Journal of neurosurgery. Spine
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The proper prehospital and inpatient management of patients with unstable spinal injuries is critical for prevention of secondary neurological compromise. The authors sought to analyze the amount of motion generated in the unstable thoracolumbar spine during various maneuvers and transfers that a trauma patient would typically be subjected to prior to definitive fixation. ⋯ Although it is unknown how much motion in the unstable spine is necessary to cause secondary neurological injury, the accepted tenet is to minimize motion as much as possible. This study has demonstrated the angular motion incurred by the unstable thoracolumbar spine as experienced by the typical trauma patient from the field to positioning in the operating room using the best and most commonly used techniques. As previously reported, using the log-roll technique consistently results in unwanted motion at the injured spinal segment.
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Spinal dural arteriovenous fistulas (SDAVFs) cause myelopathy through arterialization of the perimedullary venous plexus and venous congestion of the spinal cord. The authors hypothesized that the craniocaudal extent of engorgement of intrathecal draining veins between the fistula site and the point of drainage out of the thecal sac correlates with the degree of myelopathy. ⋯ The craniocaudal extent of enlarged intrathecal veins draining SDAVF correlates with patient functional status, providing further insight into the pathophysiology of venous hypertensive myelopathy.
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Spinal dural arteriovenous fistulas (SDAVFs) consist of a shunt with converging feeding vessels arising from radiculomeningeal arteries and draining retrogradely via a radicular vein into the perimedullary veins, thereby causing progressive myelopathy due to venous hypertension in the spinal cord. The purpose of this study was to evaluate the hypothesis that the obstruction of radicular venous outlets could be an additional factor inducing symptomatic venous hypertension due to a decreased outflow in SDAVFs. ⋯ Obstruction of the radicular venous outflow could be an important factor in inducing spinal congestive edema due to venous hypertension, as well as subsequent clinical symptoms of SDAVFs.
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The authors describe a patient who presented with acute tetraparesis and a proposed acute traumatic spinal cord injury that was the result of nitrous oxide myelopathy. This 19-year-old man sustained a traumatic fall off a 6-ft high wall. His examination was consistent with a central cord syndrome with the addition of dorsal column impairment. ⋯ Nitrous oxide abuse is increasing in prevalence. Its toxic side effects can mask vitamin B12 and folate deficiency and central cord syndrome. The patient's history and radiographic presentation are key to establishing a diagnosis.
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Spinal cord injury (SCI) is a debilitating disease. Primary SCI results from direct injury to the spinal cord, whereas secondary injury is a side effect from subsequent edema and ischemia followed by activation of proinflammatory cytokines. These cytokines activate the prosurvival molecule nuclear factor-κB and generate obstacles in spinal cord reinnervation due to gliosis. Curcumin longa is an active compound found in turmeric, which acts as an antiinflammatory agent primarily by inhibiting nuclear factor-κB. Here, the authors study the effect of curcumin on SCI recovery. ⋯ Epidural administration of curcumin resulted in improved recovery from SCI. This occurred with no adverse effects noted in experimental animals. Therefore, curcumin treatment may translate into a novel therapy for humans with SCI.