Cervical Spondylotic Myelopathy: A Common Cause of Spinal Cord Dysfunction in Older Persons

Author: William F. Young
Date: Sept 1, 2000

Cervical spondylotic myelopathy is the most common cause of spinal cord dysfunction in older persons. The aging process results in degenerative changes in the cervical spine that, in advanced stages, can cause compression of the spinal cord. Symptoms often develop insidiously and are characterized by neck stiffness, arm pain, numbness in the hands, and weakness of the hands and legs. The differential diagnosis includes any condition that can result in myelopathy, such as multiple sclerosis, amyotrophic lateral sclerosis and masses (such as metastatic tumors) that press on the spinal cord. The diagnosis is confirmed by magnetic resonance imaging that shows narrowing of the spinal canal caused by osteophytes, herniated discs and ligamentum flavum hypertrophy. Choice of treatment remains controversial, surgical procedures designed to decompress the spinal cord and, in some cases, stabilize the spine are successful in many patients. (Am Fam Physician 2000;62:1064-70,1073.)

Cervical spondylotic myelopathy (CSM) is the most common spinal cord disorder in persons more than 55 years of age in North America and perhaps in the world. As the number of older persons in the United States increases, the incidence of CSM will most likely increase. In a prospective study designed to more accurately define the incidence of CSM, 23.6 percent of 585 patients with tetraparesis or paraparesis admitted to a United Kingdom regional neuroscience center had CSM.(1) The overall prevalence in this population is unknown.

Pathophysiology of CSM

Spondylosis refers to the degenerative changes that occur in the spine, including degeneration of the joints, intervertebral discs, ligaments and connective tissue of the cervical vertebrae. There are three important pathophysiologic factors in the development of CSM: (1) static mechanical; (2) dynamic mechanical; and (3) spinal cord ischemia.(2) Static mechanical factors result in the reduction of spinal canal diameter and spinal cord compression. With aging, the intervertebral discs dry out resulting in loss of disc height. This process puts greater stress on the articular cartilage of the vertebrae and their respective end plates. Osteophytic spurs develop at the margins of these end plates (Figure 1). Osteophytes stabilize adjacent vertebrae whose hypermobility is caused by the degeneration of the disc.(3)

The disc also calcifies, further stabilizing the vertebrae. Osteophytes increase the weight-bearing surface of the end plates and, therefore, decrease the effective force being placed on them. In addition to osteophytic overgrowth, the ligamentum flavum may stiffen and buckle into the spinal cord dorsally. Osteophytic overgrowth ventrally and, in some cases, buckling of the ligamentum flavum dorsally can cause direct compression of the spinal cord resulting in myelopathy (clinically evident spinal cord dysfunction). Symptoms are believed to develop when the spinal cord has been reduced by at least 30 percent.(4)

Dynamic mechanical factors relate to the fact that the normal motion of the cervical spine may aggravate spinal cord damage precipitated by direct mechanical static compression. During flexion, the spinal cord lengthens, thus stretching over ventral osteophytic ridges. During extension, the ligamentum flavum may buckle into the spinal cord causing a reduction of available space for the spinal cord (Figure 2).

Spinal cord ischemia probably plays a role in the development of CSM, particularly in later stages.(5,6) Histopathologic changes in the spinal cord consistent with ischemia have been observed in patients with CSM. However, the precise mechanism for spinal cord ischemia is not completely understood. Other factors associated with the development of spondylosis include heavy labor, posture and genetic predisposition.(7,8) Also, 70 percent of patients with Down syndrome have an increased incidence of spondylosis by 50 years of age.(9)

Clinical History

Patients with CSM will generally have these symptoms: neck stiffness; unilateral or bilateral deep, aching neck, arm and shoulder pain; and possibly stiffness or clumsiness while walking (Table 1). CSM usually develops insidiously. In the early stages of CSM, complaints of neck stiffness are common because of the presence of advanced cervical spondylosis.(10) Other common complaints include crepitus in the neck with movement; brachialgia, which is characterized as a stabbing pain in the pre- or postaxial border of the arm, elbow, wrist or fingers; a dull "achy" feeling in the arm; and numbness or tingling in the hands.

