Secondary Logo

Journal Logo

AAPA Members can view Full text articles for FREE. Not a Member? Join today!

Diagnosis and medical and surgical management of cervical spondylotic myelopathy

SaterenZoller, Elizabeth MSPAS, PA-C; Cannella, Dominic MD; Chyatte, Douglas MD; Fogelson, Jeremy MD; Sharma, Manish MBBS

Journal of the American Academy of PAs: October 2015 - Volume 28 - Issue 10 - p 29–36
doi: 10.1097/01.JAA.0000471607.77031.03
CME: Orthopedics
Free
CME

ABSTRACT Cervical spondylotic myelopathy is a complex condition with subtle history and examination findings that mimic other conditions. Primary care physician assistants often are the first providers to evaluate these patients. This article describes cervical spondylotic myelopathy, its diagnosis and management, and recent data that offer strong evidence that patients who undergo surgical decompression show significant improvement over patients who are treated conservatively.

Elizabeth SaterenZoller practices neurosurgery at the Mayo Clinic Health System in Mankato, Minn. Dominic Cannella is a consultant neurosurgeon in the Department of Neurosurgery at Immanuel St. Joseph Hospital, part of the Mayo Clinic Health System in Mankato. Douglas Chyatte is a professor of neurosurgery at the Mayo Clinic Health System in Mankato. Jeremy Fogelson is a neurologic surgeon and assistant professor at the Mayo Clinic in Rochester, Minn. Manish Sharma is a consultant in neurologic surgery at the Mayo Clinic Health System in Mankato. The authors have disclosed no potential conflicts of interest, financial or otherwise.

Earn Category I CME Credit by reading both CME articles in this issue, reviewing the post-test, then taking the online test at http://cme.aapa.org. Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of October 2015.

Box 1

Box 1

Cervical spondylosis is a result of age-related degenerative changes of the cervical spine, and can cause structural abnormalities such as stenosis of the cervical vertebral canal, osteophytic overgrowth, intervertebral disk protrusion, and/or hypertrophy of ligamentous components. Additionally, subluxation may occur, contributing to stenosis and resulting in a kyphotic deformity.

Spondylosis is present on radiographs in 70% to 95% of patients by age 65 years, although most of these patients are asymptomatic.1,2 Symptomatic patients may present with complaints of pain in the neck or shoulders. Radiculopathy or myelopathy are present in 10% to 15% of patients with spondylosis.3 Radiculopathy results from direct compression of a nerve root and can produce pain, paresthesias, or weakness in the distribution of the nerve roots. Myelopathy, conversely, is compression of the spinal cord with or without vascular compromise. The clinical picture has a wide spectrum, ranging from radiographic evidence with mild symptoms, such as minor alterations in sensation, to quadriparesis. Pure myelopathy can be painless; it may also occur with dysesthetic funicular central pain (Table 1).

TABLE 1

TABLE 1

Back to Top | Article Outline

EPIDEMIOLOGY

Although the radiographic presence of cervical spondylosis and stenosis is nearly ubiquitous in middle age and after, the clinical syndrome of cervical spondylotic myelopathy is much less common. The average age of onset of cervical spondylotic myelopathy is between 50 and 70 years, with a mean age at diagnosis of 64 years.1 In general, men are more commonly affected than women (3:2).4,5 The natural course of the disease is variable and poorly defined without universally accepted prognostic factors. Some patients progressively decline, some present with a rapid decline followed by a lengthy period of quiescence, and still others may show spontaneous improvement.6-8

Back to Top | Article Outline

ANATOMY

The cervical spine comprises seven cervical vertebrae with the spinal cord contained within the central vertebral canal. Traversing laterally from foramina in each vertebra is a pair of spinal nerves named for the vertebra immediately caudal (for example, C6 nerve roots are immediately above the C6 vertebra). The exceptions to this rule are the C8 nerve roots, which have no corresponding cervical vertebra and lie between C7 and the first thoracic vertebra (Figure 1). Durable ligaments (anterior and posterior longitudinal ligaments, ligamentum flavum, and interspinous ligament) course the length of the spinal axis, appending the vertebrae.

Box 2

Box 2

FIGURE 1

FIGURE 1

Back to Top | Article Outline

ETIOPATHOGENESIS

As the body matures, degenerative changes take place that include disk desiccation and loss of disk height, osteophytic spurring, hypertrophy of the ligamentum flavum and facet joints, and subluxation. These changes can result in stenosis of the central vertebral canal that encloses the spinal cord and narrowing of the neural foramina through which the spinal nerves traverse (Figures 2 through 5). Static compression of the neural tissue from stenosis can cause myelopathy or radiculopathy or both (myeloradiculopathy).4 Dynamic compression of the cervical neural tissue also may produce symptoms. As the spinal cord elongates in flexion, osteophytic spurs and bulging intervertebral disks (referred to collectively as spondylotic bars) apply pressure to the anterior aspect of the cord. Conversely, in extension, the hypertrophic ligamentum flavum or facet joints impinge on the posterior surface of the cord. In addition to direct mechanical insult, the process of dynamic compression has been shown to compromise the vasculature supplying the cord, resulting in varying degrees of ischemia.1,3,7

FIGURE 2

FIGURE 2

FIGURE 3

FIGURE 3

FIGURE 4

FIGURE 4

FIGURE 5

FIGURE 5

Chronic disk degeneration is the most common cause of cervical spondylotic myelopathy in patients over age 55 years.3,4 Patients with a congenitally narrow vertebral canal (less than 13 mm anteroposterior [AP] diameter compared with the normal diameter of 17 to 18 mm) may be predisposed to cervical spondylotic myelopathy; the two conditions often occur together.7,8 The degree of compression is often proportional to the severity of the clinical presentation, yet remains unpredictable.8

Back to Top | Article Outline

CLINICAL FEATURES

A high clinical suspicion should guide further investigation. Patients with mild symptoms may present with complaints of increasing gait or balance disturbance, or difficulty negotiating fine-motor tasks such as buttoning clothing, writing, or handling a telephone or cutlery.2,7,8 Although most patients present with a pure myelopathy, as many as 41% may present with a concomitant radiculopathy, causing pain, paresthesias, or weakness in a dermatomal pattern, possibly with muscle wasting and hyporeflexia.10 Signs of pure myelopathy include upper limb hyperreflexia (depending on whether the level of compression is at or above the corresponding upper limb nerve root), atrophy of the intrinsic muscles of the hand, difficulty with rapid grip and release exercises of the hands, and a Hoffman sign (thumb and finger flexion when the nail bed of the ipsilateral long finger is flicked). Other common signs of significant myelopathy include gait disturbance with lower extremity spasticity and a scissor gait. Lower limb reflexes are generally exaggerated with an upgoing toe to plantar or lateral malleolus stimula-tion, known as Babinski and Chaddock signs, respectively. Ankle clonus also may be present.3,4,7 Patients with advanced and severe myelopathy may have bowel or, more commonly, bladder urgency and incontinence. Sensory signs and symptoms often are a less-prominent feature of myelopathic disease. When present in the upper extremities, features include signs of lateral spinothalamic tract involvement with impaired pain and/or temperature discrimination. In the lower extremities, difficulty with tandem gait, a positive Romberg sign, and/or impairment of vibratory or joint position sense indicate involvement of the dorsal column.1,7 Funicular, or central, burning, lancinating pain also may be present (Table 1).

Back to Top | Article Outline

SCORING OF SEVERITY

The Nurick, Japanese Orthopaedic Association and modified Japanese Orthopaedic Association scores, Cooper myelopathy scale, Prolo score, and European myelopathy score are commonly used scoring systems to objectively quantify disease severity. These are valuable tools in the initial assessment and subsequent evolution of a patient's condition and may be used in concert with a detailed neurologic examination.10-12

Back to Top | Article Outline

DIFFERENTIAL DIAGNOSIS

Physician assistants (PAs) must remain attuned to other disease processes with presentations similar to cervical spondylotic myelopathy. The differential diagnosis includes peripheral neuropathy, brachial or lumbar plexopathy, multiple sclerosis, and motor neuron diseases such as amyotrophic lateral sclerosis. Trauma, Lyme disease, neurosyphilis, vascular insufficiency, subacute combined degeneration of the cord secondary to pernicious anemia, and HIV-associated myelopathy also may present with myelopathic features. These conditions can be distinguished from cervical spondylotic myelopathy via history and examination, nerve conduction tests, electromyography, and/or hematobiochemical studies.1,3,6,7

