4 25.0 49.5 11 23.5
L5 35.0 53.0 10 24.0

After reasonable conservative measures have been exhausted, imaging studies for patients with chronic pain, when concordant with history and exam findings, may help guide targeted interventions or surgeries, when these are properly indicated ( Table 44.6 ).

Table 44.6
Age-Specific Prevalence of Image Findings in Asymptomatic Patients
Based on Brinjikji, W., Luetmer, P.H., Comstock, B., Bresnahan, B.W., Chen, L.E., Deyo, R.A., Jarvik, J.G., 2015. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am. J. Neuroradiol. 36(4), 811–816. http://dx.doi.org/10.3174/ajnr.A4173 .
Finding 20 years (%) 30 years (%) 40 years (%) 50 years (%) 60 years (%) 70 years (%)
Disk degeneration 37 52 68 80 88 93
Disk signal loss 17 33 54 73 86 94
Disk height loss 24 34 45 56 67 76
Disk bulge 30 40 50 60 69 77
Disk protrusion 29 31 33 36 38 40
Annular fissure 19 20 22 23 25 27
Facet degeneration 4 9 18 32 50 69
Spondylolisthesis 3 5 8 14 23 35

Management of the Patient With Chronic Pain

Chronic pain is complex, involves multiple mechanisms, and affects multiple facets of the patient’s life. As such, a multimodal approach is typically employed for the management of chronic pain. This involves pharmacological modalities, rehabilitative approach, psychological approaches, and interventional techniques, all aimed, often concomitantly, at improving patient well-being and restoring function.

Pharmacological Modalities

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