Non Specific Low Back Pain


Original Editor­ - Sam Verhelpen

Top ContributorsAnouk Van den Bossche, Andeela Hafeez, Pieter Verbeirens, Lien Hennebel and Arne De Cort

Definition

Non-specific low back pain is defined as low back pain not attributable to a recognizable, known specific pathology (eg, infection, tumour, osteoporosis, lumbar spine fracture, structural deformity, inflammatory disorder,radicular syndrome, or cauda equina syndrome).  [1]

Non-specific low back pain is usually categorized in 3 subtypes: acute, sub-acute and chronic low back pain. This subdivision is based on the duration of the back pain. Acute low back pain is an episode of low back pain for less than 6 weeks, sub-acute low back pain between 6 and 12 weeks and chronic low back pain for 12 weeks or more. [2]

Clinically Relevant Anatomy

The lumbar spine consists of 5, movable relative to each other, lumbar vertebrae (L1-L5). They are the largest segments of the vertebral column, because it supports greater weight of the body against gravity, as compared to the thoracic or cervical region. Each lumbar vertebra consists of a vertebral body, a vertebral arch and a processus spinosus, a processes transversi and facet joints. The fifth lumbar vertebra has a little bit a different morphology then the other lumbar vertebrae, it is more cuneiform which accords with the prominence of the sacrovertebral articulation. Studies also say that the integrity and the anatomy of the body of the lumbar vertebra is multifactorial. [3].

Before making a searching strategy for finding a cause of the non-specific low back pain problematic, it’s crucial to understand the functional spinal unit (=motion segment, the smallest physiological unit of the (lumbar) spine). This unit consist of 2 adjacent vertebrae and the intervertebral disc in between and they are strongly connected with all the adjoining ligaments, connecting tissues, facet joint and muscles.


The functional unit is divided in 3 compartments, which each part fulfilled a specific function:

  1. The front lumbar compartment consist the vertebral body and the discus intervertebralis (and also the ligamentum longitudinale anterius/posterius) --> function: support the biggest part of the bodyweight against gravity and also as a shock absorber. The ligaments play an important role in resisting heavy movements.
  2. The middle lumbar compartment consist the vertebral canalis --> function: protection of the spinal cord. Note: the spinal cord ends by the first lumbar vertebrae and then from the second lumbar vertebrae the spinal nerves forms the cauda equina.
  3. The rear lumbar compartment consist the vertebral arch, the processus spinosus, the processes transversi and the facet joints. --> function: protection against rotation and extreme movements + attachment site for connective tissue and muscles.

In total there are 3 motion direction possible in the lumbar spine: flexion/extension, side bending and rotation.The lumbar spine exhibits a lumbar lordosis, which is a result and a key factor of the evolution to the erect posture. This was an adaptation to the newly acquired function of axial loading. Level of evidence: 2A [3]


The back (lumbar) muscles play along with the abdominal, the glutea and the leg muscles an important role in the etiology of low back pain. Study’s suggests that that multifidus and paraspinal muscle groups are significantly smaller in patients with chronic low back pain than in control patients who are healthy and on the symptomatic side of patients with chronic unilateral low back pain compared with the asymptomatic side. Level of evidence: 2A [4]

https://www.youtube.com/watch?v=0qR-Yfw9fOI

Epidemiology/Etiology

Low back pain (LBP) is the fifth most common reason for physician visits, which affects nearly 60-80% of people throughout their lifetime[5][6]. The lifetime prevalence of low back pain is reported to be as high as 84%, and the prevalence of chronic low back pain is about 23%, with 11-12% of the population being disabled by low back pain[1].  In the 2010 Global Burden of Disease study the global age-standardised point prevalence of LBP (from 0 to 100 years of age) was estimated to be 9.4%[7]. The same study showed that prevalence in 2010 was highest in western Europe followed by North Africa/Middle East, and lowest in the Caribbean followed by central Latin America.

Economically LBP is a huge burden, LBP causes more global disability than any other condition[7]. The cost of care for LBP has been reported (in the USA) to be over $50 billion annually[8]. Despite the intense focus and formal research on the care of non-specific LBP Pransky et al[9] reported a five fold increase in the prevalence of LBP over a 15 year period. It should be noted that most of the epidemiology/economic studies have been done in the western industrialised higher resourced countries and these figures will differ globally.

Low back pain is a self limiting condition[10]:

  • 90% of people with LBP will recover in 3-4 months with no treatment.
  • 70% of people with LBP will recover in 1 month with no treatment.
  • 50% of people with LBP will recover in 2 weeks with no treatment.
  • 5% of the remaining 10% will not respond to conservative care (such as physiotherapy)
  • The final 5% are the more challenging cases that don't naturally improve that we as physiotherapists commonly see.

However these figures may be deceptive because although the pain may go away the the re-occurrence rate of LBP is extremely high and these individuals are likely to experience another episode of LBP within 3-6 months. Re-occurrence is a major problem with the re-occurrence rate being approximately 60%.

Non-specific low back pain accounts for over 90% of patients presenting to primary care[11] and these are the majority of the individuals with low back pain that present to physiotherapy.

Non-specific low back pain can caused by:

  • Traumatic injury
  • Lumbar sprain or strain
  • Postural strain

Cook et al (study ongoing 2015) studied risk factors for LBP pain: 

First occurrence Recurrent episode
Community setting
  • standing or walking >2hrs per day
  • frequent moving or lifting >25 lbs
  • widespread pain
  • limping
  • higher general health scores
  • other musculoskeletal complaints
  • sitting, standing or walking >2hrs per day
  • frequent moving or lifting >25 lbs
  • strength <50%
  • depression
  • perceived inadequacy i.e. income, job
Occupational setting
  • female
  • obesity
  • increased driving time
  • perceived heavy lifting requirements
  • slower velocity doing activities
  • poor MCS SF-12 score (i.e. higher anxiety, depression etc)
  • obesity
  • poor health
  • prior LBP
  • poor back endurance
  • frequent moving or lifting >25 lbs
  • manual jobs
  • awkward posture
  • mental distress
  • poor relationships at work

Leg pain is a frequent accompaniment to low back pain, arising from disorders of neural or musculoskeletal structures of the lumbar spine. Differentiating between different sources of radiating leg pain is important to make an appropriate diagnosis and identify the underlying pathology. Some specific causes of leg pain need to be managed in a different way to simple non-specific low back pain.

Possible Mechanisms

Any innervated structure in the lumbar spine can cause symptoms of low back and referred pain into the extremity or extremities. This long list of potential structures includes the muscles, ligaments, dura mater and nerve roots, zygapophyseal joints, annulus fibrosis, thoracolumbar fascia, and vertebrae. One might expect that improvement in the resolution of imaging technology has increased the likelihood of detecting a link between pathology and pain in the lumbar spine. However, the determination of a pathoanatomic origin of low back pain is made difficult by the rate of false-positive findings on imaging studies, that is, individuals without low back pain showing abnormal findings. For example, evidence of herniated disc material is shown on computerized tomography (CT) scans, MRI, and myelography in 20% to 76% of persons with no sciatica[12]. Furthermore, Savage et al[13] reported that 32% of their asymptomatic subjects had “abnormal” lumbar spines (evidence of disc degeneration, disc bulging or protrusion, facet hypertrophy, or nerve root compression) and only 47% of their subjects who were experiencing low back pain had an abnormality identified. In longitudinal studies, low back pain can develop in the absence of any associated change in radiographic appearance of the spine[13]. Boos et al[14] followed asymptomatic patients with a herniated disc for 5 years and determined that physical job characteristics and psychological aspects of work were more powerful than MRI-identified disc abnormalities in predicting the need for low back pain–related medical consultation. Thus, the association between clinical complaints and concurrent pathological examination with radiological findings must be considered cautiously. Further, even when abnormalities are present, establishing a direct cause and effect between the pathological finding and the patient condition has proven to be elusive and most often does not assist greatly in patient management. [12]

Characteristics/Clinical Presentation

Some characteristics/clinical presentation:

  • The cause of the problem can’t be explained by a recognizable, known specific pathology (like infection, fracture, cauda equina syndrome,…)[1]
  • All age groups can be affected by non-specific low back pain. but the impact on quality of life is lower in adolescents than in adults[1]
  • Evidence for the use of sub-grouping in the diagnosis, classification, or management of non-specific low back pain is limited[1]
  • The outcome of acute spells is obscured by frequent relapses [1] 
  • Results of large-scale epidemiological studies show that one of the main characteristics of low back pain is recurrence[1]
  • Most episodes of low back pain are self-limiting and are not associated with serious diseases, but it’s important for the clinician to distinguish the small proportion of patients with serious underlying diseases, so called red flags! Level of evidence 1A [1]
  • Risk factors for red flags are: age at onset (<20j. or > 55j.), significant trauma, unexplained weight loss and widespread neurologic changes[15]
  • Overweight/obese is a strong predictor and is often seen by non specific-low back pain. Overweight and obesity have the strongest association with seeking care for low back pain and chronic low back pain[16]
  • Studies suggests that psychosocial factors at the subacute stage are a characteristic/predictor in the development of chronic non-specific low back pain[17]
  • Studies suggests that increased lumbar spine mobility is a common clinical characteristic/ presentation in non-specific low back pain and that is a high evidence risk factor for non-specific low back pain[18]

Differential diagnoses

Low back pain is a symptom that accompanies several diseases. The diagnosis of non-specific low back pain implies no known pathoanatomical cause. Triage aims to exclude those cases in which the pain arises from either problems beyond the lumbar spine (eg, leaking aortic aneurysm); specific disorders affecting the lumbar spine (eg, epidural abscess, compression fracturespondyloarthropathymalignancy, cauda equina syndrome); or radicular pain, radiculopathy, or spinal canal stenosis. Remaining cases are non-specific low back pain. Several lumbar structures are plausible sources of pain (eg, the intervertebral disc, the facet joints), but clinical tests do not reliably attribute the pain to those structures [19]

Diagnostic procedures

Once serious spinal pathology and specific causes of back pain have been ruled out the patient is classified as having non-specific low back pain

Outcome Measures

In the study of Van der Roer et al. the main outcome measures were the Minimal Clinically Important Change (MCIC) of the pain intensity numerical rating scale (PI-NRS), the Quebec Back Pain Disability Scale (QBPDS), and the Euroqol (EQ) in patients with low back pain. The MCIC was estimated over a 12-week period, and three different methods were used: 1) mean change scores, 2) minimal detectable change, and 3) optimal cutoff point in receiver operant curves. The global perceived effect scale (GPE) was used as an external criterion. The effect of initial scores on the MCIC was also assessed. The MCIC of the PI-NRS ranged from 3.5 to 4.7 points in (sub)acute patients and 2.5 to 4.5 points in chronic patients with low back pain. The MCIC of the QBPDS was estimated between 17.5 to 32.9 points and 8.5 to 24.6 points for (sub)acute and chronic patients with low back pain. The MCIC for the EQ ranged from 0.07 to 0.58 in (sub)acute patients and 0.09 to 0.28 in patients with chronic low back pain. [20]


The study of Ferreira et al. investigated the comparison of general exercises, motor control exercises and spinal manipulative therapy for chronic low back pain. The primary outcomes in this study were patient-specific function (PSFS, 3–30) and global perceived effect (GPE, −5 to 5) at 8 weeks. These outcomes were also measured at 6 and 12 months. Follow-up was 93% at 8 weeks and 88% at 6 and 12 months. The motor control exercise group had slightly better outcomes than the general exercise group at 8 weeks (between-group difference: PSFS 2.9, 95% CI: 0.9–4.8; GPE 1.7, 95% CI: 0.9–2.4), as did the spinal manipulative therapy group (PSFS 2.3, 95% CI: 0.4–4.2; GPE 1.2, 95% CI: 0.4–2.0). The groups had similar outcomes at 6 and 12 months. Motor control exercise and spinal manipulative therapy produce slightly better short-term function and perceptions of effect than general exercise, but not better medium or long-term effects, in patients with chronic non-specific back pain. [21]

Examination

As mentioned above it is not necessary to determine the specific pain causing structure to effectively manage this patient group. Physiotherapy assessment aims to identify impairments that may have contributed to the onset of the pain, or increase the likelihood of developing persistent pain. These include biological factors (eg. weakness, stiffness), psychological factors (eg. depression, fear of movement and catastrophisation) and social factors (eg. work environment)[22]. The assessment does not focus on identifying anatomical structures (eg. the intervertebral disc) as the source of pain, as might be the case in peripheral joints such as the knee[22]. Previous research and international guidelines suggest it is not possible or necessary to identify the specific tissue source of pain for the effective management of mechanical back pain[22][23][24]

The diagnosis of non-specific low back pain implies no known pathoanatomical cause. Triage aims to exclude those cases in which the pain arises from either problems beyond the lumbar spine (eg, leaking aortic aneurysm); specific disorders affecting the lumbar spine (eg, epidural abscess, compression fracture, spondyloarthropathy, malignancy, cauda equina syndrome); or radicular pain, radiculopathy, or spinal canal stenosis. Remaining cases are non-specific low back pain. Several lumbar structures are plausible sources of pain (eg, the intervertebral disc, the facet joints), but clinical tests do not reliably attribute the pain to those structures.[25]


Diagnostic investigations have no role in the management of non-specific low back pain. Although diagnoses based on lumbar structures (discogenic low back pain, facet joint pain, sacroiliac joint pain) remain popular in some settings, the available clinical tests for these conditions have insufficient accuracy. Diagnostic investigations have a role when the clinician suspects a specific disease process that would be managed differently from non-specific low back pain. The threshold for triggering investigations should reflect both the consequence of missing or delaying the diagnosis and the clinician’s assessment of the likelihood of a more serious disease being present. [25]


Summary of Common Recommendations for Diagnosis of Low back pain

  • Diagnostic triage (non-specific low back pain, radicular syndrome, serious pathology).
  • Screen for serious pathology using red flags.
  • Physical examination for neurologic screening (including straight leg raising test).
  • Consider psychosocial factors (yellow flags) if there is no improvement.
  • Routine imaging not indicated for non-specific low back pain
  • Lumbar Examination

Movement control dysfunction [MCD] reduces active control of movements. Patients with MCD might form an important subgroup among patients with non specific low back pain. The diagnosis is based on the observation of active movements.

Tests for examination of motor control:

  • waiter's bow:Flexion of the hips in upright standing without movement (50-70° flexion) of the low back
    Rating protocol: As patients did not know the tests, only clear movement dysfunction was rated as "not correct". If the movement control improved by instruction and correction, it was considered that it did not infer a relevant movement dysfunction.
  • Sitting knee extension test for flexion dysfunction: Upright sitting with corrected lumbar lordosis; extension of the knee without movement (flexion) of low back  Rating protocol: As patients did not know the tests, only clear movement dysfunction was rated as "not correct". If the movement control improved by instruction and correction, it was considered that it did not infer a relevant movement dysfunction.
  • Pelvic tilt for extension dysfunction
  • One leg stance difference for rotational dysfunction: From normal standing to one leg stance: measurement of lateral movement of the belly button. (Position: feet one third of trochanter distance apart). Rating protocol: As patients did not know the tests, only clear movement dysfunction was rated as not correct. If the movement control improved by instruction and correction, it was considered that it did not infer a relevant movement dysfunction. [26]

Medical management

The NICE guidelines [27] for low back pain recommend advice, analgesia and imaging only in specific
circumstances.

Information, education and patient preferences [27]
Provide people with advice and information to promote self-management of their low back pain.

  1. Offer educational advice that includes information on the nature of non-specific low back pain and encourages the person to be physically active and continue with normal activities as far as possible.
  2. Include an educational component consistent with this guideline as part of other
    interventions, but do not offer stand-alone formal education programmes.
  3. Take into account the person's expectations and preferences when considering
    recommended treatments, but do not use their expectations and preferences to predict their response to treatments.

Pharmacology

No opioids, cyclooxygenase 2 (COX-2) inhibitors or tricyclic antidepressants and only some nonsteroidal anti-inflammatory drugs (NSAIDs) have a UK marketing authorisation for treating low back pain. If a drug without a marketing authorisation for this indication is prescribed, informed consent should be obtained and documented. Take into account the individual risk of side effects and patient preference.[27]First medication option should be regular paracetamol. When paracetamol alone provides insufficient pain relief, offer non-steroidal anti-inflammatory drugs (NSAIDs) and/or weak opioids (codeine and dihydrocodeine). Give due consideration to the risk of side effects from NSAIDs, especially in older people and other people at increased risk of experiencing side effects.[27]

Tricyclic antidepressants may be considered if other medications provide insufficient pain relief. Strong opioids should only be considered for short-term use to people in severe pain. Consider referral for specialist assessment for people who may require prolonged use of strong opioids.[27]

Imaging [27]

  1. Do not offer X-ray of the lumbar spine for the management of non-specific low back pain.
  2. Consider MRI when a diagnosis of spinal malignancy, infection, fracture, cauda equina syndrome or ankylosing spondylitis or another inflammatory disorder is suspected.
  3. Only offer an MRI scan for non-specific low back pain within the context of a referral for an opinion on spinal fusion.

If these treatments do not result in satisfactory improvement consider offering physiotherapy interventions such as exercise, manual therapy and acupuncture as appropriate treatment techniques.

Surgery

The place for surgery in chronic non-specific low back pain (if any) is very limited and its overuse has been criticised.[1] Failed back surgery (FBSS) is a nonspecific term that implies that the final outcome of surgery did not meet the expectations of both the patient and the surgeon that were established before surgery.[28]

Physical therapy management

The following physical therapy management strategies are from the NICE guidelines[27].  Also see Interventions for LBP.

If first line medical management of analgaesia and advice fail offer one of the following treatment options, taking into account patient preference: an exercise programme or a course of manual therapy. Consider offering another of these options if the chosen treatment does not result in satisfactory improvement.

A. Physical activity and exercise

  1. Advise people to stay active.[1]
  2. Advise people with low back pain to exercise.
  3. Consider offering a structured exercise programme tailored to the person. This should comprise up to a maximum of eight sessions over a period of up to 12 weeks. Offer a group supervised exercise programme, in a group of up to 10 people. A one-to-one supervised exercise programme may be offered if a group programme is not suitable for a particular person.
    • Exercise programmes may include the following elements:
    • aerobic activity
    • movement instruction
    • muscle strengthening
    • postural control
    • stretching.
  4. For chronic low back pain, self-management strategies for example health-promoting activities, self-monitoring of status, and decision-making are receiving increasing attention as important components in the management of low back pain. Level of evidence 1A [1]
  5. In subacute low-back pain there is some evidence that a graded activity program improves absenteeism outcomes. Level of evidence 1A [29]
  6. You can offer the patient stabilizations exercises when there is an indications of lumbar instability. These exercises for lumbar instability have been suggested that they can reduce the pain and disability outcome. However latest studies suggest that there is a strong evidence that stabilisation exercises are not more effective than any other form of active exercise in the long term. Level of evidence 1A [30]
  7. You can also offer the patient lumbar motor control exercises:
    Motor control training focuses on the activation of the deep trunk muscles and targets the restoration of control and co-ordination of these muscles, progressing to more complex and functional tasks integrating the activation of deep and global trunk muscles. There is strong evidence that MCE is not superior to other forms of exercise for both acute and chronic non-specific low back pain. Level of evidence 1A [31][32] For lumbar motor control exercises look at: www.youtube.com/watch
  8. You can also offer the patient back school programs:
    Back school programs are introduced by the Swedish back school in 1969, the goal of such a program is to reduce pain and preventing recurrent episodes of low back pain. Recent studies suggests that is uncertain if back schools are effective for acute and subacute non-specific LBP as there is only very low quality evidence available. Level of evidence 1A [33]
  9. You can also offer the patient the McKenzie Therapy:
    The McKenzie therapy is a multidimensional, classification-based treatment for patients with low back pain. The therapy consist of 3 parts: evaluation, treatment and prevention. In the treatment the exercises are based upon the direction (flexion, extension, lateral bending and rotation) and the aim is to reduce pain. Studies suggests that the McKenzie method is more effective than passive therapy for acute low back pain; however, the magnitude of the difference suggests the absence of clinically worthwhile effects. There is limited evidence for the use of McKenzie method in chronic low back pain. The effectiveness of classification-based McKenzie is yet to be established. Level of evidence 1A [34]

B. Manual therapy

Spinal manipulation therapy Level of evidence 1A [1]:

The manual therapies reviewed for the NICE Guidelines were spinal manipulation (a low-amplitude, high-velocity movement at the limit of joint range that takes the joint beyond the passive range of movement), spinal mobilisation (joint movement within the normal range of motion) and massage (manual manipulation or mobilisation of soft tissues). Consider offering a course of manual therapy, including spinal manipulation, comprising up to a maximum of nine sessions over a period of up to 12 weeks.

C. Other non-pharmacological therapies

Electrotherapy modalities

  1. Do not offer laser therapy.
  2. Do not offer interferential therapy.
  3. Do not offer therapeutic ultrasound.

D. Transcutaneous nerve stimulation

Do not offer transcutaneous electrical nerve simulation (TENS).

E. Lumbar supports

Do not offer lumbar supports.

F. Traction

Do not offer traction (this may be indicated in specific causes of low back pain such as radiculopathy).

G. Combined physical and psychological treatment programme

Cognitive behavioural interventions yield long-term improvements in pain, disability and quality of life in comparison to no treatment and other guideline-based active treatments for patients with LBP of any duration and of any age. Level of evidence 1A [35]

H. Stratified Care

Stratified care has been suggested as an appropriate approach to manage non-specific low back pain. Stratified care is the targeting of treatment to subgroups of patients based on characteristics. Foster et al suggest that there are 3 different approaches to stratification that have good evidence:[36]

  1. Patient prognosis- matching treatment to patients prognosis such as the likelihood of persistnet pain and disability (e.g. STarT Back Screening Tool [37][38]).
  2. Responsiveness to treatment - matching treatments to individuals who would benefit from that treatment (e.g. Treatment Based Classification Approach to Low Back Pain, STOPS Trials).
  3. Underlying mechanisms - matching treatment to mechanisms that drive pain and disability such as pathology, pain mechanisms, negative thoughts and behaviours (e.g. Cognitive Functional Approach[39] , McKenzie appraoch[40][41]).

The use of these different stratification approaches vary around the world and there are overlaps between these three different approaches. A perfect subgrouping approach would include all there of these approaches. These models don’t replace clinical reasoning or experience but they do warrant judicious exploration in clinical practice in appropriate settings.

Clinical Bottom Line

Non-specific low back pain is defined as low back pain not attributable to a recognizable, known specific pathology. The place for surgery in chronic non-specific low back pain is very limited and its overuse has been criticized. Level of evidence 1A [1]

For acute low back pain, most clinical practice guidelines agree on the use of reassurance, recommendations to stay active, brief education, paracetamol, non-steroidal anti-inflammatory drugs, spinal manipulation therapy, muscle relaxants (as second line drugs only, because of side-effects), and weak opioids (in selected cases). Level of evidence 1A [1]

For chronic low back pain, the use of brief education about the problem, advice to stay active, non-steroidal anti-inflammatory drugs, weak opioids (short-term use), exercise therapy (of any sort), spinal manipulation are recommended and Self-management strategies. Level of evidence 1A [1]

References

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Balagué, Federico, et al. "Non-specific low back pain." The Lancet 379.9814 (2012): 482-491. Level of evidence 1A
  2. Burton AK, Tillotson KM, Main CJ, Hollis S. Psychosocial predictors of outcome in acute and subchronic low back trouble. Spine (Phila Pa 1976). 1995 Mar 15;20(6):722-8.Level of evidence 3C
  3. 3.0 3.1 Prabhu, L. V., et al. "Vertebral body integrity: a review of various anatomical factors involved in the lumbar region." Osteoporosis international 18.7 (2007): 891-903. Level of evidence 2A
  4. Fortin, Maryse, and Luciana Gazzi Macedo. "Multifidus and paraspinal muscle group cross-sectional areas of patients with low back pain and control patients: a systematic review with a focus on blinding." Physical therapy (2013). Level of evidence 2A
  5. Burton AK, Tillotson KM, Main CJ, Hollis S. Psychosocial predictors of outcome in acute and subchronic low back trouble. Spine (Phila Pa 1976). 1995 Mar 15;20(6):722-8. Level of evidence 3C
  6. Truchon M. Determinants of chronic disability related to low back pain: towards an integrative biopsychosocial model. Disabil Rehabil. 2001 Nov 20;23(17):758-67.Level of evidence 2B
  7. 7.0 7.1 Damian Hoy, Lyn March, Peter Brooks, Fiona Blyth, Anthony Woolf, Christopher Bain, Gail Williams, Emma Smith, Theo Vos, Jan Barendregt, Chris Murray11, Roy Burstein11, Rachelle Buchbinder. The global burden of low back pain: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis 2014;73:968-974. Level of evidence 2A
  8. Liliedahl RL1, Finch MD, Axene DV, Goertz CM. Cost of care for common back pain conditions initiated with chiropractic doctor vs medical doctor/doctor of osteopathy as first physician: experience of one Tennessee-based general health insurer. J Manipulative Physiol Ther. 2010 Nov-Dec;33(9):640-3.
  9. Pransky G, Borkan JM, Young AE, Cherkin DC. Are we making progress?: the tenth international forum for primary care research on low back pain. Spine (Phila Pa 1976). 2011 Sep 1;36(19):1608-14.
  10. Gatchel RJ, Polatin PB, Mayer TG. The dominant role of psychosocial risk factors in the development of chronic low back pain disability. Spine (Phila Pa 1976). 1995 Dec 15;20(24):2702-9.
  11. Koes BW, van Tulder MW, Thomas S. Diagnosis and treatment of low back pain. BMJ 2006;332:1430–34.
  12. 12.0 12.1 Anthony Delitto, Steven Z. George, Linda Van Dillen, Julie M. Whitman, Gwendolyn Sowa, Paul Shekelle, Thomas R. Denninger, Joseph J. Godges. Low Back Pain: Clinical Practice Guidelines Linked to the International Classification of Functioning, Disability, and Health from the Orthopaedic Section of the American Physical Therapy Association. Journal of Orthopaedic and Sports Physical Therapy, 2012, 42(4) level of evidence 1A
  13. 13.0 13.1 Savage, R.A., G.H. Whitehouse, and N. Roberts, The relationship between the magnetic resonance imaging appearance of the lumbar spine and low back pain, age and occupation in males. Eur Spine J, 1997. 6(106-114).level of evidence 1A
  14. Boos N, Semmer N, Elfering A, et al. Natural history of individuals with asymptomatic disc abnormalities in magnetic resonance imaging: predictors of low back pain-related medical consultation and work incapacity. Spine (Phila Pa 1976). 2000;25:1484–1492.level of evidence 2B
  15. Koes, Bart W., et al. "An updated overview of clinical guidelines for the management of non-specific low back pain in primary care." European Spine Journal 19.12 (2010): 2075-2094. Level of evidence 1A
  16. Shiri R, Karppinen J, Leino-Arjas P, Solovieva S, Viikari-Juntura E. The association between obesity and low back pain: a meta-analysis. Am J Epidemiol 2010; 171: 135–54. Level of evidence 1A
  17. Heitz, C. A. M., et al. "Comparison of risk factors predicting return to work between patients with subacute and chronic non-specific low back pain: systematic review." European Spine Journal 18.12 (2009): 1829-1835. Level of evidence 1A
  18. Lakke, Sandra E., et al. "Risk and prognostic factors for non-specific musculoskeletal pain: a synthesis of evidence from systematic reviews classified into ICF dimensions." PAIN® 147.1 (2009): 153-164. Level of evidence 1A
