Failure of motor evoked potentials to predict neurologic outcome in experimental thoracic aortic occlusion James R. Elmore, MD, Peter Gloviczki, MD,

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Presentation transcript:

Failure of motor evoked potentials to predict neurologic outcome in experimental thoracic aortic occlusion James R. Elmore, MD, Peter Gloviczki, MD, C.Michel Harper, MD, Peter C. Pairolero, MD, Michael J. Murray, MD, Russell G. Bourchier, MB, ChB, Thomas C. Bower, MD, Jasper R. Daube, MD Journal of Vascular Surgery Volume 14, Issue 2, Pages 131-139 (August 1991) DOI: 10.1067/mva.1991.29237 Copyright © 1991 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 1 Canine model used to evaluate MEP and SEP monitoring during thoracic aortic occlusion. Journal of Vascular Surgery 1991 14, 131-139DOI: (10.1067/mva.1991.29237) Copyright © 1991 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 2 Motor evoked potential and SEP sample recordings in a control animal without CSF drainage and resultant paraplegia. Note persistence of MEPs with loss of SEPs. Somatosensory evoked potentials return after reperfusion with prolonged latencies. Journal of Vascular Surgery 1991 14, 131-139DOI: (10.1067/mva.1991.29237) Copyright © 1991 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 3 Amplitude and latency of MEPs. Amplitude data expressed as a percentage of baseline (mean ± SEM). Latency data expressed as a prolongation over baseline in milliseconds (mean ± SEM). No significant difference between neurologically injured and normal dogs. Journal of Vascular Surgery 1991 14, 131-139DOI: (10.1067/mva.1991.29237) Copyright © 1991 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 4 Amplitude and latency of SEPs. Amplitude data expressed as a percentage of baseline (mean ± SEM). Latency data expressed as a prolongation over baseline in milliseconds (mean ± SEM). No significant difference between neurologically injured and normal dogs at 30 minutes of occlusion. Ninety-five percent of injured dogs lost SEPs by 60 minutes so no data analysis at that time interval. Note significant prolongation in latencies of SEPs during reperfusion. Journal of Vascular Surgery 1991 14, 131-139DOI: (10.1067/mva.1991.29237) Copyright © 1991 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 5 Spinal cord blood flow in low thoracic and lumbar gray matter. Data expressed as median blood flow in ml/100 gm/min. Significantly decreased flow in neurologically injured dogs during the cross-clamp time. Journal of Vascular Surgery 1991 14, 131-139DOI: (10.1067/mva.1991.29237) Copyright © 1991 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 6 Light micrograph of proximal lumbar spinal cord gray matter of paraplegic control animal. Histologically there is anterior horn cell degeneration with ischemia of surrounding neural tissue. The three anterior horn cells in the top right corner are normal, whereas the three anterior horn cells in the center exhibit features of ischemic necrosis. (Hematoxylin-eosin stain; original magnification ×400.) Journal of Vascular Surgery 1991 14, 131-139DOI: (10.1067/mva.1991.29237) Copyright © 1991 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions