The importance of back and neck pain in our society is underscored by the following: (1) the cost of back pain in the United States exceeds $100 billion annually; approximately one-third of these costs are direct health care expenses, and two-thirds are indirect costs resulting from loss of wages and productivity; (2) back symptoms are the most common cause of disability in those <45 years; (3) low back pain is the second most common reason for visiting a physician in the United States; and (4) 70% of persons will have back pain at some point in their lives.
The anterior spine consists of cylindrical vertebral bodies separated by intervertebral disks and held together by the anterior and posterior longitudinal ligaments. The intervertebral disks are composed of a central gelatinous nucleus pulposus surrounded by a tough cartilaginous ring, the annulus fibrosis. Disks are responsible for 25% of spinal column length and allow the bony vertebrae to move easily upon each other (Figs. 22-1 and 22-2). Desiccation of the nucleus pulposus and degeneration of the annulus fibrosus increase with age and result in loss of disk height. The disks are largest in the cervical and lumbar regions where movements of the spine are greatest. The anterior spine absorbs the shock of bodily movements such as walking and running and, with the posterior spine, protects the spinal cord and nerve roots in the spinal canal.
Vertebral anatomy. (From A Gauthier Cornuelle, DH Gronefeld: Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998; with permission.)
Spinal column. (From A Gauthier Cornuelle, DH Gronefeld: Radiographic Anatomy Positioning. New York, McGraw-Hill, 1998; with permission.)
The posterior spine consists of the vertebral arches and processes. Each arch consists of paired cylindrical pedicles anteriorly and paired lamina posteriorly. The vertebral arch also gives rise to two transverse processes laterally, one spinous process posteriorly, plus two superior and two inferior articular facets. The apposition of a superior and inferior facet constitutes a facet joint. The posterior spine provides an anchor for the attachment of muscles and ligaments. The contraction of muscles attached to the spinous and transverse processes and lamina works like a system of pulleys and levers that results in flexion, extension, and lateral bending movements of the spine.
Nerve root injury (radiculopathy) is a common cause of neck, arm, low back, buttock, and leg pain (see Figs. 31-2 and 31-3). The nerve roots exit at a level above their respective vertebral bodies in the cervical region (e.g., the C7 nerve root exits at the C6-C7 level) and below their respective vertebral bodies in the thoracic and lumbar regions (e.g., the T1 nerve root exits at the T1-T2 level). The cervical nerve roots follow a short intraspinal course before exiting. By contrast, because the spinal cord ends at the vertebral L1 or L2 level, the lumbar nerve roots follow a long intraspinal course and can be injured anywhere from the upper lumbar spine to their exit at the intervertebral foramen. For example, disk herniation at the L4-L5 level can produce not only L5 root compression, but also compression of the traversing S1 nerve root (Fig. 22-3). The lumbar nerve roots are mobile in the spinal canal, but eventually pass through the narrow lateral recess of the spinal canal and intervertebral foramen (Figs. 22-2 and 22-3). Neuroimaging of the spine must include both sagittal and axial views to assess possible compression in either the lateral recess or intervertebral foramen.
Compression of L5 and S1 roots by herniated disks. (From AH Ropper, MA Samuels: Adams and Victor’s Principles of Neurology, 9th ed. New York, McGraw-Hill, 2009; with permission.)
Pain-sensitive structures of the spine include the periosteum of the vertebrae, dura, facet joints, annulus fibrosus of the intervertebral disk, epidural veins and arteries, and the longitudinal ligaments. Disease of these diverse structures may explain many cases of back pain without nerve root compression. Under normal circumstances, the nucleus pulposus of the intervertebral disk is not pain sensitive.
APPROACH TO THE PATIENT: Back Pain TYPES OF BACK PAIN
Delineating the type of pain reported by the patient is the essential first step. Attention is also focused on identification of risk factors for a serious underlying etiology. The most frequent causes of back pain are radiculopathy, fracture, tumor, infection, or referred pain from visceral structures (Table 22-1).
Local pain is caused by injury to pain-sensitive structures that compress or irritate sensory nerve endings. The site of the pain is near the affected part of the back.
Pain referred to the back may arise from abdominal or pelvic viscera. The pain is usually described as primarily abdominal or pelvic, accompanied by back pain and usually unaffected by posture. The patient may occasionally complain of back pain only.
Pain of spine origin may be located in the back or referred to the buttocks or legs. Diseases affecting the upper lumbar spine tend to refer pain to the lumbar region, groin, or anterior thighs. Diseases affecting the lower lumbar spine tend to produce pain referred to the buttocks, posterior thighs, calves, or feet. Referred pain can explain pain syndromes that cross multiple dermatomes without evidence of nerve root compression.
Radicular pain is typically sharp and radiates from the low back to a leg within the territory of a nerve root (see “Lumbar Disk Disease,” below). Coughing, sneezing, or voluntary contraction of abdominal muscles (lifting heavy objects or straining at stool) may elicit the radiating pain. The pain may increase in postures that stretch the nerves and nerve roots. Sitting with the leg outstretched places traction on the sciatic nerve and L5 and S1 roots because the nerve passes posterior to the hip. The femoral nerve (L2, L3, and L4 roots) passes anterior to the hip and is not stretched by sitting. The description of the pain alone often fails to distinguish between referred pain and radiculopathy, although a burning or electric quality favors radiculopathy.
Pain associated with muscle spasm, although of obscure origin, is commonly associated with many spine disorders. The spasms are accompanied by abnormal posture, tense paraspinal muscles, and dull or achy pain in the paraspinal region.
Knowledge of the circumstances associated with the onset of back pain is important when weighing possible serious underlying causes for the pain. Some patients involved in accidents or work-related injuries may exaggerate their pain for the purpose of compensation or for psychological reasons. EXAMINATION OF THE BACK
A physical examination that includes the abdomen and rectum is advisable. Back pain referred from visceral organs may be reproduced during palpation of the abdomen (pancreatitis, abdominal aortic aneurysm [AAA]) or percussion over the costovertebral angles (pyelonephritis).
The normal spine has a cervical and lumbar lordosis and a thoracic kyphosis. Exaggeration of these normal alignments may result in hyperkyphosis of the thoracic spine or hyperlordosis of the lumbar spine. Inspection may reveal a lateral curvature of the spine (scoliosis). An asymmetry in the prominence of the paraspinal muscles suggests muscle spasm. Spine pain reproduced by palpation over the spinous process reflects injury of the affected vertebrae or adjacent pain-sensitive structures.
Forward bending is often limited by paraspinal muscle spasm; the latter may flatten the usual lumbar lordosis. Flexion at the hips is normal in patients with lumbar spine disease, but flexion of the lumbar spine is limited and sometimes painful. Lateral bending to the side opposite the injured spinal element may stretch the damaged tissues, worsen pain, and limit motion. Hyperextension of the spine (with the patient prone or standing) is limited when nerve root compression, facet joint pathology, or other bony spine disease is present.
Pain from hip disease may mimic the pain of lumbar spine disease. Hip pain can be reproduced by internal and external rotation at the hip with the knee and hip in flexion or by compressing the heel with the examiner’s palm while the leg is extended (heel percussion sign).
The straight leg–raising (SLR) maneuver is a simple bedside test for nerve root disease. With the patient supine, passive flexion of the extended leg at the hip stretches the L5 and S1 nerve roots and the sciatic nerve. Passive dorsiflexion of the foot during the maneuver adds to the stretch. In healthy individuals, flexion to at least 80° is normally possible without causing pain, although a tight, stretching sensation in the hamstring muscles is common. The SLR test is positive if the maneuver reproduces the patient’s usual back or limb pain. Eliciting the SLR sign in both the supine and sitting positions can help determine if the finding is reproducible. The patient may describe pain in the low back, buttocks, posterior thigh, or lower leg, but the key feature is reproduction of the patient’s usual pain. The crossed SLR sign is present when flexion of one leg reproduces the usual pain in the opposite leg or buttocks. In disk herniation, the crossed SLR sign is less sensitive but more specific than the SLR sign. The reverse SLR sign is elicited by standing the patient next to the examination table and passively extending each leg with the knee fully extended. This maneuver, which stretches the L2-L4 nerve roots, lumbosacral plexus, and femoral nerve, is considered positive if the patient’s usual back or limb pain is reproduced. For all of these tests, the nerve or nerve root lesion is always on the side of the pain.
