In recent years, the optimal operative timing for a symptomatic SCM is still controversial. The decision to undertake surgical resection of any SCMs lesion should hinges on the underlying risk of neurological prognosis. Our study demonstrated that major predictors of outcome in patients with SCM have been identified as symptom duration, morphology of lesion, lesion size, Frankel grade and SAH at presentation. Clinician require an accurate and useful risk stratification system to advise patients and guide resection in this context.
Hemorrhage and SAH
SCM hemorrhage is frequently accompanied by neurological deficits. Some have argued that repeated hemorrhage is an absolute indication for surgery.25–27 However, they have all had at least one prior hemorrhage when they are initially recognized because it is hemoglobin that produce the features that permit their diagnosis via MRI and we have very little information on the future risk of hemorrhage in patients with a previously recognized SCM with a new hemorrhage. Increase in hemosiderin deposition around the lesion typically represents the hemorrhage transitioning from an acute to chronic phase, and the extent of hemosiderin deposition is related to the number of hemorrhage. Thus, we attempted to explore the relationship between the extent of hemosiderin deposition and prognosis, but unfortunately, our study showed it was not associated with an unfavorable outcome in patients with surgical resection of lesion. At the technical level, the general view is that if SCM with signs of acute hemorrhage on MRI, the microsurgical removal should be delayed for 2–6 weeks after neurological decline to allow for a gliotic plane to develop around the lesion, thereby facilitating safe removal.28 29 Because of edema and spinal cord vulnerability due to hemorrhage may lead to postoperative neurological deterioration, immediate operation of these lesions could be harmful for an already stressed spinal cord.
SAH was strongly associated with worse outcome.30 Presence of preoperative pain symptoms was suggested to be predictive of poor postoperative neurological recovery.22 SAH is a special manifestation of SCM hemorrhage. It is caused by the hemorrhage of SCM breaking into the central canal or subarachnoid space. At this time, the hemodynamics of SCM will be unstable, sometimes radiating, back or neck pain, followed by signs and symptoms of rapidly evolving nerve root or spinal cord compression. Based on the results of our data analysis, SAH was observed in 61 of 268 lesions (22.8%), most cases present with continually or stepwise progressive neurological deficits (32.8%). The risk of worse outcome in surgically treated patients with SAH was 7.56 times greater than that of patients without SAH. Consistent with our previous research conclusions, 30 this study once again shows that the presence of SAH is one of the key risk factors for worse outcome. Accordingly, prompt surgical removal of the SCM with SAH provides an excellent outcome.
Symptom duration and Clinical symptoms
Nonhemorrhagic causes of neurological deterioration were most likely caused by mass effect secondary to gliosis or minor bleeding episodes that gradually increased the size of the lesion. At present, it is generally accepted that patients has recurrent or progressive neurological deficits should be recommended for resection, and observation is more selected for patients with mildly symptomatic SCM.8 16 21 31 However, there is no consensus on the concept of "a limited neurological deficit or mildly symptomatic patient", which is mostly personal experience. In our study, combining symptom duration and Frankel grade allows stratification of unfavorable outcome risk in SCMs. According to the postoperative outcome, our data indicate that the negative impact of symptom duration on surgical prognosis increased significantly after 26 months. Of the patients with symptoms duration 26 months or longer, 27.3% achieved unfavorable outcome, compared with 12.2% of patients shorter than 26 months. Similarly, according to the reported review, 12 17 18 the mean preoperative symptom duration of fewer than 29 months, only 6–11% of patients were reported with deteriorated condition. This indicates that the time window of surgical intervention for patients with symptomatic SCM can be extended to 26 months. Furthermore, unlike previously reported predictors of neurological outcomes after SCM surgery, 8 32 our study demonstrated that the prognosis of patients was not related to the clinical course. There was no difference in final neurologic outcomes between patients with acute or more chronic clinical presentations of patients. On the other hand, patients with Frankel C and lower preoperatively mainly achieved an unfavorable outcome after surgery. It was dichotomized into mildly (grade D and E) and severe (grade A, B or C) symptoms as this provided a clinical distinction between patients who were independent in their activities of daily living versus those who were not. This finding is also consistent with some series reported that greater severity of preoperative neurological impairment to be associated with unfavorable outcome.31 This observation clearly shows that recovery does not mainly depend on a critical timeframe between onset of symptoms and surgical removal, but more on the extent of neurologic symptoms at onset. Therefore, based on the above conclusions, we believe that the "a limited neurological deficit or mildly symptomatic patient" of SCM can be defined as neurological function above grade C and lasting within 26 months.
Size and Morphology
Lesion size as the main indication for surgical intervention remains a significant risk factor for unfavorable outcome. However, the risk of adverse surgical outcome did not increase with the lesion enlarging, this was most prominent in lesions ≤ 5 mm in size, and in complete intramedullary lesions. The correlation between lesion size ≤ 5 mm in greatest dimension and unfavorable outcome compared with preoperative clinical status showed a statistical significance. This finding is not, however, congruent with other studies showing a no correlation of outcome with preoperative lesion size.33 34 In contrast, the risk of unfavorable outcome of resection of lesion size ≤ 5 mm was 4.4 times higher than that of lesion size ≥ 10 mm. Furthermore, it is likely that complete intramedullary lesions are considerably more surgical risks than exophytically growth lesions of a similar size. We regard the surgical exploration may easily aggravate deficiencies due to a lesion, consequently, encroachment of the lesion more anteriorly toward the motor tracts, removal of a small lesion completely located in the spinal cord, would be associated with very high surgical morbidity, as opposed to a lesser degree of parenchymal manipulation required for resection of larger lesions rising to the pial surface.
Limitations
This study has some limitations that shall be noticed. First, it is a prospective observational cohort, as with any cohort study, residual confounding due to unmeasured or unknown factors cannot be ruled out. Second, the question of how SCMs develop and progress is still not well understood. Long term conservative treatment is still an effective method to understand the natural history of SCMs. However, due to the existence of the concept of preventive surgery, there are few cases of conservative treatment of SCMs. By clarifying the factors of surgical prognosis, this study can evaluate the timing of surgery, so as to provide basis for conservative treatment.