EARLY TIME-DEPENDENT DECOMPRESSION FOR SPINAL-CORD INJURY - VASCULAR MECHANISMS OF RECOVERY

Although surgical decompression is often advocated for acute spinal co rd injury, the timing and efficacy of early treatment have not been cl inically proven. Our objectives were to determine the importance of ea rly spinal cord decompression on recovery of evoked potential conducti on under precision loading conditions and to determine if regional vas cular mechanisms could be linked to electrophysiologic recovery. Twent y-one mature beagles were anesthetized and mechanically ventilated to maintain normal respiratory and acid-base balance. Somatosensory-evoke d potentials from the upper and lower extremities were measured at reg ular intervals. The spinal cord at T-13 was loaded dorsally under prec ision loading conditions until evoked potential amplitudes had been re duced by 50%. At this functional endpoint, spinal cord displacement wa s maintained for either 30 (n = 7), 60 (n = 8), or 180 min (n = 6). Sp inal cord decompression was followed by a 3-h monitoring period. Regio nal 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 mi n after stopping dynamic compression, evoked potential signals were ab sent 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 grou p. 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. Reperfusio n flows after decompression were inversely related to duration of comp ression. Of the 7 dogs in the 30 min compression group, 5 min after de compression the blood flow was 49.1 +/- 3.1 ml/100 g/min, which was gr eater 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 sign ificantly different than baseline. Of the 8 dogs in the 60-min compres sion group, 5 who recovered evoked potential conduction revealed a low er spinal cord blood flow sampled immediately after stopping dynamic c ompression, 2.1 +/- 0.4 ml/100 g/min,compared to the 3 who did not rec over where blood flow was 8.4 +/- 2.1 ml/100 g/min (p < 0.05), Reperfu sion flows measured as the interval change in blood flow between the t ime dynamic compression was stopped to 5, 15, or 180 min after decompr ession, were significantly greater in those dogs that recovered evoked potential function (p < 0.05), Three hours after decompression, spina l cord blood flow in the 3 dogs in the 60-min compression group with n o 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 m l/100 g/min. These data illustrate the importance of early time-depend ent events following precision dynamic spinal cord loading and sustain ed compression conditions, Spinal cord decompression performed within 1 h of evoked potential loss resulted in significant electrophysiologi c recovery after 3 h of monitoring, This study showed that the degree of early reperfusion hyperemia after decompression was inversely propo rtional 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 no t recover evoked potential function after decompression suggesting a r eperfusion injury, These results indicate that, after precise dynamic spinal cord loading to a point of functional conduction deficit (50% d ecline in evoked potential amplitude), a critical time period exists w here intervention in the form of early spinal cord decompression can l ead to effective recovery of electrophysiologic function in the 1- to 3-h post-decompression period.