The neurologic examination includes a search for focal weakness or muscle atrophy, focal reflex changes, diminished sensation in the legs, or signs of spinal cord injury. The examiner should be alert to the possibility of breakaway weakness, defined as fluctuations in the maximum power generated during muscle testing. Breakaway weakness may be due to pain or a combination of pain and an underlying true weakness. Breakaway weakness without pain is almost always due to a lack of effort. In uncertain cases, electromyography (EMG) can determine if true weakness due to nerve tissue injury is present. Findings with specific lumbosacral nerve root lesions are shown in Table 22-2 and are discussed below. LABORATORY, IMAGING, AND EMG STUDIES
Laboratory studies are rarely needed for the initial evaluation of nonspecific acute (<3 months in duration) low back pain (ALBP). Risk factors for a serious underlying cause and for infection, tumor, or fracture, in particular, should be sought by history and exam. If risk factors are present (Table 22-1), then laboratory studies (complete blood count [CBC], erythrocyte sedimentation rate [ESR], urinalysis) are indicated. If risk factors are absent, then management is conservative (see “Treatment,” below)
Computed tomography (CT) scanning is superior to routine x-rays for the detection of fractures involving posterior spine structures, craniocervical and cervicothoracic junctions, C1 and C2 vertebrae, bone fragments within the spinal canal, or misalignment. CT scans are increasingly used as a primary screening modality for moderate to severe acute trauma. Magnetic resonance imaging (MRI) or CT myelography is the radiologic test of choice for evaluation of most serious diseases involving the spine. MRI is superior for the definition of soft tissue structures, whereas CT myelography provides optimal imaging of the lateral recess of the spinal canal and is better tolerated by claustrophobic patients.
Annual population surveys in the United States suggest that patients with back pain have reported progressively worse functional limitations in recent years, rather than progressive improvements, despite rapid increases in spine imaging, opioid prescribing, injections, and spine surgery. This suggests that more selective use of diagnostic and treatment modalities may be appropriate.
Spine imaging often reveals abnormalities of dubious clinical relevance that may alarm clinicians and patients alike and prompt further testing and unnecessary therapy. Both randomized trials and observational studies have suggested such a “cascade effect” of imaging may create a gateway to other unnecessary care. Based in part on such evidence, the American College of Physicians has made parsimonious spine imaging a high priority in its “Choosing Wisely” campaign, aimed at reducing unnecessary care. Successful efforts to reduce unnecessary imaging have typically been multifaceted. Some include physician education by clinical leaders and computerized decision support, to identify any recent relevant imaging tests and require approved indications for ordering an imaging test. Other strategies have included audit and feedback regarding individual rates of ordering and indications, and more rapid access to physical therapy or consultation for patients without imaging indications.
When imaging tests are reported, it may be useful to indicate that certain degenerative findings are common in normal, pain-free individuals. In an observational study, this strategy was associated with lower rates of repeat imaging, opioid therapy, and physical therapy referral.
Electrodiagnostic studies can be used to assess the functional integrity of the peripheral nervous system (Chap. 442e). Sensory nerve conduction studies are normal when focal sensory loss confirmed by examination is due to nerve root damage because the nerve roots are proximal to the nerve cell bodies in the dorsal root ganglia. Injury to nerve tissue distal to the dorsal root ganglion (e.g., plexus or peripheral nerve) results in reduced sensory nerve signals. Needle EMG complements nerve conduction studies by detecting denervation or reinnervation changes in a myotomal (segmental) distribution. Multiple muscles supplied by different nerve roots and nerves are sampled; the pattern of muscle involvement indicates the nerve root(s) responsible for the injury. Needle EMG provides objective information about motor nerve fiber injury when clinical evaluation of weakness is limited by pain or poor effort. EMG and nerve conduction studies will be normal when sensory nerve root injury or irritation is the pain source.
TABLE 22-1Acute Low Back Pain: Risk Factors for an Important Structural Cause ||Download (.pdf) TABLE 22-1Acute Low Back Pain: Risk Factors for an Important Structural Cause
|Pain worse at rest or at night |
|Prior history of cancer |
|History of chronic infection (especially lung, urinary tract, skin) |
|History of trauma |
|Age >70 years |
|Intravenous drug use |
|Glucocorticoid use |
|History of a rapidly progressive neurologic deficit |
|Unexplained fever |
|Unexplained weight loss |
|Percussion tenderness over the spine |
|Abdominal, rectal, or pelvic mass |
|Internal/external rotation of the leg at the hip; heel percussion sign |
|Straight leg– or reverse straight leg–raising signs |
|Progressive focal neurologic deficit |
TABLE 22-2Lumbosacral Radiculopathy: Neurologic Features ||Download (.pdf) TABLE 22-2Lumbosacral Radiculopathy: Neurologic Features
|Lumbosacral Nerve Roots ||Examination Findings ||Pain Distribution |
|Reflex ||Sensory ||Motor |
|L2a ||— ||Upper anterior thigh ||Psoas (hip flexors) ||Anterior thigh |
|L3a ||— ||Lower anterior thigh ||Psoas (hip flexors) ||Anterior thigh, knee |
| || ||Anterior knee ||Quadriceps (knee extensors) || |
| || || ||Thigh adductors || |
|L4a ||Quadriceps (knee) ||Medial calf ||Quadriceps (knee extensors)b ||Knee, medial calf |
| || || ||Thigh adductors ||Anterolateral thigh |
|L5c ||— ||Dorsal surface—foot ||Peronei (foot evertors)b ||Lateral calf, dorsal foot, posterolateral thigh, buttocks |
| || ||Lateral calf ||Tibialis anterior (foot dorsiflexors) || |
| || || ||Gluteus medius (hip abductors) || |
| || || ||Toe dorsiflexors || |
|S1c ||Gastrocnemius/soleus (ankle) ||Plantar surface—foot ||Gastrocnemius/soleus (foot plantar flexors)b ||Bottom foot, posterior calf, posterior thigh, buttocks |
| || ||Lateral aspect—foot ||Abductor hallucis (toe flexors)b || |
| || || ||Gluteus maximus (hip extensors) || |
TABLE 22-3Causes of Back or Neck Pain ||Download (.pdf) TABLE 22-3Causes of Back or Neck Pain
Lumbar Disk Disease
Degenerative Spine Disease
Lumbar spinal stenosis without or with neurogenic claudication
Intervertebral foraminal or lateral recess narrowing
Facet or uncovertebral joint hypertrophy
Lateral disk protrusion
Spondylosis (osteoarthritis) and spondylolisthesis
Spinal epidural abscess
Septic disk (diskitis)
Neoplasms—Metastatic, Hematologic, Primary Bone Tumors
Trauma/falls, motor vehicle accidents
Atraumatic fractures: osteoporosis, neoplastic infiltration, osteomyelitis
Strain or sprain
Metabolic Spine Disease
Osteosclerosis (e.g., Paget’s disease)
Spina bifida occulta
Tethered spinal cord
Autoimmune Inflammatory Arthritis
Other Causes of Back Pain
Referred pain from visceral disease (e.g., abdominal aortic aneurysm)
Psychiatric, malingering, chronic pain syndromes
This is a common cause of acute, chronic, or recurrent low back and leg pain (Figs. 22-3 and 22-4). Disk disease is most likely to occur at the L4-L5 or L5-S1 levels, but upper lumbar levels are involved occasionally. The cause is often unknown, but the risk is increased in overweight individuals. Disk herniation is unusual prior to age 20 years and is rare in the fibrotic disks of the elderly. Complex genetic factors may play a role in predisposing some patients to disk disease. The pain may be located in the low back only or referred to a leg, buttock, or hip. A sneeze, cough, or trivial movement may cause the nucleus pulposus to prolapse, pushing the frayed and weakened annulus posteriorly. With severe disk disease, the nucleus may protrude through the annulus (herniation) or become extruded to lie as a free fragment in the spinal canal.
Left L5 radiculopathy. A. Sagittal T2-weighted image on the left reveals disk herniation at the L4-L5 level. B. Axial T1-weighted image shows paracentral disk herniation with displacement of the thecal sac medially and the left L5 nerve root posteriorly in the left lateral recess.
The mechanism by which intervertebral disk injury causes back pain is controversial. The inner annulus fibrosus and nucleus pulposus are normally devoid of innervation. Inflammation and production of proinflammatory cytokines within a ruptured nucleus pulposus may trigger or perpetuate back pain. Ingrowth of nociceptive (pain) nerve fibers into inner portions of a diseased disk may be responsible for some chronic “diskogenic” pain. Nerve root injury (radiculopathy) from disk herniation is usually due to inflammation, but lateral herniation may produce compression in the lateral recess or at the intervertebral foramen.
A ruptured disk may be asymptomatic or cause back pain, abnormal posture, limitation of spine motion (particularly flexion), a focal neurologic deficit, or radicular pain. A dermatomal pattern of sensory loss or a reduced or absent deep tendon reflex is more suggestive of a specific root lesion than is the pattern of pain. Motor findings (focal weakness, muscle atrophy, or fasciculations) occur less frequently than focal sensory or reflex changes. Symptoms and signs are usually unilateral, but bilateral involvement does occur with large central disk herniations that compress multiple roots or cause inflammation of nerve roots within the spinal canal. Clinical manifestations of specific nerve root lesions are summarized in Table 22-2.
