Chapter 40 Low Back Pain
Low back pain has become a costly burden to society and a leading cause of disability and loss of productivity. This chapter outlines the anatomy and biomechanics of the lumbar spine and our current understanding of the physiology of low back pain. We discuss the clinical evaluation and treatment of various etiologies of low back pain and leg pain caused by lumbar spine disease.
Low back pain is a symptom, not a disease, and has many causes. It is generally described as pain between the costal margin and the gluteal folds. It is extremely common. About 40% of people say that they have had low back pain within the past 6 months.233 Studies have shown a lifetime prevalence as high as 84%.240 Onset usually begins in the teens to early 40s. Most patients have short attacks of pain that are mild or moderate and do not limit activities, but these tend to recur over many years. Most episodes resolve with or without treatment. The median time off work for a back injury is 7 days, and many people with low back pain never alter their activity. A small percentage of low back pain becomes chronic, however, and causes significant disability. In most studies about half of the sick days used for back pain are accounted for by the 15% of people who are home from work for more than 1 month. Between 80% and 90% of the health care and social costs of back pain are for the 10% who develop chronic low back pain and disability. Just over 1% of adults in the United States are permanently disabled by back pain, and another 1% are temporarily disabled.151
The percentage of patients disabled by back pain, as well as the cost of low back pain, has steadily increased during the past 30 years. This appears to be more from social causes than from a change in the conditions that cause low back pain. The two most commonly cited factors are the increasing societal acceptance of back pain as a reason to become disabled, and changes in the social system that pay benefits to patients with back pain.238
The lumbar spine has a dichotomous role in terms of function, which is strength coupled with flexibility. The spine performs a major role in support and protection (strength) of the spinal canal contents (spinal cord, conus, and cauda equina) but also give us inherent flexibility, allowing us to place our limbs in appropriate positions for everyday functions.
The strength of the spine results from the size and arrangements of the bones, as well as from the arrangement of the ligaments and muscles. The inherent flexibility results from the large number of joints placed so closely together in series. Each vertebral segment can be thought of as a three-joint complex—one intervertebral disk with vertebral end plates, and two zygapophyseal joints. The typical lordotic framework of the lumbar spine assists with this flexibility but also increases the ability of the lumbar spine to absorb shock.
The bony anatomy of the lumbar spine consists of five lumbar vertebrae. A smaller percentage of the population has four (the fifth vertebrae is sacralized) or six (the first sacral segment is lumbarized). Anatomic variants also exist consisting of a partially lumbarized S1. The lumbar vertebrae have distinct components, which include the vertebral body, the neural arch, and the posterior elements (Figure 40-1). The vertebral bodies increase in size as you travel caudally in the spine. The lower three are typically more wedge-shaped (taller anteriorly), which helps create the normal lumbar lordosis. The structure of these large vertebral bodies serves its weight-bearing function well to support axially directed loads; however, they would fracture more routinely were it not for the shock-absorbing intervertebral disks placed strategically between the vertebral bodies.
FIGURE 40-1 Lateral view of the lumbar vertebrae.
(Modified from Parke WW: Applied anatomy of the spine. In Rothman RH, Simeone FA, editors: The spine, ed 4, Philadelphia, 1999, Saunders.)
The sides of the bony neural arch are the pedicles, which are thick pillars that connect the posterior elements to the vertebral bodies. They are designed to resist bending and to transmit forces back and forth from the vertebral bodies to the posterior elements. The posterior elements consist of the laminae, the articular processes, and the spinous processes. The superior and inferior articular processes of adjacent vertebrae create the zygapophyseal joints. The pars interarticularis is a part of the lamina between the superior and inferior articular processes (Figure 40-2). The pars is the site of stress fractures (spondylolysis) because it is subjected to large bending forces. This occurs as the forces transmitted by the vertically oriented lamina undergo a change in direction into the horizontally oriented pedicle.23
FIGURE 40-2 An oblique dorsal view of an L5 vertebra, showing the parts of the vertebral arch: 1, pars interarticularis (crosshatched area); 2, pars laminaris; and 3, pars pedicularis. The dotted line indicates the most frequent site of mechanical failure of the pars interarticularis.
(Modified from Parke WW: Applied anatomy of the spine. In Rothman RH, Simeone FA, editors: The spine, ed 4, Philadelphia, 1999, Saunders.)
The intervertebral disk and its attachment to the vertebral end plate are considered a secondary cartilaginous joint, or symphysis. The disk consists of the internal nucleus pulposus and the outer annulus fibrosus. The nucleus pulposus is the gelatinous inner section of the disk. It consists of water, proteoglycans, and collagen. The nucleus pulposus is 90% water at birth. Disks desiccate and degenerate as we age and lose some of their height, which is one reason we are slightly shorter in our geriatric years.
The annulus fibrosus consists of concentric layers of fibers at oblique angles to each other, which help to withstand strains in any direction. The outer fibers of the annulus have more collagen and less proteoglycans and water than the inner fibers.19 The varying composition supports the functional role of the outer fibers in acting like a ligament to resist flexion, extension, rotation, and distraction forces.
The main function of the intervertebral disk is shock absorption (Figure 40-3). It is primarily the annulus, not the nucleus, that acts as the shock absorber. (The nucleus is primarily a liquid and is incompressible.) When an axial load occurs, the increase in force in the incompressible nucleus pushes on the annulus and stretches its fibers. If the fibers break, then a herniated nucleus pulposus results.
FIGURE 40-3 The mechanism of weight transmission in an intervertebral disk. A, Compression increases the pressure in the nucleus pulposus. This is exerted radially onto the annulus fibrosus, and the tension in the annulus increases. B, The tension in the annulus is exerted on the nucleus, preventing it from expanding radially. Nuclear pressure is then exerted on the vertebral end plates. C, Weight is borne, in part, by the annulus fibrosus and by the nucleus pulposus. D, The radial pressure in the nucleus braces the annulus, and the pressure on the end plates transmits the load from one vertebra to the next.
(Modified from Bogduk N: The inter-body joint and the intervertebral discs. In Bogduk N, editor: Clinical anatomy of the lumbar spine and sacrum, ed 3, Edinburgh, UK, 1977, Churchill Livingstone.)
The zygapophyseal joints (also known as Z joints and facet joints) are paired synovial joints, that is, they have a synovium and a capsule (Figure 40-4). Their alignment or direction of joint articulation determines the direction of motion of the adjacent vertebrae. The lumbar zygapophyseal joints lie in the sagittal plane and thus primarily allow flexion and extension. Some lateral bending and very little rotation are allowed, which limits torsional stress on the lumbar disks. Rotation is more a component of thoracic spine motion. The majority of spinal flexion and extension (90%) occurs at the L4–L5 and L5–S1 levels, which contributes to the high incidence of disk problems at these levels.