Pain following a stereotypical dermatomal distribution is referred to as a radiculopathy rather than a myelopathy. For example, in patients with a disc herniation between the sixth and seventh vertebrae, pain radiates into the shoulder, upper arm, elbow, and index and middle fingers. It is typically unilateral. Numbness and weakness follow the same distribution. Some patients will exhibit signs and symptoms of radiculopathy and myelopathy.

The hallmark symptom of CSM is weakness or stiffness in the legs.(10,11) Patients with CSM may also present with unsteadiness of gait. Weakness or clumsiness of the hands in conjunction with the legs is also characteristic of CSM. Symptoms may be asymmetric particularly in the legs. Loss of sphincter control or frank incontinence is rare; however, some patients may complain of slight hesitancy on urination.

Physical and Neurologic Examination

The physical and neurologic examination is used to confirm the presence of spinal cord dysfunction. Flexion of the neck may cause a generalized "electric shock-like" sensation down the center of the back,(10) referred to as Lhermitte's sign (Table 1). Atrophy of the hands, particularly the intrinsic musculature, may be present.

Sensory abnormalities have a variable pattern on examination. Loss of vibratory sense or proprioception in the extremities (especially the feet) can occur. Superficial sensory loss may be asymmetric and persons are variably affected. The sensory examination may be confounded by the presence of diabetes mellitus and a concurrent peripheral neuropathy.

A characteristic physical finding of CSM is hyperreflexia. The biceps and supinator reflexes (C5 and C6) may be absent, with a brisk triceps reflex (C7). This pattern is almost pathognomonic of cord compression because of cervical spondylosis at the C5-C6 interspace.(12) Ankle clonus and Babinski's sign (pathologic extension of the great toe elicited by stroking the foot) in the feet may also be revealed. Hoffmann's sign (a reflex contraction of the thumb and index finger after nipping the middle finger) is a subtle indicator of spinal cord dysfunction. A stiff or spastic gait is also characteristic of CSM in its later stages.

When cervical spondylosis is isolated to the C6-7, C7-T1 spinal levels, the arm reflexes may be normal. A hyperactive pectoralis muscle reflex elicited by tapping the pectoralis tendon in the deltopectoral groove causing adduction and internal rotation of the shoulder is a sign of cord compression in the upper cervical spine (C2-3, C3-4 spinal levels).(13) The "dynamic" Hoffmann's sign (when a typical Hoffmann's sign is elicited after having the patient flex and extend the neck multiple times) may be an indicator of early CSM.(14) Hyperreflexia may be absent in CSM patients who have concurrent diabetes, causing a peripheral neuropathy (Table 1).

Imaging and Diagnostic Studies

Magnetic resonance imaging (MRI) of the cervical spine is the procedure of choice during the initial screening process of patients with suspected CSM.15 MRI is noninvasive and provides images of the spine and spinal cord in several planes (Figure 3). In addition to giving an assessment of the degree of spinal canal stenosis, an MRI can identify intrinsic spinal cord lesions that can also present with myelopathy (e.g., tumors). High signal changes seen in the spinal cord of patients with CSM may indicate myelomalacia or permanent spinal cord damage.

Computed tomography (CT) is complementary to MRI (Table 2). CT may give a more accurate assessment of the amount of canal compromise because it is superior to MRI in evaluating bone (osteophytes).(16) Myelography or the intrathecal injection of a contrast agent is used in conjunction with CT. Since the advent of MRI, the use of myelography has decreased; however, it still provides useful information in some instances for surgical planning. Plain radiographs alone are of little use as an initial diagnostic procedure.

