Elsevier

The Lancet

Volume 398, Issue 10294, 3–9 July 2021, Pages 78-92
The Lancet

Seminar
Low back pain

https://doi.org/10.1016/S0140-6736(21)00733-9Get rights and content

Summary

Low back pain covers a spectrum of different types of pain (eg, nociceptive, neuropathic and nociplastic, or non-specific) that frequently overlap. The elements comprising the lumbar spine (eg, soft tissue, vertebrae, zygapophyseal and sacroiliac joints, intervertebral discs, and neurovascular structures) are prone to different stressors, and each of these, alone or in combination, can contribute to low back pain. Due to numerous factors related to low back pain, and the low specificity of imaging and diagnostic injections, diagnostic methods for this condition continue to be a subject of controversy. The biopsychosocial model posits low back pain to be a dynamic interaction between social, psychological, and biological factors that can both predispose to and result from injury, and should be considered when devising interdisciplinary treatment plans. Prevention of low back pain is recognised as a pivotal challenge in high-risk populations to help tackle high health-care costs related to therapy and rehabilitation. To a large extent, therapy depends on pain classification, and usually starts with self-care and pharmacotherapy in combination with non-pharmacological methods, such as physical therapies and psychological treatments in appropriate patients. For refractory low back pain, a wide range of non-surgical (eg, epidural steroid injections and spinal cord stimulation for neuropathic pain, and radiofrequency ablation and intra-articular steroid injections for mechanical pain) and surgical (eg, decompression for neuropathic pain, disc replacement, and fusion for mechanical causes) treatment options are available in carefully selected patients. Most treatment options address only single, solitary causes and given the complex nature of low back pain, a multimodal interdisciplinary approach is necessary. Although globally recognised as an important health and socioeconomic challenge with an expected increase in prevalence, low back pain continues to have tremendous potential for improvement in both diagnostic and therapeutic aspects. Future research on low back pain should focus on improving the accuracy and objectivity of diagnostic assessments, and devising treatment algorithms that consider unique biological, psychological, and social factors. High-quality comparative-effectiveness and randomised controlled trials with longer follow-up periods that aim to establish the efficacy and cost-effectiveness of low back pain management are warranted.

Introduction

Low back pain covers a spectrum of different types of pain, including nociceptive pain, neuropathic (radicular) pain that travels down the legs, and in some cases, nociplastic pain, which is caused by amplification of pain in the CNS, often falling under the umbrella of non-specific low back pain. Frequently, these pain subtypes overlap (eg, a patient with a herniated disc who has back pain can have radicular pain and diffuse symptoms outside pathoanatomical referral patterns).

The low back is anatomically defined as extending from the 12th rib to the iliac crest, and although low back pain often coexists and is conflated with buttock pain, the buttock region is anatomically distinct and comprises a region from the iliac crest to the gluteal folds. Most people have at least one episode of acute low back pain in their lifetime. This condition is usually self-limiting, but often becomes chronic.1 Studies have found that more than 60% of individuals with mechanical low back pain will continue to have pain or frequent recurrences 1 year after onset.2 For new-onset lumbar radiculopathy, between 15% and 40% of people will have chronic pain or frequent relapse.3 Chronic low back pain is a consequence of complex interactions encompassing biological, psychological, and social factors.4

It is important to understand that pain is distinct from nociception, and includes not just A delta fiber and C fiber activation, but also context-dependent emotional, cognitive, and behavioural elements.5 This distinction partly explains the poor correlation with pathology and symptoms,6 and why interventions that have no effect on degenerative processes (eg, psychological therapies or acupuncture) can have profound effects on pain and quality of life, whereas interventions that address pathology (eg, surgery) often do not provide benefit. This notion was eloquently described by Melzack and Casey7 in their landmark classification of pain into sensory–discriminative, affective–motivational, and cognitive–evaluative components. It forms the basis for a multimodal, precision medicine approach to low back pain, and is a foundation for the biopsychosocial model.8

In this Seminar, we provide a brief overview on epidemiology, and the causes and risk factors that contribute to the pathogenesis of low back pain. We also describe the clinical presentation and diagnostic evaluation of low back pain and different therapeutic options.

Section snippets

Epidemiology

A study done in 195 countries assessing the incidence, prevalence, and years lived with disability for 354 medical conditions found low back pain to be the leading cause of worldwide productivity loss as measured in years, and the top cause of years lived with disability in 126 countries.9 One systematic review of 165 studies from 54 countries estimated the point prevalence of low back pain to be 11·9% (SD 2) and 1 month prevalence to be 23·3% (SD 2·9), and to be most common in middle-aged to

Socioeconomic burden

The economic burden of low back pain is estimated to be around £2·8 billion in the UK22 and more than AU$4·8 billion in Australia23 per year. In the USA, the annual expenditures for the management of patients with low back pain are estimated to exceed US$100 billion.24 A retrospective analysis of nearly 2·5 million US patients with newly diagnosed low back or lower extremity pain between 2008 and 2015,25 revealed that 98·8% of cohorts did not undergo surgery in the year following diagnosis. The

Pathogenesis

Multifactorial causes and risk factors contribute to pathogenesis of low back pain, and this section provides an overview.

Changes in the brain

Structural and functional changes in the brain have been generating interest as they might serve as biomarkers linking anatomical changes with pain. Studies have identified common and disease-specific changes in white and grey matter brain regions in patients with chronic low back pain, such as the dorsolateral prefrontal cortex thalamus, temporal lobes, and insula and primary somatosensory cortex, indicating that chronic pain is associated with structural reorganisation.49 Functional changes,

Behavioural factors

In line with the revised International Association for the Study of Pain51 definition of pain, low back pain represents not just the sensory awareness of bodily harm, but also an emotional experience that can be influenced by other emotions (eg, fear, sadness, and anxiety). Psychologically traumatic events could precipitate or reinforce low back pain. In one study evaluating clinician-reported views on low back pain triggers (which could underestimate the incidence), 3·1% cited psychological

Genetic factors

The genetic determinants of low back pain have received increased attention in the past decade and could someday be part of precision medicine algorithms. Carvalho-E-Silva and colleagues62 found that heritability contributed 26% to lifetime prevalence of low back pain, 36% for functional limitations, and 25% to pain intensity in 1598 twins. A systematic review of 27 studies involving twins showed that the effects of heritability accounted between 21% and 67% of back pain burden.63 One question

Clinical presentation

Intervertebral disc herniation typically manifests as low back pain (ie, from annular tears and disc disruption) and leg pain (from nerve root irritation or referred pain from degenerated discs). This pain usually resolves over several weeks in patients without neurological deficits but might persist in many people. A prospective cohort study followed 605 patients with low back pain with or without sciatica for 2 years, and noted that 54% of patients had recurrent pain at 6 months and 47% had

Diagnosis of low back pain

An overview of 15 clinical practice guidelines explored diagnostic recommendations for non-specific low back pain.74 Although a large proportion of low back pain cases are non-specific or resolve without a formal diagnosis, most guidelines recommend history taking and physical examination to identify specific entities. Most guidelines (78%) endorsed neurological examination to identify patients with nerve root compression. Patients with lumbar spinal stenosis might also require vascular-focused

Imaging

Numerous guidelines have been published on the use of imaging for low back pain, high rates of use, the high prevalence rates of abnormalities in asymptomatic volunteers (most people have disc degeneration by age 40 years), and the poor correlation between symptoms and pathology.78 For acute low back pain, red flags, including severe or progressive neurological deficits, warrant imaging. For chronic low back pain, routine imaging is not recommended, although it could be considered on a

Screening

Screening tools have been developed to identify patients with acute low back pain who are prone to develop chronic pain. The Örebro Musculoskeletal Pain Screening Questionnaire,84 which assesses 24 different variables, was found to have low-to-moderate positive predictive values. The StarT Back tool85 was developed to identify subgroups of patients with low back pain requiring early prevention strategies. A large prospective study found the StarT Back tool to be acceptable for a 1 year

Prevention

Prevention of low back pain has received increased attention as governments and payers struggle to find practical solutions to implement. One reason behind the lack of progress could be the underestimation of non-anatomical aspects contributing to low back pain, such as psychosocial risk factors,89 and under-utilisation of multidimensional interventions.90 Previous studies on interventions such as exercise, education, and ergonomic modifications have yielded modest results.91 In adults, a

Behavioural management of low back pain

Due to ongoing concerns about the risk to benefit ratio of opioids and suboptimal results in clinical trials evaluating other pharmacological agents, published guidelines have proposed non-pharmacological approaches such as exercise and physical therapy as first-line treatments for low back pain. The initial encounter with patients with low back pain should take place in a primary care setting,31 and begin with familiarising an individual with their pain condition and self-management

Limitations

Conclusions from narrative reviews rely heavily on article selection, and although we prioritised systematic reviews and meta-analyses, the conclusions in these reviews vary with specialty, which introduces bias. Unlike conditions such as diabetic neuropathy, low back pain is a symptom; therefore, studies evaluating interventional treatments tailored towards a specific cause (eg, injections or surgeries) depend on accurate diagnosis, which is subject to false-positive and false-negative

Conclusions

The prevalence of chronic low back pain is expected to increase with the ageing of populations and as technological advances lead to more sedentary lifestyles. Although this Seminar focuses on specific conditions and their treatments, there is considerable overlap between contributors to low back pain in terms of presentation. There is widespread acceptance of the biopsychosocial model that emphasises multidimensional components and the diverse consequences of chronic pain that can adversely

Search strategy and selection criteria

We searched MEDLINE, Cochrane Library, and Google Scholar using the key words “back pain”, “spine OR spinal pain”, with the qualifiers “low OR lumbar”, “radicular”, “neuropathic”, “neurogenic”, “mechanical”, “axial”, “buttock”, and “non-specific” in combination with the terms “epidemiology”, “pathogenesis”, “clinical presentation”, “diagnosis”, “imaging”, “therapy”, “trials”, and “prevention” from January, 1991, to January, 2021, with no date or language restrictions. We prioritised systematic

Declaration of interests

SPC reports personal fees from SPR Therapeutics; grants and personal fees from Avanos; grants and personal fees from Scilex/Sorrento; personal fees from Persica; and personal fees from the Department of Justice, outside the submitted work. All other authors declare no competing interests.

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