The differential diagnosis covers a variety of serious and treatable conditions, including epidural abscess, hematoma, fracture, or tumor. Fever, constant pain uninfluenced by position, sphincter abnormalities, or signs of spinal cord disease suggest an etiology other than lumbar disk disease. Absence of ankle reflexes can be a normal finding in persons older than age 60 years or a sign of bilateral S1 radiculopathy. An absent deep tendon reflex or focal sensory loss may indicate injury to a nerve root, but other sites of injury along the nerve must also be considered. For example, an absent knee reflex may be due to a femoral neuropathy or an L4 nerve root injury. A loss of sensation over the foot and lateral lower calf may result from a peroneal or lateral sciatic neuropathy or an L5 nerve root injury. Focal muscle atrophy may reflect injury to the anterior horn cells of the spinal cord, a nerve root, peripheral nerve, or disuse.
A lumbar spine MRI scan or CT myelogram is necessary to establish the location and type of pathology. Spine MRIs yield exquisite views of intraspinal and adjacent soft tissue anatomy. Bony lesions of the lateral recess or intervertebral foramen are optimally visualized by CT myelography. The correlation of neuroradiologic findings to symptoms, particularly pain, is not simple. Contrast-enhancing tears in the annulus fibrosus or disk protrusions are widely accepted as common sources of back pain; however, studies have found that many asymptomatic adults have similar findings. Asymptomatic disk protrusions are also common and may enhance with contrast. Furthermore, in patients with known disk herniation treated either medically or surgically, persistence of the herniation 10 years later had no relationship to the clinical outcome. In summary, MRI findings of disk protrusion, tears in the annulus fibrosus, or hypertrophic facet joints are common incidental findings that, by themselves, should not dictate management decisions for patients with back pain.
The diagnosis of nerve root injury is most secure when the history, examination, results of imaging studies, and the EMG are concordant. The correlation between CT and EMG for localization of nerve root injury is between 65 and 73%. Up to one-third of asymptomatic adults have a lumbar disk protrusion detected by CT or MRI scans.
Management of lumbar disk disease is discussed below.
Cauda equina syndrome (CES) signifies an injury of multiple lumbosacral nerve roots within the spinal canal distal to the termination of the spinal cord at L1-L2. Low back pain, weakness and areflexia in the legs, saddle anesthesia, or loss of bladder function may occur. The problem must be distinguished from disorders of the lower spinal cord (conus medullaris syndrome), acute transverse myelitis (Chap. 456), and Guillain-Barré syndrome (Chap. 460). Combined involvement of the conus medullaris and cauda equina can occur. CES is commonly due to a ruptured lumbosacral intervertebral disk, lumbosacral spine fracture, hematoma within the spinal canal (e.g., following lumbar puncture in patients with coagulopathy), compressive tumor, or other mass lesion. Treatment options include surgical decompression, sometimes urgently in an attempt to restore or preserve motor or sphincter function, or radiotherapy for metastatic tumors (Chap. 118).
Lumbar spinal stenosis (LSS) describes a narrowed lumbar spinal canal and is frequently asymptomatic. Typical is neurogenic claudication, consisting of back and buttock or leg pain induced by walking or standing and relieved by sitting. Symptoms in the legs are usually bilateral. Unlike vascular claudication, symptoms are often provoked by standing without walking. Unlike lumbar disk disease, symptoms are usually relieved by sitting. Patients with neurogenic claudication can often walk much farther when leaning over a shopping cart and can pedal a stationary bike with ease while sitting. These flexed positions increase the anteroposterior spinal canal diameter and reduce intraspinal venous hypertension, resulting in pain relief. Focal weakness, sensory loss, or reflex changes may occur when spinal stenosis is associated with neural foraminal narrowing and radiculopathy. Severe neurologic deficits, including paralysis and urinary incontinence, occur only rarely.
LSS by itself is frequently asymptomatic, and the correlation between the severity of symptoms and degree of stenosis of the spinal canal is variable. LSS can be acquired (75%), congenital, or both. Congenital forms (achondroplasia, idiopathic) are characterized by short, thick pedicles that produce both spinal canal and lateral recess stenosis. Acquired factors that contribute to spinal stenosis include degenerative diseases (spondylosis, spondylolisthesis, scoliosis), trauma, spine surgery, metabolic or endocrine disorders (epidural lipomatosis, osteoporosis, acromegaly, renal osteodystrophy, hypoparathyroidism), and Paget’s disease. MRI provides the best definition of the abnormal anatomy (Fig. 22-5).
Axial T2-weighted images of the lumbar spine. A. The image shows a normal thecal sac within the lumbar spinal canal. The thecal sac is bright. The lumbar roots are dark punctuate dots in the posterior thecal sac with the patient supine. B. The thecal sac is not well visualized due to severe lumbar spinal canal stenosis, partially the result of hypertrophic facet joints.
Conservative treatment of symptomatic LSS includes nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, exercise programs, and symptomatic treatment of acute pain episodes. There is insufficient evidence to support the routine use of epidural glucocorticoid injections. Surgical therapy is considered when medical therapy does not relieve symptoms sufficiently to allow for resumption of activities of daily living or when focal neurologic signs are present. Most patients with neurogenic claudication who are treated medically do not improve over time. Surgical management can produce significant relief of back and leg pain within 6 weeks, and pain relief persists for at least 2 years. However, up to one-quarter develop recurrent stenosis at the same spinal level or an adjacent level 7–10 years after the initial surgery; recurrent symptoms usually respond to a second surgical decompression.
Neural foraminal narrowing with radiculopathy is a common consequence of osteoarthritic processes that cause lumbar spinal stenosis (Figs. 22-1 and 22-6), including osteophytes, lateral disk protrusion, calcified disk-osteophytes, facet joint hypertrophy, uncovertebral joint hypertrophy (cervical spine), congenitally shortened pedicles, or, frequently, a combination of these processes. Neoplasms (primary or metastatic), fractures, infections (epidural abscess), or hematomas are other considerations. These conditions can produce unilateral nerve root symptoms or signs due to compression at the intervertebral foramen or in the lateral recess; symptoms are indistinguishable from disk-related radiculopathy, but treatment may differ depending on the specific etiology. The history and neurologic examination alone cannot distinguish between these possibilities. A spine neuroimaging (CT or MRI) procedure is required to identify the anatomic cause. Neurologic findings from the examination and EMG can help direct the attention of the radiologist to specific nerve roots, especially on axial images. For facet joint hypertrophy, surgical foraminotomy produces long-term relief of leg and back pain in 80–90% of patients. The usefulness of therapeutic facet joint blocks for pain is controversial. Medical causes of lumbar or cervical radiculopathy unrelated to anatomic spine disease include infections (e.g., herpes zoster, Lyme disease), carcinomatous meningitis, and root avulsion or traction (severe trauma).
Right L5 radiculopathy. A. Sagittal T2-weighted image. There is normal high signal around the exiting right L4 nerve root in the right neural foramen at L4-L5; effacement of the high signal in the right L5-S1 foramen is present one level caudal on the right at L5-S1. B. Axial T2-weighted image. The lateral recesses are normal bilaterally; the intervertebral foramen is normal on the left, but severely stenotic on the right. *Severe right L5-S1 foraminal stenosis.
SPONDYLOSIS AND SPONDYLOLISTHESIS
Spondylosis, or osteoarthritic spine disease, typically occurs in later life and primarily involves the cervical and lumbosacral spine. Patients often complain of back pain that increases with movement, is associated with stiffness, and is better when inactive. The relationship between clinical symptoms and radiologic findings is usually not straightforward. Pain may be prominent when x-ray, CT, or MRI findings are minimal, and prominent degenerative spine disease can be seen in asymptomatic patients. Osteophytes or combined disk-osteophytes may cause or contribute to central spinal canal stenosis, lateral recess stenosis, or neural foraminal narrowing.
Spondylolisthesis is the anterior slippage of the vertebral body, pedicles, and superior articular facets, leaving the posterior elements behind. Spondylolisthesis can be associated with spondylolysis, congenital anomalies, degenerative spine disease, or other causes of mechanical weakness of the pars (e.g., infection, osteoporosis, tumor, trauma, prior surgery). The slippage may be asymptomatic or may cause low back pain and hamstring tightness, nerve root injury (the L5 root most frequently), symptomatic spinal stenosis, or CES in severe cases. Tenderness may be elicited near the segment that has “slipped” forward (most often L4 on L5 or occasionally L5 on S1). Focal anterolisthesis or retrolisthesis can occur at any cervical or lumbar level and be the source of neck or low back pain. Plain x-rays with the neck or low back in flexion and extension will reveal the movement at the abnormal spinal segment. Surgery is considered for pain symptoms that do not respond to conservative measures (e.g., rest, physical therapy) and in cases with progressive neurologic deficit, postural deformity, slippage >50%, or scoliosis.
