General Concepts

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 gives 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.

Vertebrae

The bony anatomy of the lumbar spine consists of five lumbar vertebrae. A small percentage of the population has four (the fifth vertebra is sacralized) or six (the first sacral segment is lumbarized). The lumbar vertebrae are composed of the vertebral body, the neural arch, and the posterior elements ( Figure 33-1 ). 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 the vertebral bodies and the shock-absorbing intervertebral disks function together to withstand axially directed loads. 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 between the vertebral bodies and 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 the part of the lamina between the superior and inferior articular processes ( Figure 33-2 ). 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.

Lateral view of the lumbar vertebrae.

(Modified from Parke WW: Applied anatomy of the spine. In Herkowitz HN, Garfin SR, Balderson RA, et al, editors: Rothman-Simeone: the spine , ed 4, Philadelphia, 1999, WB Saunders.)

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 Herkowitz HN, Garfin SR, Balderson RA, et al, editors: Rothman-Simeone: the spine, ed 4, Philadelphia, 1999, WB Saunders.)

Intervertebral Disk

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 older adult 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. This varying composition supports the functional role of the outer fibers to resist flexion, extension, rotation, and distraction forces.

The main function of the intervertebral disk is shock absorption ( Figure 33-3 ). It is primarily the annulus, not the nucleus, that acts as the shock absorber because the liquid properties of the nucleus render it 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.

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, editor: The inter-body joint and the intervertebral discs. In Clinical and radiological anatomy of the lumbar spine and sacrum, ed 5, Edinburgh, 2012, Churchill Livingstone.)

Because flexion loads the anterior disk, the nucleus is displaced posteriorly. 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 33-4 ). 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, thereby increasing torsional shear forces and putting the disks at risk.

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, editor: The zygapophysial joints. In Clinical and radiological anatomy of the lumbar spine and sacrum , ed 5, Edinburgh, 2012, Churchill Livingstone.)

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 33-5 demonstrates the changes in L3 disk pressure under various positions and exercises. Adding rotation to the already flexed posture increases the disk pressure substantially. Comparing lifting maneuvers, it has been shown that there is not a substantial 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). What decreases the forces on the lumbar spine is lifting the load close to your body. The farther the load is from the chest, the greater the stress on the lumbar spine.

Posterolateral intervertebral disk herniation.

Zygapophyseal Joints

The zygapophyseal joints (also known as Z joints and facet joints) are paired synovial joints with a synovium and a capsule ( Figure 33-6 ). 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.

The intermediate layer of back muscles: the erector spinae.

Ligaments

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 and the facet joints, act to restrain the spine and prevent excessive shear forces in forward bending.

Muscles

Muscles with Origins on the Lumbar Spine

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 33-7 and 33-8 ). 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 deep back muscles: the multifidi.

A, The superficial abdominal muscles. B, The deep abdominal 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.

Abdominal Musculature

The superficial abdominals include the rectus abdominis and external obliques ( Figure 33-9, A ). The deep layer consists of internal obliques and the transversus abdominis (see Figure 33-9, B ). The transversus abdominis has been the focus of considerable 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 that it has received such attention of late.

A, Relative change in pressure (or load) in the third lumbar disk in various positions in living individuals. B, Relative change in pressure (or load) in the third lumbar disk during various muscle-strengthening exercises in living individuals. Neutral erect posture is considered 100% in these figures; other positions and activities are calculated in relationship to this.

(Modified from Nachemson AL, Morris JM: In vivo measurements of intradiscal pressure, J Bone Joint Surg Am 46:1077-1092, 1964.)

Nerves

The conus medullaris ends at about 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 33-10 ). 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 innervates the zygapophyseal joints and lumbar multifidi, and is the target during radiofrequency neurotomy for presumed zygapophyseal joint pain ( Figure 33-11 ).

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 and radiological anatomy of the lumbar spine and sacrum, ed 5, Edinburgh, 2012, Churchill Livingstone.)

Observe that the innervation of the zygapophyseal joints derives from the medial branch off the dorsal primary ramus.

