Korean J Intern Med > Volume 38(1); 2023 > Article
Park, Kang, Yang, and Kim: Assessment and nonsurgical management of low back pain: a narrative review

Abstract

Low back pain (LBP) is a common condition that affects people of all ages and income levels worldwide. The etiology of LBP may be mechanical, neuropathic, systemic, referred visceral, or secondary to other causes. Despite numerous studies, the diagnosis and management of LBP remain challenging due to the complex biomechanics of the spine and confounding factors, such as trivial degenerative imaging findings irrelevant to symptoms and psychological and emotional factors. However, it is imperative to identify the crucial signs (“red flags”) indicating a serious underlying condition. While many recent guidelines emphasize non-pharmacologic management approaches, such as education, reassurance, and physical and psychological care, as the first option, LBP patients in many countries, including South Korea, are prescribed medications. Multidisciplinary rehabilitation combined with prudent use of medications is required in patients unresponsive to first-line therapy. The development of practical guidelines apposite for South Korea is needed with multidisciplinary discussion.

INTRODUCTION

Despite considerable progress in the diagnosis and treatment of low back pain (LBP), distinguishing among its many possible etiologies, and thus determining the most appropriate management approach, remains challenging [13]. Therefore, while this review does not provide standards for the management of LBP, it does present evidence-based information on its diagnosis and nonsurgical treatment. Nonetheless, it should be noted that our review is based on studies with varying levels of evidence, some of which addressed highly specific aspects of LBP. Our findings should therefore be interpreted with caution.

EPIDEMIOLOGY AND NATURAL HISTORY

LBP affects people of all ages and socioeconomic classes worldwide [46]. Previous studies have documented that 50% to 80% of people will experience LBP at least once in their lives, with a point prevalence of 15% to 30% and annual incidence of 15% to 45% [79]. Although LBP can develop in all age groups, it is most common in the working population, i.e., adults aged 35 to 55 years [2,5], with the overall prevalence and severity of LBP tending to increase over time [10,11]. LBP is the leading cause of pain and occupational disability, thus burdening patients, their families and society as a whole [1,12,13], including economically, where the medical costs associated with LBP have substantially increased [14]. In South Korea, the prevalence of LBP is 17.1% [15] and the socioeconomic cost in 2015 was approximately 6.6 billion USD. In fact, since 2010, LBP has ranked second among conditions imposing socioeconomic burden, after self-harm [16,17]. LBP was also ranked first in 2015, with the exception of indirect costs caused by productivity loss.
LBP can be classified as acute (< 4 weeks), subacute (4 to 12 weeks), or chronic (> 12 weeks), depending on the duration of symptoms. It is generally considered to be a self-limiting condition because most patients with acute LBP recover with no residual symptoms or functional loss, regardless of treatment [2,12]. A previous systematic review documented substantial improvement in patients with LBP during the first 6 weeks [18]. However, some authors reported that approximately 33% of patients with LBP experienced a recurrence within 1 year in a systematic review, and 30% to 40% of patients with LBP might experience chronic LBP [19,20]. Psychological factors, including depression, anxiety, and occupational stress, are thought to play a larger role in the transition to chronicity than organic pathologies [13,14,21]. Chronic LBP should be distinguished from acute LBP because it differs in expected course, cause, prognosis, and treatment; management and assessment of the prognosis are also more difficult.

CLINICAL PRESENTATION AND EVALUATION

Etiologies

The etiologies of LBP can be classified as mechanical, neuropathic, systemic (inflammatory), and secondary to other causes (Table 1) [13,2224]. Mechanical LBP, resulting from damage to bony structures, intervertebral discs, and ligamentous structures, is the most common cause. Neuropathic pain refers to pain originating from irritation or compression of the nerve root, and typically presents as “sharp” or “burning” pain radiating to the lower extremities, frequently below the knee [13,14]. Mechanical pain may be “aching” or “dull” and referred to the buttocks and upper thighs. Systemic conditions, including inflammatory or neoplastic conditions involving the lumbar spine, can also cause LBP. Morning pain, pain that wakes the sufferer, and pain that improves with exercise suggest an inflammatory etiology [11,23]. Pain stimuli from the abdominal or pelvic organs can be referred to the lumbar area, mimicking LBP. However, the specific etiology of LBP is rarely identified because of the complex biomechanics of the spine and confounding psychological, emotional, and occupational factors [11,12]. In fact, an exact diagnosis of LBP is made in only 15% to 20% of patients [3,25].

Medical history and physical examination

Patients with LBP often report radiating or referred pain in the lower extremities or neurological symptoms, such as motor weakness or changes in bladder or bowel habits. Obtaining a complete medical history should thus be the first step in evaluating a patient with LBP, including pain description (location, onset, duration, severity, consistency, and aggravating or relieving factors), associated symptoms (radiating pain, motor weakness or sensory change in the lower extremities, bladder or bowel symptoms, fever, and unexplained weight loss), previous medical history (malignancy, infection, osteoporosis, previous fractures, psychological history, and family history), and other details (body mass index, physical activity, socioeconomic status, occupation, psychosocial factors, and smoking status).
The physical examination consists of inspection and palpation of the lumbosacral structures to evaluate tenderness, muscle spasm, range of motion of the trunk, and alignment; assessment of the lower extremities to check motor power, sensory, and reflexes; the straight leg raise test; and rectal examination, if necessary. Information acquired during history-taking and the physical examination can reveal crucial signs (“red flags”) indicating the need for further evaluation and management rather than empirical treatment (Table 2) [2,13,26].

Imaging

The benefit of routine imaging studies is limited for most patients with LBP, given the self-limiting natural history of the pain [11]. Furthermore, since degenerative findings are frequently seen in asymptomatic individuals, imaging is likely to reveal unrelated minor abnormalities [13,27]. Several studies have shown that the early imaging of LBP has no benefit in terms of pain or function [28]. In addition, the diagnosis of nonspecific degenerative diseases may cause patients to perceive themselves as sick or disabled, which may lead to a decrease in their activities in daily life, resulting in a delay in recovery and worsening of symptoms. Thus, imaging is recommended only for patients with “red flags” or persistent symptoms after 6 weeks of sufficient conservative treatment [11,29]. However, since plain radiographs are inexpensive and easy to perform, even in primary care clinics in the South Korean healthcare environment, their use is typically not limited.
Anteroposterior (AP) and lateral standing plain radiographs are the initial imaging modalities of choice [30]. Additional dynamic flexion-extension radiographs can also be obtained to evaluate dynamic instability [31]. AP and lateral radiographs in the supine position should be considered in patients with suspected fractures. An oblique view can reveal abnormalities of the pars interarticularis [32]. These images can aid assessment of bone structures and the alignment of the spinal column.
Magnetic resonance imaging (MRI) is the most sensitive diagnostic tool, and is performed in patients with subtle spinal pathologies not detectable on radiographs, such as fractures, infections, and tumors. However, as the specificity of MRI is poor [11], care should be taken not to correlate symptoms with insignificant findings.
Computed tomography (CT) is also used in the assessment of LBP because, unlike other imaging modalities, it can provide optimal images of the bony architecture [33]. It is particularly helpful for evaluating bone-related pathologies, such as fractures, spondylolysis, facet joint osteoarthritis, and primary bone tumors [34]. It is also useful in patients with previously inserted instrumentation, as an alternative to MRI [12]. However, while CT can identify root compressive lesions, such as herniated disc and spinal stenosis, it has lower sensitivity than MRI and may lead to an incorrect diagnosis [34,35]. Moreover, the radiation dose should be considered, especially in younger patients.

NONSURGICAL TREATMENT

Nonsurgical treatment options for LBP include pharmacological and non-pharmacological therapies. As it is difficult to determine the cause of LBP in most patients, management remains challenging despite numerous treatment options. Moreover, despite the extensive literature on the management of LBP, decisive evidence supporting one modality over others is lacking. Therefore, the management strategy should be tailored to each patient and effective treatment may require a combined approach.

Education and counseling

A core component in the management of LBP is education and counseling by the treating physician [2,12,36]. Several high-quality trials and guideline reviews have demonstrated the effectiveness of educating and reassuring patients [37]. Patients should be informed of the natural history, expected course, and often favorable outcome of LBP [38,39]. It should be emphasized that the patient does not have severe disease, that symptoms will improve within several months, and that it is important to stay active, as a low level of physical activity is associated with the development of chronic LBP [40,41]. Lifestyle changes, such as smoking cessation, weight management, regular walking, and avoidance of pain-provoking activities, should also be encouraged [11,12,41]. For patients in Asian countries, sedentary behavior such as sitting or lying on the floor can be detrimental to lumbar spine health.

Physiotherapy

Physiotherapy includes exercises (strengthening, stretching, Pilates, Tai Chi, yoga), manual therapy (manipulation, mobilization, massage), and other local treatment modalities (heat, ice, ultrasound, transcutaneous electrical nerve stimulation [TENS]) [37,42].
Exercises are prescribed to improve coordination and strengthen the muscles supporting the spine and trunk. A study of patients with acute, subacute, and chronic LBP reported no difference in the effects of various exercise protocols, including motor control exercise (MCE), supervised exercise therapy, and directional exercise [37]. Although whether exercise therapy is better than usual care in terms of pain and functional outcome in patients with acute and subacute LBP is unclear [43], another study recommended exercise therapy as the first-line treatment option for patients with chronic LBP [39]. MCE consists of exercises that strengthen the core muscles supporting the spine in a neutral position [37,44]. In a previous meta-analysis of studies with short- to long-term follow-up of patients with chronic and recurrent LBP, MCE improved pain intensity and function compared with minimal intervention or general exercise [45]. Supervised exercise therapy involves patient-tailored exercises or activities performed under the guidance of healthcare professionals, including MCE, directional exercises, and strengthening exercises [44]. Although there is a paucity of evidence regarding the clinical benefit of early supervised exercise therapy in patients with recent-onset LBP, it may be effective for patients with a slow recovery or risk of developing chronic LBP [46]. Moreover, the potential positive effects of supervised exercise on general health should not be ignored [44]. Directional exercise refers to repeated spinal movements in a specific direction, and directional preference to repeated spinal movement or sustained position in a specific direction that decreases pain intensity. Although a previous systematic review found mixed results, some studies have shown that directional exercise matched with directional preference is more likely to yield a positive outcome, whereas unmatched exercise has negative outcomes [47,48]. Therefore, directional preference exercise can be considered for patients with LBP characterized by a directional preference. However, it is important to avoid directional exercise when there is a possibility of spinal fracture. Pilates, Tai Chi, and yoga can serve as adjunctive treatments for LBP, although previous results have been inconsistent and there is no clear scientific evidence supporting their utility for LBP [4951]. In general, the exercise protocol should be selected according to the patient’s symptoms, preferences, and response to therapy.
Manual therapy, such as spinal manipulation (SM) and massage, can also be considered for LBP. SM is performed manually by chiropractors, physiotherapists, and other healthcare providers. The aim is to restore joint or spinal motion and function to within normal range [52]. Previous studies have found that SM combined with usual care in patients with acute LBP is associated with a small but significant short-term effect on pain intensity or function [5355]. When combined with another active treatment, SM may also provide pain relief and improved function in patients with chronic LBP [56,57]. Although the results of previous reports were inconclusive, SM may be prescribed as a second- line or add-on modality [39]. In patients with subacute to chronic LBP, massage may provide better short-term pain relief than sham and other alternative therapies (SM, TENS, physical therapy, exercises, or education) [58]. As its effects are often small, massage can be considered as an adjunctive treatment for acute and chronic LBP, with only minor adverse effects.
In the management of acute LBP, superficial heat provides better pain relief than placebo, acetaminophen, and ibuprofen [59,60]. The combination of superficial heat therapy and exercise was shown to be more effective than exercise alone for acute LBP [61], but its efficacy in patients with chronic LBP is unclear. There is insufficient evidence regarding the effectiveness of other local treatment modalities, such as ultrasound, TENS, inferential therapy, traction, and short-wave diathermy [37,62].
As mentioned above, psychological factors are one of the most common causes of LBP and play a significant role in the development of chronic LBP. Thus, various psychological therapies, including progressive relaxation therapy, cognitive behavioral therapy, and mindfulness-based stress reduction, have been suggested for the management of chronic LBP [2,37]. For persistent LBP unresponsive to other conventional treatments, multidisciplinary rehabilitation, consisting of combined physical, educational, and psychological management, is also recommended [37]. In a previous systematic review, these biopsychosocial interventions were shown to be more effective than usual care and physical therapy in terms of pain and function in patients with chronic LBP [63].