Electromyography is rarely useful in most patients with CSM; however, it may help in the exclusion of specific syndromes such as peripheral neuropathy. Somatosensory evoked potentials (SSEPs) provide a more direct assessment of spinal cord function (e.g., dorsal column function) than electromyography.(17) However, SSEPs are nonspecific and therefore their use as a diagnostic tool is undetermined.

Differential Diagnosis

(19.) Kumar VG, Rea GL, Mervis LJ, McGregor JM. Cervical spondylotic myelopathy: functional and radiographic long-term outcome after laminectomy and posterior fusion. Neurosurgery 1999;44:771-8.

(20.) Roberts AH. Myelopathy due to cervical spondylosis treated by collar immobilization. Neurology 1966;16:951-4.

(21.) Zeidman SM, Ducker TB. Cervical disk diseases: part 1. Treatment options and outcomes. Nuerosurgy Quarterly 1992;2:116-43.

(22.) Saunders RL. Corpectomy for cervical spondylotic myelopathy. In: Menezes AH, Sonntag VK, eds. Principles of spinal surgery. New York: McGraw-Hill Companies, Health Professions Division, 1996: 559-69.

(23.) Naderi S, Ozgen S, Pamir MN, Ozek MM, Erzen C. Cervical spondylotic myelopathy: surgical results and factors affecting prognosis. Neurosurgery 1998;43:43-50.

(24.) Bucciero A, Vizioli L, Tedeschi G. Cord diameters and their significance in prognostication and decisions about management of cervical spondylotic myelopathy. J Neurosurg Sci 1993;37:223-8.

(25.) Chiles BW 3d, Leonard MA, Choudhri HF, Cooper PR. Cervical spondylotic myelopathy: patterns of neurological deficit and recovery after anterior cervical decompression. Neurosurgery 1999;44:762-70.

WILLIAM F. YOUNG, M.D., is associate professor of neurosurgery and physiology at Temple University School of Medicine, Philadelphia. He is also director of the neuro-spine program at Temple University Hospital, Philadelphia. Dr. Young received his medical degree from Cornell University Medical College, New York, N.Y., and received training in neurosurgery and spinal reconstructive surgery at Temple University Hospital.

Address correspondence to William F. Young, M.D., Temple University Hospital, 3401 N. Broad St., Philadelphia, PA 19140. Reprints are not available from the author.

TABLE 1Clinical Presentationof Cervical Spondylotic MyelopathyCommon symptomsClumsy or weak handsLeg weakness or stiffnessNeck stiffnessPain in shoulders or armsUnsteady gaitCommon signsAtrophy of the hand musculatureHyperreflexiaLhermitte's sign (electric shock-like sensation down the center of the back following flexion of the neck)Sensory lossTABLE 2Diagnostic Criteria for CervicalSpondylotic MyelopathyCharacteristic symptoms (leg stiffness, hand weakness)Characteristic signs (hyperreflexia, atrophy of hands)MRI or CT (showing spinal stenosis and cord compression as a result of osteophyte overgrowth, disc herniation, ligamentum hypertrophy)MRI = magnetic resonance imaging; CT = computed tomography.TABLE 3Differential Diagnosis: CSM vs. ALSFeature CSM ALSAge Older than 55 Older than 55MRI findings Spondylosis SpondylosisFasciculations Absent PresentAtrophy of arms Present PresentAtrophy of legs Absent PresentDenervation Absent PresentCSM = cervical spondylotic myelopathy; ALS = amyotrophic lateralsclerosis; MRI = magnetic resonance imaging.TABLE 4Conditions That Mimic CervicalSpondylotic Myelopathy on PresentationAmyotrophic lateral sclerosisExtrinsic neoplasia (metastatic tumors)Hereditary spastic paraplegiaIntrinsic neoplasia (tumors of spinal cord parenchyma)Multiple sclerosisNormal pressure hydrocephalusSpinal cord infarctionSyringomyeliaVitamin B12 deficiency

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