FIGURE 40-4 A posterior view of the L3–L4 zygapophyseal joints. On the left, the capsule of the joint (C) is intact. On the right, the posterior capsule has been resected to reveal the joint cavity, the articular cartilages (AC), and the line of attachment of the joint capsule (dashed line). The upper joint capsule (C) attaches further from the articular margin than the posterior capsule does.
(Modified from Bogduk N: The zygapophysial joints. In Bogduk N, editor: Clinical anatomy of the lumbar spine and sacrum, ed 3, Edinburgh, UK, 1977, Churchill Livingstone.)
Because flexion loads the anterior disk, the nucleus is displaced posteriorly.111 If the forces are great enough, the nucleus can herniate through the posterior annular fibers. The lateral fibers of the posterior longitudinal ligaments are thinnest, however, making posterolateral disk herniations the most common (Figure 40-5). The posterolateral portion of the disk is most at risk when there is forward flexion accompanied by lateral bending (i.e., bending and twisting). The zygapophyseal joints cannot resist rotation when the spine is in flexion. This increases torsional shear forces in the lumbar spine, making rotary movements in a forward-flexed posture probably the most risky for lumbar disks.
The two main sets of ligaments of the lumbar spine are the longitudinal ligaments and the segmental ligaments. The two longitudinal ligaments are the anterior and posterior longitudinal ligaments. They are named according to their position on the vertebral body. The anterior longitudinal ligament acts to resist extension, translation, and rotation. The posterior longitudinal ligament acts to resist flexion. Disruption of either ligament primarily occurs with rotation rather than with flexion or extension. The anterior longitudinal ligament is twice as strong as the posterior longitudinal ligament.
The main segmental ligament is the ligamentum flavum, which is a paired structure joining adjacent laminae. It is the ligament that is pierced when performing lumbar punctures. It is a very strong ligament but is elastic enough to allow flexion. Flexing the lumbar spine puts this ligament on stretch, decreasing its redundancy and making it easier to pierce during a lumbar puncture.
The other segmental ligaments are the supraspinous, interspinous, and intertransverse. The supraspinous ligaments are the strong ligaments that join the tips of adjacent spinous processes and act to resist flexion. These ligaments, along with the ligamentum flavum, act to restrain the spine and prevent excessive shear forces in forward bending. This is supported by electromyographic studies that have shown that there is no active contraction of the erector spinae and hip extensor muscles when resting in lumbar flexion.
These muscles can be divided anatomically into posterior and anterior muscles. The posterior muscles include the latissimus dorsi and the paraspinals. The lumbar paraspinals consist of the erector spinae (iliocostalis, longissimus, and spinalis), which act as the chief extensors of the spine, and the deep layer (rotators and multifidi) (Figures 40-6 and 40-7). The multifidi are tiny segmental stabilizers that act to control lumbar flexion because they cannot produce enough force to truly extend the spine. Their most important function has been hypothesized to be that of a sensory organ to provide proprioception for the spine, given the predominance of muscle spindles seen histologically in these muscles.
The anterior muscles of the lumbar spine include the psoas and quadratus lumborum. Because of the direct attachment of the psoas on the lumbar spine, tightening this muscle accentuates the normal lumbar lordosis. This can increase forces on the posterior elements and can contribute to zygapophyseal joint pain. The quadratus lumborum acts in side bending and can assist in lumbar flexion.
The superficial abdominals include the rectus abdominis and external obliques (Figure 40-8, A). The deep layer consists of internal obliques and the transversus abdominis (Figure 40-8, B). The transversus abdominis has received significant attention recently as an important muscle to train in treating low back pain. Its connection to the thoracolumbar fascia (and consequently its ability to act on the lumbar spine) has probably been the major reason it has received such attention of late.
The thoracolumbar fascia, with its attachments to the transversus abdominis and internal obliques, acts as an abdominal and lumbar “brace.” It decreases some of the shear forces that other muscles and lumbar motions create. This abdominal bracing mechanism results from contraction of these deep abdominal muscles, which creates tension in the thoracolumbar fascia, which then creates an extension force on the lumbar spine without increasing shear forces.75
The pelvic stabilizers are considered “core” muscles because of their indirect effect on the lumbar spine, even though they do not have a direct attachment to the spine. The gluteus medius stabilizes the pelvis during gait. Weakness or inhibition of this muscle results in pelvic “instability,” which introduces lumbar side bending and rotation, creating increased shear or torsional forces on the lumbar disks.
The piriformis is a hip and sacral rotator and can cause excessive external rotation of the hip and sacrum when it is tight. This can result in increased shear forces at the lumbosacral junction (i.e., the L5–S1 disk or Z joints). Some practitioners also believe that other pelvic floor muscles act to maintain proper positioning of the spine and are an important focus of some spine rehabilitation programs.
The activity of the lumbar muscles correlates well with intradiskal pressures (i.e., when back muscles contract, there is an associated increase in disk pressure). These pressures change depending on spine posture and the activity undertaken. Figure 40-9 demonstrates the changes in L3 disk pressure under various positions and exercises.149,150 Adding rotation to the already flexed posture increases the disk pressure substantially. Comparing lifting maneuvers, it has been shown that there is not a significant difference in disk pressure when lifting with the legs (i.e., with the back straight and knees bent) versus lifting with the back (i.e., with a forward-flexed back and straight legs).6,7 What decreases the forces on the lumbar spine is lifting the load close to your body because the farther the load is from the chest, the greater the stress on the lumbar spine.7
FIGURE 40-9 A, Relative change in pressure (or load) in the third lumbar disk in various positions in living subjects. B, Relative change in pressure (or load) in the third lumbar disk during various muscle-strengthening exercises in living subjects. Neutral erect posture is considered 100% in these figures; other positions and activities are calculated in relationship to this.
(Modified from Nachemson AL, Waddell G, Norlund AI: Epidemiology of neck and low back pain. In Nachemson AL, Johnsson B, editors: Neck and back pain: The scientific evidence of causes, diagnosis, and treatment, Philadelphia, 2000, Lippincott Williams & Wilkins.)
