Objective: Much new research has emerged since 1982, when the original description of spinal cord injury without radiographic abnormality (SCIWORA) as a self-contained syndrome was reported. This article reviews new and old data on SCIWORA, from the past 2 decades.
Methods: This article reviews what we have learned since 1982 about the unique biomechanical properties of the juvenile spine, the mechanisms of injuries, the profound influence of age on injury pattern and outcome, the magnetic resonance imaging (MRI) features, and management algorithms of SCIWORA.
Results: The increasing use of MRI in SCIWORA has yielded ample evidence of damage in virtually all nonbony supporting tissues of the juvenile vertebral column, including rupture of the anterior and posterior longitudinal ligaments, intervertebral disc disruption, muscular and interspinal ligament tears, tectorial membrane rupture, and shearing of the subepiphyseal growth zone of the vertebral endplates. These findings provide the structural basis for the postulated "occult instability" in the spine of a patient after SCIWORA. MRI also demonstrated five classes of post-SCIWORA cord findings: complete transection, major hemorrhage, minor hemorrhage, edema only, and normal. These "neural" findings are highly predictive of outcome: patients with transection and major hemorrhage had profoundly poor outcome, but 40% with minor hemorrhage improved to mild grades, whereas 75% with "edema only" attained mild grades and 25% became normal. All patients with normal cord signals made complete recovery. The large pool of clinical data from our own and other centers also lends statistical power to uphold most of our original assertions regarding incidence, causes of injury, pathophysiology, age-related changes in the malleability of the spine, vectors of deformation, and the extreme vulnerability of young children to severe cord injury, particularly high cervical cord injury. Thoracic SCIWORA has been identified as an important subset, comprising three subtypes involving high-speed direct impact, distraction from lap belts, and crush injury by slow moving vehicles. Computation of the sensitivities of MRI and somatosensory evoked potentials in detecting SCIWORA shows that both tests were normal in 12 to 15% of children with definite, persistent myelopathy; all of these children were nevertheless braced for 3 months because of their clinical syndrome. Children with transient deficits but abnormal MRI and/or somatosensory evoked potentials were also braced, but the 60% with transient deficits and normal MRI and somatosensory evoked potentials were not braced. This is a change from our original policy in 1982 of bracing all children with persistent or transient deficits, brought on by our new MRI and electrophysiology data.
Conclusion: Injury prevention, prompt recognition, use of MRI and electrophysiological verification, and timely bracing of SCIWORA patients remain the chief measures to improve outcome.