Delayed-onset white cord syndrome after anterior and posterior cervical decompression surgery for symptomatic ossification of spinal ligaments: illustrative cases

Abstract

BACKGROUND White cord syndrome is an extremely rare complication of cervical decompressive surgery, characterized by serious postoperative neurological deficits in the absence of apparent surgical complications. It is named after the characteristic ischemic-edematous intramedullary T2-hyperintense signal on postoperative magnetic resonance imaging and is believed to be caused by ischemic-reperfusion injury. Neurological deficits typically manifest immediately after surgery, and delayed occurrence has been reported only once. OBSERVATIONS The authors presented two cases of delayed white cord syndrome after anterior and posterior cervical decompression surgery for symptomatic ossification of the posterior longitudinal ligament and ligamentum flavum, respectively. Neurological deficits manifested on postoperative day 2 (case 1) and day 8 (case 2). The patients’ conditions were managed with high-dose corticosteroids, mean arterial pressure augmentation, and early physical therapy, after which they showed partial neurological recovery at discharge, which improved further by the 3-month follow-up visit. LESSONS The authors’ aim was to raise awareness among spine surgeons about this rare but severe complication of cervical decompressive surgery and to emphasize the mainstays of treatment based on current best evidence: high-dose corticosteroids, mean arterial pressure augmentation, and early physical therapy.

Ischemia-Reperfusion Injury After Posterior Cervical Laminectomy

“…All patients in these case reports had varying degrees of paresis or plegia (hemiplegia to complete quadriplegia) postoperatively. Their deficits presented either immediately postoperatively or up to 24 hours later, except for the two patients described by Singh et al [5] (Table 1). The authors postulated that the delayed onset could have been due to the patients having a pre-existing diagnosis of hypertension leading to endothelial damage and a decrease in nitric oxide due to aging, which may have led to subacute reperfusion and therefore delayed onset [5].…”

“…Their deficits presented either immediately postoperatively or up to 24 hours later, except for the two patients described by Singh et al [5] (Table 1). The authors postulated that the delayed onset could have been due to the patients having a pre-existing diagnosis of hypertension leading to endothelial damage and a decrease in nitric oxide due to aging, which may have led to subacute reperfusion and therefore delayed onset [5]. All patients were treated with steroids and extensive inpatient rehabilitation.…”

“…Our case shares some common characteristics with those in the existing literature, described in Table 1. None of the 11 cases describe any mechanical compromise or compression to the spinal cord during the operation itself [2][3][4][5][6][7][8][9][10]. The common themes of myelomalacia evident on preoperative MRI and hyperintensity noted on postoperative MRI are seen in all cases.…”

“…Ten cases of ischemia-reperfusion injury have been described in the literature to date [2][3][4][5][6][7][8][9][10]. Of these, three cases involved anterior [2][3][4] cervical decompression and fusion, while seven cases involved a posterior [4][5][6][7][8][9][10] approach (Table 1). All patients in these case reports had varying degrees of paresis or plegia (hemiplegia to complete quadriplegia) postoperatively.…”

“…One rare and serious complication that can arise from surgery is ischemia-reperfusion injury. Described as "white cord syndrome" due to its appearance on T2-weighted MRI, this condition has been described previously in only 10 case reports [2][3][4][5][6][7][8][9][10]. While defined as a diagnosis of exclusion, this condition is hypothesized to be mediated by reactive oxygen species, proinflammatory mediators such as cytokines and chemokines, and signaling cascades involving nitric oxide and complement following the hyperemia caused by the restoration of blood flow to a chronically ischemic spinal cord [11][12][13].…”