Back and Neck Pain
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 is ~$100 billion annually, including direct health care expenses plus costs due to loss of productivity; (2) back symptoms are the most common cause of disability in those more than 45 years; (3) low back pain is the second most common reason for visiting a physician in the United States; and (4) ~1% of the U.S. population is chronically disabled because of back pain.
Anatomy of the Spine
The anterior portion of the 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 (Figs. 16-1 and 16-2). The disks are largest in the cervical and lumbar regions where movements of the spine are greatest. The disks are elastic in youth and allow the bony vertebrae to move easily upon each other. Elasticity is lost with age. The function of the anterior spine is to absorb the shock of body movements such as walking and running.
The posterior portion of the spine consists of the vertebral arches and seven processes. Each arch consists of paired cylindrical pedicles anteriorly and paired laminae posteriorly. The vertebral arch 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 functions of the posterior spine are to protect the spinal cord and nerves within the spinal canal and to stabilize the spine by providing sites for the attachment of muscles and ligaments. The contraction of muscles attached to the spinous and transverse processes produces 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, and leg pain (Figs. 25-2 and 25-3). The nerve roots exit at a level above their respective vertebral bodies in the cervical region (the C7 nerve root exits at the C6-C7 level) and below their respective vertebral bodies in the thoracic and lumbar regions (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 commonly produces compression of the traversing S1 nerve root (Fig. 16-3).
Pain-sensitive structures in the spine include the periosteum of the vertebrae, dura, facet joints, annulus fibrosus of the intervertebral disk, epidural veins, and the posterior longitudinal ligament. Disease of these diverse structures may explain many cases of back pain without nerve root compression. The nucleus pulposus of the intervertebral disk is not pain-sensitive under normal circumstances. Pain sensation is conveyed partially by the sinuvertebral nerve that arises from the spinal nerve at each spine segment and reenters the spinal canal through the intervertebral foramen at the same level. The lumbar and cervical spine possess the greatest potential for movement and injury.
Approach to the Patient: Back Pain
Types of Back Pain
Understanding the type of pain experienced by the patient is the essential first step. Attention is also focused on identification of risk factors for serious underlying diseases; the majority of these are due to radiculopathy, fracture, tumor, infection, or referred pain from visceral structures (Table 16-1).
Local pain is caused by stretching of 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 but is 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, or rarely the calves or feet. Provocative injections into pain-sensitive structures of the lumbar spine may produce leg pain that does not follow a dermatomal distribution. This "sclerotomal" pain may explain some cases of back and leg pain without evidence of nerve root compression.
Radicular back pain is typically sharp and radiates from the lumbar spine to the 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 stretches the sciatic nerve (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 sclerotomal pain and radiculopathy.
Pain associated with muscle spasm, although of obscure origin, is commonly associated with many spine disorders. The spasms are accompanied by abnormal posture, taut paraspinal muscles, and dull pain.
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 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) or an asymmetry in the paraspinal muscles, suggesting muscle spasm. Back pain of bony spine origin is often reproduced by palpation or percussion over the spinous process of the affected vertebrae.
Forward bending is often limited by paraspinal muscle spasm; the latter may flatten the usual lumbar lordosis. Flexion of 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 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 (Patrick sign) and by tapping the heel with the examiner's palm while the leg is extended.
With the patient lying flat, 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. While flexion to at least 80° is normally possible without causing pain, tight hamstring muscles are a source of pain in some patients. The straight leg–raising (SLR) test is positive if the maneuver reproduces the patient's usual back or limb pain. Eliciting the SLR sign in the sitting position may 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 positive when flexion of one leg reproduces the pain in the opposite leg or buttocks. The crossed SLR sign is less sensitive but more specific for disk herniation than the SLR sign. The nerve or nerve root lesion is always on the side of the pain. 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 and the femoral nerve, is considered positive if the patient's usual back or limb pain is reproduced.
The neurologic examination includes a search for focal weakness or muscle atrophy, focal reflex changes, diminished sensation in the legs, and signs of spinal cord injury. The examiner should be alert to the possibility of breakaway weakness, defined as fluctuating strength during muscle testing. Breakaway weakness may be due to pain or a combination of pain and underlying true weakness. Breakaway weakness without pain is due to lack of effort. In uncertain cases, electromyography (EMG) can determine whether or not true weakness is present. Findings with specific nerve root lesions are shown in Table 16-2 and are discussed below.
aReverse straight leg–raising sign present—see "Examination of the Back."
Laboratory, Imaging, and EMG Studies
Routine laboratory studies are rarely needed for the initial evaluation of nonspecific acute (less than 3 months duration) low back pain (ALBP). If risk factors for a serious underlying cause are present, then laboratory studies [complete blood count (CBC), erythrocyte sedimentation rate (ESR), urinalysis] are indicated.
CT scanning is superior to routine x-rays for the detection of fractures involving posterior spine structures, craniocervical and craniothoracic junctions, C1 and C2 vertebrae, bone fragments within the spinal canal, or malalignment; CT scans are increasingly used as a primary screening modality for moderate to severe trauma. In the absence of risk factors, these imaging studies are rarely helpful in nonspecific ALBP. MRI and CT-myelography are the radiologic tests 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 bony lesions and is tolerated by claustrophobic patients. While the added diagnostic value of modern neuroimaging is significant, there is concern that these studies may be overutilized in patients with ALBP.
Electrodiagnostic studies can be used to assess the functional integrity of the peripheral nervous system. Sensory nerve conduction studies are normal when focal sensory loss is due to nerve root damage because the nerve roots are proximal to the nerve cell bodies in the dorsal root ganglia. The diagnostic yield of needle EMG is higher than that of nerve conduction studies for radiculopathy. Denervation changes in a myotomal (segmental) distribution are detected by sampling multiple muscles supplied by different nerve roots and nerves; 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 the clinical evaluation of weakness is limited by pain or poor effort. EMG and nerve conduction studies will be normal when only limb pain or sensory nerve root injury or irritation is present.
Causes of Back Pain
aLow back pain only.
Congenital Anomalies of the Lumbar Spine
Spondylolysis is a bony defect in the pars interarticularis (a segment near the junction of the pedicle with the lamina) of the vertebra; the etiology may be a stress fracture in a congenitally abnormal segment. The defect (usually bilateral) is best visualized on oblique projections in plain x-rays, CT scan, or single photon emission CT (SPECT) bone scan and occurs in the setting of a single injury, repeated minor injuries, or growth. Although frequently asymptomatic, it is the most common cause of persistent low back pain in adolescents and is often activity-related.
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 of the lumbosacral junction, infection, osteoporosis, tumor, trauma, prior surgery, or degenerative spine disease. It occurs more frequently in women. The slippage may be asymptomatic or may cause low back pain and hamstring tightness, nerve root injury (the L5 root most frequently), or symptomatic spinal stenosis. Tenderness may be elicited near the segment that has "slipped" forward (most often L4 on L5 or occasionally L5 on S1). A "step" may be present on deep palpation of the posterior elements of the segment above the spondylolisthetic joint. The trunk may be shortened and the abdomen protuberant as a result of extreme forward displacement of L4 on L5; in severe cases cauda equina syndrome (CES) may occur (see below). Surgery is considered for symptoms persisting for >1 year that do not respond to conservative measures (e.g., rest, physical therapy). Surgery is usually indicated for cases with progressive neurologic deficit, abnormal gait or postural deformity, slippage more than 50%, or scoliosis.
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 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. Neuroimaging studies reveal a low-lying conus (below L1-L2) and a short and thickened filum terminale.
A patient complaining of back pain and inability to move the legs may have a spinal fracture or dislocation, and, with fractures above L1, spinal cord compression. Care must be taken to avoid further damage to the spinal cord or nerve roots by immobilizing the back pending results of x-rays.
Sprains and Strains
The terms low back sprain, strain, or 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 (a pars interarticularis fracture of the L5 vertebra is common), 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.
Lumbar Disk Disease
This is a common cause of chronic or recurrent low back and leg pain (Figs. 16-3 and 16-4). Disk disease is most likely to occur at the L4-L5 and L5-S1 levels, but upper lumbar levels are involved occasionally. The cause is often unknown; the risk is increased in overweight individuals. Disk herniation is unusual prior to age 20 and is rare in the fibrotic disks of the elderly. Degeneration of the nucleus pulposus and the annulus fibrosus increases with age and may be asymptomatic or painful. Genetic factors may play a role in predisposing some patients to disk degeneration. The pain may be located in the low back only or referred to the 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.
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 the protruding or ruptured disk may trigger or perpetuate back pain. Ingrowth of nociceptive (pain) nerve fibers into inner portions of a diseased disk may be responsible for chronic "diskogenic" pain. Nerve root injury (radiculopathy) from disk herniation may be due to compression, inflammation, or both; pathologically, demyelination and axonal loss are usually present.
Symptoms of a ruptured disk include back pain, abnormal posture, limitation of spine motion (particularly flexion), 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 descending nerve roots within the spinal canal. Clinical manifestations of specific nerve root lesions are summarized in Table 16-2. There is suggestive evidence that lumbar disk herniation with a nonprogressive nerve root deficit can be managed nonsurgically. The size of the disk protrusion may naturally decrease over time.
The differential diagnosis covers a variety of serious and treatable conditions, including epidural abscess, hematoma, or tumor. Fever, constant pain uninfluenced by position, sphincter abnormalities, or signs of spinal cord disease suggest an etiology other than lumbar disk disease. Bilateral absence of ankle reflexes can be a normal finding in old age 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 a nerve root or peripheral nerve injury, an anterior horn cell disease, or disuse.
An MRI scan or CT-myelogram is necessary to establish the location and type of pathology. Spinal MRI yields 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, many studies have found that most 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 contrast enhancement are common incidental findings that, by themselves, should not dictate management decisions for patients with back pain.
There are four indications for intervertebral disk surgery: (1) progressive motor weakness from nerve root injury demonstrated on clinical examination or EMG, (2) bowel or bladder disturbance or other signs of spinal cord compression, (3) incapacitating nerve root pain despite conservative treatment for 4 weeks at a minimum, and (4) recurrent incapacitating pain despite conservative treatment. The latter two criteria are more subjective and less well established than the others. Surgical treatment should also be considered if steady pain and/or neurologic findings do not substantially improve over 4–12 weeks.
The usual surgical procedure is a partial hemilaminectomy with excision of the prolapsed disk. Fusion of the involved lumbar segments should be considered only if significant spinal instability is present (i.e., degenerative spondylolisthesis or isthmic spondylolysis). Over a recent 5-year period, the number of lumbar fusion procedures performed in the United States more than doubled, for uncertain reasons. 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.
Cauda equina syndrome (CES) signifies an injury of multiple lumbosacral nerve roots within the spinal canal. Low back pain, weakness and areflexia in the legs, saddle anesthesia, and loss of bladder function may occur. The problem must be distinguished from disorders of the lower spinal cord (conus medullaris syndrome), acute transverse myelitis and Guillain-Barré syndrome. 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
Lumbar spinal stenosis describes a narrowed lumbar spinal canal. Neurogenic claudication is the usual symptom, consisting of back and buttock or leg pain induced by walking or standing and relieved by sitting. Symptoms in the legs are usually bilateral. Lumbar stenosis, by itself, is frequently asymptomatic, and the correlation between the severity of symptoms and degree of stenosis of the spinal canal is poor. Unlike vascular claudication, symptoms are often provoked by standing without walking. Unlike lumbar disk disease, symptoms are usually relieved by sitting. Focal weakness, sensory loss, or reflex changes may occur when spinal stenosis is associated with radiculopathy. Severe neurologic deficits, including paralysis and urinary incontinence, occur rarely. Spinal stenosis can be acquired (75%), congenital, or due to a combination of these factors. 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. 16-5).
Conservative treatment of symptomatic spinal stenosis includes nonsteroidal anti-inflammatory drugs (NSAIDs), exercise programs, and symptomatic treatment of acute pain episodes. Surgical therapy is considered when medical therapy does not relieve symptoms sufficiently to allow for activities of daily living or when significant focal neurologic signs are present. Most patients with neurogenic claudication treated surgically experience at least 75% relief of back and leg pain. Up to 25% develop recurrent stenosis at the same spinal level or an adjacent level 5 years after the initial surgery; recurrent symptoms usually respond to a second surgical decompression.
Facet joint hypertrophy can produce unilateral radicular symptoms or signs due to bony compression; symptoms are often indistinguishable from disk-related radiculopathy. Stretch signs, focal motor weakness, hyporeflexia, or dermatomal sensory loss may be present. Hypertrophic superior or inferior facets can be visualized by x-rays, CT, or MRI. Surgical foraminotomy results in long-term relief of leg and back pain in 80–90% of these patients. The usefulness of therapeutic facet joint blocks for pain has not been rigorously studied.
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 is increased with movement and associated with stiffness. 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 large osteophytes can be seen in asymptomatic patients. Radiculopathy occurs when hypertrophied facets and osteophytes compress nerve roots in the lateral recess or intervertebral foramen. Osteophytes arising from the vertebral body may cause or contribute to central spinal canal stenosis. Disc degeneration may also play a role in reducing the cross-sectional area of the intervertebral foramen; the descending pedicle may compress the exiting nerve root. Rarely, osteoarthritic changes in the lumbar spine are sufficient to compress the cauda equina.
This distinctive arthritic spine disease typically presents with the insidious onset of low back and buttock pain. Patients are often males below age 40. Associated features include morning back stiffness, nocturnal pain, pain unrelieved by rest, an elevated ESR, and the histocompatibility antigen HLA-B27. Onset at a young age and back pain improving with exercise are characteristic. Loss of the normal lumbar lordosis and exaggeration of thoracic kyphosis develop as the disease progresses. Inflammation and erosion of the outer fibers of the annulus fibrosus at the point of contact with the vertebral body are followed by ossification and bony growth that bridges adjacent vertebral bodies and reduces spine mobility in all planes. Radiologic hallmarks are periarticular destructive changes, sclerosis of the sacroiliac joints, and bridging of vertebral bodies to produce the fused "bamboo spine."
Stress fractures through the spontaneously ankylosed posterior bony elements of the rigid, osteoporotic spine may produce focal pain, spinal instability, spinal cord compression, or CES. Atlantoaxial subluxation with spinal cord compression occasionally occurs. Ankylosis of the ribs to the spine and a decrease in the height of the thoracic spine may compromise respiratory function. For many patients, therapy with anti-tumor necrosis factor agents is effective in reducing disease activity. Similar to ankylosing spondylitis, restricted movements may accompany Reiter's syndrome, psoriatic arthritis, and chronic inflammatory bowel disease.
Back pain is the most common neurologic symptom in patients with systemic cancer and may be the presenting symptom. The cause is usually vertebral metastases. Metastatic carcinoma (breast, lung, prostate, thyroid, kidney, gastrointestinal tract), multiple myeloma, and non-Hodgkin's and Hodgkin's lymphomas frequently involve the spine. 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. Plain x-rays may or may not show destructive lesions in one or several vertebral bodies without disk space involvement. MRI, CT, and CT-myelography are the studies of choice when spinal metastasis is suspected. MRI is preferred, but the most rapidly available procedure is best because the patient's condition may worsen quickly. Fewer than 5% of patients who are nonambulatory at the time of diagnosis ever regain the ability to walk, thus early diagnosis is crucial.
Vertebral osteomyelitis is usually 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 exacerbated by motion and 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. Plain radiographs may show a narrowed disk space with erosion of adjacent vertebrae; however, these diagnostic changes may take weeks or months to appear. MRI and CT are sensitive and specific for osteomyelitis; CT may be more readily available in emergency settings and better tolerated by some patients with severe back pain.
Spinal epidural absces presents with back pain (aggravated by movement or palpation) and fever. Signs of nerve root injury or spinal cord compression may be present. 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 motor, sensory, or reflex changes. Causes of arachnoiditis include multiple lumbar operations, chronic spinal infections, spinal cord injury, intrathecal hemorrhage, myelography (rare), intrathecal injection of glucocorticoids or anesthetics, and foreign bodies. The MRI shows clumped nerve roots located centrally or adherent to the dura peripherally, 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, and dorsal root ganglionectomy have been tried, but outcomes have been poor. Dorsal column stimulation for pain relief has produced varying results. Epidural injections of glucocorticoids have been of limited value.
Osteoporosis and Osteosclerosis
Immobilization or underlying conditions such as osteomalacia, hyperparathyroidism, hyperthyroidism, multiple myeloma, metastatic carcinoma, or glucocorticoid use may accelerate osteoporosis and weaken the vertebral body, leading to compression fractures and pain. The most common causes of nontraumatic vertebral body fractures are postmenopausal (type 1) or senile (type 2) osteoporosis (Chap. 348). Compression fractures occur in up to half of patients with severe osteoporosis, and those who sustain a fracture have a 4.5-fold increased risk for recurrence. The sole manifestation of a compression fracture may be localized back pain or radicular pain exacerbated by movement and often reproduced by palpation over the spinous process of the affected vertebra. The clinical context, neurologic signs, and x-ray appearance of the spine establish the diagnosis. Antiresorptive drugs including bisphosphonates (e.g., alendronate), transdermal estrogen, and tamoxifen have been shown to reduce the risk of osteoporotic fractures. Fewer than one-third of patients with prior compression fractures are adequately treated for osteoporosis despite the increased risk for future fractures; rates of primary prevention among individuals at risk, but without a history of fracture, are even less. Compression fractures above the midthoracic region suggest malignancy; if tumor is suspected, a bone biopsy or diagnostic search for a primary tumor is indicated.
Interventions [percutaneous vertebroplasty (PVP), kyphoplasty] exist for osteoporotic compression fractures associated with debilitating pain. Candidates for PVP have midline back pain, palpation tenderness over the spinous process of the affected vertebral body, less than 80% loss of vertebral body height, and onset of symptoms within the prior 4 months. The PVP technique consists of injection of polymethylmethacrylate, under fluoroscopic guidance, into the affected vertebral body. Kyphoplasty adds the inflation of a balloon in the vertebral body prior to the injection of cement. Rare complications can include extravasation of cement into the epidural space (resulting in myelopathy) or fatal pulmonary embolism from migration of cement into paraspinal veins. Approximately three-quarters of patients who meet selection criteria have reported enhanced quality of life. Relief of pain following PVP has also been reported in patients with vertebral metastases, myeloma, or hemangiomas.
Osteosclerosis, an abnormally increased bone density often due to Paget's disease, is readily identifiable on routine x-ray studies and may or may not produce back pain. Spinal cord or nerve root compression may result from bony encroachment.
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 mid-lumbar 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
Peptic ulcers or tumors of the posterior wall of the stomach or duodenum typically produce epigastric pain, but midline back or paraspinal pain may occur if retroperitoneal extension is present. Fatty foods are more likely to induce back pain associated with biliary disease. Diseases of the pancreas produce back pain to the right of the spine (head of the pancreas involved) or to the left (body or tail involved). Pathology in retroperitoneal structures (hemorrhage, tumors, pyelonephritis) produces paraspinal pain that radiates to the lower abdomen, groin, or anterior thighs. A mass in the iliopsoas region often produces unilateral lumbar pain with radiation toward the groin, labia, or testicles. The sudden appearance of lumbar pain in a patient receiving anticoagulants suggests retroperitoneal hemorrhage.
Isolated low back pain occurs in 15–20% of patients with a contained rupture of an abdominal aortic aneurysm (AAA). The classic clinical triad of abdominal pain, shock, and back pain occurs in less than 20% of patients. Two of these three features are present in two-thirds of patients, and hypotension is present in half. The typical patient is an elderly male smoker with back pain. Frequently, the diagnosis is initially missed because the symptoms and signs can be nonspecific. Common 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.
Inflammatory bowel disorders (colitis, diverticulitis) or cancers of the colon may produce lower abdominal pain, midlumbar back pain, or both. The pain may have a beltline distribution around the body. A lesion in the transverse or proximal descending colon may refer pain to the mid or left back at the L2-L3 level. Lesions of the sigmoid colon may refer pain to the upper sacral or midline suprapubic regions or left lower quadrant of the abdomen.
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. The poorly localized, cramping pain can radiate 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 or nerves. 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. 91), and diseases of the kidney and ureter. Lesions of the bladder and testes do not usually 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
Postural Back Pain
There is a group of patients with nonspecific chronic low back pain (CLBP) in whom no 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. The physical examination is unrevealing except for "poor posture." Imaging studies and laboratory evaluations do not identify a specific cause. 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, chronic anxiety states, or depression. Many patients with CLBP have a history of psychiatric illness (depression, anxiety, substance abuse) 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.
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 upon neurologic signs, psychological factors, physiologic studies, and imaging studies have been devised to minimize the likelihood of unsuccessful surgery.
Back Pain: Treatment
Acute Low Back Pain (ALBP)
ALBP is defined as pain of less than 3 months' duration. Full recovery can be expected in 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).
Observational studies have been used to justify a minimalist approach to this problem. These studies share a number of limitations: (1) a true placebo control group is often lacking; (2) patients who consult different provider groups (generalists, orthopedists, neurologists) are assumed to have similar etiologies for their back pain; (3) no information is provided about the details of treatment; and (4) no attempt to tabulate structural causes of ALBP is made.
The algorithms for the treatment of back pain (Fig. 16-6) draw from published clinical practice guidelines (CPGs). However, since CPGs are based on incomplete evidence, guidelines should not substitute for clinical judgment.
