Cervical Myelopathy



Myelopathy describes damage to the white-matter tracts and central gray matter of the spinal cord. Myelopathy can be traumatic or nontraumatic, and acute or chronic. This chapter describes the most common nontraumatic causes of cervical myelopathy. It also reviews the history, pathophysiology, and current management strategies for each of these causes.


  • The most common nontraumatic cases of cervical myelopathy include:

    • a.

      Cervical spondylosis

    • b.

      Ossification of the posterior longitudinal ligament (OPLL)

    • c.

      Cervical disc herniation

  • Surgery is indicated for patients with moderate-to-severe disease in whom conservative treatment has failed.

  • Surgical approach should be tailored to each individual patient and disease pathology.

  • The anterior approach allows a more direct route of treatment, as pathology causing cervical myelopathy is most common at the anterior spinal cord; however, this approach is more difficult and risks damage to vital anterior structures such as the carotid artery.

  • The posterior approach provides a more indirect method of access and relies on mobilization of the spinal cord; this approach is easier but may be unsuccessful in patients with preoperative kyphotic or straightened cervical spines.


  • Laminoplasty has been developed as a way to decrease the kyphosis and instability associated with traditional laminectomy.

  • An anterior approach provides a more direct way to access the area of compression because the majority of it occurs at the anterior aspect of the spinal cord.

  • When considering surgical treatment of myelopathy from OPLL, excision of the calcified mass from an anterior approach is widely considered to be the procedure of choice; if multiple levels are involved, a posterior approach may be preferred.

  • Anterior cervical discectomy and fusion remains the gold standard treatment for myelopathy secondary to disc herniation.


  • Although the anterior approach is considered to be more direct than the posterior approach, it is associated with significant complications such as dysphagia, hematoma, laryngeal nerve palsy, carotid artery injury, and dural tear.

  • The complication of a progressive postoperative kyphosis and instability is greatest with a stand-alone laminectomy from a posterior approach.

  • Laminoplasty decreases the risk for postoperative instability but is itself associated with complications that include new onset of axial neck pain, dislodgement of the spacer into the spinal canal, and restenosis.



Myelopathy describes damage to the ascending and descending white-matter tracts of the spinal cord, damage to the central gray matter of the spinal cord, or both. Clinically, the physical findings associated with myelopathy are more reliable than the variety of symptoms that may be present. Myelopathy is characterized by the presence of long-tract signs or upper motor neuron findings on physical examination. Cervical myelopathy often presents with both upper and lower extremity pathology.

Damage to the spinal cord and upper motor neurons eliminates the continuous inhibition of the lower motor neurons and can result in any of the following physical findings: hyperreflexia of the deep tendon reflexes; increased muscle tone or clonus/spasticity; and pathologic reflexes including a Babinski sign, a Hoffman sign, or both. Radiographically, myelopathy may be demonstrated by spinal cord signal changes on magnetic resonance imaging (MRI) that are likely representative of spinal cord edema, swelling, damage, or bleeding. However, MRI is not predictive of the physical findings or clinical symptoms associated with myelopathy.

Myelopathy of the cervical spine can result from traumatic and nontraumatic pathology, and can be described as an acute process or as a chronic process that is either stable or progressive. This text describes the most common nontraumatic causes of cervical myelopathy, including cervical spondylosis, ossification of the posterior longitudinal ligament (OPLL), and cervical disc herniation. The natural history, pathophysiology, and current management of each cause are discussed.


Spondylosis has been defined as “vertebral osteophytosis secondary to degenerative disc disease.” Spondylosis is a natural aging process and is seen in 10% of individuals by the age of 25, and in 95% by the age of 65 years.

Cervical spondylosis describes the degenerative aging process that results in changes in the cervical spine beginning first in the intervertebral discs with resulting sequential changes in the vertebral bodies, facet joints, and ligaments of the cervical spine. Strumpell (1888), Marie (1898), and von Beckteren (1899) were the first to identify cervical disorders as a cause of neurologic deterioration. However, it was not until the 1950s that the classic anatomic studies by Brain et al. and by Payne and Spillane began to clarify and elucidate the disease process, its pathophysiology, and its effect on neural components and clinical presentation.

