Non Specific Low Back Pain


Original Editor ­ Sam Verhelpen Top Contributors - Admin, Anouk Van den Bossche, Andeela Hafeez, Pieter Verbeirens, Lien Hennebel, Arne De Cort, Michelle Lee, Kim Jackson, Vidya Acharya, Evan Thomas, Debontridder Jordy, Tarina van der Stockt, Benjamin Desmedt, Simisola Ajeyalemi, Samuel Adedigba, Wanda van Niekerk, Lucinda hampton, Vanessa Rhule, George Prudden, Isa, 127.0.0.1, Sam Verhelpen and Laura Ritchie


Definition

Non-specific (or Simple or Mechanical) low back pain is the general term that refers to any type of back pain caused by strain on muscles of the vertebral column and abnormal stress. At some point during our adult lives, most people experience bouts of back pain. Chronic back pain is pain that persists after an injury or surgery where the source is hard to determine. Acute pain can develop into Chronic Pain for a number of reasons.

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

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.177,178,192 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,319 MRI,31 and myelography161 in 20% to 76% of persons with no sciatica. Furthermore, Savage et al264 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.264 Boos et al33 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.

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). 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. 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.

Clinically relevant anatomy

• Bony: at each level of the vertebrae there’s a 3-joint complex, namely 2 facet joints and a disc interposed between 2 vertebra. Joint inflammation and degeneration is caused by rotational load of the facet joints and the disc weight-bearing transfers.
• The nucleus of the disc, facet joint capsule, anterior and posterior longitudinal ligaments, muscles, .. are the causes of the most pain.
• There are 2 important muscular groups: The anterior group: abdominal and psoas muscles.

                                                                             The posterior group: erector spinae, profundi and intersegmental muscles.

Epidemiology/etiology

Mechanical low back pain is defined as pain secondary to:

• Traumatic injury
  
• Lumbar sprain or strain: degenerative disease, discs, facet joints, diffuse idiopathic skeletal hyperostosis[[|]]
  
• Spondylolysis, Spondylolisthesis
  
• Disc Herniaton
  
• Spinal Stenosis
  
• Osteoporosis with Compression fracture (Lumbar compression fracture)
  
• Congenital disease: severe Kyphosis, severe Scoliosis
  
• Paget's Disease

The surrounding ligaments, muscles and facet joints may become irritated and inflamed. People with mechanical back pain experience pain primarily in the lower back, the pain can also radiate to the knees, thighs or buttocks. This is called sciatica, namely nerve pain from irritation of the sciatic nerve.

There are 3 types of mechanical low back pain:

• Acute
  
• Subacute
  
• Chronic
  

Possible Mechanisms

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.

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.  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. it is the first part of the vertebra to exhibit changes in response to high levels of loading and compressive force.

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.  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.”

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.

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.

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.

Characteristics/clinical presentation

This low back pain is usually aggravated by:

• Long levered activities
• Lifting heavy objects
• Levered postures (bending forward)
• Static loading of the spine (prolonged sitting or standing)

Testing:

The following tests are used when evaluating low back pain.

• Observe the patient walking into the office or examining room
• Observe the patient during the history-gathering portion of the visit for development, nutrition, deformities, and attention to grooming
• Measure blood pressure, pulse, respirations, temperature, height, and weight
• Inspect the back for signs of asymmetry, lesions, scars, trauma, or previous surgery
• Measure lumbar range of motion (ROM) in forward bending while standing (Schober test)
• Palpate the entire spine to identify vertebral tenderness that may be a nonspecific finding of fracture or other cause of low back pain
• Test for manual muscle strength in both lower extremities.
• Test for sensation and reflexes
• Imaging studies: Persistent pain may require CT scanning, diskography, and 3-phase bone scanning; electromyography and nerve conduction studies can help in the evaluation of neurologic symptoms or deficits

Diagnostic procedures

It’s difficult to reliably identify by diagnostic testing. These typically involve processes in the muscles and/or ligaments.

Differential diagnoses

• Discogenic back pain 
  
• Cauda Equina Syndrome
  
• Fracture (compression, spinosus process, stress fractures of pars)
  
• SI dysfunction
  
• Non-back pain infection (AAA, Pancreatitis, posterior penetrating ulcer and pyelonephritis)
  
• Metastatic disease (prostate, renal cell, thyroid, breast)
  

Examination

• Paraspinal muscle tenderness
• No bony tenderness
• Back pain with passive knee-to-chest stretch  
• Limited ability to forward bending as a resullt of limited ROM  
• Muscle spasm
• Negative discogenic exam

Medical management

Mechanical low back pain (LBP) is not a life-threatening illness. Unfortunately, it does have a far-reaching impact on medical care expenditures for injured workers.

Pharmacological interventions for the relief of low back pain (LBP) include acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), topical analgesics, muscle relaxants, opioids, corticosteroids, antidepressants, and anticonvulsants.

Acetaminophen remains one of the best first-line treatments of acute LBP.

Physical therapy management

The conservative treatment in the initial phase is ice massage followed by passive knee-to-chest stretch (one leg at a time then both legs together). Also daily walks followed by stretching, electrical stimulation and iontophoresis are recommended in this phase. It’s important to identify possible causes and to correct harmful activities and attitudes, to avoid further back pain problems.

In the second phase it’s necessary to continue the pain management and to be alert for ‘red flags’. The rehabilitation program exists out of stretching of the hamstrings and back (knee-chest), strengthening of back flexors and extensors and core strengthening.

Patients should be taught several correct and comfortable positions and postures (during sleeping, sitting, lying, standing, walking and lifting techniques) that are safe for the spinal structures.

Resources

http://www.allaboutbackandneckpain.com/recognizingsymptoms/causesoflowbackpain.asp

http://www.fmcpaware.org/m-n/mechanical-low-back-pain