Pathophysiology of Spondylosis

Knowledge of normal cervical spine anatomy is critical for understanding the pathologic processes that affect it. Cervical spondylosis results from progressive biomechanical stress and strain and can be compounded by repetitive trauma. The process involves noninflammatory disk degeneration (amphiarthrodial joint without a synovial membrane) and is accompanied by facet joint osteoarthritis (zygapophyseal diarthrodial joint lined with a synovial membrane), as well as pathologic changes of the posterior longitudinal ligament and ligamentum flavum such as hypertrophy, laxity, ossification. A normal disk is composed of the nucleus pulposus, which is a water-rich gel (as a result of proteoglycan aggrecan molecules that attract and entrap water) in the center of the disk, and the annulus fibrosus, which is the fibrous outer portion of the disk. The annulus fibrosus is made of type I collagen and is organized into individual sheets called lamellae that are oriented at a 60-degree angle. The very outer lamellae, also called Sharpey’s fibers, are anchored directly into the bony matrix at the periphery of each vertebral body, just outside the cartilaginous vertebral end plate. Also of note, in a healthy cervical spine, the height of the vertebral body is slightly greater anteriorly. Such a vertebral body angle, in addition to the flexible disk, ensures the naturally lordotic sagittal curvature with the center of the axial loading plane within the middle column.

As part of normal aging, degenerative biochemical changes occur in hydrophilic proteoglycan molecules that result in loss of adsorbed water. This eventually leads to a decrease in viscoelasticity of the nucleus pulposus and a reduction in its overall volume and disk height. As a result, the stress under an axial load is translated to the annulus fibrosus and it bulges, with eventual wear and tear causing thinning and further fibrosis. The weakened lamellae allow the fibrotic nuclear material to dissect through the fibers and disrupt the attachment of Sharpey’s fibers to the edges of the vertebral body bone. Subsequently, this process stimulates reactive bony growth and is the origin of early osteophyte formation. In a more acute scenario, dissection of nuclear material through the weakened annulus causes disk herniation. The recent literature shows that the delamination process of the annulus during progressive cervical disk herniation occurs within the lamellae rather than between them, without evidence of any annulus rupture or failure.¹

Early reactive bone growth ultimately causes osteophyte spur and ridge formation, which leads to infolding and peeling of the posterior longitudinal ligament from the bone and secondary hypertrophy and ossification. In addition, the loss of disk space height causes initial straightening of the normally lordotic sagittal curvature of the cervical spine. As the center of axial loading shifts anteriorly, a cycle of further degeneration contributes to the chronic compressive vertebral body changes that eventually result in a kyphotic deformity.² These changes lead to abnormal cervical spine biomechanics and subsequently to hypertrophy or laxity of the facet joint and ligamentum flavum. The cervical spine hypermobility or instability is pathologically stabilized by osteophyte bar formation and uncovertebral joint degeneration. Multiple studies have demonstrated a significant decrease in mobility with advanced age.³ In a more recent study by Miyazaki and colleagues, magnetic resonance imaging (MRI) was performed on patients with degrees of spondylosis ranging from very mild to very severe.⁴ The early degenerative process affected the mobility of the functional spinal unit, which changed from a normal disk to a more unstable phase with increased mobility. As the degeneration entered later phases, the motion segment stabilized and became more ankylosed. The C4-5 and C5-6 segments were shown to contribute most of the total angular mobility, but their contribution to total angular mobility decreased significantly after severe degeneration. This degenerative cascade eventually leads to neuroforaminal or spinal canal stenosis, or both.

Pathophysiology of Pain

Patients can have clinically significant neurological symptoms or objective findings during any of the aforementioned stages. Symptoms can range from mild axial neck pain to severe cervical myelopathy. Even though the actual source of pain in cervical spondylosis is controversial, there is consensus that it originates from degeneration of the cervical disk or facet joint (or both).⁵ Multiple studies have demonstrated very rich innervation, both somatic and autonomic, of the cervical intervertebral disk and facet joint.

As the cervical nerve root exits the neuroforamina, it splits into ventral and dorsal rami, which are the source of somatic, proprioceptive, and nociceptive input. The small branches (somatic root) of the ventral ramus join the vertebral nerve (autonomic root) to form the sinuvertebral nerve. The vertebral nerves are formed by the gray rami communicantes, which are branches of the sympathetic trunk and the stellate ganglion. The sinuvertebral nerve arborizes superiorly and inferiorly as it enters the cervical canal through a neuroforamen and supplies the posterior aspect of the annulus (up to the posterior third), the posterior longitudinal ligament, and the dura. The anterior longitudinal ligament and anterior annulus are innervated by the sympathetic trunk and recurrent branches of the gray rami communicantes. It is reasonable to conclude that an annular tear can cause increased afferent output that can be the source of axial neck pain. Moreover, Bogduk and coworkers have proposed that intervertebral disks, especially when under significant stress, can be the source of pain even without obvious annular rupture or herniation.⁶ An internal annular rupture would suffice because it can cause enough inflammatory changes as it encroaches on the deep and rich innervation of the annulus fibrosus.

In addition to the cervical disk being a source of axial neck pain, the cervical facet joint can also be an important source. The dorsal rami of the cervical nerve roots supply most of the innervation to the facet joints, which are rich in mechanoreceptors and nociceptive nerve endings. Studies by Dwyer and associates have confirmed that stimulation of the facet joint produces a clinically distinguishable, characteristic pattern of pain that enables the construction of pain charts.⁷ Practitioners can use these charts to isolate the symptomatic joint in patients with cervical zygapophyseal pain. Some authors believe that facet joint pain could be of primary importance, especially in neck pain associated with whiplash injury.⁸

Pathophysiology of Radiculopathy

The pathologic changes in patients with cervical radiculopathy can be divided into acute and chronic. Acute radiculopathy is usually secondary to soft disk herniation and occurs in a younger patient group. The inflammatory process, which involves a cytokine-mediated response, leads to a decrease in the number of large-diameter myelinated axons. This finding can be seen within the first week⁹ and results in relatively more prominent motor findings. Chronic radiculopathy, in contrast, usually causes predominantly sensory complaints and is more commonly seen in an older patient group. Chronic radiculopathy is associated with cervical spondylosis. Jancalek and Dubovy showed that changes include thickening of the dura mater and arachnoid membrane around the affected nerve root with associated alteration of the blood-nerve barrier, which eventually leads to nerve root dysfunction as a result of chronic compression.¹⁰

Pathophysiology of Myelopathy

Multiple pathologic processes that eventually lead to similar pathologic cervical cord changes in the white and gray matter can cause cervical myelopathy. Even acute cervical cord injury (despite representing a different mechanism and manifestation) has been shown to result in similar pathologic cord findings as those of indolent cervical spondylosis.¹¹

The pathogenesis of myelopathy in patients with cervical spondylosis should be subdivided into three main components that are responsible for the final cord changes.¹² The first consists of static factors, which are processes that lead to cervical canal stenosis and cord compression. The second consists of dynamic factors caused by repetitive movement of the compressed cord, which is associated with decreased elasticity and susceptibility to stretch-associated injury. The third component is the final cord changes that are seen histopathologically and include vascular rearrangement, arterial- or venous-induced ischemia and infarction (or both), oligodendrocyte apoptosis, and other cytotoxic cell changes.

The static factors that contribute to decreased canal diameter include acquired spondylosis of the disk, facet, vertebral bodies, and ligaments and subsequent loss of the lordotic curvature. In addition, other less common conditions can contribute, such as congenital cervical stenosis, ossification of the posterior longitudinal ligament, and ossification of the ligamentum flavum. Patients with congenital cervical stenosis are initially asymptomatic but eventually progress to severe cord compression and usually become symptomatic by the third decade. The normal sagittal cervical canal diameter has been identified as being approximately 17 to 18 mm. Based on multiple studies, the canal is considered stenotic when smaller than 13 mm,¹³ which is associated with a high risk for the development of cord compression with myelopathic changes.

The dynamic factors resulting in cervical cord injury are multifactorial. First, the movements of a severely compressed cord are restricted. Second, flexion of the spine results in overstretching of the cord. This effect is more severe in the setting of a prominent ventral osteophyte complex or with a kyphotic deformity. Conversely, extension causes posterior cord compression by buckling of the ligamentum flavum and shingling of the laminae. Some studies, including MRI, show both flexion- and extension-induced compression, with extension-associated injury causing more severe compression. Panjabi and White^13a showed that axial rotation and lateral bending do not cause as significant cord indentations as do sagittal movements. As mentioned earlier, the spondylotic spine can become unstable and result in repetitive cord injury during flexion-extension movements. Furthermore, the spinal cord’s ability to tolerate stretch decreases with age, and thus older adults become extremely susceptible to stretch injury.¹⁴ In animal studies, Shi and Pryor confirmed three types of conduction block resulting from and correlating with the extent of stretch injury in the absence of pathologic variables related to vascular damage¹⁵: an immediate, spontaneously reversible component that may result from a transient increase in membrane permeability that affects ionic distribution; a second component that may be due to perturbation of the myelin sheath and was reversible with the use of a potassium channel blocker; and a third component that was irreversible and resulted from profound axolemmal disruption.

Finally, the last well-described pathogenesis of myelopathy is cord ischemia. Spondylotic cord compression causes the pathologic butterfly pattern of cord ischemia that affects the gray and medial white matter. This pattern is also consistent with a vascular hypoperfusion injury. The compression probably affects flow in the small pial and intramedullary arterioles, as well as the larger anterior spinal artery. Venous congestion may also play a role and lead to venous infarction. All these processes can result in cord cavitation and delayed syringomyelia and are probably similar to traumatic syrinx formation. In further support of this ischemic theory, oligodendrocytes have been shown to undergo apoptosis, similar to the pathologic changes in traumatic cord injury.

Cervical Pain

Patients with chronic pain as a result of a degenerated cervical disk usually complain of axial neck pain that is exaggerated with flexion. As a consequence of facet degeneration or instability, or both, any movement of the sensitive joint can cause pain that has a reproducible regional pattern.

Cervical Radiculopathy

When radiculopathy is suspected, a thorough examination is needed. As mentioned earlier, younger patients generally exhibit greater motor involvement from acute soft disk herniation. In contrast, older patients with extensive spondylosis usually have primarily sensory and fine motor problems. Moreover, their disease tends to be multilevel. The Spurling and abduction relief signs also help confirm the radicular nature of the disease.

Radiculopathy is usually characterized by level-specific clinical findings, as outlined in the following list:

Cervical Myelopathy

Identifying signs of cervical myelopathy is critical in evaluating any patient with spondylosis because it can affect the treatment strategy. Because the etiology of cord compression is primarily chronic degeneration, patients rarely have acute signs as they would in a traumatic setting.

Cervical myelopathy is most commonly seen in the setting of progressive chronic spondylosis causing cord compression. Symptoms can be subdivided on the basis of upper or lower motor neuron injury. Lower motor neuron injury is secondary to alpha motor neuron or exiting nerve root compression (or both). Patients complain of dermatomal weakness, tingling, numbness, and decreased fine motor coordination. Examination reveals atrophy and weakness of the arms or hands, diminished pinprick sensation in the fingers, and decreased deep tendon reflexes. Upper motor neuron injury is secondary to long tract compression and subsequent dysfunction. The primary tracts responsible for symptoms in patients with cervical compression myelopathy are the corticospinal (motor), spinothalamic (pain and temperature), dorsal column (vibration and proprioception), and spinocerebellar (motor tone and coordination) tracts. The usual complaints are unsteady/clumsy gait, leg rigidity, altered sensation, and bowel and bladder dysfunction (in the late stages). Physical examination reveals lower extremity spasticity and diffuse hyperreflexia with the possible presence of the Babinski, clonus, or Hoffman reflexes, or any combination of these reflexes (Hoffman’s sign is present if the cord compression is higher than C7/C8 and is causing long tract injury). The deterioration in gait is generally the result of overall lower extremity spasticity rather than weakness.

Roentgenography

Even though multiple other imagining modalities have been developed that are better than plain films, radiography still has an important role in imaging the cervical spine in patients with spondylosis. Plain radiographs provide a detailed rendering of the bony anatomy. Fractures of the vertebral body, pedicle, and lamina can be diagnosed. Pathologic bone changes such as spondylosis (osteophytes), erosive lesions (infection, tumors), or trauma (fractures) can easily be seen. Sagittal canal diameter can be measured. The anteroposterior and lateral views provide important information on the overall alignment in any posture. Flexion and extension lateral radiographs are still the primary means of identifying instability.

Computed Tomography

With sagittal, coronal, and three-dimensional reconstructions, computed tomography (CT) is a very useful way of looking at normal and abnormal cervical spine bony anatomy. The hyperdense signal of bone algorithm CT allows visualization of the vertebral body, pedicle, lateral mass, laminae, and spinous process in exquisite detail. Fractures are seen as radiolucencies that (along with distortions in surrounding soft tissue anatomy) allow a more specific diagnosis and decrease the risk of missing pathology. Any abnormal bone growth (osteophyte, ligament ossification), erosions, and distortion are easily seen. The hypodense appearance of the neuroforamina and canal allow more accurate visualization and correlation with the bony anatomy than possible with plain radiography. Unfortunately, CT alone is of little value in assessing the soft tissues, but CT-myelography (CTM) (with water-soluble intrathecal contrast material injected before CT), however, is invaluable in evaluating either cord or nerve root compression. Instillation of contrast material into the subarachnoid space around the spinal cord and nerve roots allows very high sensitivity regardless of the cause of the compression. CTM can actually be superior to MRI in some patients, especially those with postoperative scars or instrumentation or those who are claustrophobic or cannot undergo MRI for other reasons (e.g., indwelling pacemaker). With the technique of double-contrast CTM, in which an intravenous contrast agent is given in addition to intrathecal contrast, one can significantly increase both sensitivity and specificity for the diagnosis of radiculopathy. In patients in whom the subarachnoid space of the cervical root sleeve does not extend into the neuroforamina, the intravenous contrast–enhancing periradicular epidural veins appear hyperdense. If neuroforaminal compression is present, the absence of hyperdense signal would confirm the diagnosis because of compression of the extradural periradicular space.

Magnetic Resonance Imaging

MRI revolutionized the management of cervical spine pathology. Before MRI, there was no way of actually looking at both the neural structures and surrounding tissues, including cerebrospinal fluid, ligaments, disks, facets, and vertebral bodies. Some studies report an accuracy of MRI in diagnosing surgical pathology as high as 98% (i.e., cervical disk herniation). With the different signal acquisition techniques (e.g., T1 or T2), we not only can see unique anatomic details but can also see the changes within specific tissues, such as a dehydrated black disk. One can also appreciate the relationship between two or more different structures because of different signals, such as a herniated disk and nerve root. In myelopathy, MRI allows visualization of the changes in signal within the cord and thereby aids in diagnosis and treatment planning.

Neurophysiologic Studies

In patients with a clinical syndrome of cervical radiculopathy and confirmatory imaging (MRI or CTM), neurophysiologic studies are not usually needed. However, when one is not certain about the patient’s examination and the imaging findings are of little value, neurophysiology becomes an important adjunct, especially in differentiating cervical radiculopathy from peripheral nerve processes. The test consists of a nerve conduction study (NCS) and needle electromyography (EMG). NCS has four components: motor NCS, sensory NCS, F-wave study, and H reflex. The measured latency, amplitude, persistence, and conduction velocities are analyzed and correlated with findings on EMG. Needle EMG, in contrast, records and analyzes the signal in the muscle of a specific cervical myotome, with the presence of fibrillation potentials and positive sharp waves being indicative of muscle fiber denervation. It usually takes 3 weeks for EMG-detectable changes to develop in the denervated muscle, so one should wait at least 3 weeks from the time of initial symptoms to perform the test. Sensory evoked potentials and transcranial motor evoked potentials are of no value in diagnosing radiculopathy or peripheral nerve pathology but can be used for evaluation of intramedullary processes or intraoperative monitoring.

Diskography

Diskography in the cervical spine remains very controversial, and there is weak medical evidence to support fusion of diskography-positive disks for the treatment of axial neck pain. In patients with chronic axial neck pain but without any definite or conclusive imaging findings to implicate a specific level, diskography may add useful information. The specific indication for the test should be to confirm or evaluate suspected one- or two-level disk disease, generally in patients with de novo axial neck pain that fails conservative treatment. To be used appropriately, concordant pain should be carefully correlated with both the clinical and imaging findings. A recent systematic literature review by Buenaventura and associates showed strong evidence that intradiskal distention (by injecting a small amount of fluid) can produce pain and moderate evidence supporting its use in identifying patients with chronic cervical diskogenic pain.¹⁶

Epidemiology

The goal of any treatment should first of all be guided by the natural history of the disease. Cervical spondylosis is a chronic degenerative process, so one should expect to see its prevalence increase significantly with age. Multiple radiographic studies have looked into the epidemiology of cervical spondylosis, and one of the earliest, by Lawrence in 1969, showed that the prevalence based on cervical plain radiographs increases with age¹⁷: the prevalence of spondylosis (grades 1 to 4) increased from 15% at 34 years of age, to 60% at 54 years, and to 90% at 65 years and older, with moderate to severe spondylosis (grades 2 to 4) in 8%, 55%, and 85%, respectively (Fig. 278-1). The peak prevalence of symptomatic pain, defined as neck-shoulder-brachial pain, was 9%. A history of nerve root involvement was noted in just 1.7% of the 662 patients studied with moderate to severe cervical spondylosis. Other studies have confirmed the increasing prevalence of cervical spondylosis with age. More recently, Boden and coworkers substantiated the earlier findings with an MRI-based study. Evidence of cervical degeneration was observed in 90% of men older than 50 years and 90% of women older than 60.¹⁸

FIGURE 278-1 Prevalence of disk degeneration based on radiographic findings.

(From Lawrence JS. Disc degeneration. Its frequency and relationship to symptoms. Ann Rheum Dis. 1969;28:121-138.)

Cervical Pain

The symptoms of chronic neck pain or neurological dysfunction, or both, are less common than the correlative imaging findings. The prevalence of chronic neck pain (duration longer than 6 months in most studies) is approximately 10% in large population studies from Norway and Finland.¹⁹ As mentioned earlier, degeneration of the disk and facet joint is probably responsible for the chronic pain in most cases, with other possible causes including radiculopathy, myelopathy, and spondylotic instability. C3 and C4 radiculopathy can also be manifested as trapezoidal and posterior scapular pain, which may require surgical decompression. Confirmatory findings on imaging usually include the dehydrated disk with or without annular tears or facet joint hypertrophy. Treatment is almost exclusively conservative. A nonsteroidal anti-inflammatory drug (NSAID) is a good initial choice. If the pain becomes severe, opioid analgesics and muscle relaxants may be started. Most types of axial neck pain should respond to medical management, especially in those with a history of traumatic whiplash. If there is still no relief and significant disability is present, further differentiation is needed. Provocative diskography and facet joint anesthetic blocks can identify the sensitive component. Based on the findings, one should proceed with either facet joint injection or disk blocks. Physical therapy, primarily isometric exercises, have also been shown to help. If the pain is posterior (dorsal rami) in origin and has a good response to facet joint injection, radiofrequency ablation may provide longer relief of pain. Only patients who fail extensive conservative treatment with correlative imaging and diskographic findings should be considered for surgery. These authors emphasize, however, that there is little medical evidence to support the use of cervical fusion for the treatment of axial neck pain (even if thought to be due to disk degeneration).

Cervical Radiculopathy

Cervical radiculopathy is less common than axial neck pain and occurs in 0.5% to 3% of individuals, with a peak incidence around the age of 50. In 1963, Lees and Turner showed that in about half of patients, the radicular symptoms resolve even though some of these patients might have one temporary recurrence.²⁰ About 25% had improved but persisting symptoms, and in about 20% of patients the symptoms persist or worsen. In a prospective nonrandomized multicenter study by Sampath and colleagues, 246 patients with a primary symptom of cervical radiculopathy were monitored.²¹ Of these, 155 (63%) returned for follow-up, with 58 (37%) undergoing surgical treatment. When comparing the results in both groups, the surgically treated patients had better overall outcomes with greater average patient recovery despite having significantly worse symptomatology and overall disability initially. Patient satisfaction was higher in the surgically treated patients (80% versus 60%), and even though 75% of the surgically treated patients were reported as being “cured” of their radiculopathy, 26% continued to report significant pain with some neurological deficits, thus limiting their work ability. Also, Boden and coauthors reported a high incidence of asymptomatic disk herniation, with true disk herniation found in 10% of asymptomatic patients younger than 40 years as opposed to just 5% of those older than 40.¹⁸ One should conclude that the natural course of radiculopathy is more benign than that of myelopathy, but not as benign as cervical pain alone. A significant proportion of radiculopathy patients, especially those with milder symptoms, readily respond to an initial course of conservative treatment.