Aging Spine: A Degenerative Cascade

Kirkaldy-Willis et al. have supplied us with the most accepted theory describing the cascade of events in degenerative lumbar spine disease that results in disk herniations, spondylotic changes, and eventually multilevel spinal stenosis. 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 zygapophyseal joints, leading to the common degenerative changes seen over time. Torsional stress can injure the zygapophyseal joints and the disks, which in turn leads to increased stress on both these elements. It appears that commonly these changes begin first in the disks. By studying multiple magnetic resonance images (MRIs) of aging spines, evidence of disk degeneration is seen first, and can precede zygapophyseal joint disease by as much as 20 years. When these degenerative changes affect one level, 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.

To simplify discussion of the degenerative cascade, we will separate our discussion of the changes that occur in the zygapophyseal joints from those in the disk, fully realizing that they both can occur simultaneously and affect each other ( Figure 33-12 ).

The spectrum of degenerative change that leads from minor strains to marked spondylosis and stenosis.

(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.)

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.

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 the resultant capsular laxity, the joint can become unstable, and with the subsequent repetitive abnormal joint motion, bony hypertrophy results, thus narrowing the central canal and lateral recesses and potentially impinging nerve roots.

These changes are commonly described clinically as segmental dysfunction. 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 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. Structural changes from tissue damage, such as 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 crucial component of spinal stability, and is one area of potential intervention through exercise. In normal situations, only a small amount of muscular coactivation (approximately 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. 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. Alternatively, some segments are thought to be too stiff, because of osteoarthritis and ligamentous thickening in the spine, which is also considered to be a source of low back pain.

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 occurrence of back pain and the anatomic changes in the spine associated with aging. 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. One theory is that this is related to differences in muscular activation and neural control.

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 pain. Motor systems and their adaption to back pain appear to vary greatly between individuals and range from subtle changes in muscle activation to redistribute forces, to complete avoidance of activity. Studies have shown abnormal firing patterns in the deep stabilizers of the spine and transversus abdominis 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. These motor adaptations may have persistent long-term consequences.

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. Recovery of the multifidi does not appear to occur spontaneously with the resolution of back pain. Biopsies of multifidi in patients with low back pain also show abnormalities. Multifidi biopsies collected at the time of surgery for disk herniation showed type 2 muscle atrophy and type 1 fiber structural changes. On repeat biopsy 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.

Centralization and Pain

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 facilitatory 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.

Psychosocial Factors and Low Back Pain

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 37 ), as these issues are shared by multiple painful conditions and not just low back pain.

History

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. 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 33-2 ). When these are present, further workup is necessary ( Table 33-1 ).

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 33-3 ). 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 psychological 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.

Physical Examination

Table 33-2 outlines a thorough examination of the lumbar spine.

Observation

Observation should include a survey of the skin, muscle mass, and bony structures, as well as observation of overall posture ( Figures 33-13 and 33-14 , Table 33-3 ) and the position of the lumbar spine in particular. Gait should also be observed for clues regarding etiology and contributing factors.

Four types of postural alignment. A, Ideal alignment. B, Kyphosis-lordosis posture. C , Flat back posture, D , Sway-back posture.

(Modified from Kendall FP, McCreary EK: Trunk muscles in muscle testing and function, Philadelphia, 1983, Lippincott Williams & Wilkins.)

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. A, Tilting the pelvis backward reduces the sacral angle and flattens the lumbar spine. B, During relaxed standing, the sacral angle is about 30 degrees. C, Tilting the pelvis forward increases the sacral angle and accentuates the lumbar lordosis.

(Modified from Sahrmann SA: Movement impairment syndromes of the lumbar spine: diagnosis and treatment of movement impairment syndromes, St Louis, 2002, Mosby.)

Table 33-3

Factors That Affect Posture

Reason for Abnormality	Clinical Example
Bone structure	Compression fractures
	Scheuermann disease
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

 

Orthopedic Special Tests to Assess for Relative Strength and Flexibility

Back pain may be caused by deconditioning, poor endurance, and muscle imbalances. Identifying inefficient or abnormal movement patterns of muscles that control the movement of the spine and the position of the pelvis help direct the exercise prescription.