Back pain is the most common neurologic symptom in patients with systemic cancer and is the presenting symptom in 20%. The cause is usually vertebral body metastasis but can also result from spread of cancer through the intervertebral foramen (especially with lymphoma), from carcinomatous meningitis, or from metastasis to the spinal cord. Cancer-related back pain tends to be constant, dull, unrelieved by rest, and worse at night. By contrast, mechanical low back pain usually improves with rest. MRI, CT, and CT myelography are the studies of choice when spinal metastasis is suspected. Once a metastasis is found, imaging of the entire spine reveals additional tumor deposits in one-third of patients. MRI is preferred for soft tissue definition, but the most rapidly available imaging modality is best because the patient’s condition may worsen quickly without intervention. Fewer than 5% of patients who are nonambulatory at the time of diagnosis ever regain the ability to walk; thus, early diagnosis is crucial. The management of spinal metastasis is discussed in detail in Chap. 118.
Vertebral osteomyelitis is often caused by staphylococci, but other bacteria or tuberculosis (Pott’s disease) may be responsible. The primary source of infection is usually the urinary tract, skin, or lungs. Intravenous drug use is a well-recognized risk factor. Whenever pyogenic osteomyelitis is found, the possibility of bacterial endocarditis should be considered. Back pain unrelieved by rest, spine tenderness over the involved spine segment, and an elevated ESR are the most common findings in vertebral osteomyelitis. Fever or an elevated white blood cell count is found in a minority of patients. MRI and CT are sensitive and specific for early detection of osteomyelitis; CT may be more readily available in emergency settings and better tolerated by some patients with severe back pain. The intervertebral disk can also be affected by infection (diskitis) and, very rarely, by tumor.
Spinal epidural abscess (Chap. 456) presents with back pain (aggravated by movement or palpation), fever, radiculopathy, or signs of spinal cord compression. The subacute development of two or more of these findings should increase the index of suspicion for spinal epidural abscess. The abscess may track over multiple spinal levels and is best delineated by spine MRI.
Lumbar adhesive arachnoiditis with radiculopathy is due to fibrosis following inflammation within the subarachnoid space. The fibrosis results in nerve root adhesions and presents as back and leg pain associated with focal motor, sensory, or reflex changes. Causes of arachnoiditis include multiple lumbar operations, chronic spinal infections (especially tuberculosis in the developing world), spinal cord injury, intrathecal hemorrhage, myelography (rare), intrathecal injections (glucocorticoids, anesthetics, or other agents), and foreign bodies. The MRI shows clumped nerve roots or loculations of cerebrospinal fluid within the thecal sac. Clumped nerve roots may also occur with demyelinating polyneuropathy or neoplastic infiltration. Treatment is usually unsatisfactory. Microsurgical lysis of adhesions, dorsal rhizotomy, dorsal root ganglionectomy, and epidural glucocorticoids have been tried, but outcomes have been poor. Dorsal column stimulation for pain relief has produced varying results.
A patient complaining of back pain and an inability to move the legs may have a spine fracture or dislocation; with fractures above L1 the spinal cord is at risk for compression. Care must be taken to avoid further damage to the spinal cord or nerve roots by immobilizing the back or neck pending the results of radiologic studies. Vertebral fractures frequently occur in the absence of trauma in association with osteoporosis, glucocorticoid use, osteomyelitis, or neoplastic infiltration.
The terms low back sprain, strain, and mechanically induced muscle spasm refer to minor, self-limited injuries associated with lifting a heavy object, a fall, or a sudden deceleration such as in an automobile accident. These terms are used loosely and do not clearly describe a specific anatomic lesion. The pain is usually confined to the lower back, and there is no radiation to the buttocks or legs. Patients with paraspinal muscle spasm often assume unusual postures.
Traumatic Vertebral Fractures
Most traumatic fractures of the lumbar vertebral bodies result from injuries producing anterior wedging or compression. With severe trauma, the patient may sustain a fracture-dislocation or a “burst” fracture involving the vertebral body and posterior elements. Traumatic vertebral fractures are caused by falls from a height, sudden deceleration in an automobile accident, or direct injury. Neurologic impairment is common, and early surgical treatment is indicated. In victims of blunt trauma, CT scans of the chest, abdomen, or pelvis can be reformatted to detect associated vertebral fractures.
Osteoporosis and Osteosclerosis
Immobilization, osteomalacia, the postmenopausal state, renal disease, multiple myeloma, hyperparathyroidism, hyperthyroidism, metastatic carcinoma, or glucocorticoid use may accelerate osteoporosis and weaken the vertebral body, leading to compression fractures and pain. Up to two-thirds of compression fractures seen on radiologic imaging are asymptomatic. The most common nontraumatic vertebral body fractures are due to postmenopausal or senile osteoporosis (Chap. 425). The risk of an additional vertebral fracture at 1 year following a first vertebral fracture is 20%. The presence of fever, weight loss, fracture at a level above T4, or the conditions described above should increase suspicion for a cause other than senile osteoporosis. The sole manifestation of a compression fracture may be localized back or radicular pain exacerbated by movement and often reproduced by palpation over the spinous process of the affected vertebra.
Relief of acute pain can often be achieved with acetaminophen or a combination of opioids and acetaminophen. The role of NSAIDs is controversial. Both pain and disability are improved with bracing. Antiresorptive drugs, especially bisphosphonates (e.g., alendronate), have been shown to reduce the risk of osteoporotic fractures and are the preferred treatment to prevent additional fractures. Less than one-third of patients with prior compression fractures are adequately treated for osteoporosis despite the increased risk for future fractures; even fewer at-risk patients without a history of fracture are adequately treated. Given the negative results of sham-controlled studies of percutaneous vertebroplasty (PVP) and of kyphoplasty for osteoporotic compression fractures associated with debilitating pain, these procedures are not routinely recommended.
Osteosclerosis, an abnormally increased bone density often due to Paget’s disease, is readily identifiable on routine x-ray studies and can sometimes be a source of back pain. It may be associated with an isolated increase in alkaline phosphatase in an otherwise healthy older person. Spinal cord or nerve root compression can result from bony encroachment. The diagnosis of Paget’s disease as the cause of a patient’s back pain is a diagnosis of exclusion.
For further discussion of these bone disorders, see Chaps. 424, 425, and 426e.
AUTOIMMUNE INFLAMMATORY ARTHRITIS
Autoimmune inflammatory disease of the spine can present with the insidious onset of low back, buttock, or neck pain. Examples include rheumatoid arthritis (Chap 380), ankylosing spondylitis, reactive arthritis, psoriatic arthritis, or inflammatory bowel disease (Chap. 384).
CONGENITAL ANOMALIES OF THE LUMBAR SPINE
Spondylolysis is a bony defect in the vertebral pars interarticularis (a segment near the junction of the pedicle with the lamina); the cause is usually a stress microfracture in a congenitally abnormal segment. It occurs in up to 6% of adolescents. The defect (usually bilateral) is best visualized on plain x-rays, CT scan, or bone scan and is frequently asymptomatic. Symptoms may occur in the setting of a single injury, repeated minor injuries, or during a growth spurt. Spondylolysis is the most common cause of persistent low back pain in adolescents and is often associated with sports-related activities.
Scoliosis refers to an abnormal curvature in the coronal (lateral) plane of the spine. With kyphoscoliosis, there is, in addition, a forward curvature of the spine. The abnormal curvature may be congenital due to abnormal spine development, acquired in adulthood due to degenerative spine disease, or occasionally progressive due to neuromuscular disease. The deformity can progress until ambulation or pulmonary function is compromised.
Spina bifida occulta is a failure of closure of one or several vertebral arches posteriorly; the meninges and spinal cord are normal. A dimple or small lipoma may overlie the defect. Most cases are asymptomatic and discovered incidentally during an evaluation for back pain.
Tethered cord syndrome usually presents as a progressive cauda equina disorder (see below), although myelopathy may also be the initial manifestation. The patient is often a young adult who complains of perineal or perianal pain, sometimes following minor trauma. MRI studies reveal a low-lying conus (below L1 and L2) and a short and thickened filum terminale.
REFERRED PAIN FROM VISCERAL DISEASE
Diseases of the thorax, abdomen, or pelvis may refer pain to the posterior portion of the spinal segment that innervates the diseased organ. Occasionally, back pain may be the first and only manifestation. Upper abdominal diseases generally refer pain to the lower thoracic or upper lumbar region (eighth thoracic to the first and second lumbar vertebrae), lower abdominal diseases to the midlumbar region (second to fourth lumbar vertebrae), and pelvic diseases to the sacral region. Local signs (pain with spine palpation, paraspinal muscle spasm) are absent, and little or no pain accompanies routine movements of the spine.
