Cervical Spondylosis with Minimal Myelopathy: To Decompress or Not to Decompress

Published on 27/03/2015 by admin

Filed under Neurosurgery

Last modified 27/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1756 times

Chapter 214 Cervical Spondylosis with Minimal Myelopathy

To Decompress or Not to Decompress

To Decompress

With the advent and widespread use of modern neuroradiologic evaluation, many patients are being identified with spinal cord compression without obvious clinical signs of neurologic deterioration. Such patients often are referred for neurosurgical consultation and an opinion regarding surgical intervention. The management of such patients remains controversial, primarily due to the lack of understanding of their natural history in this specific clinical and imaging context. This chapter reviews the relevant literature regarding the natural history of cervical spondylotic myelopathy and contrasts it with the natural history of cervical stenosis, reviews the risk factors that may be associated with early progression of myelopathy, and makes suggestions regarding surgical decision making for such patients.

The development of an algorithm for the employment of surgical decompression early in the course of cervical spondylotic myelopathy (CSM) necessitates answering three fundamental questions regarding the disease process. The first and foremost question to be addressed is whether the expected clinical course of CSM is sufficiently morbid that some specific treatment is required. If the answer to this is that the untreated clinical course of CSM is not benign, should the appropriate therapeutic intervention be nonoperative, or does surgical treatment provide a more favorable outcome? The third question to be answered concerns the optimal timing for any proposed treatment. When in the clinical course of CSM is a specific therapy likely to have its greatest benefit? In short, is there a window of opportunity for any given treatment?

Regarding the first issue, is it possible to determine the probability that patients with asymptomatic cervical spondylosis or early mild CSM will experience disease progression resulting in functionally significant neurologic deficits? Secondly, can we identify risk factors that indicate a high likelihood of disease progression? Finally, can we identify neurologic manifestations, which may be defined qualitatively and quantitatively, that are most likely to be favorably affected by our treatment, whether nonoperative or surgical? The importance of correctly answering each of these questions is great, considering that cervical spondylotic spinal cord compression exists in 16% of asymptomatic patients under the age of 64 years and in 26% of those patients older than 64 years.1

Incidence of Cervical Spondylosis, Cervical Stenosis, and Cervical Spondylotic Myelopathy

Cervical spondylosis is a complex degenerative process of the cervical spine. The plain radiographic findings include disc space collapse, end plate sclerosis, osteophytosis, facet joint hypertrophy, and ligamentous hypertrophy. Cervical spondylosis is best viewed as a ubiquitous process of aging, with an increasing incidence with increasing age. Most of the population show no symptoms, but a smaller percentage may present with complaints of axial neck pain, cervical radiculopathy, and cervical myelopathy. Cervical spondylosis may be associated with cervical stenosis.

Cervical stenosis is defined as narrowing of the spinal canal and represents an anthropometric measurement, not a clinical entity. Cervical stenosis can be congenital but is often associated with cervical spondylosis. Whereas the normal spinal canal diameter between C3 and C7 is about 17 to 18 mm, cervical stenosis historically has been defined as an area less than 11 to 13 mm on plain lateral radiographs. Adams and Logue noted that the canal diameter in patients with cervical myelopathy averaged 11.8 mm.2 Teresi et al. studied 100 asymptomatic subjects and identified spinal cord impingement seen on MR in 16% of subjects under 64 years of age and 26% of those over 64 years.1 Odor et al. calculated the ratios of sagittal canal to vertebral body on cervical spine lateral radiographs in 124 professional and 100 rookie football players.3 Of these, 32% of the professional football players and 34% of the rookies had a ratio of less than 0.80 at one or more levels from C3 to C6, suggesting spinal stenosis. Lee et al. reviewed 469 randomly selected adult cervical spine specimens.4 Using a definition of cervical stenosis as 12 mm, 22% of the general population, 29% of specimens from patients older than 50 years, and 34% of specimens of patients older than 70 years were found to be stenotic. In summary, cervical spinal stenosis is observed in a large number of aging patients.