Because of its stabilizing effect on the spine, abdominal muscle strength and endurance is important. Several different methods can be used to measure abdominal muscle strength and control ( Figures 33-15 and 33-16 ). One grading system assesses if the patient is able to maintain a neutral spine position while adding increasingly more challenging leg movements ( Figure 33-17 ).

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 and McCreary ¹¹⁴ state 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, Lippincott Williams and Wilkins.)

Leg lowering: grading. In the second test, the patient raises the legs one at a time to a right angle, and then flattens the low 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 and McCreary ¹¹⁴ note that this second test is more important than the first (see Figure 33-15 ) 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.)

Abdominal strength grading. A, The patient lies supine with the knees bent (supine hook 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, and 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.

Imaging Studies

Imaging of the lumbar spine should be used in the evaluation of low back pain if specific pathology needs to be confirmed after a thorough history and physical examination.

Plain Radiography

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. 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 33-18 ). Lateral flexion-extension views are obtained to check for dynamic instability, although the literature does not support their usefulness. They are potentially most helpful from a surgical screening perspective when evaluating a spondylolisthesis. They are commonly obtained in patients after trauma or surgery.

Oblique drawing of the lumbosacral junction, outlining the “Scottie dog” and the area of spondylolysis.

Magnetic Resonance Imaging

MRI is the preeminent imaging method for evaluating degenerative disk disease, disk herniations, and radiculopathy ( Figure 33-19 ). 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.

Disk extrusion in a 48-year-old woman with back and left leg pain. A and B, Sagittal T2-weighted 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. demonstrated that one third of 67 individuals who were asymptomatic were found to have a “substantial abnormality” on MRI of the lumbar spine. Of the individuals younger than 60 years, 20% had a disk herniation, and 36% of those older than 60 years 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. demonstrated that only 36% of 98 patients had normal disks. They found that bulges and protrusions were very common in individuals who were asymptomatic, but that extrusions were not. In a study in 2001, Jarvik et al. confirmed these findings.

Myelography

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 33-20 ). 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 presurgical screening tool but has been used less with the advancement of MRI.

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.

Laboratory Studies

Blood tests are rarely used in isolation as a diagnostic strategy for low back pain. They may be helpful as an adjunct in diagnosing inflammatory disease of the spine (with markers of inflammation such as sedimentation rate and C-reactive protein), as well as some neoplastic disorders, such as multiple myeloma with serum and urine protein electrophoresis.

Nonspecific Low Back Pain

Nearly 85% of those who seek medical care for low back pain do not receive a specific diagnosis. The majority of these patients are likely to 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; nonspecific low back pain, simple backache, mechanical low back pain, lumbar strain, and spinal degeneration are a few of the common names for this condition. By definition, the history and physical examination do not suggest a more specific diagnosis, and diagnostic tests used to exclude other likely causes of the symptoms are negative. Risk factors remain difficult to discern. So far, researchers have been able to show that obesity, smoking, a very sedentary lifestyle, very vigorous physical activity (i.e., both extremes of the activity continuum), and genetic effects have all been found to be risk factors for nonspecific low back pain. Interestingly, neither abnormalities on MRI nor work-related activities such as lifting, twisting, standing, and awkward positions have been found to be risk factors. Treatment is discussed in a subsequent section.

Lumbar Spondylosis

In an attempt to arrive at a more specific diagnosis and to determine subgroups of patients who may respond to different treatments, rather than using the term nonspecific low back pain, the diagnosis of lumbar spondylosis is often used for older patients with back pain. Because degenerative disease of the zygapophyseal joints generally coexists with degenerative disk disease, it is difficult to separate the two entities. Both can cause axial back pain. Both can also cause referred pain into the buttocks and legs. Mooney and Robertson and McCall et al. have studied the sclerotomal distribution of zygapophyseal joint pain in detail. Zygapophyseal joint pain has even been reported to refer below the knee in some cases.

