Management of Cervical Spondylotic Myelopathy

Introduction

Cervical spondylotic myelopathy (CSM) is caused by a reduction of the sagittal diameter of the cervical spinal canal as a result of congenital and/or degenerative changes in the cervical spine. It is the most common type of spinal cord dysfunction in patients over the age of 55 years and it is the most common cause of acquired spastic paraparesis and tetra- or quadriparesis in the adult population. ^, Risk factors for spondylosis include age, cigarette smoking, frequent lifting, and diving.

CSM is a manifestation of chronic and repetitive trauma from spondylosis to the spinal cord, taking the form of compression, distraction, and/or angular distortion, resulting in neurological dysfunctions. ^{, ,} Degenerative changes of cervical spondylosis occur in the five articulations that comprise the cervical motion segment: the intervertebral disc, the two facet joints, and the two uncovertebral joints of Luschka. The normal aging process of the spine results initially in disc desiccation, leading to loss of disc height. This change brings the uncovertebral joints into contact, thereby disrupting the normal biomechanics of the facet joints. Osteophyte formation, ligamentum flavum hypertrophy, and facet and uncovertebral joint eburnation may then occur as a reaction to the abnormal biomechanics. ^, These degenerative changes most commonly occur at C5–C6 and C6–C7. White and Panjabi classify such spondylotic changes as “static” factors involved in the pathogenesis of CSM. Other etiologies and risk factors include congenital spinal canal stenosis with less than 13 mm anteroposterior (AP) diameter, and disc herniation. White and Panjabi also describe “dynamic” factors, which are abnormal forces placed on the spinal column and cord during flexion and extension under normal physiologic loads. For example, repetitive traumatic compression of the spinal cord against an osteophyte during normal flexion and extension of the cervical spine is defined as a dynamic factor. ^{, ,}

In addition to the direct mechanical compression of neural elements, CSM may also be the result of spinal cord ischemia. Ischemia can result from compression of large arterial feeders to the spinal cord such as the anterior spinal artery, reduced flow through the penetrating arteries of the spinal cord or the pial plexuses, or impairment in venous outflow resulting in venous hypertension. ^,

The natural history of CSM appears to be one of progressive disability. ^, It should be noted that there are some limitations in determining this natural history; studies are hampered by bias, heterogeneous patient populations, lack of long-term follow-up, and the use of qualitative rather than quantitative outcome measures. In fact, Clarke and Robinson asserted that once the disorder was recognized, neurologic function did not return to normal. In their series, 75% had episodic progression; 20% had slow, steady progression; and 5% had a rapid onset of symptoms followed by a prolonged period of stable disease. Nurick observed that younger patients with mild disability tended to have a better prognosis, while patients over the age of 60 years tended to progress. Moreover, patients who have had symptoms longer than 2 years show no improvement despite treatment. ^,

Symptom duration may have a negative impact on natural history. Sadasivan and colleagues reported on 22 patients with symptomatic CSM for an average of 6.3 years. All patients were reported to be Nurick II myelopathy at diagnosis. All progressed over the study period, one to grade III, 17 to grade IV, and 4 to grade V. Gait was involved in 100%, weakness in 45%, and dexterity in 72% of patients.

Pathologic Anatomy and Cervical Spondylotic Myelopathy

The patient with cervical spondylosis presents to the physician with complaints of neck pain related to degenerative changes, neurologic symptoms from spinal cord and nerve root compression, or a combination of complaints. CSM is the clinical result of spinal cord compression, and there are many factors with the potential to contribute to decreased space available for the spinal cord within the spinal canal.

There are static, degenerative factors, including intervertebral disc bulging, dorsal vertebral body osteophytes, ossified posterior longitudinal ligament (OPLL), uncovertebral and facet joint hypertrophy, ligamentum flavum, and facet joint capsule laxity and infolding. Collapse of the intervertebral disc space can potentially lead to a degenerative cascade. As the disc-space height decreases, the uncovertebral joints approximate and are loaded abnormally, increasing the likelihood of degenerative spurring. Disc-space collapse also causes a rostral–caudal translation, leading to similar degenerative spurring in the facet joints and laxity and buckling of the facet capsules and ligamentum flavum. All of these contribute to static narrowing of the spinal canal ( Fig. 138.1 ).

Dynamic factors include abnormal translation or angulation during flexion and extension of the cervical spine. Flexion can increase spinal cord compression in the presence of disc protrusions or posterior vertebral body osteophytes as the cord is draped over these structures. Extension/hyperextension may narrow the spinal canal and increase compression on the cord as well by infolding or buckling of the ligamentum flavum and facet joint capsules. If there is existing loss of disc-space height, this dorsal soft-tissue buckling is usually exaggerated. The morphology of the spinal cord has been shown to change with flexion and extension. Flexion tends to stretch the spinal cord, which can be magnified in the presence of disc protrusions and vertebral body osteophytes. Cervical spine extension causes the spinal cord to shorten and thicken, making it more susceptible to compression from buckling of the ligamentum flavum, scar tissue from previous surgeries, and previous injuries leading to anatomical changes.

In addition to these static and dynamic causes for spinal cord compression, congenital narrowing can be associated with myelopathy. Congenital cervical spine stenosis is said to exist if the ventrodorsal diameter of the spinal canal is less than 13 mm. The normal adult canal diameter in the subaxial cervical spine is approximately 17 to 18 mm. Congenital stenosis, with superimposed degenerative and/or dynamic compressive pathology, increases the likelihood of developing myelopathy. Recognizing the presence of congenital stenosis with diagnostic images in a setting of significant degenerative changes is crucial, as it may affect the surgical decision-making process.

The normal cervical lordosis is formed due to the thicker disc space in the ventral aspect than the dorsal. Degenerative process involving disc herniation in the dorsal direction, along with the loss of disc height and structural integrity, lead to the development of kyphosis. In addition, as the loss of lordosis induces the loading forces to be placed on the ventral aspect of the vertebral bodies even more, increasing stress concentration with a higher tendency toward compression, the height of the vertebral bodies tends to decrease more in the ventral aspect, exacerbating the kyphotic deformity and leading to further progression of CSM.

Patient Presentation and Physical Examination

The patient with CSM can present with any number of subjective complaints and objective findings related to spinal cord compression. Subjective findings can range from subtle paresthesias of the hands to significant problems with upper extremity dexterity and gait/balance difficulties. Often, the patient will attribute early symptoms such as numbness in the fingers or mild balance disturbance to expected aging changes. The patient may also complain of axial neck pain due to the degenerative changes of spondylosis.

Cervical spondylosis can be divided into three groups based on clinical presentation: (1) myelopathy, (2) radiculopathy, and (3) myeloradiculopathy. Vascular or ischemic pathology is also a known cause of CSM; however, this chapter will discuss myelopathy and myeloradiculopathy secondary to spondylosis. CSM is related to spinal cord compression manifested by vague paresthesias and upper motor neuron signs. The patient with myeloradiculopathy presents with a combination of findings due to myelopathy and radiculopathy (nerve root compression and other related lower motor neuron findings).

During the assessment of the patient with suspected CSM, a directed review of systems is an important portion of the clinical evaluation, since patients may dismiss and not voluntarily report pertinent findings. Questions are generally directed toward the upper extremity, lower extremity, and bladder function. This is consistent with the myelopathy grading system described by Benzel and colleagues (modification of the myelopathy scale devised by the Japanese Orthopaedic Association). Upper extremity dysfunction can be ascertained by assessing for handwriting deterioration, increasing frequency of dropping objects, difficulty with fine motor skills such as fastening clasps or buttons, and the feeling of numbness and tingling in the hands. The term “myelopathy hand” has been used to describe nondermatomal paresthesias in the hands, a sense of clumsiness in the hands, and interosseous wasting. ^, Myelopathy hand can be confused with peripheral nerve compression syndromes such as carpal tunnel, cubital tunnel, and thoracic outlet syndrome. Questioning regarding lower extremity function is directed toward balance and gait dysfunction, which is secondary in part to spasticity. Paresthesias and weakness in the lower extremities may also be a prominent complaint. Finally, inquiring about bladder function is important. Bladder dysfunction is not as common a finding as extremity problems but may be present in the form of incontinence or retention.

The physical examination of the patient with suspected CSM includes a generalized neurologic examination, which should be more focused specifically based on the history. A thorough examination can differentiate CSM from the etiologies stemming rostral and caudal to the cervical spine, as well as from motor neuron disease and peripheral neuropathy. The examination begins with observation of the patient’s posture, gait, and general appearance and fluidity of movements. Posture assessment may demonstrate sagittal and/or coronal imbalances. Gait examination may show a wide-based, spastic gait, and subtle changes may manifest only when the patient is asked to increase the pace of walking. Cranial nerve evaluation is included. Extremity function includes a motor and sensory examination from C4 to T1 and L2 to S1 bilaterally. Note that when assessing thoracic sensory levels, patients with CSM can have variable sensory levels localizing to the thoracic spine. Deep tendon reflexes (DTRs) are typically hyperactive. This is not always the case, as concomitant peripheral neuropathy from diabetes can alter DTRs. Coexisting lumbar spinal stenosis can present with hyperactive upper extremity reflexes but normal or hypoactive lower extremity reflexes. Additional reflexes include Babinski reflex and clonus in the lower extremities, and Hoffman reflex, the inverted radial reflex, and finger escape sign in the upper extremities. Other reflexes that may help localize the site of compression are the pectoralis reflex, scapulohumeral reflex, and jaw jerk. Finally, cervical spine range of motion may be restricted. Associated findings may include a positive Spurling sign and Lhermitte sign.

Radiologic Evaluation

Once a thorough history and physical examination are completed, a radiographic assessment is needed to complete and confirm the evaluation. Imaging studies by themselves do not diagnose myelopathy, because the levels of spondylosis and cord compression do not always correlate clinically with patient complaints and physical findings. Imaging studies used in the workup of CSM include plain radiographs, magnetic resonance imaging (MRI), and computed tomography (CT) scan with or without myelography.

Plain radiographs are still an important part of the evaluation of the patient with CSM. The views obtained include AP, lateral, flexion/extension, and obliques. AP radiographs allow for the evaluation of coronal alignment (scoliosis) and for the presence of anomalies such as cervical ribs or large C7 transverse processes (sometimes associated with fibrous bands). The lateral view provides the most information. It demonstrates the sagittal balance or the amount of lordosis/kyphosis. The lateral view also demonstrates the amount of disc-space narrowing, vertebral body osteophytes, the AP diameter of the spinal canal, and sometimes the OPLL. The Pavlov ratio, defined as the ratio of the sagittal diameter of the spinal canal to the sagittal diameter of the vertebral body, is determined using lateral radiographs. A ratio of less than 0.8 has been associated with an increased risk for developing myelopathy. Lateral flexion/extension views evaluate for translation and angulation abnormalities, which can provide information regarding dynamic cord compression. Flexion/extension views, combined with a static lateral view, demonstrate the ability of the patient to achieve lordosis, either globally or focally, which can be important for deciding between surgical approaches. Lastly, oblique views provide information about foraminal narrowing, particularly due to uncovertebral joint hypertrophy.

MRI is essential for the evaluation of soft tissue compressive structures as well as the assessment of the spinal cord itself. The intervertebral disc and ligamentous and capsular structures are all well visualized in the axial and sagittal planes. Perhaps the greatest advantage of MRI in CSM is its ability to directly visualize the spinal cord. Parenchymal changes, such as myelomalacia with cord signal changes and syrinx formation, are readily identified ( Fig. 138.2 ). MRI may also have a prognostic role. High-signal-intensity abnormalities on T2-weighted images and low-signal-intensity changes on T1-weighted MRIs are not uncommon findings in patients with CSM. A recent retrospective review correlating MRI findings to operative outcomes suggested that low-signal-intensity changes on the T1-weighted images preoperatively indicated a poor prognosis. A recent guideline article focusing on predictors of outcome found consensus that the presence of low signal of preoperative T1-weighted images, multisegment and focal high signal on T2-weighted images, and the presence of cord atrophy are indicators of poor outcome. ^, The addition of gadolinium is useful in cases of suspected infection, tumor, and scar tissue in a setting of prior spine surgery.

Myelography combined with CT can serve several important roles. The myelogram can be evaluated with the cervical spine in flexed and extended postures, providing details regarding dynamic compression. CT provides the most detailed information about bony pathology such as osteophytes and OPLL, and in the case of significant OPLL, CT can influence the decision on surgical approach. It is more effective at differentiating bony from soft tissue than MRI, and it has been suggested that CT myelography and MRI should be considered complementary, not interchangeable.