Low Thoracic or Lumbar Pain with Abdominal Disease
Tumors of the posterior wall of the stomach or duodenum typically produce epigastric pain (Chaps. 109 and 348), but midline back or paraspinal pain may occur if retroperitoneal extension is present. Fatty foods occasionally induce back pain associated with biliary disease. Diseases of the pancreas can produce right or left paraspinal back pain. Pathology in retroperitoneal structures (hemorrhage, tumors, pyelonephritis) can produce paraspinal pain that radiates to the lower abdomen, groin, or anterior thighs. A mass in the iliopsoas region can produce unilateral lumbar pain with radiation toward the groin, labia, or testicle. The sudden appearance of lumbar pain in a patient receiving anticoagulants suggests retroperitoneal hemorrhage.
Isolated low back pain occurs in some patients with a contained rupture of an abdominal aortic aneurysm (AAA). The classic clinical triad of abdominal pain, shock, and back pain occurs in <20% of patients. The typical patient at risk is an elderly male smoker with back pain. The diagnosis may be missed because the symptoms and signs can be nonspecific. Misdiagnoses include nonspecific back pain, diverticulitis, renal colic, sepsis, and myocardial infarction. A careful abdominal examination revealing a pulsatile mass (present in 50–75% of patients) is an important physical finding. Patients with suspected AAA should be evaluated with abdominal ultrasound, CT, or MRI (Chap. 301).
Sacral Pain with Gynecologic and Urologic Disease
Pelvic organs rarely cause low back pain, except for gynecologic disorders involving the uterosacral ligaments. The pain is referred to the sacral region. Endometriosis or uterine cancers may invade the uterosacral ligaments. Pain associated with endometriosis is typically premenstrual and often continues until it merges with menstrual pain. Uterine malposition may cause uterosacral ligament traction (retroversion, descensus, and prolapse) or produce sacral pain after prolonged standing.
Menstrual pain may be felt in the sacral region sometimes with poorly localized, cramping pain radiating down the legs. Pain due to neoplastic infiltration of nerves is typically continuous, progressive in severity, and unrelieved by rest at night. Less commonly, radiation therapy of pelvic tumors may produce sacral pain from late radiation necrosis of tissue. Low back pain that radiates into one or both thighs is common in the last weeks of pregnancy.
Urologic sources of lumbosacral back pain include chronic prostatitis, prostate cancer with spinal metastasis (Chap. 115), and diseases of the kidney or ureter. Lesions of the bladder and testes do not often produce back pain. Infectious, inflammatory, or neoplastic renal diseases may produce ipsilateral lumbosacral pain, as can renal artery or vein thrombosis. Paraspinal lumbar pain may be a symptom of ureteral obstruction due to nephrolithiasis.
OTHER CAUSES OF BACK PAIN
There is a group of patients with nonspecific chronic low back pain (CLBP) in whom no specific anatomic lesion can be found despite exhaustive investigation. These individuals complain of vague, diffuse back pain with prolonged sitting or standing that is relieved by rest. Exercises to strengthen the paraspinal and abdominal muscles are sometimes helpful.
CLBP may be encountered in patients who seek financial compensation; in malingerers; or in those with concurrent substance abuse. Many patients with CLBP have a history of psychiatric illness (depression, anxiety states) or childhood trauma (physical or sexual abuse) that antedates the onset of back pain. Preoperative psychological assessment has been used to exclude patients with marked psychological impairments that predict a poor surgical outcome from spine surgery.
The cause of low back pain occasionally remains unclear. Some patients have had multiple operations for disk disease but have persistent pain and disability. The original indications for surgery may have been questionable, with back pain only, no definite neurologic signs, or a minor disk bulge noted on CT or MRI. Scoring systems based on neurologic signs, psychological factors, physiologic studies, and imaging studies have been devised to minimize the likelihood of unsuccessful surgery.
TREATMENT Back Pain HEALTH CARE FOR POPULATIONS OF BACK PAIN PATIENTS: A CLINICAL CARE SYSTEMS VIEW
There are increasing pressures to contain health care costs, especially when expensive care is not based on sound evidence. Physicians, patients, the insurance industry, and government providers of health care will need to work together to ensure cost-effective care for patients with back pain.
Surveys in the United States indicate that patients with back pain have reported progressively worse functional limitations in recent years, despite rapid increases in spine imaging, opioid prescribing, injections, and spine surgery. This suggests that more selective use of diagnostic and treatment modalities may be appropriate.
Spine imaging often reveals abnormalities of dubious clinical relevance that may alarm clinicians and patients and prompt further testing and unnecessary therapy. Both randomized trials and observational studies have suggested a “cascade effect” of imaging, which may create a gateway to other unnecessary care. Based in part on such evidence, the American College of Physicians has made parsimonious spine imaging a high priority in its “Choosing Wisely” campaign, aimed at reducing unnecessary care. Successful efforts to reduce unnecessary imaging have included physician education by clinical leaders, computerized decision support to identify recent imaging tests and eliminate duplication, and requiring an approved indication to order an imaging test. Other strategies have included audit and feedback regarding individual practitioners’ rates of ordering and indications and facilitating rapid access to physical therapy for patients who do not need imaging. When imaging tests are reported, it may also be useful to routinely note that some degenerative findings are common in normal, pain-free individuals. In an observational study, this strategy was associated with lower rates of repeat imaging, opioid therapy, and referral for physical therapy.
Mounting evidence of morbidities from long-term opioid therapy (including overdose, dependency, addiction, falls, fractures, accident risk, and sexual dysfunction) has prompted efforts to reduce use for chronic pain, including back pain (Chap. 18). Safety may be improved with automated reminders for high doses, early refills, or overlapping opioid and benzodiazepine prescriptions. Greater access to alternative treatments for chronic pain, such as tailored exercise programs and cognitive-behavioral therapy, may also reduce opioid prescribing.
The high cost, wide geographic variations, and rapidly increasing rates of spinal fusion surgery have prompted scrutiny over appropriate indications. Some insurance carriers have begun to limit coverage for the most controversial indications, such as low back pain without radiculopathy. Finally, educating patients and the public about the risks of imaging and excessive therapy may be necessary. A successful media campaign in Australia provides a successful model for this approach. ALBP WITHOUT RADICULOPATHY
ALBP is defined as pain of <3 months in duration. Full recovery can be expected in more than 85% of adults with ALBP without leg pain. Most have purely “mechanical” symptoms (i.e., pain that is aggravated by motion and relieved by rest).
The initial assessment excludes serious causes of spine pathology that require urgent intervention including infection, cancer, or trauma. Risk factors for a serious cause of ALBP are shown in Table 22-1. Laboratory and imaging studies are unnecessary if risk factors are absent. CT, MRI, or plain spine films are rarely indicated in the first month of symptoms unless a spine fracture, tumor, or infection is suspected.
The prognosis is generally excellent. Many patients do not seek medical care and improve on their own. Even among those seen in primary care, two-thirds report being substantially improved after 7 weeks. This spontaneous improvement can mislead clinicians and researchers about the efficacy of treatment interventions unless subjected to rigorous prospective trials. Many treatments commonly used in the past but now known to be ineffective, including bed rest, lumbar traction, and coccygectomy, have been largely abandoned.
Clinicians should reassure patients that improvement is very likely and instruct them in self-care. Education is an important part of treatment. Satisfaction and the likelihood of follow-up increase when patients are educated about prognosis, treatment methods, activity modifications, and strategies to prevent future exacerbations. Patients who report that they did not receive an adequate explanation for their symptoms are likely to request further diagnostic tests. In general, bed rest should be avoided for relief of severe symptoms or kept to a day or two at most. Several randomized trials suggest that bed rest does not hasten the pace of recovery. In general, the best activity recommendation is for early resumption of normal physical activity, avoiding only strenuous manual labor. Possible advantages of early ambulation for ALBP include maintenance of cardiovascular conditioning, improved disk and cartilage nutrition, improved bone and muscle strength, and increased endorphin levels. Specific back exercises or early vigorous exercise have not shown benefits for acute back pain, but may be useful for chronic pain. Use of heating pads or blankets is sometimes helpful.
Evidence-based guidelines recommend over-the-counter medicines such as acetaminophen and NSAIDs as first-line options for treatment of ALBP. In otherwise healthy patients, a trial of acetaminophen can be followed by NSAIDs for time-limited periods. In theory, the anti-inflammatory effects of NSAIDs might provide an advantage over acetaminophen to suppress inflammatory changes that accompany many causes of ALBP, but in practice, there is no clinical evidence to support the superiority of NSAIDs. The risk of renal and gastrointestinal toxicity with NSAIDs is increased in patients with preexisting medical comorbidities (e.g., renal insufficiency, cirrhosis, prior gastrointestinal hemorrhage, use of anticoagulants or steroids, heart failure). Skeletal muscle relaxants, such as cyclobenzaprine or methocarbamol, may be useful, but sedation is a common side effect. Limiting the use of muscle relaxants to nighttime only may be an option for patients with back pain that interferes with sleep.