The conus medullaris ends at about bony level L2, and below this level is the cauda equina. The cauda equina consists of the dorsal and ventral rootlets, which join together in the intervertebral neuroforamen to become the spinal nerves (Figure 40-10). The spinal nerve gives off the ventral primary ramus. The ventral primary rami from multiple levels form the lumbar and lumbosacral plexus to innervate the limbs. The dorsal primary ramus, with its three branches (medial, intermediate, and lateral), innervates the posterior half of the vertebral body, the paraspinal muscles, and the zygapophyseal joints, and provides sensation to the back. The medial branch is the most important to remember because it innervates the zygapophyseal joints and lumbar multifidi and is the target during radiofrequency neurotomy for presumed zygapophyseal joint pain (Figure 40-11).24
FIGURE 40-10 A lumbar spinal nerve, its roots, and meningeal coverings. The nerve roots are invested by pia mater, and covered by arachnoid and dura as far as the spinal nerve. The dura of the dural sac is prolonged around the roots as their dural sleeve, which blends with the epineurium of the spinal nerve.
(Modified from Bogduk N: Nerves of the lumbar spine. In Bogduk N, editor: Clinical anatomy of the lumbar spine and sacrum, ed 3, Edinburgh, UK, 1977, Churchill Livingstone.)
Kirkaldy-Willis et al.108 have supplied us with the most accepted theory describing the cascade of events in degenerative lumbar spine disease that results in spondylotic changes, disk herniations, and eventually multilevel spinal stenosis (Figure 40-12). At the heart of this theory is the fact that, although the posterior zygapophyseal joints and the anterior intervertebral disks are separated anatomically, forces and lesions affecting one certainly alter and affect the other. For example, axial compressing injuries can damage the vertebral end plates, which can lead to degenerative disk disease, which eventually stresses the posterior joints, leading to the common degenerative changes seen in them over time. Torsional stress can injure the posterior joints and the disks, which in turn leads to increased stress on both these elements, resulting in further degenerative changes over time. When these degenerative changes affect one level, such as L4–L5, a chain reaction occurs, placing stress on the levels above and below the currently affected level, and eventually resulting in more generalized multilevel spondylotic changes.
(Modified from Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al: Pathology and pathogenesis of lumbar spondylosis and stenosis, Spine 3:319-328, 1998, with permission of Lippincott Williams & Wilkins.)
In studying lumbar degenerative disease, the question of which came first (disk degeneration or zygapophyseal joint degeneration) always arises. Fujiwara67 has answered this by studying multiple magnetic resonance images (MRIs) of aging spines. He hypothesizes that disk degeneration precedes zygapophyseal joint osteoarthritis, and that it might take 20 years for zygapophyseal joint disease to occur after the onset of disk degeneration.
To describe the degenerative cascade in more detail, we will separate our discussion of the changes that occur in the posterior joints from those in the disk, but fully realizing that they both can occur simultaneously and affect each other (see Figure 40-12). The degenerative changes that occur in the zygapophyseal joints from aging and repetitive microtrauma are similar to those that occur in the appendicular skeletal joints. The process begins with synovial hypertrophy, which eventually results in cartilage degeneration and destruction. With lessened and weakened cartilage and capsular laxity, the joint can become unstable. With the repetitive abnormal joint motion that results from this instability, the bony joint hypertrophies. This narrows the central canal and lateral recesses, potentially impinging nerve roots.
A similar process occurs anteriorly at the disk level from repetitive microtrauma of primarily shearing forces. Tears in the annulus are thought to be the first anatomic sign of degenerative wear. When the annulus is weakened enough, typically posterolaterally, the internal nucleus pulposus can herniate. Internal disk disruption can occur without herniation, however, because age and repeated stresses acting on the spine cause the gelatinous nucleus to become more fibrous over time. Tears in the annulus can progress to tears in the fibrous disk material, resulting in “internal disk disruption” without frank herniation. All this results in a loss of disk height, which causes instability (because the end-plate connection to the disk is degenerated), as well as lateral recess and foraminal narrowing and potential nerve root impingement. The loss of disk height also places new stresses on the posterior elements, resulting in further instability of the zygapophyseal joints and further degeneration and nerve root impingement.
Although this theory offers an explanation as to how the spine ages, it is still unclear why there is such a marked disconnect between the anatomic changes in the spine associated with aging, and back pain. Many patients with normal spine anatomy suffer from back pain, occasionally disabling pain, and many patients with marked degenerative changes on imaging are nearly or fully pain free. As a result, several theories have been developed to explain the occurrence of back pain.
Many patients with radicular pain have no neural impingement noted on MRI. Studies have shown that disk herniations can cause an inflammatory response.131,136,187 The mechanism stems from the fact that the nucleus pulposus is highly antigenic as a result of being in an immunoprotected setting in nonpathologic states. When the fluid of the nucleus pulposus is exposed to neural tissue of the spinal canal and neuroforamen through a defect in the annular fibers, an autoimmune-mediated inflammatory cascade begins. The inflammatory mediators generated can cause swelling of the nerves. This can alter their electrophysiologic function, sensitizing these neurons and enhancing pain generation without specific mechanical compression.
The mechanism of mechanical compression of the nerve roots has been studied as well.13,184,185 Compression of nerve roots can induce structural and vascular changes as well as inflammation.150 Neural compression can result in impairment of intraneural blood flow, subsequently decreased nutrient supply to the neural tissue, local ischemia, and formation of intraneural edema. This can set off an inflammatory cascade similar to that described above. Mechanical stimulation of lumbar nerve roots has also been shown to stimulate production of substance P, the neuropeptide known to modulate sensory nociceptive feedback.13 With these biochemical reactions, the local structural effects of mechanical compression (demyelination and axonal transport block) just compound the symptomatic response.
If mechanical compression were the sole problem in spinal stenosis, decompressive surgeries would be the only needed cure. We know that this is untrue, and consequently alternative theories on the pathogenesis of symptomatic spinal stenosis have been studied. Two theories supporting a vascular component to symptoms of spinal stenosis are the venous engorgement and arterial insufficiency theories.1
In the venous engorgement theory, the spinal veins of patients with stenosis dilate, causing venous congestion and stagnating blood flow.45 This pooling of blood in the spinal veins increases epidural and intrathecal pressures, leading to a microcirculatory, neuroischemic insult (i.e., an ischemic neuritis), which in turn leads to the typical neurogenic claudication symptoms of stenosis.
The arterial insufficiency theory of spinal stenosis is based on the arterial dilatation of the lumbar radicular vessels during lower limb exercise to provide increased blood flow and nourishment to the nerve roots. In patients with spinal stenosis, this reflex dilatation might be defective.14Because patients with spinal stenosis are typically elderly, they are also at higher risk for atherosclerosis, which in turn just amplifies the arterial insufficiency.
The low back is an anatomically diverse set of structures, and there are many potential sources of pain. One useful strategy to clarify these potential sources of pain is learning what low back structures are innervated (and can transmit pain through neural pain fibers) and what structures have no innervation (Box 40-1).
The sinuvertebral nerve innervates the anterior vertebral body, the external annulus, and the posterior longitudinal ligament. The posterior longitudinal ligament is a highly innervated structure and can play a significant role in low back pain perception with lumbar disk herniations. The medial branch of the dorsal primary ramus innervates the zygapophyseal joints and interspinous ligaments, as well as the lumbar multifidi. The other small branches of the dorsal primary ramus innervate the posterior vertebral body and other lumbar paraspinal musculature and fascia. The anterior longitudinal ligament is innervated by the gray rami communicans, which branch off the lumbar sympathetic chain. The internal annulus fibrosus and nucleus pulposus do not have innervation and in nondisease states cannot transmit pain.
Because many structures are potentially a source of pain, theories have been developed to help practitioners determine the cause of a particular patient’s pain. Some of the most common ones are described below.
Segmental dysfunction can occur when either a segment is too stiff or too mobile. A segment encompasses the disk, the vertebrae on each side of the disk, and the muscles and ligaments that act across this area. Excessive stiffness is thought to be caused by arthritic and ligamentous changes. Excessive mobility, also called instability, or potentially better termed “functional instability,” can be the result of tissue damage, poor muscular endurance, or poor muscular control, and is usually a combination of all three factors. Structural changes from tissue damage, such as strained or failed ligaments that cause joint laxity, vertebral end-plate fractures, and loss of disk height, can lead to segmental dysfunction because of the altered anatomy. Muscles also provide a critical component of spinal stability. This is of particular interest to the physiatrist because it can be affected by exercise. In normal situations, only a small amount of muscular coactivation (about 10% of maximal contraction) is needed to provide segmental stability. In a segment damaged by ligamentous laxity or disk disease, slightly more muscle coactivation might be needed. Because of the relatively gentle forces required to perform the activities of daily living, muscular endurance is more important than absolute muscle strength for most patients. Some strength reserve, however, is needed for unpredictable activities such as a fall, a sudden load to the spine, or quick movements. In sports and heavy physical work, both strength and endurance needs increase. For example, in rapid breathing caused by exertion, there is rhythmic contraction and relaxation of the abdominal wall. A fit person can simultaneously provide spine support with abdominal wall muscles and meet breathing demands, but a less-fit person might not be able to do so and therefore could more easily become injured or have pain.139 This biomechanical model is particularly complex in the spine because of the presence of global movement patterns and segmental movement patterns. Two interrelated muscular tasks must be carried out at the same time: maintaining overall posture and position of the spine, and control of individual intersegmental relationships. Sufficient but not excessive joint stiffness is required at the segmental level to prevent injury and allow for efficient movement. This stiffness is achieved with specific patterns of muscle activity, which differ depending on the position of the joint and the load on the spine. The inability to achieve this stiffness, and the resulting segmental problems, is thought to be a factor in low back pain.178
There appear to be consistent muscular problems in patients with chronic low back pain. Some of these factors might exist preinjury and make the spine more susceptible to injury, and some are adaptations to injury. Just as is seen in other areas of the body (such as the knee), muscle function and strength around the spine are altered after injury.177 Studies have shown abnormal firing patterns in the deep stabilizers of the spine and transversus abdominus with activities such as limb movements, accepting a heavy load, and responding to balance challenges. Other researchers have found strength ratio abnormalities and endurance deficits in patients with low back pain, such as abnormal flexion to extension strength ratios and lack of endurance of torso muscles.140
Studies of lumbar paraspinals have found several abnormalities in patients with low back pain. Multiple imaging studies have demonstrated paraspinal muscle atrophy, particularly of the multifidi, in patients with chronic low back pain.178 Recovery of the multifidi does not appear to occur spontaneously with the resolution of back pain.91 Biopsies of multifidi in patients with low back pain also show abnormalities. Atrophy of type 2 muscle fibers is found, and internal structural changes of type 1 fibers that give them a moth-eaten appearance are seen. In a study of patients undergoing surgery for lumbar disk herniations with duration of symptoms from 3 weeks to 1 year, multifidi biopsies collected at the time of surgery showed type 2 muscle atrophy and type 1 fiber structural changes. Biopsies were repeated 5 years postoperatively. Type 2 fiber atrophy was still found in all patients, in both those who had improved with surgery and those who had not. In the positive outcome group, however, the percentage of type 1 fibers with abnormal structures had decreased, and in the negative outcome group there was a marked increase in abnormal type 1 fibers.175 Increasingly strong scientific support is found for the multifactorial nature of low back pain, which includes both structural and dynamic factors.
This gives a theoretical basis for treatment aimed at improving spine biomechanics as a means of treating low back pain, along with other treatments aimed at pain management. The research in this area is intriguing but not yet conclusive. It is unclear whether these muscular abnormalities are the result of back pathology that leads to pain, or the cause of back pain. Study results conflict regarding consistent deficits in patients with back pain. This again reflects the heterogeneous nature of the group of patients classified as having low back pain, and that different factors predominate for different patients.
Pain is an individual experience, and biomechanical and neurologic factors alone do not explain much of the variance seen clinically in patients with back pain. Multiple psychosocial factors have been found to play a role in low back pain. This is briefly discussed here and more thoroughly discussed in the chapter on chronic pain (see Chapter 42), as these issues are shared by multiple painful conditions and not just low back pain.
