Hyperextension cervical spine injuries and traumatic central cord syndrome

Abstract

Traumatic central cord syndrome (TCCS), regardless of its biomechanics, is the most frequently encountered incomplete spinal cord injury. Patients with TCCS present with disproportionate weakness of the upper extremities, and variable sensory loss and bladder dysfunction. Fractures and/or subluxations, forced hyperextension, and herniated nucleus pulposus are the main pathogenetic mechanisms of TCCS. Nearly 50% of patients with TCCS suffer from congenital or degenerative spinal stenosis and sustained their injuries during hyperextension as originally described by Schneider in 1954. Immunohistochemical and imaging studies indicate mild to moderate insult to axons and their ensheathing myelin in the lateral funiculi culminating in cytoskeletal injury and impaired conduction. More than one-half of these patients enjoy spontaneous recovery of motor weakness; however, as time goes on, lack of manual dexterity, neuropathic pain, spasticity, bladder dysfunction, and imbalance of gait render their activities of daily living nearly impossible. Based on the current level of evidence, there is no clear indication of the timing of decompression for relief of sustained spinal cord compression in hyperextension injuries. Future research, taking advantage of validated digital imaging data such as maximum canal compromise, maximum spinal cord compression, and lesion length on the CT and MR images, as well as more sensitive measures of bladder and hand function, spasticity, and neuropathic pain may help tailor surgery for a specific group of these patients.