Cervical spondylotic myelopathy is defined as a clinical syndrome of spinal cord dysfunction that is attributable only to cervical spondylosis. It is the most common cause of spinal cord dysfunction in North America. The clinical history and examination findings can vary significantly. The history and examination can then be used to determine whether the patient has mild, moderate, or severe neurologic impairment. As described in the next section, the natural history of cervical stenosis and cervical myelopathy is not well understood and may be difficult to predict in an individual patient.

Natural History of Cervical Spondylotic Myelopathy and Cervical Stenosis

In 1956, cervical myelopathy was recognized by Clarke and Robinson as a potentially devastating and irreversible neurologic condition.5 Their study of 120 patients indicated that once symptoms developed, patients were unable to return to a neurologically normal state. Although half of the study subjects experienced some improvement in their symptomatology with conservative therapy, the remaining 50% of patients progressed in a slow, steady manner with short episodes of rapid worsening. Several subsequent studies have corroborated the ominous nature of this disease and noted the need for aggressive intervention.68

A review of the Joint Guidelines Committee of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons demonstrates the relative lack of data regarding the natural history of cervical spondylotic myelopathy, especially in the context of modern imaging, objective myelopathy scoring, and blinded outcome.9 Indeed the authors’ key issues statement summarizes the problem nicely:

The same committee suggested an appropriately powered prospective randomized trial; however, to date, such a trial has yet to be performed. Hence, this systematic review, unfortunately, does not include a more recent study for which to base clinical decision making with respect to patients with minimal myelopathy and cervical stenosis.

Best Evidence to Date

Recently, Bednarík et al.10 reported their findings in a group of 199 patients with “presymptomatic spondylotic cervical cord compression” who were followed for a minimum of 2 years. Forty-five (22.6%) of the patients developed clinical evidence of myelopathy and 18 (9.0%) were offered surgical intervention. Significantly, slightly more than one third of these patients who developed clinical myelopathy did so within the first year of observation. The best predictors of early progression to myelopathy were symptomatic cervical radiculopathy and abnormal motor-evoked potentials (MEPs) or somatosensory-evoked potentials (SEPs). The best predictor of late progression to myelopathy was MRI hyperintensity. It is clear that most patients with MRI evidence of cord compression can likely be followed expectantly. It appears that at least about 20% of patients with no or minimal myelopathic signs or symptoms but with MRI evidence of cervical cord compression or those with only mild CSM will progress to some degree during a 2-year follow-up period of observation. The next task is to identify factors that predict probable worsening of cervical spondylotic myelopathy.

Risk Factors for Progression of Neurologic Dysfunction

Numerous factors in the radiologic, clinical, electrophysiologic, and genetic realms have been considered in attempting to predict which patients will develop progressive cervical spondylotic myelopathy. Some of the positive predictive factors in neurologic worsening are considered in the following sections.

Cervical Spinal Cord Diameter

There is a strong correlation between the severity of cervical spondylotic spinal cord compression and the likelihood of progressive clinical myelopathy.

The extent of the spatial compromise of the cervical spinal canal and the consequent severity of spinal cord compression correlates with the severity of the initial clinical presentation of CSM. A congenitally narrow spinal canal results in the development of CSM in 40% to 47% of these patients, which is a much higher rate than is seen in the general population.14,15 Long periods of severe cervical stenosis over many years result in demyelination of the spinal cord’s white matter and in necrosis of both the gray and white matter, leading to potentially irreversible neurologic deficits.9 In patients with more severe MRI evidence of cord compression and/or MRI evidence of spinal cord atrophy, functional neurologic deficits with lower postoperative modified Japanese Orthopaedic Association (mJOA) scores were seen more consistently.16,17 In a prospective, randomized 3-year clinical study of stable or very slowly progressing mild and moderate clinical SCM (mJOA ≥12), several factors were associated with good outcome in conservatively treated, nonoperative patients. Patients demonstrating lower rates of stenosis of the spinal canal in the anteroposterior (AP) dimension were less likely to show progression of their myelopathy. Also, a slightly larger spinal cord transverse area was found to have a positive predictive power for favorable response to conservative treatment.18 Although the correlation between the severity of cervical spondylotic cord compression and the likelihood of rapidly progressive myelopathy appears strong, not every study correlates this finding.19

