|
| A) | men than women. | ||
| B) | those with higher family income. | ||
| C) | persons 18 to 44 years of age compared with those 45 to 64 years of age. | ||
| D) | non-high school graduates than those with a Bachelor's degree or higher. |
In 2018, 29% of adults reported LBP in the past three months. The prevalence was slightly greater for women (30.7%) than men (27.4%) and among those with lower educational attainment (33.9%), defined as non-high school graduates, compared with those with a Bachelor's degree or higher (25.5%) [9]. Persons older than 75 years of age were more likely to report past-three-month LBP (37.3%) compared with 36.5% of adults 65 to 74 years of age and 33.0% of adults 45 to 64 years of age. This is followed by adults 18 to 44 years of age, of whom 24.4% reported LBP. Lower family income (35.1% in ≤$35,000, 23.8% in ≥$100,000) and poverty status (35.6% in poor, 27.3% in non-poor) also appear to be factors, likely related (at least in part) to the type of work typical of the group [9]. White women are more likely to report LBP (32.2%) compared with African American women (31.2%) and Hispanic women (28.5%). Among men, the highest prevalence of LBP occurs among White men (29.2%) compared with Hispanic men (25.7%) and African American men (22.2%) [9].
| A) | 0.1% to 0.2% | ||
| B) | 2% to 5% | ||
| C) | 12% to 15% | ||
| D) | 32% to 35% |
An estimated 12% to 15% of annual healthcare provider visits in the United States are related to LBP [18]. The estimated 8% of patients whose LBP is chronic and debilitating account for 50% of direct medical expenditures for back pain, estimated at $85 billion [13,19]. Together with costs from decreased wages and lost productivity, the total is $100 to $200 billion [20].
| A) | Obesity | ||
| B) | Poverty | ||
| C) | Smoking | ||
| D) | Job dissatisfaction |
Risk factors for developing LBP can be generally categorized as nonmodifiable, such as old age, female sex, poverty, and lower education level, and modifiable, including higher body mass index (BMI), smoking, lower perceived general health status, physical activity (e.g., bending, lifting, twisting), repetitive tasks, job dissatisfaction, and depression. The greatest contributors to LBP episodes are single-event or repetitive exposures to mechanical stress and age-related degenerative spinal changes. With chronic LBP, mechanical and biophysiologic factors play a minimal secondary role to the primary contribution from psychosocial factors [25].
| A) | Obesity is more likely to predate LBP. | ||
| B) | There is no relationship between obesity and LBP. | ||
| C) | Obesity is more likely to follow the development of LBP. | ||
| D) | Obesity and LBP occur in tandem as the pain becomes chronic. |
Obesity contributes to factors that promote the development of some pain states, including LBP. Persons with LBP exhibit abnormal movement patterns that include gait and postural dysfunction, increased thoracolumbar stiffness, decreased proprioception, and alteration in abdominal and extensor muscle activation. Pain can result from joint or structural damage due to aberrant or increased biomechanical forces over time. These processes are accelerated by obesity, and regardless of age, obesity contributes to chronic LBP, mobility impairment, and ultimately physical disability. The relationship between obesity-related LBP and functional decline is mediated by skeletal muscle strength deterioration, systemic inflammation, and psychosocial characteristics, such as pain catastrophizing, kinesiophobia, and depression. Morbid obesity greatly alters biomechanical forces on lower back tissues to accelerate the development of chronic back pain syndromes [27].
Overweight and obesity are risk factors for both lumbar radicular pain and sciatica, and a direct relationship exists between BMI and low back pathology and pain in men and women. A meta-analysis of 28 studies found overweight and obesity were associated with lumbar radicular pain, increased the risk of hospitalization for sciatica, and increased the risk of lumbar disk herniation surgery. These associations were similar for men and women [28]. Clarification of whether or not LBP precedes obesity was addressed by an 11-year longitudinal study of 25,450 individuals. Among those without LBP at baseline, a significant positive association was found between BMI ≥30 and risk of LBP in men and women, and risk of chronic LBP recurrence in women, but not men. In contrast, LBP at baseline had little effect on later changes in BMI [29].
| A) | calcium. | ||
| B) | vitamin C. | ||
| C) | vitamin D. | ||
| D) | vitamin E. |
Interest in the role of vitamin D deficiency in pain was spurred by findings of highly prevalent vitamin D deficiency among primary care patients with persistent, nonspecific musculoskeletal pain refractory to pharmacotherapy [34]. Pain patients with vitamin D deficiency also require twice the opioid dosing for substantially greater duration versus non-deficient patients [35].