The initial assessment excludes serious causes of spine pathology that require urgent intervention, including infection, cancer, and trauma. Risk factors for a serious cause of ALBP are shown in Table 16-1. Laboratory studies are unnecessary if risk factors are absent. Plain spine films or CT are rarely indicated in the first month of symptoms unless a spine fracture is suspected.
Clinical trials have shown no benefit of more than 2 days of bed rest for uncomplicated ALBP. There is evidence that bed rest is also ineffective for patients with sciatica or for acute back pain with signs of nerve root injury. Similarly, traction is not effective for ALBP. 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. One trial of early vigorous exercise was negative, but the value of less vigorous exercise or other exercise programs are unknown. Early resumption of normal physical activity (without heavy manual labor) is likely to be beneficial.
Proof is lacking to support the treatment of acute back and neck pain with acupuncture, transcutaneous electrical nerve stimulation, massage, ultrasound, diathermy, magnets, or electrical stimulation. Cervical collars can be modestly helpful by limiting spontaneous and reflex neck movements that exacerbate pain. Evidence regarding the efficacy of ice is lacking; heat may provide a short-term reduction in pain and disability. These interventions are optional given the lack of negative evidence, low cost, and low risk. Biofeedback has not been studied rigorously. Facet joint, trigger point, and ligament injections are not recommended for acute treatment.
A role for modification of posture has not been validated by rigorous clinical studies. As a practical matter, temporary suspension of activity known to increase mechanical stress on the spine (heavy lifting, prolonged sitting, bending or twisting, straining at stool) may be helpful.
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. In one study, patients who felt they did not receive an adequate explanation for their symptoms wanted further diagnostic tests. Evidence for the efficacy of structured education programs ("back school") is inconclusive; there is modest evidence for a short-term benefit, but evidence for a long-term benefit is lacking. Randomized studies of back school for primary prevention of low back injury and pain have failed to demonstrate any benefit.
NSAIDs and acetaminophen (see Table 12-1) are effective over-the-counter agents for ALBP. Muscle relaxants (cyclobenzaprine, 10 mg PO qhs as initial dose, up to 10 mg PO tid) provide short-term (4–7 days) benefit, particularly at night if sleep is affected, but drowsiness limits daytime use. Opioid analgesics are no more effective than NSAIDs or acetaminophen for initial treatment of ALBP, nor do they increase the likelihood of return to work. Short-term use of opioids may be necessary in patients unresponsive to or intolerant of acetaminophen or NSAIDs. There is no evidence to support the use of oral glucocorticoids or tricyclic antidepressants for ALBP.
Epidural glucocorticoids may occasionally produce short-term pain relief in ALBP with radiculopathy, but proof is lacking for pain relief beyond 1 month. Epidural glucocorticoids, anesthetics, or opioids are not indicated in the initial treatment of ALBP without radiculopathy. 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 anesthesia of the sinuvertebral nerve. Therapeutic nerve root blocks with injection of glucocorticoids and a local anesthetic should be considered only after conservative measures fail, particularly when temporary relief of pain is necessary.
A short course of lumbar spinal manipulation or physical therapy (PT) for symptomatic relief of uncomplicated ALBP is a reasonable option. Prospective, randomized studies are difficult to perform in part because there is no consensus about what constitutes an adequate placebo control. Specific PT or chiropractic protocols that may provide benefit have not been fully defined.
Chronic Low Back Pain
CLBP, defined as pain lasting more than 12 weeks, 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. Combinations of these premorbid factors have been used to predict which individuals with ALBP are likely to develop CLBP. The initial approach to these patients is similar to that for ALBP. Treatment of this heterogeneous group of patients is directed toward the underlying cause when known; the ultimate goal is to restore function to the maximum extent possible.
Many conditions that produce CLBP can be identified by a combination of neuroimaging and electrophysiologic studies. Spine MRI and CT-myelography are almost always the imaging techniques of choice. Imaging studies should be performed only in circumstances when the results are likely to influence management.
Injection studies can be used diagnostically to help determine the anatomic source of back pain. Reproduction of the patient's typical pain with diskography has been used as evidence that a specific disk is the pain generator. Pain relief following a foraminal nerve root block or glucocorticoid injection into a facet has been similarly used as evidence that the facet joint or nerve root is the source. However, the possibility that the injection response was a placebo effect or due to systemic absorption of the glucocorticoids is usually not considered. The value of these procedures in the treatment of CLBP or in the selection of candidates for surgery is largely unknown despite their widespread use. The value of thermography in the assessment of radiculopathy also has not been rigorously studied.
