Back and Neck Pain

The importance of back and neck pain in our society is underscored by the following: (1) the annual societal cost of back pain in the United States is estimated to be between $20 and $50 billion; (2) back symptoms are the most common cause of disability in patients under 45 years of age; (3) 50% of working adults, in one survey, admitted to having a back injury each year; and (4) approximately 1% of the U.S. population is chronically disabled because of back pain.

The enormous economic pressure to provide rational and efficient care of patients with back pain has resulted in clinical practice guidelines (CPGs) for these patients. CPGs are algorithms which guide evaluation or treatment at specific steps in patient care. CPGs for acute low back pain (ALBP) are based upon incomplete evidence (see algorithms, Fig. 16-6) but represent an attempt to standardize common medical practice. Major revisions in CPGs for back pain can be anticipated in the future. Management of patients with chronic low back pain (CLBP) is complex and not amenable to a simple algorithmic approach at this time.

Figure 16-6 Figure 16-6

 



Figure 16-6: Algorithms for management of acute low back pain, age 0x00226518 years. A. Symptoms <3 months, first 4 weeks. B. Possible serious etiology.figure-continued1><<016>> C. Management weeks 4-12. 10x0025cb, entry point from Algorithm D postoperatively or if patient declines surgery. D. Surgical options. (NSAIDs, nonsteroidal anti-inflammatory drugs; CBC, complete blood count; ESR, erythrocyte sedimentation rate; UA, urinalysis; EMG, electromyography; NCV, nerve conduction velocity studies; MRI, magnetic resonance imaging; CT, computed tomography; CNS, central nervous system.)

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 cartilagenous 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 typical body movements such as walking and running.

Figure 16-1

Figure 16-1: Vertebral anatomy.



Figure 16-2

Figure 16-2: Spinal column.

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 (Fig. 16-1). The vertebral arch gives rise to two transverse processes laterally, one spinous process posteriorly, plus two superior and two inferior articular facets. 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. Normal upright posture in humans places the center of gravity anterior to the spine. The graded contraction of well-developed paraspinal muscles attached to the laminae, transverse processes, and spinous processes is necessary to maintain normal upright posture.

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 spinal cord ends at the L1 or L2 level of the bony spine. Consequently, 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, it is common for disk herniation at the L4-L5 level to produce compression of the S1 nerve root (Fig. 16-3). In contrast, cervical nerve roots follow a short intraspinal course and exit at the level of their respective spinal cord segments (upper cervical) or one segment below the corresponding levels (lower cervical cord). Cervical spine pathology can result in spinal cord compression, but lumbar spine pathology cannot.


Approach to the Patient

Types of Back Pain

An understanding of the nature of the pain as described by the patient is the essential first step in evaluation. Attention is also focused on identification of risk factors for serious underlying diseases that require specific evaluation.

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 spine (diskography) may produce leg pain that does not follow a dermatomal distribution. The exact pathogenesis of this "sclerotomal" pain is unclear, but it may explain many instances in which combined back and leg pain is unaccompanied by evidence of nerve root compression.

Radicular back pain is typically sharp and radiates from the 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 clearly 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.

Back pain at rest or unassociated with specific postures should raise the index of suspicion for an underlying serious cause (e.g., spine tumor, fracture, infection, or referred pain from visceral structures). 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) or percussion over the costovertebral angles (pyelonephritis, adrenal disease, L1-L2 transverse process fracture).

The normal spine (Fig. 16-2) displays a thoracic kyphosis, lumbar lordosis, and cervical lordosis. Exaggeration of these normal alignments may result in hyperkyphosis (lameback) of the thoracic spine or hyperlordosis (swayback) of the lumbar spine. Spasm of lumbar paraspinal muscles results in flattening of the usual lumbar lordosis. Inspection may reveal lateral curvature of the spine (scoliosis) or an asymmetry in the appearance of the paraspinal muscles, suggesting muscle spasm. Taut paraspinal muscles limit the motion of the lumbar spine. Back pain of bony spine origin is often reproduced by palpation or percussion over the spinous process of the affected vertebrae.

Forward bending is frequently limited by paraspinal muscle spasm. 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 or bony spine disease is present.

Pain from hip disease may mimic the pain of lumbar spine disease. The first movement is typically internal rotation of the hip. Manual internal and external rotation at the hip with the knee and hip in flexion (Patrick sign) may reproduce the pain, as may percussion of the heel (of an outstretched leg) with the palm of the examiner's hand.

In the supine position passive flexion of the thigh on the abdomen while the knee is extended produces stretching of the L5 and S1 nerve roots and the sciatic nerve because the nerve passes posterior to the hip. 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 hamstrings commonly limit motion, may result in pain, and are readily identified by the patient. This straight leg-raising (SLR) sign 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 performance of the maneuver on one leg reproduces the patient's pain symptoms in the opposite leg or buttocks. 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 while the patient continues to stand. This maneuver stretches the L2-L4 nerve roots and the femoral nerve because the nerves pass anterior to the hip. The reverse SLR test is positive if the maneuver reproduces the patient's usual back or limb pain.

The neurologic examination includes a search for weakness, muscle atrophy, focal reflex changes, diminished sensation in the legs, and signs of spinal cord injury. Findings with specific nerve root lesions are shown in Table 16-1 and are discussed below.

Table 16-1: Lumbosacral Radiculopathy-Neurologic Features

 

Examination Findings

 

 

 

Lumbosacral Nerve Roots

Reflex

Sensory

Motor

Pain Distribution

L2a

-

Upper anterior thigh

Psoas (hip flexion)

Anterior thigh

L3a

-

Lower anterior thigh
Anterior knee

Psoas (hip flexion)
Quadriceps (knee extension)
Thigh adduction

Anterior thigh, knee

L4a

Quadriceps (knee)

Medial calf

Quadriceps (knee extension)b
Thigh adduction
Tibialis anterior (foot dorsiflexion)

Knee, medial calf

L5c

-

Dorsal surface-foot
Lateral calf

Peroneii (foot eversion)b
Tibialis anterior (foot dorsiflexion)
Gluteus medius (hip abduction)
Toe dorsiflexors

Lateral calf, dorsal foot, posterolateral thigh, buttocks

S1c

Gastrocnemius/soleus (ankle)

Plantar surface-foot
Lateral aspect-foot

Gastrocnemius/soleus (foot plantar flexion)b
Abductor hallucis (toe flexors)b
Gluteus maximus (hip extension)

Bottom foot, posterior calf, posterior thigh, buttocks


aReverse straight leg-raising sign present-see 'Examination of the Back.'
bThese muscles receive the majority of innervation from this root.
cStraight leg-raising sign present-see 'Examination of the Back.'



Laboratory Studies

Routine laboratory studies such as a complete blood count, erythrocyte sedimentation rate, chemistry panel, and urinalysis are rarely needed for the initial evaluation of acute (<3 months), nonspecific, low back pain. If risk factors for a serious underlying disease are present, then laboratory studies (guided by the history and examination) are indicated (Fig. 16-6B).

Plain films of the lumbar or cervical spine are helpful when risk factors for vertebral fracture (trauma, chronic steroid use) are present. In the absence of risk factors, routine x-rays of the lumbar spine in the setting of acute, nonspecific, low back pain are expensive and rarely helpful. Magnetic resonance imaging (MRI) and computed tomography (CT)-myelography have emerged as the radiologic tests of choice for evaluation of most serious diseases involving the spine. In general, the definition of soft tissue structures by MRI is superior, whereas CT-myelography provides optimal imaging of bony lesions in the region of the lateral recess and intervertebral foramen and is tolerated by claustrophobic patients. With rare exceptions, conventional myelography and bone scan are inferior to MRI and CT-myelography.

Electromyography (EMG) can be used to assess the functional integrity of the peripheral nervous system (Chap. 357) in the setting of back pain. 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. Mixed nerve somatosensory evoked potentials and F-wave studies are of uncertain value in the evaluation of radiculopathy.

Causes of Back Pain

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 of the defect may be a stress fracture in a congenitally abnormal segment. The defect (usually bilateral) is best visualized on oblique projections in plain x-rays or by CT scan and occurs in the setting of a single injury, repeated minor injuries, or growth.

Spondylolisthesis is the anterior slippage of the vertebral body, pedicles, and superior articular facets, leaving the posterior elements behind. Spondylolisthesis is associated with spondylolysis and degenerative spine disease and occurs more frequently in women. The slippage may be asymptomatic but may also cause low back pain, 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 degrees of spondylolisthesis. In these cases, cauda equina syndrome may occur (Chap. 368).

 

Figure 16-3

Figure 16-3: Locations of compression of lumbar and sacral roots by herniated disks.

Pain-sensitive structures in the spine include the vertebral body periosteum, dura, facet joints, annulus fibrosus of the intervertebral disk, epidural veins, and the posterior longitudinal ligament. Damage to these nonneural structures may cause pain. The nucleus pulposus of the intervertebral disk is not pain-sensitive under normal circumstances. Pain sensation is conveyed 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. Disease of these diverse pain-sensitive spine structures may explain many cases of back pain without nerve root compression. The lumbar and cervical spine possess the greatest potential for movement and injury.

Trauma

Trauma is an important cause of acute low back pain. 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. In such cases care must be taken to avoid further damage to the spinal cord or nerve roots. The back should be immobilized pending results of plain x-rays.

Sprains and Strains

The terms low back sprain, strain, or mechanically induced muscle spasm are used for minor, self-limited injuries associated with lifting a heavy object, a fall, or a sudden deceleration such as occurs 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 low back pain and paraspinal muscle spasm often assume unusual postures.

Vertebral Fractures

Most traumatic fractures of the lumbar vertebral bodies result from compression or flexion injuries producing anterior wedging or compression. With more severe trauma, the patient may sustain a fracture-dislocation or a "burst" fracture involving not only the vertebral body but posterior elements as well. 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 commonly associated with these injuries, and early surgical treatment is indicated (Chap. 369).

When fractures are atraumatic, the bone is presumed to be weakened by a pathologic process. The cause is usually postmenopausal (type 1) or senile (type 2) osteoporosis (Chap. 342). Underlying systemic disorders such as osteomalacia, hyperparathyroidism, hyperthyroidism, multiple myeloma, metastatic carcinoma, or glucocorticoid use may also weaken the vertebral body. The clinical context, neurologic signs, and x-ray appearance of the spine establish the diagnosis. Antiresorptive drugs including biphosphatonates, alendronate, transdermal estrogen, and tamoxifen have been shown to reduce the risk of osteoporotic fractures.

Lumbar Disk Disease

This disorder is a common cause of chronic or recurrent low back and leg pain. Disk disease is most likely to occur at the L4-L5 and L5-S1 levels, but upper lumbar levels are involved occasionally. The cause of the disk injury is often unknown; the risk is increased in overweight individuals. Degeneration of the nucleus pulposus and the annulus fibrosus increases with age and may be asymptomatic or painful. A sneeze, cough, or trivial movement may cause the nucleus pulposus to prolapse, pushing the frayed and weakened annulus posteriorly. In 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 pulposis 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 diseased intervertebral disk may be responsible for chronic "diskogenic" pain. Nerve root injury (radiculopathy) from disk herniation may be due to compression, inflammation, or both; pathologically, varying degrees of demyelination and axonal loss are usually present.

