Early time-dependent decompression for spinal cord injury: vascular mechanisms of recovery.

Although surgical decompression is often advocated for acute spinal cord injury, the timing and efficacy of early treatment have not been clinically proven. Our objectives were to determine the importance of early spinal cord decompression on recovery of evoked potential conduction under precision loading conditions and to determine if regional vascular mechanisms could be linked to electrophysiologic recovery. Twenty-one mature beagles were anesthetized and mechanically ventilated to maintain normal respiratory and acid-base balance. Somatosensory-evoked potentials from the upper and lower extremities were measured at regular intervals. The spinal cord at T-13 was loaded dorsally under precision loading conditions until evoked potential amplitudes had been reduced by 50%. At this functional endpoint, spinal cord displacement was maintained for either 30 (n = 7), 60 (n = 8), or 180 min (n = 6). Spinal cord decompression was followed by a 3-h monitoring period. Regional spinal cord blood flow was measured with fluorescent microspheres at baseline (following laminectomy) immediately after stopping dynamic cord compression, 5, 15, and 180 min after decompression. Within 5 min after stopping dynamic compression, evoked potential signals were absent in all dogs. We observed somatosensory-evoked potential recovery in 6 of 7 dogs in the 30-min compression group, 5 of 8 dogs in the 60-min compression group, and 0 of 6 dogs in the 180-min compression group. Recovery in the 30- and 60-min groups varied significantly from the 180-min group (p < 0.05). Regional spinal cord blood flow at baseline, 21.4+/-2.2 ml/100/g/min (combined group mean +/- SE) decreased to 4.1+/-0.7 ml/100 g/min after stopping dynamic compression. Reperfusion flows after decompression were inversely related to duration of compression. Of the 7 dogs in the 30 min compression group, 5 min after decompression the blood flow was 49.1+/-3.1 ml/100 g/min, which was greater than two times baseline. In the 180-min compression group early post-decompression blood flow, 19.8+/-6.2 ml/100 g/min, was not significantly different than baseline. Of the 8 dogs in the 60-min compression group, 5 who recovered evoked potential conduction revealed a lower spinal cord blood flow sampled immediately after stopping dynamic compression, 2.1+/-0.4 ml/100 g/min, compared to the 3 who did not recover where blood flow was 8.4+/-2.1 ml/100 g/min (p < 0.05). Reperfusion flows measured as the interval change in blood flow between the time dynamic compression was stopped to 5, 15, or 180 min after decompression, were significantly greater in those dogs that recovered evoked potential function (p < 0.05). Three hours after decompression, spinal cord blood flow in the 3 dogs in the 60-min compression group with no recovery, 11.1+/-2.1 ml/100 g/min, was significantly less than the spinal cord blood flow of the recovered group (n = 5), 20.5+/-2.2 ml/100 g/min. These data illustrate the importance of early time-dependent events following precision dynamic spinal cord loading and sustained compression conditions. Spinal cord decompression performed within 1 h of evoked potential loss resulted in significant electrophysiologic recovery after 3 h of monitoring. This study showed that the degree of early reperfusion hyperemia after decompression was inversely proportional to the duration of spinal cord compression and proportional to electrophysiologic recovery. Residual blood flow during the sustained compression period was significantly higher in those dogs that did not recover evoked potential function after decompression suggesting a reperfusion injury. These results indicate that, after precise dynamic spinal cord loading to a point of functional conduction deficit (50% decline in evoked potential amplitude), a critical time period exists where intervention in the form of early spinal cord decompression can lead to effective recovery of electrophysiologic function in the 1- to 3-h post-decompression p