Advertisement
Feature

A Patient-Centered Approach to Low Back Pain: Science and Strategies

Pooja Amy Shah, MD

Author:
Pooja Amy Shah, MD

Citation:
Shah PA. A patient-centered approach to low back pain: science and strategies. Consultant. 2017;57(12):685-690.


 

ABSTRACT: Low back pain (LBP) is common, very costly, and presents a diagnostic and treatment challenge. This article offers strategies for primary care providers in evaluating patients with LBP, including the crucial components of a comprehensive history and physical examination. It offers an approach to triaging patients’ symptoms as acute, subacute, or chronic, and then classifying LBP as specific, radicular, or nonspecific. It discusses the development of multimodal treatment plans that include patient education, self-care, and pharmacologic and nonpharmacologic therapies, and it proposes the adoption of a more patient-centered approach to the evaluation and treatment of patients with LBP.

KEYWORDS: Low back pain, acute low back pain, chronic low back pain, specific low back pain, nonspecific low back pain, radicular low back pain, patient-centered medicine


 

Low back pain (LBP) is ubiquitous and costly and poses a great burden to society worldwide.1 Studies suggest that as much as 80% of the population will experience LBP at some time in their life.2 In 2012, the National Institutes of Health estimated that more than half of all US adults had a musculoskeletal pain disorder, of whom one-fifth reported having LBP.3 In developed and developing countries alike, LBP is the leading cause of disability.4 Nevertheless, most LBP episodes are self-limiting and are not related to serious disease. More than 85% of patients seen in primary care will have nonspecific LBP, meaning that the LBP is without an identifiable specific underlying condition.5

The overarching definition of LBP is unambiguous: pain, muscle tension, or stiffness, with or without radicular symptoms, localized below the costal margin and above the inferior gluteal folds. However, that is where any straightforwardness ends. LBP is actually a symptom—similar to dizziness, cough, or headaches—and is not a disease entity within itself.6 The anatomy of the back and spinal structures is complex and includes bones, facet joints, intervertebral disks, ligaments, tendons, spinal cord and nerve roots, paravertebral muscles, fascia, and blood vessels. The risk factors for developing back pain are pervasive and multidimensional and include biomechanical determinants, general medical and psychological health, socioeconomic status, and occupational environmental factors.7 It is now commonly accepted that the correlation is weak between a patient’s symptoms and pathological changes revealed on imaging. Furthermore, pain physiology is complicated, deeply connecting the external environment with the body and mind.8 Individual patients’ belief systems about pain, as well as biological and psychosocial factors, have been shown to have a significant impact on the persistence of pain and the development of disability.9,10

Because of all of these factors, LBP is a diagnostic and treatment challenge for primary care providers and specialists alike. The dearth of clear anatomical correlation with LBP symptoms makes diagnostic evaluation frustrating for clinicians and patients. It is well known that patients seek care for LBP from not only their primary care physicians, but also a number of medical and nonmedical specialists, including sports medicine physicians, neurologists, physiatrists, orthopedic surgeons, neurosurgeons, rheumatologists, physical therapists, chiropractors, acupuncturists, massage therapists, bodyworkers, and yoga therapists.

This article offers strategies for primary care providers in evaluating patients with LBP. It provides an approach to triaging patients’ symptoms into a time-based framework of symptom duration, and then classifying the LBP into 3 categories: specific, radicular, and nonspecific. It discusses the development of multimodal treatment plans and proposes the adoption of a more patient-centered approach to the evaluation and treatment of patients with LBP.

Acute, Subacute, or Chronic LBP

Most authorities recommend staging LBP into time-dependent categories: acute, subacute, and chronic. Acute LBP is defined in most of the literature as pain lasting less than 6 weeks, although some studies use the 4-week mark. Subacute LBP lasts from 6 to 12 weeks. Chronic LBP persists for greater than 12 weeks.

When approaching acute LBP, health care providers must keep in mind that among patients who seek medical care, the pain and disability generally improve within the first month.11 Approximately two-thirds of people who recover from a first episode of acute LBP will have another episode within 12 months.12 Estimates in the literature suggest that approximately 10% to 15% of people affected by acute LBP develop chronic LBP with persistent symptoms at 1 year.13

The caveat here is that the literature and epidemiologic data also suggest that there is a need to revise common views regarding the course of LBP. Given that most persons with a first-time occurrence of LBP will have another episode, the designations of acute, subacute, and chronic pain may not be adequate to fully describe the nature of LBP. It may be helpful to think of any recurrent LBP as being on a chronic disease spectrum, fluctuating over time, with recurrences or exacerbations and periods of relative freedom from pain. Furthermore, it is also important to consider that LBP may be part of a larger, more widespread pain problem, such as fibromyalgia.1

NEXT: History

History

Obtaining a clear history from the patient with LBP is crucial. The clinician should document not only the common assessments of pain (eg, location, onset, quality, severity, timing, etc), but also several other components at each visit. These assessments include the following:

Subjective pain rating. Generally speaking, single-item pain-screening tools such as the numeric pain rating scale provide very limited information. In patients with chronic LBP, a multidimensional but still relatively rapid validated pain assessment tool, such as the 3-item PEG scale,14 is useful. The acronym PEG stands for average pain intensity (P), interference with enjoyment of life (E), and interference with general activity (G). It helps assess chronic pain intensity, emotional function, and physical function quickly in the primary care setting.

Functional status of the patient. This assessment includes evaluation of the patient’s ability to perform tasks that are required for living. It may include simple inquiry into how the patient gets out of bed, gets up and down stairs and to a chair; the patient’s ambulation status; and how the patient manages at work. It may also delve further to include a discussion of activities of daily living and instrumental activities of daily living, depending on the severity of the LBP.

Presence or absence of red flags. Red flags are indicators used when evaluating LBP to assess whether a patient needs referral and/or urgent treatment for potentially dangerous etiologies.15 A caveat here is that with any multifactorial entity such as LBP, considering single clinical features in isolation can be problematic. Red flag false-positives may be misleading, which are illustrated well in a 2009 study in which 80% of patients with acute LBP had at least 1 red flag present, but less than 1% had a medically serious disease.16 Relying on a combination of clinical features to identify individuals who require further diagnostic workup may be a more effective strategy and is recommended.17 Red flags include the following12:

  • Risk factors for neoplastic disease, such as a history of cancer with new-onset LBP; age greater than 50 years; unexplained weight loss; and failure to improve after 4 to 6 weeks of conservative therapy. Notably, cancer-associated LBP often does not improve with rest or recumbent posture and is often worse at night.18
  • Risk factors for spinal infection, such as intravenous drug use, immunosuppression, urinary infection, temperature greater than 38°C for more than 48 hours, and active tuberculosis or a history of tuberculosis.
  • Signs of cauda equina syndrome, such as new-onset urinary incontinence, painless urinary retention (if retention is absent, the likelihood of cauda equina syndrome is as low as 1 in 100019 to 1 in 10,00012), saddle anesthesia, and sensory or motor deficits.
  • Risk factors for fracture, such as osteoporosis, immunosuppression, history of prolonged corticosteroid use, older age, serious accident or injury with evidence of a contusion or abrasion, or fall or injury in the elderly patient.20,21

Psychosocial indicators. These include assessments of employment/disability status, substance abuse history (including tobacco), arc of pain recurrence or chronicity, and yellow flags. Yellow flags are historical psychosocial factors that are useful in identifying patients with chronic LBP who have a poor prognosis and that often indicate long-term chronicity and disability.22 Yellow flags include the following22:

  • The attitude that back pain is harmful or potentially severely disabling
  • Fear avoidance behavior and reduced activity levels
  • Expectation that passive treatment rather than active treatment will be beneficial
  • A tendency toward depression, low/negative morale, and social withdrawal
  • Social or financial problems or a history of trauma

Previous imaging and treatment. Assessment of prior imaging studies and prior treatments and responses to them is an important component of a patient’s LBP history.

