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Volume 3, Issue 1, Pages 68-81 (January 2003)


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Cervical myelopathy: current diagnostic and treatment strategies☆☆

Charles C Edwards II, MDa, K.Daniel Riew, MDb, Paul A Anderson, MDc, Alan S Hilibrand, MDd, Alexander F Vaccaro, MDCorresponding Author Informationd

Received 3 July 2002; accepted 23 September 2002.

Abstract 

Cervical myelopathy is a varied clinical syndromes resulting from spinal cord dysfunction. Underlying causes are numerous, but spondylosis at one or more levels is the most common etiology. Natural history studies have demonstrated a variable clinical course with gradual neurologic deterioration in a majority of patients. While prospective clinical comparisons are limited, existing literature suggests that operative management reliably arrests the progression of myelopathy and may lead to functional improvement in a majority of patients. The selection of surgical procedures must be carefully individualized based on specific clinical and radiographic factors. Whereas anterior decompression and fusion procedures at one or two motion segments have predictable results, procedures involving three or more levels are associated with increased morbidity. Newer techniques for the treatment of multilevel cervical myelopathy include anterior decompression with 360-degree fusion, hybrid corpectomy/anterior cervical discectomy and fusion techniques and the use of dynamic anterior cervical plates. An alternative technique for patients with a lordotic sagittal alignment is laminoplasty, which has a proven track record of long-term good to excellent results.

Article Outline

Abstract

Introduction

Pathogenesis

Evaluation

Diagnostic studies

Natural history

Nonoperative treatment

Operative treatment

Operative techniques

Anterior approaches

Anterior cervical discectomy and fusion

Corpectomy

Complications with anterior decompression procedures

Posterior approaches

Laminectomy

Laminectomy and fusion

Laminoplasty

Complications with posterior decompression procedures

Comparative studies

Conclusions

References

Copyright

Introduction 

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Dysfunction of the spinal cord results in a clinical syndrome known as myelopathy. Signs and symptoms of myelopathy may vary significantly based on the location and severity of the spinal cord dysfunction. Cord dysfunction may manifest in subtle symptoms, such as diminished balance and dexterity, or profound sequelae, such as paralysis and incontinence. The most common etiology for cervical myelopathy is canal stenosis resulting from spondylosis. Other etiologies commonly encountered include ossification of the posterior longitudinal ligament (PLL), trauma and tumors. The natural history of myelopathy is varied with neurologic improvement in some patients and deterioration in function in others. Patients with chronic or progressive symptoms and those failing to respond to nonoperative treatment should be considered candidates for surgical intervention. Operative treatment is directed toward expansion of the spinal canal and relief of cord compression. The selection of procedure is individualized according to specific clinical and radiographic factors. The results of surgery are generally favorable with arrest of myelopathic progression and improvement in function in the majority of patients. This article addresses the pathogenesis, diagnosis and natural history of cervical myelopathy as well as indications for treatment with currently available procedures.

Pathogenesis 

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The normal cervical spinal canal provides adequate space for the neural elements, meninges, ligaments and epidural fat. The normal canal diameter from C3 to C7 is 17 to 18 mm with some variation between sexes [1]. The occurrence of cervical myelopathy is strongly correlated with decreased sagittal diameter of the spinal canal. Canal stenosis may result from static and dynamic factors. Static factors producing stenosis may include a congenitally narrow canal and cervical spondylosis as well as some less common sources, such as ossification of the PLL or tumors.

A congenitally narrow canal lowers the threshold at which trivial trauma or early degenerative changes encroach on the spinal cord and cause myelopathy 1, 2. A 1955 pathologic study by Arnold [3] demonstrated that a sagittal diameter of 12 mm or less was critical in the production of myelopathy. Other authors have confirmed the presence of significant stenosis with sagittal diameters 10 to 14 mm or less 4, 5. Absolute measurements of canal dimensions, however, may be inaccurate because of radiograph magnification variability. A ratio of the spinal canal to vertebral body sagittal diameter for the assessment of the severity of canal stenosis has been recommended. Pavlov et al. [6] established a 92% accuracy for the diagnosis of canal stenosis when the ratio was less than 0.82 (normal ≥ 1.0).

Spondylosis with resultant cord compression is the pathogenic factor in approximately 55% of cervical myelopathy cases [2]. The degenerative cascade begins with deterioration of the intervertebral disc [7]. This process is insidious and frequently does not produce symptoms [8]. Decrease in the height of the disc leads to an increase in its sagittal diameter with various degrees of bulging into the canal. Microinstability leads to reactive hyperostosis (hypertrophy and osteophyte formation) at the level of the vertebral end plates. Osteophytes can project posteriorly into the canal and thus further reduce the space available for the spinal cord and its blood supply. Narrowing of the disc space also leads to overriding of the uncovertebral and facet joints. Osteophytes arising from the uncovertebral joints and facets may also project into the canal, resulting in incrementally less space available for the cord. Hypertrophy of the facet capsules and ligamentum flavum along with the other mentioned changes lead to a circumferential decrease in canal dimensions.

Additional static factors that may further diminish the cross-sectional area of the spinal canal are herniation of the intervertebral disc, facet cysts and buckling of the ligamentum flavum. Distinct from the degenerative cascade are the less common processes, such as ossification of the PLL and of the ligamentum flavum, which likewise may result in spinal stenosis and myelopathy.

Dynamic factors also have a significant effect on the dimensions of the spinal canal. With normal spine kinematics, coupled motion of adjacent vertebrae during extension produces a decrease in the diameter of the spinal canal (pincer effect) 9, 10. In the presence of advanced intervertebral degeneration, the degree of dynamic stenosis with a normal arc of flexion and extension may increase [10]. With hyperextension, the ligamentum flavum buckles into the canal and the degenerated disc may bulge posteriorly, further decreasing the space available for the cord. This phenomena may become clinically apparent when an asymptomatic patient with advanced cervical spondylosis experiences a hyperextension injury. A central cord syndrome may follow with motor weakness greater in the arms than the legs.

With deterioration of the intervertebral disc, translation of one vertebra on its neighboring vertebra often occurs [11]. The magnitude of this listhesis, whether anterior or posterior, rarely exceeds 2 to 3 mm but may play a significant additive role in the circumferential encroachment on the spinal canal [12]. Loss of disc height leads to decreased cervical lordosis. If a kyphotic sagittal alignment ensues, the cord may become tented anteriorly over prominent osteochondral spurs, resulting in further mechanical compression and vascular embarrassment.

