CHAPTER 47

Neck and Back Pain

Patients with primary orthopedic or musculoskeletal problems may have symptoms and signs that simulate neurologic disease. Such patients are frequently referred for neurologic consultation, particularly for electromyography (EMG). It is important to be able to recognize musculoskeletal disease in order to provide the appropriate evaluation. In addition, patients with neurologic disease, primarily radiculopathy, may present with pain patterns that can be confused with primary musculoskeletal processes. Patients with neck and arm pain, and back and leg pain, are frequent visitors to the neurologist. This chapter focuses on the clinical characteristics and differential diagnosis of cervical and lumbosacral radiculopathy (LSR), and the following chapter covers common musculoskeletal conditions that often arise in the differential diagnosis of neurologic illness.

Clinical Pathoanatomy of the Spine

The vertebrae are separated by intervertebral discs, which are composed of an outer fibrous ring, the annulus fibrosus, and an inner gelatinous core—the nucleus pulposus (NP). The “posterior elements” of the vertebral bodies spread out to encircle the spinal cord and form the spinal canal. Extending backward from the vertebral body, with varying degrees of slant, are the pedicles. The pedicles end in a bony mass, which has smooth upper and lower surfaces—the superior and inferior articulating facets, which are separated by the pars interarticularis. From the facet masses, the transverse processes jut laterally, and the laminae extend backward to join in the midline and complete the circle. From the junction point of the laminae, the spinous process extends backward a bit farther (Figure 47.1). The lateral recess is the corner formed by the pedicle, vertebral body, and superior articular facet (Figure 47.2).

FIGURE 47.1 Lateral view of the cervical spine. Shows the vertebral bodies separated by intervertebral discs, the pedicles merging into the facet joint with its superior and inferior facets, and intervening pars interarticularis. The facets are oblique in the cervical region and more vertical in the lumbosacral spine. The uncovertebral joints are not true joints but just the opposing surfaces of the vertebral bodies. The uncovertebral processes may form osteophytes, or “spurs,” which then project into the foramen. (From Campbell WW. Essentials of Electrodiagnostic Medicine. Philadelphia: Lippincott Williams & Wilkins, 1999. Reprinted with permission of Dr. William W. Campbell.)

FIGURE 47.2 Cross section of a vertebral body with one pedicle cut away to show the contents of the intervertebral foramen, with the dorsal root ganglion lying in the midzone. Note the location of the multifidus muscle compartment and the innervation of the paraspinal muscles by the posterior primary ramus. The posterior longitudinal ligament is incomplete laterally, and disc ruptures tend to occur in a posterolateral direction. When a facet joint becomes enlarged because of osteoarthritis, it may encroach on the lateral recess, where the nerve root is entering the foramen. (From Campbell WW. Essentials of Electrodiagnostic Medicine. Philadelphia: Lippincott Williams & Wilkins, 1999. Reprinted with permission of Dr. William W. Campbell.)

The mixed spinal nerve passes outward from the spinal canal through the intervertebral foramen. The foramen is a passageway formed by the vertebral body anteriorly; pedicles above and below; and the facet mass and its articulation, the zygapophyseal joint, posteriorly. The neural foramen has an entrance, a middle zone, and an exit. The lateral recess of the spinal canal merges into the entry zone of the foramen. The dorsal root ganglion (DRG) occupies the midzone. The uncovertebral joints (of Luschka), which are not true joints, are the points where the posterolateral surface of a cervical vertebra comes into apposition with a neighboring vertebra. Degenerative osteophytes projecting into the intervertebral foramen from the uncovertebral “joints” may narrow it and cause radiculopathy (Figure 47.1). The uncovertebral joints are not present in the lumbosacral spine.

The tough anterior longitudinal ligament (ALL) extends lengthwise along the anterior aspect of the vertebral column, providing anterior reinforcement for the annulus. The posterior longitudinal ligament (PLL) extends along the posterior aspect of the vertebral bodies and reinforces the discs posteriorly. Compared with the ALL, the PLL is weak and flimsy and narrows as it descends. Disc herniations tend to occur posterolaterally, especially in the lumbosacral region, in part because of the lateral incompleteness of the PLL. In the cervical region, the PLL may ossify and contribute to spondylotic narrowing. The ligamentum flavum extends along the posterior aspect of the spinal canal. It buckles and folds during neck extension and may also contribute to canal narrowing.

The static anatomy of the spine provides only a partial understanding of the changes that occur on motion. Direct measurements have shown that the pressure within a lumbar disc varies markedly with different postures and activities. It is lowest when lying supine, increases by fourfold on standing, and increases a further 50% when leaning forward. The pressure is 40% higher sitting than standing. The higher pressure when sitting is clinically relevant, as patients with lumbosacral disc ruptures characteristically have more pain sitting than standing. The intradiscal pressure during a sit-up is astronomical.

The size of the intervertebral foramina decreases with extension and with ipsilateral bending. In extension, the facet joints draw closer together and the posterior quadrants of the spinal canal narrow. Cervical roots stretch with flexion and may angulate at the entrance to the foramen. The intraspinal subarachnoid pressure varies with respiration and increases markedly with Valsalva or restriction of venous outflow. The epidural and radicular veins change in size with posture and respiration. These dynamic changes, which are especially relevant in the presence of pathology, form the basis for clinical tests and historical questions useful for distinguishing the various causes for back and neck pain.

The Intervertebral Disc

The annulus provides circumferential reinforcement for the disc; the spherical NP allows the vertebral bodies above and below to glide and slip across it, like a ball bearing. The NP is eccentrically placed, closer to the posterior aspect of the disc (Figure 47.2). The relative thinness of the annulus posteriorly is another factor contributing to the tendency of disc herniations to occur in that direction. The great majority of the weight-bearing function of a normal disc is borne by the NP, which contains proteoglycans, macromolecules that heartily imbibe fluid. Early in life, the NP is 90% water, but it undergoes progressive desiccation over time. With desiccation of the nucleus and loss of compressibility, the annulus must assume more of the weight burden. This increased load, in the face of its own degenerative weakening, then makes the annulus prone to tears.

The Spinal Roots

The anatomy of the spinal nerve is shown in Figure 24.3. Myotomal anatomy is discussed in Chapter 27 and dermatomal anatomy in Chapters 31 and 36. In the cervical spine, the nerve root exits over the vertebral body of like number until the C8 root exits beneath C7; all subsequent roots exit beneath the vertebral body of like number (Figure 24.1). In contrast to LSR, where disease usually affects the spinal root exiting one vertebral level lower, that is, disease at the L4-L5 level affects the L5 root, cervical radiculopathy (CR) tends to affect the nerve root laterally at its level of exit. Disease at the C5-C6 vertebral level affects the C6 root and at the C6-C7 level, the C7 root. When the cord terminates at the level of L1-L2, the remaining roots drop vertically downward in the cauda equina to their exit foramina. The L5 nerve root exiting at the L5-S1 interspace has arisen as a discrete structure at L1-L2 and had to traverse the interspaces at L2-L3, L3-L4, and L4-L5 before exiting at L5-S1, sliding laterally all the while. The L5 root could be injured by a central disc at L2-L3 or L3-L4, a posterolateral disc at L4-L5, or a far lateral disc or lateral recess stenosis at L5-S1 (Figure 47.3). A posterolateral disc at L4-L5 is the most likely culprit but not the sole suspect. The clinician must correlate the clinical localization of a given root lesion with the radiographic and clinical information to deduce the vertebral level involved and the proper course of action.

FIGURE 47.3 Posterior view of the cauda equina with exiting nerve roots. The nerve roots move laterally en route to their exit foramina. A posterolateral herniation of the nucleus pulposus (HNP) has compressed the S1 root as it passes by the L5-S1 interspace. A central HNP at any interspace could affect multiple roots. (From Campbell WW. Essentials of Electrodiagnostic Medicine. Philadelphia: Lippincott Williams & Wilkins, 1999. Reprinted with permission of Dr. William W. Campbell.)

With aging and recurrent micro- and macrotrauma, degenerative spine disease develops. This involves both the disc (degenerative disc disease or DDD) and the bony structures and joints (degenerative joint disease or DJD). These processes are separate but related. Together, DDD and DJD are referred to as spondylosis. Small tears in the annulus may cause nonspecific, nonradiating neck or back pain. More extensive tears lead to disc bulging or protrusion, in which the disc herniates but remains beneath the PLL. Frank ruptures breach the PLL and allow a full-blown herniation of the nucleus pulposus (HNP) into the epidural space. Most HNPs occur in a posterolateral direction; occasionally, they are directly lateral or central. Which nerve roots are damaged depends largely on the direction of the herniation. In the face of disc herniation, the root may be damaged not only by direct compression but also by an inflammatory process induced by intradiscal proteoglycans, ischemia due to pressure, and adhesions and fibrosis.

The anterior elements, vertebral body and pedicles, normally bear 80% to 90% of the weight. As degenerative changes advance with desiccation and loss of disc height, the posterior elements (facets, pars, and laminae) may come to carry up to 50% of the weight-bearing function. This increases the work of the posterior elements and accelerates their degenerative changes. They react to the increased weight-bearing role by becoming hypertrophic and elaborating osteophytes. Osteoarthritis and synovitis of the facet joints is another point of pathology. In response to the increased loading attendant on loss of disc height and shift of weight bearing posteriorly, the facet joints develop degenerative changes: laxity of the capsule, instability, subluxation, and bony hypertrophy with osteophyte formation. The friction induced by minor instability and microtrauma leads to the formation of osteophytes. In the cervical spine, there is the added element of hypertrophy of the uncinate processes and the development of uncovertebral spurs. Degenerative osteophytes arising simultaneously from the uncus and from the vertebral body end-plate region may become confluent and create a spondylotic bar or ridge that stretches across the entire extent of the spinal canal. Like any arthritic joint, the facet may enlarge, impinging on the intervertebral foramen or the spinal canal, especially in the lateral recess. Loss of disc height causes the PLL and the ligamentum flavum to buckle and bulge into the canal. The degenerative changes in the discs and bony elements eventually produce cervical or lumbar spondylosis and may culminate in the syndrome of spinal stenosis.

All these degenerative changes leave less room for the neural elements. In the sagittal plane, the average cervical spinal cord is about 8 mm and the average cervical spinal canal about 14 mm. A sagittal canal diameter less than 10 mm may put the spinal cord at risk. The epidural space is normally occupied primarily by epidural fat and veins. When disc herniations and osteophytes intrude into the space, the resultant clinical manifestations depend in large part on how much room there is to accommodate them. Patients blessed by nature with capacious spinal canals can asymptomatically harbor a surprising amount of pathology. Patients with congenitally narrow canals and those who have undergone past spinal fusion procedures are at increased risk for developing spinal stenosis. Compression of vascular structures may introduce an additional complication of cord and/or root ischemia.

Several different clinical syndromes may ensue from degenerative spine disease, including the following: simple, single-level radiculopathy; multilevel radiculopathy; cauda equina syndrome; cervical myelopathy; cervical radiculomyelopathy; neurogenic claudication; lateral recess syndrome; and occasionally, a central cord or Brown-Séquard syndrome. Rarely, radiculopathy results from other processes, such as tumor (e.g., neurofibroma, meningioma, metastasis), arachnoid or synovial cysts, infection (e.g., Lyme disease, CMV, epidural abscess), infiltration (e.g., meningeal neoplasia, sarcoidosis), epidural block, irradiation, or ischemia (e.g., diabetes). A common cause of noncompressive radiculopathy is herpes zoster. Reactivation of a latent varicella-zoster virus resident in DRG cells triggers a herpes zoster outbreak (“shingles”). Affected patients develop an extremely painful vesicular rash in the distribution of the involved dorsal root ganglia, usually a single dermatome. Although thoracic segments are involved most often, zoster can strike anywhere. Severe myotomal weakness may result when herpes zoster strikes in the cervical or lumbar enlargements (Figure 4.7). Zoster may also cause plexopathy, mononeuropathy, or radiculoplexus neuropathy. Acute and chronic inflammatory demyelinating polyradiculoneuropathies produce marked abnormalities of the roots.

Because of the varied pathology involved, different types of radiculopathy occur in degenerative spine disease. The process is frequently multifactorial, involving some combination of disc herniation and spondylosis. The most straightforward clinical syndrome is unilateral “soft disc” rupture, an HNP. A similar clinical picture can result from a foraminal osteophyte, a “hard disc,” or spur. Some patients have soft disc superimposed on hard disc. It is clinically, radiologically, and sometimes surgically difficult to distinguish between soft disc and hard disc. Osteophytes, spurs, and foraminal stenosis are more common than simple soft disc in the etiology of CR. In Radhakrishnan et al.’s series, soft disc (i.e., not present in association with significant spondylosis) was responsible in only 22%; the remainder had hard disc or a combination. As a general rule, soft disc is more likely in younger patients. A central HNP may compress the spinal cord or cauda equina.

In compressive radiculopathy, sensory loss occurs in a dermatomal distribution and weakness in a myotomal distribution. Dermatomal sensory loss is less than expected because of extensive overlap in the innervation zones of spinal roots. Investigators used very different techniques to obtain the available dermatome maps (see Chapter 31 and Figure 36.5). The maps of Keegan and Garrett most closely approximate clinical reality. Sensory loss is most readily demonstrated in the signature zones of the major roots. Weakness in radiculopathy is also usually less than expected for a given myotome because most muscles receive multisegmental innervation (see Chapter 27). Disease affecting multiple levels causes much more severe weakness.

Neck and Arm Pain

Pain in the neck or upper extremity is a common clinical problem. Pain may involve the neck, shoulder, arm, forearm, or hand in virtually any combination. Potential causes of neck and arm pain are many. Common neurologic etiologies are CR, degenerative spine disease, brachial plexopathy, and peripheral nerve entrapment. Neck and arm pain of musculoskeletal origin is also common. Neurologic and musculoskeletal etiologies may be difficult to separate.

Cervical Radiculopathy

The population-based study of CR by Radhakrishnan et al. provided a wealth of interesting information. The incidence was highest at ages 50 to 54, with a mean age of 47, a male predominance, and a decline in incidence after age 60. There was a history of physical injury or exertion in only 15%; the most common precipitants were shoveling snow or playing golf. The onset was acute in half, subacute in a quarter, and insidious in a quarter, with the majority of patients symptomatic for about 2 weeks prior to diagnosis. Surgery was done in 26%. The disease tends to recur—some 31% of patients had a previous history of CR, and 32% had a recurrence during follow-up. At last follow-up, 90% of the patients had minimal to no symptoms. Others have noted this favorable long-term prognosis.

A number of clinical conditions may be confused with CR. These primarily include brachial plexopathies, entrapment neuropathies, and nonneuropathic mimickers. The more common musculoskeletal conditions causing confusion include shoulder pathology (bursitis, tendonitis, impingement syndrome), lateral epicondylitis, and de Quervain’s tenosynovitis (see Chapter 48). Cervical myofascial pain, facet joint disease, and cervical vertebral body pathology can cause neck pain with referred pain to the arm. Pain can be referred to the neck, arm, or shoulder from the heart, lungs, esophagus, or upper abdomen.

Clinical Signs and Symptoms in Cervical Radiculopathy

The classic articles by Yoss et al. and Murphey et al. detail the history and examination findings in CR. Yoss et al. evaluated 100 patients with surgically confirmed single-level cervical radiculopathies. The highly and suggestively localizing findings from these 100 patients are summarized in Table 47.1. Murphey et al. reviewed 648 cases of surgically treated single-level cervical radiculopathies. Findings in terms of pain radiation and neurologic deficits were similar to Yoss et al. Murphey et al. emphasized the occurrence of pain in the pectoral region in 20% of their cases; they opined that neck, periscapular, and pectoral region pain was referred from the disc itself and that arm pain was the result of nerve root compression.

TABLE 47.1 Clinical Findings in 100 Cervical Radiculopathy (CR) Patients

In the Radhakrishnan et al. series, cervicobrachial pain was present at the onset in 98% and was radicular in 65%. Paresthesias were reported by 90%, almost identical to the Yoss series. Pain on neck movement was present in 98%, paraspinal muscle spasm in 88%, decreased reflexes in 84% (triceps 50%, biceps or brachioradialis 34%), weakness in 65%, and sensory loss in 33%. In the Levin et al. series, 70% had motor and sensory symptoms, 12% had motor symptoms only, and 18% had sensory symptoms only.

The history, especially patterns of pain radiation and paresthesias, can provide localizing information in suspected CR. Radiating pain on coughing, sneezing, or straining at stool (Dejerine’s sign) is significant but seldom elicited. Increased pain on shoulder motion suggests nonradicular pathology. Relief of pain by resting the hand atop the head is reportedly characteristic of CR, but the author has seen this phenomenon with a Pancoast tumor. Hand paresthesias at night suggest carpal tunnel syndrome, but carpal tunnel syndrome can occur in association with CR (“double crush syndrome”), so nocturnal acroparesthesias do not exclude coexistent radiculopathy.

Physical examination in patients with suspected CR should include an assessment of the range of motion of the neck and arm, a search for root compression signs, detailed examination of strength and reflexes, a screening sensory examination, and probing for areas of muscle spasm or trigger points ( Video 47.1). Patients with either weakness or reduced reflexes on physical examination are up to five times more likely to have an abnormal electrodiagnostic study. A normal physical examination by no means excludes CR (negative predictive value 52%).

The cervical spine range of motion is highly informative. Patients should be asked to put chin to chest and to either shoulder, each ear to shoulder, and to hold the head in full extension; these maneuvers all affect the size of the intervertebral foramen. Pain produced by movements that narrow the foramen suggests CR. Pain on the symptomatic side on putting the ipsilateral ear to the shoulder suggests radiculopathy, but increased pain on leaning or turning away from the symptomatic side suggests a myofascial origin. Radiating pain or paresthesias with the head in extension and tilted slightly to the symptomatic side is highly suggestive of CR (Spurling’s sign or maneuver, foraminal compression test); brief breath holding or gentle Valsalva in this position will sometimes elicit the pain if positioning alone is not provocative. The addition of axial compression by pressing down on the crown of the head does not seem to add much. Spurling’s test is specific but not very sensitive. Light digital compression of the jugular veins until the face is flushed and the patient is uncomfortable will sometimes elicit radicular symptoms: unilateral shoulder, arm, pectoral or scapular pain, or radiating paresthesias into the arm or hand (Viets’ sign). A slight cough while the face is suffused may increase the sensitivity. In the past, clinicians sometimes went so far as to put a blood pressure cuff around the patient’s neck to occlude the jugular veins (Naffziger’s sign). The two eponyms are often used interchangeably, and more often Naffziger’s sign is used for both techniques. Jugular compression is thought to engorge epidural veins or the cerebrospinal fluid reservoirs, which in the normal individual is harmless. But when some element of foraminal narrowing and nerve root pressure exists, the additional compression causes the acute development of symptoms. The same mechanism likely underlies the exacerbation of root pain by coughing, sneezing, and straining. Like Spurling’s test, Viets/Naffziger’s sign is specific but insensitive. It is less useful in LSR than in CR.

An occasional CR patient has relief of pain with manual upward neck traction, particularly with the neck in slight flexion (cervical distraction test). Likely related to the occasional relief of pain by resting the hand on top of the head, some patients have a decrease in pain with shoulder abduction (Bakody’s sign, shoulder abduction relief test, arm abduction sign); this sign is more likely to occur with soft disc herniation. Flexion of the neck may cause Lhermitte’s sign in patients with cervical spondylosis or large disc herniations. Pain or limitation of motion of any upper-extremity joint should signal the possibility of nonradicular pathology. The differentiation of CR from primary shoulder disease (e.g., bursitis, capsulitis, tendonitis, or impingement syndrome) can be particularly difficult (see Chapter 48).

A focused but detailed strength exam should at least assess the power in the deltoids, spinati, biceps, triceps, pronators, wrist extensors, finger extensors, thenar muscles, and interossei. Testing muscles in a position of mechanical disadvantage may help detect mild weakness (see Chapter 27). The sensory exam should concentrate on the hand, and particularly assess touch, because the large, myelinated fibers conveying light touch are more vulnerable to pressure injury than the smaller fibers carrying pain and temperature. Reflex exam should include not only the standard upper-extremity reflexes but the knee and ankle jerks and plantar reflexes as well. Increased lower-extremity reflexes and extensor plantar responses suggest myelopathy complicating the radiculopathy.

Based on the foregoing, Table 47.2 outlines the clinical data that favor the diagnosis of CR.

TABLE 47.2 Clinical Signs and Symptoms That Favor a Diagnosis of Cervical Radiculopathy

Individual Root Lesions

In the cervical spine, C7 root lesions are the most common (±60%), C6 next most common (±20%), with C5 and C8 lesions making up about equal proportions of the remainder. Involvement of the upper cervical roots is rare. In C5 lesions, weakness is most easily detected in the supra- and infraspinatus, deltoid, biceps, and brachioradialis. The rhomboids may also be weak but are difficult to examine. The biceps and brachioradialis reflexes may be depressed. The signature zone for sensory loss lies over the mid-deltoid region. In C6 lesions, weakness is most likely in the biceps, pronator teres, flexor carpi radialis, brachioradialis, and wrist extensors. The biceps and brachioradialis reflexes may be depressed. If there is concomitant myelopathy, along with reflex depression, spread to the finger flexors or frank “inversion” of the reflex may occur (see Chapter 38). The signature zone for sensory loss lies along the radial aspect of the forearm and the thumb. In C7 lesions, detectable weakness is most common in the triceps (use mechanical advantage), pronator teres, flexor carpi radialis, and wrist and finger extensors. Weakness of the triceps and pronator teres is pathognomonic, because C7 is their only common innervation. Depression of the triceps may be present, and with concomitant myelopathy, it may be inverted (i.e., elbow flexion occurs). The signature zone for sensory loss lies over the middle finger. In C8 lesions, expect weakness in the flexor digitorum profundus and superficialis, flexor pollicis longus, flexor carpi ulnaris, pronator quadratus, extensor indicis, extensor pollicis longus and brevis, and all hand intrinsics. The finger flexor reflex, and rarely the triceps, may be depressed. The signature zone for sensory loss is the small finger and medial forearm.

A study of 69 patients with magnetic resonance imaging (MRI) confirmed C6 and C7 nerve root compression found that arm pain and sensory symptoms were diffuse and not distinctly different for C6 or C7 radiculopathy. Weakness was reported by 41% of patients, and the specific pattern of weakness had only limited value in discriminating between the levels.

Lumbosacral Radiculopathy

About 70% of humans suffer from at least an occasional episode of low back pain (LBP), but clinically significant radiculopathy occurs in only 4% to 6% of the population. Abnormalities on imaging studies are common in asymptomatic subjects and only loosely associated with symptoms and signs. Most benign self-limited episodes of LBP arise from musculoligamentous structures, and discomfort is localized to the low back region. There are numerous pain-sensitive structures that can underlie a clinical episode of LBP: the intervertebral disc, especially the outer fibers of the annulus; the facet joints; other bony structures; subcutaneous tissues; the meninges; the paravertebral muscles and ligaments; and spinal nerve roots. Pain can also be referred to the lower back from visceral structures in the abdomen and pelvis. The back may also be involved in systemic diseases, such as spondyloarthropathies.

Involvement of some of these pain-sensitive structures can produce referred pain that radiates to the extremity (buttock, hip, thigh) and can simulate the radiating pain of nerve root origin. In some patients, there is referred pain to one or both lower extremities that arises from within the disc or other structures, without actual nerve root compression. Considerable pain can be referred to the buttock and thigh with disease limited to the disc, the facet joint, or the sacroiliac joint. A study of 1,293 cases of LBP concluded that referred pain to the lower limb most often originated from sacroiliac and facet joints. Referred pain to the extremity occurred nearly twice as often as true radicular pain and frequently mimicked the clinical presentation of radiculopathies. A study of 92 patients with chronic LBP concluded that 39% had annular tears or other forms of internal disc disruption as the etiology of their pain.

Clinical Signs and Symptoms in Lumbosacral Radiculopathy

Deyo et al. reviewed the information that could be obtained from the history and physical examination in patients with LBP and suggested three basic questions: (a) is there a serious, underlying systemic disease present? (b) is there neurologic compromise that might require further evaluation? and (c) are there psychological factors leading to pain amplification? Things that suggest underlying systemic disease include the following: a history of cancer, unexplained weight loss, pain lasting longer than 1 month, pain unrelieved by bed rest, fever, focal spine tenderness, morning stiffness, improvement in pain with exercise, and failure of conservative treatment. Other symptoms suggesting serious pathology include bowel and bladder disturbances, perineal sensory loss, and a history of violent trauma.

Pain radiating below the knee is more likely of true radicular origin than pain radiating only to the posterior thigh. The relationship of the pain to position and exercise is important. The pain of an HNP is typically more severe when the patient is seated than when standing but is usually increased by activity, particularly bending, twisting, lifting, or stooping, especially when the knees are extended. Other common causes of LBP, such as muscle strain, osteoarthritis, and spinal stenosis cause pain that is worse when standing. Nonmechanical pain is unrelated to posture, position, or activity. Pain that is constant, progressive, and nonmechanical is more likely to indicate serious underlying pathology. Radicular pain is characteristically intensified by coughing, straining, and sneezing. The pain of a spinal cord tumor may also be aggravated by increasing the intracranial or intraspinal pressure but is typically more severe when the patient is lying down than when seated.

The utility, or lack thereof, of various physical examination findings has been studied. The straight leg raising (SLR, Lasègue) test remains the mainstay in detecting radicular compression. The test is performed by slowly raising the symptomatic leg with the knee extended (Figure 47.4, Video 47.2). Pain caused by flexing the hip with the knee bent is suggestive of hip disease. The FABERE or Patrick’s test also checks for hip disease (see Chapter 48). During SLR, tension is transmitted to the nerve roots between about 30 and 70 degrees and pain increases. Pain at less than 30 degrees raises the question of nonorganicity, and some discomfort and tightness beyond 70 degrees is routine and insignificant. There are various degrees or levels of positivity. Ipsilateral leg tightness is the lowest level; pain in the back, more significant; and radiating pain in the leg, highly significant. When raising the good leg produces pain in the symptomatic leg (crossed SLR), the likelihood of a root lesion is very high. Rarely, SLR may even cause numbness and paresthesias in the distribution of the affected nerve root. The buckling sign is knee flexion during SLR to avoid sciatic nerve tension. Kernig’s sign is an alternate way of stretching the root (see Chapter 52).

FIGURE 47.4 Method of eliciting straight leg raising (Lasègue’s sign).

Various SLR modifications may provide additional information; all of these variations are referred to as root stretch signs. The pain may be more severe, or elicited sooner, if the test is carried out with the thigh and leg in a position of adduction and internal rotation (Bonnet phenomenon). The SLR can be enhanced by passively dorsiflexing the patient’s foot (Bragard’s sign) or great toe (Sicard’s sign) just at the elevation angle at which the increased root tension begins to produce pain (Figure 47.5). The term Spurling’s sign is also used for either of these. A quick snap to the sciatic nerve in the popliteal fossa just as stretch begins to cause pain (bowstring sign or popliteal compression test) accomplishes the same end and may cause pain in the lumbar region, in the affected buttock, or along the course of the sciatic nerve. In severe cases, pain may be elicited merely by dorsiflexion of the foot or great toe as the patient lies supine with legs extended. A similar modification may be carried out by flexing the thigh to an angle just short of that necessary to cause pain and then flexing the neck; this may produce the same exacerbation of pain that would be brought about by further flexion of the hip (Brudzinski’s sign). Occasionally, the pain may be brought on merely by passive flexion of the neck when the patient is recumbent with legs extended. The pain with SLR should be the same with the patient supine or seated. Failure of a patient with a positive supine SLR to complain or lean backward when the extended leg is brought up while in the seated position (e.g., under the guise of doing the planter response) suggests nonorganicity. In the sitting position, the patient may be able to extend each leg alone but extending both together causes radicular pain (Bechterew’s test).

FIGURE 47.5 Accentuation of straight leg raising by dorsiflexion of either the foot or the great toe.

In O’Connell’s test, SLR is first carried out on the sound limb, and the angle of flexion and site of pain are recorded; the pain may be on the opposite side. Then, SLR is carried out on the affected limb, and the angle and site of pain again noted. Then, both thighs are flexed simultaneously, keeping the knees extended. The angle of flexion permitted may be greater than that allowed when either the affected limb or the sound limb is flexed alone. Finally, with both thighs flexed to an angle just short of that which produces pain, the sound limb is lowered; this may result in a marked exacerbation of pain, sometimes associated with paresthesias. The patient may be able to do a sit-up with the knees flexed but not extended (Kraus-Weber test).

The reverse SLR (femoral stretch or Ely test) is a way of eliciting root stretch in the evaluation of high lumbar radiculopathy (Figure 47.6). The patient lies prone, and the knee is pulled into maximum flexion, or the examiner pulls upward on the extended knee to passively extend the hip. In the bent knee pulling test, the patient’s knee is flexed and the examiner pulls upward on the ankle while pushing the buttock forward (in the same way as for eliciting the psoas sign used in the diagnosis of appendicitis). In all these variations, the normal individual should complain only of quadriceps tightness. With disc disease, there is pain in the back or in the femoral nerve distribution on the side of the lesion.

FIGURE 47.6 Reverse straight leg raising (femoral nerve stretch test) for evaluation of suspected high lumbar radiculopathy. (Modified with author’s permission from Reeves AG, Swenson RS. Disorders of the Nervous System: A Primer. New Haven: Dartmouth Medical School, 2004. Retrieved on August 28, 2018. http://www.dartmouth.edu/~dons/index.html. Copyright © 2008 Reeves.)

The examiner should also look for abnormalities of posture, deformities, tenderness, and muscle spasm. With radiculopathy, there may be loss of the normal lumbar lordosis because of involuntary spasm of the paravertebral muscles. In addition, there is often a lumbar scoliosis, with a compensatory thoracic scoliosis. Most commonly, the list of the body is away from the painful side, and the pelvis is tilted so that the affected hip is elevated (Figure 47.7). The patient attempts to bear weight mostly on the sound leg. The list and scoliosis may sometimes be toward the painful side, and the patient’s body may be bent forward and toward that side to avoid stretching the involved root. With very severe sciatic pain, the patient will avoid complete extension at the knee and may place only the toes on the floor because dorsiflexion of the foot aggravates the pain by stretching the nerve. The patient may walk with small steps and keep the leg semiflexed at the knee. In bending forward, she flexes the knee to avoid stretching the nerve (Neri’s sign). When sitting, she keeps the affected leg flexed at the knee and rests her weight on the opposite buttock. She may rise from a seated position by supporting herself on the unaffected side, bending forward, and placing one hand on the affected side of the back (Minor’s sign). There may be areas of tenderness in the lumbosacral region, and manipulation or percussion over the spinous processes, or pressure just lateral to them, may reproduce or exacerbate the pain. A sharp blow with a percussion hammer on or just lateral to the spinous processes while the patient is bending forward may bring out the pain. There may be spasm not only of the paravertebral muscles but also of the hamstrings and calf muscles. Flexion, extension, and lateral deviation of the spine are limited; the pain is usually accentuated with passive extension of the lumbar spine toward the affected side while the patient is standing erect. There may be localized tenderness at the sciatic notch and along the course of the sciatic nerve. Pelvic and rectal examination may be necessary in some instances.

FIGURE 47.7 Curvature of the vertebral column associated with unilateral paraspinal muscle spasm. Unilateral spasm causes the spine to curve with the concavity toward the spasm (B). Because of the broad attachment of the paraspinal muscles to the sacrum and the ilium at the lumbosacral junction, the convexity appears on the side of the spasm (A). (Modified from Reeves AG, Swenson RS. Disorders of the Nervous System: A Primer. New Haven: Dartmouth Medical School, 2004. Retrieved on August 28, 2018. http://www.dartmouth.edu/~dons/index.html)

The neurologic examination should include assessment of power in the major lower-extremity muscle groups, but especially the dorsiflexors of the foot and toes and the evertors and invertors of the foot. Plantar flexion of the foot is so powerful that manual testing rarely suffices. Having the patient do 10 toe raises with either foot is a better test. As the patient is standing on one leg, look for Trendelenburg’s sign (Chapter 27). Normally, the pelvis remains level or slants upward toward the unsupported leg. With a positive Trendelenburg, the hip moves laterally and up and the shoulder moves down on the weight-bearing side, and the pelvis sags toward the unsupported leg (see Video Link 47.1). On walking, weakness of the hip abductors, primarily the L5-S1 innervated gluteus medius, causes the weight-bearing leg to adduct and the hip to jut laterally on the affected side (Trendelenburg gait, gluteus medius lurch). Trendelenburg’s sign or gait may occur with other processes causing hip abductor weakness, for example, superior gluteal neuropathy or myopathy, and may also occur with musculoskeletal disease, such as hip dislocation, fracture of the femoral head, or coxa vara. The peroneal reflex is sometimes useful (see Video Link 47.2).

In addition to assessing power, it is important to look for atrophy and fasciculations. Sensation should be tested in the signature zones of the major roots. The status of knee and ankle reflexes reflects the integrity of the L3-L4 and S1 roots, respectively. There is no good reflex for the L5 root, but the hamstring reflexes are sometimes useful (see Chapter 38). An occasional L5 radiculopathy produces a clear selective diminution of the medial hamstring reflex.

Tests for nonorganicity are useful in the evaluation of LBP ( Video 47.2). Waddell et al. identified a set of eight nonorganic signs in 1980, and the overall Waddell score is considered positive if at least three of the signs are positive. The usefulness of the Waddell score remains controversial, and it suggests at least the possibility of somatic amplification and the contribution of psychosocial factors to the clinical picture. Imaging studies show that while there is more overall pathology in patients without Waddell signs, many of these patients have significant spinal pathology. Pain during simulated spinal rotation, pinning the patient’s hands to the sides while rotating the hips (no spine rotation occurs as shoulders and hips remain in a constant relationship) suggests somatic amplification. Also useful are a discrepancy between the positivity of the SLR between the supine and seated position, pain in the back on pressing down on top of the head, widespread and excessive “tenderness” (touch-me-not sign), general overreaction during testing, and nondermatomal/nonmyotomal neurologic signs.

The major lumbosacral radicular syndromes include HNP, lateral recess stenosis, and spinal stenosis with cauda equina compression. Virtually all patients with radiculopathy have sciatica. The odds of a patient without sciatica having radiculopathy have been estimated at 1:1,000. With HNP or lateral recess stenosis, leg pain usually predominates over back pain. With HNP, the pain is typically worse when sitting, better when standing, better still when lying down, and generally worse in flexed than extended postures—all reflecting the known changes in intradiscal pressure that occur in these positions. With lateral recess stenosis, the pain is worse with standing or walking because of spinal extension, relieved by sitting with the torso flexed or by lying down. Patients with HNP tend to have a positive SLR, those with recess stenosis do not. The essence of the recess stenosis picture then is pain on standing, lack of pain on sitting, and a negative SLR. The essence of the HNP picture is pain worse on sitting, lessened with standing, and a positive SLR. Patients with HNP are usually in the 30 to 55 age range, and those with lateral recess stenosis are a bit older. As with CR, pain may exacerbate with cough, sneeze, or Valsalva.

Individual Root Lesions

In LSR, the root is most often compromised at the level above its level of exit, but foraminal pathology at the exit level or a central disc at levels above may cause damage as the root exits or passes by in its descent.

The most common LSRs involve either L5 or S1. Upper lumbar radiculopathies are rare. Disease of S2-S5 is usually part of a cauda equina syndrome (see below). In L5 lesions, weakness primarily occurs in the tibialis anterior, extensor hallucis longus, tibialis posterior, and extensor digitorum longus and brevis. When severe the patient may have a footdrop. In this setting, the presence or absence of involvement of the tibialis posterior is critical in distinguishing between an L5 radiculopathy and a peroneal nerve palsy. Involvement of the tibialis posterior suggests radiculopathy. Careful examination may reveal weakness of the gluteus medius, tensor fascia lata, flexor digitorum longus, and hamstrings. The knee and ankle reflexes are normal, but the medial hamstring and peroneal reflexes are sometimes depressed. The signature zone for sensory loss is over the dorsum of the foot. Rarely, neurogenic hypertrophy of the tibialis anterior occurs.

In S1 lesions, weakness occurs primarily in the gastrosoleus. Because this muscle is so powerful, hand strength testing often fails to detect weakness (see above). Further testing may reveal weakness of the gluteus maximus, hamstrings, and toe flexors. The ankle reflex and the plantar stretch reflex (see Chapter 38) are often depressed; the subtlest evidence is asymmetry of the ankle reflexes on very careful testing as by having the patient in a kneeling position. The signature zone for sensory loss is along the lateral border of the foot. Neurogenic hypertrophy of the calf happens rarely.

Spinal Stenosis

As patients mature into the seventh decade and beyond, the liability to disc rupture decreases, but degenerative spine disease attacks in a different form. Osteophytic spurs and bars; bulging discs; thickened laminae and pedicles; arthritic, hypertrophied facets; and thickened spinal ligaments all combine to narrow the spinal canal and produce the syndrome of spinal stenosis. Because of the diffuse involvement, there is commonly evidence of multilevel LSR. An extension posture contributes to spinal stenosis by causing narrowing of the foramina and dorsal quadrants and buckling of the ligamentum flavum. Narrowing of the canal compresses neural and possibly vascular structures. Flexing the spine, as by leaning forward, stooping over, or sitting down opens the canal and decreases the symptomatology.

A common feature of lumbar spondylosis is neurogenic claudication (claudication of the cauda equina, pseudoclaudication), generally attributed to mechanical pressure on the nerve roots and blood vessels of the cauda equina. Such pain in the legs on walking can be easily confused with vascular claudication. Patients with spinal stenosis and neurogenic claudication experience pain, weakness, numbness, and paresthesias/dysesthesias when standing or walking. Prolonged standing, as at a cocktail party, often exacerbates the symptoms. An occasional patient will have a bizarre symptom, such as spontaneous erections or fecal incontinence brought on by walking. Differentiation from vascular claudication is made by the wide distribution of symptoms, the neurologic accompaniments, and the necessity to sit down for relief (Table 47.3). Vascular claudication tends to produce focal, intense, crampy pain in one or both calves, and the pain subsides if the patient just stops and stands. Patients with vascular claudication have even more symptoms walking uphill because of the increased leg work. Neurogenic claudication may decrease when walking uphill because of the increased spinal flexion in forward leaning. Patients with vascular claudication have as much trouble riding a bicycle as walking because of the leg work involved, whereas forward flexion on the bicycle opens up the spinal canal, allowing patients with neurogenic claudication to ride a bike with greater ease than they can walk. Vespers (L. “evening”) curse, a rare but interesting manifestation of spinal stenosis, often with coincidental CHF, mimics restless legs syndrome (see Chapter 30). The essential difference between neurogenic and vascular claudication is the symptoms are evoked by spine extension in the former and leg exertion in the latter. Table 47.3 lists differential points helpful in distinguishing vascular from neurogenic claudication. Helpful points in the differential diagnosis of back and leg pain are summarized in Table 47.4.

TABLE 47.3 Differential Diagnostic Points in Neurogenic versus Vascular Claudication

TABLE 47.4 Differential Diagnostic Points in Patients with Low Back Pain Syndromes

From Campbell WW. Essentials of Electrodiagnostic Medicine. Philadelphia: Lippincott Williams & Wilkins, 1999. Reprinted with permission of Dr. William W. Campbell.

The table outlines what is generally true; it is not a statement of absolutes.

AH, abductor hallucis; EDB, extensor digitorum brevis; EDL, extensor digitorum longus; EHL, extensor hallucis longus; FDL, flexor digitorum longus; GMD, gluteus medius; GMX, gluteus maximus; HNP, herniated nucleus pulposus; IP, iliopsoas; LHS, lateral hamstring; MHS, medial hamstring; PL, peroneus longus; RF, rectus femoris; SLR, straight leg raising; TA, tibialis anterior; TFL, tensor fascia lata; TP, tibialis posterior.

Conus Medullaris and Cauda Equina Lesions

In conus medullaris lesions, the pathology is limited to the parenchyma of the terminal spinal cord; in cauda equina lesions, the pathology involves multiple nerve roots. A conus lesion is intramedullary; a cauda equina lesion is extramedullary. Some processes may involve both structures, and it is not always possible to make a clear clinical distinction, as many of the manifestations are similar. Favoring a lesion of the conus are prominent and early bowel, bladder, and sexual dysfunction; mild, symmetric lower-extremity motor involvement; and a relative lack of pain. In lesions of the cauda equina, pain is more prominent; bowel, bladder, and sexual dysfunction are less prominent; and motor, sensory, and reflex loss tend to be asymmetric and suggestive of nerve root involvement (Table 47.5).

TABLE 47.5 Signs and Symptoms Differentiating Between Lesions of the Conus Medullaris and Cauda Equina

Thoracic Radiculopathy

Thoracic radiculopathy is most often due to either diabetes (diabetic truncal radiculoneuropathy or thoracoabdominal neuropathy) or herpes zoster. True neurogenic thoracic outlet syndrome primarily affects the T1 root fibers. Compressive radiculopathy occurs very rarely. A lesion of the T1 root may cause weakness of the hand intrinsics, especially the abductor pollicis brevis. The primary representation of the T1 myotome is in the APB. Sensory loss occurs over the medial forearm and in the axilla. Neoplastic invasion of the T1 root may present as relentless axillary pain. Depression of the finger flexor reflex and a Horner’s syndrome may aid in localization. The primary neurologic manifestation of other thoracic radiculopathies is sensory loss in the distribution of the involved root. Rare motor manifestations include abdominal pseudohernia. Notalgia paresthetica causes pain, paresthesias, and pruritus in the distribution of the posterior primary rami of T2-T6 between the spine and the medial border of the scapula; it is relatively common.

MRI has shown that thoracic disc herniations occur much more frequently than previously thought. Still, compressive thoracic radiculopathies occur rarely.

Video Links

Video Link 47.1. Trendelenburg’s sign. https://www.youtube.com/watch?v=DkSTr7K-eAo

Video Link 47.2. The peroneal reflex. http://neurosigns.org/wiki/Peroneal_reflex

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