It is important that the historical evaluation is robust and that documentation is precise so that the clinician’s assessment can be accurate and a clear groundwork can be laid for future LBP recurrences. The Institute for Clinical Systems Improvement’s 2012 guideline makes the following consensus statement12: “The initial exam should document evidence that would suggest the presence or absence of findings that would influence medical decision-making (neurologic deficits, muscle weakness, mental status affecting recovery, comorbid conditions) as well as establish a baseline for future comparisons.” Additionally, the clinician should attempt to take a wide-angle view of the patient’s pain history and document a comprehensive, gestalt assessment of the LBP.

Physical Examination

A full physical examination should be performed on initial evaluation and as indicated (to rule out nonback causes of LBP such as aortic aneurysm, nephrolithiasis, pyelonephritis, perinephric abscess, prostatitis, endometriosis, chronic pelvic inflammatory disease, pancreatitis, cholecystitis, penetrating ulcer, cardiac or pericardial disease, pulmonary or pleural disease, and pregnancy), and focused physical examinations should be performed subsequently.

The physical examination also includes informal observation—for example, a patient’s posture, facial expressions, pain behavior, asymmetric movements, and inconsistencies—and a focused examination of the back, including assessment of the following:

  • Stance and posture
  • Gait and mobility, including toe and heel raises and transitions between sitting, lying, and standing
  • Palpation to assess for localized tenderness, tightness, adhesions, scar tissue, and trigger points
  • Range of motion (flexion, extension, lateral flexion, and axial rotation)
  • Bilateral straight-leg raise tests (SLRs), a type of neural tension testing (Figure 1). The SLR is the primary test used to help diagnose lumbar disk herniation. A positive test reproduces the patient’s radicular pain symptoms. A negative SLR result is useful in ruling out a diskogenic source of pain, while a positive test result only provides supporting evidence of a disk pathology or nerve root pathology.12 Furthermore, a crossed (contralateral) SLR has higher specificity but lower sensitivity than the ipsilateral SLR, so combining the 2 tests may enable a better assessment of the patient’s radicular pain symptoms.23

Lower Back Pain

Figure 1: In the straight-leg raise test, an ipsilateral positive result occurs with reproduction of pain when the straight leg on the affected side is passively lifted to an angle between 30° and 70°. A cross or contralateral positive result occurs with reproduction of pain when the straight leg on the contralateral side is passively lifted to an angle between 30° and 70°.

In addition, a neurologic evaluation that includes focus on sensation, strength, and reflexes should be performed, along with psychosocial evaluation, including screening for depression and substance abuse.

NEXT: Diagnostic Triage

Diagnostic Triage

With careful history taking and physical examination, the primary care provider can distinguish between specific LBP (ie, the pain symptom has a specific cause), radicular nerve-root pain (ie, the pain is associated with specific historical and clinical findings consistent with radicular pain), and nonspecific LBP (ie, the pain has no clear pathoanatomical cause). The reason for this differentiation is crucial: Some etiologies of specific LBP and radicular pain are serious and warrant imaging, rapid referral, and immediate treatment. After serious conditions and specific causes of LBP have been ruled out, the primary care provider can safely approach the patient from the perspective of nonspecific LBP using a multimodal treatment approach.

Specific Pain

Specific LBP, including radicular etiologies, accounts for a minority (approximately 15%) of back pain cases.24 Less than 1% of these patients will have a serious systemic cause, such as metastatic cancer, spinal infection (eg, spinal epidural abscess, vertebral osteomyelitis), or spinal cord compression including cauda equina syndrome.24 Other less-serious nonradicular specific causes of LBP include osteoarthritis, vertebral compression fracture, ankylosing spondylitis, spinal curve deformities (eg, scoliosis), and congenital bony deformities. Some authors also include the controversial diagnosis of sacroiliac joint dysfunction as a specific cause of LBP.