The symptoms of a ruptured intervertebral disk include back pain, abnormal posture, limitation of spine motion (particularly flexion), or radicular pain. A dermatomal pattern of sensory loss or a reduction in or loss of a deep tendon reflex is more suggestive of a specific root lesion than the pattern of pain. Motor findings (focal weakness, muscle atrophy, or fasciculations) occur less frequently than sensory or reflex changes, but a myotomal pattern of involvement can suggest specific nerve root injury. Lumbar disk disease is usually unilateral (Fig. 16-4), but bilateral involvement does occur with large central disk herniations that compress several nerve roots at the same level. Clinical manifestations of specific lumbosacral nerve root lesions are summarized in Table 16-1. There is evidence to suggest that lumbar disk herniation with a nonprogressive nerve root deficit can be managed conservatively (i.e., nonsurgically) with a successful outcome. The size of the disk protrusion may naturally decrease over time.



Figure 16-4

Figure 16-4: Lumbar herniated disk; left S1 radiculopathy. Sagittal T1-weighted image on the left with arrows outlining disk margins. Sagittal T2 image on the right reveals a protruding disk at the L5-S1 level (arrows), which displaces the central thecal sac.

Degeneration of the intervertebral disk without frank extrusion of disk tissue may give rise to low back pain only. There may be referred pain in the leg, buttock, or hip with little or no discomfort in the back and no signs of nerve root involvement. Lumbar disk syndromes are usually unilateral, but large central disk herniations can cause bilateral symptoms and signs and may produce a cauda equina syndrome.

Breakaway weakness describes a variable power of muscle contraction by a patient who is asked to provide maximal effort. The 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; patients who exhibit breakaway weakness should be asked if testing a specific muscle is painful. In uncertain cases, EMG can determine whether or not true weakness is present.

The differential diagnosis of lumbar disk disease includes 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 reflect 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 rather than an L4 nerve root injury. A focal decrease in sensation over the foot and distal lateral calf may result from a peroneal or lateral sciatic neuropathy rather than an L5 nerve root injury. Focal muscle atrophy may reflect loss of motor axons from 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. Simple MRI yields exquisite views of intraspinal and adjacent soft tissue anatomy and is more likely to establish a specific anatomic diagnosis than plain films or myelography. Bony lesions of the lateral recess or intervertebral foramen may be seen with optimal clarity on CT-myelographic studies.

The correlation of neuroradiologic findings to symptoms, particularly pain, is often problematic. As examples, contrast-enhancing tears in the annulus fibrosus or disk protrusions are widely accepted as common sources of back pain. However, one recent study found that over half of asymptomatic adults have annular tears on lumbar spine MR imaging, nearly all of which demonstrate contrast enhancement. Furthermore, asymptomatic disk protrusions are common in adults, and many of these abnormalities enhance with contrast. These observations strongly suggest that 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. The presence or absence of persistent disk herniation 10 years after surgical or conservative treatment has no bearing on a successful clinical outcome.

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 disease, (3) incapacitating nerve root pain despite conservative treatment for at least 4 weeks, 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 the pain and/or neurologic findings do not substantially improve over 4 to 12 weeks.

Surgery is preceded by MRI scan or CT-myelogram to define the location and type of pathology. The usual surgical procedure is a partial hemilaminectomy with excision of the involved and prolapsed intervertebral disk. Arthrodesis of the involved lumbar segments is considered only in the presence of significant spinal instability (i.e., degenerative spondylolisthesis or isthmic spondylolysis).

Other Causes of Low Back Pain

Spinal stenosis is an anatomic diagnosis reflecting a narrowed lumbar or cervical spinal canal. Classic neurogenic claudication occurs in the setting of moderate to severe spinal stenosis and typically consists of back and buttock or leg pain induced by walking or standing. The pain is relieved by sitting. Symptoms in the legs are usually bilateral. Focal weakness, sensory loss, or reflex changes may occur when associated with radiculopathy. Unlike vascular claudication, the symptoms are often provoked by standing without walking. Unlike lumbar disk disease, the symptoms are usually relieved by sitting. Severe neurologic deficits, including paralysis and urinary incontinence, occur rarely. Spinal stenosis usually results from acquired (75%), congenital, or mixed acquired/congenital factors. Congenital forms (achondroplasia, idiopathic) are characterized by short, thick pedicles that produce both spinal canal and lateral recess stenosis. Acquired factors that may contribute to spinal stenosis include degenerative diseases (spondylosis, spondylolisthesis, scoliosis), trauma, spine surgery (postlaminectomy, fusion), metabolic or endocrine disorders (epidural lipomatosis, osteoporosis, acromegaly, renal osteodystrophy, hypoparathyroidism), and Paget's disease. MRI or CT-myelography provide the best definition of the abnormal anatomy (Fig. 16-5).



Figure 16-5

Figure 16-5: Spinal stenosis. Sagittal T2 fast spin echo magnetic resonance imaging of a normal (left) and stenotic (right) lumbar spine, revealing multifocal narrowing (arrows) of the cerebrospinal fluid spaces surrounding the nerve roots within the thecal sac.

Conservative treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs), exercise programs, and symptomatic treatment of acute pain exacerbations. Surgical therapy is considered when medical therapy does not relieve pain sufficiently to allow for activities of daily living or when significant focal neurologic signs are present. Between 65 and 80% of properly selected patients treated surgically experience >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, due to bony compression, that are indistinguishable from disk-related radiculopathy. Patients may exhibit stretch signs, focal motor weakness, hyporeflexia, or sensory loss. Hypertrophic superior or inferior facets can often be visualized radiologically. Foraminotomy results in long-term relief of leg and back pain in 80 to 90% of patients.