Medications

Although there are various classes of medications for LBP, pharmacological therapy does not necessarily provide better outcomes than non-pharmacological management [1]. Indeed, several guidelines recommend non-pharmacological interventions as first-line treatment and pharmacological therapy only in unresponsive patients [37]. However, medications are frequently prescribed during the first visit, either for pain relief or patient satisfaction.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the first-line and most commonly used medications for LBP [2,14]. They are more effective than placebo for improving symptoms in acute LBP [64] and can also provide short-term relief of chronic LBP [65,66]. There are two types of NSAIDs: non-selective NSAIDs, which inhibit both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and selective COX- 2 inhibitors. There is no evidence of a difference between them in terms of pain relief in LBP [67], and the response to a particular agent can vary among patients. However, NSAIDs are also associated with several adverse effects, such as gastrointestinal, renal, and cardiovascular complications [68]. A selective COX-2 inhibitor was developed to reduce gastrointestinal side effects (e.g., gastric ulcer, perforation, bleeding, and obstruction). Since all NSAIDs at therapeutic doses differ in their selectivity for COX-1 and COX-2, physicians should keep in mind that NSAIDs with greater COX-2 than COX-1 selectivity generally have a lower risk of gastrointestinal adverse events than those with lower COX-2 selectivity. By contrast, both non-selective and COX-2 selective NSAIDs have been associated with an increased risk of cardiovascular complications, such as hypertension, myocardial infarction, stroke, and heart failure, especially at high doses [69]. Since the risk of adverse events is often dose- and duration-dependent, NSAIDs should be used at the lowest effective dose and for the shortest duration [68,70,71]. In addition, their co-administration with aspirin or other antiplatelet/anticoagulation drugs should be avoided if possible, due to the risk of adverse drug interactions [68]. Therefore, the specific NSAID should be chosen based on the recommended dose/schedule, as well as the patient’s clinical history (e.g., gastrointestinal and cardiovascular risk factors), response to each drug, and preference. A previous study found no evidence that acetaminophen is superior to placebo [65]. However, because it is inexpensive and safe, it is a reasonable option for patients with contraindications to other medications and might also be useful because of its opioid-sparing and synergistic effects [72].
Tramadol, a centrally acting non-narcotic analgesic, is commonly used to treat LBP. Given its positive effect on pain and function and less potential for abuse than narcotic drugs, it is a useful option, especially for patients with chronic LBP [2,37].
Skeletal muscle relaxants (SMRs), a class of heterogeneous drugs with different chemical structures and mechanisms of action, can be classified as antispastic (e.g., baclofen and dantrolene) or antispasmodic (e.g., carisoprodol, chlorzoxazone, and cyclobenzaprine) [73]. Antispastic agents act on upper motor symptoms by resisting exaggerated reflexes and reducing muscle rigidity, with the mechanism varying among agents [74]. Antispasmodic agents can be prescribed for peripheral muscle pain and spasm, but their precise mechanism of action is unclear; however, it likely includes sedative effects on the central nervous system [74]. SMRs were shown to be more efficacious than placebo in acute LBP [75] and may offer additional benefits when used in combination with NSAIDs [76]. Although the interobserver reliability of muscle spasm on physical examination is relatively low [76], SMRs could theoretically be effective in acute LBP associated with paraspinal muscle spasm. However, there is no evidence of their efficacy for treating chronic LBP [37]. Potential side effects, including drowsiness, somnolence, and dizziness, should also be considered. Therefore, when prescribing these drugs their benefits and risks should be weighed.
Given their minimal benefits and potential risks, the routine use of opioids is not recommended [39]. Nonetheless, opioids are one of the most frequently prescribed medications for LBP worldwide, including in South Korea, and their use in acute LBP has been advocated despite their unclear efficacy [77,78]. In patients with chronic LBP, opioids may provide short-term pain relief, but their efficacy is generally considered clinically insignificant and evidence of long-term effectiveness is lacking [7981]. Adverse effects of opioids include dizziness, drowsiness, nausea, vomiting, constipation, abuse and misuse potential, and overdose-related death [12,78]. There is a guideline for prescribing opioids for chronic pain in South Korea [82], which could be applied to patients with LBP. In brief, opioid prescriptions should be limited to a short period of time or restricted to patients in whom conventional medications have failed.
Antidepressants serve as an alternative or adjuvant option for the management of LBP, especially in patients with comorbid mood disorders [12,83,84]. Because mood and LBP are closely related [13,85], antidepressants can provide significant pain relief, especially in patients with chronic LBP, as documented in previous studies and guidelines [2,75,86,87]. Two classes of antidepressants are frequently used in the management of LBP: tricyclic antidepressants (TCA) and serotonin and norepinephrine reuptake inhibitor (SNRI) antidepressants [37,88]. TCA can be considered for patients with LBP and sleep disturbances, which are often associated with mood disorders [89]. The SNRI duloxetine was shown to provide pain relief and functional improvement in the management of LBP [9092]. However, antidepressants can be associated with nausea, dizziness, fatigue, and somnolence [83].
Anticonvulsant agents, such as pregabalin and gabapentin, are generally used to control neuropathic pain. In a prospective randomized trial, pregabalin combined with celecoxib was more effective than monotherapy for chronic LBP [93]. However, the evidence supporting a beneficial effect of these medications for patients with LBP or sciatica is insufficient [9496].
Topical analgesics refer to agents rubbed (e.g., cream or gel) or stuck (e.g., patches or plasters) on the skin. This class of agents includes topical NSAIDs, salicylate-containing rubefacients, capsaicin, and lidocaine [97]. They are used to treat acute or chronic painful conditions, including LBP. A 5% lidocaine patch was reported to be effective for pain relief in patients with acute, subacute, and chronic LBP [98,99]. Topical capsicum is recommended on a short-term basis for chronic LBP, including neuropathic LBP associated with radiculopathy [99,100]. However, patients should be closely monitored for the development of common side effects of topical agents, including localized erythema, rash, or a burning sensation [101].
As there are no definitive recommendations or guidelines regarding the pharmacological management of LBP, clinicians should be familiar with the fundamental principles and indications of each drug and consider patient-tailored pharmaceutical therapy.

Intervention

LBP arising from organic causes can be classified as somatic pain (facet joint, sacroiliac joint, myofascial, and discogenic pain) or radicular pain (disc herniation, annulus tear, and spinal stenosis), depending on its origin. Although the etiology of LBP is often multifactorial, damage to the facet joint (zygapophyseal joint) and sacroiliac joint is a major cause [102]. Facet joint pain can be managed by therapeutic interventions such as medial branch block (MBB), facet joint injection (FJI), and radiofrequency ablation (RFA) [103,104]. MBB, which blocks the medial branch of the dorsal ramus innervating the facet joints, can be performed for diagnostic purposes to identify target lesions before RFA, and for therapeutic purposes to provide long-lasting pain relief [105]. Miyakoshi et al. [106] suggested conventional MBB with a large volume of local anesthetics to block all three branches (medial, lateral, and intermediate) of the dorsal ramus and thus reduce LBP originating from both the facet joints and myofascial structures. In FJI, the anesthetic agents are injected intra-articularly, while in RFA the innervating nerves are denatured to stop pain signals from injured joints reaching the brain. Pain arising from the sacroiliac joint can be managed with intra-articular injections and RFA. Caudal epidural injection can exert both short- and long-term effects on chronic LBP (with or without radiculopathy) caused by discogenic sources, spinal stenosis, or post-spinal surgery syndrome [107].

LIMITATIONS

This review had several limitations. First, it was a narrative rather than systematic review or meta-analysis. Therefore, bias in the literature search or selection cannot be ruled out. In addition, the treatment modalities were not graded according to the level of evidence. Second, LBP is an extremely broad comprehensive category, such that its mechanisms, etiologies, examinations, and management protocols remain controversial. Third, given the lack of conclusive evidence supporting any one treatment option unconditionally, we cannot provide definitive recommendations for the management of LBP. Despite these limitations, this review provided an overview of the LBP management process and can thus act as a guide for physicians involved in the treatment of this common condition.

CONCLUSIONS

Despite a plethora of studies, trials, and clinical guidelines regarding the nonsurgical management of LBP, gaps remain between their recommendations and actual practice, depending on the health system and economic status of a given country, as well as patient behaviors and demographics. In South Korea, the lack of apposite guidelines often results in inappropriate imaging or drug prescriptions and subsequent substantial and unnecessary medical costs. Multidisciplinary discussions with clinicians from various departments, researchers, pharmaceutical companies, and lawmakers are required to devise practical guidelines. Ultimately, it is essential to comply with the basic principles of care, taking into account the benefits and potential risks of treatment.

Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Table 1
Etiologies of low back pain
Mechanical (most common)
 Lumbar strain/sprain (muscle/ligament injury)
 Vertebral contusion or fracture
 Facet degeneration
 Disc degeneration (discogenic pain)
 Instability including spondylolisthesis
 Spondylolysis
 Deformity (scoliosis, kyphosis)
 Bertolotti’s syndrome (transitional vertebra)
 Baastrup’s disease
Neuropathic
 Herniated disc
 Spinal stenosis
 Annular fissure with disc degeneration
Systemic (inflammatory)
 Inflammatory conditions
  Spondyloarthropathy (ankylosing spondylitis, enteropathic arthritis, reactive arthritis)
  Rheumatoid arthritis
  Infection (osteomyelitis, discitis, abscess)
 Neoplasia
  Metastatic carcinoma
  Hematologic malignancy (multiple myeloma, lymphoma, leukemia)
  Primary spinal tumor (vertebral tumor, spinal cord tumor)
Other causes
 Visceral (referred)
  Abdominal aortic aneurysm
  Gastrointestinal disease (pancreatitis, cholecystitis, peptic ulcer disease)
  Renal disease (pyelonephritis, kidney stone)
  Pelvic organ disease (endometriosis, chronic pelvic inflammatory disease, prostatitis, neoplasm)
 Fibromyalgia
 Somatoform disorder (somatization disorder, hypochondriasis, pain disorder)
 Malingering
Table 2
“Red flags” indicating serious conditions in patients with low back pain
Historical or physical findings Possible condition(s)
History
 Age > 50 years (plus other red flags signs)
 Unexplained weight loss Malignancy
 Prolonged use of corticosteroid Fracture
 Severe trauma relative to age Fracture
 History of osteoporosis Fracture
 Bladder and bowel symptoms: retention or incontinence Cauda equina syndrome
 Prolonged use of immunosuppressive drugs Infection
 History of recent infection Infection
 History of recent spinal procedures Infection
 Sharp, sudden, severe pain spreading downward Abdominal aortic aneurysm
Physical examination
 Presence of a contusion or abrasion Fracture
 Fever and/or chills Infection, malignancy
 Progressive neurologic signs: marked motor and sensory deficit, saddle anesthesia, diminished sphincter tone and reflexes Cauda equina syndrome
 Localized pain or focal tenderness Malignancy, infection
 Morning stiffness: typically improve with activity or exercise Spondyloarthropathy

