The effects of spinal cord injury induced by shortening on motor evoked potentials and spinal cord blood flow

An experimental study in swine

Hitesh N. Modi, Seung-Woo Suh, Jae-Young Hong, Jae Hyuk Yang

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background: Spinal cord injury due to spinal shortening is disastrous, but the amount that the spine can be shortened without injury is unknown. We assessed spinal cord injury and changes in spinal cord blood flow after spinal shortening in swine. Methods: Ten pigs underwent pedicle screw instrumentation between T10 and T13 followed by a T11 and T12 vertebrectomy resulting in spinal shortening. Spinal cord function and spinal cord blood flow were monitored simultaneously with use of transcranial motor evoked potentials and laser Doppler flowmetry, respectively. A staged shortening procedure was performed: phase 1 resulted in no morphological change in the spinal cord, phase 2 resulted in buckling of the spinal cord, and phase 3 resulted in kinking of the spinal cord. After loss of motor evoked potential signals, which was considered to indicate spinal cord injury, the spinal instrumentation was tightened. The motor evoked potentials and spinal cord blood flow were monitored for an additional thirty minutes, and a wake-up test was then performed. Finally, a spinal cord specimen was obtained and evaluated histologically. Results: The motor evoked potential data demonstrated no evidence of spinal cord injury during phases 1 and 2. However, the signals were lost during phase 3, indicating spinal cord injury. The mean shortening was 35 ± 2.7 mm, which was similar to the mean vertebral body height at the thoracolumbar level (33.6 ± 1.9 mm), indicating that spinal cord injury resulted from shortening equivalent to the height of one vertebra. Spinal shortening did not cause injury if the amount of shortening was less than the mean segmental height of the entire spinal column (27.7 ± 1.6 mm for T1-L6). The spinal cord blood flow increased slightly (by 11.6% ± 20.6%) during phase 2, but decreased by 43.1% ± 11.4% during phase 3. The wake-up test performed after thirty minutes revealed no movement in the lower limbs. Conclusions: Spinal shortening of ≥104.2% of one vertebral body height at the thoracolumbar level caused spinal cord injury, but shortening of ≤73.8% did not result in injury. Clinical Relevance: This study provides guidelines for the mean amount of spinal shortening that will result in spinal cord injury in swine.

Original languageEnglish
Pages (from-to)1781-1789
Number of pages9
JournalJournal of Bone and Joint Surgery - Series A
Volume93
Issue number19
DOIs
Publication statusPublished - 2011 Oct 5

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Motor Evoked Potentials
Fetal Blood
Spinal Cord Injuries
Spinal Cord
Swine
Spine
Body Height
Wounds and Injuries
Laser-Doppler Flowmetry
Lower Extremity
Guidelines