Delineating a degenerative zygapophyseal joint as the primary pain generator in axial low back pain, however, is difficult. Imaging studies are not particularly useful because many people who are asymptomatic have spondylotic changes in their spines. This diagnosis is also made more commonly in older patients. Older individuals have multiple findings in their history, in their physical examination, and on imaging studies that complicate arriving at specific diagnosis or specific pain generators as the cause of their complaints. Spondylotic zygapophyseal joints are seen commonly with other potential sources of low back pain, such as degenerative disks and lumbar stenosis. On physical examination, patients with these imaging findings commonly have postural abnormalities, poor pelvic girdle mechanics, and potentially multiple myofascial sources for pain. They typically have an accentuated lumbar lordosis, in part because of tight hip flexors, which exacerbates the problem by increasing stress on the posterior elements.

From biomechanical studies and knowledge of anatomy, we know that lumbar extension and rotation increase forces placed on the posterior zygapophyseal joints. This specific maneuver, however, has not been shown to be diagnostic for zygapophyseal joint pain in clinical settings (by either history or examination). No unique identifying features are found in the history, physical examination, or radiologic imaging that are diagnostic for zygapophyseal joint pain. The only diagnostic maneuvers for zygapophyseal joint pain are fluoroscopically guided zygapophyseal joint injections with local anesthetic and medial branch blocks (i.e., local anesthetic blocks of the medial branches of the dorsal primary rami that innervate the zygapophyseal joints). With these injection techniques, the prevalence of facet-mediated pain in chronic low back pain sufferers has been estimated to be 15% in the younger population and 40% in older age groups. In a study in 1994, Schwarzer et al. demonstrated that the vast majority of lumbar zygapophyseal joint pain originates from the L4-L5 and L5-S1 zygapophyseal joints.

More conservative management options for the spondylotic spine and facet-mediated pain should be tried before resorting to invasive procedures such as intraarticular zygapophyseal joint corticosteroid injections or medial branch neurotomies. The conservative treatments are similar to treatments for osteoarthritic joints and can be categorized as lifestyle and activity modification, medications, and exercise, and are described in the section on treatment later.

Lumbar Disk Disease

Identifying diskogenic causes of low back pain is another attempt to separate patients from the nonspecific low back pain group. These can be divided into three categories: degenerative disk disease, internal disk disruption, and disk herniation. Diskogenic pain is classically described as bandlike and exacerbated by lumbar flexion, but this is not always the case. It can be unilateral, can radiate to the buttock, and can even be worsened by extension or side bending (depending on the site of disk pathology).

Internal Disk Disruption

Bogduk defines internal disk disruption as a condition in which the internal architecture of the disk is disrupted, but its external surface remains essentially normal (i.e., there is no bulge or herniation). It is characterized by degradation of the nucleus pulposus and radial fissures that extend to the outer third of the annulus (high-intensity zone areas on MRI). Diagnosis requires reproduction of pain on diskography and annular fissure on postdiskography CT. Although the use of diskography is controversial, most believe that annular tears (especially those that reach the outer third of the annulus, i.e., the innervated fibers) can be a source of low back pain. It must be remembered, however, that similar to most abnormalities on lumbar spine imaging, annular tears or high-intensity zones are seen commonly in individuals who are asymptomatic.

The proposed mechanisms for pain generation from internal disk disruption are chemical nociception from inflammatory mediators and mechanical stimulation.

Disk Herniation

The terminology used to describe disk material that extends beyond the intervertebral disk space is confusing. Herniated disk, herniated nucleus pulposus, disk bulge, disk protrusion, ruptured disk, and prolapsed disk are all commonly used terms, and sometimes are incorrectly used synonymously. Displaced disk material can be initially classified as a bulge (disk material is displaced greater than 50% of its circumference) or as a herniation (less than 50% of its circumference) ( Figure 33-21 ). Disk herniations can then be subclassified into protrusions or extrusions. A disk protrusion is defined as a herniation with the distance of the edges of the herniated material less than the distance of the edges at its base. A disk extrusion occurs when the distance of the edges of the herniated material is greater than the distance of the edges at its base. A disk extrusion can be further subclassified as sequestrated if the extruded disk material has no continuity with the disk of origin. Disk herniations can also be described as contained or uncontained depending on the integrity of the outer annular fibers. If the outer annular fibers are still intact, it is described as a contained disk herniation. This classification has no relevance to the integrity of the posterior longitudinal ligament.

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