REFERENCES

1. Gianola S, Bargeri S, Del Castillo G, et al. Effectiveness of treatments for acute and subacute mechanical non-specific low back pain: a systematic review with network meta-analysis. Br J Sports Med 2022;56:41–50.
crossref pmid pmc
2. Shen FH, Samartzis D, Andersson GB. Nonsurgical management of acute and chronic low back pain. J Am Acad Orthop Surg 2006;14:477–487.
crossref pmid
3. Casazza BA. Diagnosis and treatment of acute low back pain. Am Fam Physician 2012;85:343–350.
pmid
4. Hoy D, Bain C, Williams G, et al. A systematic review of the global prevalence of low back pain. Arthritis Rheum 2012;64:2028–2037.
crossref pmid
5. Hartvigsen J, Christensen K, Frederiksen H. Back pain remains a common symptom in old age. a population-based study of 4486 Danish twins aged 70–102. Eur Spine J 2003;12:528–534.
crossref pmid pmc pdf
6. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 2016;388:1545–1602.
pmid pmc
7. Andersson GB. Epidemiology of low back pain. Acta Orthop Scand Suppl 1998;281:28–31.
crossref pmid
8. Frymoyer JW, Pope MH, Clements JH, Wilder DG, MacPherson B, Ashikaga T. Risk factors in low-back pain: an epidemiological survey. J Bone Joint Surg Am 1983;65:213–218.
crossref pmid
9. Hong JY, Song KS, Cho JH, Lee JH, Kim NH. An updated overview of low back pain management. Asian Spine J 2021. Dec. 30. [Epub]. https://doi.org/10.31616/asj.2021.0371 .
crossref pmid
10. Hoy D, Brooks P, Blyth F, Buchbinder R. The epidemiology of low back pain. Best Pract Res Clin Rheumatol 2010;24:769–781.
crossref pmid
11. Patrick N, Emanski E, Knaub MA. Acute and chronic low back pain. Med Clin North Am 2014;98:777–789.
crossref pmid
12. Brodke DS, Ritter SM. Nonoperative management of low back pain and lumbar disc degeneration. J Bone Joint Surg 2004;86:1810–1818.
crossref
13. Cohen SP, Argoff CE, Carragee EJ. Management of low back pain. BMJ 2008;337:a2718.
crossref pmid
14. Will JS, Bury DC, Miller JA. Mechanical low back pain. Am Fam Physician 2018;98:421–428.
pmid
15. Lee S, Nam CM, Yoon DH, et al. Association between low-back pain and lumbar spine bone density: a population-based cross-sectional study. J Neurosurg Spine 2013;19:307–313.
crossref pmid
16. Kim TE, Lee RG, Park SY, Oh IH. Measuring trends in the socioeconomic burden of disease in Korea, 2007–2015. J Prev Med Public Health 2022;55:19–27.
crossref pmid pmc pdf
17. Lee YR, Cho B, Jo MW, et al. Measuring the economic burden of disease and injury in Korea, 2015. J Korean Med Sci 2019;34(Suppl 1):e80.
crossref pmid pmc pdf
18. da C Menezes Costa L, Maher CG, Hancock MJ, McAuley JH, Herbert RD, Costa LO. The prognosis of acute and persistent low-back pain: a meta-analysis. CMAJ 2012;184:E613–E624.
crossref pmid pmc
19. da Silva T, Mills K, Brown BT, Herbert RD, Maher CG, Hancock MJ. Risk of recurrence of low back pain: a systematic review. J Orthop Sports Phys Ther 2017;47:305–313.
crossref
20. Henschke N, Maher CG, Refshauge KM, et al. Prognosis in patients with recent onset low back pain in Australian primary care: inception cohort study. BMJ 2008;337:a171.
crossref pmid pmc
21. Pincus T, Burton AK, Vogel S, Field AP. A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain. Spine (Phila Pa 1976) 2002;27:E109–E120.
crossref pmid
22. Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363–370.
crossref pmid
23. Manusov EG. Evaluation and diagnosis of low back pain. Prim Care 2012;39:471–479.
crossref pmid
24. Crane J, Cragon R, O’Neill J, et al. A comprehensive update of the treatment and management of Bertolotti’s syndrome: a best practices review. Orthop Rev (Pavia) 2021;13:24980.
crossref pmid pmc
25. Frymoyer JW. Back pain and sciatica. N Engl J Med 1988;318:291–300.
crossref pmid
26. 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.
crossref pmid pmc
27. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002;137:586–597.
crossref pmid
28. 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;289:2810–2818.
crossref pmid
29. Patel ND, Broderick DF, Burns J, et al. ACR appropriateness criteria low back pain. J Am Coll Radiol 2016;13:1069–1078.
crossref pmid
30. Simmons ED Jr, Guyer RD, Graham-Smith A, Herzog R. Radiographic assessment for patients with low back pain. Spine (Phila Pa 1976) 1995;20:1839–1841.
pmid
31. Russo R, Cook P. Diagnosis of low back pain: role of imaging studies. Occup Med 1998;13:83–96.
pmid
32. van Tulder MW, Assendelft WJ, Koes BW, Bouter LM. Spinal radiographic findings and nonspecific low back pain: a systematic review of observational studies. Spine (Phila Pa 1976) 1997;22:427–434.
pmid
33. Kalichman L, Kim DH, Li L, Guermazi A, Hunter DJ. Computed tomography-evaluated features of spinal degeneration: prevalence, intercorrelation, and association with self-reported low back pain. Spine J 2010;10:200–208.
crossref pmid pmc
34. Maus T. Imaging the back pain patient. Phys Med Rehabil Clin N Am 2010;21:725–766.
crossref pmid
35. van Rijn RM, Wassenaar M, Verhagen AP, et al. Computed tomography for the diagnosis of lumbar spinal pathology in adult patients with low back pain or sciatica: a diagnostic systematic review. Eur Spine J 2012;21:228–239.
crossref pmid pmc
36. Albaladejo C, Kovacs FM, Royuela A, del Pino R, Zamora J, Spanish Back Pain Research Network. The efficacy of a short education program and a short physiotherapy program for treating low back pain in primary care: a cluster randomized trial. Spine (Phila Pa 1976) 2010;35:483–496.
pmid
37. Qaseem A, Wilt TJ, McLean RM, et al. Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med 2017;166:514–530.
crossref pmid
38. Hagen KB, Hilde G, Jamtvedt G, Winnem M. Bed rest for acute low-back pain and sciatica. Cochrane Database Syst Rev 2004;4:CD001254.
crossref pmid
39. Foster NE, Anema JR, Cherkin D, et al. Prevention and treatment of low back pain: evidence, challenges, and promising directions. Lancet 2018;391:2368–2383.
crossref pmid
40. Citko A, Gorski S, Marcinowicz L, Gorska A. Sedentary lifestyle and nonspecific low back pain in medical personnel in North-East Poland. Biomed Res Int 2018;2018:1965807.
crossref pmid pmc pdf
41. Park SM, Kim HJ, Jeong H, et al. Longer sitting time and low physical activity are closely associated with chronic low back pain in population over 50 years of age: a cross-sectional study using the sixth Korea National Health and Nutrition Examination Survey. Spine J 2018;18:2051–2058.
crossref pmid
42. Bernstein IA, Malik Q, Carville S, Ward S. Low back pain and sciatica: summary of NICE guidance. BMJ 2017;356:i6748.
crossref pmid
43. Chou R, Huffman LH, American Pain Society; American College of Physicians. Nonpharmacologic therapies for acute and chronic low back pain: a review of the evidence for an American Pain Society/American College of Physicians clinical practice guideline. Ann Intern Med 2007;147:492–504.
crossref pmid
44. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Eur Spine J 2018;27:60–75.
crossref pmid pdf
45. Bystrom MG, Rasmussen-Barr E, Grooten WJ. Motor control exercises reduces pain and disability in chronic and recurrent low back pain: a meta-analysis. Spine (Phila Pa 1976) 2013;38:E350–E358.
pmid
46. Chou R, Deyo R, Friedly J, et al. Noninvasive Treatments for Low Back Pain. Rockville (MD): Agency for Healthcare Research and Quality (US), 2016.