It appears that between 30% and 40% of those with chronic back pain also have depression.115 This rate is so high because depressed patients are more likely to develop back pain and to become more disabled by pain, and because some patients with persistent pain become depressed. Patients who are depressed are at increased risk of developing back and neck pain. In a recent analysis of factors leading to the onset of back and neck pain, those in the highest quartile for depression scores had a fourfold increased risk of developing low back pain than those in the lowest quartile for depression scores.39 Strong evidence also shows that psychosocial factors are closely linked to the transition from acute pain to chronic pain and disability. In a study of 1628 patients with back pain seen at a pain clinic, those with a comorbid diagnosis of depression were more than 3 times more likely to be in the worst quartiles of physical and emotional functioning on the 36-Item Short-Form Health Survey than those who were not depressed.70 Multiple other studies have found that depression, anxiety, and distress are strongly related to pain intensity, duration, and disability.118
Research has also shown a high correlation with anger measurements and pain, thought to be related to deficient opioid modulation in those with high anxiety, anger, and fear reactivity.32 Patients with posttraumatic stress disorder have a high incidence of chronic low back pain as well.201
Beliefs about back pain can be highly individual and are often not based on facts. Some patients with back pain, especially those with chronic low back pain that keeps them from working, have a great deal of fear about back pain. These include fears that their pain will be permanent, that it is related to activity, and that exercise will damage their back. This set of beliefs is referred to as fear avoidance. For example, studies have found that patients with chronic low back pain who perform poorly on treadmill exercise tests,191 walk slower on treadmill tests,2 and perform more poorly on spinal isometric exercise testing3 were the ones with more anticipation of pain than those who did well on these tests. Fear-avoidance beliefs rather than actual pain during testing predicted their performance. Fear-avoidance levels explain self-reported disability and time off work more accurately than actual pain levels or medical diagnosis does.127 This finding has led Waddell and other experts to state that “the fear of pain may be more disabling than pain itself.”234
A large, population-based study found that subjects with high levels of pain catastrophizing, characterized by excessively negative thoughts about pain and high fear of movement and injury or reinjury (kinesophobia), who had back pain at baseline were much more likely to have especially severe or disabling pain at follow-up evaluation compared with those who did not catastrophize. For those without back pain at the initial questionnaire, catastrophizers were more likely to have developed low back pain with disability at follow-up evaluation than noncatastrophizers.171 Thought processes, such as the presence of catastrophizing, are not limited to back pain and are often part of a larger pattern of relationships and thought processes.
Patients’ beliefs about pain and their approach to dealing with pain have been consistently found to affect outcomes. Fortunately, changes in these beliefs and cognitive patterns are possible. Multidisciplinary pain programs have proven effective in decreasing fear-avoidant beliefs and catastrophizing (see Chapter 42).205
These changes in beliefs can also improve function. For example, a study in which a group of patients with chronic low back pain underwent a cognitive behavioral treatment program found that, although there were not significant changes in pain intensity, those with reductions of fear-avoidance beliefs had significant reductions in disability. Changes in fear-avoidant beliefs accounted for 71% of the variance in reduction in disability in this study.252
The experience of nociception is processed by the body in complex ways. The theory that pain is a simple loop from injury to perception of injury is much too simplistic. Pain processing begins in the spinal cord and continues extensively in the brain, and the ultimate pain that someone experiences is the sum of multiple descending and ascending faciliatory and inhibitory pathways. Extensive evidence now supports the theory that persistent pain might be caused by central sensitization, which could help explain why often no pain generator is found in chronic low back pain.46
A complete history and physical examination is important in the evaluation of low back pain to determine the cause of the symptoms, rule out serious medical pathology, and determine whether further diagnostic evaluation is needed.
As with any pain history, features of back pain that should be explored include location; character; severity; timing, including onset, duration, and frequency; alleviating and aggravating factors; and associated signs and symptoms. Each of these features can assist the clinician in obtaining a diagnosis and prognosis and determining the appropriate treatment. The causes of back pain are often very difficult to determine. For as many as 85% of patients, no specific cause for back pain is found.50 One of the main purposes of the history is to rule out rare but serious causes of back pain. Elements of historical information that suggest a serious underlying condition as the cause of the pain such as cancer, infection, long tract signs, and fracture are called red flags (Box 40-2). When these are present, further workup is necessary (Table 40-1).
Modified from Nachemson A, Vingard E: Assessment of patients with neck and back pain: A best-evidence synthesis. In Nachemson AL, Johnsson B, editors: Neck and back pain: the scientific evidence of causes, diagnosis, and treatment, Philadelphia, 2001, Lippincott Williams & Wilkins.
Besides determining a diagnosis, a purpose of the history is to explore the patient’s perspective and illness experience. Certain psychosocial factors are valuable in determining prognosis (Box 40-3). Factors such as poor job satisfaction, catastrophic thinking patterns about pain, the presence of depression, and excessive rest or downtime are much more common in patients in whom back pain becomes disabling. These are called yellow flags because the clinician should proceed with caution, and further psychologic evaluation or treatment should be considered if they are present. Some of these psychosocial factors are addressed by specific questions, and some become evident through statements that patients make during the history as they describe their illness experience. Questions about, for example, what patients believe is causing the pain, their fear and feelings surrounding this belief, their expectations about the pain and its treatment, and how back pain is affecting their lives (including work and home life) can yield valuable information. Many of these yellow flags are better prognostic indicators than the more traditional medical diagnoses.235
Table 40-2 outlines a thorough examination of the lumbar spine.
|Examination Component||Specific Activity||Reason for This Part of the Examination|
|Observation||Observation of overall posture||Determine whether structural abnormality or muscle imbalances are present|
|Observation of lumbar spine||Further define muscle imbalance and habitual posture|
|Observation of the skin||Search for diagnoses such as psoriasis, shingles, or vascular disease as cause of the pain|
|Observation of gait||Screen the kinetic chain and determine whether muscular, neurologic, or joint problems are contributing to symptoms|
|Palpation||Bones||Search for bony problems such as infection or fracture|
|Facet joints||Identify whether specific levels are tender|
|Ligaments and intradiskal spaces||Determine whether these are tender|
|Muscles||Search for trigger points, muscle spasms, muscle atrophy|
|Active range of motion||Forward flexion||Amount, quality if painful|
|Side bending||Same, also side to side differences|
|Neurologic examination||Manual muscle testing of L1–S1 myotomes||Determine weakness|
|Pinprick and light touch sensation, L1–S1 dermatomes||Determine sensory loss|
|Reflexes: patellar, hamstring, Achilles||Test injury to L4, L5, or S1 roots if diminished, upper motor neuron disease if brisk|
|Balance and coordination testing||Signs of upper motor neuron disease|
|Straight leg raise||Neural tension at L5 or S1|
|Femoral nerve arch||Neural tension at L3 or L4|
|Orthopedic special tests||Abdominal muscle strength||Determines weakness and deconditioning|
|Pelvis stabilizer strength, i.e., gluteus medius, maximus, etc.||Determines weakness and deconditioning|
|Tightness or stiffness of hamstrings||Determines areas of poor flexibility|
|Tightness or stiffness of hip flexors||—|
|Tightness or stiffness of hip rotators||—|
|Prone instability test||Signs of instability|
Observation should include a survey of the skin, muscle mass, and bony structures, as well as observation of overall posture (Figures 40-13 and 40-14), and the position of the lumbar spine in particular. Gait should also be observed for clues regarding etiology and contributing factors.
(Modified from Kendall FP, McCreary EK: Trunk muscles in muscle testing and function, Philadelphia, 1983, Williams & Wilkins.)
