Usefulness of full spine computed tomography in cases of high-energy trauma: a prospective study.

INTRODUCTION: At this hospital, computed tomography (CT) of the full spine is performed on all patients who have sustained high-energy trauma because spinal fractures can be overlooked by referring only to clinical findings and plain X-rays of the spine. The goal of this study is to prospectively detect the occurrence of spinal fractures in cases of high-energy trauma using full spine CT and to evaluate the usefulness of it. MATERIALS AND METHODS: Subjects were 179 patients (134 male, 45 female) who were deemed to have sustained high-energy trauma in the 21-month period starting in September 2007. Spinal fractures initially revealed by CT were studied in detail. RESULTS: Spinal fractures were found in 54 patients (30.2 %); 19 patients had stable fractures, and 41 had unstable fractures. Forty patients had concomitant injuries to organs in addition to spinal injury; these patients had an average Injury Severity Score of 20.2 (4-70). Of 16 patients with a cervical fracture, 6 (37.5 %) had a fracture that did not appear on plain X-rays of the cervical and that was first identified by CT. Of 43 patients with a thoracolumbar fracture, 6 (14.0 %) had a fracture that would have been difficult to detect if a full spine CT had not been done. CONCLUSION: In patients who have sustained high-energy trauma, spinal fractures may be overlooked during primary care by a diagnosis based only on plain X-rays and clinical manifestations. Therefore, patients who have sustained high-energy trauma should be evaluated with full spine CT during primary care.

Hypothermia suppresses excitatory synaptic transmission and neuronal death induced by experimental ischemia in spinal ventral horn neurons.

STUDY DESIGN: Whole-cell patch-clamp recordings were performed from the ventral horn neurons obtained from the rat spinal cord slices. OBJECTIVE: This study investigated the effects of hypothermia on excitatory synaptic transmission and ischemia-induced neuronal death. SUMMARY OF BACKGROUND DATA: Hypothermia has long been recognized as a promising physical strategy against both ischemic and traumatic spinal cord injuries. However, the mechanism of hypothermia-mediated neuroprotective action in the spinal cord is still not fully understood at the single cell level. METHODS: Whole-cell patch-clamp recordings were performed from ventral horn neurons obtained from the spinal cord slices. Ischemia was simulated by superfusing an oxygen- and glucose-deprived medium [ischemia simulating medium (ISM)]. RESULTS: When the temperature of the superfusing artificial cerebrospinal fluid solution was changed from normothermia (36 degrees C) to hypothermia (32 degrees C, 28 degrees C, and 24 degrees C), the frequency of spontaneous excitatory postsynaptic currents was significantly decreased in a temperature-dependent manner. Surperfusing the ISM generated an agonal inward current which consisted of a slow and subsequent rapid inward current in all of the neurons tested. The latencies of the slow and rapid inward currents after the ISM exposures were significantly longer at hypothermia than at normothermia. Hypothermia decreased the slope of the ISM-induced slow inward current, although it did not affect the slope of the rapid inward current. Moreover, the glutamate receptor antagonists slightly prolonged the latencies of the slow and rapid inward currents that were induced by ISM and significantly decreased their slopes. CONCLUSION: These results suggest that hypothermia reduces the excitatory synaptic activities and ischemic neuronal death in the spinal ventral horn. This finding may help in achieving a better understanding of the mechanisms of hypothermia-mediated neuroprotection in the spinal cord.