| A) | Excessive focus on pain | ||
| B) | Adaptive coping strategies | ||
| C) | Low levels of "fear avoidance" behaviors | ||
| D) | Expectation that active treatment is beneficial |
Psychosocial factors for developing chronicity include [39,40,41,42]:
Negative belief that pain is harmful or potentially severely disabling
High levels of "fear avoidance" behaviors
Poor or maladaptive coping strategies
Expectation that passive, rather than active, treatment is beneficial
Excessive focus on pain
High emotional distress levels
Depressed mood, low morale, and social withdrawal
Resistance to change
Low self-efficacy
Family reinforcement of illness behavior
Concurrent social or financial problems
Troubled childhood (e.g., abuse, parental death, addiction)
| A) | modestly improved outcome. | ||
| B) | double the rates of negative outcome. | ||
| C) | no effect on rates of positive outcome. | ||
| D) | roughly double the rates of positive outcome. |
Psychosocial factors of poor outcomes in lumbar surgery include mood disorders, unresolved litigation or claims, history of child abuse, and maladaptive pain coping or beliefs [53]. The predictive power of these variables on surgical outcomes surpasses radiographic findings, neurologic signs, and other medical indices. Psychologic screening of implantable neuromodulation device candidates increased successful outcomes from 33% to 70% and is now standard protocol. In outcome studies of spinal cord stimulation in patients with failed back surgery syndrome, inadequate psychologic screening was associated with 50% short-term and 35% long-term benefit, while adequate psychologic screening led to 85% short-term and 60% long-term success rates [53].
| A) | By 12 weeks, 80% to 90% attain remission. | ||
| B) | Most patients with favorable prognosis do not seek medical care. | ||
| C) | Very few patients with persistent pain at three months recover after one year. | ||
| D) | Only 10% of patients with LBP who initially improve following medical care experience recurring pain episodes. |
The most commonly cited short-term prognosis data state that most patients with acute LBP recover in a matter of weeks with limited or no therapy; specifically, 60% to 70% of patients recover by 6 weeks and 80% to 90% by 12 weeks [25,56]. These early prognosis projections are at variance with data derived from a study of patients presenting to primary care providers with nonspecific acute LBP [57]. This study found that 33% of patients experienced spontaneous resolution by 3 months, 57% still had problematic pain at 6 months, and 65% reported some degree of pain at 12 months after onset. Of patients with persistent pain at 3 months, only 1% to 7% experienced recovery 3 to 12 months from onset [57].
This study confirmed the impression of experienced clinicians that the clinical course of most patients with acute LBP in a primary care practice does not conform to the conventional notion that nonspecific acute LBP has a favorable natural history and resolves within several weeks [58]. The reason for this discrepancy may be that most patients who develop acute LBP with favorable prognosis do not seek medical care [59]. In those seeking care, pain and disability can be ongoing and recurrent pain episodes may be common. Up to 70% of patients who initially improve following medical care experience recurring pain episodes [58].
| A) | is a symptom of a larger disease process. | ||
| B) | is now understood to be a unifactorial entity. | ||
| C) | severity is determined by the extent of peripheral tissue damage. | ||
| D) | reflects the uncoupling of pain from its original peripheral origin. |
Chronic LBP reflects the uncoupling of pain from its original peripheral origin; it is a distinct disease process rather than a symptom [61]. Likewise, the extent of peripheral tissue damage is no longer viewed as the sole determinant of pain presence, severity, and duration. Chronic LBP is now understood as a multifactorial entity determined by inputs from numerous and complex electrochemical, biocellular, cognitive, and emotional factors. The broad range of individual pain responses to stimuli reflects the highly individualistic phenomenon of pain [63,64].
| A) | a physiologic response to tissue injury. | ||
| B) | the result of central nervous system injury. | ||
| C) | strictly pathologic and has no adaptive function. | ||
| D) | a perception that arises from activation of the immune response. |
Pain is broadly categorized as nociceptive, inflammatory, neuropathic, or centralized. Nociceptive and inflammatory pain overlap and result from peripheral tissue injury, damage, or disease. Both are protective and adaptive for survival when acute but are considered pathologic when pain continues after peripheral tissue healing. Neuropathic pain results from injury, damage, or disease to peripheral nervous structures or sensory pathways in the spinal cord or brain, and regardless of duration, it is pathologic. Centralized pain reflects aberrant function in various CNS pathways and is now thought to account for fibromyalgia, irritable bowel syndrome, and other chronic conditions [65,66]. Centralized pain is not associated with any common back pain condition or peripheral tissue injury and therefore is not discussed further in this course. These pain subcategories are not distinct and do not account for individual variations. Many cases of chronic LBP represent a mixture of pain subcategories [65].
| A) | Pain severity accurately reflects tissue state. | ||
| B) | Pain is modulated only by peripheral nociceptive signaling. | ||
| C) | The relationship between pain and tissue state strengthens as pain persists. | ||
| D) | Pain represents a conscious correlate of the implicit perception that tissue is in danger, not the actual tissue state. |
Neuroscience findings have refuted previous assumptions of back pain pathophysiology. Healthcare providers should understand these changes in how pain is conceptualized, because the management of LBP can hinge on proper matching of pain pathophysiology and treatment mechanism. Effective chronic LBP management requires replacement of several entrenched paradigms with the following [67]:
Pain is not an accurate measure of tissue state.
