Practice Essentials

Mechanical low back pain (LBP) remains the second most common symptom-related reason
for seeing a physician in the United States. Of the US population, 85% will experience an
episode of mechanical LBP at some point during their lifetime. Fortunately, the LBP resolves
for the vast majority within 2-4 weeks.

The image below illustrates a herniated nucleus pulposus at multiple levels, one of the causes
of LBP.

Magnetic resonance image of the lumbar spine. This image

demonstrates a herniated nucleus pulposus at multiple levels.

See Back Pain: Find the Cause, Watch for the Comeback, a Critical Images slideshow, to
help diagnose and manage this common problem.

Signs and symptoms

An important part of the physical examination is the general observation of the patient. The
patient presents with pain in the low back region and often places his or her whole hand
against the skin to indicate a regional pain; however, in some cases the patient may indicate a
more precise location.

Interruption in bowel or bladder function should be a reminder to consider more serious

causes of back pain such as a tumor, infection, or fracture.

Patients generally present with a history of an inciting event that produced immediate low
back pain. The most commonly reported histories include the following:
  Lifting and/or twisting while holding a heavy object (eg, box, child, nursing home
resident, a package on a conveyor)
 Operating a machine that vibrates
 Prolonged sitting (eg, long-distance truck driving, police patrolling)
 Involvement in a motor vehicle collision
 Falls

See Clinical Presentation for more detail

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
 Note chest expansion: If < 2.5 cm, this finding can be specific, but not sensitive, for
ankylosing spondylitis
 Take measurements of the calf circumferences (at midcalf). Differences of less than 2
cm are considered normal variation
 Measure lumbar range of motion (ROM) in forward bending while standing (Schober
test)
 Neurologic examination should test 2 muscles and 1 reflex representing each lumbar
root to distinguish between focal neuropathy and root problems
 Measure leg lengths (anterior superior iliac spine to medial malleolus) if side-to-side
discrepancy is suspected
 Use the inclinometer to measure forward, backward, and lateral bending. With the
goniometer positioned over the head, measure trunk rotation
 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

See Workup for more detail.

Management

Management of mechanical low back pain can be outlined in the following 6 steps:

1. Control of pain and the inflammatory process

2. Restoration of joint ROM and soft tissue extensibility
3. Improvement of muscular strength and endurance
4. Coordination retraining
5. Improvement of general cardiovascular condition
6. Maintenance exercise programs
Surgical interventions for mechanical low back pain (LBP) are the last choice for treatment.

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

See Treatment and Medication for more detail.

Background
Mechanical low back pain (LBP) remains the second most common symptom-related reason
for seeing a physician in the United States. Of the US population, 85% will experience an
episode of mechanical LBP at some point during their lifetime. Fortunately, the LBP resolves
for the vast majority within 2-4 weeks.

For individuals younger than 45 years, mechanical LBP represents the most common cause of
disability and is generally associated with a work-related injury. For individuals older than 45
years, mechanical LBP is the third most common cause of disability, and a careful history
and physical examination are vital to evaluation, treatment, and management.[1]

Numerous treatment guidelines have been written regarding the evaluation, treatment, and
management of LBP.[2, 3] Perhaps the most widely reviewed (and controversial) guideline was
published in 1994 by the Agency for Health Care Policy and Research titled "Acute Lower
Back Problems in Adults: Clinical Practice Guidelines."[4]

At the beginning of the 21st century, 750 national and international organizations partnered to
create the Bone and Joint Decade (2002-2011).[5] This initiative involves patient and
professional health care organizations, government agencies, and industries working
collaboratively to increase the awareness of bone and joint diseases while increasing the
information and research to address this major health care issue. Because 1 in 5 Americans
will be age 65 or older by 2030, 65 million people (20% of the total population) will be
affected by musculoskeletal impairments, with LBP ranking among the most common
problems. Already, total direct and indirect costs for the treatment of LBP are estimated to be
$100 billion annually.

