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Pathophysiology, Natural History, and Clinical EvaluationNeck Pain, Cervical Radiculopathy, and Cervical Myelopathy :

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Neck Pain, Cervical Radiculopathy, and

Cervical MyelopathyPATHOPHYSIOLOGY, NATURAL HISTORY, AND CLINICAL EVALUATION

BY RAJ RAO, MD

An Instructional Course Lecture, American Academy of Orthopaedic Surgeons

Cervical spondylosis is a common and occasionally disabling condition, oc-curring as a natural consequence of aging in the vast majority of the adult population. A clinical approach to symptomatic cervical spondylosis can be simplified by dividing the findings at presentation into the categories of axial neck pain, radiculopathy, myelopathy, or some combination of these three. While the pathogenesis of radiculopathy and myelopathy in cervical spondylosis is better under-stood, the source of neck pain remains controversial. The aim of this lecture is to review the pathophysiology and natural history of each of these con-ditions and to describe the pertinent clinical features of cervical disc pathology.

PathophysiologyNeck PainIn a substantial number of patients, axial neck pain is a result of muscular or ligamentous factors related to pos-ture, poor ergonomics, stress, and/or chronic muscle fatigue. Neck muscle pain can develop secondarily as a re-sult of postural adaptations to a pri-mary source of pain in the shoulder,

the craniovertebral junction, or the temporomandibular joint. The physi-ology of this pain process in the in-volved muscles is unclear. Patients with chronic myofascial pain have been shown to have a lower level of high-energy phosphates in the in-volved muscle tissue1. It is unclear whether this causes the pain or is a result of the pain. Unencapsulated free nerve endings in muscle serve as chemonociceptive and mechanonoci-ceptive units. Chemonociceptive nerve endings may respond to metabolites that accumulate during anaerobic me-tabolism in fatigued muscle, or they may respond to non-neurogenic pain mediators released by injury or is-chemia, such as bradykinin, hista-mine, serotonin, and potassium ions. Mechanonociceptive nerve endings re-spond to stretch or pressure. Sensitiza-tion of these nerve endings may be a primary source of muscle pain.

Attributing axial neck pain to degenerative changes in the cervical discs or facet joints is a source of con-troversy, primarily because of the ubiquitous nature of such changes in the spine. Nevertheless, it does appear that cervical discs and facet joints can

be pain generators. Nerve fibers and nerve endings found in the peripheral portions of the disc2,3 offer a possible mechanism by which degenerated cer-vical discs can produce pain directly. The disc is innervated by the sinuver-tebral nerve, formed by branches from the ventral nerve root and the sympa-thetic plexus3 (Fig. 1). Once formed, the nerve turns back into the inter-vertebral foramen along the posterior aspect of the disc, supplying portions of the annulus, the posterior longi-tudinal ligament, the periosteum of the vertebral body and pedicle, and the adjacent epidural veins. A recent re-view of the findings of cervical discog-raphy performed over a twelve-year period suggested that reliable patterns of pain are produced by stimulation of each cervical disc4 (Fig. 2). The au-thors reported a high percentage of patients in whom multiple discs were concurrently responsible for axial neck pain.

The facet joint is also recognized as a source of axial neck pain. Provo-cative injections into the facet joints in asymptomatic volunteers produce a reproducible pattern of axial neck pain and pain in the shoulder girdle5





(Fig. 3). This pattern of facet-joint-induced pain can be accurately treated by anesthetic injections into the facet joint6, or by blocking the dorsal primary rami7, further suggesting that the facet joints do indeed play a role in the devel-opment of axial neck pain.

Patients with degenerative arthri-tis in the upper cervical joints can present with severe suboccipital pain that radiates down into the neck or to the back of the ear. Injection of the at-lantooccipital and atlantoaxial joints re-sults in a reproducible pain pattern in this region8. Wächli et al. 9 reported uni-lateral headaches and atypical facial pain as a result of degenerative changes at the second and third cervical level. In some patients, suboccipital headaches are presumed to be a result of irritation of the greater occipital nerve, which originates from the posterior rami at the second, third, and fourth cervical levels. Another potential source of sub-occipital pain is the sinuvertebral nerves

from the first, second, and third cervical levels, which ascend cephalad to inner-vate the atlantoaxial ligaments, the tec-torial membrane, and the dura mater of the upper cervical cord and posterior cranial fossa3.

