Anterior Approach for Cervical Spondylotic Myelopathy

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CHAPTER 280 Anterior Approach for Cervical Spondylotic Myelopathy

The progression of cervical spondylosis can be insidious, and symptoms can range from relatively asymptomatic or minor findings to significant spinal cord compression with associated myelopathic findings. These symptoms result from degenerated cervical intervertebral disks, herniated disks, bulging disks, or disk-osteophyte complexes. The radiographic incidence of cervical spondylosis has been quoted as 20% to 25% in the population 50 years or younger and 70% to 95% in the 65-year-old age group.1,2 Despite radiographic findings suggestive of degenerative cervical disk disease, relatively few patients are symptomatic and most have transient episodes that respond to conservative measures.

Recent developments in diagnostic imaging, surgical techniques, and spinal instrumentation have changed the management of degenerative cervical spondylosis and intervertebral disk disease, but the most appropriate surgical approach and management of this condition continue to be debated. This chapter addresses the pathophysiology of degenerative cervical disk disease, the associated clinical symptoms, diagnostic imaging modalities, and anterior operative treatment of cervical disease and spondylosis.

Historical Perspective

At the turn of the 20th century, Elliot first reported how arthritis in the cervical spine appeared to be responsible for the development of radicular symptoms caused by compression at the neural foramina.3 Stookey later revealed pathologic syndromes caused by cervical disk herniations that were incorrectly attributed to chondromas.4 Stookey divided the compression of these extradural chondromas into three regions: (1) those compressing half of the ventral aspect of the spinal cord, (2) those compressing both halves of the spinal cord, and (3) those compressing laterally on the nerve roots. Elsberg classified these chondroma-like lesions as ecchondrosis and local hyperplasia of the cartilage.5 Stookey and Elsberg were the first surgeons to address the surgical removal of chronic degenerated cervical disks. The classic paper by Mixter and Barr first presented the correlation between radicular symptoms and lateral herniation of the lumbar disks.6 This observation propelled an intense interest in the role of cervical disk degeneration and herniation in the development of cervical radiculopathy and myelopathy.

The surgical approach to the treatment of cervical disk disease was refined in the 20th century. In 1955, Smith and Robinson described their anterior approach for removing the disk and performing an arthrodesis with a horseshoe-shaped bone graft7 and later expanded the success of this technique.8,9 In 1958, Cloward presented his technique for removing the disk and performing an interbody fusion with a cylindrical bone graft.10 In 1960, Bailey and Badgley introduced interbody fusion through a keystone technique.11 In the late 1960s, Verbiest expanded the anterior approach to incorporate a more anterolateral exposure for resecting the foramen transversarium and controlling the vertebral artery.12 These procedures have enjoyed a tremendous amount of success in the treatment of cervical spondylosis and degenerative disk disease. The advent of new imaging modalities has further improved understanding of the natural history of cervical spondylosis. Moreover, new spinal instrumentation permits safe and extensive decompression with excellent clinical outcomes.

Cervical Spine Anatomy

The cervical segment of the spine consists of seven vertebrae. Within the cervical spine, there are three distinct anatomic, physiologic, and biomechanical regions. Because the cervical vertebrae bear the least weight of any spinal region, the cervical vertebral bodies are small in relation to their respective arch and transverse foramina. In addition, the transverse diameter is greater than the anteroposterior (AP) diameter. Except for the upper two cervical vertebrae, each vertebra articulates with adjoining vertebrae at the intervertebral disk interspace and at the facet joints posteriorly. The disks are wider anteriorly than posteriorly, and this configuration creates a natural lordotic posture. Within the intervertebral space, the superior surfaces of the vertebrae turn sharply upward in a superolateral direction to form the uncinate processes.

A unique feature of the cervical vertebrae is the transverse foramen, which perforates the transverse processes. The anterior aspect of the transverse process represents a fused costal joint that arises from the vertebral body. The lateral portion of the transverse process contains two projections referred to as the anterior and posterior tubercles. The anterior tubercle serves as the origin of the anterior cervical musculature, whereas the posterior tubercle serves as the origin and insertion of the posterior musculature. The spinal nerves exit through a deep groove within the tubercles. As it traverses from C6 to the skull base, the vertebral artery is located anterior to the spinal nerve roots.