Radicular Pain

Radicular pain differs from other types of pain by its quality. It is important to keep in mind that like most patients with acute LBP, patients with radiculopathic symptoms will have substantial improvements in their pain and function in the first 4 weeks.11 The most common cause of radicular pain is disk herniation, while disk rupture and spinal stenosis are more insidious causes. Studies suggest that within 8 weeks of onset, the majority of disk herniations regress or reabsorb.12

Inflammation of the affected nerve seems to be the critical pathophysiologic process of radicular pain.25 Physiologically, radicular pain is evoked by impulses flowing from a dorsal nerve root or its ganglion, it usually has a lancinating quality, and it travels along the length of the lower limb in a band approximately 5 to 8 cm wide.26 Squeezing or pulling normal nerve roots does not produce radicular pain; if nerve roots have previously been inflamed, mechanical stimulation of them can evoke radicular pain.25

When radicular pain is present in addition to acute or chronic LBP, clinicians may be more likely to order unnecessary diagnostic imaging studies.27 Imaging and referral to a spine specialist should be ordered only when patients are experiencing progressive or severe neurologic deficits.12 Guidelines suggest that clinicians order magnetic resonance imaging or computed tomography in a patient with chronic LBP with radiculopathy or possible spinal stenosis only if the patient is a potential candidate for surgery or epidural corticosteroid injection.28

Nonspecific Pain

Nonspecific LBP is defined as LBP of unknown cause (ie, not attributable to a recognizable or known specific pathology), and it accounts for the vast majority (approximately 85%) of LBP cases seen in primary care and specialist offices. As in other chronic musculoskeletal pain disorders, many factors have been identified as possible causes of nonspecific LBP; it is multifactorial, and psychosocial factors have a large role.

Chronic nonspecific LBP may include diverse conditions affecting muscles, bones, and/or joints of the limbs or the spine.29 In addition, inflammation, fascial conditions, and specific factors such as tumor necrosis factor α and nerve growth factors also have been implicated, all of which need further research to illuminate direct causal mechanisms.30,31

Mechanical factors do not seem to have a large causal role in LBP, contrary to common belief. A 2012 report on nonspecific LBP highlighted 8 systematic reviews and concluded that it was “unlikely that occupational sitting, awkward postures, standing and walking, manual handling or assisting patients, pushing or pulling, bending and twisting, lifting, or carrying were independently causative of LBP in the populations of workers studied.”13 Despite these findings, nonspecific LBP is often attributed to imprecise causes such as “sprain” or “strain.”

Imaging in Nonspecific LBP

Over the past 20 years, studies have concluded that diagnostic imaging investigations have no role in the management of nonspecific LBP because of the poor association between symptoms and anatomical findings. Indiscriminate imaging is costly and time-consuming, can cause unnecessary exposure to radiation, and may cause unnecessary harm to the patient.32,33

Most clinical guidelines for LBP propose that clinicians should not order imaging for any patient with nonspecific LBP. These guidelines are based on a number of studies, including a 2009 systematic review and meta-analysis of 6 trials showing that lumbar imaging for LBP without indications of serious underlying conditions does not improve clinical outcomes.34 Imaging is a direct cause of increasing LBP costs due to the cost of the radiologic studies as well as downstream cascading effects—it can lead to additional tests, follow-up, and referrals; improper labeling of the causative mechanism of the patient’s pain; and invasive or surgical procedures of limited or questionable benefit.35-37 During the clinical encounter, special focus should be placed on educating patients, managing their expectations, and addressing any biases in favor of unnecessary imaging.