Lumbar adhesive arachnoiditis with radiculopathy is the result of a fibrotic process following an inflammatory response to local tissue injury within the subarachnoid space. The fibrosis results in nerve root adhesions, producing back and leg pain associated with motor, sensory, and reflex changes. Myelography-induced arachnoiditis has become rare with the abandonment of oil-based contrast. Other causes of arachnoiditis include multiple lumbar operations, chronic spinal infections, spinal cord injury, intrathecal hemorrhage, intrathecal injection of steroids and anesthetics, and foreign bodies. The spine MRI appearance of arachnoiditis includes nerve roots clumping together centrally and adherent to the dura peripherally, or loculations of cerebrospinal fluid (CSF) within the thecal sac that obscure nerve root visualization. Treatment is often unsatisfactory. Microsurgical lysis of adhesions, dorsal rhizotomy, and dorsal root ganglionectomy have resulted in poor outcomes. Dorsal column stimulation for pain relief has produced varying results. Epidural steroid injections have been of limited value.

Arthritis

Arthritis is a major cause of spine pain.

Spondylosis

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 by motion and associated with stiffness or limitation of motion. The relationship between clinical symptoms and radiologic findings is usually not straightforward. Pain may be prominent when x-ray findings are minimal; alternatively, large osteophytes can be seen in asymptomatic patients in middle and later life. Hypertrophied facets and osteophytes may 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. Loss of intervertebral disk height reduces the vertical dimensions of the intervertebral foramen; the descending pedicle may compress the nerve root exiting at that level. Osteoarthritic changes in the lumbar spine may rarely compress the cauda equina.

Ankylosing Spondylitis

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 sedimentation rate, and the histocompatibility antigen HLA-B27. The differential diagnosis includes tumor and infection. Onset at a young age and back pain characteristically improving with exercise suggest ankylosing spondylitis. Loss of the normal lumbar lordosis and exaggeration of thoracic kyphosis are seen 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 bone growth. Bony growth (syndesmophyte) bridges adjacent vertebral bodies and results in reduced spine mobility in all planes. The radiologic hallmarks of the disease are periarticular destructive changes, sclerosis of the sacroiliac joints, and bridging of vertebral bodies by bone to produce the fused "bamboo spine." Similar restricted movement may accompany Reiter's syndrome, psoriatic arthritis, and chronic inflammatory bowel disease. Stress fractures through the spontaneously ankylosed posterior bony elements of the rigid, osteoporotic spine may result in focal spine pain, spinal cord compression or cauda equina syndrome. Occasional atlantoaxial subluxation with spinal cord compression occurs. Bilateral ankylosis of the ribs to the spine and a decrease in the height of axial thoracic structures may cause marked impairment of respiratory function.

Other Destructive Diseases

Neoplasm

Back pain is the most common neurologic symptom among patients with systemic cancer. One-third of patients with undiagnosed back or neck pain and known systemic cancer have epidural extension or metastasis of tumor, and one-third have pain associated with vertebral metastases alone. About 11% have back pain unrelated to metastatic disease. Metastatic carcinoma (breast, lung, prostate, thyroid, kidney, gastrointestinal tract), multiple myeloma, and non-Hodgkin's and Hodgkin's lymphomas frequently involve the spine. Back pain may be the presenting symptom because the primary tumor site may be overlooked or asymptomatic. The pain tends to be constant, dull, unrelieved by rest, and worse at night. In contrast, mechanical low back pain is usually improved with rest. Plain x-rays usually, though not always, show destructive lesions in one or several vertebral bodies without disk space involvement. MRI or CT-myelography are the studies of choice in the setting of suspected spinal metastasis, but the trend of evidence favors the use of MRI. The procedure of choice is the study most rapidly available because the patient may worsen during a diagnostic delay.

Infection

Vertebral osteomyelitis is usually caused by staphylococci, but other bacteria or the tubercle bacillus (Pott's disease) may be the responsible organism. A primary source of infection, most often from the urinary tract, skin, or lungs, can be identified in 40% of patients. Intravenous drug use is a well-recognized risk factor. Back pain exacerbated by motion and unrelieved by rest, spine tenderness over the involved spine segment, and an elevated erythrocyte sedimentation rate are the most common findings. Fever or elevated white blood cell count are found in a minority of patients. Plain radiographs may show a narrowed disk space with erosion of adjacent vertebrae; these diagnostic changes may take weeks or months to appear. MRI and CT are sensitive and specific for osteomyelitis; MRI definition of soft tissue detail is exquisite. CT scan may be more readily available and better tolerated by some patients with severe back pain.

Spinal epidural abscess (Chap. 368) presents with back pain (aggravated by palpation or movement) and fever. The patient may exhibit nerve root injury or spinal cord compression accompanied by a sensory level, incontinence, or paraplegia. The abscess may track over multiple spinal levels and is best delineated by spine MRI.

Osteoporosis and Osteosclerosis

Considerable loss of bone may occur with or without symptoms in association with medical disorders, including hyperparathyroidism, chronic glucocorticoid use, or immobilization. Compression fractures occur in up to half of patients with severe osteoporosis. The risk of osteoporotic vertebral fracture is 4.5 times greater over 3 years among patients with a baseline fracture compared with osteoporotic controls. The sole manifestation of a compression fracture may be focal lumbar or thoracic aching (often after a trivial injury) that is exacerbated by movement. Other patients experience thoracic or upper lumbar radicular pain. Focal spine tenderness is common. When compression fractures are found, treatable risk factors should be sought. Compression fractures above the midthoracic region suggest malignancy.