The conservative treatment modalities for cervical radiculopathy should consist of rest, medications (NSAIDs, steroids), a cervical collar, physical therapy, patient education, and local injections. The initial period of rest should be restricted, with immobility limited to a few days to avoid deconditioning and decreased recovery potential. Because the inflammatory cytokine-mediated process is responsible for some of the pain in patients with acute soft disk herniation, NSAIDs or steroids (or both) should be a good first line of treatment. A short course of steroids can have a profound effect, especially on acute motor neurological recovery. Cervical epidural injection can deliver steroids locally and has been shown to produce a good temporary response. An opioid analgesic can be used to treat severe pain. Muscle relaxants are used for muscle spasms, and neuropathic anticonvulsants (i.e., gabapentin) can provide neuropathic pain relief. Multiple exercise modalities have been developed to treat radiculopathic pain, in addition to traction, which can help by opening the neuroforamen. Patients should have a good response to treatment, especially with steroids. Indications for surgery include any of the following: acutely worsening neurological status, persistence or progression of neurological deterioration despite conservative treatment, or persistent or recurrent arm pain for longer than 6 weeks with confirmatory imaging findings.

Cervical Myelopathy

Because the pathophysiology of cervical myelopathy includes three components—static, dynamic, and cord ischemia—minimizing any of these components would slow progression of the myelopathy. Most of the literature in support of conservative treatment recommends intermittent cervical immobilization for at least 8 hours a day to affect the dynamic component, with some variations.^22–24 These studies were conducted over a very short period with a small number of patients. They showed marginal improvement in some patients, with worsening symptoms developing in a significant proportion. In one frequently quoted example, Matsumoto and coworkers in 2001 subjected 27 patients to conservative treatment, with 17 of the 27 showing improvement in Japanese Orthopedic Association scores from 16.2 to 13.6, but 10 patients underwent surgery because of neurological worsening.²² These results certainly raise questions about the utility of intermittent cervical immobilization to treat a lifelong progressive disease.

Lees and Turner²⁰ in 1963 and Nurick²⁵ in 1972 showed the progressive nature of cervical myelopathy, especially in the group older than 60 years. Instead of steady worsening, most patients exhibited long quiescent periods with phases of deterioration. Notably, a significant number of patients with very mild symptoms did not progress over very long-term follow-up (up to 14 years). There have been no good prospective randomized studies that evaluated surgical versus conservative treatment of cervical myelopathy. A prospective nonrandomized trial by Sampath and colleagues showed decreased overall pain and improved functional outcome with surgical treatment, but no comparative neurological improvement.²⁶ However, multiple retrospective studies have demonstrated neurological improvement after surgery. Based on these findings, one cannot predict the course of symptoms for a single patient with mild cervical myelopathy. Careful follow-up studies and neurological examination are therefore necessary, and patients who progress should be considered for surgery.

Cervical Pain

The sinuvertebral nerve arborizes over the posterior longitudinal ligament and extends at least one level above and one level below as it enters the cervical canal through the neuroforamen at every level. As a result, pain originating from three adjacent disks can potentially be contained in one specific sinuvertebral nerve complex, or conversely, one disk can be innervated by two or three overlapping nerves. Such a diffuse distribution of neuronal sensory output is probably the reason for the overlapping pain pattern results seen with diskometry. It has also been shown that stimulation of the sinuvertebral nerve causes a spasmodic response of the surrounding musculature, thereby complicating the interpretation of results. Nonetheless, discordant pain within normal-appearing adjacent disks is not inconsistent with good surgical outcomes for fusion of disks with concordant pain.^27,28 Furthermore, patients who undergo analgesic diskography (injection of lidocaine into the disk) and have relief of symptoms may be good candidates for surgery. In a study of axial neck pain published in 1976, Roth reported 93% good or excellent results 2 years after surgery.²⁹ This group of patients with primarily diskogenic pain who failed conservative treatment and had characteristic imaging findings can be considered for one- or two-level anterior cervical diskectomy and fusion (ACDF). In some patients, however, facet joint disease can be partially responsible for the axial pain. The reproducible regional pattern of pain generated on stimulation of a facet joint includes an axial component of pain. Unfortunately, even though facet blocks or other ablative (percutaneous radiofrequency neurotomy) procedures have been shown to be somewhat beneficial, considerable controversy remains. In patients who are shown to have a facet joint pain pattern, posterior fusion could be considered. Nonetheless, despite some of its drawbacks, diskography is our primary method of evaluating axial neck pain clinically. In most centers, however, fusion is seldom recommended for the treatment of axial neck pain without associated radiculopathy or myelopathy.