There is no good evidence to support the use of opioid analgesics or tramadol as first-line therapy for ALBP. Their use is best reserved for patients who cannot tolerate acetaminophen or NSAIDs or for those with severe refractory pain. As with muscle relaxants, these drugs are often sedating, so it may be useful to prescribe them at nighttime only. Side effects of short-term opioid use include nausea, constipation, and pruritus; risks of long-term opioid use include hypersensitivity to pain, hypogonadism, and dependency. Falls, fractures, driving accidents, and fecal impaction are other risks. Clinical efficacy of opioids beyond 16 weeks of use is unproven.
There is no evidence to support use of oral or injected glucocorticoids for ALBP without radiculopathy. Similarly, therapies for neuropathic pain, such as gabapentin or tricyclic antidepressants, are not indicated for ALBP.
Nonpharmacologic treatments for ALBP include spinal manipulation, exercise, physical therapy, massage, acupuncture, transcutaneous electrical nerve stimulation, and ultrasound. Spinal manipulation appears to be roughly equivalent to conventional medical treatments and may be a useful alternative for patients who wish to avoid or who cannot tolerate drug therapy. There is little evidence to support the use of physical therapy, massage, acupuncture, laser therapy, therapeutic ultrasound, corsets, or lumbar traction. Although important for chronic pain, back exercises for ALBP are generally not supported by clinical evidence. There is no convincing evidence regarding the value of ice or heat applications for ABLP; however, many patients report temporary symptomatic relief from ice or frozen gel packs, and heat may produce a short-term reduction in pain after the first week. Patients often report improved satisfaction with the care that they receive when they actively participate in the selection of symptomatic approaches that are tried. CLBP WITHOUT RADICULOPATHY
CLBP is defined as pain lasting >12 weeks; it accounts for 50% of total back pain costs. Risk factors include obesity, female gender, older age, prior history of back pain, restricted spinal mobility, pain radiating into a leg, high levels of psychological distress, poor self-rated health, minimal physical activity, smoking, job dissatisfaction, and widespread pain. In general, the same treatments that are recommended for ALBP can be useful for patients with CLBP. In this setting, however, the long-term benefit of opioid therapy or muscle relaxants is less clear.
Evidence supports the use of exercise therapy, and this can be one of the mainstays of treatment for CLBP. Effective regimens have generally included a combination of gradually increasing aerobic exercise, strengthening exercises, and stretching exercises. Motivating patients is sometimes challenging, and in this setting, a program of supervised exercise can improve compliance. In general, activity tolerance is the primary goal, while pain relief is secondary. Supervised intensive physical exercise or “work hardening” regimens have been effective in returning some patients to work, improving walking distance, and reducing pain. In addition, some forms of yoga have been evaluated in randomized trials and may be helpful for patients who are interested. A long-term benefit of spinal manipulation or massage for CLBP is unproven.
Medications for CLBP may include acetaminophen, NSAIDs, and tricyclic antidepressants. Trials of tricyclics suggest benefit even for patients without evidence of depression. Trials do not support the efficacy of selective serotonin reuptake inhibitors (SSRIs) for CLBP. However, depression is common among patients with chronic pain and should be appropriately treated.
Cognitive-behavioral therapy is based on evidence that psychological and social factors, as well as somatic pathology, are important in the genesis of chronic pain and disability. Cognitive-behavioral therapy includes efforts to identify and modify patients’ thinking about their pain and disability. A systematic review concluded that such treatments are more effective than a waiting list control group for short-term pain relief; however, long-term results remain unclear. Behavioral treatments may have effects similar in magnitude to exercise therapy.
Back pain is the most frequent reason for seeking complementary and alternative treatments. The most common of these for back pain are spinal manipulation, acupuncture, and massage. The role of most complementary and alternative medicine approaches remains unclear. Biofeedback has not been studied rigorously. There is no convincing evidence that either spinal manipulation or transcutaneous electrical nerve stimulation (TENS) is effective in treating CLBP. Rigorous recent trials of acupuncture suggest that true acupuncture is not superior to sham acupuncture, but that both may offer an advantage over routine care. Whether this is due entirely to placebo effects provided even by sham acupuncture is uncertain. Some trials of massage therapy have been encouraging, but this has been less well studied than spinal manipulation or acupuncture.
Various injections, including epidural glucocorticoid injections, facet joint injections, and trigger point injections, have been used for treating CLBP. However, in the absence of radiculopathy, there is no evidence that these approaches are effective.
Injection studies are sometimes used diagnostically to help determine the anatomic source of back pain. The use of discography to provide evidence that a specific disk is the pain generator is not recommended. Pain relief following a glucocorticoid injection into a facet is commonly used as evidence that the facet joint is the pain source; however, the possibility that the response was a placebo effect or due to systemic absorption of the glucocorticoids is difficult to exclude.
Another category of intervention for chronic back pain is electrothermal and radiofrequency therapy. Intradiskal therapy has been proposed using both types of energy to thermocoagulate and destroy nerves in the intervertebral disk, using specially designed catheters or electrodes. Current evidence does not support the use of these intradiskal therapies.
Radiofrequency denervation is sometimes used to destroy nerves that are thought to mediate pain, and this technique has been used for facet joint pain (with the target nerve being the medial branch of the primary dorsal ramus), for back pain thought to arise from the intervertebral disk (ramus communicans), and radicular back pain (dorsal root ganglia). A few small trials have produced conflicting results for facet joint and diskogenic pain. A trial in patients with chronic radicular pain found no difference between radiofrequency denervation of the dorsal root ganglia and sham treatment. These interventional therapies have not been studied in sufficient detail to draw conclusions of their value for CLBP.
Surgical intervention for CLBP without radiculopathy has been evaluated in a small number of randomized trials, all conducted in Europe. Each of these studies included patients with back pain and a degenerative disk, but no sciatica. Three of the four trials concluded that lumbar fusion surgery was no more effective than highly structured, rigorous rehabilitation combined with cognitive-behavioral therapy. The fourth trial found an advantage of fusion surgery over haphazard “usual care,” which appeared to be less effective than the structured rehabilitation in other trials. Given conflicting evidence, indications for surgery for CLBP without radiculopathy have remained controversial. Both U.S. and British guidelines suggest considering referral for an opinion on spinal fusion for people who have completed an optimal nonsurgical treatment program (including combined physical and psychological treatment) and who have persistent severe back pain for which they would consider surgery.
Lumbar disk replacement with prosthetic disks is U.S. Food and Drug Administration approved for uncomplicated patients needing single-level surgery at the L3-S1 levels. The disks are generally designed as metal plates with a polyethylene cushion sandwiched in between. The trials that led to approval of these devices compared them to spine fusion and concluded that the artificial disks were “not inferior.” Serious complications are somewhat more likely with the artificial disk. This treatment remains controversial for CLBP.
Intensive multidisciplinary rehabilitation programs may involve daily or frequent physical therapy, exercise, cognitive-behavioral therapy, a workplace evaluation, and other interventions. For patients who have not responded to other approaches, such programs appear to offer some benefit. Systematic reviews suggest that the evidence is limited and benefits are incremental.
Some observers have raised concern that CLBP may often be overtreated. For CLBP without radiculopathy, new British guidelines explicitly recommend against use of SSRIs, any type of injection, TENS, lumbar supports, traction, radiofrequency facet joint denervation, intradiskal electrothermal therapy, or intradiskal radiofrequency thermocoagulation. These treatments are also not recommended in guidelines from the American College of Physicians and the American Pain Society. On the other hand, exercise therapy and treatment of depression appear to be useful and underused. LOW BACK PAIN WITH RADICULOPATHY
A common cause of back pain with radiculopathy is a herniated disk with nerve root impingement, resulting in back pain with radiation down the leg. The term sciatica is used when the leg pain radiates posteriorly in a sciatic or L5/S1 distribution. The prognosis for acute low back and leg pain with radiculopathy due to disk herniation is generally favorable, with most patients showing substantial improvement over months. Serial imaging studies suggest spontaneous regression of the herniated portion of the disk in two-thirds of patients over 6 months. Nonetheless, there are several important treatment options to provide symptomatic relief while this natural healing process unfolds.
Resumption of normal activity is recommended. Randomized trial evidence suggests that bed rest is ineffective for treating sciatica as well as back pain alone. Acetaminophen and NSAIDs are useful for pain relief, although severe pain may require short courses of opioid analgesics.
Epidural glucocorticoid injections have a role in providing temporary symptom relief for sciatica due to a herniated disk. However, there does not appear to be a benefit in terms of reducing subsequent surgical interventions. Diagnostic nerve root blocks have been advocated to determine if pain originates from a specific nerve root. However, improvement may result even when the nerve root is not responsible for the pain; this may occur as a placebo effect, from a pain-generating lesion located distally along the peripheral nerve, or from effects of systemic absorption. The utility of diagnostic nerve root blocks remains a subject of debate.