Osteosclerosis is readily identifiable on routine x-ray studies (e.g., Paget's disease) and may or may not produce back pain. Spinal cord or nerve root compression may result from bony encroachment on the spinal canal or intervertebral foramina. Single dual-beam photon absorptiometry or quantitative CT can be used to detect small changes in bone mineral density. For further discussion of these bone disorders, see Chaps. 341 to 343.

Referred Pain from Visceral Disease

Diseases of the pelvis, abdomen, or thorax may produce referred pain to the posterior portion of the spinal segment that innervates the diseased organ. Occasionally, back pain may be the first and only sign. In general, pelvic diseases refer pain to the sacral region, lower abdominal diseases to the lumbar region (around the second to fourth lumbar vertebrae), and upper abdominal diseases to the lower thoracic or upper lumbar region (eighth thoracic to the first and second lumbar vertebrae). Local signs (pain with spine palpation, paraspinal muscle spasm) are absent, and minimal or no pain accompanies normal spine movements.

Low Thoracic and Upper Lumbar Pain in Abdominal Disease

Peptic ulcer or tumor of the posterior stomach or duodenum typically produces epigastric pain (Chaps. 285 and 90), but midline back or paraspinal pain may occur if retroperitoneal extension is present. Back pain due to peptic ulcer may be precipitated by ingestion of an orange, alcohol, or coffee and relieved by food or antacids. Fatty foods are more likely to induce back pain associated with biliary disease. Diseases of the pancreas may 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) may produce paraspinal pain with radiation 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 testicle. The sudden appearance of lumbar pain in a patient receiving anticoagulants suggests retroperitoneal hemorrhage.

Isolated low back pain occurs in 15 to 20% of patients with a contained rupture of an abdominal aortic aneurysm (AAA). The classic clinical triad of abdominal pain, shock, and back pain in an elderly man occurs in fewer than 20% of patients. Two of these three features are present in two-thirds of patients, and hypotension is present in half. Ruptured AAA has a high mortality rate; the typical patient is an elderly male smoker with back pain. The diagnosis is initially missed in at least one-third of patients 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 to 75% of patients) is an important physical finding.

Lumbar Pain with Lower Abdominal Diseases

Inflammatory bowel disorders (colitis, diverticulitis) or colonic neoplasms may produce lower abdominal pain, midlumbar back pain, or both. The pain may have a beltlike distribution around the body. A lesion in the transverse or initial descending colon may refer pain to the middle or left back at the L2-L3 level. Sigmoid colon disease may refer pain to the upper sacral or midline suprapubic regions or left lower quadrant of the abdomen.

Sacral Pain in 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 carcinoma may invade the uterosacral ligaments; malposition of the uterus may cause uterosacral ligament traction. The pain associated with endometriosis begins during the premenstrual phase and often continues until it merges with menstrual pain. Malposition of the uterus (retroversion, descensus, and prolapse) may lead to sacral pain after standing for several hours.

Menstrual pain may be felt in the sacral region. The poorly localized, cramping pain can radiate down the legs. Other pelvic sources of low back pain include neoplastic invasion of pelvic nerves, radiation necrosis, and pregnancy. Pain due to neoplastic infiltration of nerves is typically continuous, progressive in severity, and unrelieved by rest at night. Radiation therapy of pelvic tumors may produce sacral pain from late radiation necrosis of tissue or nerves. Low back pain with radiation into one or both thighs is common in the last weeks of pregnancy.

Urologic sources of lumbosacral back pain include chronic prostatitis, prostate carcinoma with spinal metastasis, and diseases of the kidney and ureter. Lesions of the bladder and testes do not usually produce back pain. The diagnosis of metastatic prostate carcinoma is established by rectal examination, spine imaging studies (MRI or CT), and measurement of prostate-specific antigen (PSA) (Chap. 95). Infectious, inflammatory, or neoplastic renal diseases may result in ipsilateral lumbosacral pain, as can renal artery or vein thrombosis. Ureteral obstruction due to renal stones may produce paraspinal lumbar pain.

Postural Back Pain

There is a group of patients with chronic, nonspecific low back pain in whom no anatomic or pathologic 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 are normal. Exercises to strengthen the paraspinal and abdominal muscles are sometimes therapeutic.

 

Psychiatric Disease

Chronic low back pain (CLBP) may be encountered in patients with compensation hysteria, malingering, 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 impairment who are at high risk for a poor surgical outcome. It is important to be certain that the back pain in these patients does not represent serious spine or visceral pathology in addition to the impaired psychological state.

Unidentified

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 surgical explorations and to avoid selection of patients with psychological profiles that predict poor functional outcomes.

Treatment

Acute Low Back Pain

A practical approach to the management of low back pain is to consider acute and chronic presentations separately. ALBP is defined as pain of less than 3 months' duration. Full recovery can be expected in 85% of adults with ALBP unaccompanied by leg pain. Most of these patients exhibit "mechanical" symptoms-pain that is aggravated by motion and relieved by rest.

Observational, population-based studies have been used to justify a minimalist approach to individual patient care. 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 within each provider group or between provider groups; and (4) no attempt to tabulate serious causes of ALBP is made. The appropriateness of specific diagnostic procedures or therapeutic interventions for low back pain cannot be assessed from these studies.

The proposed algorithms (Fig. 16-6) for management of ALBP in adults draw considerably from published guidelines. However, it must be emphasized that current CPGs for the treatment of low back pain are based on incomplete evidence-for example, there is a paucity of well-designed studies documenting the natural history of disk lesions associated with a focal neurologic deficit. Guidelines should not substitute for sound clinical judgment.