The articulation between vertebral bodies is formed by the disks. Intervertebral disks consist of a semifluid gelatinous matrix, the nucleus pulposus, surrounded by the annulus fibrosus. The intervertebral disk adheres firmly to the vertebral bodies via the cartilaginous end plate. More posteriorly, the position of the nucleus pulposus is slightly eccentric. In younger age groups, the nucleus pulposus has a high water content. With time, however, it dehydrates, thereby leading to degeneration. The annulus fibrosus consists of well-defined fibrous lamellae that adhere strongly to the vertebral end plate. In addition to containing the nucleus pulposus, the annulus fibrosus withstands considerable shearing and tensile forces from all directions. The annulus fibrosus is innervated by the sinuvertebral nerve, which might play a role in the origin of diskogenic pain.13

The intervertebral disk is supported by the anterior longitudinal ligament and the posterior longitudinal ligament (PLL). The former is stronger than the latter. The PLL is formed by two bands of fibers. The superficial fibers extend through several vertebral bodies and are attached to their posterior midline. A deeper band extends no more than two vertebral segments and attaches itself firmly into the disks. Laterally, the PLL becomes thinner and does not extend completely to the lateral margins of the disk. These features make this region more susceptible to disk herniation. Lateral disk herniations can compress the exiting nerve roots and cause radiculopathy. Central compression of the spinal cord can occur with central disk herniation and the concomitant development of osteophytes from adjacent vertebral bodies. In some cases, multisegmental ossification of the PLL can also cause severe spinal cord compression.

Pathophysiology: the Degenerative Process

Most reports on the natural history of cervical spondylosis and myelopathy were published before the advent of contemporary imaging techniques and do not accurately represent the true natural history of cervical spondylosis.1521 New imaging techniques, however, are improving our understanding of the natural history and progression of symptomatic cervical spondylosis and its pathophysiology. Gore and coauthors1 reported that the radiographic incidence of cervical spondylosis in asymptomatic patients was about 95% in men and 70% in women in the seventh decade of life.

In 1963, Lees and Turner reported their data on a group of patients suffering from cervical stenosis with and without myelopathy.18 They found that the development of symptoms was typically followed by periods of improvement or stabilization. Of the 44 patients with myelopathy, only 5 showed progressive symptoms at the time of last follow-up. In contrast, in 1967 Symon and Lavender reported that 67% of their patients with conservatively treated cervical myelopathy had a steadily progressive course.22

More recent studies have also described a more worrisome course for cervical myelopathy. Shimomura and associates observed 56 patients after nonsurgical treatment of cervical spondylotic myelopathy as defined by a Japanese Orthopedic Association score of 13 or higher.23 Although most patients remained stable, 11 deteriorated and suffered moderate or severe symptoms. In contrast to partial compression, circumferential compression of the spinal cord was predictive of deterioration.

The onset of symptoms is generally in the sixth decade, and men are affected more than women. C5-6 and C6-7 are the levels most involved because of their relatively extensive range of motion. The onset of symptoms is usually insidious, with long periods of stabilization and intermittent episodes of decline. The outcome of symptomatic cervical spondylosis depends on the severity of the radiculopathy and myelopathic signs and the age of patients when they seek treatment.15,16,19,21

The development of cervical spondylosis is a consequence of disk degeneration and dynamic processes. The vertebrae of the cervical spine contain five joints: two zygapophyseal (facets) joints, two neurocentral (Luschka) joints, and the intervertebral disk. As mentioned, the anatomic configuration of the facet joints allows a significant degree of motion in flexion and extension and some lateral bending. Moreover, the shape of the intervertebral disk in conjunction with its interface with the end plates of the adjacent vertebra permits flexion, extension, lateral bending, and shearing motion. The neurocentral joints are located laterally. They confine the intervertebral disk and closely abut the superior end plate of the adjacent vertebral body with little cushioning. Progressive degeneration of these joints leads to compression of the exiting nerve root and clinical symptoms of radiculopathy.

The anatomy of the cervical spine and its relationship to the neural elements are unique in comparison to other regions of the spine. The cross-sectional area of the cervical spinal canal is almost entirely occupied by the spinal cord and exiting nerve roots. In contrast, the lumbar region is mostly occupied by nerve roots. This anatomic relationship, coupled with increasing cervical motion, makes the cervical spine vulnerable to small degenerative changes that might become manifested clinically.24,25

Degeneration of any disk is a dynamic process that begins with loss of the absorptive and viscoelastic properties as a result of dehydration and changes in proteoglycans. Events that increase motion, chronic heavy use, and smoking can accelerate these degenerative changes. Disk dehydration alters the biomechanical properties. The resulting loss of height and annular bulging make the disk and end plates more vulnerable to injury. Altered physical demands on the disk produce gradual fibrocartilaginous changes that blur the boundaries between the nucleus pulposus and the annulus fibrosus until they are indistinguishable. Moreover, these biomechanical changes can increase segmental motion and thereby accelerate the degeneration.

As degeneration ensues, fissures in the annulus make the disk more susceptible to herniation and narrow its height. As the disk narrows, the facet joints override each other, and the neurocentral joints rub against the superior end plates. Reparative efforts between adjacent end plates and the joints cause sclerosis of subchondral bone and the formation of osteophytes. As the extent of contact surfaces and the transfer of force to equilibrate the new biomechanical demands increase, the surfaces expand and form disk-osteophyte complexes that constrict the neural foramen and spinal canal.19,2527

Unlike the lumbar nerve roots, which exit the foramen after a long oblique course, the cervical nerve roots exit through the neural foramen in a shorter, more direct transverse route. Moreover, the cervical neural foramen is mostly filled by the nerve root. These features make it difficult for the nerve roots to accommodate a decrease in the surface area of their foraminal exit. Consequently, clinical radiculopathy can be associated with an insignificantly small to moderately sized bone spur. Another potential cause of a disk-osteophyte complex is calcified herniated disk material.28 Overt trauma might exacerbate the symptoms of cervical spondylosis; however, its association with the development of cervical spondylosis has not been clearly established.29

As a degenerating disk fails biomechanically, load shared by the facets increases. Together with the ligamentum flavum, these structures become hypertrophied, thus further compromising the spinal canal posteriorly and the neural foramen.30 As the facet joints degenerate, this region becomes incompetent to shear stress, thereby leading to spondylolisthesis or retrolisthesis. Posterior disk-osteophyte complexes form from the inferior articular joint and may further constrict the dimensions of the intervertebral foramen and cause clinical symptoms.31 Occasionally, disk-osteophyte complexes become quite large and yet are clinically silent. However, in individuals with congenital cervical stenosis, relatively small osteophytes can compromise a large percentage of the spinal canal and produce significant clinical findings. In patients with spinal canals larger than 13 mm in the AP dimension, symptomatic cervical myelopathy rarely develops.32,33

In addition to anatomic constraints, the area of the cervical canal changes during flexion and extension.30,34 During flexion, the spinal cord lengthens and bows anteriorly such that it abuts the posterior surfaces of the vertebral column.35 In the presence of a posteriorly displaced osteophytic complex, the spinal cord stretches over these bars. As documented in autopsy studies, chronic changes develop.30,35 Local changes in areas of significant compression might affect the physiologic state of local neurons or axons via compressive forces or vascular compromise (venous or arterial).30,32,36

During extension, the posterior elements become a critical factor in the development of cervical stenosis. Extension of the cervical spine allows the ligamentum flavum to buckle inward and shortens the cross-sectional area available for the spinal cord. The spinal cord also shortens during extension, which increases its cross-sectional area and further compromises the cervical canal.32,37 In patients with degenerated disks, loss of height, disk-osteophyte complexes, and hypertrophied joints, as seen in older adults, extension injuries can be neurologically devastating.38

The overriding hypertrophied facets narrow the foramen and impale the exiting nerve roots. The size of the foramen can be further compromised by lateral bending and flexion, which causes radicular symptoms.32