Cervical Radiculopathy and MyelopathyNeurologic symptoms in cervical spondylosis are the result of a cascade of degenerative changes that most likely begin at the cervical disc. Age-related changes in the chemical composition of the nucleus pulposus and annulus fi-brosus result in a progressive loss of their viscoelastic properties. The disc loses height and bulges posteriorly into the canal. With this loss of height, the vertebral bodies drift toward one an-other. Posteriorly, there is infolding of the ligamentum flavum and facet joint capsule, causing a decrease in canal and foraminal dimensions. Osteophytes form around the disc margins and at the uncovertebral and facet joints. The posteriorly protruded disc material, os-teophytes, or thickened soft tissue within the canal or foramen results in extrinsic pressure on the nerve root or spinal cord.

Mechanical distortion of the nerve root may lead to motor weakness or sensory deficits. The exact pathogen-esis of radicular pain is unclear, but it is generally thought that, in addition to the compression, an inflammatory re-sponse of some kind is necessary for pain to develop. Within the com-pressed nerve root intrinsic blood ves-sels show increased permeability, which secondarily results in edema of the nerve root. Chronic edema and fibrosis within the nerve root can alter the re-

Fig. 1

Cross-sectional view showing the cervical nerve root, dorsal and ventral primary rami, recurrent

meningeal or sinuvertebral nerve, and sympathetic plexus. Note the proximity of the disc space,

vertebral artery, and facet joints. (Reprinted, with permission, from: Cramer GD, Darby SA,

editors. Basic and clinical anatomy of the spine, spinal cord and ANS. St. Louis: Mosby Year-

Book; 1995. p 141.)

TABLE I Chemical Mediators of Spinal Pain7

Neurogenic Non-Neurogenic

Substance P Bradykinin

Somatostatin Serotonin

Cholecystokinin-like substance Histamine

Vasoactive intestinal peptide Acetylcholine

Calcitonin gene-related peptide Prostaglandin E1

Gastrin-releasing peptide Prostaglandin E2

Dynorphin Leukotrienes

Enkephalin DiHETE

Gelanin

Neurotensin

Angiotensin II





sponse threshold and increase the sen-sitivity of the nerve root to pain10. Neurogenic chemical mediators of pain released from the cell bodies of the sensory neurons and non-neurogenic mediators released from disc tissue may play a role in initiating and perpetuat-ing this inflammatory response11 (Table I). The dorsal root ganglion has been implicated in the pathogenesis of radic-ular pain. Prolonged discharges origi-nate from the cell bodies of the dorsal root ganglion as a result of brief pres-sure. In addition to the chemicals pro-duced by the cell bodies of the dorsal root ganglion, the membrane sur-rounding the dorsal root ganglion is more permeable than that around the nerve root, allowing a more florid local inflammatory response.

Certain positions of the arm may decrease stress within the nerve root and relieve radicular pain. Davidson et al. described the shoulder abduction signi.e., relief of severe radicular pain when the patient rests the hand on the

top of the head12. Davidson et al. theo-rized that, in addition to decreasing tension within the nerve root, this position may lift the sensory root or

dorsal root ganglion directly cephalad or lateral to the source of compression, and decompression of epidural veins may contribute to pain relief.

Fig. 3

Composite map of axial pain patterns

produced by injections into the facet

joints at the second through seventh

cervical levels. (Reprinted, with permis-

sion, from Dwyer A, Aprill C, Bogduk N.

Cervical zygapophyseal joint pain pat-

terns I: a study in normal volunteers.

Spine. 1990;15:453-7.)

Fig. 2

Axial pain patterns provoked during disco-

graphy at each cervical level. A = level

between second and third cervical verte-

brae, B = level between third and fourth

cervical vertebrae, C = level between

fourth and fifth cervical vertebrae, D =

level between fifth and sixth cervical verte-

brae, and E = level between sixth and

seventh cervical vertebrae. (Reprinted,

with permission, from: Grubb SA, Kelly

CK, Bogduk N. Cervical discography: clini-

cal implications from 12 years of experi-

ence. Spine. 2000; 25:1382-9.)





Cervical spondylotic myelopathy is the manifestation of long-tract signs resulting from a decrease in the space available for the cervical spinal cord. In addition to the spondylotic processes that contribute to the extrinsic pressure (Fig. 4), certain factors are thought to be important in the development of myelopathy; these include the anterior-posterior diameter of the spinal canal, dynamic cord compression, dynamic changes in the intrinsic morphology of the spinal cord, and the vascular supply of the spinal cord.

A congenital decrease in the anterior-posterior diameter of the spinal canal can play a role in the de-velopment of cervical myelopathy. The anterior-posterior diameter of the sub-axial spine in normal adults measures 17 to 18 mm, and the diameter of the spinal cord is approximately 10 mm in this region. Individuals with an anterior-posterior diameter of the spinal canal of <13 mm are considered to have congen-ital cervical stenosis. There is a strong association between flattening of the cord within the narrowed spinal canal and the development of cervical my-elopathy. Penning et al.13 believed that symptoms of cord compression oc-curred when the transverse area of the cord was <60 mm2. Houser et al. thought that the shape and degree of

flattening of the spinal cord could be an indicator of neurologic deficit; 98% of their patients with severe stenosis and a banana-shaped spinal cord had clinical evidence of myelopathy14. Ono et al. de-scribed an anterior-posterior cord-compression ratio that was calculated by dividing the anterior-posterior di-ameter of the cord by the transverse di-ameter of the cord15 (Fig. 5). Patients with substantial flattening of the cord, suggested by an anterior-posterior ra-tio of <0.40 tended to have worse neu-rologic function. Ogino et al. thought that an increase in this ratio to ≥0.40 or an increase in the transverse area to >40 mm2 was a strong predictor of recovery following surgery16.

Dynamic factors in the cervical spinal column affect the degree of cord compression. Hyperextension narrows the spinal canal by shingling the lami-

nae and buckling the ligamentum fla-vum. Translation or angulation between vertebral bodies in flexion or extension can result in narrowing of the space available for the cord. Patients who do not have cord compression stat-ically may compress the cord dynami-cally, leading to the development of myelopathic symptoms17. Retrolisthesis of a vertebral body can result in pinch-ing of the spinal cord between the inferior-posterior margin of a vertebral body and the superior edge of the lam-ina caudad to it (Fig. 6). This compres-sion may be aggravated in extension, and it may be relieved in flexion as the retrolisthesis tends to reduce. Forward slippage of a vertebral body may cause compression of the spinal cord between the superior-posterior margin of the vertebral body below and the lamina above. This is aggravated by flexion of

Fig. 4

Degenerative changes that contribute to compression of the

spinal cord in cervical myelopathy. OPLL = ossification of the

posterior longitudinal ligament. (Reprinted from: Bernhardt

M, Hynes RA, Blume HW, White AA. Current concepts review:

cervical spondylotic myelopathy. J Bone Joint Surg Am.

1993;75:119-28.)

Fig. 5

Determination of the anteroposterior

compression ratio (AP) in patients with

myelopathy. AP = b/a × 100. (Reprinted,

with permission, from: Ono K, Ota H,

Tada K, Yamamoto T. Cervical myelop-

athy secondary to multiple spondylotic

protrusion: a clinico-pathologic study.

Spine. 1977;2:109-25.)





the spinal column. Hypermobility cephalad to a degenerated and stiffened segment is commonly seen at the third and fourth cervical levels in elderly individuals, and it may result in myelopathy18.

Morphologic changes also occur within the spinal cord itself with flex-ion and extension. Breig et al. showed that the spinal cord stretches with flex-ion of the cervical spine and shortens and thickens with extension19. Thicken-ing of the cord in extension makes it more susceptible to pressure from the infolded ligamentum flavum or lam-ina. In flexion, the stretched cord may be prone to higher intrinsic pressure if it is abutting against a disc or a vertebral body anteriorly.

In 1924, Barre was apparently the first to propose that vascular factors play a role in the development of cer-vical myelopathy20. Acute or subacute development of myelopathy in the ab-sence of a mechanical compression of the spinal cord is thought to be pathog-nomonic in these patients21. There is some experimental evidence to support a role for vascular factors in the patho-genesis of myelopathy. Cervical cord is-chemia superimposed on compression of the cord resulted in dramatic neuro-logic findings in two separate experi-ments involving canines22,23. The effects of compression and ischemia were thought to be additive and responsible for the clinical manifestation of my-elopathy. In a separate study, obstruc-tion of the peripial arterial plexus in dogs caused structural changes within the spinal cord24. The classic study by

Breig et al. showed that blood flow through the anterior spinal artery and anterior radicular arteries may be re-duced when those vessels are tented over a disc or a vertebral body, but flow through the tortuous posterior spinal arteries is not substantially affected in this position19. Vessels that are thought to be most prone to reduced flow are the transverse intramedullary arterioles arising from the anterior sulcal arteries. These vessels perfuse the gray matter and adjacent lateral columns25.

Severe compression results in de-generative changes in the spinal cord. The central gray matter and the lateral columns show the most changes, with cystic cavitation, gliosis, and demyeli-nation most prominent caudad to the site of compression. The posterior col-umns and posterolateral tracts show wallerian degeneration cephalad to the site of compression. These irreversible changes may explain why some pa-tients do not recover following decom-pressive surgery.

Natural HistoryThere are few population-based studies on the prevalence of neck pain. A recent study of a Saskatchewan adult popula-tion showed that neck pain is more prevalent than commonly perceived: 66% of adults experienced neck pain during their lifetime, with 54% having experienced it during the past six months and 5% highly disabled by it26. Another population study demon-strated a 9% point prevalence of neck and shoulder pain27. The prevalence of neck pain appears to be higher in better

educated individuals with a history of injury, headaches, or low-back pain28.

DePalma et al. found that most patients with axial symptoms from cer-vical spondylosis do reasonably well29. They reported that, following three months of nonoperative care, 21% of patients had complete relief of symp-toms, 49% had partial relief, and 22% had no relief. Rothman and Rashbaum found that 23% of a similar group of patients remained partially or totally disabled at the end of five years30. In the same study, they found no substantial difference between that group of nonoperatively treated patients and another group of patients with “pre-dominantly” axial neck pain who had undergone surgery. They recommended nonoperative management for axial symptoms.

In 1963, Lees and Turner re-ported on the natural history and prog-nosis of cervical spondylosis31. Fifty-one patients in their “non-myelopathic group” had pain in the neck, shoulders, arms, or hands. Patients were treated with a collar, exercises, traction, manip-ulation, and rest. Of ten patients who were followed for ten to nineteen years, three had no symptoms after the first few months of treatment, three contin-ued to have mild symptoms, and four had more troublesome symptoms. Of forty-one patients who were followed for two to ten years, nineteen had no symptoms, twelve had intermittent symptoms, and ten had moderate dis-ability. Myelopathic symptoms did not develop in any of the patients during the course of the nineteen-year follow-up period. It appears that, while approxi-mately 45% of patients with non-myelopathic symptoms have good reso-lution of those symptoms shortly after onset, the remaining 55% continue to have minor or moderate long-term morbidity. Nonoperative treatment ap-peared to alleviate symptoms without influencing the eventual outcome.

Gore et al. carried out a clinical and radiographic study of 205 patients who had presented with axial neck pain or radicular symptoms in the upper extremities32. One hundred and sixty-one of these patients were treated with

Fig. 6

Dynamic compression of the spinal cord with flexion and extension of the spinal column. (Re-

printed from: Bernhardt M, Hynes RA, Blume HW, White AA. Current concepts review: cervical

spondylotic myelopathy. J Bone Joint Surg Am. 1993;75:119-28.)





rest, traction, a collar, medications, or combinations of these modalities. At the time of follow-up at ten to twenty-five years, 43% had complete resolution of pain, 25% had mild residual pain, and 32% had moderate or severe residual pain. Patients with radicular symptoms or findings had a less favorable progno-sis. Treatment did not appear to influ-ence the eventual outcome. The pain could not be correlated to the degenera-tive changes seen on radiographs. Gore et al. concluded that many patients with this condition have long-term symp-toms that may be moderately disabling.

The true natural history of cervi-cal myelopathy may be difficult to de-termine because in the vast majority of cases the symptoms are attributed to age or other neurologic conditions. Thus, knowledge of the natural history of this condition has been derived from a select population in whom the dis-ease was already diagnosed and possibly was well established. In 1952, Spillane and Lloyd reported that the course of cervical myelopathy in their patients appeared to be one of progressive disability33. In a 1956 report on 120 pa-tients with cervical spondylotic myelop-athy, Clarke and Robinson stated their belief that, once the disorder was recog-nized, neurologic function never re-turned to normal34. Of their patients, 75% had episodic progression, 20% showed slow steady progression, and 5% had a rapid onset of symptoms fol-lowed by a lengthy period of stability. Sensory and bladder changes tended to be transient, but motor changes tended to persist and to progress over time. A soft collar helped to decrease nerve-root symptoms and improve gait for 50% of their patients.

Lees and Turner reported on a group of forty-four patients who had had symptoms of myelopathy for three to forty years31. They thought that long periods of nonprogressive disability were the rule and progressive deteriora-tion was the exception. Neither the age at the onset of symptoms nor treat-ment with a collar or surgery appeared to influence the eventual prognosis. Nurick reported similar findings: he ob-served that the disability was estab-

lished early in the course of the disease and was followed by static periods last-ing many years35. The prognosis was better for patients who presented with mild disease, and disability tended to progress in patients older than sixty years of age. Symon and Lavender36 re-viewed the results reported by Lees and Turner and found that, when disability was used as a criterion, only 18% of pa-tients showed improvement. In their own series, they reported steady, pro-gressive deterioration in 67% of pa-tients with cervical spondylotic myelopathy. Phillips also thought that the prognosis was poor; only one-third of his patients obtained improvement from treatment with a soft collar, and patients who had had symptoms for more than two years showed no improvement37. A recent multicenter, nonrandomized study by the Cervical Spine Research Society suggested a sim-ilarly poor outcome of nonsurgical management of cervical myelopathy38. In that study of forty-three patients, twenty underwent surgery and twenty-three received medical treatment. The surgically treated patients had de-creased neurologic symptoms and over-all pain and improved functional status, but the nonsurgically treated patients had a decrease in their ability to per-form activities of daily living with wors-ening of neurologic symptoms.

Clinical EvaluationAxial Neck PainNeck pain is an extremely common but nonspecific presenting symptom. The pain or soreness is usually in the para-median neck muscles posteriorly, with radiation toward the occiput or into the shoulder and periscapular regions. The patient reports stiffness in one or more directions, and headaches are common39. The neck pain may be ac-companied by radiating “referred” pain in the shoulder or arm that does not follow a dermatomal distribution. Re-ferred pain can be associated with a sensation of warmth or tingling and with autonomic phenomena such as pi-loerection and sweating. Localized areas of tenderness in the muscle may be present. Deep palpation of some of

these areas, known as trigger points, re-sults in reproducible patterns of re-ferred pain.

In the absence of radicular symp-toms or findings, determining the source of neck pain can be a diagnostic challenge. Identifying a position of maximal discomfort may provide a clue to the underlying pathology. Anterior neck pain along the sternocleidomas-toid muscle belly that is aggravated by rotation to the contralateral side is most often a result of muscular strain. Pain in the posterior neck muscles that is wors-ened by flexion of the head suggests a myofascial etiology. Pain in the poste-rior aspect of the neck that is aggravated by extension, especially with rotation of the head to one side, suggests the possi-bility of a discogenic component. Pa-tients who present with severe pain in the suboccipital region often have pathological changes in the upper cervi-cal spine. The pain in these patients may radiate to the back of the ear or the caudad part of the neck. Rotation of the neck is often markedly restricted.

Pain in the neck and shoulder gir-dle can develop as a result of adapta-tions stemming from an initial source of pain. The initial source of pain may resolve, but postural adaptations and compensatory overuse of normal tis-sues in the neck and shoulder girdle can result in new pain patterns. It is impor-tant to obtain an accurate history re-garding how the pain initially presented and how it might have changed with time.

Pathological changes in the shoulder can present with localized pain or pain referred to the neck. The pain may radiate down the anterior or lateral aspect of the arm. Careful exami-nation of the shoulder will help to dif-ferentiate this cause from pathological changes in the neck. Pain in the neck and shoulder girdle can also be referred from the heart, lungs, viscera, and tem-poromandibular joint. A detailed and accurate history and examination will help to rule out the possibility that pain in the neck is being referred from an-other region. Morning stiffness, pol-yarticular involvement, rigidity, or cutaneous manifestations suggest an in-





flammatory arthritic component. Fe-ver, weight loss, or nonmechanical neck pain may point to an infectious or neo-plastic process.

Cervical RadiculopathyCervical radiculopathy refers to symp-toms in a specific dermatomal distribu-tion in the upper extremity. Patients describe sharp pain and tingling or burning sensations in the involved area. There may be sensory or motor loss cor-responding to the involved nerve root, and reflex activity may be diminished.

Patients typically have severe neck and arm pain that prevents them from getting into a comfortable position. They may hold the arm over the head, typically resting the wrist or forearm on top of the head (the shoulder abduction sign12) and sometimes tilting the head to the contralateral side. The symptoms are usually aggravated by extension or lateral rotation of the head to the side of the pain (the Spurling maneuver). Ag-gravation of the symptoms by neck ex-tension often helps to differentiate a radicular etiology from muscular neck pain or a pathological condition of the shoulder with secondary muscle pain in the neck. It is also important to remem-ber that multiple sources of pain in the neck and upper extremity are common and that the nerve structures may be compressed at more than one site40,41. Patients with metabolic disorders, such as diabetes, who have neuropathy may be more susceptible to radiculopathy and compressive neuropathy. Adapta-tions to the initial radiculopathy may result in secondary pathological changes in the shoulder, carpal tunnel syndrome, or ulnar nerve irritation, which may persist long after the initial radiculopathy has resolved. Henderson et al. reviewed the clinical presenta-tions of cervical radiculopathy in 736 patients42: 99.4% had arm pain, 85.2% had sensory deficits, 79.7% had neck pain, 71.2% had reflex deficits, 68% had motor deficits, 52.5% had scapular pain, 17.8% had anterior chest pain, 9.7% had headaches, 5.9% had anterior chest and arm pain, and 1.3% had left-sided chest and arm pain (cervical angina). Neurologic deficits corre-

sponded with the offending disc level in approximately 80% of patients.

Radiculopathy of the third cervi-cal nerve root results from pathological changes in the disc between the second and third cervical levels and is unusual. The posterior ramus of the third cervi-cal nerve innervates the suboccipital re-gion, and involvement of that nerve causes pain in this region, often extend-ing to the back of the ear. An isolated motor deficit from radiculopathy of the third cervical nerve root cannot be de-tected clinically.

Radiculopathy of the fourth cer-vical nerve root may be an unexplained cause of neck and shoulder pain. Numbness extending from the caudad aspect of the neck to the superior aspect of the shoulder may be present. Dia-phragmatic involvement may result from involvement of the third, fourth, and fifth cervical nerve roots43,44. Motor deficits in the diaphragm manifest as paradoxical respiration, and they may be confirmed by fluoroscopic evalua-tion of the abdomen.

Radiculopathy of the fifth cervical nerve root can present with numbness in an “epaulet” distribution, beginning at the superior aspect of the shoulder and extending laterally to the midpart of the arm. The deltoid muscle is inner-vated primarily by the fifth cervical nerve, and involvement of that nerve can result in profound weakness of this muscle. The absence of pain with a range of motion of the shoulder and the absence of impingement signs at the shoulder help to differentiate radicu-lopathy of the fifth cervical nerve root from a pathological shoulder condition. The biceps reflex is innervated by the fifth and sixth cervical nerves and may be affected.

Radiculopathy of the sixth cervical nerve root presents with pain radiating from the neck to the lateral aspect of the biceps, to the lateral aspect of the fore-arm, to the dorsal aspect of the web space between the thumb and index finger, and into the tips of those digits. Numbness occurs in the same distribution. Motor deficits are best elicited in the wrist ex-tensors, but they also may be elicited by elbow flexion and forearm supination.

The brachioradialis and biceps reflexes may be lost or diminished. The sensory symptoms may mimic carpal tunnel syn-drome, which typically involves the ra-dial three and a half digits and causes weakness in the thenar musculature.

The seventh cervical nerve root is the most frequently involved by cervi-cal radiculopathy. The patient has pain radiating along the back of the shoul-der, often extending into the scapular region, down along the triceps, and then along the dorsum of the forearm and into the dorsum of the long finger. The patient usually pronates the fore-arm while trying to describe the loca-tion of the symptoms, and this is a useful observation when the physician is trying to differentiate the hand symp-toms from those of sixth cervical radic-ulopathy and carpal tunnel syndrome. Motor weakness is best appreciated in the triceps, wrist flexors, and finger ex-tensors. The triceps reflex may be lost or diminished. Entrapment of the pos-terior interosseus nerve may be mis-taken for the motor component of seventh cervical radiculopathy and pre-sents with weakness in the extensor dig-itorum communis, extensor pollicis longus, and extensor carpi ulnaris. Sen-sory changes are absent, however, and the triceps and wrist flexors show nor-mal strength.

Radiculopathy of the eighth cer-vical nerve root usually presents with symptoms extending down the medial aspect of the arm and forearm and into the medial border of the hand and the ulnar two digits. Numbness usually in-volves the dorsal and volar aspects of the ulnar two digits and hand and may extend up the medial aspect of the forearm. The patient reports difficulty with using the hands for routine daily activities. It is important to differenti-ate eighth cervical radiculopathy from ulnar nerve weakness. The function of the flexor digitorum profundus in the index and long fingers and of the flexor pollicis longus in the thumb can be af-fected by eighth cervical radiculopathy, but they are not affected by ulnar nerve entrapment. With the exception of the adductor pollicis, the short the-nar muscles are spared with ulnar





nerve involvement but involved with eighth cervical or first thoracic radic-ulopathy. Entrapment of the anterior interosseus nerve may masquerade as eighth cervical or first thoracic ra-diculopathy, but it does not cause the sensory changes or have thenar muscle involvement.

Patients occasionally present with symptoms that simulate radiculopathy but result from nonspondylotic patho-logical changes (Table II). Schwanno-mas usually arise from the intradural portion of the sensory root and may cause severe pain in a dermatomal dis-tribution. Meningiomas can similarly cause radicular or myelopathic symp-toms, depending on their size and pre-cise location. Benign or malignant vertebral body tumors usually present with nonmechanical neck pain that progresses to severe radiculopathy, and even myelopathy, as the amount of bone destruction increases. A Pancoast tumor of the apical lung can involve the caudad cervical nerve roots and, addi-tionally, involve the sympathetic chain. Idiopathic brachial plexus neuritis is thought to be viral in nature and pre-sents with severe arm pain that resolves and leaves behind polyradicular motor deficits. Polyradicular involvement may also be seen with epidural abscesses. Re-flex sympathetic dystrophy occasion-ally occurs following trauma to the upper extremity, and it presents as dif-fuse burning pain or paresthesias ac-companied by discoloration, edema, or other autonomic phenomena.