Surgical intervention is indicated for patients who have progressive motor weakness due to nerve root injury demonstrated on clinical examination or EMG. Urgent surgery is recommended for patients who have evidence of CES or spinal cord compression, generally suggested by bowel or bladder dysfunction, diminished sensation in a saddle distribution, a sensory level on the trunk, and bilateral leg weakness or spasticity.
Surgery is also an important option for patients who have disabling radicular pain despite optimal conservative treatment. Sciatica is perhaps the most common reason for recommending spine surgery. Because patients with a herniated disk and sciatica generally experience rapid improvement over a matter of weeks, most experts do not recommend considering surgery unless the patient has failed to respond to 6–8 weeks of maximum nonsurgical management. For patients who have not improved, randomized trials indicate that, compared to nonsurgical treatment, surgery results in more rapid pain relief. However, after the first year or two of follow-up, patients with sciatica appear to have much the same level of pain relief and functional improvement with or without surgery. Thus, both treatment approaches are reasonable, and patient preferences and needs (e.g., rapid return to employment) strongly influence decision making. Some patients will want the fastest possible relief and find surgical risks acceptable. Others will be more risk-averse and more tolerant of symptoms and will choose watchful waiting if they understand that improvement is likely in the end.
The usual surgical procedure is a partial hemilaminectomy with excision of the prolapsed disk (diskectomy). Fusion of the involved lumbar segments should be considered only if significant spinal instability is present (i.e., degenerative spondylolisthesis). The costs associated with lumbar interbody fusion have increased dramatically in recent years. There are no large prospective, randomized trials comparing fusion to other types of surgical intervention. In one study, patients with persistent low back pain despite an initial diskectomy fared no better with spine fusion than with a conservative regimen of cognitive intervention and exercise. Artificial disks have been in use in Europe for the past decade; their utility remains controversial in the United States.
PAIN IN THE NECK AND SHOULDER
Neck pain, which usually arises from diseases of the cervical spine and soft tissues of the neck, is common. Neck pain arising from the cervical spine is typically precipitated by movement and may be accompanied by focal tenderness and limitation of motion. Many of the prior comments made regarding causes of low back pain also apply to disorders of the cervical spine. The text below will emphasize differences. Pain arising from the brachial plexus, shoulder, or peripheral nerves can be confused with cervical spine disease (Table 22-4), but the history and examination usually identify a more distal origin for the pain. Cervical spine trauma, disk disease, or spondylosis with intervertebral foraminal narrowing may be asymptomatic or painful and can produce a myelopathy, radiculopathy, or both. The same risk factors for serious causes of low back pain also apply to neck pain with the additional feature that neurologic signs of myelopathy (incontinence, sensory level, spastic legs) may also occur. Lhermitte’s sign, an electrical shock down the spine with neck flexion, suggests involvement of the cervical spinal cord.
TRAUMA TO THE CERVICAL SPINE
Trauma to the cervical spine (fractures, subluxation) places the spinal cord at risk for compression. Motor vehicle accidents, violent crimes, or falls account for 87% of cervical spinal cord injuries (Chap. 456). Immediate immobilization of the neck is essential to minimize further spinal cord injury from movement of unstable cervical spine segments. The decision to obtain imaging should be based on the nature of the injury. The NEXUS low-risk criteria established that normally alert patients without palpation tenderness in the midline; intoxication; neurologic deficits; or painful distracting injuries were very unlikely to have sustained a clinically significant traumatic injury to the cervical spine. The Canadian C-spine rule recommends that imaging should be obtained following neck region trauma if the patient is >65 years old or has limb paresthesias or if there was a dangerous mechanism for the injury (e.g., bicycle collision with tree or parked car, fall from height >3 feet or five stairs, diving accident). These guidelines are helpful but must be tailored to individual circumstances; for example, patients with advanced osteoporosis, glucocorticoid use, or cancer may warrant imaging after even mild trauma. A CT scan is the diagnostic procedure of choice for detection of acute fractures following severe trauma; plain x-rays can be used for lesser degrees of trauma. When traumatic injury to the vertebral arteries or cervical spinal cord is suspected, visualization by MRI with magnetic resonance angiography is preferred.
Whiplash injury is due to rapid flexion and extension of the neck, usually in automobile accidents. The exact mechanism of the injury is unclear. This diagnosis should not be applied to patients with fractures, disk herniation, head injury, focal neurologic findings, or altered consciousness. Up to 50% of persons reporting whiplash injury acutely have persistent neck pain 1 year later. Once personal compensation for pain and suffering was removed from the Australian health care system, the prognosis for recovery at 1 year from whiplash injury improved also. Imaging of the cervical spine is not cost-effective acutely but is useful to detect disk herniations when symptoms persist for >6 weeks following the injury. Severe initial symptoms have been associated with a poor long-term outcome.
Herniation of a lower cervical disk is a common cause of pain or tingling in the neck, shoulder, arm, or hand. Neck pain, stiffness, and a range of motion limited by pain are the usual manifestations. Herniated cervical disks are responsible for ~25% of cervical radiculopathies. Extension and lateral rotation of the neck narrow the ipsilateral intervertebral foramen and may reproduce radicular symptoms (Spurling’s sign). In young adults, acute nerve root compression from a ruptured cervical disk is often due to trauma. Cervical disk herniations are usually posterolateral near the lateral recess. Typical patterns of reflex, sensory, and motor changes that accompany cervical nerve root lesions are summarized in Table 22-4. Although the classic patterns are clinically helpful, there are numerous exceptions because (1) there is overlap in sensory function between adjacent nerve roots, (2) symptoms and signs may be evident in only part of the injured nerve root territory, and (3) the location of pain is the most variable of the clinical features.
TABLE 22-4Cervical Radiculopathy: Neurologic Features ||Download (.pdf) TABLE 22-4Cervical Radiculopathy: Neurologic Features
|Cervical Nerve Roots ||Examination Findings ||Pain Distribution |
|Reflex ||Sensory ||Motor |
|C5 ||Biceps ||Lateral deltoid ||Rhomboidsa (elbow extends backward with hand on hip) ||Lateral arm, medial scapula |
| || || ||Infraspinatusa (arm rotates externally with elbow flexed at the side) || |
| || || ||Deltoida (arm raised laterally 30–45° from the side) || |
|C6 ||Biceps ||Thumb/index finger; ||Bicepsa (arm flexed at the elbow in supination) ||Lateral forearm, thumb/index fingers |
| || ||Dorsal hand/lateral forearm ||Pronator teres (forearm pronated) || |
|C7 ||Triceps ||Middle fingers ||Tricepsa (forearm extension, flexed at elbow) ||Posterior arm, dorsal forearm, dorsal hand |
| || ||Dorsal forearm ||Wrist/finger extensorsa || |
|C8 ||Finger flexors ||Palmar surface of little finger ||Abductor pollicis brevis (abduction of thumb) ||Fourth and fifth fingers, medial hand and forearm |
| || ||Medial hand and forearm ||First dorsal interosseous (abduction of index finger) || |
| || || ||Abductor digiti minimi (abduction of little finger) || |
|T1 ||Finger flexors ||Axilla and medial arm ||Abductor pollicis brevis (abduction of thumb) ||Medial arm, axilla |
| || || ||First dorsal interosseous (abduction of index finger) || |
| || || ||Abductor digiti minimi (abduction of little finger) || |
Osteoarthritis of the cervical spine may produce neck pain that radiates into the back of the head, shoulders, or arms, or may be the source of headaches in the posterior occipital region (supplied by the C2-C4 nerve roots). Osteophytes, disk protrusions, or hypertrophic facet or uncovertebral joints may alone or in combination compress one or several nerve roots at the intervertebral foramina; these causes together account for 75% of cervical radiculopathies. The roots most commonly affected are C7 and C6. Narrowing of the spinal canal by osteophytes, ossification of the posterior longitudinal ligament (OPLL), or a large central disk may compress the cervical spinal cord and produce signs of radiculopathy and myelopathy in combination (myeloradiculopathy). When little or no neck pain accompanies cervical cord involvement, other diagnoses to be considered include amyotrophic lateral sclerosis (Chap. 452), multiple sclerosis (Chap. 458), spinal cord tumors, or syringomyelia (Chap. 456). The possibility of cervical spondylosis should be considered even when the patient presents with symptoms or signs in the legs only. MRI is the study of choice to define anatomic abnormalities of soft tissues in the cervical region including the spinal cord, but plain CT is adequate to assess bony spurs, foraminal narrowing, lateral recess stenosis, or OPLL. EMG and nerve conduction studies can localize and assess the severity of nerve root injury.