FIGURE 40-14 Faulty pelvic alignment as a result of weak and long abdominal muscles (A), short and stiff hip flexors (B), apparent anterior tilt (C), and posterior tilt (D). The effect of pelvic tilting on the inclination of the base of the sacrum to the transverse plane (sacral angle) during upright standing is shown. E, Tilting the pelvis backward reduces the sacral angle and flattens the lumbar spine. F, During relaxed standing, the sacral angle is about 30 degrees. G, Tilting the pelvis forward increases the sacral angle and accentuates the lumbar spine.
(Modified from Sahrmann SA: Movement impairment syndromes of the lumbar spine: diagnosis and treatment of movement impairment syndromes, St Louis, 2002, Mosby.)
Palpation should begin superficially and progress to deeper tissues. It can be done with the patient standing. To ensure that the back muscles (Figure 40-15) are fully relaxed, palpation is often done with the patient lying prone, perhaps with a pillow under the abdomen to slightly flex the spine into a position of comfort. It should proceed systematically to determine what structures are tender to palpation.
Several methods can be used to measure spinal range of motion (ROM). These include using a single or double inclinometer; measuring the distance of fingertips to floor; and, for forward flexion, the Schober test (measuring distraction between two marks on the skin during forward flexion). Of these methods, the double inclinometer has been shown to correlate the closest to measurements on radiographs.77,210 Fingertip to floor has good interrater and intrarater reliability, but this takes into account the movement of the pelvis and is affected by structures outside the spine, such as tight hamstrings.168 The Schober test is commonly used to assess a decrease in forward flexion in ankylosing spondylitis. It is sensitive for this condition but is not specific. General figures for normal ROM are forward flexion, 40 to 60 degrees; extension, 20 to 35 degrees; lateral flexion, 15 to 20 degrees; and rotation, 3 to 18 degrees. Studies to determine normal ROM in asymptomatic adults have found large variations within the normal range.165 It is unclear what the significance of decreased ROM is in patients with back pain because many people without back pain also have limited range. ROM can also change depending on the time of day, the effort the patient expends, and many other factors.255
The examiner should record whether there are abnormalities in the patient’s movement pattern during ROM, such as a “catch” in the range or whether it causes pain. This might give clues to the diagnosis. For example, pain with forward flexion can signify disk disease, and pain with extension can indicate spondylolisthesis, zygapophyseal joint disease, or spinal stenosis.
The neurologic examination of the lower limbs can rule out clinically significant nerve root impingement and other neurologic causes of leg pain (Tables 40-3 and 40-4). The physical examination should logically proceed to discover whether a particular root level is affected by combining the findings of weakness, sensory loss, diminished or absent reflexes, and special tests such as straight leg-raising sign. Upper motor neuron abnormalities should also be ruled out. The accuracy of the neurologic examination in diagnosing herniated disk is moderate. The accuracy can be increased considerably, however, with combinations of findings.50 The sensitivity and specificity of different findings for lumbar radiculopathy have been well studied (Table 40-5).
|Reason for Abnormality||Clinical Example|
|Bone structure||Compression fractures|
|Ligamentous laxity||Hyperextension of the knees, elbows|
|Muscle and fascial length||Tight hamstrings that cause a posterior pelvic tilt|
|Weak and long abdominal muscles that allow an anterior pelvic tilt|
|Body habitus||Obesity or pregnancy causes changes in force and increased lumbar lordosis|
|Neurologic disease||Spasticity causes an extension pattern of the lower limb|
|Mood||Depression causes forward slumped shoulders|
|Habit||Long-distance cyclists have increased thoracic kyphosis and flat spine from prolonged positioning while riding|
Back pain can be caused by deconditioning, poor endurance, and muscle imbalances. This makes it important to identify any inefficient or abnormal movement patterns of muscles that control the movement of the spine and the position of the pelvis.
Because of their stabilizing effect on the spine, abdominal muscle strength and endurance is important. Several different ways can be used to measure abdominal muscle strength and control (Figures 40-16 and 40-17). One grading system assesses whether the patient is able to maintain a neutral spine position while adding increasingly more challenging leg movements(Figure 40-18).
FIGURE 40-16 Trunk raising forward: grading. The curl trunk sit-up is performed with the patient lying supine and with the leg extended. The patient posteriorly tilts the pelvis and flexes the spine, and slowly completes a curled trunk sit-up. Kendall states that the “crucial point in the test for the abdominal muscle strength is at the moment the hip flexors come into strong action. The abdominal muscle at this point must be able to oppose the force of the hip flexors in addition to maintain the trunk curl.” At the point where the hip flexors strongly contract, patients with weak abdominal muscles will tilt the pelvis anteriorly and extend the low back. A, A 100% or normal grade is the ability to maintain spinal flexion and come into the sitting position with the hands clasped behind the head. B, An 80% or good grade is the ability to do this with the forearms folded across the chest. C, A 60% or fair grade is the ability to do this with the forearms extended forward. A 50% or fair grade is the ability to begin flexion but not maintain spinal flexion with the forearms extended forward.
(Modified from Kendall FP, McCreary EK: Trunk muscles in muscle testing and function, Philadelphia, 1983, Williams and Wilkins.)
FIGURE 40-17 Leg lowering: grading. In the second test, the patient raises the legs one at a time to a right angle, and then flattens them back on the table. The patient slowly lowers the legs while holding the back flat. A 100% or normal grade is the ability to hold the low back flat on the table as the legs are lowered to the fully extended position. An 80% or good grade is the ability to hold the low back flat and lower the legs to a 30-degree angle. A, A 60% or fair plus grade is the ability to lower the legs to 60 degrees with the low back flat. B, The pelvis tilted anteriorly and the low back arched as the legs were lowered. C, The final position. Kendall notes that this second test is more important than the first (see Figure 40-16) in grading muscles essential to proper posture, and that often patients who do well on the first test do poorly on the second.
(Modified from Kendall FP, McCreary EK: Trunk muscles in muscle testing and function, Philadelphia, 1983, Williams and Wilkins.)
FIGURE 40-18 Abdominal strength grading. A, The patient lies supine with the knees bent (supine crook lying). The physician cues the patient to activate the transversus abdominis (“Pull your belly button toward your backbone”), and a very slight lumbar lordosis is maintained in a neutral position in which the spine is neither flexed nor extended. The ability to maintain the neutral spine is progressively challenged by loading the spine via lower extremity movements. Grading is as follows. B, Grade 1: The patient is able to maintain a neutral spine while extending one leg by dragging the heel along the table; the other leg remains in the starting position. C, Grade 2: The patient is able to maintain a neutral spine while holding both legs flexed 90 degrees at the hip and 90 degrees at the knee, and touching one foot to the mat and then the other. D, Grade 3: The patient is able to maintain a neutral spine while extending one leg by dragging the heel along the table. The other leg is off the mat and flexed 90 degrees at the hip and 90 degrees at the knee. E, Grade 4: The patient is able to maintain a neutral spine while extending one leg hovered an inch or two above the table, while the other leg is off the mat and flexed 90 degrees at the hip and 90 degrees at the knee. Grade 5: The patient is able to extend both legs a few inches off the mat and back again while maintaining the spine in neutral.