Cervical Spondylotic MyelopathyCervical spondylotic myelopathy is the most common cause of acquired spas-tic paraparesis in adults. The patient may present with subtle findings that have been present for years or with quadriparesis that developed over the course of a few hours. Perhaps the most unique feature of the condition is its subtle and varied presentation, and the fact that its diagnosis requires a high in-dex of suspicion.

The clinical picture varies, de-pending on the anatomic portion of the cord that is primarily involved. Crandall and Batzdorf described five broad cate-gories of cervical spondylotic myelop-athy45: (1) transverse lesion syndrome, in which the corticospinal, spinothalamic, and posterior cord tracts were involved with almost equal severity and which was associated with the longest duration of symptoms, suggesting that this cate-gory may be an end stage of the disease; (2) motor system syndrome, in which corticospinal tracts and anterior horn cells were involved, resulting in spastic-ity; (3) central cord syndrome, in which motor and sensory deficits affected the upper extremities more severely than the lower extremities; (4) Brown-Séquard syndrome, which consisted of ipsilateral motor deficits with contralateral sensory deficits and which appeared to be the least advanced form of the disease, and (5) brachialgia and cord syndrome, which consisted of radicular pain in the upper extremity along with motor and/or sensory long-tract signs.

Ferguson and Caplan divided cer-vical spondylotic myelopathy into four syndromes21: (1) medial syndrome, con-sisting primarily of long-tract symp-toms; (2) lateral syndrome, consisting primarily of radicular symptoms; com-

bined medial and lateral syndrome, which is the most common clinical pre-sentation; and (4) vascular syndrome, which presents with a rapidly progres-sive myelopathy and is thought to rep-resent vascular insufficiency of the cervical spinal cord.

The findings in cervical spondy-lotic myelopathy vary from patient to patient. Patients typically present with the insidious onset of clumsiness in the hands and lower limbs. They may re-port worsening handwriting in the past few months or weeks, difficulty with grasping and holding, or diffuse numb-ness in the hands. They frequently have had increasing difficulty with balance that they attribute to age or arthritic hips, and relatives may volunteer that their gait has become increasingly awkward. Nurick developed a system for grading the disability in cervical spondylotic myelopathy on the basis of gait abnormality35 (Table III). On physi-cal examination, the findings that es-tablish the diagnosis are brisk reflexes, clonus, or pathological reflexes con-firming an upper-motor-neuron le-sion. Myelopathy resulting from a region of the cord cephalad to the third cervical level may result in a hyperactive scapulohumeral reflex46i.e., tapping of the spine of the scapula or acromion results in scapular elevation and/or ab-duction of the humerus. This is thought to be a stretch reflex of the trapezius muscle. Superficial reflexes such as the abdominal or cremasteric reflex are of-ten diminished or absent in the pres-ence of upper-motor-neuron lesions. The pathological reflexes that are typi-cally elicited are the inverted radial re-flex, the Hoffmann reflex, and the extensor plantar reflex. Muscle weak-ness and wasting in the lower extremi-

TABLE III Nurick35 Classification of Disability from Cervical Myelopathy

Grade I No difficulty in walking

Grade II Mild gait involvement not interfering with employment

Grade III Gait abnormality preventing employment

Grade IV Able to walk only with assistance

Grade V Chairbound or bedridden

TABLE II Differential Diagnosis of Radiculopathy

Peripheral entrapment syndromes

Rotator cuff/shoulder pathology

Brachial plexitis

Herpes zoster

Thoracic outlet syndrome

Sympathetic mediated pain syndrome

Intraspinal or extraspinal tumor

Epidural abscess

Cardiac ischemia





ties with superimposed loss of proprioception result in an unsteady, broad-based gait.

Sensory findings in cervical spondylotic myelopathy vary. Pain, temperature, proprioception, vibra-tory, and dermatomal sensations may all be diminished, depending on the ex-act area of the cord or the nerve-root that is compromised. Sphincter distur-bances are not usually presenting symp-toms. Patients may complain of urinary urgency, hesitation, and frequency and rarely of urinary incontinence or reten-tion. Fecal incontinence is unusual. In a study of sixty-two patients with cervi-cal spondylotic myelopathy by Crandall and Batzdorf 45, neck pain was present in fewer than half of the patients and asso-ciated radicular pain was present in 38%. The Lhermitte sign with shock-like sensations in the torso and limbs resulting from quick flexion or exten-sion of the neck was present in 27% of the patients, and sphincter distur-bances were present in 44%.

Hand dysfunction in cervical spondylosis has, in the past, been attrib-uted primarily to radicular pathology. Several recent reports have shown findings specific to the “myelopathy hand.”47,48 Diffuse numbness in the hands is extremely common and is often misdiagnosed as peripheral neu-ropathy or carpal tunnel syndrome. Clumsiness of the hands results in an inability to carry out fine motor tasks. Marked wasting of the intrinsic hand muscles is usually present49. Ono et al.47 described two specific signs of myelopa-thy hand: (1) the finger-escape sign (when the patient is asked to fully ex-tend the digits with the palm facing down, the ulnar digits tend to drift into abduction and flexion) and (2) the grip-and-release test (weakness and spasticity of the hand result in a de-creased ability to rapidly open and close the fist). Many neurologic conditions can mimic cervical spondylotic myelop-athy (Table IV). Multiple sclerosis, a de-myelinating disorder of the central nervous system, causes both motor and sensory symptoms, but it typically has remissions and exacerbations, involve-ment of the cranial nerves, and charac-

teristic plaques that can be seen on magnetic resonance imaging of the brain and spinal cord. Amyotrophic lat-eral sclerosis results in upper and lower motor-neuron symptoms, with no al-teration in sensation. Subacute com-bined degeneration seen with vitamin-B12 deficiency results in corticospinal tract and posterior tract symptoms, with greater sensory involvement in the lower extremities. Patients with meta-bolic or idiopathic peripheral neuropa-thy have sensory symptoms that mimic those of myelopathy.

Atypical Presentations of Cervical SpondylosisCervical angina, a symptom constella-tion mimicking ischemic heart disease but produced by cervical radiculopa-thy, is a well-known entity. Women with pain of cervical radicular origin may present with chronic breast pain50. Facial pain or paresthesias may be sec-ondary to involvement of the spinal nu-cleus of the trigeminal nerve and may result from pressure on the cephalad and middle parts of the cervical spinal cord. Marked spurring along the ante-rior aspects of the vertebral bodies as a result of proliferative degenerative changes may manifest as dysphagia, dyspnea, or dysphonia as a result of pressure on the esophagus, larynx, or trachea. Similar hypertrophic spurs re-sulting from the uncovertebral joints and facet joints can occlude the verte-bral artery in its foramen and result in thrombosis of the vertebral artery. If the thrombosis spreads to the posterior in-ferior cerebellar artery, it may lead to palsy of the ipsilateral V, IX, X, and XI cranial nerves, Horner syndrome, cere-bellar ataxia, and possibly deatha

constellation known as Wallenberg syn-drome. Sympathetic chain involvement can result in atypical symptoms such as dizziness, blurring of vision, tinnitus, retroocular pain, facial pain, or jaw pain51. Cervical spondylotic myelopa-thy has also been reported to present with hemiparesis52.

Radiculopathy occasionally pre-sents in association with myelopathy. It is important not to let overriding radicular deficits obscure an underly-ing myelopathy. Patients with cervical myelopathy occasionally may have con-comitant peripheral neuropathy or lumbar stenosis53, which might mask the lower-extremity hyperreflexia typi-cally expected from the myelopathy.

OverviewDegenerative cervical disc disease is a common condition that is, for the most part, asymptomatic. When symptoms do develop, they can be easily grouped into axial neck pain, radiculopathy, and myel-opathy. An understanding of the patho-physiology of these conditions makes it possible to determine clinically whether the symptoms are likely a result of cervi-cal spinal pathology and, in many cases, to further localize a specific level within the neck. The natural history of these conditions suggests that patients with axial symptoms usually are best treated without surgery, although some patients with radiculopathy continue to be dis-abled by pain and may be candidates for operative treatment. Patients with myel-opathy are unlikely to have substantial improvement and, in most cases, show stepwise deterioration. Surgical decom-pression and stabilization should be con-sidered for these patients.

Raj Rao, MDDepartment of Orthopaedic Surgery, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee, WI 53226

The author did not receive grants or outside funding in support of his research or prepara-tion of this manuscript. He did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any ben-

TABLE IV Differential Diagnoses of Cervical Spondylotic Myelopathy

Peripheral polyneuropathy

Motor neuron disease

Multiple sclerosis

Cerebrovascular disease

Syringomyelia





efits to any research fund, foundation, educa-tional institution, or other charitable or nonprofit organization with which the author is affiliated or associated.

Printed with the permission of the American Academy of Orthopaedic Surgeons. This arti-cle, as well as other lectures presented at the Academy’s Annual Meeting, will be available in

March 2003 in Instructional Course Lectures, Volume 52. The complete volume can be ordered online at www.aaos.org, or by calling 800-626-6726 (8 A.M.-5 P.M., Central time).

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