Cervical Myelopathy: Ventral Approach

Edward R. Anderson III

Garrick W. Cason

Harry N. Herkowitz

INTRODUCTION AND PATHOPHYSIOLOGY

Cervical myelopathy is one of the most common disorders treated by spine surgeons (1). It is characterized as a dysfunction of the cervical cord caused by extrinsic compression on the spinal cord and/or obstruction of its vascular supply (2). Cervical disk degeneration with disk protrusion, dorsal vertebral and uncovertebral osteophytosis, olisthesis/instability, disk herniation, ossification of the posterior longitudinal ligament (OPLL), and hypertrophy/infolding of the ligamentum flavum are features of cervical spondylosis that can manifest clinically as radiculopathy, myelopathy, or myeloradiculopathy. Soft disk herniation, tumor, trauma, and vertebral osteomyelitis can manifest clinically as myelopathy in the absence of spondylosis. While each of these factors alone can contribute to the pathogenesis of cervical myelopathy, the additive synergy of each, especially when combined with congenital stenosis, can present with a profound degree of spinal cord compression with clinical manifestations.

Described by Brain (3) and Clark and Robinson (4) in the 1950s, the etiologies of cervical myelopathy are most commonly related to degenerative processes and present in the sixth decade of life (3,5, 6 and 7). Its pathogenesis is multifactorial (5), exhibiting static, dynamic, and vascular etiologic factors (8). Ferguson and Caplan (9) described four distinct cervical syndromes: lateral/radicular, medial/myelopathic, combined, and vascular syndromes. The combined syndrome represents the most common manifestation, with the vascular syndrome being the rarest.

The average adult cervical spinal cord is 12 mm in sagittal diameter. Nurick (10) demonstrated that the minimum cervical canal sagittal diameter must be 11 mm in men and 9.9 mm in women. Absolute stenosis is present at diameters of 10 mm or less. In the aged, the etiology of cervical stenosis is related to bony compression (osteophyte formation, spondylolisthesis) and disk dehydration causing disk height loss with annular protrusion ventrally and dorsal flaval infolding with hypertrophy dorsally. The osteology of the spondylotic subaxial cervical spine contributes to the loss of cervical lordosis. The uncovertebral joints favor development of spondylotic kyphosis by blocking dorsal disk space height loss upon apposition of the zygapophyseal joints. The loss of lordosis contributes to the relative stenosis of the spondylotic cervical spine.

Dynamic etiologic factors of stenosis in the cervical spine are related primarily to postural and rotational movements of the subaxial spine. Hyperextension of the spondylotic cervical spine increases the pressure exerted upon the cervical cord through a pincer mechanism (Fig. 78.1) due to a local decrease in anteroposterior diameter of the cervical canal (11, 12 and 13). Infolding of the ligamentum flavum increases with cervical extension resulting in dynamic dorsal spinal cord compression/stenosis (10,14). While there is a relative increase in sagittal diameter with flexion, the cord can be stretched over and flattened against spondylotic osteophyte/disk complexes projecting from the dorsal vertebral bodies (15).

Vascular factors related to compression of the anterior spinal artery have been demonstrated experimentally in vitro, histopathologically, and suggested as an etiologic factor in cervical myelopathy (16, 17, 18, 19, 20, 21, 22 and 23). The anterior spinal artery supplies the ventral two-thirds of the spinal cord, whereas the posterior columns are supplied by paired posterior spinal arteries. Chronic compression by the dorsal vertebral osteophytes has been demonstrated histopathologically to primarily affect the region of the spinal cord dependent upon the anterior spinal artery for its blood supply (22). Chronic vascular insufficiency has been suggested as an etiology of the radiographic finding myelomalacia on magnetic resonance imaging (MRI), which manifests histopathologically as cavitation and gliosis of the spinal cord. Furthermore, flattening deformation of the cervical spinal cord results in attenuation of the lateral tributaries of the anterior spinal artery, which supply the lateral corticospinal tracts, providing a teleologic explanation for the susceptibility of the corticospinal tracts to insult in the setting of myelopathy (24).

Figure 78.1. Dynamic cord compression associated with nutation/flexion and extension. From Law MD Jr, Bernhardt M, White AA III. Cervical spondylotic myelopathy: a review of surgical indications and decision making. Yale J Biol Med 1993;66(3):165-177.

CLINICAL PRESENTATION AND EVALUATION

An evaluation, to include the systematic performance of a history, physical examination, and review of diagnostic imaging, is critical to the workup of the myelopathic patient. The classic clinical presentation, characterized by Clark and Robinson (4), is a stooped, broad-based, spastic gait with lower extremity weakness. Most commonly, the presentation includes an upper extremity radicular component (lower motor neuron findings), combined with the lower extremity weakness, gait disturbance, and the presence of long tract signs (upper motor neuron findings: crossed/inverted radial and Shimizu reflexes, Hoffmann sign, dysdiadochokinesia, Babinski sign, sustained clonus, dynamic Romberg sign, Lhermitte sign, and/or hyperreflexia). The performance of a graded motor examination of both the upper and lower extremities is paramount. Cervical pain is often but not always present.

Radiographic evaluation should begin with a standard x-ray evaluation of the cervical spine to include anteroposterior, lateral, oblique, and flexion/extension views. The radiographs should be scrutinized for the presence of bony sources of compression and instability such as congenital stenosis, OPLL, uncovertebral/retrovertebral osteophytosis, olisthesis, tumor, and osteomyelitis. MRI is the modality of choice for evaluating the soft tissue factors contributing to compression of the spinal cord (Fig. 78.2A,B). If performance of an MRI is contraindicated due to factors such as the presence of a non-MRI-compatible pacemaker or automated implantable defibrillator, a cervical computerized tomography (CT) myelogram may be performed. In the setting of a bony source of compression such as OPLL, olisthesis, tumor, and osteomyelitis, CT is often a useful adjunct to MRI for the purpose of preoperative planning if surgery is indicated.

Neuroelectrophysiologic testing has not been a routine diagnostic modality employed in the evaluation of cervical myelopathy. Due to its low sensitivity and specificity, it is not suitable as a screening measure. Bednarik et al. (25) concluded that the development of myelopathy is associated with the coexistence of radiculopathy and premorbid electromyography (EMG) and somatosensory evoked potential (SSEP) abnormalities in patients with spondylotic cervical stenosis. In their study, the presence of a radiculopathy was the most sensitive screening tool, being present in 92% of patients who went on to develop myelopathy versus only 24% of those who did not. EMG abnormalities were less sensitive but demonstrated in 61% of patients developing myelopathy versus only 11% who did not. Similarly, SSEPs demonstrated abnormalities in 38.5% of patients who developed myelopathy versus only 9.4% with abnormalities in patients who did not.

NATURAL HISTORY

The natural history of cervical myelopathy is mixed (26). Cervical myelopathy has been characterized both as having a slow stepwise progression punctuated by episodes of neurologic deterioration (4,27) and as having a quiescent/seemingly static clinical course (28) in which a small subgroup may improve (29,30). Many authors have reported on the natural history of cervical myelopathy (4,28,31), but their respective study groups have been heterogenous, retrospectively reviewed, and have lacked validated longitudinal outcome assessment tools.

The Nurick (10,32) scale, the Japanese Orthopaedic Association (JOA) scale (33,34), and its modifications (35,36) are the most commonly employed systems for classifying the severity of myelopathy and can be useful in the longitudinal analysis of therapeutic response and prognosis based upon the patient’s initial presentation. Nurick (Table 78.1) classifies patients based on the degree of gait ataxia, whereas the JOA (Table 78.2) system examines the impairment of myelopathy on the patient’s activities of daily living (degree of ataxia, ability to feed oneself,
micturition control, and upper/lower extremity sensory and motor function). The classic JOA scale was modified by Chiles et al. (35) and Benzel et al. (36), in order to extend its utility to Western cultures, where chopstick use is less common (Table 78.3).

Figure 78.2. A,B: Sagittal and axial MRI demonstrating cervical stenosis at C4-C5 with compression.

In a clinicopathologic study of five patients with cervical myelopathy, Ono et al. (37) demonstrated that the severity of the clinical presentation correlated with the degree of cord compression as measured by the anteroposterior compression ratio. The anteroposterior compression ratio is calculated by dividing the AP cord diameter by the diameter of the spinal cord in the coronal plane (37) (Fig. 78.3). The severity of cord compression correlates clinically with regard to disability (10,32) and pathologically to the destruction of both gray and white matter extending cephalad and caudad to the inciting cervical cord lesions (37,38). The lesions can occur at any level in the subaxial cervical spine but most commonly occur at C4-C5, C5-C6, and C6-C7, with C5-C6 being the most prevalent (39).

TABLE 78.1 Nurick Grade

Grade	Nurick Grade for Cervical Myelopathy
0	Signs or symptoms of root involvement but without evidence of spinal cord disease
1	Signs of spinal cord disease, but no difficulty in walking
2	Slight difficulty in walking, which did not prevent full-time employment
3	Difficulty in walking, which prevented full-time employment or the ability to do all housework, but which was not so severe as to require someone else’s help to walk
4	Able to walk only with someone else’s help or with the aid of a walking frame
5	Chair bound or bedridden
Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain. 1972;95(1):87-100.

NONOPERATIVE MANAGEMENT

Because dynamic compression plays a role in the clinical manifestation of cervical myelopathy, immobilization with a rigid cervical orthosis represents the mainstay of nonoperative management (40). Other modalities of nonoperative managements include physical therapy, muscle relaxants, oral steroids, nonsteroidal anti-inflammatory medications, and judicious use of analgesics. Nonoperative management does not alter the natural history of the disease process and is unlikely to result in clinical improvement in patients with moderate to severe progressive myelopathy as most will demonstrate a progressive neurologic deterioration over time (40). Nonoperative
management is considered for two groups of patients. The first group consists of younger patients (<75 years) with mild to moderate disability (mJOA > 12). Kadanka et al. (41) reported on a prospective randomized controlled trial of 48 patients comparing conservative treatment (27 patients) to surgery (21 patients) in patients with mild to moderate disease. Outcomes at 3 years demonstrated stable mJOA scores and yielded equivalent results in both the surgically and conservatively managed groups. This approach remains controversial because an mJOA of 12 can present with a moderate impairment of gait, urinary incontinence, decreased hand function, or in combination (42). Furthermore, long-term natural history data are still lacking. The question remains, will the conservatively managed group remain stable beyond 3 years? The second group for which nonoperative management is reasonable includes patients with relative contraindications for surgical management such as an unacceptably high perioperative risk (elderly, high-risk/multiple comorbidity, or quadriparetic). Indicators of poor outcomes include a preoperative cord area of less than 30 mm² (43) and radiographic evidence of cord atrophy (44).

TABLE 78.2 JOA Assessment for Cervical Myelopathy

Motor Dysfunction Scores of the Upper Extremity
0	Inability to feed oneself	Chiles’ modification of the JOA assessment scale
1	Unable to handle chopsticks, able to eat with a spoon	Unable to use knife and fork, able to eat with a spoon
2	Ability to handle chopsticks, but with much difficulty	Able to use knife and fork with much difficulty
3	Ability to handle chopsticks, but with slight difficulty	Able to use knife and fork with slight difficulty
4	None
Motor Dysfunction Scores of the Lower Extremity
0	Inability to walk
1	Ability to walk on flat floor with walking aid
2	Ability to walk up and/or down stairs with hand rail
3	Lack of stability and smooth reciprocation
4	None
Sensory Deficit Scores of the Upper Extremity
0	Severe sensory loss or pain
1	Mild sensory loss
2	None
Sensory Deficit Scores of the Lower Extremity
0	Severe sensory loss or pain
1	Mild sensory loss
2	None
Sensory Deficit Scores of the Trunk
0	Severe sensory loss or pain
1	Mild sensory loss
2	None
Sphincter Dysfunction Scores
0	Inability to void
1	Marked difficulty in micturition
2	Difficulty in micturition
3	None
Total individual item scores for assessment of severity
From Ogino H, Tada K, Okada K, et al. Canal diameter, anteroposterior compression ratio, and spondylotic myelopathy of the cervical spine. Spine (Phila Pa 1976) 1983;8(1):1-15; Chiles BW III, Leonard MA, Choudhri HF, et al. Cervical spondylotic myelopathy: patterns of neurological deficit and recovery after anterior cervical decompression. Neurosurgery 1999;44(4):762-769; discussion 769-770.

SURGICAL INDICATIONS

Surgery is indicated for patients with moderate to severe myelopathy (mJOA ≤ 12), an acceptable perioperative risk profile, and positive prognostic indicators (42). Progressive neurologic deterioration, the presence of a static deficit (>6 months) significantly affecting quality of life, an anteroposterior compression ratio greater than or equal to 0.4, or a cervical cord transverse area less than 40 mm² (43) represent indications for surgical decompression (40). Young age (≤65 years), symptom duration less than 1 year, and the presence of a Lhermitte sign are positive predictors of neurologic improvement following decompression (45). Patients older than 75 years exhibit an increased risk for postoperative complications (45).

TABLE 78.3 Chiles’ Modified JOA Assessment for Cervical Myelopathy

Motor Dysfunction Scores of the Upper Extremity
0	Inability to feed oneself
1	Unable to use knife and fork, but able to eat with a spoon
2	Ability to use knife and fork, but with much difficulty
3	Ability to use knife and fork, but with slight difficulty
4	None
Motor Dysfunction Scores of the Lower Extremity
0	Inability to walk
1	Ability to walk on flat floor with walking aid
2	Ability to walk up and/or down stairs with handrail
3	Lack of stability and smooth reciprocation
4	None
Sensory Deficit Scores of the Upper Extremity
0	Severe sensory loss or pain
1	Mild sensory loss
2	None
Sensory Deficit Scores of the Lower Extremity
0	Severe sensory loss or pain
1	Mild sensory loss
2	None
Sensory Deficit Scores of the Trunk
0	Severe sensory loss or pain
1	Mild sensory loss
2	None
Sphincter Dysfunction Scores
0	Inability to void
1	Marked difficulty in micturition
2	Difficulty in micturition
3	None
Total individual item scores for assessment of severity

SURGICAL OPTIONS

The approach to the treatment of cervical myelopathy is predicated on multiple factors: site of compression, number of levels involved, degree of kyphosis, and the presence of congenital stenosis. The site of spinal cord compression, in general, directs the surgical approach ventrally or dorsally. Ventral options include anterior cervical discectomy and fusion (ACDF), anterior cervical corpectomy and fusion (ACCF), and cervical disk replacement (CDR). Dorsal surgical options include cervical laminectomy (Chapter 76-A) with/without fusion, and laminoplasty (Chapter 76-B). Because of the relatively low morbidity associated with the ventral approach, ACDF is preferred for the treatment of myelopathy involving one or two levels (46,47). The presence of clinically significant congenital stenosis is best approached with a dorsal decompression and fusion either alone or combined with a ventral procedure.

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