Perfusion-limited recovery of evoked potential function after spinal cord injury

• Published in: Spine (Philadelphia, Pa. 1976) Pa. 1976), 2000-05, Vol.25 (10), p.1218-1226
• Main Authors: Carlson, G D, Gorden, C D, Nakazowa, S, Wada, E, Warden, K, LaManna, J C
• Format: Article
• Language: English
• Subjects: Animals; Blood Pressure; Decompression, Surgical; Disease Models, Animal; Dogs; Evoked Potentials, Somatosensory - physiology; Monitoring, Physiologic; Regional Blood Flow; Reperfusion Injury - physiopathology; Space life sciences; Spinal Cord - blood supply; Spinal Cord - physiopathology; Spinal Cord Compression - physiopathology; Spinal Cord Compression - surgery; Weight-Bearing
• ISSN: 0362-2436
• DOI: 10.1097/00007632-200005150-00004

The current study was designed to determine whether progressive spinal cord damage during residual compression is caused by low blood flow and ischemia. The purpose of this experiment was to determine the effects of sustained spinal cord compression on regional blood flow and evoked potential recovery after time-dependent decompression. Spinal cord injury after trauma is commonly associated with residual cord compression. Although decreased blood flow has been reported after spinal cord contusion, the effect of residual spinal cord displacement on reperfusion of blood flow or recovery of neurologic function remains unclear. Eighteen beagles were anesthetized, and the spinal cord at T13 was loaded dorsally under precision loading conditions until evoked potential amplitudes were reduced by 50%. At this function endpoint, spinal cord displacement was maintained for 90 minutes. Somatosensory-evoked potentials were measured at regular intervals until 3 hours after decompression. Regional spinal cord blood flow was measured with a fluorescent microsphere technique at regular time points during and after spinal cord decompression. Within 5 minutes after dynamic cord compression was discontinued, evoked potential signals were absent in all dogs. Evoked potential recovery was observed after decompression in 7 of 18 dogs. Regional spinal cord blood flow at baseline, 21.8 +/- 1.9 mL/100 g. min (mean +/- SE), decreased to 3.9 +/- 0.9 mL/100 g. min after dynamic compression was discontinued. Although spinal cord-piston interface pressure dissipated by 87% of maximum interface pressure during sustained compression, mean blood flow recovered to only 34% of baseline flow. In the 7 dogs that recovered evoked potential function, blood flow increased to 11.3 +/- 2.7 mL/100g. min immediately before decompression (P < or = 0.05). In the 11 dogs that did not recover evoked potential function after decompression, regional blood flow did not improve during sustained compression. Recovery of evoked potential function after decompression corresponded with a greater return of blood flow during sustained displacement and greater reperfusion of blood flow associated with decompression.