47. Long A, May S, Fung T. The comparative prognostic value of directional preference and centralization: a useful tool for front-line clinicians? J Man Manip Ther 2008;16:248–254.
crossref pmid pmc
48. Surkitt LD, Ford JJ, Hahne AJ, Pizzari T, McMeeken JM. Efficacy of directional preference management for low back pain: a systematic review. Phys Ther 2012;92:652–665.
crossref pmid pdf
49. Wajswelner H, Metcalf B, Bennell K. Clinical pilates versus general exercise for chronic low back pain: randomized trial. Med Sci Sports Exerc 2012;44:1197–1205.
pmid
50. Hall AM, Maher CG, Lam P, Ferreira M, Latimer J. Tai chi exercise for treatment of pain and disability in people with persistent low back pain: a randomized controlled trial. Arthritis Care Res (Hoboken) 2011;63:1576–1583.
crossref pmid
51. Cramer H, Lauche R, Haller H, Dobos G. A systematic review and meta-analysis of yoga for low back pain. Clin J Pain 2013;29:450–460.
crossref pmid
52. Ernst E, Canter PH. A systematic review of systematic reviews of spinal manipulation. J R Soc Med 2006;99:192–196.
crossref pmid pmc pdf
53. Rubinstein SM, Terwee CB, Assendelft WJ, de Boer MR, van Tulder MW. Spinal manipulative therapy for acute low-back pain. Cochrane Database Syst Rev 2012;2012:CD008880.
crossref pmid pmc
54. Cruser dA, Maurer D, Hensel K, Brown SK, White K, Stoll ST. A randomized, controlled trial of osteopathic manipulative treatment for acute low back pain in active duty military personnel. J Man Manip Ther 2012;20:5–15.
crossref pmid pmc
55. Hancock MJ, Maher CG, Latimer J, et al. Assessment of diclofenac or spinal manipulative therapy, or both, in addition to recommended first-line treatment for acute low back pain: a randomised controlled trial. Lancet 2007;370:1638–1643.
crossref pmid
56. Rubinstein SM, van Middelkoop M, Assendelft WJ, de Boer MR, van Tulder MW. Spinal manipulative therapy for chronic low-back pain: an update of a Cochrane review. Spine (Phila Pa 1976) 2011;36:E825–E846.
pmid
57. Licciardone JC, Stoll ST, Fulda KG, et al. Osteopathic manipulative treatment for chronic low back pain: a randomized controlled trial. Spine (Phila Pa 1976) 2003;28:1355–1362.
pmid
58. Furlan AD, Giraldo M, Baskwill A, Irvin E, Imamura M. Massage for low-back pain. Cochrane Database Syst Rev 2015;2015:CD001929.
crossref pmid pmc
59. French SD, Cameron M, Walker BF, Reggars JW, Esterman AJ. Superficial heat or cold for low back pain. Cochrane Database Syst Rev 2006;2006:CD004750.
crossref pmid pmc
60. Nadler SF, Steiner DJ, Erasala GN, et al. Continuous low-level heat wrap therapy provides more efficacy than Ibuprofen and acetaminophen for acute low back pain. Spine (Phila Pa 1976) 2002;27:1012–1017.
crossref pmid
61. Mayer JM, Ralph L, Look M, et al. Treating acute low back pain with continuous low-level heat wrap therapy and/or exercise: a randomized controlled trial. Spine J 2005;5:395–403.
crossref pmid
62. UK National Guideline Centre. Low back pain and sciatica in over 16s: assessment and management [Internet] London (UK): National Institute for Health and Care Excellence, 2016. [cited 2022 Nov 1]. Available from: https://www.nice.org.uk/guidance/ng59 .