Somatosensory and Motor-Evoked Potential Monitoring

Somatosensory evoked potential (SSEP) and motor-evoked potential (MEP) as well as electromyography (EMG) recordings have been used as tools of prognostic indication for CSM. Lyu and colleagues performed preoperative MEP and SSEP in 39 patients with CSM who were to undergo surgical decompression. ^, The authors judged improvement postoperatively by using pre- and postoperative JOA scores and 6-month neurologic recovery rates. The mean recovery rate was 51%, and this did not correlate with sex, arm or leg MEP, or SSEP recordings. Neurological recovery rate, however, significantly correlated with normal SSEP results. Morshita and colleagues performed pre- and postoperative median nerve SSEPs in 14 patients with CSM who underwent cervical decompression. The authors demonstrated a statistically significant correlation between 1-week postoperative improvement in median nerve SSEPs and 12-week postoperative JOA score for recovery rate. On the other hand, a lack of improvement in the median nerve SSEP in the early decompression period was associated with a poor neurological outcome. Such data provide class II evidence supporting the use of median nerve SSEPs in predicting the outcomes following treatment of CSM.

The use of EMG has not been shown to be convincingly predictive of recovery in CSM. It should be noted that the EMG evidence of radiculopathy has been shown to be predictive of developing myelopathy in patients with asymptomatic cervical stenosis.

Nonsurgical Treatment

Controversy exists regarding the natural history of patients with CSM. This stems from the lack of randomized prospective studies on the issue and the reflection that the majority of studies that exist in the literature contain a heterogeneous population of patients. The natural history of CSM is a slow, stepwise progressive deterioration. Lees and Turner reported episodic and stepwise deterioration in 75% of their patients. Patients with mild symptoms had the best prognosis in regard to lack of progression.

Conservative treatment consists of measures aimed at decreasing symptoms and increasing function. Options include cervical orthosis, physical therapy, medication, and epidural steroid injections. Medications include nonsteroidal antiinflammatory drugs (NSAIDs), analgesics (opioids), muscle relaxants, and steroids. Some or all of these conservative measures may lead to some improvement in 30% to 50% of patients, depending on the grading criteria utilized. ^, This is especially true for those with only mild symptoms, that is, mild hand and arm symptoms but no impairment of daily tasks.

Conservative management with close follow-up may be considered for those with mild myelopathy, but caution should be taken with those with moderate to severe symptoms. No difference at 2 years was observed between those who received surgical treatment and those who did not due to mild myelopathy. In contrast, those with severe myelopathy rarely improved with conservative measures. Fourteen out of 15 patients with severe myelopathy treated nonsurgically remained disabled without improvement in one series.

Conservative treatment is an effective treatment for patients without cervical disc herniation, and with mild compression with no or mild myelopathy. ^, In general, favorable outcomes from nonsurgical treatment can be expected if a median- or diffuse-type soft disc herniation is found on MRI. ^, Conservative, nonoperative management is only appropriate for mild, nonprogressive CSM, and surgical treatment is warranted for progressive, moderate-to-severe CSM. ^{, ,} In a multicenter prospective cohort study, surgical decompression in severe CSM patients was found to be associated with improvement in functional status, disability, and health-related quality of life (HR-QOL), at 1 year follow-up. The majority of complications in the surgical cohort of CSM patients were treatable and without long-term effect, and moreover, surgical treatment was associated with significant improvement in health utilities and cost effectiveness, as compared to those treated conservatively. ^,

Ultimately, most patients with CSM undergo surgery. Those with moderate or severe symptoms should undergo early surgical decompression. Many surgical studies have demonstrated that shortening symptom duration prior to decompression results in improved outcomes. Patients with only mild symptoms may be closely followed and decompression performed when there is deterioration or lack of improvement.

Operative Management

Ventral Approach

The ventral approach to the cervical spine to address spondylosis has been successfully performed for nearly 50 years. This approach provides direct access for spinal cord and nerve root decompression secondary to herniated intervertebral discs, dorsal vertebral body osteophytes, OPLL, and uncovertebral joint hypertrophy. Another important benefit of the ventral approach is the ability to correct kyphotic deformity through discectomy and/or corpectomy. Although some advocate ventral discectomy without arthrodesis in certain clinical situations, decompression in the setting of CSM is accompanied by a stabilization procedure with the goal of arthrodesis (artificial disc placement would be an exception). Ventral decompression options include discectomy (either single or multiple levels), corpectomy (either single or multiple levels), or a combination of both. Arthrodesis can be accomplished by using autograft or allograft bone, or a combination of both, with or without instrumentation. A variety of metallic and carbon fiber cages have been used, typically packed with autograft or allograft bone, and all of these options can be performed with or without a ventral cervical plate ( Fig. 138.3 ).