Monitoring somatosensory evoked potentials in spinal cord ischemia-reperfusion injury

Abstract

It remains unclear whether spinal cord ischemia-reperfusion injury caused by ischemia and other non-mechanical factors can be monitored by somatosensory evoked potentials. Therefore, we monitored spinal cord ischemia-reperfusion injury in rabbits using somatosensory evoked potential detection technology. The results showed that the somatosensory evoked potential latency was significantly prolonged and the amplitude significantly reduced until it disappeared during the period of spinal cord ischemia. After reperfusion for 30-180 minutes, the amplitude and latency began to gradually recover; at 360 minutes of reperfusion, the latency showed no significant difference compared with the pre-ischemic value, while the somatosensory evoked potential amplitude in-creased, and severe hindlimb motor dysfunctions were detected. Experimental findings suggest that changes in somatosensory evoked potential latency can reflect the degree of spinal cord ischemic injury, while the amplitude variations are indicators of the late spinal cord reperfusion injury, which provide evidence for the assessment of limb motor function and avoid iatrogenic spinal cord injury.

Keywords: abdominal aorta occlusion model; grants-supported paper; histopathology; iatrogenic spinal cord injury; ischemia; latency; neural regeneration; neuroregeneration; reperfusion; somatosensory evoked potentials; spinal cord; spinal cord injury.

Figure 1

N-wave peak time (L1) of somatosensory evoked potential latency in rabbits with spinal cord ischemia-reperfusion injury. ^aP < 0.05, vs. normal state before occlusion. Data are expressed as mean ± SD, n = eight rabbits per time point of occlusion, one-way analysis of variance and least significant difference test. min: Minutes.

Figure 2

P-wave trough time (L2) of somatosensory evoked potential latency in rabbits with spinal cord ischemia-reperfusion injury. ^aP < 0.05, vs. normal state before occlusion. Data are expressed as mean ± SD, n = eight rabbits per time point of occlusion, one-way analysis of variance and least significant difference test. min: Minutes.

Figure 3

Spinal cord tissue at 360 minutes in rabbits with spinal cord ischemia-reperfusion injury (hematoxylin-eosin staining, optical microscopy, × 100). (A) In the normal control group, spinal nerve cells showed a complete structure. (B) At 40 minutes after abdominal aorta occlusion, the nuclei of spinal nerve cells had dissolved and disappeared. (C) At 360 minutes after reperfusion, spinal nerve cell edema was observed, nuclear boundaries were unclear, and some cells degenerated and became necrotic, with apparent hemorrhage loci.