Back to Top | Article Outline

DIAGNOSTIC TESTING

Plain radiographs of the cervical spine often are the first diagnostic test acquired. Radiographs are useful for assessing degree of spondylosis, spondylolisthesis, loss of lordosis, spontaneous fusion, osteophyte formation, and ossification of the ligamentum flavum or posterior longitudinal ligament.1,4,7 Radiographs obtained in flexion and extension are important to evaluate for cervical spine instability that can cause dynamic compression of the spinal cord or nerve roots. Stenosis also can be noted with plain radiographs by measuring the vertebral canal AP diameter; a measurement of less than 10 mm is considered absolute stenosis.7 Relative stenosis is defined as less than 13 mm diameter; normal sagittal diameter is 17 to 18 mm.7 The Torg-Pavlov ratio often is used to evaluate stenosis by measuring ratio of the AP diameter of the vertebral canal at the mid vertebral body level to the AP dimension of the vertebral body at the same level. A Torq-Pavlov a ratio of less than 0.82 indicates stenosis.13

Oblique radiographs allow direct visualization of the neural foramen to diagnose bony foraminal stenosis. The gold standard for diagnostic testing in cervical spondylotic myelopathy is MRI because of its ability to direct-ly demonstrate the degree and location of spinal cord compression. In reviewing the relationship between bony structures, intervertebral disks, and neural tissue, the level or levels of compression can be confirmed. The MRI also allows visualization of ligamentous hypertrophy and edema in the spinal cord.4 In patients with a contraindication to MRI or metallic imaging artifact, CT with myelography may be used. This test is more invasive than MRI and involves the injection of contrast dye into the subarachnoid space via the lumbar or cervical spine.

Back to Top | Article Outline

TREATMENT

The natural history of cervical spondylotic myelopathy remains incompletely understood. This makes it difficult to predict the effectiveness of conservative treatment. Conservative therapy options consist of a rigid cervical collar, physiotherapy, pharmacotherapy, behavior modification, a “wait and watch” strategy of clinical and radiographic surveillance, or any combination of these options.1,4,6,7 Conservative therapy generally is reserved for patients who are mildly affected, stable, and without significant neurologic signs. This therapy also is reserved for neurologically stable patients with serious comorbid conditions that would place them at increased surgical risk.1,7

The decision to proceed with surgery requires an open and comprehensive discussion with the patient, explaining that the objective of surgery is to prevent disease progression and to stabilize the cervical spine; returning the patient to prepathology baseline is sometimes an unattainable outcome. This is especially true in patients with nonprogressive disease. A prime indication for surgical intervention or spinal cord decompression is progressive, symptomatic myelopathy—that is, worsening neurologic deficit with radiologic confirmation of cervical spondylotic myelopathy and exclusion of other possible contributing pathologies.1,4,6,7,9 An upgoing plantar response is another important sign of the need for surgery.

Decompressive surgery for treatment of cervical spondylotic myelopathy can be performed either via anterior or posterior approaches and may require spinal fusion. In general, the accepted trend is that patients with ventral compression, kyphosis, and/or pathology at one to three levels be treated anteriorly.1,7,9,10,14 Anterior decompression necessitates removal of the intervertebral disk. Historically, fusion was not always performed and patients would do well until they developed disk space collapse with subsequent kyphosis and foraminal stenosis, leading to recurrent symptoms. Contemporary anterior decompression includes anterior fusion to prevent late failures. The disk or vertebral body is replaced with an intervertebral cadaveric bone graft or iliac crest autograft. A rigid cervical collar can be considered on one-level anterior diskectomies, but internal fixation via anterior plating eliminates the need for an orthosis, and most patients choose to have anterior plating (Figures 4 and 5).

For multilevel anterior fusions, instrumentation advances have led to better fusion rates. More complex pathology consisting of irreducible kyphosis with or without significant osteophytic involvement, particularly of the posterior longitudinal ligament, may require a corpectomy. Corpectomy involves removal of a vertebral body, to be subsequently replaced with a graft or cage to maintain vertebral height and maintain lordosis. This is followed by anterior plating.1,4,7,9,14 Several choices for vertebral body replacement are used and include iliac crest autograft, fibular allograft, and polyetheretherketone (PEEK) or titanium cages.