Together these static and dynamic factors may result in a significant encroachment on the spinal canal and produce vascular and intrinsic changes to the spinal cord. In 1977 Ono et al. [13] reported the necropsy findings of five patients with known cervical myelopathy. He found that compression of the spinal cord was associated with extensive destruction of both gray and white matter and ascending and descending demyelinization. Interestingly, the anterior column was consistently spared from infarction. These findings were confirmed by a similar necropsy report by Ogino et al. [14] and an animal experimental model by Bohlman et al. [15].

The extent to which direct mechanical compression of the neural elements and neuroischemia contribute to these pathologic findings remains unclear. The anterior spinal artery supplies 65% to 70% of the spinal cord. With progressive anterior compression, blood flow through the terminal branches of the anterior spinal artery within the spinal cord is interrupted [16]. If impairment of the blood supply becomes chronic, the ischemia ultimately produces demyelinization and nerve cell damage as well as loss of axoplasmic flow [17].

Evaluation 

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Patients with cervical myelopathy can present with a broad spectrum of signs and symptoms. Depending on the magnitude of spinal cord dysfunction and its chronicity, patients may be asymptomatic or severely disabled. Early symptoms include diminished dexterity and subtle changes in balance and gait. Difficulty manipulating small objects, such as buttons and eating utensils, is typical. Compromised bladder or bowel function is less common but when present is associated with greater disease severity. Myelopathy often occurs concomitantly with radiculopathy resulting from advanced cervical spondylosis causing foraminal stenosis. Symptoms referable to coexisting lumbar spinal stenosis are also common [18]. Patients with severe lumbar stenosis should, therefore, be carefully evaluated for the presence of cervical myelopathy.

Physical examination often reveals a mixed picture of myelopathy and radiculopathy. Upper motor neuron findings (spasticity) may be present in the arms and legs, whereas lower motor neuron dysfunction (fasciculations and hyporeflexia) occurs at the level of cord or root compression. Pathologic reflexes, such as Hoffman sign, inverted radial reflex, Babinski sign and clonus, are long tract signs consistent with cord compression. Coordinated motor function may be evaluated by asking the patient to perform heel-toe tightrope gait, and rapidly repeated grip and release. Slow or clumsy performance of these tests is consistent with cervical cord compression. Cranial nerve abnormalities and a hyperactive jaw jerk reflex, when present, may suggest the presence of a brainstem or intracranial lesion. If tapping on the chin of a relaxed mandible produces hyperactive mandible flexion, a positive jaw-jerk is present.

Sensory changes vary widely according to the location and extent of spinal cord dysfunction. Altered vibratory sense and proprioceptive changes are often present in cases with chronic or severe myelopathy. Loss of a normal vibratory sense however, may also occur in association with peripheral neuropathy resulting from diabetes, thyroid disease, heavy alcohol use or metal toxicity.

Loss of ambulatory function was graded by Nurick [19] as an indicator of the severity of myelopathy (Table 1). The resultant classification proceeds from Grade 1 (signs of myelopathy, normal gait) to Grade 5 (severe myelopathy, nonambulatory). Although the Nurick scale has been widely used as a research tool, its utility is limited because of its exclusive focus on lower extremity function. The Japanese Orthopaedic Association (JOA) [20] developed an objective scale to quantitate the severity of myelopathy based on upper and lower extremity motor dysfunction, degree of sensory deficits and sphincter dysfunction (Table 2). The maximum score of 17 reflects normal function. The JOA recovery rate was described by Hirabayashi and Satomi [21] as a means of comparing the relative magnitude of recovery experienced by different patients.

Table 1.

Nurick classification for severity of myelopathy

GradeMyelopathic signsGaitEmployment/regular activities
0NoNoneNot limited
1YesNoneNot limited
2YesSlight difficultyNot limited
3YesSignificant difficultyRestricted
4YesOnly with AssistanceImpossible
5YesChairbound or bedriddenImpossible
Table 2.

Criteria for evaluation of the operative results of patients with cervical myelopathy by the Japanese Orthopaedic Association

FunctionScore*Remarks
Motor function of upper extremity4 3 2 1 0Normal Able to feed with chopsticks regularly, but slightly awkwardly Able to feed with chopsticks regularly, but awkardly Able to feed with a spoon, but not with chopsticks Unable to feed oneself with either spoon or chopsticks
Motor function of lower extremity4 3 2 1 0Normal Able to walk on a level surface or climb stairs without cane or support, but awkwardly Able to walk on a level surface without a cane or support, but unable to climb stairs without either of them Needs a cane or support even when walking on a level surface Nonambulatory
Sensory
Upper extremities2Normal
1Slight sensory loss or numbness
0Definite sensory loss
Lower extremities2Normal
1Slight sensory loss or numbness
0Definite sensory loss
Trunk2Normal
1Slight sensory loss or numbness
0Definite sensory loss
Bladder function3Normal
2Mild dysuria
1Severe dysuria
0Complete retention of urine
*

Maximum score = 17.

Diagnostic studies 

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Anteroposterior, lateral and oblique radiographs should be performed on patients suspected of having cervical myelopathy. Spondylotic changes, such as narrowing of the disc space, osteophyte formation and listhesis, may be appreciated. The lateral radiograph should be critically reviewed for evidence of decrease in the sagittal dimension of the osseous canal resulting from congenital stenosis, spondylosis or ossification of the PLL. Any decrease in the segmental and global lordosis from C2 to T1 should be recognized, because it may influence treatment options. Lateral flexion and extension radiographs are a useful means of assessing range of motion, the presence of ankylosed segments and instability [17]. Oblique radiographs are helpful for defining the amount of foraminal stenosis resulting from osteophytes.

The absolute sagittal diameter of the spinal canal of 13 mm or less as measured from the posterior aspect of the midvertebral body to the spinolaminar line is indicative of patients with a developmentally narrow canal 12, 17, 22. A spinal canal to vertebral body sagittal diameter ratio of 0.8 or less has also been demonstrated to correlate with an increased risk of developing myelopathy [6].

Magnetic resonance imaging (MRI) is a useful adjunct for evaluation of the soft tissues and spinal cord [23]. Nonosseous stenosing sources, such as disc protrusions, hypertrophied ligamentum flavum and facet cysts, may be well visualized. The effect of such stenosing processes on the size and shape of the spinal cord are assessed on both axial and sagittal images. In cases of severe stenosis, low signal intensity changes to the spinal cord parenchyma on T1-weighted sequences, and hyperintense cord changes on T2-weighted images are often present. A recent study by Morio et al. [24] demonstrated that low signal intensity changes on T1-weighted sequences, when present, portend the worst prognosis for recovery.

Myelography followed by computed tomography (CT) imaging provides additional information regarding the bony architecture and stenosing osseous structures, such as osteophytes and ossified PLL (Fig. 1). Myelogram images obtained in relative positions of flexion and extension help to clarify the presence of dynamic cord compression [9].


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Fig. 1. Computed tomography myelogram demonstrating cord compression resulting from spondylotic changes superimposed on congenital stenosis.


Although imaging studies usually confirm clinical suspicion that the pathogenesis of cervical myelopathy is related to cervical stenosis, occasionally an alternative etiology is identified. Although cervical stenosis is the most common cause of cervical myelopathy, a broad differential diagnosis should be considered, including intracranial pathology, intradural tumor or syrinx, multiple sclerosis and other nerve-related disease, such as Guillain Barre or amyotrophic lateral sclerosis.

Natural history 

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The prognosis for patients with cervical myelopathy is highly variable with complete resolution infrequently observed. In 1952, Brain [9a] first established cervical myelopathy resulting from spondylosis as a distinct clinical entity. Four years later, Clarke and Robinson [25] reported their experience with 120 patients. In their nonoperative series, no patient experienced complete recovery, and spontaneous regression was observed in only two patients. Episodic worsening with neurologic deterioration occurred in 75%; 20% experienced slow steady progression; and 5% had a rapid onset of symptoms without further worsening. Clarke and Robinson also noted that nonoperative management, including immobilization and periods of bed rest, had the potential to improve symptoms. In 1963, Lees and Turner [26] reviewed the natural history of 44 patients treated nonoperatively. They observed that patients symptomatic for more than 10 years were more severely disabled, often with diminished ambulatory potential. Patients experienced stepwise neurologic deterioration with periods of quiescent stability between exacerbations. In 1973 Phillips [27] reviewed the data of Lees and Turner and found that 57% of patients had severe disability with few experiencing improvement. Roberts [28] studied 24 patients with cervical myelopathy for 6.5 years and found that one-third improved, one-third remained the same, and one-third deteriorated. Motor symptoms tended to be much more progressive and less likely to improve than sensory abnormalities. Based on these studies, it appears that the clinical course of cervical myelopathy is variable with some patients experiencing a benign clinical course with potential for neurologic improvement. A majority of patients presenting with cervical myelopathy, however, do not experience spontaneous improvement and are subject to deterioration in their neurologic status over time.

Nonoperative treatment 

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The success of nonoperative modalities in altering the natural history of cervical myelopathy is largely unknown. In Clark and Robinson's [25] 1956 report, various nonsurgical measures, including a soft collar, were found to provide some degree of symptom relief in approximately 50% of patients. Over time, however, progressive neurologic deterioration was observed in a majority of patients. Alternative modalities, such as epidural steroid injections, physical therapy and nonsteroidal medications, have been advocated, but studies documenting their efficacy are lacking. Manipulation and traction are contraindicated, because extension of the neck causes narrowing of an already tight canal and foramina 17, 25.

Nonoperative management of cervical myelopathy may be recommended in select circumstances. Patients presenting with the new onset of subtle myelopathic findings and radiographic evidence of a soft disc herniation [29] may be initially treated nonoperatively and are followed carefully at frequent intervals to evaluate for progression or remission of symptoms. Patients who are unwilling or unfit to undergo operative treatment as well as those undergoing preoperative evaluation are prescribed a soft cervical collar and often a neck-conditioning program. Indicators for a poor prognosis with nonoperative treatment are advanced age, duration of symptoms, severity of myelopathy and severity of stenosis with a spinal canal to vertebral ratio of 0.8 or less [30].

Operative treatment 

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Kadanka et al. [31] reported the results of the first randomized prospective study comparing the results of nonoperative and surgical treatment for mild to moderate forms of cervical myelopathy. Forty-eight patients with mild cervical spondylotic myelopathy, JOA scores of 12 or greater, were randomized to operative or nonoperative treatment. Outcome measures were JOA score, timed walk, activities of daily living assessment and patient subjective score. At 2-year follow-up, the functional improvement for patients receiving surgery was not statistically better than patients receiving nonoperative treatment.

The short-term results of a prospective multicenter nonrandomized comparison of operative and nonoperative treatment for cervical myelopathy were recently reported by Sampath et al. [32] using the Cervical Spine Research Society database. Twenty patients underwent surgery, and 23 received medical treatment. At a mean follow-up of 11 months, patients treated nonoperatively had a significant worsening of their ability to perform activities of daily living with progression of neurologic symptoms. Patients treated surgically experienced significant improvement in functional status and neurologic symptoms.

Results of recent studies demonstrate the ability of various procedures to arrest the progression of myelopathy and provide for functional improvement in a majority of patients. Clinical results vary based on the severity of myelopathy, the extent of the disease process and patient factors [33]. The rate of neurologic improvement after either anterior or posterior decompressive procedures ranges from 47% to 100%, with most reports indicating some degree of neurologic recovery in more than 90% of patients [34]. The results of surgical treatment seem to differ markedly from the natural history of untreated cervical myelopathy wherein a high percentage of patients (more than 50%) progress to severe disability. Optimal results are obtained when decompression is performed within 6 months to 1 year after the onset of symptoms in patients with mild myelopathy [35] and in those in whom the transverse area of the spinal cord is greater than 40 mm2.

Operative techniques 

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Selection of the appropriate operative strategy is based on a complete understanding of the factors responsible for the cord dysfunction. As abnormal radiographic findings are common in even asymptomatic patients [36], clinicians need to be careful to correlate the patient's complaints, physical examination and imaging results to discern the precise diagnosis. Operative intervention of cervical myelopathy is focused on decompression of the spinal cord to halt neurologic deterioration and promote functional improvement. The decision to use either an anterior or posterior approach and which specific procedure is based on multiple factors, including the source of spinal cord compression, the number of vertebral segments involved in the disease process, cervical alignment, the magnitude of coexisting neck pain, patient comorbidities and the surgeon's familiarity with various techniques.

Anterior decompression procedures are well suited for cases in which the stenosing pathology is ventral to the spinal cord. An anterior approach provides for direct visualization and removal of the offending pathology without manipulation of the cord. When a neutral or kyphotic cervical sagittal alignment is present, anterior procedures may also serve to restore physiologic lordosis. Restoration of lordosis allows for shifting of the cord dorsally to diminish the effect of anterior compression. After anterior decompression, spinal column stability is restored through segmental arthrodesis. The arthrodesis may have the added benefit of eliminating painful motion from the spondylotic motion segment.

The optimal procedure for the treatment of cervical myelopathy resulting from stenosis at three or more levels remains controversial. Anterior arthrodesis of three or more motion segments is associated with a higher incidence of nonunion and graft-related problems than one- or two-level procedures 37, 38, 39. Alternative motion-preserving procedures, such as laminectomy and laminoplasty, have been proposed for patients with multilevel stenosis in the absence of kyphosis. As existing techniques continue to be refined and new technology emerges, recommendations for the treatment of cervical myelopathy will continue to evolve. The purpose of the following review is to examine the success of operative strategies commonly employed in the management of cervical myelopathy in light of historical evidence and recent advances.

Anterior approaches 

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Anterior cervical discectomy and fusion 

The anterior approach to the cervical spine was developed in the 1950s by Baily and Badgley [40], Smith and Robinson [41] and Cloward [42]. Since that time, anterior decompression and fusion has been applied to the treatment of cervical stenosis resulting from herniated discs, spondylosis or ossification of the PLL. When the pathologic process occurs at the level of the intervertebral disc, anterior cervical discectomy and fusion (ACDF) usually provides sufficient access to the stenotic focus. Clinical series have demonstrated successful arthrodesis in 92% to 96% of patients after single-level ACDF with satisfactory clinical results 43, 44, 45.

The extent to which decompression should include the posterior osteophytes and the PLL remains controversial. Bohlman [46] reported a series of 17 patients that underwent ACDF without removal of either the PLL or osteophytes. All but one patient experienced a good to excellent outcome. Other authors advocate the removal of osteophytes with the hope of accelerating neurologic recovery. Kadoya et al. [47] demonstrated that osteophyte removal could be safely performed in his series of 43 patients with myelopathy who underwent decompression using a microscope. The extent of decompression is dictated by the degree of stenosis present on preoperative imaging studies and local anatomic landmarks. Using microscopic visualization, posterior end plate osteophytes are thinned with a high-speed burr until only a wafer-thin cortical remnant remains. The remaining cortex and chondral fragments are then dissected off the PLL and excised with a curved micro curette.

When foraminal stenosis is present, wide foraminotomies are performed to remove uncinate spurs. The entire uncinate region is carefully cleaned of all disc material, and the lateral margin is determined by palpation with a blunt probe. The posterior portion of the uncinate region is then decompressed with a burr and micro curettes until the foramen is wide open. A micro curette or probe can be used to ascertain the patency of the foramen.

For cord compression at multiple levels, numerous anterior decompressive options exist, including multilevel ACDF, corpectomy and hybrid procedures. Although the rate of neurologic improvement remains high for multilevel ACDFs [49], the incidence of nonunion increases with the number of levels being fused. The recently reported fusion rate for a one-level ACDF using autograft iliac crest without plating (two graft–host sites) was 96% [50]. This decreased to a 75% fusion rate when a two-level ACDF was performed and to a 56% fusion rate with a three-level ACDF (six graft–host sites) [51].

Morbidity associated with autogenous bone graft harvest from the ileum and fibula spurred interest in the use of structural allograft with ACDF. Numerous studies have demonstrated the pseudarthrosis rate after single-level uninstrumented ACDF using structural allograft (2% to 20%) to be similar to that obtained with autograft. For uninstrumented multilevel ACDF, however, the incidence of nonunion is higher with allograft [45].

The introduction of anterior cervical plating has led to an improvement in the fusion rate observed after ACDF. Wang et al. [51] recently reported on 60 patients who underwent a two-level ACDF. Thirty-two patients were treated with plating and 28 without plating. Solid arthrodesis was observed in all patients with plates and 75% without. In a separate study by Wang et al. [51], the fusion rate for three-level ACDF was 82% with plating and 63% without. Improved fusion rates using plates were also demonstrated by Geck et al. [52] in their report on 205 ACDF procedures. A three-fold improvement in the fusion rate was noted (11.8% vs. 3.6%) with the plated group.

Corpectomy 

An alternate means of improving the fusion rate after multilevel decompression is the use of corpectomy. In addition to improving the fusion rate, corpectomy provides for a more extensive decompression and serves as a source of autograft. Stenosis at two adjacent levels can be decompressed with a single-level corpectomy (two graft–host interfaces) as compared with two ACDFs (four graft–host interfaces). Swank compared the fusion rate after ACDF and corpectomy. The nonunion rate in the one-level corpectomy group was 10% compared with 36% for patients undergoing two-level ACDF procedures [37]. Hilibrand reported on 131 patients undergoing multilevel ACDF and 59 patients undergoing corpectomy (one to four levels). Patients in the ACDF group had a 34% incidence of nonunion. Patients undergoing corpectomy had a 7% nonunion rate and six graft dislodgements, four requiring revisions [39]. Based on these factors, corpectomy may be considered preferable to multilevel ACDF, especially in higher-risk patients, such as recent smokers, diabetics or revision cases. If corpectomy is performed in a patient without compression behind the vertebral body, then 2 to 3 mm of the posterior cortex can be left intact. This provides a posterior buttress to prevent the graft retropulsion into the canal. For conditions with diffuse canal stenosis, corpectomy and removal of the entire posterior cortex is the only viable alternative. Examples include ossification of the PLL, malunited fractures with persistent canal stenosis and postlaminectomy kyphosis.

Static plates, buttress plates and most recently dynamic plates have been introduced with the intended purpose of decreasing the rate of nonunion and to prevent anterior strut graft dislodgement after corpectomy 53, 54, 55. The early experience with static plating with multilevel corpectomies, however, suggested that such plates may predispose to an increased incidence of strut graft dislodgment. Vaccaro et al. [38] reported a multicenter experience of 45 patients undergoing two-level (33 patients) and three-level (12 patients) corpectomies with plating. Strut graft dislodgement was observed in 9% of the two-level corpectomy group and 50% of the three-level corpectomy group, despite adjunctive halo application in 10 of 12 three-level corpectomy patients.

Foley et al. [56] evaluated the biomechanical rationale of anterior plating as an adjunct to strut grafting. They determined that with strut graft alone, cervical flexion increased the load applied to the graft, whereas extension decreased the load. With addition of an anterior static plate, a paradoxical mechanical effect was observed. Cervical extension substantially increased the load on the graft beyond that produced by extension without a plate. In contrast, cervical flexion in the presence of static plate consistently unloaded the strut graft.

Anterior cervical buttress plates were designed to prevent graft dislodgment while allowing for physiologic patterns of force application through the anterior column. Unfortunately, failure at the implant–host bone interface and subsequent strut graft dislodgement were observed after multilevel corpectomies [57]. In order to prevent these sequelae, supplementation with posterior fusion is recommended when multilevel strut graft fusion with buttress plate fixation is employed.

A new generation of “dynamic” anterior cervical plates has been developed to avoid the failures of static and buttress plates. A recent in vitro model demonstrated that these devices accommodate the normal settling of the strut graft–host bone interface, avoid stress shielding of the anterior column and provide for normal strut graft loads [58]. Critical analysis of the early experience with the dynamic plate is required in order to determine its role in multilevel anterior decompression procedures.

An alternative means of addressing the challenges of multilevel anterior decompression and fusion is to perform a combination of a corpectomy and discectomy procedures (Fig. 2). For a patient with stenosis involving three contiguous levels, the top two involved disc spaces may be addressed by a single-level corpectomy. A discectomy is then performed at the most caudad disc space. Two bone grafts are then placed to span the defects. An anterior cervical plate is then placed over the entire construct. This compromise between a two-level corpectomy and three-level discectomy preserves much of the structural integrity of the cervical spine and limits the necessary healing surfaces to four. In addition, because four screws around an ACDF anchor the inferior end of the plate, the plate is less apt to dislodge. This technique cannot be employed if there is stenosis behind the inferior vertebral body, because it is left intact. A disadvantage of such hybrid procedures is the added operative and anesthetic time resulting from the fashioning of two or more grafts. Hybrid ACDF and corpectomy procedures may also be used in patients with four-level disease. One can perform a two-level corpectomy to address the top three disc levels, along with a single-level discectomy for the lowest level. An alternative reconstructive strategy for patients with stenosis at four levels is to perform two single-level corpectomies separated by a noncorpectomy level. (Fig. 3).


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Fig. 2. Postlaminectomy kyphosis in an elderly woman with rheumatoid arthritis and osteoporosis was treated with corpectomies of C4 and C5, anterior cervical discectomy and fusion at C6–C7, a spanning anterior plate from C3 to C7 and lateral mass plating from C3 to C7. Corpectomy and discectomy defects were reconstructed with a combination of allograft fibula and autologous cancellous iliac crest autograft.



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Fig. 3. Double single-level corpectomy at C4 and C6.


Anterior decompression with circumferential fusion has been advocated for cases involving decompression and fusion of three or more segments. Addition of a posterior segmental fusion has been demonstrated to increase the rate of fusion and decrease the incidence of graft and implant-related problems [59]. The addition of posterior segmental fusion to an anterior decompression and fusion procedure should be considered in cases of multilevel (three or more) spondylosis or ossification of the PLL requiring extensive decompression, multilevel spondylosis with congenital stenosis, multilevel spondylosis with degenerative kyphosis, postlaminectomy kyphosis and an S-shaped curve and posttraumatic kyphosis [60].

Complications with anterior decompression procedures 

Complications occurring with anterior decompression and fusion procedures may be related to the soft tissue structures, bone graft and the neurologic system. One of the most common unintended sequelae of anterior procedures is postoperative dysphagia. Although the incidence of esophageal perforation is very low (0.2% to 0.9%) [61], postoperative dysphagia has been observed in 2% to 48% of patients [62]. Symptoms are frequently transient, with chronic dysphagia reported in up to 12% of patients. The etiology may be multifactorial, including hematoma formation, prolonged retraction and denervation of the upper esophagus by injury to the pharyngeal plexus [63].

Temporary hoarseness is reported in 3% to 11% of patients, with permanent hoarseness occurring in 0.33% 64, 65. The etiology of postoperative dysphonia is postulated to be related to direct injury to the recurrent or superior laryngeal nerves, the length of the procedure and force of retraction. A recent study by Apfelbaum et al. [64] suggested that the incidence of dysphonia after anterior cervical spine surgery may be partly the result of injury of the recurrent laryngeal resulting from the endotracheal tube. Monitoring of endotracheal tube cuff pressure and release after retractor placement was found to dramatically decrease the incidence of dysphonia in their study of 900 consecutive patients. Historically, rates of dysphonia are reported to be higher with right-sided cervical approaches because of the varied course of the recurrent laryngeal nerve. In contrast to previous reports, a recent study by Butler et al. [66] found no difference in the incidence of recurrent laryngeal nerve injury when comparing right- and left-sided approaches. A higher incidence of nerve injury was noted with increased levels of decompression and revision surgery.

Harris et al. [67] recently presented an anatomical study on the course of the superior laryngeal nerve. They found that the sensory branch of this nerve, which innervates a portion of the larynx and vocal cords, is located most consistently between the C2 and C3 vertebra. Injury to this nerve or its branches during higher anterior cervical approaches may result in postoperative voice changes or sensory changes, leading to a diminished aspiration protective response.

Iatrogenic injury to the vertebral artery during anterior cervical procedures, although exceedingly rare, can be a devastating complication. A recent study by Burke et al. [67a] demonstrated an incidence of vertebral artery injury to be 0.03% (6 of 1,976 patients). Various treatment options have been described, including repair, ligation and tamponade. In the series of six patients, four were asymptomatic, one experienced a vertebral artery dissection with resultant lateral medullar infarct, and one died intraoperatively because of hypovolemia. An anatomic study by Thomas et al. [68] demonstrated that the incidence of brainstem infarction was 1.8% after occlusion of the right vertebral artery and 3.1% after the left was occluded.

The fate of motion segments adjacent to anterior cervical fusions remains a subject of continued investigation. It has been theorized that fused segments accelerate the degenerative process at neighboring levels. Hilibrand et al. [69] recently reported a retrospective long-term disease-free survivorship analysis in 374 patients undergoing 409 anterior cervical fusions. They found a relatively consistent incidence of adjacent segment disease of 3% per year. Degeneration was most likely at C5–C6 and C6–C7 and occurred more frequently after single-level rather than multilevel fusion.

A potentially lethal complication of anterior cervical surgery is postoperative airway obstruction caused by edema or hematoma formation. Emery et al. [70] recommend that all patients with severe myelopathy be kept intubated postoperatively. A recent study involving a large number of patients who underwent anterior cervical procedures [71] suggests that the operative time and numbers of levels of decompression are the most important factors in determining whether the patient should be kept intubated postoperatively. The authors advocate extubating patients when the total cervical retraction time is less than 2.5 hours or when the total operative time is less than 3 hours. For patients who are difficult to intubate, the authors recommend extubation if the operative time is less than 90 minutes. Using these parameters, the authors found that airway difficulties resulting from edema were not encountered. Respiratory distress resulting from hematoma formation was encountered in 4 of 256 patients 30 to 48 hours postoperatively. Each of the 4 patients was each reintubated and underwent hematoma evacuation.

If a patient is kept intubated postoperatively, a cuff-leak test should be performed before extubation. The cuff-leak test is performed by occluding the endotracheal tube lumen with the cuff balloon deflated. If the patient can breathe around the tube, then there is adequate space between the tube and the larynx. If the patient cannot breathe around the tube, then they should be kept intubated and the cuff leak test repeated in 24 hours.

Posterior approaches 

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Although the posterior approach has been advocated to address one or two levels of canal stenosis [72], posterior procedures are most commonly used for the management of cervical myelopathy involving three or more levels.

Laminectomy was first described in 1901 for the management of trauma. It has since been broadly employed for the decompression of cervical stenosis resulting from spondylosis with satisfactory results in a high percentage of patients. The success of laminectomy, however, has been limited by its tendency to produce segmental instability and late neurologic deterioration in a subset of patients. Concern regarding the destabilizing potential of laminectomy prompted some authors to advocate the use of laminectomy with concurrent posterior fusion for the treatment of multilevel cervical myelopathy 73, 74, 75. Limitations associated with laminectomy spurred the evolution of an alternative posterior strategy in Japan. Laminoplasty was described in 1973 as a canal expansive procedure that provided for spinal cord decompression, retention of the posterior elements and maintenance of segmental motion. An extensive body of literature since then has documented the efficacy and the limitations of laminoplasty 76, 77, 78. An advantage shared by these procedures is the benefit of an extensile exposure of the entire cervical spine with relative safety. Through the same posterior approach, each procedure may provide for canal decompression at multiple levels and foraminotomies where indicated. Posterior approaches avoid the technical problems encountered with anterior cervical approaches resulting from obesity, a short neck, barrel chest, anterior soft tissue pathology and a previous anterior surgery. Posterior procedures also avoid the potential for injury to the esophagus, trachea and laryngeal nerves. An important prerequisite to the successful performance of a posterior procedure, however, is the presence of a neutral to lordotic sagittal alignment. Lordosis is necessary to allow dorsal migration of the cord away from impinging anterior elements. In the event that a kyphotic alignment exists, but lordosis is re-established in extension, then a posterior decompression and fusion may be successfully performed [79].

Laminectomy 

Historically, laminectomy has been regarded as the standard posterior procedure for the treatment of multilevel cervical myelopathy. Laminectomy is a straightforward technique that provides for an extensile posterior decompression and excellent visualization of the neural elements. A recent study by Kaptain et al. [80] evaluated the success of laminectomy in the management of cervical spondylotic myelopathy in 46 patients. With an average of 4 years of follow-up, the function for 29% of patients was improved compared with preoperative levels, in 42% it was unchanged, and in 29% it was worse. The presence of a kyphotic sagittal alignment was present in 9% of patients before surgery and in 28% of patients at latest follow-up. Overall, good to excellent results have been reported in 40% to 85% of patients after laminectomy. In a subset of patients, however, the results tend to worsen over time 81, 82, 83. The deterioration in results after laminectomy has been attributed to multiple causes, including the development of a scar membrane around the dura, segmental instability and kyphosis [84]. Postoperative cervical kyphosis after laminectomy is directly related to the amount of facet joint resection. Raynor et al.[85] have shown that a 50% facetectomy allows a visualization of 3 to 5 mm of nerve root, whereas a 70% resection allows visualization of 8 to 10 mm. These authors concluded that resection of greater than 50% of the facet joint significantly compromises facet strength . Zdeblick and Ducker [45] noted that segmental hypermobility of the cervical spine results if a foraminotomy involves resection of more than 50% of the facet. A biomechanical study by Nowinski et al. [86] concluded that as little as a 25% facetectomy affects stability after multilevel laminectomy. Hypermobility produced by a decompressive laminectomy may result in segmental listhesis and angular kyphosis. In addition to the production of a postural deformity and axial discomfort, a hypermobile cervical spine with a kyphotic alignment may result in recurrent cord dysfunction with neurologic deterioration.

If postlaminectomy kyphosis occurs, an extensive reconstruction is generally necessary to halt the progression of both the sagittal deformity and myelopathy. In postlaminectomy patients, corpectomy and fusion alone as a reconstructive option should be avoided, because it results in complete disassociation of the lateral pillars and results in severe instability (Fig. 4). Surgical correction of a postlaminectomy kyphosis, therefore, requires anterior strut graft placement to re-establish a more normal sagittal alignment followed by posterior stabilization (360-degree fusion).


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Fig. 4. Computed tomography myelogram after cervical corpectomy was performed for the treatment of postlaminectomy kyphosis. Note the complete disassociation of the two lateral masses.


Laminectomy and fusion 

The frequency of instability and loss of lordosis after laminectomy has prompted some authors to advocate prophylactic fusion of decompressed cervical levels 73, 74, 75, 87. Concurrent lateral mass plating has the advantages of stabilizing the decompressed segment in a lordotic posture and preventing segmental instability (Fig. 5). Fusion also permits a more expansive laminectomy and foraminal decompression without jeopardizing stability. Instrumentation is used in all but the stiffest spines to maintain segmental stability and lordosis while the arthrodesis takes place. Various facet-wiring techniques have been employed for three decades. Presently, lateral mass plating is most commonly used for more rigid internal fixation. Arthrodesis typically spans the decompressed levels but may be extended to the subjacent level at the cervicothoracic junction. The few published reports describing the results of laminectomy and fusion reflect a high rate of functional improvement. Limitations of the procedure relate principally to attempts at fusion: nonunion, hardware failure, adjacent segment degeneration, loss of lordosis and autograft harvest site discomfort [88]. While potential problems related to posterior plating with screws include injury of the vertebral artery or cervical nerve roots, such complications are fortunately uncommon 88, 89.


View full-size image.

Fig. 5. Computed tomography myelogram after laminectomy and instrumented fusion with lateral mass plates. (Courtesy of Gerald Rodts, MD.)


Laminoplasty 

In Japan, poor outcomes associated with cervical laminectomy spawned the evolution of a different strategy for achieving posterior decompression. In 1973 Oyama [90] introduced a canal-expansive laminoplasty procedure. Many modifications of the procedure have been reported since then 78, 91, 92. Laminoplasty strategies have taken two forms: eccentric expansion with a unilateral hinge and symmetric expansion with bilateral hinges. The common purpose of all laminoplasty procedures is the increase in canal area through reconfiguring of the posterior bony arch (Fig. 6). Fusion of decompressed levels should be avoided except in those cases in which segmental instability is noted preoperatively. Decompression of neuroforamina may also be achieved by performing a laminoforaminotomy before expansion of the posterior arch or through direct decompression of the neuroforamina after the expansion of the posterior arch.


View full-size image.

Fig. 6. Lateral radiograph after open-door laminoplasty from C3 to C7 demonstrating an expanded canal and suture anchors in the lateral masses.


Success of various laminoplasty procedures in decompressing the spinal cord and producing a functional improvement in patients with cervical myelopathy has been well documented 72, 77, 78, 93. A recent study by Kawaguchi et al. [48] evaluated the results of laminoplasty in 133 patients with a minimum 10-year follow-up after laminoplasty. They found that the functional recovery rate of 58.3% was well maintained over time (55.1%). Laminoplasty has also been demonstrated to be successful in the management of cervical spondylotic myelopathy in the elderly [94], diabetics [95] and patients on dialysis [96]. Radiographic and anatomic studies have demonstrated laminoplasty's ability to expand the cross-sectional area of the canal and decompress the spinal cord 93, 97, 98. Cord decompression occurs as the spinal cord migrates dorsally away from impinging anterior structures. The success of laminoplasty in decompressing the cord, however, is contingent on the presence of a neutral to lordotic sagittal alignment [99]. Laminoplasty performed on patients with cervical kyphosis has been shown to result in less cord enlargement and functional recovery than those patients with a lordotic alignment. Additional factors associated with inferior outcomes are cord atrophy, long symptom duration, advanced age, severe cord compression and radiculopathy 33, 100. Although laminoplasty is not considered a fusion procedure, most patients experience a significant loss of subaxial motion after the procedure [93]. Satomi et al. [77] reported a 47% decrease in cervical motion in the sagittal plane at 1 year, which increased to 56% at final follow-up (7.8 years), after open-door laminoplasty. Edwards et al. [93] reported a 38% decrease in cervical motion after spinous process–splitting laminoplasty in North American patients with mean 2-year follow-up. Spontaneous segmental fusion at laminoplasty hinge sites is believed to be the causative factor in most cases. Our current practice is to apply bone wax to the exposed cancellous surface at the hinge site to prevent intersegmental bone formation and subsequent ankylosis. Bone graft is not placed at the hinge site, as has been previously described. Early motion is encouraged, starting the day of surgery.

Posterior arch closure after laminoplasty has been reported [93] but may be avoided using a combination of techniques. For open-door laminoplasty, we prefer to keep the posterior arch open with a nonresorbable braided suture attached to a suture-anchor placed into the hinge-side lateral mass. Before the posterior arch is hinged open, a transverse hole is made at the base of the spinous process as for a spinous process wire. The sutures are passed through this hole and tied down (Fig. 6). When spinous process–splitting laminoplasty is performed, immediate stability is achieved by suturing the bone graft strut in place between the two hinged laminae.

Complications with posterior decompression procedures 

Neurologic complications observed after posterior decompressive procedures include iatrogenic cord or root trauma, nerve root dysfunction and late neurologic deterioration. Laminectomy in the past featured significant complications resulting from direct damage to the cord by a rongeur introduced into the spinal canal where stenosis is severe. Fortunately, with the introduction of en block laminectomy techniques, such devastating iatrogenic complications are rare [101]. Nerve root palsy, especially C5, has been observed to develop in the first few days after both laminectomy and laminoplasty. Dai et al. [102] reported on a series of 287 consecutive patients undergoing laminectomy in which 12.9% developed postoperative radiculopathy, principally at C5 and C6. Large laminoplasty series have documented a prevalence of nerve palsy after laminoplasty ranging from 3% to 8%, with the C5 root being most commonly involved 48, 78, 103. In a series of 203 laminoplasty procedures reported by Yonenobu et al. [104], 12 patients developed fifth or sixth nerve root palsy, 3 patients had seventh nerve root involvement, and 1 had an eighth root complication. Patients often have a normal examination immediately after surgery. The onset of motor weakness generally develops within 1 to 5 days postoperatively. Sensation typically remains intact. Motor weakness for most patients resolves substantially or completely within one year. Explanations concerning the apparent predisposition of the C5 nerve root to dysfunction after posterior decompression principally center around three factors: the C5 segment is usually the midpoint of decompression and the extent of shifting at this segment is greater than that at other segments, and the C5 root is shorter than those of other segments. Moreover, because the deltoid receives sole C5 innervation, C5 palsy is more likely to be clinically evident than roots with shared motor functions [105].

A decrease in cervical lordosis has been reported after each of these posterior decompressive procedures. With laminectomy, nominal soft tissue capsule removal around the facet and less than 50% facetectomy minimizes destabilization. Recent reports suggest that the incidence of kyphotic deformity after laminectomy currently ranges from 21% to 33% 80, 106. At greatest risk are children, adults with a preexisting neutral to kyphotic alignment and those patients who have undergone a wide laminectomy without surgical stabilization 105, 107, 108. A decrease in lordosis after laminectomy and fusion or laminoplasty is less common than after laminectomy and tends to occur principally at the upper and lower extents of decompression where the ligamentum flavum and interspinous ligaments have been disrupted or are left unreconstructed 88, 109.

Patients commonly report axial symptoms, such as neck pain, stiffness, fatigue or shoulder discomfort, after posterior decompressive procedures. The causes of these symptoms are not well understood. Hosono et al. [110] reported a prevalence of axial symptoms in 60% of 72 patients after laminoplasty. Symptoms were of such severity as to require some form of analgesics in 13% of patients. Fortunately, symptoms resolved in a majority of patients within 1 year. In a matched cohort study of laminoplasty and laminectomy with fusion, the incidence of axial symptoms (69%) and the need for postoperative analgesics were identical for both procedures [88]. The prevalence of axial symptoms experienced after laminectomy was reported by Yonenobu et al. [103] to be 27.2%. The causes of such symptoms after posterior decompressive procedures are not well understood and merit further investigation. A study presented by Asano et al. [111] investigated the effect of early motion without immobilization after spinous-splitting laminoplasty. The authors found that early motion without immobilization resulted in markedly less axial pain with significantly better maintenance of lordosis as compared with a control group. Our current practice after laminoplasty is to place patients in a soft collar for use on an as-needed basis. Patients are directed to remove the collar several times per day for cervical range of motion exercises beginning on postoperative day 1.

Comparative studies 

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The optimal procedure for the treatment of cervical myelopathy involving three or more motion segments in the presence of a lordotic sagittal alignment remains controversial. The results of various posterior procedures have been compared using clinical series [84] and animal models 112, 113. A radiographic analysis of cervical alignment after laminectomy and laminoplasty in humans was performed by Matsunaga et al. [84]. They found that at an average of 6 years after surgery, segmental kyphosis was present in 33% of laminectomy patients and 6% of laminoplasty patients.

Heller et al. [88] reported the results of a comparison of laminectomy with fusion and laminoplasty. In this study two cohorts of patients were matched for preoperative prognostic factors: patient age, duration of symptoms and severity of myelopathy. Subjective and objective measures of functional improvement were similar for the two cohorts, but patients undergoing laminectomy and fusion had a significantly increased frequency of complications.

In 1985 Yonenobu et al. [106] compared the results of laminectomy with corpectomy and ACDF for the treatment of multilevel cervical spondylotic myelopathy. From their follow-up of 95 patients, multilevel corpectomy was found to have a significantly greater rate of recovery and decreased late neurologic deterioration compared with laminectomy. Multilevel corpectomy also had a superior maximum neurologic recovery compared with ACDF. In 1992 Yonenobu et al. [76] compared the results of laminoplasty with subtotal corpectomy. No differences were found in either the maximum JOA recovery rate or the final recovery rate for the two techniques. A notable difference observed was the overall incidence of complications (corpectomy, 29%; laminoplasty, 7%). The authors concluded that laminoplasty should be considered the treatment of choice for multilevel cervical myelopathy.

Edwards et al. [114] recently reported a comparison of corpectomy and laminoplasty for the treatment of cervical myelopathy in patients with stenosis at three or more levels and a lordotic sagittal alignment. Cohorts were carefully matched according to preoperative criteria of known prognostic significance. Patients undergoing both procedures enjoyed a similar degree of subjective and objective neurologic improvement, but the incidence of complications was significantly higher for patients in the corpectomy cohort.

Wada et al. [115] reported the results of corpectomy and laminoplasty for multilevel cervical spondylotic myelopathy with minimum 10-year follow-up. At latest follow-up, both procedures had similar rates of maintained neurologic improvement. Disadvantages noted for the two procedures were pseudarthrosis (26%) and asymptomatic adjacent segment degeneration in a majority of patients after corpectomy; and decreased range of motion and axial discomfort (40%) after laminoplasty.

Conclusions 

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Cervical myelopathy has a varied clinical course. Surgical management should be considered for patients with chronic or progressive symptoms and those not responding to nonoperative treatment. Surgical treatment of cervical myelopathy must be tailored to each patient's specific clinical and radiographic scenario. Myelopathy resulting from stenosis at one level may be managed reliably by ACDF with a high degree of success. Corpectomies alone or in combination with ACDF are best suited for the canal decompression at two or three levels. For stenosis at three or more levels, an anterior decompression with circumferential fusion or laminoplasty is recommended, depending on the patient's sagittal alignment.

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a Maryland Spine Center, Mercy Hospital, 301 St. Paul Place, Baltimore, MD 21202 USA

b Department of Orthopedic Surgery, Washington University, 660 S. Euclid, St. Louis, MO 63110-1010 USA

c Orthopedic Surgery and Rehabilitation Medicine, Spine Medicine, University of Wisconsin Medical School, Research Park Clinic–Spine Medicine, 621 Science Drive, Madison, WI 53711-1074 USA

d The Rothman Institute and Jefferson Medical College, 925 Chestnut Street, 5th Floor, Philadelphia, PA 19107-4216 USA

Corresponding Author InformationCorresponding author. Alexander R. Vaccaro, MD, The Rothman Institute, 925 Chestnut Street, 5th Floor, Philadelphia, PA 19107, USA. Tel.: (215) 955-5367; fax: (215) 503-0580

 This Contemporary Concepts review article has been reviewed by the Board of the North American Spine Society (NASS). As such, it represents the current position of the state of knowledge of the above subject in spine care. This series is edited by Alexander Vaccaro, MD. Prior to entering the review process for The Spine Journal, the authors were assisted by members of the NASS Committee on Contemporary Concepts, Alexander Vaccaro, MD, Chair.

☆☆ FDA device/drug status: not applicable.

 Nothing of value received from a commercial entity related to this research.

PII: S1529-9430(02)00566-1


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