The critical size of the spinal canal and foramen responsible for clinical symptoms is difficult to characterize with current imaging modalities. Individual anatomic and local biomechanical factors are responsible for the development of these symptoms and must be evaluated carefully on an individual basis.30,39 Excessive motion can cause ligamentous laxity and segmental instability and thereby contribute to myelopathic symptoms. The ligaments become incompetent and hypertrophied, and this condition is usually seen adjacent to surgically or degenerated fused levels. Excessive segmental loading results in degenerative subluxation, which further compromises the spinal canal.29

The actual pathophysiologic mechanism of myelopathy is not fully understood. Proposed theories include direct compression of the neural elements, ischemia from compromise of the vasculature, and repetitive microtrauma to the spinal cord with neck movements. The actual mechanism is probably a combination of direct microtrauma and vascular compromise. A study using a canine model of chronic cervical compression showed the characteristic irreversible pathologic findings of large motor neuron loss, necrosis, and cavitation in the region of the anterolateral gray matter at the level of greatest compression.40 There were also potentially reversible changes such as edema and demyelination. The authors postulated that changes in the dimensions of the spinal cord and canal in response to movement pinches the cord when the neck is in certain positions. The pinching then interferes with the microvasculature and causes ischemia in watershed areas.

Clinical Manifestations

Clinical symptoms of cervical spondylosis can develop in an insidious fashion and may include myelopathy, axial neck pain, occipital pain, shoulder pain, and radiculopathy. Myelopathic patients typically exhibit subtle changes in their gait, which tends to be broad-based, stumbling, spastic, and ataxic. Patients report difficulty going up an incline, buckling of their legs, and sensory disturbances in their proximal extremities. They may also report profound weakness and clumsiness of their hands, difficulty with writing and joint position sense, fine tremor, chronic and ill-defined numbness, and intrinsic musculature dysfunction. Bowel or bladder dysfunction characterized by urinary incontinence or retention can also be present. During flexion and extension, patients often report electrical shock–like sensations up and down the spine, a myelopathy known as Lhermitte’s sign. This sign usually indicates severe spinal cord compression and a dynamic component, possibly with incompetent structural support.

Physical findings in myelopathic patients include lower motor neuron disease at the level of the lesion and upper motor neuron disease below the level of the lesion. Hoffman’s sign may be elicited by flicking the middle finger and observing flexion contractions of the thumb and index finger. Reflex abnormalities can include hyporeflexia at the level of the compromised nerve root and hyperreflexia distally. Other findings may include altered suspended sensory disturbances, diffuse spasticity, diffuse hand weakness, proximal lower extremity weakness, clonus, and Babinski’s sign. The differential diagnosis of patients with symptoms of cervical spondylosis who may have myelopathy can include intrinsic medullary tumors, syringomyelia, multiple sclerosis, extramedullary tumors in the cervical or thoracic spine, subacute combined degeneration, hereditary spastic paraplegia, amyotrophic lateral sclerosis, normal-pressure hydrocephalus, and arteriovenous malformations.2,20,29,4143

Axial neck pain can result from segmental instability caused by disk degeneration and from direct nerve root compression. Myofascial syndromes have also been implicated in the development of axial neck pain.44 Occipital pain has been attributed to arthritic changes or instability at the C1 and C2 junction causing compression of the exiting C2 nerve root.45 Shoulder pain may be related to cervical disk degeneration, brachial neuritis, or nerve root compression at C3, C4, or C5.4649

The symptoms of cervical radiculopathy follow a specific dermatomal pattern corresponding to the involved nerve root. These features can include loss of motor strength, decreased reflexes, loss of sensation, and well-delineated pain along the dermatome of the nerve root. The most common radiculopathies involve the C5, C6, and C7 nerve roots (also see Chapter 278).24,50

In all cases of radiculopathy, the clinician can attempt to elicit radiating symptoms with provocative maneuvers. Spurling’s maneuver, performed by slight extension with lateral bending toward the symptomatic side and axial compression, can exacerbate and elicit radicular symptoms along a compromised nerve root.

