Dorsal Spinal Cord Herniation Following Thoracic Laminectomy for Medulloblastoma Metastasis: A Case Report and Literature Review

Discussion

Postoperative dorsal spinal cord herniation is a rare iatrogenic complication, distinctly less common than the idiopathic ventral subtype. In contrast to ventral herniation—where the pathophysiology is often attributed to congenital dural defects or idiopathic dural thinning—dorsal herniation almost exclusively follows direct surgical manipulation, dural opening, or postoperative dural instability. In the postoperative context, the mechanism is believed to involve dural discontinuity, arachnoid violation, and subsequent cord displacement driven by CSF pulsation and tethering forces over time.

In the present case, several intraoperative and postoperative factors likely contributed to dorsal cord herniation. The patient underwent multilevel thoracic laminectomy and intradural tumor debulking for metastatic medulloblastoma. Due to the tumor’s adherence to the spinal cord, arachnoid, and vascular structures, complete separation was not feasible at any level. Upon dural opening, the tumor mass and dorsal cord immediately protruded beyond the midline dural margins. Because of the residual tumor burden and significant cord edema, primary dural closure was not achievable; therefore, an onlay dural graft was placed to prevent compression while avoiding excessive manipulation.

This surgical necessity, however, created a dural environment with inadequate posterior containment. In the postoperative period, persistent CSF pulsations, lack of posterior osseoligamentous support secondary to laminectomy, and progressive arachnoid scarring likely generated traction forces that gradually drew the cord dorsally. These findings support the increasingly recognized hypothesis that an unrepaired dural defect—even if covered with a patch graft—may predispose a patient to progressive dorsal cord displacement and herniation.

It is important to acknowledge that causality between the laminectomy and dorsal herniation in this case, while highly plausible, cannot be attributed to surgical factors alone. This patient harbored several additional variables that may have independently or synergistically contributed to the development of herniation. Extensive leptomeningeal metastatic disease creates abnormal CSF dynamics, increasing pulsatile pressure transmitted across dural defects and potentially accelerating cord displacement. Craniospinal irradiation, received in the months preceding laminectomy, is well recognized to induce dural fibrosis, microvascular compromise, and impaired tissue healing—factors that may have rendered the dura inherently fragile and less capable of forming an effective biological seal despite the onlay graft. Furthermore, direct tumor adherence to the cord and arachnoid at the time of surgery likely disrupted the normal meningeal barrier, contributing to subsequent scar formation and tethering. The interplay of these surgical, oncological, and radiation-related factors likely created a uniquely vulnerable dural environment in this patient—one that would not be encountered in the typical degenerative or traumatic surgical context. This multifactorial constellation should be recognized as a distinct and high-risk subset when counseling patients and planning surgical strategy in the setting of leptomeningeal malignancy.

Only a small number of similar postoperative cases have been described in the literature (Table). Historical reports by Cobb,2 Burres,3 and Mizuno4 primarily involved cervical decompression procedures, with most patients demonstrating neurological improvement after dural repair. Later publications documented dorsal cord herniation following Chiari decompression, pseudomeningocele formation, and tumor resections (Belen 20098 Moriyama 20139; Zakaria 201310;). More recent analysis by Nakashima et al15 further emphasized that delayed presentation is common, often occurring months to years after laminoplasty, particularly when dural defects are unrecognized or not adequately reconstructed.

Compared with the reported literature, our case is distinguished by 3 characteristics: this patient represents the youngest known individual to develop postoperative dorsal cord herniation; the precipitating pathology was metastatic medulloblastoma rather than degenerative or traumatic disease; and the dura was intentionally left open to accommodate swollen neural tissue, as opposed to an incidental or inadequately repaired dural tear.

MRI remains the gold-standard diagnostic modality, identifying dorsal cord displacement, absence of circumferential CSF, and focal tethering to the dural margins. Differentiation from arachnoid webs or dorsal arachnoid cysts is critical; in ambiguous cases, computed tomography myelography or cine-MRI may assist in delineating CSF dynamics and confirming communication with the subarachnoid space.

Management strategies reported across the literature are generally uniform and align with the approach utilized in this patient. Essential operative principles include complete exposure of the herniation site, microsurgical release of adhesions, restoration of cord mobility, and watertight dural reconstruction. Intraoperatively, decompression of the anterior arachnoid cyst permitted spontaneous and immediate cord realignment, which was radiographically confirmed postoperatively.

Prevention of postoperative dorsal spinal cord herniation hinges on meticulous dural management at the time of index surgery. Primary watertight dural closure remains the gold standard and should be attempted in all cases.14,15 When primary closure is not achievable—as in the present case due to cord edema and residual tumor burden—several adjunctive strategies should be considered. Dural substitutes such as collagen matrix or bovine pericardium allografts can be used as onlay patches, ideally secured with fibrin glue sealant to minimize CSF egress and create a more robust barrier against cord displacement.14,16 As demonstrated by the cases reported by Nakashima et al, even partial dural repair with fibrin glue alone may prove insufficient to prevent subsequent cord herniation, underscoring the importance of achieving the most robust closure possible.8 In oncologic cases where radiation-induced dural fragility is anticipated, the surgeon should plan for dural reconstruction from the outset rather than relying on tissue quality encountered intraoperatively. Postoperative positioning with the operative site elevated and avoidance of activities that increase intrathoracic pressure may also reduce early pulsatile forces on vulnerable dural repairs in the immediate postoperative period. Close surveillance with early postoperative MRI in high-risk patients—particularly those with leptomeningeal disease, prior irradiation, or documented dural compromise—allows prompt identification of early cord displacement before irreversible neurological injury supervenes.15

Although neurological recovery was limited in the immediate postoperative period, early recognition and surgical reduction likely prevented further neurological decline. Across published reports, patients who underwent timely repair demonstrated significantly better outcomes than those in whom diagnosis was delayed. Thus, this case reinforces the critical principle consistently highlighted in prior literature: early diagnosis, prompt operative correction, and restoration of dural integrity are key determinants of neurological recovery.