Combined Spinal Cord Injury Research Articles

Risk factors for damage to the dura mater in thoracic and lumbar spine injury

Objective. To clarify a significance of the risk factors for damage to the dura mater (DM) in fractures of the thoracic and lumbar spine.Material and Methods. The study is based on the analysis of examination data and surgical treatment results of 350 patients with spinal cord injury (SCI). Fractures of the thoracic spine were observed in 124 patients, and those of the lumbar spine in 226. The study included 167 operated patients who underwent posterior decompression at the fracture level using laminectomy and transpedicular fixation of the injured spinal motion segment. There were two groups of patients: study group included 55 patients with DM rupture and control one – 112 patients without damage to the DM.Results. Damage to the DM was found in 32.9 % of patients, the rupture was localized on the posterior surface of the dural sac. In patients with rupture of the dura mater, ASIA type A and B neurological disorders were significantly more common (p = 0.00065). The DM damage occurs significantly more often in patients with type C fracture according to the AOSpine classification, with multilevel spinal injuries and combined SCI (Injury Severity Score more than 27.58 ± 9.46 points). The most significant risk factors for the development of DM ruptures are narrowing of the spinal canal at the fracture level by more than 50 %, a fracture of the vertebral arch, an increase in the relative interpedicular distance of more than 20 %, and diastasis between the fragments of the arches by more than 2.5 mm.Conclusion. The damage to the dura mater is a common complication of vertebral fracture. The prediction of dura mater rupture will allow optimizing surgical approach and improving the treatment outcome.

Mechanistic insights into posttraumatic syringomyelia based on a novel in vivo animal model

Although posttraumatic syringomyelia (PTS) develops in up to 30% of patients after spinal cord injury (SCI), the pathophysiology of this debilitating complication is incompletely understood. To provide greater insight into the mechanisms of this degenerative sequela of SCI, the authors developed and characterized a novel model of PTS. The spinal cords of 64 female Wistar rats were injured by 35-g modified aneurysm clip compression at the level of T6-7. Kaolin (5 microl of 500 mg/ml solution) was then injected into the subarachnoid space rostral to the site of the injury to induce inflammatory arachnoiditis in 22 rats. Control groups received SCI alone (in 21 rats), kaolin injection alone (in 15 rats), or laminectomy and durotomy alone without injury (sham surgery in 6 rats). The combination of SCI and subarachnoid kaolin injection resulted in a significantly greater syrinx formation and perilesional myelomalacia than SCI alone; SCI and kaolin injection significantly attenuated locomotor recovery and exacerbated neuropathic pain (mechanical allodynia) compared with SCI alone. We observed that combined SCI and kaolin injection significantly increased the number of terminal deoxytransferase-mediated deoxyuridine triphosphate nick-end labeled-positive cells at 7 days after injury (p<0.05 compared with SCI alone) and resulted in a significantly greater extent of astrogliosis and macrophage/microglial-associated inflammation at the lesion (p<0.05). The combination of compressive/contusive SCI with induced arachnoiditis results in severe PTS and perilesional myelomalacia, which is associated with enhanced inflammation, astrogliosis, and apoptotic cell death. The development of delayed neurobehavioral deficits and neuropathic pain in this model accurately reflects the key pathological and clinical conditions of PTS in humans.