Cervical myelopathy guidelines
by Nathan Wei, MD, FACP, FACR
Nathan Wei is a board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
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Cervical Myelopathy is a condition where the spinal cord gets compressed in the neck. While the this can occur as a result of a herniated disc alone, it is usually in combination with bone spurs in the spinal canal (cervical spondylosis) or a developmentally narrow spinal canal (spinal stenosis).
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. 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. 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. Osteophytes stabilize adjacent vertebrae whose hypermobility is caused by the degeneration of the disc. 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.
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 . CSM usually develops insidiously. In the early stages of CSM, complaints of neck stiffness are common because of the presence of advanced cervical spondylosis. 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. 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.
History is of neck and arm pain, and paresthesias (pins-and-needles sensations) may be present. There is clumsiness or difficulty using the hands and legs. Bowel or bladder control problems are often reported, as is sexual dysfunction. The symptoms may vary. There may be a central spinal cord syndrome, with weakness in the arms, even greater weakness in the legs, and arm reflexes that are depressed corresponding to the level of compression. A Brown-Sequard syndrome may be seen, as one-sided spinal cord dysfunction, weakness on one side, and loss of sensation on the opposite side. Another possible clinical picture is an anterior spinal artery syndrome (blockage of the artery by a centrally herniated disc), with a loss of sensory and motor function below the level of spinal cord compression. With a herniated disc, all these symptoms appear acutely, but, with spondylosis, the onset can be very gradual.
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, referred to as Lhermitte's sign. 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 (reflexes very brisk). 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. 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). 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. Hyperreflexia may be absent in CSM patients who have concurrent diabetes, causing a peripheral neuropathy.
Magnetic resonance imaging (MRI) of the cervical spine is the procedure of choice during the initial screening process of patients with suspected CSM. MRI is noninvasive and provides images of the spine and spinal cord in several planes. 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). 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. However, SSEPs are nonspecific and therefore their use as a diagnostic tool is undetermined.
A list of other diagnoses to exclude...
Amyotrophic lateral sclerosis Extrinsic neoplasia (metastatic tumors) Hereditary spastic paraplegia Intrinsic neoplasia (tumors of spinal cord parenchyma) Multiple sclerosis Normal pressure hydrocephalus Spinal cord infarction Syringomyelia Vitamin B12 deficiency
A tumor in the spinal canal or an epidural abscess can also produce symptoms of spinal cord compression, as can a transverse myelitis or degenerative disease of the spinal cord.
Conservative treatment is recommended only if the disease is not progressive. This includes a cervical collar to limit neck movement, physical therapy, and anti-inflammatory medication.
Surgery is necessary if symptoms and signs progress, and is aimed at decompressing the spinal cord. If spondylosis is present, a cervical spinal fusion may also be done.
Permanent nerve damage can occur up to complete paralysis. If surgery is done, there can possibly be an increase in nerve damage, but this is unusual (one to three percent).
Treatment will stop the progression of nerve damage, but there is less likelihood that it will improve the individual's condition. Results are best if the history is short and progressive, less than a few months; the best outcome is with the Brown-Sequard syndrome. If surgery is performed, half may return to full employment, 40% to light employment, and ten percent remain disabled, even though improved.
Work may need to be modified to allow for weakness in the arms and/or legs, decreased dexterity, and an abnormal gait. The work modification may be temporary or permanent. Overhead work (neck extension) should be avoided.
Physical therapy should be performed three times a week for a period of two to four weeks.
Disability will depend on the severity and duration of spinal cord compression, and the response to treatment.
Medical treatment. Duration depends on position of neck (when extended) at work and job requirements for use of arms elevated over shoulder level. Even with improvement after treatment, myelopathy is usually incompatible with heavy work.
Surgical treatment. Laminectomy. Myelopathy, even successfully treated with laminectomy, is not compatible with return to heavy work. Disability may be permanent.
Surgical treatment. Fusion. Disability may be permanent.
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