63. Kamper SJ, Apeldoorn AT, Chiarotto A, et al. Multidisciplinary biopsychosocial rehabilitation for chronic low back pain: Cochrane systematic review and meta-analysis. BMJ 2015;350:h444.
crossref pmid pmc
64. Herrmann WA, Geertsen MS. Efficacy and safety of lornoxicam compared with placebo and diclofenac in acute sciatica/lumbo-sciatica: an analysis from a randomised, double-blind, multicentre, parallel-group study. Int J Clin Pract 2009;63:1613–1621.
crossref pmid
65. Saragiotto BT, Machado GC, Ferreira ML, Pinheiro MB, Abdel Shaheed C, Maher CG. Paracetamol for low back pain. Cochrane Database Syst Rev 2016;2016:CD012230.
crossref pmid pmc
66. Kivitz AJ, Gimbel JS, Bramson C, et al. Efficacy and safety of tanezumab versus naproxen in the treatment of chronic low back pain. Pain 2013;154:1009–1021.
crossref pmid
67. Roelofs PD, Deyo RA, Koes BW, Scholten RJ, van Tulder MW. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev 2008;1:CD000396.
crossref pmid
68. Brune K, Patrignani P. New insights into the use of currently available non-steroidal anti-inflammatory drugs. J Pain Res 2015;8:105–118.
crossref pmid pmc
69. Coxib and traditional NSAID Trialists’ (CNT) Collaboration; Bhala N, et al.; Emberson J. Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials. Lancet 2013;382:769–779.
crossref pmid pmc
70. Castellsague J, Riera-Guardia N, Calingaert B, et al. Individual NSAIDs and upper gastrointestinal complications: a systematic review and meta-analysis of observational studies (the SOS project). Drug Saf 2012;35:1127–1146.
crossref pmid pmc
71. Pepine CJ, Gurbel PA. Cardiovascular safety of NSAIDs: additional insights after PRECISION and point of view. Clin Cardiol 2017;40:1352–1356.
crossref pmid pmc pdf
72. Barkin RL. Acetaminophen, aspirin, or Ibuprofen in combination analgesic products. Am J Ther 2001;8:433–442.
crossref pmid
73. See S, Ginzburg R. Choosing a skeletal muscle relaxant. Am Fam Physician 2008;78:365–370.
pmid
74. Chou R, Peterson K, Helfand M. Comparative efficacy and safety of skeletal muscle relaxants for spasticity and musculoskeletal conditions: a systematic review. J Pain Symptom Manage 2004;28:140–175.
crossref pmid
75. Deyo RA. Drug therapy for back pain. Which drugs help which patients? Spine (Phila Pa 1976) 1996;21:2840–2850.
pmid
76. Cherkin DC, Wheeler KJ, Barlow W, Deyo RA. Medication use for low back pain in primary care. Spine (Phila Pa 1976) 1998;23:607–614.
crossref pmid
77. Chung SS, Park CK, Cho KJ, et al. A nationwide retrospective study of opioid management patterns in 2,468 patients with spinal pain in Korea. Asian Spine J 2016;10:1122–1131.
crossref pmid pmc pdf
78. Deyo RA, Von Korff M, Duhrkoop D. Opioids for low back pain. BMJ 2015;350:g6380.
crossref pmid pmc
79. Martell BA, O’Connor PG, Kerns RD, et al. Systematic review: opioid treatment for chronic back pain: prevalence, efficacy, and association with addiction. Ann Intern Med 2007;146:116–127.
crossref pmid
80. Chaparro LE, Furlan AD, Deshpande A, Mailis-Gagnon A, Atlas S, Turk DC. Opioids compared to placebo or other treatments for chronic low-back pain. Cochrane Database Syst Rev 2013;8:CD004959.
crossref pmid
81. Abdel Shaheed C, Maher CG, Williams KA, Day R, McLachlan AJ. Efficacy, tolerability, and dose-dependent effects of opioid analgesics for low back pain: a systematic review and meta-analysis. JAMA Intern Med 2016;176:958–968.
crossref pmid
82. Kim ED, Lee JY, Son JS, et al. Guidelines for prescribing opioids for chronic non-cancer pain in Korea. Korean J Pain 2017;30:18–33.
crossref pmid pmc pdf
83. Yabuki S, Ip AK, Tam CK, et al. Evidence-based recommendations on the pharmacological management of osteoarthritis and chronic low back pain: an asian consensus. Asian J Anesthesiol 2019;57:37–54.
pmid
84. Tsuji O, Kosugi S, Suzuki S, et al. Effectiveness of duloxetine for postsurgical chronic neuropathic disorders after spine and spinal cord surgery. Asian Spine J 2021;15:650–658.
crossref pdf
85. Park SM, Kim HJ, Jang S, et al. Depression is closely associated with chronic low back pain in patients over 50 years of age: a cross-sectional study using the sixth Korea National Health and Nutrition Examination Survey (KNHANES VI-2). Spine (Phila Pa 1976) 2018;43:1281–1288.