A spinal cord transverse area of less than 50 mm2 at the level of maximum compression significantly correlated with clinical symptoms by mJOA.20 In the same study, this correlation was strengthened if these areas of maximal spinal cord compression were associated with hyperintensities on T2-weighted MR imaging within the spinal cord. Other studies examining the AP dimensions of the cervical canal have demonstrated significant differences in functional neurologic status; patients with a 7.1-mm AP canal diameter were more likely to have clinical myelopathy, whereas patients with a 10.8-mm canal were more likely to be nonmyelopathic.21 In a study of mild and moderate CSM (mJOA ≥12), Kadanka et al. randomized patients to either early surgery or nonoperative management and found that patients with less significant spinal cord compression responded more favorably to surgery.18 Considering this potential postoperative improvement, if cervical stenosis is permitted to progress preoperatively, is there a point where surgical results will be suboptimal? If so, and if that point can be identified, then treatment prior to that time may prevent the occurrence of irreversible symptoms. Several groups have attempted to identify the exact degree of spinal cord compression that will best predict the optimal timing of surgery, but despite promising data, these results have rarely been consistent.2224 It has been demonstrated, however, that spinal cord architecture appears to be well restored by decompression in these patients with mild-to-moderate cervical myelopathy.23

Intramedullary Spinal Cord Signal Intensity

Cervical intramedullary signal changes, especially when accompanied by significant stenosis, can help identify a patient who will have a favorable surgical outcome. Once these changes span multiple levels or include hypointensity on T1-weighted MR imaging, however, the prognosis worsens.

The observation that severe cervical stenosis and cord compression often result in intramedullary spinal cord signal intensities in CSM patients has prompted the evaluation of a possible relation between these signal changes and the severity of cervical myelopathy. Although the results of such studies have produced promising results, the exact correlation and the strength of its predictive value remain unclear.

Bednarík et al. suggested that MRI hyperintensity, when present in patients with asymptomatic cervical spondylosis, may predict a delayed (>12 months) progression to symptomatic CSM.25 The influence on surgical outcome of these signal intensities has become an area of immense interest. Overall, there appears to be a significant correlation between surgical result and the preoperative presence of intramedullary signal alteration.20,2630 The best results occur in those patients with either no signal changes or hyperintensity on T2-weighted MRI.2630 When T2 hyperintensity occurs at a single segment, this single finding does not portend a poor surgical outcome; these changes are reversible.2731 When hyperintensity onT2-weighted imaging spans multiple levels or is coupled with T1-weighted hypointensity, however, the surgical prognosis is significantly less favorable.2731 Unlike T2-weighted changes, T1-weighted hypointensities are not reversible,28 but they never exist as an isolated finding (i.e., without accompanying T2-weighted hyperintensities).30 There does not appear, however, to be a relationship between the duration of observed signal intensity and outcome.28

As mentioned previously, a review of the cross-sectional transverse area and signal change on MRI found that a T2-weighted MRI of a cross-sectional area of the spinal cord between 50 and 60 mm2 in association with hyperintensities was a critical point of significant disability as identified by the mJOA score.20 In addition, differentiating between mild and pronounced spinal cord hyperintensities produced a significant difference in mJOA scores of patients with CSM.20 Although decompressive surgery can result in the rapid resolution of these imaging abnormalities, clinical improvement does not always accompany these radiologic changes.31 Suri et al., however, were able to demonstrate that patients who experienced regression of any intramedullary signal changes were statistically likely to experience better surgical outcomes.30

Electrophysiologic Abnormalities

Electrophysiologic examination may be helpful in identifying candidates for early surgery. Surgical results will be best in those with normal or mildly abnormal studies. In the setting of cervical stenosis, an abnormal electromyelogram (EMG) or clinical radiculopathy should prompt strong consideration for decompression due to the ominous association with the development of symptomatic myelopathy.