Besides determining the strength of the abdominals, strength testing of the back muscles and pelvic stabilizers, such as the hip abductors, can be useful. Assessing for areas of relative inflexibility is also important. Commonly performed tests are hip flexor flexibility, hamstring flexibility, other hip extensors’ length, and gastrocnemius/soleus length. Balance challenges, such as the ability to maintain single-footed stance, the ability to lunge or squat, and other functional tests are also helpful to determine a patient’s baseline status.
Many clinicians and researchers believe that one cause of mechanical low back pain is segmental instability that responds to specific stabilization treatments. Therefore accurately identifying this group from other forms of low back pain could be important. These special tests include passive intervertebral motion testing and the prone instability test.
The patient lies prone, with the torso on the examining table and the legs over the edge of the table with the feet resting on the floor. The examiner performs passive intervertebral motion testing at each level and notes provocation of pain. Then the patient lifts the legs off the floor, and the painful levels are repeated. A positive test is when the pain disappears when the legs are lifted off the table. This is because the extensors are able to stabilize the spine in this position.90,138
Generally in musculoskeletal medicine, the joint above and the joint below the painful area should be assessed to make sure nothing is missed. This is a good idea for the examination of the lumbar spine as well. ROM of the hip joints should be assessed, and a quick screen of the knee and ankle joint can determine whether pathology in these areas is contributing to the back problem. The thoracic spine can be quickly screened as well during ROM and palpation.
Multiple reasons can explain why patients with back pain might display symptoms out of proportion to injury. Illness behaviors are learned behaviors and are responses that some patients use to convey their distress. Several studies have found that patients with chronic low back pain and chronic pain syndrome experience significant anxiety during the physical examination, even to the level experienced during panic attacks. This complicates the assessment by altering the clinical presentation of the condition. This anxiety is generally manifest as avoidance behavior, such as decreased ROM or poor effort with muscle testing.81 Other reasons for illness behavior include a desire to prove to physicians how disabling the pain is and malingering. One way to assess for illness behavior on physical examination is to perform parts of the examination to search for Waddell’s signs. Waddell’s signs are forms of illness behavior.234 They are nonorganic findings on physical examination that correlate with psychologic distress. They are as follows:
Findings in three of these five categories suggest psychologic distress and also suggest that other parts of the physical exam that require patient effort or reporting of symptoms might be inaccurate.
Conventional radiographs are indicated in trauma to evaluate for fracture and to look for bony lesions such as tumor when red flags are present in the history. As an initial screening tool for lumbar spine pathology, however, they have very low sensitivity and specificity.73 Anterior–posterior and lateral views are the two commonly obtained views. Oblique views can be obtained to examine for a spondylolysis by visualizing the pars interarticularis and the “Scottie dog” appearance of the lumbar spine (Figure 40-19). Lateral flexion–extension views are obtained to check for dynamic instability, although the literature does not support their usefulness.55 They are potentially most helpful from a surgical screening perspective when evaluating a spondylolisthesis. They are commonly obtained in posttrauma and postsurgical patients.
MRI is the preeminent imaging method for evaluating degenerative disk disease, disk herniations, and radiculopathy (Figure 40-20) (see also Chapter 7). On T2-weighted imaging, the annulus can be differentiated from the internal nucleus, and annular tears can be seen as high-intensity zones. These zones are of unclear clinical significance but are thought to be potential pain generators.
FIGURE 40-20 Disk extrusion in a 48-year-old woman with back and left leg pain. A and B, Sagittal T2– and T1-weighted magnetic resonance image (MRI) showing L5–S1 disk extrusion with caudal extension. C, Axial T2-weighted MRI showing the extrusion is left paracentral in the lateral recess, occupying the space where the S1 root resides.
Adding gadolinium contrast enhancement helps to identify structures with increased vascularity. Contrast is always indicated in evaluating for tumor or infection or to determine scar tissue (vascular) versus recurrent disk herniation (avascular) in postsurgical patients with recurrent radicular symptoms.
The downside of MRI is that, although it is a very sensitive test, it is not very specific in determining a definite source of pain. It is well established that many people without back pain have degenerative changes, disk bulges, and protrusions on MRI. Boden et al.21 demonstrated that one third of 67 asymptomatic subjects were found to have a “substantial abnormality” on MRI of the lumbar spine. Of the subjects younger than 60 years, 20% had a disk herniation, and 36% of those older than 60 had a disk herniation and 21% had spinal stenosis. Bulging and degenerative disks were even more commonly found. In another study of lumbar MRI findings in people without back pain, Jensen et al.97 demonstrated that only 36% of 98 patients had normal disks. They found that bulges and protrusions were very common in asymptomatic subjects, but that extrusions were not. In a more recent study in 2001, Jarvik confirmed these findings.96
Because of the resolution of anatomic structures in MRI, it has essentially replaced computed tomography (CT) scanning as the imaging study of choice for low back pain and radiculopathy. CT scanning is still more useful than MRI, however, in evaluating bony lesions. CT scans are also useful in the postsurgical patient with excessive hardware that can obscure MRIs, and in patients with implants (aneurysm clips or pacemakers) that preclude MRI.
In myelography, contrast dye is injected into the dural sac and plain radiographs are performed to produce images of the borders and contents of the dural sac (Figure 40-21). CT images can also be obtained after contrast injection to produce axial cross-sectional images of the spine that enhance the distinction between the dural sac and its surrounding structures. This is typically reserved as a potential presurgical screening tool but has been used less with the advancement of MRI.
FIGURE 40-21 Anteroposterior (A) and lateral (B) myelograms of a 59-year-old woman with severe L4–L5 central stenosis caused by a large left L4–L5 zygapophyseal joint synovial cyst. Note the obvious filling defect at the L4–L5 level. She had symptoms of cauda equina syndrome and regained full neurologic function after decompression surgery.