Pain is modulated by multiple factors across somatic, psychologic, and social domains.
The relationship between pain and tissue state further weakens as pain persists.
Pain represents a conscious correlate of the implicit perception that tissue is in danger, not the actual tissue state and not the actual threat to tissue.
| A) | GABA | ||
| B) | NMDA | ||
| C) | Serotonin | ||
| D) | Sodium channel |
The process of central sensitization begins when post-synaptic terminals of ascending neurons in the dorsal horn become altered by nociceptive barrage. The surge of excitatory signaling transmitters and modulators (e.g., glutamate, substance P, CGRP, BDNF) bind to receptors on spinal cord neurons and activate intracellular signaling pathways, which phosphorylate membrane channels of the glutamate receptors N-methyl-D-aspartate receptor (NMDA) and AMPA. This lowers the threshold and opening characteristics of the channels and results is increased CNS neuron excitation, substantial increase in pain transmission, and the development of central sensitization. The greatest contribution to initiation of central sensitization comes from post-synaptic NMDA receptor activation in the spinal cord and, subsequently, in the thalamus, limbic system, and cerebral cortex [87,88,89,90].
| A) | relying on others to resolve the pain. | ||
| B) | active participation in one's pain management. | ||
| C) | exaggerated negative thoughts and emotions surrounding pain. | ||
| D) | exaggerated complaints regarding one's pain in order to obtain opioids. |
The contribution of psychologic factors to chronic LBP is essential to consider, as discussed. Depressive symptoms, pain catastrophizing, and fear avoidance in LBP are thought to enhance pain facilitatory pathways in the CNS, resulting in sensitization of dorsal horn spinal cord neurons and the development of exaggerated pain perception [86]. Pain catastrophizing refers to exaggerated negative thoughts and emotions surrounding pain, and this pain coping style significantly contributes to variability in pain perception. Catastrophizing adversely impacts pain by inducing an aroused, negative emotional state that worsens pain and fosters helplessness that decreases adaptive pain responding. This promotes the alteration of neural processes related to pain attention and response. People with trauma histories are more likely to catastrophize, suggesting that catastrophizing may mediate the effects of earlier psychologic stress on pain [62].
| A) | lumbar radiculopathy. | ||
| B) | lumbar spinal stenosis. | ||
| C) | myofascial pain syndrome. | ||
| D) | degenerative lumbar disk disease. |
Lumbar spinal stenosis: Narrowing of the central or lateral recesses of the spinal canal and/or the neural foramina [127].
| A) | Central sensitization | ||
| B) | Altered biomechanics | ||
| C) | Improper surgical technique | ||
| D) | Normal age-related structural changes |
Failed back surgery syndrome: Failed back surgery syndrome is not a single entity, but a complex syndrome with multiple potential causalities, including structural pathogenesis, improper surgical technique, altered biomechanics, and/or central sensitization [55,124].
| A) | The majority of LBP cases lack apparent etiology. | ||
| B) | Most LBP cases are associated with serious pathology. | ||
| C) | Roughly 85% of LBP is the result of bulging lumbar disk. | ||
| D) | LBP is associated with specific, defining radiographic abnormalities. |
Roughly 85% of LBP lacks apparent etiology and is termed nonspecific. Clinical practice guidelines for LBP recommend assessment of new patients by triage, with LBP grouped as nonspecific, potentially serious, associated with radiculopathy or spinal stenosis. Several LBP syndromes and conditions have been studied with radiographic imaging (usually MRI) in an effort to establish causality. These include lumbago, myofascial syndrome, muscle spasm, mechanical LBP, lumbar strain, facet joint dysfunction, and bulging lumbar disk. No specific, defining radiographic abnormality has been identified. These conditions, often presenting as acute LBP, are considered vague and nonspecific, and imaging studies are of limited value in establishing the cause, directing therapy, or predicting the clinical course. As an example, many persons with lumbar spine degenerative change or disk protrusion evident on MRI are not experiencing LBP. Thus, some abnormalities detected by MRI are nonspecific and of uncertain relevance to the patient's complaint. A diagnostic imaging workup does not improve clinical outcomes in most patients with acute LBP [60].