NEXT: Multimodal Treatment Strategies

Multimodal Treatment Strategies

LBP treatments span the gamut from high-touch, hands-on approaches, to passive and active patient interventions, to oral, topical, and injected medications. Because nonspecific LBP does not have a known pathoanatomical cause, and because most people who experience it are likely to improve, treatment must be both accessible and acceptable to the individual patient. Rather than attempting to repair a cause of pain or eliminate it entirely, treatment strategies should focus on reducing pain, improving quality of life and overall function, and cultivating well-being (Figure 2). Management must be multimodal, consisting of reassurance and education, self-care, medications, nonpharmacologic therapies, and timely follow-up.

Lower Back Pain

Newer guidelines, such as the 2017 American College of Physicians (ACP) guideline on noninvasive treatments for acute, subacute, and chronic LBP, suggest that treatment of all patients with LBP should begin with nonpharmacologic approaches and, if desired, pharmacologic treatments can be considered initially only in cases of acute LBP.38 Studies of pharmacologic and nonpharmacologic treatment strategies most often have been small in size and of variable methodological quality.39 When compared with placebo, the effect sizes for most LBP treatments are small for both acute and chronic LBP.40 This may be in part related to the tendency of researchers to treat nonspecific LBP as a single homogenous condition rather than a heterogeneous entity that may preferentially respond to different treatment strategies.41 Keeping this information in mind, rather than viewing available treatment options as inefficacious, the clinician can view the options as a palette of treatment strategies that can be provided in a patient-centered way. Treatments can be selected based on the disposition of the patient and the availability of resources.

Patient Self-Care

All patients should be educated and encouraged to participate in self-care, which includes advice to stay active (avoid bed rest) and the application of superficial heat.38 Given that patients’ expectations are known to influence the outcome of treatment, patients require reassurance during every clinical encounter that the natural history of LBP is favorable.42 Reframing the pain from “How do we fix this problem?” to “How can we manage this problem?” is key.

Expectations about the use of diagnostic imaging should be managed aggressively using evidence-based data. Depending on patients’ literacy and interest, the use of up-to-date and accurate educational handouts and other materials can help to educate and manage expectations. One example of a useful handout is “Back Pain Tests and Treatments” from the Choosing Wisely campaign, an initiative of the American Board of Internal Medicine Foundation.43

NEXT: Nonpharmacologic Treatments

Nonpharmacologic Treatments

A plethora of nonpharmacologic LBP treatment options encompass manual/physical, psychobehavioral, and procedural therapies. A detailed discussion of these entities is beyond the scope of this article, but examples of nonpharmacologic treatments include massage, acupuncture, spinal manipulation (osteopathic and chiropractic), exercise therapy, multidisciplinary rehabilitation, tai chi, yoga and yoga therapy, motor control exercise, progressive relaxation, electromyography biofeedback, low-level laser therapy, operant conditioning therapy, spinal manipulation, myofascial bodywork, and dry needling. Trigger point injections, either with saline or lidocaine, may also be considered.44 Psychological and mind-body interventions such as mindfulness-based stress reduction and cognitive behavioral therapy have shown promise for significantly improving chronic pain management.45

Medications

Medications for LBP are geared toward analgesia and symptom management. A variety of oral and topical medications are used, with varying levels of efficacy, possible adverse effects, and potential for abuse. Choosing from among these agents requires a patient-centered approach, keeping in mind the patient’s other comorbidities, medications, and previously trialed treatments. Examples of these drugs include nonsteroidal anti-inflammatory drugs (NSAIDs), skeletal muscle relaxants, opioid and opioid-like medications, serotonin and norepinephrine reuptake inhibitors, and various topical agents.

Low-quality data show that acetaminophen is equivalent to placebo in efficacy for the treatment of acute LBP, and insufficient data exist for a clear recommendation for the use of acetaminophen in chronic and radicular LBP.46 Systemic corticosteroids are generally not recommended for acute, chronic, or radicular LBP.38 A discussion on opioids, cannabinoids, and low-dose naltrexone treatments is beyond the scope of this article, but they may be useful in a small subset of patients when their risks and benefits are carefully weighed.

The 2017 ACP guideline on noninvasive treatment of LBP suggests that only NSAIDs and spinal muscle relaxants should be used if a pharmacologic approach to acute LBP is chosen.38 Insufficient evidence exists to determine the effectiveness of opioids, antiseizure medications, antidepressants, and benzodiazepines in patients with acute or subacute LBP.38 The same guideline states that a patient with chronic LBP should start medications only if the patient has had an inadequate response to nonpharmacologic management.38 The decision-making process for the pharmacologic approach to chronic LBP can be thought of in a tiered manner: if no contraindications exist, start with NSAIDs; second-line therapy recommendations are tramadol or duloxetine; opioids should be used as a last resort and only after a careful assessment and discussion with the patient.38

A number of nonopioid topical medications are available, including many that are over-the-counter, but data are limited on their efficacy. This likely is why topical analgesics are popular among patients but do not have a good reputation among clinicians.47 The 2 most studied are topical capsaicin and topical NSAIDs, which have differing mechanisms of action. They can be trialed alone or in conjunction with the other therapies outlined above, as long as the clinician instructs patients on proper use, and the combination of topical and oral NSAIDs is avoided. Counterirritant medications such as menthol and camphor, and local anesthetics such as lidocaine, are also available over-the-counter.

Summary

Most LBP evades direct cause-and-effect diagnostic and treatment pathways, thus making it a challenging entity in medicine. LBP is common and very costly. Approaches to evaluation and treatment argue for a paradigm shift away from the default method of solely using imaging, medications, and surgery for the evaluation and treatment of pain. Comprehensive and well-documented patient histories and physical examinations are crucial, including assessments of red flags and yellow flags.

In most cases, acute LBP will improve on its own, but a small percentage of patients will move on to chronic pain. If a patient shows signs of chronic LBP, it is best for the clinician to ensure adequate focus on psychosocial and quality of life factors. Clinicians must always keep in mind that most LBP is nonspecific.

Using the patient-centered lens, clinicians have a large variety of tools with which to approach LBP. These include direct patient education, nonpharmacologic treatments (such as acupuncture, mindfulness-based stress reduction, and trigger point injections), and oral and topical medications. For the combination of LBP treatments to be as efficacious as possible, shared decision-making is key, ensuring that the chosen treatments are both accessible and acceptable to the patient. 

Pooja Amy Shah, MD, is an assistant professor, director of Integrative Medicine, and director of Musculoskeletal Education at the Columbia University College of Physicians and Surgeons Center for Family and Community Medicine in New York, New York.

REFERENCES:

  1. van Tulder M, Koes B, Bombardier C. Low back pain. Best Pract Res Clin Rheumatol. 2002;16(5):761-775.
  2. Rubin Dl. Epidemiology and risk factors for spine pain. Neurol Clin. 2007;​25(2):353-371.
  3. Clarke TC, Nahin RL, Barnes PM, Stussman BJ. Use of complementary health approaches for musculoskeletal pain disorders among adults: United States, 2012. Natl Health Stat Rep. 2016;(98):1-12.
  4. Hoy D, March L, Brooks P, et al. The global burden of low back pain: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014;73(6):968-974.
  5. Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344(5):363-370.
  6. van Tulder M, Becker A, Bekkering T, Breen A, et al; COST B13 Working Group on Guidelines for the Management of Acute Low Back Pain in Primary Care. Chapter 3. European guidelines for the management of acute nonspecific low back pain in primary care. Eur Spine J. 2006;15 suppl 2:​S169-S191.
  7. Rubin Dl. Epidemiology and risk factors for spine pain. Neurol Clin. 2007;​25(2):353-371.
  8. Osterweis M, Kleinman A, Mechanic D, eds. Pain and Disability: Clinical, Behavioral, and Public Policy Perspectives. Institute of Medicine Committee on Pain, Disability, and Chronic Illness Behavior. Washington, DC: National Academy Press; 1987.
  9. Turk DC, Flor H. Chronic pain: a biobehavioral perspective. In: Gatchel RJ, Turk DC, eds. Psychosocial Factors in Pain: Critical Perspectives. New York, NY: Guilford Press; 1999:18-34.
  10. Vlaeyen JW, Kole-Snijders AM, Boeren RG, van Eek H. Fear of movement/(re)injury in chronic low back pain and its relation to behavioral performance. Pain. 1995;62(3):363-372.
  11. Pengel LHM, Herbert RD, Maher CG, Refshauge KM. Acute low back pain: systematic review of its prognosis. BMJ. 2003;327(7410):323.
  12. Goertz M, Thorson D, Bonsell J, et al. Health Care Guideline: Adult Acute and Subacute Low Back Pain. 15th ed. Bloomington, MN: Institute for Clinical Systems Improvement; 2012.
  13. Balagué F, Mannion AF, Pellisé F, Cedraschi C. Non-specific low back pain. Lancet. 2012;379(9814):482-491.
  14. Krebs EE, Lorenz KA, Bair MJ, et al. Development and initial validation of the PEG, a three-item scale assessing pain intensity and interference. J Gen Intern Med. 2009;24(6):733-738.
  15. Greenhalgh S, Selfe J. A qualitative investigation of red flags for serious spinal pathology. Physiotherapy. 2009;95(3):224-227.
  16. Henschke N, Maher CG, Refshauge KM, et al. Prevalence of and screening for serious spinal pathology in patients presenting to primary care settings with acute low back pain. Arthritis Rheum. 2009;60(10):3072-3080.
  17. Underwood M, Buchbinder R. Red flags for back pain. BMJ. 2013;347:​f7432.
  18. Siemionow K, Steinmetz M, Bell G, Ilaslan H, McLain RF. Identifying serious causes of back pain: cancer, infection, fracture. Cleve Clin J Med. 2008;​75(8):557-566.
  19. Greenberg M. Handbook of Neurosurgery. 6th ed. New York, NY: Thieme; 2004.
  20. Downie A, Williams CM, Henschke N, et al. Red flags to screen for malignancy and fracture in patients with low back pain: systematic review. BMJ. 2013;347:f7095.
  21. Della-Giustina D. Acute low back pain: recognizing the “red flags” in the workup. Consultant. 2013;53(6):436-440.
  22. Kendall, NAS, Linton, SJ, Main, CJ. Guide to Assessing Psychosocial Yellow Flags in Acute Low Back Pain: Risk Factors for Long-Term Disability and Work Loss. Wellington, New Zealand: Accident Rehabilitation and Compensation Insurance Corporation of New Zealand and the National Health Committee; 1997.
  23. van der Windt DAWM, Simons E, Riphagen II, et al. Physical examination for lumbar radiculopathy due to disc herniation in patients with low-back pain. Cochrane Database Syst Rev. 2010;(2):CD007431. doi:10.1002/14651858.CD007431.pub2
  24. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760-765.
  25. Bogduk M. On the definitions and physiology of back pain, referred pain, and radicular pain. Pain. 2009;147(1-3):17-19.
  26. Merskey H, Bogduk N, eds; Task Force on Taxonomy of the International Association for the Study of Pain. Classification of Chronic pain: Descriptions of Chronic Pain Syndromes and Definition of Pain Terms. 2nd ed. Seattle, WA: IASP Press; 1994:14.