ASJC Scopus subject areas

  • Surgery
  • Orthopedics and Sports Medicine

Cite this

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title = "The effects of spinal cord injury induced by shortening on motor evoked potentials and spinal cord blood flow: An experimental study in swine",
abstract = "Background: Spinal cord injury due to spinal shortening is disastrous, but the amount that the spine can be shortened without injury is unknown. We assessed spinal cord injury and changes in spinal cord blood flow after spinal shortening in swine. Methods: Ten pigs underwent pedicle screw instrumentation between T10 and T13 followed by a T11 and T12 vertebrectomy resulting in spinal shortening. Spinal cord function and spinal cord blood flow were monitored simultaneously with use of transcranial motor evoked potentials and laser Doppler flowmetry, respectively. A staged shortening procedure was performed: phase 1 resulted in no morphological change in the spinal cord, phase 2 resulted in buckling of the spinal cord, and phase 3 resulted in kinking of the spinal cord. After loss of motor evoked potential signals, which was considered to indicate spinal cord injury, the spinal instrumentation was tightened. The motor evoked potentials and spinal cord blood flow were monitored for an additional thirty minutes, and a wake-up test was then performed. Finally, a spinal cord specimen was obtained and evaluated histologically. Results: The motor evoked potential data demonstrated no evidence of spinal cord injury during phases 1 and 2. However, the signals were lost during phase 3, indicating spinal cord injury. The mean shortening was 35 ± 2.7 mm, which was similar to the mean vertebral body height at the thoracolumbar level (33.6 ± 1.9 mm), indicating that spinal cord injury resulted from shortening equivalent to the height of one vertebra. Spinal shortening did not cause injury if the amount of shortening was less than the mean segmental height of the entire spinal column (27.7 ± 1.6 mm for T1-L6). The spinal cord blood flow increased slightly (by 11.6{\%} ± 20.6{\%}) during phase 2, but decreased by 43.1{\%} ± 11.4{\%} during phase 3. The wake-up test performed after thirty minutes revealed no movement in the lower limbs. Conclusions: Spinal shortening of ≥104.2{\%} of one vertebral body height at the thoracolumbar level caused spinal cord injury, but shortening of ≤73.8{\%} did not result in injury. Clinical Relevance: This study provides guidelines for the mean amount of spinal shortening that will result in spinal cord injury in swine.",
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N2 - Background: Spinal cord injury due to spinal shortening is disastrous, but the amount that the spine can be shortened without injury is unknown. We assessed spinal cord injury and changes in spinal cord blood flow after spinal shortening in swine. Methods: Ten pigs underwent pedicle screw instrumentation between T10 and T13 followed by a T11 and T12 vertebrectomy resulting in spinal shortening. Spinal cord function and spinal cord blood flow were monitored simultaneously with use of transcranial motor evoked potentials and laser Doppler flowmetry, respectively. A staged shortening procedure was performed: phase 1 resulted in no morphological change in the spinal cord, phase 2 resulted in buckling of the spinal cord, and phase 3 resulted in kinking of the spinal cord. After loss of motor evoked potential signals, which was considered to indicate spinal cord injury, the spinal instrumentation was tightened. The motor evoked potentials and spinal cord blood flow were monitored for an additional thirty minutes, and a wake-up test was then performed. Finally, a spinal cord specimen was obtained and evaluated histologically. Results: The motor evoked potential data demonstrated no evidence of spinal cord injury during phases 1 and 2. However, the signals were lost during phase 3, indicating spinal cord injury. The mean shortening was 35 ± 2.7 mm, which was similar to the mean vertebral body height at the thoracolumbar level (33.6 ± 1.9 mm), indicating that spinal cord injury resulted from shortening equivalent to the height of one vertebra. Spinal shortening did not cause injury if the amount of shortening was less than the mean segmental height of the entire spinal column (27.7 ± 1.6 mm for T1-L6). The spinal cord blood flow increased slightly (by 11.6% ± 20.6%) during phase 2, but decreased by 43.1% ± 11.4% during phase 3. The wake-up test performed after thirty minutes revealed no movement in the lower limbs. Conclusions: Spinal shortening of ≥104.2% of one vertebral body height at the thoracolumbar level caused spinal cord injury, but shortening of ≤73.8% did not result in injury. Clinical Relevance: This study provides guidelines for the mean amount of spinal shortening that will result in spinal cord injury in swine.

AB - Background: Spinal cord injury due to spinal shortening is disastrous, but the amount that the spine can be shortened without injury is unknown. We assessed spinal cord injury and changes in spinal cord blood flow after spinal shortening in swine. Methods: Ten pigs underwent pedicle screw instrumentation between T10 and T13 followed by a T11 and T12 vertebrectomy resulting in spinal shortening. Spinal cord function and spinal cord blood flow were monitored simultaneously with use of transcranial motor evoked potentials and laser Doppler flowmetry, respectively. A staged shortening procedure was performed: phase 1 resulted in no morphological change in the spinal cord, phase 2 resulted in buckling of the spinal cord, and phase 3 resulted in kinking of the spinal cord. After loss of motor evoked potential signals, which was considered to indicate spinal cord injury, the spinal instrumentation was tightened. The motor evoked potentials and spinal cord blood flow were monitored for an additional thirty minutes, and a wake-up test was then performed. Finally, a spinal cord specimen was obtained and evaluated histologically. Results: The motor evoked potential data demonstrated no evidence of spinal cord injury during phases 1 and 2. However, the signals were lost during phase 3, indicating spinal cord injury. The mean shortening was 35 ± 2.7 mm, which was similar to the mean vertebral body height at the thoracolumbar level (33.6 ± 1.9 mm), indicating that spinal cord injury resulted from shortening equivalent to the height of one vertebra. