Low Back Pain: Difference between revisions

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However, in its narrow focus on the disc, the spine field may have overlooked other potential keys to the understanding of low back pain, including one immediately adjacent to the disc. <ref>BackLetter, When It Comes to Back Pain Causation, Has the Spine Field Missed the Forest for the Trees? Vol. 27, No. 9, September 2012</ref>  
However, in its narrow focus on the disc, the spine field may have overlooked other potential keys to the understanding of low back pain, including one immediately adjacent to the disc. <ref>BackLetter, When It Comes to Back Pain Causation, Has the Spine Field Missed the Forest for the Trees? Vol. 27, No. 9, September 2012</ref>  


The vertebral endplate has been somewhat understudied as a potential cause of low back pain. Some of this relates to its size and structure. Over the past century, most theories of back pain causation have been based on abnormalities that could be visualized—with the naked eye or with imaging. <ref>Lutz GK et al., Looking back on back pain: Trial and error of diagnoses in the 20th  century, Spine, 2003; 28:1899–905.</ref>&nbsp;The thin vertebral endplate—and the various injuries and diseases that affect it—have been difficult to visualize and classify with traditional imaging methods. <br>The endplate appears to play a vital role in the health of both the disc and the vertebrae. The endplate acts a buffer, a barrier, and a conduit for blood vessels and the diffusion of nutrients into the disc. Its structure and function vary by age and skeletal maturity—and in response to various injuries and stages of disc degeneration. (See Moore, 2006; Adams et al., 2006.) it is the first part of the vertebra to exhibit changes in response to high levels of loading and compressive force. (See Adams et al., 2006.)
The vertebral endplate has been somewhat understudied as a potential cause of low back pain. Some of this relates to its size and structure. Over the past century, most theories of back pain causation have been based on abnormalities that could be visualized—with the naked eye or with imaging. <ref>Lutz GK et al., Looking back on back pain: Trial and error of diagnoses in the 20th  century, Spine, 2003; 28:1899–905.</ref>&nbsp;The thin vertebral endplate—and the various injuries and diseases that affect it—have been difficult to visualize and classify with traditional imaging methods. <br>The endplate appears to play a vital role in the health of both the disc and the vertebrae. The endplate acts a buffer, a barrier, and a conduit for blood vessels and the diffusion of nutrients into the disc. Its structure and function vary by age and skeletal maturity—and in response to various injuries and stages of disc degeneration.<ref>Moore RJ, The vertebral endplate: Disc degeneration, disc regeneration, European Spine Journal, 2006; 15 (Suppl 3): S333–S337.</ref><ref>Adams M et al., The Biomechanics of Back Pain. Edinburgh: Churchill Livingstone; 2006:149–50.</ref>&nbsp;it is the first part of the vertebra to exhibit changes in response to high levels of loading and compressive force.<ref>Adams M et al., The Biomechanics of Back Pain. Edinburgh: Churchill Livingstone; 2006:149–50.</ref>


Unlike the adjacent disc, the vertebral endplate has an ample nerve supply in the form of interosseous nerves (i.e. nerves that run into the bony part of the endplate). And it would appear that both the blood and the nerve supply of the endplate may increase in response to disc degeneration. This could be an attempt at tissue repair that paradoxically results in an increased risk for back pain. (See Moore, 2006.) As M.F. Brown, MD, et al. noted in a 1997 study, “The increase in the density of sensory nerves, and the presence of endplate cartilage defects, strongly suggest that the endplates and vertebral bodies are sources of pain.” (See Brown et al., 1997.) <br>It is often stated that “the intervertebral discs are the shock absorbers of the spine”. The scientific evidence supports a different understanding which seems to be important in treatment decisions about how to treat mechanical low back pain. Mechanical pain distinguishes itself from pain related to tumor growth, infection or obvious trauma related pain. <br>The vertebral bodies appear to play a dominant role in performing the function of shock absorber…not the disc. A healthy disc is isotropic and transmits load evenly over the endplate of the vertebral bodies. The endplates are deformable and elastic in the center. The nucleus is incompressible. Cancellous bone inside the vertebrae body is made up of trabeculae; columns of bone from endplate to endplate tied together with smaller transverse trabeculae. With axial compression these columns bend. Under excessive load the transverse trabeculae fracture and columns buckle, but return to 95% when the load is removed This architecture affords elastic deformation, even after marked damage, and then regains its original structure function as it heals. Damaged cancellous fractures appear to heal quickly compared to collagenous tissues.<br>The cause of mechanical low back pain is the focus of ongoing studies. Professor Robert Mulholland finds that the current science is convincing that pain from the spine is related to how the disc and vertebrae take on load, rather than from aberrant movement (instability). Disc degeneration is mainly genetically determined and in itself is not painful. There is an association between disc degeneration and back pain but not between the severity of disc degeneration and the severity of low back pain. As discs degenerate there are often changes in the pattern of movement in the disc that can be seen on repeated studies of flexion and extension x-ray films. However these changes could not be used to distinguish painless degenerative discs from painful ones. <br>The degenerated discs become non-isotropic. That is to say they transmit load variably over the endplate and hence within the vertebral body. McNally and Shackleford in Nottingham showed that patients with painful discs had patterns of load transmission which differed from painless degenerated discs. Mulholland points out the dissatisfaction with spinal fusion occurs often with both technically adequate posterior fusions and anterior fusions. In the case of posterior fusions no movement occurs but the disc is still required to take a load and that mechanism is not improved by the fusion. In the case of anterior fusions the load is often concentrated under the cage or bone implant and therefore pain persists. The Cochrane report suggested that there was no scientific evidence to support the use of fusion for mechanical back pain and results were not improved with the use of rigid fixation. <br>The relevance for physical therapists is that there seems to be clear scientific support for treatment that may change spinal loading patterns. Mulholland comments that prescribing exercise and fitness regimes which currently are so central to the management of back pain, has a certain logic as it may alter the loading patterns, and certainly such therapies would appear illogical if we were treating a movement related problem. <br>There are many options available to physical therapists and other exercise trainers for teaching patients to modify how an individual carries load through their spine. Muscle reeducation, restoring flexibility, postural training, and spinal manipulation is done by a variety of practitioners from different schools of thought. The fact that there are so many approaches used would seem to indicate that each works on some patients but not on others. The key seems to be specifically targeting an approach to the specific patient’s spinal load bearing dysfunction. <br>The benefits of taking a specific exercise approach seems to be efficacious on several levels. First, it addresses a mechanical load-bearing problem with a mechanical load-altering solution. Secondly exercise elicits the patient as an active participant in resolving their problem; thereby enhancing self-efficacy (a person’s perceived ability to manage essential life circumstances.) <br>From clinical experience even patients that report continued chronic pain after technically successfully fusion can improve symptoms and progress using a well designed rehabilitation that focuses on altering spinal loading and facilitating self-efficacy. Perhaps outcomes could be improved, and surgery avoided if exercise programs were improved in several key areas.  
Unlike the adjacent disc, the vertebral endplate has an ample nerve supply in the form of interosseous nerves (i.e. nerves that run into the bony part of the endplate). And it would appear that both the blood and the nerve supply of the endplate may increase in response to disc degeneration. This could be an attempt at tissue repair that paradoxically results in an increased risk for back pain. <ref>Moore RJ, The vertebral endplate: Disc degeneration, disc regeneration, European Spine Journal, 2006; 15 (Suppl 3): S333–S337.</ref>&nbsp;As M.F. Brown, MD, et al. noted in a 1997 study, “The increase in the density of sensory nerves, and the presence of endplate cartilage defects, strongly suggest that the endplates and vertebral bodies are sources of pain.” <ref>Brown MF et al., Sensory and sympathetic innervation of the vertebral endplate in patients with degenerative disc disease, Journal of Bone and Joint Surgery (Brit), 1997; 79:147–53.</ref><br>It is often stated that “the intervertebral discs are the shock absorbers of the spine”. The scientific evidence supports a different understanding which seems to be important in treatment decisions about how to treat mechanical low back pain. Mechanical pain distinguishes itself from pain related to tumor growth, infection or obvious trauma related pain. <br>The vertebral bodies appear to play a dominant role in performing the function of shock absorber…not the disc. A healthy disc is isotropic and transmits load evenly over the endplate of the vertebral bodies. The endplates are deformable and elastic in the center. The nucleus is incompressible. Cancellous bone inside the vertebrae body is made up of trabeculae; columns of bone from endplate to endplate tied together with smaller transverse trabeculae. With axial compression these columns bend. Under excessive load the transverse trabeculae fracture and columns buckle, but return to 95% when the load is removed This architecture affords elastic deformation, even after marked damage, and then regains its original structure function as it heals. Damaged cancellous fractures appear to heal quickly compared to collagenous tissues.<ref>McGill, S.M. Low back disorders: Evidence based prevention and rehabilitation, Human Kinetics Publishers, Champaign, IL, U.S.A., 2002</ref>
 
The cause of mechanical low back pain is the focus of ongoing studies. Professor Robert Mulholland finds that the current science is convincing that pain from the spine is related to how the disc and vertebrae take on load, rather than from aberrant movement (instability). Disc degeneration is mainly genetically determined and in itself is not painful. There is an association between disc degeneration and back pain but not between the severity of disc degeneration and the severity of low back pain. As discs degenerate there are often changes in the pattern of movement in the disc that can be seen on repeated studies of flexion and extension x-ray films. However these changes could not be used to distinguish painless degenerative discs from painful ones.<ref>Mulholland R. Activity related back pain: a new concept for the millennium, McKenzie Journal Vol 9, No.4</ref><br>The degenerated discs become non-isotropic. That is to say they transmit load variably over the endplate and hence within the vertebral body. McNally and Shackleford in Nottingham showed that patients with painful discs had patterns of load transmission which differed from painless degenerated discs. Mulholland points out the dissatisfaction with spinal fusion occurs often with both technically adequate posterior fusions and anterior fusions. In the case of posterior fusions no movement occurs but the disc is still required to take a load and that mechanism is not improved by the fusion. In the case of anterior fusions the load is often concentrated under the cage or bone implant and therefore pain persists. The Cochrane report suggested that there was no scientific evidence to support the use of fusion for mechanical back pain and results were not improved with the use of rigid fixation.  
 
The relevance for physical therapists is that there seems to be clear scientific support for treatment that may change spinal loading patterns. Mulholland comments that prescribing exercise and fitness regimes which currently are so central to the management of back pain, has a certain logic as it may alter the loading patterns, and certainly such therapies would appear illogical if we were treating a movement related problem. <br>There are many options available to physical therapists and other exercise trainers for teaching patients to modify how an individual carries load through their spine. Muscle reeducation, restoring flexibility, postural training, and spinal manipulation is done by a variety of practitioners from different schools of thought. The fact that there are so many approaches used would seem to indicate that each works on some patients but not on others. The key seems to be specifically targeting an approach to the specific patient’s spinal load bearing dysfunction. <br>The benefits of taking a specific exercise approach seems to be efficacious on several levels. First, it addresses a mechanical load-bearing problem with a mechanical load-altering solution. Secondly exercise elicits the patient as an active participant in resolving their problem; thereby enhancing self-efficacy (a person’s perceived ability to manage essential life circumstances.) <br>From clinical experience even patients that report continued chronic pain after technically successfully fusion can improve symptoms and progress using a well designed rehabilitation that focuses on altering spinal loading and facilitating self-efficacy. Perhaps outcomes could be improved, and surgery avoided if exercise programs were improved in several key areas.  


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.<ref name="Burton" />
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.<ref name="Burton" />

Revision as of 12:56, 3 October 2012

Original Editors - Fauve simoens

Lead Editors Bo Hellinckx - 

Introduction[edit | edit source]

File:Interactive Spine - Lumbar Vertebral Spine - L7F19.jpg
© Primal Pictures

There are different definitions of low back pain depending on the choice of the source. According to the European Guidelines for prevention of low back pain, low back pain is defined as “pain and discomfort , localized below de costal margin and above the inferior gluteal folds, with or without leg pain"[1]  Another definition, according to S.Kinkade - resembles a lot on the one above of the European guidelines – is that low back pain is “ pain that occurs posteriorly in the region between the lower rib margin and the proximal thighs”.[2]
The most common form of low back pain is the one that is called “non-specific low back pain” and is defined as “ low back pain not attributed to recognizable, known specific pathology”.[1]

After decades of research, the relationship of low back pain to disc degeneration is poorly understood. Most cases of low back pain can’t be clearly attributed to the disc. And the treatment of “discogenic pain” hasn’t proven to be a panacea for chronic low back pain.

However, in its narrow focus on the disc, the spine field may have overlooked other potential keys to the understanding of low back pain, including one immediately adjacent to the disc. [3]

The vertebral endplate has been somewhat understudied as a potential cause of low back pain. Some of this relates to its size and structure. Over the past century, most theories of back pain causation have been based on abnormalities that could be visualized—with the naked eye or with imaging. [4] The thin vertebral endplate—and the various injuries and diseases that affect it—have been difficult to visualize and classify with traditional imaging methods.
The endplate appears to play a vital role in the health of both the disc and the vertebrae. The endplate acts a buffer, a barrier, and a conduit for blood vessels and the diffusion of nutrients into the disc. Its structure and function vary by age and skeletal maturity—and in response to various injuries and stages of disc degeneration.[5][6] it is the first part of the vertebra to exhibit changes in response to high levels of loading and compressive force.[7]

Unlike the adjacent disc, the vertebral endplate has an ample nerve supply in the form of interosseous nerves (i.e. nerves that run into the bony part of the endplate). And it would appear that both the blood and the nerve supply of the endplate may increase in response to disc degeneration. This could be an attempt at tissue repair that paradoxically results in an increased risk for back pain. [8] As M.F. Brown, MD, et al. noted in a 1997 study, “The increase in the density of sensory nerves, and the presence of endplate cartilage defects, strongly suggest that the endplates and vertebral bodies are sources of pain.” [9]
It is often stated that “the intervertebral discs are the shock absorbers of the spine”. The scientific evidence supports a different understanding which seems to be important in treatment decisions about how to treat mechanical low back pain. Mechanical pain distinguishes itself from pain related to tumor growth, infection or obvious trauma related pain.
The vertebral bodies appear to play a dominant role in performing the function of shock absorber…not the disc. A healthy disc is isotropic and transmits load evenly over the endplate of the vertebral bodies. The endplates are deformable and elastic in the center. The nucleus is incompressible. Cancellous bone inside the vertebrae body is made up of trabeculae; columns of bone from endplate to endplate tied together with smaller transverse trabeculae. With axial compression these columns bend. Under excessive load the transverse trabeculae fracture and columns buckle, but return to 95% when the load is removed This architecture affords elastic deformation, even after marked damage, and then regains its original structure function as it heals. Damaged cancellous fractures appear to heal quickly compared to collagenous tissues.[10]

The cause of mechanical low back pain is the focus of ongoing studies. Professor Robert Mulholland finds that the current science is convincing that pain from the spine is related to how the disc and vertebrae take on load, rather than from aberrant movement (instability). Disc degeneration is mainly genetically determined and in itself is not painful. There is an association between disc degeneration and back pain but not between the severity of disc degeneration and the severity of low back pain. As discs degenerate there are often changes in the pattern of movement in the disc that can be seen on repeated studies of flexion and extension x-ray films. However these changes could not be used to distinguish painless degenerative discs from painful ones.[11]
The degenerated discs become non-isotropic. That is to say they transmit load variably over the endplate and hence within the vertebral body. McNally and Shackleford in Nottingham showed that patients with painful discs had patterns of load transmission which differed from painless degenerated discs. Mulholland points out the dissatisfaction with spinal fusion occurs often with both technically adequate posterior fusions and anterior fusions. In the case of posterior fusions no movement occurs but the disc is still required to take a load and that mechanism is not improved by the fusion. In the case of anterior fusions the load is often concentrated under the cage or bone implant and therefore pain persists. The Cochrane report suggested that there was no scientific evidence to support the use of fusion for mechanical back pain and results were not improved with the use of rigid fixation.

The relevance for physical therapists is that there seems to be clear scientific support for treatment that may change spinal loading patterns. Mulholland comments that prescribing exercise and fitness regimes which currently are so central to the management of back pain, has a certain logic as it may alter the loading patterns, and certainly such therapies would appear illogical if we were treating a movement related problem.
There are many options available to physical therapists and other exercise trainers for teaching patients to modify how an individual carries load through their spine. Muscle reeducation, restoring flexibility, postural training, and spinal manipulation is done by a variety of practitioners from different schools of thought. The fact that there are so many approaches used would seem to indicate that each works on some patients but not on others. The key seems to be specifically targeting an approach to the specific patient’s spinal load bearing dysfunction.
The benefits of taking a specific exercise approach seems to be efficacious on several levels. First, it addresses a mechanical load-bearing problem with a mechanical load-altering solution. Secondly exercise elicits the patient as an active participant in resolving their problem; thereby enhancing self-efficacy (a person’s perceived ability to manage essential life circumstances.)
From clinical experience even patients that report continued chronic pain after technically successfully fusion can improve symptoms and progress using a well designed rehabilitation that focuses on altering spinal loading and facilitating self-efficacy. Perhaps outcomes could be improved, and surgery avoided if exercise programs were improved in several key areas.

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.[1]

Low back related leg pain
[edit | edit source]

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. Schäfer et al[12] proposed that low back-related leg pain be divided into four subgroups according to the predominating pathomechanisms involved:

  1. central sensitization with mainly positive symptoms such as hyperalgesia
  2. denervation with significant axonal damage showing predominantly negative sensory symptoms and possibly motor loss
  3. peripheral nerve sensitization with enhanced nerve trunk mechanosensitization
  4. somatic referred pain from musculoskeletal structures, such as the intervertebral disc or facet joints.

Each group presents with a distinct pattern of symptoms and signs although there may be considerable overlap between the classifications. The importance of distinguishing low back-related leg pain into these four groups is to facilitate diagnosis and provide a more effective, appropriate treatment.

Diagnostic procedures[edit | edit source]

The diagnostic process is mainly focused on the triage of patients with specific or non-specific low back pain.This triage is focused on identification of “red flags” as indicators of possible underlying pathology, including nerve root problems.

"Red Flags":

Prevention of low back pain[edit | edit source]

Prevention is also categorized in 3 types of prevention. Primary prevention is defined as “specific practices for the prevention of disease or mental disorders in susceptible individuals or populations. These include health promotion, including mental health; protective procedures, such as communicable disease control; and monitoring and regulation of environmental pollutants. Primary prevention is to be distinguished from secondary prevention and tertiary prevention.”[16]  Secondary prevention is defined as “the prevention of recurrences or exacerbations of a disease that already has been diagnosed. This also includes prevention of complications or after-effects of a drug or surgical procedure”[16]  and tertiary prevention as “measures aimed at providing appropriate supportive and rehabilitative services to minimize morbidity and maximize quality of life after a long-term disease or injury is present”.[16]

The guidelines discuss different possibilities to prevent low back pain, and most of them are supported by other articles. Physical exercise is recommended to prevent consequences of low back pain, such as absence of work and occurrence of further episodes. With physical exercises is especially mend training of back extensors en trunk flexors beside regular en aerobe training. There is no specific recommendation of exercise frequency or intensity.[1][2][17] Regard the back school programs, a high intensity program is advised in patients with recurrent and lasting low back pain but not in preventing low back pain. The program consists of exercises and an educational and skills program. Education and information alone or based on biomechanical model has only a small effect. Education and information in combination with other interventions, in a treatment setting an based on biopsychosocial model effect has a better effect. Information based on biopsychosocial model is focused on beliefs in low back pain and reducing work loss caused by low back pain. This attitude of giving information has a positive effect on back beliefs.[1]  It is important to know that individually tailored programs and intervention may have more results as to group interventions.[17] Lumbar supports, back belts and shoe insoles are not recommended in the prevention of low back pain. Lumbar supports and back belts have also a negative effect on back pain beliefs and are therefore not recommended in preventing low back pain.[1][2] Specific mattresses and chairs for prevention have no evidence in favor or against. Medium mattresses may decrease existing persistent symptoms of low back pain.[1] Ergonomic adjustments regarding work environment can be necessary and useful to achieve earlier return to work.[1][18]