The physiatrist represents one type of medical specialist who can evaluate, diagnose, treat,
and manage LBP by using medical and nonsurgical procedures and interventions. The
physiatrist may have the best functional understanding of all specialists in the treatment and
management of mechanical LBP.[6, 7]

Lambeek et al assessed the efficacy of an integrated care program for chronic LBP against
that of a more conventional care program, as a means of helping patients with this condition
return to work. In the study, 66 patients received integrated care from a team made up of a
clinical occupational physician, a physical therapist, an occupational therapist, and a medical
specialist. Treatment included workplace intervention involving participatory ergonomics, as
well as a graded activity program. Another 68 patients received the usual type of care for
chronic back pain, administered by a medical specialist, general practitioner, occupational
physician, and/or allied health care professionals.
Members of the integrated care group achieved a full, sustainable return to work in a median
period of 88 days, while the same was accomplished in the conventional care group after a
median 208 days. By 12-month follow-up, the integrated care group had experienced
significantly greater improvement in functional status than had the conventional care patients.
However, the investigators found no significant difference in pain reduction between the 2
groups at 12 months.[8]

Pathophysiology
Causes of mechanical low back pain (LBP) generally are attributed to an acute traumatic
event, but they may also include cumulative trauma as an etiology.[9] The severity of an acute
traumatic event varies widely, from twisting one's back to being involved in a motor vehicle
collision. Mechanical LBP due to cumulative trauma tends to occur more commonly in the
workplace.

In a systematic study review, Chen et al investigated whether a sedentary lifestyle (which the
authors defined as including sitting for prolonged periods at work and during leisure time) is
a risk factor for LBP.[10] Examining journal articles published between 1998 and 2006, they
identified 8 high-quality reports (6 prospective cohort and 2 case-control studies). While 1 of
the cohort studies reported a link between sitting at work and the development of LBP, the
other investigations did not find a significant connection between a sedentary lifestyle and
LBP. Chen and coauthors concluded that a sedentary lifestyle alone does not lead to LBP.

In a birth cohort study from 1980-2008, Rivinoja et al investigated whether lifestyle factors,
such as smoking, being overweight or obese, and participating in sports, at age 14 years
would predict hospitalizations in adulthood for LBP and sciatica.[11] The authors found that
119 females and 254 males had been hospitalized at least once because of LBP or sciatica.
Females who were overweight had an increased risk of second-time hospitalization and
surgery. Smoking in males was linked with an increased risk of first-time nonsurgical
hospitalization and second-time hospitalization for surgical treatment.

The pathophysiology of mechanical LBP remains complex and multifaceted. Multiple

anatomic structures and elements of the lumber spine (eg, bones, ligaments, tendons, disks,
muscle) are all suspected to have a role. (See the images below.) Many of these components
of the lumber spine have sensory innervation that can generate nociceptive signals
representing responses to tissue-damaging stimuli. Other causes could be neuropathic (eg,
sciatica). Most chronic LBP cases most likely involve mixed nociceptive and neuropathic
etiologies.
 Diskogram showing examples of
an intact disk and a disrupted disk at the lumbar level.

Degenerative changes of the lumbar spine,

including decreased signal intensity and disk bulging at the L-3/4, L-4/5 and L-5/S-1 disks.

Biomechanically, the movements of the lumbar spine consist of the cumulative motions of
the vertebrae, with 80-90% of the lumbar flexion/extension occurring at the L4-L5 and L5-S1
intervertebral disks. The lumbar spine position most at risk for producing LBP is forward
flexion (bent forward), rotation (trunk twisted), and attempting to lift a heavy object with out-
stretched hands. Axial loading of short duration is resisted by annular collagen fibers in the
disk. Axial loading of a longer duration creates pressure to the annulus fibrosis and increased
pressure to the endplates. If the annulus and endplate are intact, the loading forces can be
adequately resisted. However, compressive muscular forces may combine with the loading
forces to increase intradiskal pressure that exceeds the strength of the annular fibers.

Repetitive, compressive loading of the disks in flexion (eg, lifting) puts the disks at risk for
an annular tear and internal disk disruption. Likewise, torsional forces on the disks can
produce shear forces that may induce annular tears. (Degenerative disk forces are
demonstrated in the image below.) The contents of the annulus fibrosis (nucleus pulposus)
may leak through these tears. Central fibers of the disk are pain free, so early tears may not be
painful. Samples of disk material taken at the time of autopsy reveal that the cross-linked
profile of pentosidine, a component of the collagen matrix, declines. This may indicate the
presence of increased matrix turnover and tissue remodeling.

The various forces placed on the

disks of the lumbar spine that can result in degenerative changes.

In lumbar flexion, the highest strains are recorded within the interspinous and supraspinous
ligaments, followed by the intracapsular ligaments and the ligamentum flavum. In lumbar
extension, the anterior longitudinal ligament experiences the highest strain. Lateral bending
produces the highest strains in the ligaments contralateral to the direction of bending.
Rotation generates the highest strains in the capsular ligaments.