Evaluation of patients with cervical spondylotic myelopathy in various electrophysiologic (EP) studies has yielded promising results. In general, when these results are normal, a more favorable clinical course is likely and these patients will likely respond well to nonsurgical management.10,18 In contrast, in a study of 30 asymptomatic patients with spondylotic cervical cord compression, one-third of those demonstrating an initial EP abnormality eventually developed CSM during the study’s 2-year follow-up.10 In a subsequent study analyzing the utility of SEPs and MEPs in predicting and monitoring the effect of therapy in spondylotic cervical myelopathy, however, the same authors were unable to demonstrate as strong a correlation between these EP studies and the clinical status.32

In their 2004 study involving a 2-year prospective follow-up of 66 patients with MRI-demonstrated spondylotic cervical cord compression but without clinical myelopathy, Bednarík et al. identified several variables significantly associated with the development of myelopathy. Among these were the presence of symptomatic cervical radiculopathy, which was present in 92% of patients eventually developing CSM versus 24% who did not develop myelopathy (P = .0001), electromyelographic signs of an anterior horn lesion (61% vs. 11.3%, P < .01), and abnormal SEPs (38.5% vs. 9.4%, P < .02).19 These authors also noted that the presence of symptomatic cervical radiculopathy and electrophysiologic abnormalities of cervical cord dysfunction detected by SEPs or MEPs were associated with the early development (<12 months) of CSM.25 Using the combination of these two parameters, radiculopathy, and EP abnormalities, early progression could be predicted accurately in over 80% of patients.25 In fact, in a recent meta-analysis of the CSM literature, class I evidence suggested that in the setting of cervical stenosis without myelopathy but with either an abnormal EMG or clinical radiculopathy, decompression should be strongly considered due to the association with the development of symptomatic myelopathy.9

The value of additional electrophysiologic parameters for the detection, evaluation, and treatment of CSM has been examined.3335 In general, these studies demonstrated a correlation between the severity of the cervical myelopathy and the degree of EP abnormalities. This relationship indicates that as EP studies worsen, surgical intervention should be more readily employed as a treatment option to prevent further myelopathic progression.34 There may be, however, a point of diminishing return in which the EP abnormalities are so severe that a patient may not improve clinically despite the treatment modality, including surgery. Both Hu et al. and Yu et al. have shown that the absence of any SEP waveform is correlated with impairment that is least likely to improve with operative intervention.36,37

Symptom Severity and Duration

Patients with no or mild myelopathic symptoms will respond better to surgery than those with more severe disease. Once permitted to progress, cervical myelopathy becomes more refractory to surgical intervention. Adjunctive tests (e.g., 30-meter timed walk test, nine-hole-peg test) may help objectify clinical symptoms and can be used to follow patients treated operatively or nonoperatively.

In identifying those patients with no or mild CSM symptoms who will benefit from early surgery, both the severity and the duration of symptoms must be identified. Perhaps the most important predictive factor for surgical intervention is the pretreatment neurologic condition.38,39 Whereas 70% of patients with mild myelopathy (mJOA ≥12) had good outcomes with surgery, only 55% of those with more severe symptoms (mJOA <7) fared as well.3840 Additionally, multiple reports have suggested the negative prognostic impact of surgical treatment performed “too late.”* There is a significant correlation between the duration of symptoms and neurologic condition after surgery, that is, a longer duration of symptoms portends a poorer prognosis. The point at which patients will begin to experience this negative effect is unclear. Some studies have suggested that those patients who have had preoperative myelopathic symptoms for more than 12 months have a worse postoperative prognosis.28,40 Others, however, found a significant difference only at the 2-year time point.11,30 Regardless, it is clear that patients have a better outcome when treated earlier in the disease course.

The difficulty arises in the quantitative assessment of myelopathy and determining what exactly “early” is in terms of signs and symptoms. The limitation of existing functional scales such as the mJOA score, Nurick score, or the myelopathy disability index is that they the lack the true objectivity that many clinicians emphasize.42 Attempts have been made to try and develop testing that can fill this void. Focusing on hyperreflexia and pathologic reflexes, Houten and Noce noted that patients with mild myelopathy (mJOA 14–16) less frequently demonstrated either Hoffman (46%) or Babinksi (10%) signs than did patients with more clinically significant CSM (mJOA ≤10; 81% and 83%, respectively). Reviewing patients with MRI evidence of cervical spinal cord compression, a Hoffman sign existed unilaterally in 50% and bilaterally in 91%.43

Buy Membership for Neurosurgery Category to continue reading. Learn more here