The initial assessment excludes serious causes of spine pathology that require urgent intervention, including infection, cancer, and trauma. Risks factors for a possible serious underlying cause of back pain include: age > 50 years, prior diagnosis of cancer or other serious medical illness, bed rest without relief, duration of pain >1 month, urinary incontinence or recent nocturia, focal leg weakness or numbness, pain radiating into the leg(s) from the back, intravenous drug use, chronic infection (pulmonary or urinary), pain increasing with standing and relieved by sitting, history of spine trauma, and glucocorticoid use. Clinical signs associated with a possible serious etiology include unexplained fever, well-documented and unexplained weight loss, positive SLR sign or reverse SLR sign, crossed SLR sign, percussion tenderness over the spine or costovertebral angle, an abdominal mass (pulsatile or nonpulsatile), a rectal mass, focal sensory loss (saddle anesthesia or focal limb sensory loss), true leg weakness, spasticity, and asymmetric leg reflexes. Laboratory studies are unnecessary unless a serious underlying cause (Fig. 16-6, Algorithms A and B) is suspected. Plain spine films are rarely indicated in the first month of symptoms unless a spine fracture is suspected.

The roles of bed rest, early exercise, and traction in the treatment of acute uncomplicated low back pain have been the subject of recent prospective studies. Clinical trials fail to demonstrate any benefit of prolonged (>2 days) bed rest for ALBP. There is evidence that bed rest is also ineffective for patients with sciatica or for acute back pain with findings of nerve root injury. Theoretical 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. A recent trial did not show benefit from an early vigorous exercise program, but the benefits of less vigorous exercise or other exercise programs remain unknown. The early resumption of normal physical activity (without heavy manual labor) is likely to be beneficial. Well-designed clinical studies of traction that include a sham traction group have failed to show a benefit of traction for ALBP. Despite this knowledge, one survey of physicians' perceptions of effective treatment identified strict bed rest for >3 days, trigger point injections (see below), and physical therapy (PT) as beneficial for more than 50% of patients with ALBP. In many instances, the behavior of treating physicians does not reflect the current medical literature.

Proof is lacking to support the treatment of acute back and neck pain with acupuncture, transcutaneous electrical nerve stimulation, massage, ultrasound, diathermy, 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 or heat is lacking, but 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 in the treatment of ALBP.

A beneficial role for specific exercises or 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.

Patient education is an important part of treatment. Studies reveal that patient 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 more diagnostic tests. Evidence for the efficacy of structured education programs ("back school") is inconclusive; in one controlled study, patients attending back school had a shorter duration of sick leave during the initial episode but not during subsequent episodes. Recent large, controlled, randomized studies of back school for primary prevention of low back injury and pain have failed to demonstrate a benefit.

Medications used in the treatment of ALBP include NSAIDs, acetaminophen, muscle relaxants, and opioids. NSAIDs are superior to placebo for back pain relief. Acetaminophen is superior to placebo in the treatment of other types of pain but has not been compared against placebo for low back pain. Muscle relaxants provide short-term (4 to 7 days) benefit compared with placebo, but drowsiness often limits their daytime use. The efficacy of muscle relaxants compared to NSAIDs or in combination with NSAIDs is unclear. Opioid analgesics have not been shown to be more effective than NSAIDs or acetaminophen for relief of ALBP or likelihood of return to work. Short-term use of opioids in selected patients unresponsive to or intolerant of acetaminophen or NSAIDs may be helpful. There is no evidence to support the use of oral glucocorticoids or tricyclic antidepressants in treatment of ALBP.

The role of diagnostic and therapeutic nerve root blocks for patients with acute back or neck pain remains controversial. Equivocal data suggests that epidural steroids may occasionally produce short-term pain relief in patients with ALBP and radiculopathy, but proof is lacking for pain relief beyond 1 month. Epidural anesthetics, steroids, or opioids are not indicated as initial treatment for ALBP without radiculopathy. Diagnostic selective nerve root blocks have been advocated to determine if pain originates from a nerve root. However, these studies may be falsely positive due to a placebo effect, in patients with a painful lesion located distally along the peripheral nerve, or from anesthesia of the sinuvertebral nerve. Therapeutic selective nerve root blocks are an option after brief conservative measures fail, particularly when temporary relief of pain may be important for patient function. Needle position is confirmed under fluoroscopic guidance with nonionic contrast before injection of glucocorticoid and local anesthetic.

A short course of spinal manipulation or PT for symptomatic relief of uncomplicated ALBP is an option. A prospective, randomized study comparing PT, chiropractic manipulation, and education interventions for patients with ALBP found modest trends toward benefit with both PT and chiropractic manipulation at 1 year. Costs per year were equivalent in the PT/chiropractic group and ~$280 less for the group treated with the education booklet alone. The extent to which this modest improvement in symptoms and outcome is worth the cost must be determined for each patient. Extended duration of treatment or treatment of patients with radiculopathy is of unknown value and carries potential risk. The appropriate frequency or duration of spinal manipulation has not been addressed adequately.

Chronic Low Back Pain

CLBP is defined as pain lasting longer than 12 weeks. Patients with CLBP account for 50% of back pain costs. Overweight individuals appear to be at particular risk. Other risk factors include: 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, and the differential diagnosis of CLBP includes most of the conditions described in this chapter. Treatment of this heterogeneous group of patients is directed toward the underlying cause when possible; the ultimate goal is to restore function to the greatest extent possible.

Many conditions that produce CLBP can be identified by the combination of neuroimaging and electrophysiologic studies. Spine MRI or CT-myelography are the techniques of choice but are generally not indicated within the first month after initial evaluation in the absence of risk factors for a serious underlying cause. Imaging studies should be performed only in circumstances where the results are likely to influence surgical or medical treatment.

Diskography is of questionable value in the evaluation of back pain. No additional anatomic information is provided beyond what is available by MRI. Reproduction of the patient's typical pain with the injection is often used as evidence that a specific disk is the pain generator, but it is not known whether this information has any value in selecting candidates for surgery. There is no proven role for thermography in the assessment of radiculopathy.

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 and pain increases the likelihood of an unsuccessful outcome.

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 type II muscle fiber atrophy in paraspinal muscles and strengthen trunk extension. Supervised, 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; compliance with the exercise regimen strongly influences outcome. The role of manipulation, back school, or epidural steroid injections in the treatment of CLBP is unclear. Up to 30% of "blind" epidural steroid injections miss the epidural space even when performed by an experienced anesthesiologist. There is no strong evidence to support the use of acupuncture or traction in this setting. A reduction in sick leave days, long-term health care utilization, and pension expenditures may offset the initial expense of multidisciplinary treatment programs. In one study comparing 3 weeks of hydrotherapy versus routine ambulatory care, hydrotherapy resulted in diminished duration and intensity of back pain, reduced analgesic drug consumption, improved spine mobility, and improved functional score. Functional score returned to baseline at the 9-month follow-up, but all other beneficial effects were sustained. Percutaneous electrical nerve stimulation (PENS) has been shown to provide significant short-term relief of CLBP, but additional studies regarding long-term efficacy and cost are necessary.

 

Pain in the Neck and Shoulder

Approach to the Patient

In one recent epidemiologic survey, the 6-month prevalence of disabling neck pain was 4.6% among adults. Neck pain commonly arises from diseases of the cervical spine and soft tissues of the neck. Neck pain arising from the cervical spine is typically precipitated by neck movements and may be accompanied by focal spine 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

Unlike injury to the low back, 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, which can have devastating consequences (Chap. 369). Emergency immobilization of the neck prior to complete assessment is mandatory to minimize further spinal cord injury from movement of unstable cervical spine segments.

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, or altered consciousness. One prospective study found that 18% of patients with whiplash injury had persistent injury-related symptoms 2 years after the car accident. Such patients were older, had a higher incidence of inclined or rotated head position at impact, greater intensity of initial neck and head pain, greater number of initial symptoms, and more osteoarthritic changes on cervical spine x-rays at baseline compared to patients who ultimately recovered. Objective data on the pathology of neck soft tissue injuries is lacking. Patients with severe initial injury are at increased risk for poor long-term outcome.

Cervical Disk Disease

Herniation of a lower cervical disk is a common cause of neck, shoulder, arm, or hand pain. Neck pain (worse with movement), stiffness, and limited range of neck motion are common. With nerve root compression, pain may radiate into a shoulder or arm. Extension and lateral rotation of the neck narrows the intervertebral foramen and may reproduce radicular symptoms (Spurling's sign). In young individuals, acute cervical nerve root compression from a ruptured disk is often due to trauma. Subacute radiculopathy is less likely to be related to a specific traumatic incident and may involve both disk disease and spondylosis. Cervical disk herniations are usually posterolateral near the lateral recess and intervertebral foramen. The usual patterns of reflex, sensory, and motor changes that accompany specific cervical nerve root lesions are listed in Table 16-2. When evaluating patients with suspected cervical radiculopathy it is important to consider the following: (1) overlap in function between adjacent nerve roots is common, (2) the anatomic pattern of pain is the most variable of the clinical features, and (3) the distribution of symptoms and signs may be evident in only part of the injured nerve root territory.

Table 16-2: Cervical Radiculopathy-Neurologic Features

 

Examination Findings

 

 

 

Cervical Nerve Roots

Reflex

Sensory

Motor

Pain Distribution

C5

Biceps

Over lateral deltoid

Supraspinatusa (initial arm abduction)
Infraspinatusa (arm external rotation)
Deltoida (arm abduction)
Biceps (arm flexion)

Lateral arm, medial scapula

C6

Biceps

Thumb, index fingers
Radial hand/forearm

Biceps (arm flexion)
Pronator teres (internal forearm rotation)

Lateral forearm, thumb, index finger

C7

Triceps

Middle fingers
Dorsum forearm

Tricepsa (arm extension)
Wrist extensorsa
Extensor digitoruma (finger extension)

Posterior arm, dorsal forearm, lateral hand

C8

Finger flexors

Little finger
Medial hand and forearm

Abductor pollicis brevis (abduction D1)
First dorsal interosseous (abduction D2)
Abductor digiti minimi (abduction D5)

4th and 5th fingers, medial forearm

T1

Finger flexors

Axilla and medial arm

Abductor pollicis brevis (abduction D1)
First dorsal interosseous (abduction D2)
Abductor digiti minimi (abduction D5)

Medial arm, axilla


aThese muscles receive the majority of innervation from this root.



Surgical management of cervical herniated disks usually consists of an anterior approach with diskectomy followed by anterior interbody fusion. A simple posterior partial laminectomy with diskectomy is an alternative approach. The risk of subsequent radiculopathy or myelopathy at cervical segments adjacent to the fusion is 3% per year and 26% at 10 years. Although the risk is sometimes portrayed as a late complication of cervical surgery, it may also reflect the natural history of degenerative cervical spine disease in this subpopulation of patients.