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 disk protrusion detected by CT or MRI scans. Thus, surgical intervention based solely upon radiologic findings increases the likelihood of an unsuccessful outcome.
An unblinded study in patients with chronic sciatica found that surgery could hasten relief of symptoms by ~2 months; however, at 1 year there was no advantage of surgery over conservative medical therapy, and nearly all patients (95%) in both groups made a full recovery regardless of the treatment approach.
CLBP can be treated with a variety of conservative measures. Acute and subacute exacerbations are managed with NSAIDs and comfort measures. There is no good evidence to suggest that one NSAID is more effective than another. Bed rest should not exceed 2 days. Activity tolerance is the primary goal, while pain relief is secondary. Exercise programs can reverse atrophy in paraspinal muscles and strengthen extensors of the trunk. Intensive physical exercise or "work hardening" regimens (under the guidance of a physical therapist) have been effective in returning some patients to work, improving walking distances, and diminishing pain. The benefit can be sustained with home exercise regimens. It is difficult to endorse one specific exercise or PT regimen given the heterogeneous nature of this patient group. The role of manipulation, back school, or epidural steroid injections in the treatment of CLBP is unproven. There is no strong evidence to support the use of acupuncture or traction. A reduction in sick leave days, long-term health care utilization, and pension expenditures may offset the initial expense of multidisciplinary treatment programs. Studies of hydrotherapy for CLBP have yielded mixed results; however, given its low risk and cost, hydrotherapy can be considered as a treatment option. Transcutaneous electrical nerve stimulation (TENS) has not been adequately studied in CLBP.
Pain in the Neck and Shoulder
aThese muscles receive the majority of innervation from this root.
Neck pain, which usually arises from diseases of the cervical spine and soft tissues of the neck, is common (4.6% of adults in one study). Neck pain arising from the cervical spine is typically precipitated by movement and may be accompanied by focal tenderness and limitation of motion. Pain arising from the brachial plexus, shoulder, or peripheral nerves can be confused with cervical spine disease, but the history and examination usually identify a more distal origin for the pain. Cervical spine trauma, disk disease, or spondylosis may be asymptomatic or painful and can produce a myelopathy, radiculopathy, or both. The nerve roots most commonly affected are C7 and C6.
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 spinal cord injuries. Immediate immobilization of the neck is essential to minimize further spinal cord injury from movement of unstable cervical spine segments. A CT scan is the diagnostic procedure of choice for detection of acute fractures. Following major trauma to the cervical spine, injury to the vertebral arteries is common; most lesions are asymptomatic and can be visualized by MRI and angiography.
Whiplash injury is due to trauma (usually automobile accidents) causing cervical musculoligamental sprain or strain due to hyperflexion or hyperextension. This diagnosis should not be applied to patients with fractures, disk herniation, head injury, focal neurologic findings, or altered consciousness. Imaging of the cervical spine is not cost-effective acutely but is useful to detect disk herniations when symptoms persist for more than 6 weeks following the injury. Severe initial symptoms have been associated with a poor long-term outcome.
Cervical Disk Disease
Herniation of a lower cervical disk is a common cause of neck, shoulder, arm, or hand pain or tingling. Neck pain, stiffness, and a range of motion limited by pain are the usual manifestations. A herniated cervical disk is responsible for ~25% of cervical radiculopathies. Extension and lateral rotation of the neck narrows the ipsilateral intervertebral foramen and may reproduce radicular symptoms (Spurling's sign). In young persons, acute nerve root compression from a ruptured cervical disk is often due to trauma. Cervical disk herniations are usually posterolateral near the lateral recess and intervertebral foramen. Typical patterns of reflex, sensory, and motor changes that accompany specific cervical nerve root lesions are summarized in Table 16-4; however, (1) overlap in function between adjacent nerve roots is common, (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.
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, and hypertrophic facet or uncovertebral joints may compress one or several nerve roots at the intervertebral foramina (Fig. 16-7); this compression accounts 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. Combinations of radiculopathy and myelopathy may also be present. Spinal cord involvement is suggested by Lhermitt's symptom, an electrical sensation elicited by neck flexion and radiating down the spine from the neck. When little or no neck pain accompanies cord compression, the diagnosis may be confused with amyotrophic lateral sclerosis, multiple sclerosis, spinal cord tumors, or syringomyelia. 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 the anatomic abnormalities, but plain CT is adequate to assess bony spurs, foraminal narrowing, or OPLL. EMG and nerve conduction studies can localize and assess the severity of the nerve root injury.
Other Causes of Neck Pain
Rheumatoid arthritis (RA) of the cervical apophyseal joints produces neck pain, stiffness, and limitation of motion. In advanced RA, synovitis of the atlantoaxial joint (C1-C2; Fig. 16-2) 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 30% of patients with RA. Not surprisingly, 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.
Ankylosing spondylitis can cause neck pain and less commonly atlantoaxial subluxation; surgery may be required to prevent spinal cord compression. Acute herpes zoster 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. Neck pain may also be referred from the heart with coronary artery ischemia (cervical angina syndrome).
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. True neurogenic thoracic outlet syndrome (TOS) results from compression of the lower trunk of the brachial plexus or ventral rami of the C8 or T1 nerve roots by an anomalous band of tissue connecting an elongate transverse process at C7 with the first rib. Signs include weakness of intrinsic muscles of the hand and diminished sensation on the palmar aspect of the fourth and fifth digits. 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; the compression results in poststenotic dilatation of the artery and 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 or vein. Disputed TOS includes a large number of patients with chronic arm and shoulder pain of unclear cause. The lack of sensitive and specific findings on physical examination or laboratory markers for this condition frequently 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 pain of cervical spine origin. Neoplastic infiltration of the lower trunk of the brachial plexus may produce shoulder pain radiating down the arm, numbness of the fourth and fifth fingers, and weakness of intrinsic hand muscles innervated by the ulnar and median nerves. Postradiation fibrosis (most commonly from treatment of breast cancer) may produce similar findings, although pain is less often present. A Pancoast tumor of the lung is another cause and should be considered, especially when a Horner's syndrome is present. Suprascapular neuropathy may produce severe shoulder pain, weakness, and wasting of the supraspinatous and infraspinatous muscles. Acute brachial neuritis is often confused with radiculopathy; the acute onset of severe shoulder or scapular pain is followed over days to weeks by weakness of the proximal arm and shoulder girdle muscles innervated by the upper brachial plexus. The onset is often preceded by an infection. The suprascapular and long thoracic nerves are most often affected; the latter results in a winged scapula. Brachial neuritis may also present as an isolated paralysis of the diaphragm. Complete recovery occurs in 75% of patients after 2 years and in 89% after 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.
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, and 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 abduction, internal rotation, or extension of the arm. Pain from shoulder disease may radiate into the arm or hand, but sensory, motor, and reflex changes are absent.
Neck Pain: Treatment
There are few well-designed clinical trials that address optimal treatment of neck pain or cervical radiculopathy. Relief of pain, prevention of recurrence, and improved neurologic function are reasonable goals. Symptomatic treatment includes the use of analgesic medications and/or a soft cervical collar. Most treatment recommendations reflect anecdotal experience, case series, or conclusions derived from studies of the lumbar spine. Controlled studies of oral prednisone or transforaminal glucocorticoid injections have not been performed. Reasonable indications for cervical disk surgery include a progressive radicular motor deficit, pain that fails to respond to conservative management and limits activities of daily living, or cervical spinal cord compression. Surgical management of herniated cervical disks usually consists of an anterior approach with diskectomy followed by anterior interbody fusion. A simple posterior partial laminectomy with diskectomy is an acceptable alternative approach. Another surgical approach involves implantation of an artificial disk; in one prospective trial, outcomes after 2 years favored the implant over a traditional anterior cervical discectomy with fusion. The artificial disk is not yet approved for general use in the United States. The risk of subsequent radiculopathy or myelopathy at cervical segments adjacent to the 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.
Nonprogressive cervical radiculopathy due to a herniated cervical disk may be treated conservatively, even if a focal neurologic deficit is present, with a high rate of success. However, if the cervical radiculopathy is due to bony compression from cervical spondylosis, then surgical decompression is generally indicated to forestall the progression of neurologic signs.
Cervical spondylotic myelopathy is typically managed with either anterior decompression and fusion or laminectomy in order to forestall progression of the myelopathy known to occur in 20–30% of untreated patients. However, one prospective study comparing surgery vs. conservative treatment for mild cervical spondylotic myelopathy showed no difference in outcome after 2 years of follow-up.