While most LBP cases lack serious pathology, each case is deserving of a careful clinical assessment for symptoms and signs (termed "red flags") associated with serious pathology. Patients with red flags are redirected to urgent diagnostic workup and intervention. Patients without red flags should be assessed for the possibility of radiculopathy and lumbar spinal stenosis, which, with diagnostic confirmation, may require early specialist referral. LBP may be classified as nonspecific when there are no red-flag indicators, radiculopathy, or suspicion of lumbar spinal stenosis. Once red flag indicators are excluded, all patients should be evaluated for risk factors of poor prognosis and chronicity ("yellow flags"). Patients with yellow flags should receive psychosocial intervention to minimize chronification and disability. Patients with painful recurrence following LBP remission require assessment of new-onset LBP [41,124,138].
| A) | Saddle anesthesia | ||
| B) | Gait disturbances | ||
| C) | Age older than 70 years | ||
| D) | Unexplained weight loss in the past six months |
RED FLAG ASSESSMENT IN PATIENTS WITH LOW BACK PAIN
| Possible Etiology | Red Flags | ||||||
|---|---|---|---|---|---|---|---|
| Malignancy |
| ||||||
| Vertebral fracture |
| ||||||
| Cauda equina syndrome |
| ||||||
| Vertebral infection |
|
| A) | malignancy. | ||
| B) | vertebral fracture. | ||
| C) | vertebral infection. | ||
| D) | cauda equina syndrome. |
RED FLAG ASSESSMENT IN PATIENTS WITH LOW BACK PAIN
| Possible Etiology | Red Flags | ||||||
|---|---|---|---|---|---|---|---|
| Malignancy |
| ||||||
| Vertebral fracture |
| ||||||
| Cauda equina syndrome |
| ||||||
| Vertebral infection |
|
| A) | Positive tests with distraction | ||
| B) | Non-anatomic motor or sensory loss | ||
| C) | Non-anatomic superficial tenderness | ||
| D) | Verbal over-reaction or exaggerated body language |
In addition, there is a group of physical signs that may indicate an underlying non-organic or psychologic basis for LBP. This group of signs, termed Waddell signs, includes [41]:
Non-anatomic superficial tenderness
Positive simulation tests (i.e., pain from axial loading and en bloc rotation)
Non-positive tests with distraction (e.g., no pain with full knee extension while seated, but supine straight leg raise is markedly positive)
Non-anatomic motor or sensory loss
Verbal over-reaction or exaggerated body language
| A) | Differentiation is straight-forward. | ||
| B) | The definition of radicular pain is inconsistent. | ||
| C) | This patient grouping scheme relies heavily on pain mechanism. | ||
| D) | None of the above |
Most guidelines for chronic LBP recommend a diagnostic triage to group patients by nonspecific, specific, and radicular LBP. This differentiation is not straightforward; patients with disk herniation are either grouped as specific with radicular pain or nonspecific with degenerative disk disease without radicular pain. Also, the definition of radicular pain is inconsistent.
To address these and other limitations with the triage approach, an alternative classification system for chronic LBP was developed to differentiate patients with pain of nociceptive, peripheral neuropathic, or central sensitization origin using a mechanism-based classification of LBP signs and symptoms [155]. The system was developed and validated using data from 464 patients with a range of back and leg symptoms; the majority had pain duration longer than three months (chronic). Factors with the greatest predictive ability for each of the three back pain mechanisms include [155,156,157]:
Clear and proportionate mechanical/anatomical nature to aggravating and easing factors
Usually intermittent and sharp with movement or mechanical provocation
At rest, tends to be a constant dull ache or throbbing pain
The absence of dysesthesia, disturbed sleep, antalgic postures, and pain of a burning, shooting, or electric shock-like quality
Pain referred in a dermatomal or cutaneous distribution
History of nerve injury, pathology, or mechanical compromise
Pain or symptom provocation with mechanical or movement tests that move, load, or compress neural tissue
Disproportionate, nonmechanical, unpredictable pattern of pain provocation by multiple nonspecific aggravating or easing factors
Pain disproportionate to the extent of injury or pathology
Strongly associated with maladaptive psychosocial factors, such as negative emotions, poor self-efficacy, and maladaptive pain beliefs and behaviors
Diffuse non-anatomic areas of pain tenderness on palpation
| A) | The absence of dysesthesia and antalgic postures | ||
| B) | Pain disproportionate to the extent of injury or pathology | ||
| C) | History of nerve injury, pathology, or mechanical compromise | ||
| D) | Pain usually intermittent and sharp with movement or mechanical provocation |
To address these and other limitations with the triage approach, an alternative classification system for chronic LBP was developed to differentiate patients with pain of nociceptive, peripheral neuropathic, or central sensitization origin using a mechanism-based classification of LBP signs and symptoms [155]. The system was developed and validated using data from 464 patients with a range of back and leg symptoms; the majority had pain duration longer than three months (chronic). Factors with the greatest predictive ability for each of the three back pain mechanisms include [155,156,157]:
Clear and proportionate mechanical/anatomical nature to aggravating and easing factors
Usually intermittent and sharp with movement or mechanical provocation
At rest, tends to be a constant dull ache or throbbing pain
The absence of dysesthesia, disturbed sleep, antalgic postures, and pain of a burning, shooting, or electric shock-like quality
Pain referred in a dermatomal or cutaneous distribution
History of nerve injury, pathology, or mechanical compromise
Pain or symptom provocation with mechanical or movement tests that move, load, or compress neural tissue
Disproportionate, nonmechanical, unpredictable pattern of pain provocation by multiple nonspecific aggravating or easing factors
Pain disproportionate to the extent of injury or pathology
Strongly associated with maladaptive psychosocial factors, such as negative emotions, poor self-efficacy, and maladaptive pain beliefs and behaviors
Diffuse non-anatomic areas of pain tenderness on palpation
| A) | Avoid twisting and bending. | ||
| B) | Stay active and avoid bed rest. | ||
| C) | Use heat or ice packs, whichever provides the most comfort. | ||
| D) | All of the above |
When a patient presents with LBP of less than four to six weeks, the mainstays of management are patient education, reassurance, and advice on self-management. Patients should be assured that prognosis is generally good, often resolving with little intervention. Self-care recommendations include [1,40,41,138,140]:
Stay active, avoid bed rest, and return to normal activities as tolerated.
Avoid twisting and bending.
Use heat or ice packs, whichever provides the most comfort.
| A) | tramadol. | ||
| B) | long-acting opioids. | ||
| C) | NSAIDs and muscle relaxants. | ||
| D) | benzodiazepines combined with ibuprofen or amitriptyline. |
The pharmacotherapy with the strongest evidence for myofascial pain is benzodiazepines combined with ibuprofen or amitriptyline (not as monotherapy) [130,172,173]. Second-line options include topical methyl salicylate, menthol, and diclofenac patch. Although antiepileptics, antidepressants, muscle relaxants, NSAIDs, and tramadol are widely used, they are largely lacking evaluation.
| A) | NSAIDs | ||
| B) | Imipramine | ||
| C) | Amitriptyline | ||
| D) | Acetaminophen |
Acetaminophen is recommended for initial and ongoing treatment of persistent musculoskeletal back pain in older patients [176]. There is a strong recommendation against the use of NSAIDs, amitriptyline, and imipramine due to the possible adverse effects. Systemic corticosteroids should only be used in pain from systemic inflammatory disease or metastatic bone pain.
| A) | It is intended for use in patients with central sensitization. | ||
| B) | It explains to patients with chronic LBP the mechanism that underlies their pain problem. | ||
| C) | It strives to reframe chronic LBP as resulting from CNS hypersensitivity, not tissue damage. | ||
| D) | All of the above |
With central sensitization present in chronic LBP, the brain produces pain, fatigue, and other "warning signs" of tissue harm without actual tissue damage or nociception. Explaining the mechanism of central sensitization with evidence from neuroscience to patients with chronic LBP is a therapeutic strategy known as therapeutic pain neuroscience education or TPNE [98,99].
TPNE helps patients with chronic pain understand their pain and make sense of the lack of objective biomarkers or imaging findings. A main goal is changing pain beliefs through the reconceptualization pain. This involves patient knowledge that pain persists without tissue damage, is disproportionate to tissue damage and/or that tissue damage (and nociception) does not by itself result in pain. The distinction between "hurting versus harming" is addressed [98,99].
Exercises and physical activity are introduced under time-contingent (e.g., perform for five minutes regardless of pain) instead of symptom-contingent (e.g., stop when painful) conditions. Research shows that symptom-contingent approaches can facilitate brain production of nonspecific warning signs, while time-contingent approaches can deactivate brain-orchestrated top-down pain facilitatory pathways. Reduced CNS hyperexcitability and increased prefrontal cortical volume have also been found in response to time-contingent therapy [179,180].
To reconceptualize pain and convince patients that CNS hypersensitivity, rather than tissue damage, is the likely cause of pain symptoms, TPNE is delivered in two to three sessions over two to three weeks. Potential patient misunderstanding of being told the pain is "all in their head" can be prevented by front-end coverage of pain neurophysiology and chronic pain, before discussing potential sustaining factors such as emotions, stress, illness perceptions, pain cognitions, and pain behavior [181].
| A) | To completely eradicate pain | ||
| B) | To improve patient-clinician communication | ||
| C) | To promote patient understanding, acceptance, and self-management | ||
| D) | To identify core brain regions that mediate effective pain management |
Interventions that use CBT include creative visualization, imagery, progressive muscle relaxation techniques, and problem-solving techniques. The goal of CBT is to promote patient understanding, acceptance, and self-management of chronic LBP through the development of adaptive coping behaviors and strategies, which eventually empowers the patient. CBT is effective for subacute and chronic LBP, and there is moderate-to-strong evidence for CBT use early in recovery in patients with specific biopsychosocial issues. Strong evidence indicates that CBT should be used in most patients with nonspecific LBP lasting longer than 12 weeks. Comparable outcomes have been found between fear-avoidance training and spinal fusion in chronic LBP. CBT is cost effective, adds 20% efficacy to usual rehabilitation, and reduces the duration of recurrence [60,201,202].
Studies have identified core brain regions that mediate effective cognitive interventions. These include increased rostral anterior cingulate cortex activation and decreased dorsal anterior cingulate cortex activation with cognitive distraction; involvement of the ventral lateral prefrontal cortex, mid-cingulate cortex, thalamus, amygdala, and post-central gyrus with cognitive reappraisal; and correlation of right anterolateral prefrontal cortex and the dorsal anterior cingulate cortex activation with increased self-control over pain [203,204,205].
| A) | physiatry. | ||
| B) | a pain specialist. | ||
| C) | an addiction specialist. | ||
| D) | a behavioral health specialist. |
BIOPSYCHOSOCIAL ASSESSMENT AND REFERRAL OF PATIENTS WITH CHRONIC LOW BACK PAIN
| Domain | Instrument | Measurement-Based Score | Step Care Referral | ||
|---|---|---|---|---|---|
| Pain intensity | Intensity numerical rating scale (1–10) | Score ≥7 without diagnosis/plan | Pain specialist | ||
| Pain interference | Interference numerical rating scale (1–10) | Score >4 | Physiatry, occupational therapy, and/or physical therapy or vocational rehabilitation | ||
| Mood | PHQ-4, PHQ-9, or PC-PTSD | PHQ-4 score ≥6 or PC-PTSD score ≥3a | Behavioral health specialist | ||
| Sleep quality | STOP-BANG | STOP-BANG score ≥3, high morphine equivalent dose, or the use of opioids and sedatives | Sleep specialist | ||
| Risk of opioid misuse | ORT | ORT score ≥8, more than four minor urinary drug test aberrancies, or any serious aberrancies | Addiction specialist | ||
| |||||
| A) | Education | ||
| B) | Physical reconditioning | ||
| C) | Medical and behavioral therapy | ||
| D) | All of the above |
Multidisciplinary pain programs are used for chronic LBP with the goal of restoring and improving physical and emotional functioning and quality of life. In contrast to other pain programs, multidisciplinary pain programs provide interdisciplinary care, with collaboration by providers from different program components to develop and implement patient care. Core components of multidisciplinary pain programs are medical and behavioral therapy, physical reconditioning, and education; adjunctive modalities can be added. Multidisciplinary pain programs are often viewed as the last resort for intractable pain, and many enrolled patients have exhausted most other non-invasive options. However, they may be considered earlier in the disease course. Multidisciplinary pain programs may improve chronic LBP outcomes by simultaneously addressing multiple contributing factors to chronic pain [214]. These programs cause few if any adverse effects, in contrast to surgery or long-term opioid therapy [215]. The biopsychosocial model of chronic pain (the theoretical basis of multidisciplinary pain programs) describes psychosocial factors as part of a complex system with dynamic and reciprocal inter-relationships between biologic, psychologic, and sociocultural factors that shape patient pain experience and therapeutic response [216].
| A) | placebo effect. | ||
| B) | endorphin release. | ||
| C) | stimulation of the fascia. | ||
| D) | inhibition of lipid peroxidation. |
According to the Colorado Division of Workers' Compensation, true and sham acupuncture improves function in patients with chronic low back pain as compared to usual care. Acupuncture reduces pain in patients with acute and chronic low back pain, as compared to sham acupuncture. Individuals with positive expectations of acupuncture likely experience enhanced treatment benefit.
(https://codwc.app.box.com/v/rule-17-exhibit-1 Last Accessed: July 25, 2022)Level of Evidence: Expert Opinion/Consensus Statement
Acupuncture is a Chinese medicine technique whereby needles are slightly inserted in particular points on the body to stimulate energy fields and meridians. There is now greater understanding of the mechanisms that mediate successful acupuncture therapy, specifically stimulation of the fascia, a web of connective tissue that envelops muscle fiber and surrounds, separates, and connects organs and allows them to slide past one another when necessary [233]. Thoracolumbar fascia mediates force transfer, and disruption of its self-regulatory features may contribute to LBP. Stimulation by acupuncture needles inserted into muscle fascia induces the realignment of fibroblasts [234,235,236].
A review of acupuncture randomized controlled trials in chronic LBP found significant reductions in pain and disability with acupuncture or sham acupuncture versus conventional therapy or no therapy; a significant difference in acupuncture versus no treatment or routine care at 8- and 12-week follow-up; and a significant improvement in pain, function, and quality of life with acupuncture versus routine care at three months. The results suggest benefit from acupuncture beyond improvement from usual care in chronic LBP [237]. Acupuncture was also evaluated in a low-income, urban healthcare setting in 226 patients with chronic pain (60% with chronic back pain). Treatment once weekly up to 18 weeks led to statistically significant but clinically modest improvements in pain and physical well-being [238]. Acupuncture has been found to be a cost-effective therapy for sub-acute or chronic LBP [195].
| A) | was free of risk for potential injury. | ||
| B) | showed a medium-to-large effect size in reducing disability and pain. | ||
| C) | was associated with a slight reduction in pain but no improvements in disability. | ||
| D) | found widely different treatment outcomes dependent on differences in yoga style. |
Yoga is an ancient discipline, originating in the Indian subcontinent, designed to restore balance and health to the physical, mental, emotional, and spiritual dimensions of the practitioner. Yoga has gained popularity in the United States, and proponents claim benefits from yoga that include reduced inflammation and decreased heart rate and blood pressure [244]. Yoga has also become increasingly used in patients with chronic musculoskeletal pain, including back pain, and has been investigated in several trials [245]. A review of randomized controlled trials in chronic LBP found that yoga showed a medium-to-large effect size in reducing disability and pain. The same benefits remained at follow-up, with somewhat smaller effect sizes. Despite differences in yoga style and duration in the reviewed trials, treatment outcomes were consistent [246]. Little is known of the mechanisms in yoga benefit [247]. Generalizability to diverse populations was assessed in 95 low-income urban minorities with moderate-to-severe chronic LBP. Following 12 weeks of once- or twice-weekly yoga classes, both groups showed significant reductions in pain (30% and 36%, respectively) and disability (36% for both) [248].
Yoga is not free of potential injury. A survey of 1,336 yoga instructors found the most frequent and severe injuries involved the neck, lower back, shoulder, wrists, and knees. Risk factors for yoga injury include poor technique or alignment, previous injury, excessive effort, and improper instruction. Specific yoga forms were associated with specific injuries, including neck injuries from headstand and shoulder stand, and low back injuries from forward bends, twists, and backbends. Recommendations to reduce yoga injuries include population-specific instructor training, appropriate placement of new students, improved understanding of appropriate effort levels, improved teacher detection of overzealous students and improper alignment, and the use of assistants to watch for overzealous and poorly aligned students in large classes [249].
| A) | deep breathing exercises and guided imagery. | ||
| B) | exercise therapy in a room with an oxygen- ozone gas mixture. | ||
| C) | the percutaneous administration of an oxygen-ozone gas mixture. | ||
| D) | the topical application of corn or nut oil subjected to an accelerated peroxidation process. |
Ozone (O3) is an allotropic form of oxygen primarily used in Europe as an alternative treatment option for patients with LBP from disk herniation. Ozone is administered percutaneously as an oxygen-ozone gas mixture at nontoxic concentrations of 1–40 mcg ozone per mL of oxygen. Proposed mechanisms of analgesia include anti-inflammatory and antioxidant action on the nucleus pulposus. The safety and efficacy of percutaneous ozone injection in LBP secondary to disk herniation was reviewed using four randomized controlled trials and eight observational studies. Based on pain reduction at six-month follow-up, the authors strongly recommended intradiscal and paravertebral ozone therapy [263].
| A) | unrelated to outcome. | ||
| B) | a negative predictor of outcome. | ||
| C) | modestly associated with outcome. | ||
| D) | directly responsible for positive outcomes. |
Likewise, in acupuncture-naïve patients with chronic LBP, higher pre-treatment expectations for success did not predict pain or functional improvement. An association did develop with ongoing treatments, but positive pre-treatment attitude toward acupuncture was not associated with superior outcomes [270].
| A) | Non-selective NSAIDs are more effective than coxibs. | ||
| B) | NSAIDs are effective in reducing acute, but not chronic, LBP. | ||
| C) | A small proportion of patients (about 10%) preferentially respond to a specific NSAID. | ||
| D) | NSAIDs have a ceiling effect, where further dose escalation increases side effects but not analgesia. |
NSAIDs are effective in reducing acute LBP and pain associated with several chronic LBP conditions, though no benefit has been found in LBP with radiating symptoms [284]. The data on acute LBP are less convincing than with non-radicular chronic LBP, but, given the toxicity potential with acetaminophen, NSAIDs seem preferable in acute LBP [273]. NSAIDs have a ceiling effect, where further dose escalation increases side effects but not analgesia [285]. Analgesic efficacy between coxibs and non-selective NSAIDs is comparable, and consistent differences in pain reduction for specific NSAIDs have not been found [284]. For unknown reasons, up to 70% to 80% of patients preferentially respond to a specific NSAID. Response cannot be predicted, but some patients lacking response to one NSAID will achieve full benefit from another [286].
| A) | Doxepin | ||
| B) | Imipramine | ||
| C) | Nortriptyline | ||
| D) | Amitriptyline |
In chronic LBP, nortriptyline and desipramine are preferred over amitriptyline and imipramine as they show fewer side effects with comparable efficacy. TCA advantages include once-daily dosing and low cost [289]. However, TCAs exhibit a wide range of adverse effects, which differ among the various agents. Common adverse effects include anticholinergic effects, antihistaminergic effects, and orthostatic hypotension (α-1 adrenergic receptor blockade). Anticholinergic side effects include urinary retention, dry mouth, and constipation. Cardiac complications are described as a possible TCA side effect in patients with a history of coronary artery disease, more likely with doses greater than 100 mg/day. Potential side effects and overdose risks should be considered when prescribing antidepressants for chronic LBP; in TCAs, risks include weight gain, driving impairment, falls, and greater overdose lethality potential than other analgesic antidepressants [285,291].
