2000SpineRequires access

Perfusion-Limited Recovery of Evoked Potential Function After Spinal Cord Injury

Gregory D. Carlson, Carey Gorden, Shigenobu Nakazowa, Eiji Wada, KAREN E. WARDEN, Joseph C. LaManna

Open publisher page 27 citations

Abstract

STUDY DESIGN: The current study was designed to determine whether progressive spinal cord damage during residual compression is caused by low blood flow and ischemia. OBJECTIVES: 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. SUMMARY OF BACKGROUND DATA: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

About this research paper

What this paper is about

STUDY DESIGN: The current study was designed to determine whether progressive spinal cord damage during residual compression is caused by low blood flow and ischemia. OBJECTIVES: 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. SUMMARY OF BACKGROUND DATA: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Why it matters

OpenAlex reports 27 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

STUDY DESIGN: The current study was designed to determine whether progressive spinal cord damage during residual compression is caused by low blood flow and ischemia. OBJECTIVES: 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. SUMMARY OF BACKGROUND DATA: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Key concepts: Medicine, Spinal cord, Anesthesia, Spinal cord injury, Cord, Blood flow, Decompression, Spinal cord compression

Related papers

Back to paper searchBrowse research topicsOriginal source
Perfusion-Limited Recovery of Evoked Potential Function After Spinal Cord Injury — Research Paper | ScholarLens