  27. Webster BS, Courtney TK, Huang Y-H, Matz S, Christiani DC. Physicians’ initial management of acute low back pain versus evidence-based guidelines: influence of sciatica. J Gen Intern Med. 2005;20(12):1132-1135.
  28. Chou R, Qaseem A, Snow V, Casey D, et al; Clinical Efficacy Assessment Subcommittee of the American College of Physicians and the American College of Physicians/American Pain Society Low Back Pain Guidelines Panel. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med. 2007;147(7):478-491.
  29. Ramond-Roquin A, Bouton C, Bègue C, Petit A, Roquelaure Y, Huez J-F. Psychosocial risk factors, interventions, and comorbidity in patients with non-specific low back pain in primary care: need for comprehensive and patient-centered care. Front Med. 2015;2:73.
  30. Wang H, Schiltenwolf M, Buchner M. The role of TNF-α in patients with chronic low back pain—a prospective comparative longitudinal study. Clin J Pain. 2008;24(3):273-278.
  31. Yamauchi K, Inoue G, Koshi T, et al. Nerve growth factor of cultured medium extracted from human degenerative nucleus pulposus promotes sensory nerve growth and induces substance P in vitro. Spine. 2009;34(21):2263-2269.
  32. Maher C, Underwood M, Buchbinder R. Non-specific low back pain. Lancet. 2017;389(10070):736-747.
  33. Fisher ES, Welch HG. Avoiding the unintended consequences of growth in medical care: how might more be worse? JAMA. 1999;281(56):446-453.
  34. Chou R, Fu R, Carrino JA, Deyo RA. Imaging strategies for low-back pain: systematic review and meta-analysis. Lancet. 2009;373(9662):463-472.
  35. Deyo RA. Cascade effects of medical technology. Annu Rev Public Health. 2002;23:23-44.
  36. Chou R, Qaseem A, Owens DK, Shekelle P; Clinical Guidelines Committee of the American College of Physicians. Diagnostic imaging for low back pain: advice for high-value health care from the American College of Physicians. Ann Intern Med. 2011;154(3):181-189.
  37. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low back pain: a randomized controlled trial. JAMA. 2003;289(21):2810-2818.
  38. Qaseem A, Wilt TJ, McLean RM, Forciea MA; Clinical Guidelines Committee of the American College of Physicians. Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166(7):514-530.
  39. van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspecific low back pain: a systematic review of randomized controlled trials of the most common interventions. Spine. 1997;22(18):2128-2156.
  40. Machado LAC, Kamper SJ, Herbert RD, Maher CG, McAuley JH. Analgesic effects of treatments for non-specific low back pain: a meta-analysis of placebo-controlled randomized trials. Rheumatology. 2009;48(5):520-527.
  41. Hancock M, Herbert RD, Maher CG. A guide to interpretation of studies investigating subgroups of responders to physical therapy interventions. Phys Ther. 2009;89(7):698-704.
  42. Finniss DG, Kaptchuk TJ, Miller F, Benedetti F. Biological, clinical, and ethical advances of placebo effects. Lancet. 2010;375(9715):686-695.
  43. Back pain tests and treatments: what you should consider beforehand. Choosing Wisely, an Initiative of the ABIM Foundation. http://www.choosingwisely.org/patient-resources/back-pain-tests-and-treatments. Updated March 2016. Accessed November 17, 2017.
  44. Alvarez DJ, Rockwell PG. Trigger points: diagnosis and management. Am Fam Physician. 2002;65(4):653-660.
  45. Cherkin DC, Sherman KJ, Balderson BH, et al. Effect of mindfulness-based stress reduction vs cognitive behavioral therapy or usual care on back pain and functional limitations in adults with chronic low back pain: a randomized clinical trial. JAMA. 2016;315(12):1240-1249.
  46. Williams CM, Maher CG, Latimer J, et al. Efficacy of paracetamol for acute low-back pain: a double-blind, randomised controlled trial. Lancet. 2014;​384(9954):1586-1596.
  47. Tramèr MR. It’s not just about rubbing—topical capsaicin and topical salicylates may be useful as adjuvants to conventional pain treatment. BMJ. 2004;328(7446):998.