In the prevention of acute low back pain becoming chronic low back pain Kinkade refers to the European guidelines and suggest to exercise and to not use back belts or lumbar supports. Important in preventing acute low back pain of becoming chronic is to mention the interest of psychosocial factors that correlate with the development of chronic low back pain.[2]
- disputed compensation claims
- fear avoidance (exaggerated pain or fear that activity will cause permanent damage)
- job dissatisfaction
- pending or past litigation related to back pain
- psychological distress and depression
- reliance on passive treatments rather than active patient participation
- somatization

Further on, there is still more research needed.[17]  

Guidelines[edit | edit source]

See Low Back Pain Guidlines

Related Pages[edit | edit source]

Presentations[edit | edit source]

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 Exercise and Low Back Pain: Where do we Stand

This presentation, created by Jason Steere as part of the Evidence In Motion OMPT Fellowship in 2011, discusses the basis and evidence for specific stabilisation exercises for low back pain.

View the presentation


Recent Related Research (from Pubmed)[edit | edit source]

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 References
[edit | edit source]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Burton AK. European guidelines for prevention in low back pain. COST B13 Working Group. 2004: 1-53. (Level 1A)
  2. ↑ 2.0 2.1 2.2 2.3 Kinkade S. Evaluation and treatment of acute low back pain. Am Ac of Family Phys. 2007: 1182-1188.
  3. ↑ BackLetter, When It Comes to Back Pain Causation, Has the Spine Field Missed the Forest for the Trees? Vol. 27, No. 9, September 2012
  4. ↑ Lutz GK et al., Looking back on back pain: Trial and error of diagnoses in the 20th century, Spine, 2003; 28:1899–905.
  5. ↑ Moore RJ, The vertebral endplate: Disc degeneration, disc regeneration, European Spine Journal, 2006; 15 (Suppl 3): S333–S337.
  6. ↑ Adams M et al., The Biomechanics of Back Pain. Edinburgh: Churchill Livingstone; 2006:149–50.
  7. ↑ Adams M et al., The Biomechanics of Back Pain. Edinburgh: Churchill Livingstone; 2006:149–50.
  8. ↑ Moore RJ, The vertebral endplate: Disc degeneration, disc regeneration, European Spine Journal, 2006; 15 (Suppl 3): S333–S337.
  9. ↑ Brown MF et al., Sensory and sympathetic innervation of the vertebral endplate in patients with degenerative disc disease, Journal of Bone and Joint Surgery (Brit), 1997; 79:147–53.
  10. ↑ McGill, S.M. Low back disorders: Evidence based prevention and rehabilitation, Human Kinetics Publishers, Champaign, IL, U.S.A., 2002
  11. ↑ Mulholland R. Activity related back pain: a new concept for the millennium, McKenzie Journal Vol 9, No.4
  12. ↑ Axel Schäfer, Toby Hall and Kathy Briffa. Classification of low back-related leg pain—A proposed patho-mechanism-based approach. fckLRManual Therapy, 2009;14(2):222-230
  13. ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 13.7 B W KOES, M W VAN TULDER, S THOMAS. Diagnosis and treatment of low back pain. BMJ 2006;332:1430–4 (Level of evidence: 2B)
  14. ↑ 14.0 14.1 14.2 14.3 14.4 14.5 14.6 Humphreys SC, Eck JC. Clinical evaluation and treatment options for herniated fckLRlumbar disc. Am Fam Physician. 1999 Feb 1;59(3):575-82, 587-8 (Level of evidence: 2B)
  15. ↑ 15.0 15.1 15.2 15.3 15.4 15.5 Bigos SJ. Acute low back problems in adults. Rockville, Md.: U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994; AHCPR publication no. 95-0642.(Level of evidence: 1B)
  16. ↑ 16.0 16.1 16.2 National Center of Biotechnology Information [www.ncbi.nlm.nih.gov]. Brussels [cited 2011 Apr 17]. Available from: http://www.ncbi.nlm.nih.gov/mesh/.
  17. ↑ 17.0 17.1 17.2 van Poppel MNM , WE. An update of a systematic review of controlled clinical trials on the primary prevention of back pain at the workplace. Occupational Medicine. 2004: 345-352. (Level 1A)
  18. ↑ Van Nieuwenhuyse, P. G. The role of physical workload and pain related fear in the development of low back pain in young workers: evidence from the BelCoBack Study; results after one year of follow up. Occup Environ Med. 2006: 45-52. (Level 2B)

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