Patients with multilevel disease, significant ligamentum flavum hypertrophy, or a congenitally narrow vertebral canal are more likely candidates for a posterior approach.1,7,9,10 Posterior decompression may be completed by laminectomy (often with fusion) or laminoplasty. A laminectomy involves removing the posterior elements including bilateral laminae, spinous processes, and ligamentum flavum in order to maximize the vertebral canal diameter. This often is accompanied by placement of lateral mass screws and connecting rods to accomplish a fusion for stability. Fusion is especially important to consider in patients with kyphosis, loss of lordosis, or if instability has been demonstrated on dynamic radiographs preoperatively (Figure 3). In patients with well-preserved lordosis, a laminoplasty may be an effective choice. A laminoplasty similarly expands the vertebral canal diameter, but rather than removing vertebral elements, the laminae are hinged open, displaced laterally or posterolaterally, and held open either by incorporating a graft or fixing the lamina to the adjacent structures with sutures or plates. This maintains both mobility and a level of protection to the thecal sac posteriorly.1,4,7,10,14

Laminectomy or laminoplasty may be performed as standalone procedures in patients with maintained cervical lordosis and no evidence of instability. Although some experts have suggested that laminoplasty offers an advantage in preservation of lordosis compared with laminectomy, meta-analysis data suggest that patients undergoing either of these procedures are at risk of developing kyphotic deformity postoperatively. This risk can be eliminated by pairing laminectomy or laminoplasty with a fusion via lateral mass screws and rods.14,15

In some cases, combining an anterior and posterior approach is indicated (Figure 5). These more difficult cases include patients with compressive pathology both anteriorly and posteriorly; those who need a multilevel corpectomy; those with significant kyphotic deformity, compromised bone integrity due to osteoporosis, renal disease, diabetes, or a history of tobacco smoking; and those with other factors resulting in diffuse vertebral involvement contributing to cervical spondylotic myelopathy.14,16

Significant risks associated with either anterior or posterior approaches must be taken into consideration, including permanent neurologic deficit, osteomyelitis or diskitis, cerebrospinal fluid leak, meningitis, pseudoarthrosis, gait disturbance, bowel or bladder dysfunction, injury to the carotid and/or vertebral arteries, injury to the trachea and/or esophagus, recurrent laryngeal nerve palsy, dislodgement of bone grafts, dislodgement of plates and screws, adjacent segment disease, need for future surgery, or failure of the operative procedure to improve symptoms.1,7,14,16 Higher rates of complications are associated with perioperative blood loss, increased intraoperative time, combined anterior and posterior approach, and increased patient age.1,14,17

Back to Top | Article Outline

PROGNOSIS

Several studies concluded that, over time, there was no significant difference in outcome in patients who were treated conservatively versus those treated surgically.1,3,6,18,19 However, other studies have found that the patients with cervical spondylotic myelopathy who undergo surgical decompression of the cervical spine, anteriorly, posteriorly, or circumferentially, show significant improvement, even in patients over age 75 years.14,20-22 The conflicting outcomes may be related to the highly variable constellation of signs and symptoms, degree of disease progression at the time of patient presentation, and unpredictable clinical course, all of which present challenges for researchers. Current practice appears to be trending toward earlier surgical intervention. Most recently, a prospective multicenter study revealed a 75% positive response rate in patients treated surgically, defined as a more than 2-point increase in modified Japanese Orthopaedic Association score, and a 49% success rate, defined as an increase to 17 or 18 on the scoring system at 12 months postoperatively.14,20,23 Improvement was demonstrated in all outcome measures including an average 2.88-point improvement in modified Japanese Orthopaedic Association score and 1.59-point improvement in Nurick grade. Improvement in modified Japanese Orthopaedic Association scores was significantly higher in patients with severe disease versus mild or moderate disease; no significant difference in degree of improvement in other outcome measures was found between patient groups.20

Positive predictors of postoperative outcome include younger age, shorter duration of symptomatic pathology, increased compression ratio (defined as a greater than 40% increase in postoperative AP diameter of the spinal cord), and resolution of abnormal spinal cord signal change on postoperative MRI of the cervical spine.1,4,6,14

The general consensus is that patients with clinically progressive myelopathic signs and symptoms in addition to radiographic evidence of cervical spondylotic myelopathy are candidates for decompressive surgery. In the instances of patients continuing to deteriorate neurologically postoperatively, despite MRI evidence of adequate and complete decompression, further investigations may be required to rule out additional causes.

Back to Top | Article Outline

REFERENCES

1. Tracy JA, Bartleson JD. Cervical spondylotic myelopathy. Neurologist. 2010;16(3):176–187.
2. Youmans JR. Neurological Surgery. W.B. Saunders Co.; 1996:2253–2261.
3. Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy. Spine. 2002;27(7):736–747.
4. Malcolm GP. Surgical disorders of the cervical spine: presentation and management of common disorders. J Neurol Neurosurg Psychiatry. 2002;73(suppl 1):i34–i41.
5. Northover JR, Wild JB, Braybrooke J, Blanco J. The epidemiology of cervical spondylotic myelopathy. Skeletal Radiol. 2012;41(12):1543–1546.
6. Kadanňka Z, Bednařík J, Novotný O, et al. Cervical spondylotic myelopathy: conservative versus surgical treatment after 10 years. Eur Spine J. 2011;20(9):1533–1538.
7. Lebl DR, Hughes A, Cammisa FP Jr, O'Leary PF. Cervical spondylotic myelopathy: pathophysiology, clinical presentation, and treatment. HSS J. 2011;7(2):170–178.
8. Matz PG, Anderson PA, Holly LT, et al. The natural history of cervical spondylotic myelopathy. J Neurosurg Spine. 2009;11(2):104–111.
9. Cusick JF. Pathophysiology and treatment of cervical spondylotic myelopathy. Clin Neurosurg. 1991;37:661–681.
10. Hukuda S, Mochizuki T, Ogata M, et al. Operations for cervical spondylotic myelopathy. A comparison of the results of anterior and posterior procedures. J Bone Joint Surg Br. 1985;67(4):609–615.
11. Dalitz K, Vitzthum HE. Evaluation of five scoring systems for cervical spondylogenic myelopathy. Spine J. [e-pub Sep. 5, 2008]
    12. Benzel EC, Lancon J, Kesterson L, Hadden T. Cervical laminectomy and dentate ligament section for cervical spondylotic myelopathy. J Spinal Disord. 1991;4(3):286–295.
    13. Pavlov H, Torg JS, Robie B, Jahre C. Cervical spinal stenosis: determination with vertebral body ratio method. Radiology. 1987;164(3):771–775.
    14. Muthukumar N. Surgical management of cervical spondylotic myelopathy. Neurol India. 2012;60(2):201–209.
    15. Hsu W, Dorsi MJ, Witham TF. Surgical management of cervical spondylotic myelopathy. Neurosurg Q. 2009;19(4):302–307.
    16. Mummaneni PV, Haid RW, Rodts GE Jr. Combined ventral and dorsal surgery for myelopathy and myeloradiculopathy. Neurosurgery. 2007;60(1 supp1 1):S82–S89.
    17. Fehlings MG, Smith JS, Kopjar B, et al. Perioperative and delayed complications associated with the surgical treatment of cervical spondylotic myelopathy based on 302 patients from the AOSpine North America Cervical Spondylotic Myelopathy Study. J Neurosurg Spine. 2012;16(5):425–432.
    18. Bednarík J, Kadanka Z, Vohánka S, et al. The value of somatosensory- and motor-evoked potentials in predicting and monitoring the effect of therapy in spondylotic cervical myelopathy. Prospective randomized study. Spine. 1999;24(15):1593–1598.
    19. Kadanka Z, Mares M, Bednaník J, et al. Approaches to spondylotic cervical myelopathy: conservative versus surgical results in a 3-year follow-up study. Spine. 2002;27(20):2205–2210.
    20. Fehlings MG, Wilson JR, Kopjar B, et al. Efficacy and safety of surgical decompression in patients with cervical spondylotic myelopathy: results of the AOSpine North America prospective multi-center study. J Bone Joint Surg Am. 2013;95(18):1651–1658.
    21. Holly LT, Moftakhar P, Khoo LT, et al. Surgical outcomes of elderly patients with cervical spondylotic myelopathy. Surg Neurol. 2008;69(3):233–240.
    22. Matsuda Y, Shibata T, Oki S, et al. Outcomes of surgical treatment for cervical myelopathy in patients more than 75 years of age. Spine. 1999;24(6):529–534.
    23. Fehlings MG, Kopjar B, Yoon TS, et al. Predictors of success in the surgical treatment for cervical spondylotic myelopathy: analysis of the AOSpine North America multi-center prospective study in 260 patients. Paper presented at the annual meeting of the American Association of Neurological Surgeons, Denver, CO; 2011.
    Keywords:

    cervical spondylotic myelopathy; spine; central vertebral canal; stenosis; decompressive surgery; laminectomy

    Copyright © 2015 American Academy of Physician Assistants