 

Cervical Spondylosis

Osteoarthritis of the cervical spine may produce neck pain that radiates into the back of the head, shoulders, or arms. Arthritic or other pathologic conditions of the upper cervical spine may be the source of headaches in the posterior occipital region (supplied by the C2-C4 nerve roots). Cervical spondylosis with osteophyte formation in the lateral recess or hypertrophic facet joints may produce a monoradiculopathy (Fig. 16-7). Narrowing of the spinal canal by osteophytes, ossification of the posterior longitudinal ligament, or a large central disk may compress the cervical spinal cord. In some patients, a combination of radiculopathy and myelopathy occur. An electrical sensation elicited by neck flexion and radiating down the spine from the neck (Lhermitte's symptom) usually indicates cervical or upper thoracic (T1-T2) spinal cord involvement. When little or no neck pain accompanies the cord compression, the diagnosis may be confused with amyotrophic lateral sclerosis (Chap. 365), multiple sclerosis (Chap. 371), spinal cord tumors (Chap. 368), or syringomyelia (Chap. 368). The possibility of this treatable cervical spinal cord disease must be considered even when the patient presents with leg complaints only. Furthermore, lumbar radiculopathy or polyneuropathy may mask an associated cervical myelopathy. MRI or CT-myelography can define the anatomic abnormalities, and EMG and nerve conduction studies can quantify the severity and localize the levels of motor nerve root injury.

Other Causes of Neck Pain

Rheumatoid arthritis (RA) (Chap. 312) of the cervical apophyseal joints results in neck pain, stiffness, and limitation of motion. In typical cases with symmetric inflammatory polyarthritis, the diagnosis of RA is straightforward. 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 neurologic assessment is important to identify early signs of myelopathy. Occasional patients develop high spinal cord compression leading to quadriparesis, respiratory insufficiency, and death. Although low back pain is common among RA patients, the frequency of facet disease, fracture, and spondylolisthesis is no greater than among age- and sex-matched controls with mechanical low back pain.

Ankylosing spondylitis can cause neck pain and on occasion atlantoaxial subluxation; when spinal cord compression is present or threatened, surgical intervention is indicated. Herpes zoster produces neck and posterior occipital pain in a C2-C3 distribution prior to the outbreak of vesicles. Neoplasms metastatic to the cervical spine, infections (osteomyelitis and epidural abscess), and metabolic bone diseases may also be the cause of neck pain. Neck pain may also be referred from the heart in the setting of coronary artery ischemia (cervical angina syndrome).

Thoracic Outlet

The thoracic outlet is an anatomic region containing the first rib, the subclavian artery and vein, the brachial plexus, the clavicle, and the lung apex. Injury to these structures may result in posture or task-related pain around the shoulder and supraclavicular region. There are at least three subtypes of thoracic outlet syndrome (TOS). True neurogenic TOS results from compression of the lower trunk of the brachial plexus by an anomalous band of tissue connecting an elongate transverse process at C7 with the first rib. Neurologic deficits 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. Definitive treatment consists of surgical division of the anomalous band compressing either the lower trunk of the brachial plexus or ventral rami of the C8 or T1 nerve roots. The weakness and wasting of intrinsic hand muscles typically does not improve, but surgery halts the insidious progression of weakness. The 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. Noninvasive ultrasound techniques confirm the diagnosis. Treatment is with thrombolysis or anticoagulation (with or without embolectomy) and surgical excision of the cervical rib compressing the subclavian artery or vein. The 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; conservative approaches often include multidisciplinary pain management. Treatment is often unsuccessful.

Brachial Plexus and Nerves

Pain from injury to the brachial plexus or arm peripheral nerves can occasionally be confused with 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 (breast carcinoma is the most common setting) or a Pancoast tumor of the lung (Chap. 88) may produce similar findings. A Horner's syndrome is present in two-thirds of patients with a Pancoast tumor. Suprascapular neuropathy may produce severe shoulder pain, weakness, and wasting of the supraspinatous and infraspinatous muscles. Acute brachial neuritis is often confused with radiculopathy. It consists of the acute onset of severe shoulder or scapular pain followed over days to weeks by weakness of the proximal arm and shoulder girdle muscles innervated by the upper or middle trunks or cords of the brachial plexus. The onset is often preceeded by an infection or immunization. Separation of this syndrome from cervical radiculopathy is important because slow, complete recovery of brachial neuritis occurs in 75% of patients after 2 years and in 89% after 3 years. Occasional cases of carpal tunnel syndrome produce pain and paresthesia 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 nerves. For further discussion of peripheral nerve disorders, see Chap. 377.

Shoulder

Pain in the shoulder region can be difficult to separate clearly from neck pain. If the 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. The pain of shoulder disease may at times radiate into the arm or hand, but the sensory, motor, and reflex changes that indicate disease of the nerve roots, plexus, or peripheral nerves are absent.

Treatment

A paucity of well-designed clinical trials exists for the treatment of neck pain. Symptomatic treatment of neck pain can include the use of analgesic medications and/or a soft cervical collar. Current indications for cervical disk surgery are similar to those for lumbar disk surgery; because of the risk of spinal cord injury with cervical spine disease, an aggressive approach is generally indicated whenever spinal cord injury is threatened. Surgical management of cervical herniated 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. The cumulative risk of subsequent radiculopathy or myelopathy at cervical segments adjacent to the fusion is approximately 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 spine disease. Nonprogressive cervical radiculopathy (associated with a focal neurologic deficit) due to a herniated cervical disk may be treated conservatively with a high rate of success. Cervical spondylosis with bony, compressive cervical radiculopathy is generally treated with surgical decompression to interrupt the progression of neurologic signs. Cervical spondylotic myelopathy is typically managed with either anterior decompression and fusion or laminectomy. Outcomes in both surgical groups vary, but late functional deterioration occurs in 20 to 30% of patients; a prospective, controlled study comparing different surgical interventions is sorely needed.

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