Cervical spondylosis can result in three different types of pathologic disease based on its effect on the neural components: cervicalgia, cervical radiculopathy, and cervical myelopathy. Each can occur separately or together in a clinical presentation. Cervicalgia, or neck pain, can be acute or chronic, is confined to the neck, and does not radiate to the upper extremities. The pathophysiology of cervicalgia from cervical spondylosis is not fully elucidated, and theories abound regarding the cause(s) of such pain. One common theory is that it is related to “discogenic” neck pain caused by the activation of pain fibers within the annulus fibrosis after disc degeneration, but this is far from a consensus. Cervical radiculopathy is a pathologic process involving the cervical nerve root(s), and is the consequence of compression and inflammation of the nerve root or roots near the cervical neural foramen. It can be classified as acute, subacute, or chronic. Although the degenerative changes of cervical spondylosis can produce radiculopathy, the most common cause of cervical radiculopathy is cervical disc herniation. Cervical spondylotic myelopathy (CSM), the compression of the spinal cord from cervical spondylosis, is typically a slowly progressive process. CSM is the most common cause of spinal dysfunction in the elderly and is the most common cause of nontraumatic myelopathy. In one series, 23.6% of all patients with nontraumatic myelopathic symptoms were found to have CSM.

Symptoms and Signs of Cervical Spondylotic Myelopathy

Clinically, patients with CSM can display a variety of symptoms including neck pain, paresthesias in a nondermatomal pattern in the upper extremities, loss of fine motor control of the upper extremities, arm or leg weakness with involvement of the proximal muscles more than the distal muscle groups, and difficulty with gait and balance involving the lower extremities. Physical findings and signs associated with CSM are the same as those previously described for myelopathy, and include hyperreflexia of the deep tendon reflexes, increased muscle tone or clonus/spasticity, and pathologic reflexes including a Babinski sign, a Hoffman sign, or both.

Natural History of Cervical Spondylotic Myelopathy

Patients with CSM typically present in their sixth or seventh decades of life. Reported ages of affected patients range from the third to the tenth decades of life, with the median age in the mid-50s. Clarke and Robinson and Lees and Turner provided the first descriptions of the natural history of CSM. Clarke and Robinson observed 120 patients with the disease and categorized them into 3 categories. They showed that, in 75% of the patients, the disease process occurred in a stepwise or episodic pattern of clinical exacerbations where new signs and symptoms persisted after each episode. In these patients, the conditions of 67% were found to deteriorate slowly between the obvious periods of exacerbation, and in 33% of these patients, the neurologic deterioration remained stable between the obvious periods of exacerbation. Overall, Clarke and Robinson observed that 20% of patients had a slow, steady progression of symptoms and signs without a stable period, whereas 5% had rapid deterioration of neurologic function followed by long periods where new symptoms did not appear.

Lees and Turner’s description of the natural history of CSM was similar and found that patients had an exacerbation of symptoms followed by long periods where neurologic function was mostly stable. In some cases, they observed a reversal of symptoms and improvement in function, but that was uncommon. Regardless, Lees and Turner did not observe continuous progression of symptoms as deterioration of patients’ conditions occurred in a more stepwise manner.

Once clinically apparent, the progression of CSM follows an unpredictable time course and a variable rate. In some patients, signs and symptoms progress in a more rapid, stepwise fashion, whereas in other patients, symptoms and signs may be stable for many years only to worsen after many years of stability. However, no known clinical or radiographic signs predict such progression. Generally, once moderate signs and symptoms of myelopathy develop, the ultimate prognosis is poor.

Pathophysiology and Pathoanatomy of Cervical Spondylotic Myelopathy

CSM occurs as a result of three pathophysiologic factors that include static-mechanical factors, dynamic-mechanical factors, and spinal cord ischemia. Static-mechanical factors begin with disc desiccation and degeneration. On a macroscopic level, the aging intervertebral disc demonstrates breakdown, fragmentation, and collapse. At the cellular and biochemical level, the intervertebral disc loses water content and demonstrates a relative increase in the ratio of keratin sulfate to chondroitin sulfate. Ultimately, annular bulging results from the loss of elasticity, total disc substance, and loss of disc height.

It is hypothesized that disc degeneration leads to increased mechanical stresses that occur at the end plates of the adjacent vertebral body, which leads to the formation of chondro-osseous spurs that can compress the spinal cord along the ventral aspect of the spinal canal. Additional hypertrophy of the uncovertebral joints may lead to foraminal stenosis. Dorsally, the posterior zygapophyseal joints can become arthritic and cause dorsal foraminal narrowing, whereas thickening and buckling of the ligamentum flavum can result in central canal ( Fig. 7-1 ). This decrease in spinal canal diameter is particularly a problem in patients with congenitally narrowed spinal canals (10–13 mm) who are predisposed to development of CSM.


Preoperative magnetic resonance imaging showing multilevel cervical stenosis at C3-4, C4-5, and C5-6 with some preservation of lordosis.

Dynamic-mechanical factors can be another cause of cord impingement. Cervical spondylosis commonly produces a stiffening of the spinal motion segments, and in some cases, segments adjacent to the stiffened segments can become hypermobile, a process termed compensatory subluxation . Loss of normal cervical lordosis or cervical kyphosis can occur in patients with significant spondylotic changes. This deformity will aggravate the degree of compression because the spinal cord becomes draped over the posterior aspect of the discs and degenerative vertebral bodies. Furthermore, in flexion, the spinal cord is stretched and flattened over the anterior osteophytes, whereas extension results in more pronounced buckling of the ligamentum flavum.

The direct compressive effects and dynamic effects of spondylosis on neural tissue can also result in ischemia from decreased flow in the microcirculation of the spinal cord. As the anteroposterior diameter of the spinal cord becomes narrowed, the cervical spinal cord becomes flattened and widened. The vasculature of the cord is affected by this distortion, the pial vessels become more tortuous, and the arteries of the lateral column are elongated, narrowed, and flattened. Venous congestion also results, adding to the ischemia.

Pathologic specimens have been examined and correlated with clinical findings on examination. Degeneration of the lateral white-matter tracts has been noted in mild-to-moderate compression. The demyelination of the corticospinal tracts occurs from the additional damage to the oligodendroglia present in the spinal cord. Additional histologic changes associated with myelopathy include axonal demyelinization followed by cell necrosis and gliosis or scarring from impairment of intracellular energy metabolism, free radical–mediated injury, and apoptosis. Recently, the extent of spinal cord changes present before surgery on T2-weighted MRI has been found to correlate to the ultimate clinical outcome when surgical intervention is undertaken.


OPLL is the replacement of the posterior longitudinal ligament (PLL) by compact lamellar bone and has also been described as a cause of cervical myelopathy, with or without the presence of spondylotic changes. OPLL generally occurs in patients older than 40 years and is extremely uncommon until the third decade of life. It is hypothesized that the aging process may be crucial in ossification of the ligament; however, the cause of this condition is unknown. OPLL has a greater incidence and is a major disorder of compressive myelopathy in certain Asian populations, such as the Japanese. Therefore, a genetic component most likely plays a large role in the pathophysiology of this process.

OPLL can be classified by its anatomic arrangement into four major groups. The ossification can be focal at the posterior margin of one vertebral level. It can involve “skip-type” segmental ossification at multiple vertebral levels such that the ossified ligament does not extend beyond the intervertebral disc at any of the levels involved. It can be classified as a continuous formation of bone involving multiple vertebral levels. Finally, it can be classified as any of the above in a mixed-type ossification.

The ossified ligament is often not a thin strip but a larger mass that can extend from the midline laterally and rostral and caudal to the intervertebral disc ( Fig. 7-2 ). It can occur in conjunction with cervical spondylosis and often produces severe anterior compression of the spinal cord. Over time, OPLL can fuse and become adherent and continuous with the adjacent anterior dura. With an anterior surgical decompression, one must be careful because this may result in spinal fluid leak secondary to a large iatrogenic dural defect, which may ultimately form a spinal fluid fistulae.


Preoperative cervical axial T2 magnetic resonance imaging demonstrating ossification of the posterior longitudinal ligament and significant cervical stenosis at the above level.


Single-level or multilevel cervical disc herniation may result in cervical myelopathy, often in a younger cohort than traditionally seen with CSM. This population also differs in the acuity of the lesion, with large central “soft disc” herniations resulting in a presentation of myeloradiculopathy. Although occasionally traumatic in nature, the degenerative soft disc herniation may also present with relatively abrupt onset of bilateral upper motor neuron and lower motor neuron findings. The treatment of acute myelopathy associated with cervical disc herniation is typically different than that undertaken for acute cervical radiculopathy. Profound neurologic deficits or progressive neurologic deficits, or both, are an indication for surgical intervention.

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Mar 22, 2019 | Posted by in ORTHOPEDIC | Comments Off on Cervical Myelopathy
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