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.⁶^–⁸

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:

It is evident that there is a need for a randomized clinical trial examining patients with mild CSM (cervical spondylotic myelopathy) and comparing operative and nonoperative treatment. There is sufficient evidence indicating that patients with severe symptoms and a long duration of symptoms will generally not improve, and attempts at randomizing these patients to different treatment groups may not be ethically feasible.

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.

Surgical Decision Making for Patients with Presymptomatic Spinal Cord Compression

Given the current lack of data regarding the relative benefits of surgical versus nonsurgical treatment for minimal myelopathy, it becomes very difficult to counsel patients. The main question remains, in what setting is operative treatment best? Knowing when to intervene prevents unnecessary surgery in those whose symptoms are unlikely to progress and, conversely, treats appropriate patients prior to a point of significant debilitation. Attempting to identify CSM patients would be a negligible exercise if a successful treatment option was not available. It is clear, however, that surgical decompression does produce favorable results ¹¹^–¹³ and should be used early in the disease course. Failing to aggressively treat this group of patients with operative intervention will result in clinical worsening, which at some point will become irreversible.

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 mm ² 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.²²^–²⁴ 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.^20,²⁶^–³⁰ The best results occur in those patients with either no signal changes or hyperintensity on T2-weighted MRI.²⁶^–³⁰ When T2 hyperintensity occurs at a single segment, this single finding does not portend a poor surgical outcome; these changes are reversible.²⁷^–³¹ When hyperintensity onT2-weighted imaging spans multiple levels or is coupled with T1-weighted hypointensity, however, the surgical prognosis is significantly less favorable.²⁷^–³¹ 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 mm ² 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.³³^–³⁵ 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.³⁸^–⁴⁰ 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 In comparison, a positive Hoffman sign exists as a normal variant in only 12% of the population. It is possible, therefore, to develop a correlation between physical findings, symptomatology, and radiologic abnormalities.

In view of the fact that the predominant symptoms in CSM involve gait stability and manual dexterity, a focus recently has been placed on tests to quantify deficits in these areas. A 30-meter walking time test has been utilized to show gait deficits in patients with myelopathy.⁴⁴ Upper extremity and hand dysfunction has been characterized by a nine-hole-peg test as well as by a score calculated from a battery of tests aimed at evaluating manual dexterity.^45,⁴⁶ The findings of each of these tests have been shown to be sensitive for the detection of cervical myelopathy and correlate significantly with other measures of CSM, including mJOA and Nurick scores. Also, these tests can be used to evaluate the effects of therapy, as examination with each study showed improvement when patients responded favorably to intervention.

Patient Age

Younger patients will respond better to early surgery, whereas older patients probably should be treated in a more conservative fashion.

As with many other disease processes, age is an integral factor in determining response to therapy in patients with CSM. In general, younger patients fare better after surgical intervention in nearly all studies evaluating operative decompression in myelopathy.^12,^21,^23,^24,^30,³⁵ The age at which unfavorable surgical results become significantly more predominant varies widely, between 60 and 75 years.

Genetic Factors

Genetic analysis shows great promise in identifying both patients who will develop cervical myelopathy and those who will respond to surgery.

Recently, genetic factors related to progressive myelopathy have been examined. The apolipoprotein E gene polymorphism, which previously has been identified as involved in repair and plasticity processes after CNS lesions, may play a role in the pathology of CSM. Patients with spinal cord compression who are carriers of the ε4 allele are at four- to six-fold increased risk of developing cervical myelopathy.²¹ In a prospective analysis of patients with CSM treated with ventral decompression, occurrence of the ε4 allele was a significant independent predictor for no improvement after anterior cervical discectomy and fusion.⁴⁷ In the future, such genetic analysis may be of value in determining which patients are at greater risk for progressive cervical myelopathy and will therefore benefit most from surgery.

Threshold for Treatment

Although CMS rarely is completely cured, surgery has produced favorable outcomes in the course of the disease. Reviews of its effect have shown variable surgical results, with reports of improvement in 50% to 92% of patients.⁴⁸^–⁵⁴ We believe that there are thresholds that should prompt surgical intervention. In the setting of significant cervical stenosis, especially with spinal cord compression, use of some combination of the following factors as the threshold for surgery early in the course of CSM will provide a significant improvement in surgical prognosis:

• Spinal cord hyperintensity isolated to a single spinal segment on T2-weighted MRI only

• Minimal impairment on electrophysiologic studies, especially SEPs and MEPs

• An abnormal EMG or clinical radiculopathy

• Mild myelopathic symptoms (e.g., mJOA ≥12) of a short duration (<1 year)

• Younger age (<60 years)

Likewise, there are other findings in CSM that should prompt less aggressive surgical treatment, because the prognosis with any intervention is sufficiently poor to make intervention less useful. These include the following:

• Spinal cord hyperintensities on T1-weighted MRI or spanning multiple levels on T2-weighted MRI

• Significant impairment on electrophysiologic studies

• Significant myelopathic symptoms (e.g., mJOA <7) of an extended duration (>1–2 years)

• Older age (>75 years)

Overall Approach to Patients

Patients who present with either mild myelopathy or significant cervical stenosis undergo a thorough history and neurologic examination. As part of the history, both a physician-derived mJOA score and Nurick grade are calculated. Patients also receive a more quantitative assessment with 12-hole peg testing and a timed 25-foot walk. Counseling involves a discussion of the risk of neurologic deterioration based on their clinical presentation and imaging studies. The patient is offered electrodiagnostic testing to further refine a risk assessment. Finally, the patient is counseled that both surgical intervention and observation are reasonable treatment options. If the patient opts for surgical intervention, this is scheduled routinely. If the patient opts for observation, he or she is asked to return to the clinic in 6 months. A change in Nurick grade, a drop of 2 points or more in the physician-derived mJOA score, a significant change in a 12-hole peg test time, and/or a significant change in the timed 25-foot walk may prompt further discussion of surgery. We emphasize that surgery should be used early in the course of cervical myelopathy. In those patients who will both develop progressive CSM and respond favorably to surgical decompression using the factors detailed earlier, conservative, nonoperative therapy is a mistake and should not be used. Although not yet clearly defined in the myelopathic literature, there probably is a therapeutic window of opportunity that, when ignored, will result in a suboptimal clinical outcome.

Yoshimatsu et al. summarized our approach by indicating that for CSM patients, “to anticipate symptomatic relief by conservative [nonoperative] treatment, it should be carried out intensively in cases with a short disease duration.”⁴⁰ Such cases should be rigorously overseen with close neurologic follow-up. In the event of any clinical progression, further attempts at conservative therapy should be halted, and surgical intervention should be instituted. In cases where conservative treatment is most likely to fail, surgery should be considered as the first choice of therapy.

Key References

Bednarík J., Kadanka Z., Dusek L., et al. Presymptomatic spondylotic cervical myelopathy: an updated predictive model. Eur Spine J. 2008;17:421-431.

Kadanka Z., Bednarík J., Vohanka S., et al. Conservative treatment vs surgery in spondylotic cervical myelopathy: prospective randomized study. Eur Spine J. 2000;9:538-544.

Mastronardi L., Elsawaf A., Roperto R., et al. Prognostic relevance of the postoperative evolution of intramedullary spinal cord changes in signal intensity on magnetic resonance imaging after anterior decompression for cervical spondylotic myelopathy. J Neurosurg Spine. 2007;7:615-622.

Matz P., Anderson P., Holly L., et al. The natural history of cervical spondylotic myelopathy. J Neurosurg Spine. 2009;11:104-111.

Olindo S., Signate A., Richech A., et al. Quantitative assessment of hand disability by the Nine-Hole-Peg test (9-HPT) in cervical spondylotic myelopathy. J Neurol Neurosurg Psychiatry. 2008;79:965-967.

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Not to Decompress

Eloy Rusafa, Thomas E. Mroz

Cervical spondylosis is a relatively straightforward degenerative process involving: (1) degeneration of the disc interspace with dorsal anular bulging and/or disc herniation and, in advanced stages, osteophyte formation; (2) hypertrophy of the facet joints, resulting in dorsolateral impingement on the dural sac and nerve roots; (3) soft tissue and ligamentous hypertrophy, resulting in dorsal impingement on the dural sac; and, in some cases, (4) loss of lordosis or kyphosis. Cervical spondylosis is an anatomic and pathophysiologic process. It is not synonymous with neurologic symptoms; rather, it is a normal part of aging that often is asymptomatic. When long-tract neurologic symptoms accompany the well-described anatomic and pathologic changes, as outlined previously, the process is termed cervical spondylotic myelopathy (CSM). Unfortunately, CSM is the most common cause of spinal cord impairment worldwide, and data on management approaches and outcomes for this disease are relatively sparse.

Brain et al. defined the pathophysiology and etiology of this degenerative condition in relation to neurologic injury and degeneration ¹ in order to characterize the best treatment for these patients. Other authors also have reported on the natural history of cervical spondylosis.²^–⁵ Some authors observed that untreated patients do not necessarily develop progressive disability.^5,⁶ Others have reported that surgery-related benefits are not clear in long-term trials in patients with mild myelopathy, and that surgery has a role in the treatment of progressive myelopathy and for older myelopathic patients.^7,⁸ Further, functional ability and quality of life in patients with mild myelopathy have been reported to improve with conservative treatment algorithms.⁹

Clark and Robinson ⁴ evaluated 120 patients with CSM confirmed by myelography, operation, or autopsy (mean age, 53 years) to analyze how these patients evolve over time. Patients were stratified into three groups according to outcome patterns. Seventy-five percent of the patients had a stepwise worsening. In one third of study patients, the clinical conditions remained the same between periods of exacerbations that varied from a few weeks to several years, and two thirds of patients had a progressive impairment. Twenty percent of the studied patients had a slow, steady progression, and 5% experienced rapid onset of symptoms with a long period or periods of quiescence. However, these authors analyzed a very heterogeneous group, and of the 16 patients who underwent conservative treatment with a collar, 8 improved and 8 remained stable. The authors concluded that when subsequent progression of the disease occurred, it often was very slow. Using myelography, Roberts et al.¹⁰ evaluated 24 patients with CSM who were treated with bedrest and cervical collar immobilization. They were assessed with a four-tiered scale similar to the Nurick scale, and the authors concluded that 8 patients worsened over a period of months, 9 patients were unchanged, and 7 improved.

Several others have evaluated outcomes of patients with early myelopathy, providing a collection of data that validates nonoperative care for this spectrum of the disease. In 2002, Kadanka et al.¹¹ compared two groups of patients with an average age of 54 years with mild or moderate myelopathy, defined as mJOA score higher than 12 and correlative pathology on MRI. One group (33 patients) was treated surgically, whereas the other (35 patients) was treated conservatively, with NSAIDs, intermittent collar immobilization, and bedrest. At 6 and 36 months there was no difference between those two groups in functional outcome as assessed by the mJOA scale, but there was a small but significant difference in favor of the conservative group when they were assessed by timed 10-meter walk. At the 6-month follow-up, the conservative group walked 10 meters in 7.2 seconds, whereas the surgical group required 8.7 seconds (P = .02). At 12 months, the groups walked in 7.4 and 9.9 seconds (P = .03), respectively, and at the 24- and 36-month follow-up examinations, the times were 7.5 and 11.7 seconds (P = .003), and 7.5 and 9.4 seconds (P = .03), respectively. At 1- and 2-year follow-up, patients treated conservatively were significantly better compared with the surgically treated patients. However, those treated surgically felt better at 6 months postoperatively on a self-evaluation scale ranging from −3 (poor) to 3 (excellent). A conclusion from a review published in 2010 by the Cochrane Library¹² about Kadanka’s paper was that there is little or no difference in function and quality of life between those who were treated conservatively and those who were treated with surgery. Kadanka and colleagues concluded that finding the predictive factor to neurologic deterioration would be more important. The shortcomings of this study are well recognized. It involved a small number of patients, and while the patients were randomized, the surgical group presented with a low mJOA score and longer disease duration. However, this study provides very reasonable evidence in favor of nonsurgical management for mild and moderate forms of myelopathy, at least during the first 3 years of follow-up. It used validated functional outcomes scores and clearly demonstrates at least equivalent outcomes between surgical and nonsurgical treatment.

Other authors have provided evidence for nonsurgical treatment in patients with early myelopathy. Matsumoto and colleagues performed two studies with patients with mild and moderate myelopathy (JOA score >10). In a retrospective review ¹³ of 27 patients, 17 were treated conservatively with bracing and activity restriction for 6 months, whereas 10 underwent decompression because of worse neurologic status. Follow-up included JOA scores, patient satisfaction, and evaluation of MRI studies. The average follow-up was 3.9 years, and at the end of the observation period the final JOA score was 16.0 in the surgery group and 16.2 in the conservative group. Spontaneous regression of the disc herniation was reported in 10 of 17 patients (59%) treated nonoperatively. Based on the results of this review, the authors concluded that nonoperative treatment is an effective strategy for myelopathy caused by soft disc herniations. In 1998, Nakamura et al.¹⁴ retrospectively reviewed 64 patients with CSM treated conservatively with Crutchfield tongs, plaster casts, traction, and bracing. Of these, 55% improved in the upper extremities and 57% in lower extremities, and only 3% showed deterioration. The remaining patients were stable clinically. Follow-up was a minimum of 1 year, with an average of 6 years. Younger patients and patients with mild disability were more likely to improve when treated conservatively.

Predictive factors of treatment outcome for myelopathy include duration of symptoms, patient age, preoperative functional status, spinal alignment, severity of spinal cord compression (expressed by the ratio of the anterior-posterior diameter of the spinal canal to transverse diameter of the spinal cord at the level of the maximal compression), congenital diameter of the spinal canal (Pavlov’s index), number of stenotic levels, spinal cord signal change on MRI, method of decompression, and alterations in neurophysiologic function. Range of motion and sex were considered in the literature as predictive outcome factors, but in a heterogeneous population without truly objective outcome measures.^15,¹⁶ Those predictive factors can be helpful in making the decision about when to operate or not in patients with mild and moderate myelopathy.

Among the negative predictive factors, three pathologic studies indicated that progression appears to worsen with disease duration and AP compression. Demyelination of white matter, gray matter neuronal loss, and cavitation can occur.¹⁷^–¹⁹ Ogino et al.¹⁸ followed nine patients with an average duration of symptoms of 18.2 years. They found a correlation between the degree of compression and demyelination. When the compression was 40% to 44% of normal, there was mild demyelination with flattening of gray matter. At 22% to 39% of normal, diffuse demyelination and gray matter cavitation occurred, and at 12% to 19% of normal, gray matter necrosis with white matter gliosis was noted. Other authors have demonstrated that if the compression of the spinal canal is submaximal (<40 mm²), then surgery does not have a beneficial effect.^20,²¹ In 2005, Kadanka et al.²² evaluated predictive factors for a worse outcome in 66 myelopathic patients. They concluded that patients treated conservatively had a better prognosis if their spinal cord area at the level of compression was larger and if they had higher Pavlov index values (i.e., with a congenitally wider spinal canal). However, the same was not a predictive factor in the surgically treated group. The spinal cord transverse area was 66.8 (59.2; 74.4) mm², and the Pavlov index was 0.65 (0.58; 0.76) in patients who were nonresponders to conservative treatment, compared with 76.1 (70.7; 84.1) mm² and 0.92 (0.81; 1.02) in responders. In the surgery group these values were 75.2 and 70.9, respectively, with no differences in the Pavlov index.¹⁶ Therefore, a congenitally narrow canal was a common finding in myelopathic patients, appearing in 40% to 47% of study patients (much higher than in the general population), and it predisposed them to develop symptomatic spinal cord compression.^22,²³ Bednarík et al.²⁴ found no correlation between severity of compression rates and development of CSM. The authors defined congenital stenosis as a Pavlov ratio lower than 0.8 and spondylotic compression as an AP:width ratio below 0.4.²⁴

Electrophysiologic abnormalities have been associated with myelopathy. Bednarík et al.²⁴ evaluated short-latency somatosensory-evoked potentials (SEPs) from the median and tibial nerves, and motor-evoked potentials (MEPs) with transcranial and root magnetic stimulation and muscular activity with EMG in 66 patients with asymptomatic cervical stenosis confirmed by MRI. These patients were evaluated every 6 months, with a minimum follow-up period of 24 months (median, 4 years; range, 2–8 years). The authors reported that patients with radiculopathy and with abnormalities in EMG and SEPs more often developed CSM, as defined by clinical examination and loss of 1 point on the mJOA scale. Clinical radiculopathy was present in 92% of the patients who developed myelopathy and in 24% of those who did not (P < .0001). SEPs were altered in 38.5% of patients with CSM and 9.4% of the patients without the disease (P < .02). EMG revealed abnormalities in 61% of patients who developed CSM and 11.3% of those who did not (P < .01).^22,²⁴ Similarly, in the series by Kadanka et al.,²² none of the 15 patients without abnormalities on EMG developed CSM, whereas one third of the patients with abnormalities did develop CSM.²² Therefore, alterations in EMG, SEPs, and clinical radiculopathy can predict development of CSM in asymptomatic cervical stenosis. On the other hand, those with normal values of central motor conduction time to upper extremities were better responders to conservative treatment.¹⁶

The clinical significance of MRI abnormalities (i.e., cord signal changes) is controversial. MRI is excellent in defining pathoanatomy, but it is difficult to infer the degree of spinal cord dysfunction from MRI images. Increased signal intensity (ISI) on T2-weighted MR probably indicates edema, inflammation, vascular ischemia, gliosis, or myelomalacia,²⁵ each of which represents a different pathologic stage of CSM, therefore making it difficult to differentiate between reversible and irreversible lesions. The correlation between ISI on T2-weighted MRI and the severity of myelopathy is less significant, because ISI probably indicates a lesion of the gray matter, affecting predominantly the upper extremities. However, low intensity on T1-weighted images has been attributed to late stages of myelomalacia,²⁵ cystic necrosis, or secondary syrinx,^26,²⁷ and, therefore, has not been associated with mild myelopathy. Corroborating such assertions, Bednarík et al.¹⁶ did not find an ISI in T2-weighted MRI to be a predictive factor for development of myelopathy in asymptomatic patients. In their second work, Matsumoto et al.²⁸ evaluated 52 patients with mild and moderate myelopathy and tried to find a correlation between clinical worsening and ISI in the cervical spinal cord on T2-weighted MRI. Fifty-two patients were treated with cervical immobilization 8 hours a day for 3 months, and 34 of the 52 patients had a focal or segmental ISI. They found good results, considered as JOA >15 or improved function, in 63% of the patients with focal ISI, 70% with multisegmental ISI, and 78% without ISI. They concluded that this alteration on MRI does not play a role in the outcome of myelopathic patients treated conservatively. Morio et al.²⁹ and Kadanka et al.¹⁶ came to the same conclusion in their respective studies. Conversely, other authors have found a correlation between the outcome of surgical or conservative treatment and ISI on T2-weighted images.^25,^26,^30,³¹ Because the literature lacks consistency, it is difficult to make definitive conclusions about the clinical significance of cord signal changes and their predictive impact on surgical or nonsurgical outcomes.

Another controversial aspect of myelopathy is the number of involved stenotic cervical levels. The number of compressed levels was demonstrated to predict the severity of deterioration functionally, electrophysiologically, and histologically, as postulated by Shinomiya et al.³² However, Kadanka et al.¹⁶ found no correlation between multilevel or single-level compression and change in prognosis.

Age has been postulated by some to be an important prognostic factor. Nurick et al.⁶ noticed that patients younger than 60 years of age had a better prognosis, and other authors have come to the same conclusion.^21,³³ Conversely, however, Irvine and Strachan³⁴ found no correlation between age and prognosis for myelopathic patients, and Kadanka et al.¹⁶ had better results with older patients when they were treated conservatively. Thus, the relationship between age and outcome is controversial.

After a careful consideration of the literature, several predictive factors have been defined that can be used to predict positive outcomes following nonoperative care for myelopathy (Table 214-1). These include normal electrophysiologic conduction, absence of radiculopathy, higher Pavlov index, higher spinal cord area at the level of compression, higher mJOA scores, and shorter time in 10-meter walk.

TABLE 214-1 Predictive Factor of Conservative Treatment Outcome in Patients with Cervical Spondylotic Myelopathy

Positive Predictors	Negative Predictors	Not Defined as Predictors
Normal eletrophysiologic conduction	Alterations in electrophysiologic studies	Increased signal intensity on T2-weighted MRI
Absence of radiculopathy	Radiculopathy	Number of levels of compression
Higher Pavlov index	Lower Pavlov index	Range of motion
Higher spinal cord area at the level of compression	Higher compression rates and lower transverse area of spinal cord	Sex
Higher mJOA score	Lower mJOA score	Age
Slightly shorter time in 10-m walk	Slightly longer time in 10-m walk	—