A review study by Raastad et al of radiographic features in patients with LBP found that in
community- and occupation-based studies, such pain was significantly associated with disk-
space narrowing. LBP was also significantly linked with the presence of spondylolisthesis,
but in occupation-based studies only. The review, which involved 28 studies (26,107 subjects
total), also indicated that LBP has only a weak association with spondylosis and osteophytes
and a nonsignificant association with endplate sclerosis.[12]

Research since the late 20th century suggests that chemical causes may play a role in the
production of mechanical LBP. Components of the nucleus pulposus, most notably the
enzyme phospholipase A2 (PLA2), have been identified in surgically removed herniated disk
material. This PLA2 may act directly on neural tissue, or it may orchestrate a complex
inflammatory response that manifests as LBP.

Glutamate, a neuroexcitatory transmitter, has been identified in degenerated disk

proteoglycan and has been found to diffuse to the dorsal root ganglion (DRG) affecting
glutamate receptors. Substance P (pain) is present in afferent neurons, including the DRG,
and is released in response to noxious stimuli, such as vibration and mechanical compression
of the nerve. Steady, cyclic, or vibratory loading induces laxity and creep in the viscoelastic
structures of the spinal elements. This creep does not recover fully in the in vivo cat model,
even when rest periods are equal in duration to the loading period.

The concept of a biomechanical degenerative spiral has an appealing quality and is gaining
wider acceptance. This concept postulates the breakdown of the annular fibers allows PLA2
and glutamate, and possibly other as-yet unknown compounds, to leak into the epidural space
and diffuse to the DRG. The weakened vertebra and disk segment become more susceptible
to vibration and physical overload, resulting in compression of the DRG and stimulating
release of substance P. Substance P, in turn, stimulates histamine and leukotriene release,
leading to an altering of nerve impulse transmission. The neurons become sensitized further
to mechanical stimulation, possibly causing ischemia, which attracts polymorphonuclear cells
and monocytes to areas that facilitate further disk degeneration and produce more pain.

Epidemiology
Frequency

United States

The lifetime prevalence of mechanical low back pain (LBP) in the United States is 60-80%.
The prevalence of serious mechanical LBP (persisting >2 wk) is 14%. The prevalence of true
sciatica (pain radiating down one or both legs) is approximately 2%.

Of all cases of mechanical LBP, 70% are due to lumbar strain or sprain, 10% are due to age-
related degenerative changes in disks and facets, 4% are due to herniated disks, 4% are due to
osteoporotic compression fractures, and 3% are due to spinal stenosis. All other causes
account for less than 1% of cases.

Mechanical LBP is the most common cause of work-related disability in persons younger
than 45 years in the United States.

International

Mechanical low back pain (LBP) exists in every culture and country. Worldwide, more
disability is caused by LBP than by any other condition.[13, 14, 15] Estimates by numerous
investigators indicate that at some point in their lives, 80% of all human beings experience
LBP. Mechanical LBP becomes more prevalent in countries with higher per capita income
and where more liberal policies and adequate funds provide for compensation (eg, Germany,
Sweden, Belgium).

In Sweden, the level of insurance benefits for disabling LBP is 100%, compared with a range
of 0-80% in the United States. In 1987, the percentage of the work force placed on a sick list
for diagnoses associated with back pain was 8% in Sweden versus 2% in the United States. In
the same year, the average number of days of back-related absence from work per patient per
year in Sweden was 40, versus 9 in the United States.

Mortality/Morbidity
While mechanical low back pain is not associated with mortality, morbidity in terms of lost
productivity, use of medical services, and cost to society is staggering. Total workers'
compensation costs for cases occurring in 1989 in the United States amounted to $11.4
billion, making it the most costly ailment for working-age adults. No evidence has been
found to indicate that these costs are declining.

Race

No published information suggests that race is a factor in the prevalence of mechanical low
back pain.

Sex

The impact of sex on prevalence of low back pain (LBP) has not been established as well as
the roles of other risk factors in LBP (eg, previous LBP, age). A reported 50-90% of women
develop symptoms of LBP in the course of pregnancy. Discomfort generally develops in the
very early weeks, more commonly in the third trimester. Age, race, occupation, baby's
weight, prepregnancy maternal weight, weight gain, number of children, exercise habits,
sleeping posture, mattress type, and history of previous LBP have not shown any correlation
with the development of LBP symptoms during pregnancy.

Age

Age has been shown to be associated more consistently with mechanical low back pain (LBP)
than with sex. The prevalence of LBP during pregnancy appears to increase 5% for every 5
years of patient age. Sciatica (pain that radiates down one or both legs) is usually reported in
persons aged 40-59 years. Women aged 60 years or older also report more low back
symptoms.