| A) | Nausea | ||
| B) | Diarrhea | ||
| C) | Sialorrhea | ||
| D) | Weight gain |
The use of opioids to manage acute and cancer pain is established and relatively straightforward, but their appropriateness for chronic pain is sometimes disputed [215]. The most common side effects are dry mouth, constipation, and nausea. A substantial minority of subjects in randomized controlled trials of opioids for chronic noncancer pain drop out due to side effects (20% to 30% with opioids vs. 5% to 15% with placebo) [215].
| A) | Piroxicam | ||
| B) | Ketoprofen | ||
| C) | Diclofenac | ||
| D) | Indomethacin |
Of all topical NSAIDs, diclofenac has the most evidence supporting its use and is the sole NSAID with FDA approval for topical use. Approved formulations include diclofenac sodium 1% and 3% gel, diclofenac sodium 1.5% topical solution in 45.5% dimethyl sulfoxide, diclofenac epolamine topical patch 1.3%, and diclofenac sodium topical solution 2% [328,338]. Topical diclofenac has shown efficacy in pain reduction superior to placebo; comparable to topical NSAIDs indomethacin, ketoprofen, and piroxicam; and comparable to oral NSAIDs diclofenac, ibuprofen, and naproxen. The effectiveness, safety, and tolerability of topical diclofenac support its use for a variety of inflammatory chronic back pain conditions [335,339]. Randomized controlled trials of diclofenac applied three times daily showed that benefits began at 1 week, were fully apparent by 4 weeks, and were maintained to 12 weeks [340].
| A) | highly effective for spinal stenosis. | ||
| B) | the preferred option for refractory LBP. | ||
| C) | not a useful modality for any type of LBP. | ||
| D) | possibly effective for chronic, predominantly unilateral LBP. |
A single-blind, randomized clinical trial study of 50 patients with refractory chronic LBP similarly assigned patients to receive either botulinum toxin or saline injections in the paraspinal muscles where the pain localized [367]. After four weeks, 76% of the participants receiving botulinum reported improvements in pain, compared with 20% of patients receiving saline. After eight weeks, the botulinum treatment group was significantly more likely to report improvements in functionality (68% vs. 12%) [367]. The American Academy of Neurology has concluded botulinum toxin A is possibly effective for chronic, predominantly unilateral LBP, but its role in chronic LBP treatment should be clarified by larger randomized controlled trials in homogenous populations [368,369].
| A) | muscle spasm. | ||
| B) | herniated disk. | ||
| C) | cauda equina syndrome or severe or progressive motor weakness. | ||
| D) | strain of a ligament supporting the back. |
Roughly 80% of patients evaluated by neurosurgeons are referred for spinal pain, but surgery is indicated in fewer than 10% [383]. In many cases, primary care providers lack an understanding of back pain amenable to surgery. Patients in pain may wait for extended periods for initial consult, only to be sent back to primary care; improved knowledge can limit inappropriate patient referral. Spinal surgery in acute LBP is limited to patients with severe or progressive motor weakness or cauda equina syndrome. Surgical options and appropriate chronic LBP indications include spinal compression surgery, fusion surgery, and disk arthroplasty [383,384].
| A) | spinal stenosis. | ||
| B) | herniated disk. | ||
| C) | non-radicular chronic LBP. | ||
| D) | failed back surgery syndrome. |
Epidural steroid injection involves corticosteroid plus local anesthetic injection into the space between the dura and the spine. Arachidonic acid release from tissues is induced by phospholipase A2. Metabolism of arachidonic acid by the COX and lipoxygenase pathways generates prostaglandins, prostacyclins, thromboxanes, and leukotrienes. Prostaglandins and other arachidonic acid byproducts initiate or exacerbate pain by inducing inflammation and sensitizing peripheral nociceptors. Corticosteroids inhibit phospholipase A2, accounting for their anti-inflammatory properties. Steroids may also inhibit pain by suppressing ectopic discharge from injured nerve fibers and blocking conduction of normal unmyelinated C fiber [385].
| A) | Pain provider reimbursement | ||
| B) | Poor evidence base in most treatment approaches | ||
| C) | Declining access to multidisciplinary pain programs | ||
| D) | All of the above |
The International Association for the Study of Pain has identified areas of crisis in pain care in the United States: poor evidence base in most treatment approaches; inadequate primary care provider pain education; the unknown value of opioid therapy for chronic pain; pain provider reimbursement; and declining access to multidisciplinary pain programs [5].