  19. Chris Maher, et al. "Non-specific low back pain." The Lancet (2016). Level of evidence 1A
  20. Van Tulder M., et al.” An updated overview of clinical guidelines for the management of non-specific low back pain in primary care.”, Eur Spine J (2010) 19:2075–2094. Level of evidence A1
  21. Ferreira, Manuela L., et al. "Comparison of general exercise, motor control exercise and spinal manipulative therapy for chronic low back pain: a randomized trial." Pain 131.1 (2007): 31-37. Level of evidence A2
  22. 22.0 22.1 22.2 Hancock MJ, Maher CG, Latimer J, et al. Systematic review of tests to identify the disc, SIJ or facet joint as the source of low back pain. Eur Spine J 2007;16:1539–50.level of evidence 1A
  23. Koes BW, van Tulder M, Lin C-WC, Macedo LG, McAuley J, Maher C. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J 2010;19:2075–94. level of evidence 1A
  24. van Tulder M, Becker A, Bekkering T, et al. Chapter 3. European guidelines for the management of acute nonspecific low back pain in primary care. Eur Spine J 2006;15(Suppl 2):S169–91.level of evidence 1A
  25. 25.0 25.1 E. B. ROUX, et al.,” Medical approach to low back pain.”, Bailli~re's Clinical Rheumatology-- Vol. 6, No. 3, October 1992. Level of evidence C
  26. Chris Maher, et al. "Non-specific low back pain." The Lancet (2016). Level of evidence 1A
  27. 27.0 27.1 27.2 27.3 27.4 27.5 27.6 Low back pain: Early management of persistent non-specific low back pain. NICE guidelines [CG88], May 2009 Level of evidence 2C
  28. Schofferman, Jerome, et al. "Failed back surgery: etiology and diagnostic evaluation." The Spine Journal 3.5 (2003): 400-403. Level of evidence 2C
  29. Hayden, Jill, et al. "Exercise therapy for treatment of non‐specific low back pain." The Cochrane Library (2005). Level of evidence 1A
  30. Smith, Benjamin E., Chris Littlewood, and Stephen May. "An update of stabilisation exercises for low back pain: a systematic review with meta-analysis." BMC musculoskeletal disorders 15.1 (2014): 1. Level of evidence 1A
  31. Macedo, Luciana G., et al. "Motor control exercise for acute non‐specific low back pain." The Cochrane Library (2016). Level of evidence 1A
  32. Saragiotto, Bruno T., et al. "Motor control exercise for chronic non‐specific low‐back pain." The Cochrane Library (2016). Level of evidence 1A
  33. Poquet, Nolwenn, et al. "Back schools for acute and subacute non‐specific low‐back pain." The Cochrane Library (2016). Level of evidence 1A
  34. Machado, Luciana Andrade Carneiro, et al. "The McKenzie method for low back pain: a systematic review of the literature with a meta-analysis approach." Spine 31.9 (2006): E254-E262. Level of evidence 1A
  35. Richmond, Helen, et al. "The effectiveness of cognitive behavioural treatment for non-specific low back pain: a systematic review and meta-analysis." PloS one 10.8 (2015): e0134192. Level of evidence 1A
  36. Foster N.E, Hill J.C, O'Sullivan P, Childs J.D, Hancock M.J. Stratified models of care for low back pain. WCPT Congress, Singapore, 2015
  37. Hill JC, Dunn KM, Lewis M, Mullis R, Main CJ, Foster NE, Hay EM. A primary care back pain screening tool: identifying patient subgroups for initial treatment. Arthritis Care and Research 2008;59:632-41. level of evidence 2B
  38. Hill JC, Whitehurst DG, Lewis M, Bryan S, Dunn KM, Foster NE, Konstantinou K, Main CJ, Mason E, Somerville S, Sowden G, Vohora K, Hay EM. Comparison of stratified primary care management for low back pain with current best practice (STarT Back): a randomised controlled trial. Lancet 2011;378:1560-71. level of evidence 2B
  39. K Vibe Fersum, P O’Sullivan,2 JS Skouen, A Smith, and A Kvåle1. Efficacy of classification-based cognitive functional therapy in patients with non-specific chronic low back pain: A randomized controlled trial. Eur J Pain. 2013 Jul; 17(6): 916–928. level of evidence 2B
  40. Helen Clare, Roger Adams, Chris G Maher. A systematic review of efficacy of McKenzie therapy for spinal pain. THE AUSTRALIAN JOURNAL OF PHYSIOTHERAPY 50(4):209-16 • FEBRUARY 2004 Level of evidnce 1A
  41. Tom Petersen. Non-specific Low Back Pain: Classification and treatment. Lund University, 2003. level of evidence 5