Elena Montes1, Jesús Burgos2, Carlos Barrios3, Gema de Blas1, Eduardo Hevia4, Jerónimo Forteza5. 1. Department of Clinical Neurophysiology, Hospital Ramón y Cajal, Madrid, Spain. 2. Division of Pediatric Orthopedics, Hospital Ramón y Cajal, Madrid, Spain. 3. Institute for Research on Musculoskeletal Disorders, Valencia Catholic University, Quevedo 2, 46001, Valencia, Spain. carlos.barrios@ucv.es. 4. Spine Surgery Unit, Hospital La Fraternidad-Muprexpa, Madrid, Spain. 5. Instituto Valenciano de Patología, Valencia Catholic University, Valencia, Spain.
Abstract
PURPOSE: To evaluate the degree of acute or progressive lateral compression needed to cause neurologic injury to the spinal cord assessed by electrophysiological monitoring. METHODS: In five domestic pigs, the spinal cord was exposed and compressed between T8-T9 roots using a precise compression device. Two sticks placed on both sides of the spinal cord were sequentially brought together (0.5 mm every 2 min), causing progressive spinal cord compression. Acute compression was reproduced by a 2.5-mm displacement of the sticks. Cord-to-cord evoked potentials were obtained with two epidural catheters. RESULTS: Increasing latency and decreasing amplitude of the evoked potentials were observed after a mean progressive displacement of the sticks of 3.2 ± 0.9 mm, disappearing after a mean displacement of 4.6 ± 1.2 mm. The potential returned after compression removal (16.8 ± 3.2 min). The potentials disappeared immediately after an acute compression of 2.5 ± 0.3 mm, without any sign of recovering after 30 min. CONCLUSIONS: The experimental model replicates the mechanism of a spinal cord injury caused by medially displaced screws into the spinal canal. The spinal cord had more ability for adaptation to progressive and slow compression than to acute mechanisms.
PURPOSE: To evaluate the degree of acute or progressive lateral compression needed to cause neurologic injury to the spinal cord assessed by electrophysiological monitoring. METHODS: In five domestic pigs, the spinal cord was exposed and compressed between T8-T9 roots using a precise compression device. Two sticks placed on both sides of the spinal cord were sequentially brought together (0.5 mm every 2 min), causing progressive spinal cord compression. Acute compression was reproduced by a 2.5-mm displacement of the sticks. Cord-to-cord evoked potentials were obtained with two epidural catheters. RESULTS: Increasing latency and decreasing amplitude of the evoked potentials were observed after a mean progressive displacement of the sticks of 3.2 ± 0.9 mm, disappearing after a mean displacement of 4.6 ± 1.2 mm. The potential returned after compression removal (16.8 ± 3.2 min). The potentials disappeared immediately after an acute compression of 2.5 ± 0.3 mm, without any sign of recovering after 30 min. CONCLUSIONS: The experimental model replicates the mechanism of a spinal cord injury caused by medially displaced screws into the spinal canal. The spinal cord had more ability for adaptation to progressive and slow compression than to acute mechanisms.
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