pmid
86. Urquhart DM, Hoving JL, Assendelft WW, Roland M, van Tulder MW. Antidepressants for non-specific low back pain. Cochrane Database Syst Rev 2008;2008:CD001703.
crossref pmid pmc
87. Hong JY, Song KS, Cho JH, Lee JH. An updated overview of low back pain management in primary care. Asian Spine J 2017;11:653–660.
crossref pmid pmc pdf
88. Ferreira GE, McLachlan AJ, Lin CC, et al. Efficacy and safety of antidepressants for the treatment of back pain and osteoarthritis: systematic review and meta-analysis. BMJ 2021;372:m4825.
crossref pmid pmc
89. Harman K, Pivik RT, D’Eon JL, Wilson KG, Swenson JR, Matsunaga L. Sleep in depressed and nondepressed participants with chronic low back pain: electroencephalographic and behaviour findings. Sleep 2002;25:775–783.
crossref pmid
90. Weng C, Xu J, Wang Q, Lu W, Liu Z. Efficacy and safety of duloxetine in osteoarthritis or chronic low back pain: a systematic review and meta-analysis. Osteoarthritis Cartilage 2020;28:721–734.
crossref pmid
91. Skljarevski V, Zhang S, Desaiah D, et al. Duloxetine versus placebo in patients with chronic low back pain: a 12-week, fixed-dose, randomized, double-blind trial. J Pain 2010;11:1282–1290.
crossref pmid
92. Skljarevski V, Ossanna M, Liu-Seifert H, et al. A double-blind, randomized trial of duloxetine versus placebo in the management of chronic low back pain. Eur J Neurol 2009;16:1041–1048.
crossref pmid
93. Romano CL, Romano D, Bonora C, Mineo G. Pregabalin, celecoxib, and their combination for treatment of chronic lowback pain. J Orthop Traumatol 2009;10:185–191.
crossref pmid pmc pdf
94. Mathieson S, Maher CG, McLachlan AJ, et al. Trial of pregabalin for acute and chronic sciatica. N Engl J Med 2017;376:1111–1120.
crossref pmid
95. Shanthanna H, Gilron I, Rajarathinam M, et al. Benefits and safety of gabapentinoids in chronic low back pain: a systematic review and meta-analysis of randomized controlled trials. PLoS Med 2017;14:e1002369.
crossref
96. McCleane GJ. Does gabapentin have an analgesic effect on background, movement and referred pain?: a randomised, double-blind, placebo controlled study. Pain Clin 2001;13:103–107.
crossref
97. Derry S, Wiffen PJ, Kalso EA, et al. Topical analgesics for acute and chronic pain in adults: an overview of Cochrane Reviews. Cochrane Database Syst Rev 2017;5:CD008609.
crossref pmid pmc
98. Gimbel J, Linn R, Hale M, Nicholson B. Lidocaine patch treatment in patients with low back pain: results of an open-label, nonrandomized pilot study. Am J Ther 2005;12:311–319.
crossref pmid
99. Peck J, Urits I, Peoples S, et al. A comprehensive review of over the counter treatment for chronic low back pain. Pain Ther 2021;10:69–80.
crossref pmid pmc pdf
100. Frerick H, Keitel W, Kuhn U, Schmidt S, Bredehorst A, Kuhlmann M. Topical treatment of chronic low back pain with a capsicum plaster. Pain 2003;106:59–64.
crossref pmid
101. Wagner T, Poole C, Roth-Daniek A. The capsaicin 8% patch for neuropathic pain in clinical practice: a retrospective analysis. Pain Med 2013;14:1202–1211.
crossref pmid pmc
102. Helbig T, Lee CK. The lumbar facet syndrome. Spine (Phila Pa 1976) 1988;13:61–64.
crossref pmid
103. Boswell MV, Colson JD, Sehgal N, Dunbar EE, Epter R. A systematic review of therapeutic facet joint interventions in chronic spinal pain. Pain Physician 2007;10:229–253.
crossref pmid
104. Baroncini A, Maffulli N, Eschweiler J, Knobe M, Tingart M, Migliorini F. Management of facet joints osteoarthritis associated with chronic low back pain: a systematic review. Surgeon 2021;19:e512–e518.
crossref pmid
105. Liu M, Shaparin N, Nair S, Kim RS, Hascalovici JR. Chronic low back pain: the therapeutic benefits of diagnostic medial branch nerve blocks. Pain Physician 2021;24:E521–E528.
pmid
106. Miyakoshi N, Shimada Y, Kasukawa Y, Saito H, Kodama H, Itoi E. Total dorsal ramus block for the treatment of chronic low back pain: a preliminary study. Joint Bone Spine 2007;74:270–274.
crossref pmid
107. Parr AT, Manchikanti L, Hameed H, et al. Caudal epidural injections in the management of chronic low back pain: a systematic appraisal of the literature. Pain Physician 2012;15:E159–E198.
crossref pmid
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