Unusual manifestations of cervical spondylosis can include Brown-Séquard syndrome with ipsilateral hemiparesis, contralateral loss of pain and temperature sensation, and ipsilateral loss of joint perception.51 Although rare, an anterior spinal artery syndrome can result from thrombosis caused by compression of this vessel. This syndrome is associated with complete loss of motor function and sensation below the lesion with preserved joint and vibratory sensation. Vertebrobasilar insufficiency, manifested by nausea, vertigo, dizziness, and visual disturbances, has also resulted from osteophytic overgrowth in the transverse foramen.52,53 Anterior osteophytic spurs can grow quite large and cause dysphagia. This condition, however, is rare because osteophytes grow slowly and the esophagus is flexible and mobile.54,55

Diagnostic Studies

The diagnosis of cervical spondylotic myelopathy and radiculopathy includes the use of radiologic or electrophysiologic studies. Radiographic evaluation of cervical disease begins with comprehensive plain radiographic studies that include AP, lateral, and oblique views. Swimmer’s views are used to assess the cervicothoracic junction. Flexion and extension views can be helpful in patients with a history of trauma, evidence of spondylolisthesis, and previous surgical fusions. Plain radiographs must be evaluated carefully for the presence of congenital stenosis, misalignment, degenerative changes, and instability. A spinal canal less than 12 mm in diameter is considered to be abnormally narrow. One difficulty in relying on plain radiographs is the almost ubiquitous findings of cervical spondylosis in the aging population and the presence of degenerative changes in asymptomatic patients.1,34,56,57 Moreover, plain radiographs are inadequate for the assessment of soft tissue compression, such as ligamentous and disk herniation.

Magnetic resonance imaging (MRI) has become the mainstay for assessing cervical degenerative changes. It is rapid and accurate and does not involve the use of ionizing radiation. It is now the preferred method for screening patients suspected of having radiculopathy or myelopathy (Fig. 280-1).5860 MRI clearly visualizes the neural elements, as well as ligamentous and soft tissue structures. High-intensity signals within the spinal cord occur in areas of severe compression and suggest intrinsic neural damage, which has implications for postoperative prognosis.36,6163 MRI can provide excellent visualization of ligamentous disruption caused by trauma.64 This modality images the cervical spine in a multiplanar fashion, thereby facilitating visualization and anatomic definition of the disks and neural foramina and their compressive relationship to the exiting nerve roots. MRI can visualize bone marrow changes that suggest neoplastic, degenerative, inflammatory, or infectious processes. Moreover, MRI is a valuable tool for postoperative evaluation. However, it cannot adequately assess bony or osseous features, which should be imaged with computed tomography (CT).

CT provides cross-sectional views of the cervical spine, which allows clear visualization of disk-osteophyte complexes and calcified ridges. Myelography via injection of a water-soluble contrast agent into the subarachnoid space can be used to visualize the spinal cord and segmental nerve roots. Lateral and AP radiographs provide limited definition of compressive lesions. However, the combination of cervical myelography with postmyelography CT provides excellent definition of osteophytic ridges, herniated disks, and their relationship to the nerve roots and spinal cord. In cases of severe compression, CT-myelography allows visualization distal to myelographic blocks.65 CT-myelography is complementary to MRI for patients suffering from an ossified PLL and for those who have previously undergone instrumented fusion. In some cases, CT-myelography has provided enough definition to avoid vertebrectomy, thereby providing another point of fixation for the instrumentation and enhancing stability.

Electrodiagnostic studies can also be used to evaluate patients with radiculopathy or myelopathy. Such tests include electromyography (EMG), nerve conduction velocity (NCV), and somatosensory evoked potentials (SSEPs). These studies are usually performed when there are discrepancies between the clinical and radiographic findings or when other underlying conditions such as amyotrophic lateral sclerosis, multiple sclerosis, or peripheral neuropathy are suspected. EMG and NCV are performed concomitantly and can differentiate among radiculopathy, peripheral nerve pathology, and brachial plexus pathology. All of these electrodiagnostic tools suffer from a lack of specificity and sensitivity in localizing or grading the extent of compression. In selected cases, changes in SSEPs may serve as an objective measure of the progression of cervical spondylosis.66 In their model of chronic spinal cord compression, Al-Mefty and coworkers36 found that changes in SSEPs were present almost immediately before or at the time of initial neurological evaluation.

Preoperative diagnostic images must be evaluated carefully to ensure appropriate surgical planning.

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