OTHER CAUSES OF NECK PAIN
Rheumatoid arthritis (RA) (Chap. 380) of the cervical facet joints produces neck pain, stiffness, and limitation of motion. Synovitis of the atlantoaxial joint (C1-C2; Fig. 22-2) may damage the transverse ligament of the atlas, producing forward displacement of the atlas on the axis (atlantoaxial subluxation). Radiologic evidence of atlantoaxial subluxation occurs in up to 30% of patients with RA. The degree of subluxation correlates with the severity of erosive disease. When subluxation is present, careful assessment is important to identify early signs of myelopathy. Occasional patients develop high spinal cord compression leading to quadriparesis, respiratory insufficiency, and death. Surgery should be considered when myelopathy or spinal instability is present. MRI is the imaging modality of choice. Ankylosing spondylitis can cause neck pain and less commonly atlantoaxial subluxation; surgery may be required to prevent spinal cord compression.
Acute herpes zoster can presents as acute posterior occipital or neck pain prior to the outbreak of vesicles. Neoplasms metastatic to the cervical spine, infections (osteomyelitis and epidural abscess), and metabolic bone diseases may be the cause of neck pain, as discussed above among causes of low back pain. Neck pain may also be referred from the heart with coronary artery ischemia (cervical angina syndrome).
THORACIC OUTLET SYNDROMES
The thoracic outlet contains the first rib, the subclavian artery and vein, the brachial plexus, the clavicle, and the lung apex. Injury to these structures may result in postural or movement-induced pain around the shoulder and supraclavicular region, classified as follows.
True neurogenic thoracic outlet syndrome (TOS) is an uncommon disorder resulting from compression of the lower trunk of the brachial plexus or ventral rami of the C8 or T1 nerve roots, caused most often by an anomalous band of tissue connecting an elongate transverse process at C7 with the first rib. Pain is mild or may be absent. Signs include weakness and wasting of intrinsic muscles of the hand and diminished sensation on the palmar aspect of the fifth digit. An anteroposterior cervical spine x-ray will show an elongate C7 transverse process (an anatomic marker for the anomalous cartilaginous band), and EMG and nerve conduction studies confirm the diagnosis. Treatment consists of surgical resection of the anomalous band. The weakness and wasting of intrinsic hand muscles typically does not improve, but surgery halts the insidious progression of weakness.
Arterial TOS results from compression of the subclavian artery by a cervical rib, resulting in poststenotic dilatation of the artery and in some cases secondary thrombus formation. Blood pressure is reduced in the affected limb, and signs of emboli may be present in the hand. Neurologic signs are absent. Ultrasound can confirm the diagnosis noninvasively. Treatment is with thrombolysis or anticoagulation (with or without embolectomy) and surgical excision of the cervical rib compressing the subclavian artery.
Venous TOS is due to subclavian vein thrombosis resulting in swelling of the arm and pain. The vein may be compressed by a cervical rib or anomalous scalene muscle. Venography is the diagnostic test of choice.
Disputed TOS accounts for 95% of patients diagnosed with TOS; chronic arm and shoulder pain are prominent and of unclear cause. The lack of sensitive and specific findings on physical examination or specific markers for this condition results in diagnostic uncertainty. The role of surgery in disputed TOS is controversial. Multidisciplinary pain management is a conservative approach, although treatment is often unsuccessful.
BRACHIAL PLEXUS AND NERVES
Pain from injury to the brachial plexus or peripheral nerves of the arm can occasionally mimic referred pain of cervical spine origin including cervical radiculopathy. Neoplastic infiltration of the lower trunk of the brachial plexus may produce shoulder or supraclavicular pain radiating down the arm, numbness of the fourth and fifth fingers or medial forearm, and weakness of intrinsic hand muscles innervated by the ulnar and median nerves. Delayed radiation injury may produce similar findings, although pain is less often present and almost always less severe. A Pancoast tumor of the lung (Chap. 107) is another cause and should be considered, especially when a concurrent Horner’s syndrome is present. Suprascapular neuropathy may produce severe shoulder pain, weakness, and wasting of the supraspinatus and infraspinatus muscles. Acute brachial neuritis is often confused with radiculopathy; the acute onset of severe shoulder or scapular pain is followed typically over days by weakness of the proximal arm and shoulder girdle muscles innervated by the upper brachial plexus. The onset may be preceded by an infection, vaccination, or minor surgical procedure. The long thoracic nerve may be affected resulting in a winged scapula. Brachial neuritis may also present as an isolated paralysis of the diaphragm with or without involvement of other nerves of the upper limb. Recovery may take up to 3 years.
Occasional cases of carpal tunnel syndrome produce pain and paresthesias extending into the forearm, arm, and shoulder resembling a C5 or C6 root lesion. Lesions of the radial or ulnar nerve can mimic a radiculopathy at C7 or C8, respectively. EMG and nerve conduction studies can accurately localize lesions to the nerve roots, brachial plexus, or peripheral nerves.
For further discussion of peripheral nerve disorders, see Chap. 459.
Pain arising from the shoulder can on occasion mimic pain from the spine. If symptoms and signs of radiculopathy are absent, then the differential diagnosis includes mechanical shoulder pain (tendonitis, bursitis, rotator cuff tear, dislocation, adhesive capsulitis, or rotator cuff impingement under the acromion) and referred pain (subdiaphragmatic irritation, angina, Pancoast tumor). Mechanical pain is often worse at night, associated with local shoulder tenderness and aggravated by passive abduction, internal rotation, or extension of the arm. Pain from shoulder disease may radiate into the arm or hand, but focal neurologic signs (sensory, motor, or reflex changes) are absent.
TREATMENT Neck Pain without Radiculopathy
The evidence regarding treatment for neck pain is less complete than that for low back pain, but the approach is remarkably similar in many respects. As with low back pain, spontaneous improvement is the norm for acute neck pain. The usual goals of therapy are to promote a rapid return to normal function and provide symptom relief while healing proceeds.
The evidence in support of nonsurgical treatments for whiplash-associated disorders is generally of limited quality and neither supports nor refutes the common treatments used for symptom relief. Gentle mobilization of the cervical spine combined with exercise programs may be beneficial. Evidence is insufficient to recommend for or against the routine use of acupuncture, cervical traction, TENS, ultrasound, diathermy, or massage. Some patients obtain modest relief using a soft neck collar; there is little risk or cost.
For patients with neck pain unassociated with trauma, supervised exercise with or without mobilization appears to be effective. Exercises often include shoulder rolls and neck stretches. The evidence for the use of muscle relaxants, analgesics, and NSAIDs in acute and chronic neck pain is of lower quality and less consistent than for low back pain.
Low-level laser therapy directed at areas of tenderness, local acupuncture points, or a grid of predetermined points is a controversial approach to the treatment of neck pain. A 2009 meta-analysis suggested that this treatment may provide greater pain relief than sham therapy for both acute and chronic neck pain, but comparison to other conservative and less expensive treatment measures is needed.
Although some surgical studies have proposed a role for anterior diskectomy and fusion in patients with neck pain, these studies generally have not been rigorously conducted. A systematic review suggested that there was no valid clinical evidence to support either cervical fusion or cervical disk arthroplasty in patients with neck pain without radiculopathy. Similarly, there is no evidence to support radiofrequency neurotomy or cervical facet injections for neck pain without radiculopathy.
TREATMENT Neck Pain with Radiculopathy
The natural history of neck pain with acute radiculopathy due to disk disease is favorable, and many patients will improve without specific therapy. Although there are no randomized trials of NSAIDs for neck pain, a course of NSAIDs, acetaminophen, or both, with or without muscle relaxants, is reasonable as initial therapy. Other nonsurgical treatments are commonly used, including opioid analgesics, oral glucocorticoids, cervical traction, and immobilization with a hard or soft cervical collar. However, there are no randomized trials that establish the effectiveness of these treatments. Soft cervical collars can be modestly helpful by limiting spontaneous and reflex neck movements that exacerbate pain.
As for lumbar radiculopathy, epidural glucocorticoids appear to provide short-term symptom relief in cervical radiculopathy, but rigorous studies addressing this question have not been conducted. If cervical radiculopathy is due to bony compression from cervical spondylosis with foraminal narrowing, periodic follow-up to assess for progression is indicated and consideration of surgical decompression is reasonable.
Surgical treatment can produce rapid pain relief, although it is unclear whether long-term outcomes are improved over nonsurgical therapy. Indications for cervical disk surgery include a progressive radicular motor deficit, functionally limiting pain that fails to respond to conservative management, or spinal cord compression.
Surgical treatments include anterior cervical diskectomy alone, laminectomy with diskectomy, or diskectomy with fusion. The risk of subsequent radiculopathy or myelopathy at cervical segments adjacent to a fusion is ~3% per year and 26% per decade. Although this risk is sometimes portrayed as a late complication of surgery, it may also reflect the natural history of degenerative cervical disk disease.