Radionuclear bone scanning is a fairly sensitive but not specific imaging modality that can be used to detect occult fractures, bony metastases, and infections. To increase anatomic specificity, single-photon emission computed tomography (SPECT) bone scanning is used to obtain bone scans with axial slices. This allows the diagnostician to differentiate uptake in the posterior elements from more anterior structures of the spine. The diagnostic use of this study with regard to altering clinical decision-making is controversial. Studies have been published demonstrating that the use of SPECT can help identify patients with low back pain who might benefit from Z-joint injections.172
Electromyography is useful in evaluating radiculopathy because it provides a physiologic measure for detecting neurogenic changes and denervation with good sensitivity and high specificity. It can help to provide information as to which anatomic lesions found in imaging studies are truly physiologically significant.181 See Chapters 9 through 11 for further details.
Blood tests are rarely used in isolation as a diagnostic strategy for low back pain. Some blood tests are helpful as an adjunct in diagnosing inflammatory disease of the spine (with such markers of inflammation as sedimentation rates and C-reactive proteins), as well as some neoplastic disorders, such as multiple myeloma with a serum protein electrophoresis and urine protein electrophoresis.
Nearly 85% of those who seek medical care for low back pain do not receive a specific diagnosis.50 The majority of these patients most probably have a multifactorial cause for back pain, which includes deconditioning; poor muscle recruitment; emotional stress; and changes associated with aging and injury such as disk degeneration, arthritis, and ligamentous hypertrophy. This type of back pain can be given many names; simple backache, nonspecific low back pain, lumbar strain, and spinal degeneration are a few of the common names for this condition. The name given to a condition sends certain messages to the patient who receives the diagnosis. The term simple backache might cause a patient to think that the physician misunderstands because, from the patient’s perspective, the pain is not simple if it has not resolved in a few days. The label nonspecific low back pain can cause the patient to continue to seek care from multiple providers to receive a specific diagnosis. Lumbar strain suggests that the condition was caused by overactivity, which is often not the case, and that further physical activity would cause it to recur, which is not true. Spinal degeneration sends the message that the changes are permanent and will probably worsen.235 The term mechanical low back pain is perhaps the best term for this multifactorial axial backache. It suggests the mechanism of injury better than terms such as strain or sprain, and it does not imply permanence.
The biomechanics of the spine are not unlike the biomechanics of other systems, in that longevity of the components and efficiency of the system depend on precise movements of each segment. In the spine, this means both an alignment in sustained postures and movement patterns that reduce tissue strain and allow for efficient muscle action without trauma to the joints or soft tissue.189 Clinicians and researchers alike theorize that when alignment and movement patterns deviate from the ideal, degeneration and tissue overload is more likely. This is analogous to the abnormal tire wear that occurs on a car when the wheels are out of alignment. Unlike machinery, the body can adapt over the course of time to stress on the segments. This adaptation can be the healthy response of tissue to loading (as is seen with exercise), such as muscle hypertrophy or increased bone density. It can also, however, begin a cycle of microtrauma that can lead to macrotrauma.125,140,189 The theoretic model for this approach is strong, and research is beginning to validate many of these concepts, although this is not easy given the complex nature of the system.
Most studies of the various treatments for low back pain, particularly chronic low back pain, unfortunately have shown limited efficacy. Even the most commonly prescribed treatments, such as medications, exercise, and manipulation, in large trials tend to show improvements of only 10 to 20 points on a 100-point pain visual analogue scale. For this reason, most clinicians use multiple treatments on a particular patient in the hope that their cumulative effect will provide sufficient pain relief and an improvement in symptoms. The most common treatments for low back pain are discussed below.
Education should include providing as much of an explanation as patients need in terms they can understand. The physician should also provide empathy and support and impart a positive message. Reassurance that there is no serious underlying pathology, that the prognosis is good, and that the patient can stay active and get on with life despite the pain can help counter negative thoughts and misinformation that the patient might have about back pain.235
Strong evidence from systematic reviews indicates that the advice to continue ordinary activity as normally as possible fosters faster recovery and can lead to less disability than the advice to rest and “let pain be your guide.”236 It is controversial whether patients with low back pain fare better with a specific diagnosis or not. Education and explanations, however, should be adequate. As Waddell states in his book The Back Pain Revolution, “Simply saying that ‘I can’t find anything wrong’ might imply that you are not sure and make patients worry more!”235 On the other hand, some diagnoses carry negative messages to patients that suggest permanent damage and the need to “get fixed,” such as degenerative disk disease or arthritis.235 Mechanical low back pain is a useful diagnostic term because it implies the mechanism of the pain and the way it is best treated without suggesting permanence.
Beyond a diagnosis, there is other information that patients want about low back pain. In a study of patients who presented with low back pain to their primary care doctors in a health maintenance organization setting, the information that patients wanted from their doctor included the likely course of their back pain, how to manage their pain, how to return to usual activity quickly, and how to minimize the frequency and severity of recurrences. They ranked each of these areas of education a higher priority than finding a cause or receiving a diagnosis for their pain.235 Providing this information in an amount and in a way that patients can understand helps build a therapeutic doctor–patient relationship and, it is hoped, helps reduce anxiety and speed recovery.
The term back school is generally used for group classes that provide education about back pain. The content and length of these classes varies a great deal, but generally they include information about the anatomy and function of the spine, common sources of low back pain, proper lifting technique and ergonomic training, and sometimes advice about exercise and remaining active. Studies have generally found back schools to be effective in reducing disability and pain for those with chronic low back pain.224
No well-controlled studies show that exercise is effective for the treatment of acute low back pain. Many practitioners believe that exercise for patients with acute low back pain is appropriate to prevent deconditioning, to reduce the chance of recurrence of symptoms, and to reduce the risk of the development of chronic pain and disability. This is consistent with rehabilitation principles for other acute injuries, such as sports-related injuries or rehabilitation after joint replacement surgery.239 This principle is not yet supported by scientific research, perhaps because of problems with long-term exercise compliance, the overall favorable prognosis for each episode of acute back pain, or the outcome measures used.
Multiple high-quality studies have found, however, that exercise results in positive outcomes in the treatment of chronic low back pain.226 This includes pain relief (although this relief is modest, with a recent metaanalysis of 43 trials showing a mean difference of 10 points on a 100-point scale), improvement in function, and slightly reduced sick leave.43,87 It appears that the most effective exercise for low back pain includes an individualized regimen learned and performed under supervision that includes stretching and strengthening.87 This is not surprising because it is generally believed that the purpose of exercises for the treatment of low back pain is to strengthen and increase endurance of muscles that support the spine and improve flexibility in areas where this is lacking. This is combined with motor retraining to establish normal patterns of muscle activity, and treatment of deficits of the kinetic chain that interfere with biomechanical efficiency. One reason that studies have not been able to determine what exercises are best for patients with low back pain could be that multiple forms of exercise can achieve the goal of restoring function and regaining physical fitness.116,225,239