Cervical Radiculopathy

The goal of surgery for primarily radicular symptoms should be decompression of the affected nerve root or roots. As mentioned earlier, surgery is indicated for patients who exhibit acute deterioration, progressive neurological worsening, or persistent arm pain despite a trial of conservative treatment. It is critical to identify patients who might also have evidence of myelopathy on examination or have radiographic changes that might predispose them to myelopathy because the treatment strategy may be different. Two primary approaches have been well described: posterolateral laminoforaminotomy and anterior cervical diskectomy with or without fusion. It should be noted that one-level or multilevel laminectomy is rarely indicated for typical radiculopathy. When it is considered, evaluation of sagittal cervical spine alignment is critical. The presence of a cervical kyphotic deformity should be recognized as a relative contraindication to comprehensive posterior decompression.

Cervical Myelopathy

Even though some of the surgical techniques for the treatment of cervical myelopathy are similar to those for radiculopathy or axial neck pain, the objective of surgery is different. The goal of surgery for cervical myelopathy is decompression of the spinal cord, restoration of sagittal alignment, and stabilization of any instability.

In choosing an approach for any patient with cervical myelopathy, a few important factors have to be evaluated. The most important are the sagittal curvature and the site of compressive pathology. Naderi and associates defined the difference in sagittal cervical curvature (from effective lordosis, to straightened, to a kyphotic spine).⁵⁴ In evaluating the intrinsic curvature, a line is drawn from the dorsocaudal aspect of the C2 vertebral body to the same C7 point to create the associated gray zone (Fig. 278-2). Effective lordosis is defined when the shaded gray zone is posterior to any of the vertebral bodies. A straightened cervical spine occurs when the posterior-most aspect of the vertebral body is within the gray zone. Effective kyphosis is seen when any portion of the vertebral bodies is posterior to the shaded gray area. In addition to the sagittal curvature, the location of the compressive pathology is critical (Fig. 278-3). In a patient with fewer than three levels of ventral disease, the anterior approach is preferred. Patients with more than three levels of compression are generally treated by posterior decompression, especially with preserved lordotic curvature. A multilevel laminectomy is less demanding overall than an equivalent anterior approach and is associated with shorter operative times and fewer perioperative complications. Laminoplasty should be considered when multilevel posterior decompression is planned, particularly if lordosis is preserved. Preoperative dynamic cervical radiographs should be obtained. In patients with marked stiffening or ankylosis (as commonly seen in older adults), posterior decompression alone might suffice. Younger patients with full range of motion in flexion and extension are at risk for a delayed swan neck deformity after laminectomy, so the surgeon should consider including concomitant lateral mass fixation and posterolateral fusion. Additionally, patients with mobile subluxation at one or several levels should be considered for posterior instrumentation and fusion when multilevel laminectomy is performed.

FIGURE 278-2 Progression of sagittal alignment in patients with cervical spondylosis from lordosis (left), to straightened (center), to kyphosis (right).

(From Naderi S, Benzel EC, Baldwin NG. Cervical spondylotic myelopathy: Surgical decision making. Neurosurg Focus. 1996;1(6):e1.)

FIGURE 278-3 Surgical treatment algorithm for cervical spondylotic myelopathy.

The presence of posterior ligamentous hypertrophy is directly dealt with during posterior decompression. In the presence of cervical lordosis, posterior decompression will lead to dorsal migration of the spinal cord away from the ventral pathology and result in indirect decompression (see Fig. 278-2). The posterior approach is contraindicated in patients with kyphosis but can be used as additional stabilization in those who require aggressive, long-segment (greater than two-level vertebrectomies) anterior correction and decompression. Clinical and surgical judgment is critical in assessing patients with cervical myelopathy (see Fig. 278-3). The major advantages and disadvantages of the anterior and posterior approaches are summarized in Table 278-1.

TABLE 278-1 Advantages and Disadvantages of the Anterior and Posterior Approaches to Cervical Myelopathy

From Clark CR, ed. The Cervical Spine, 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2004.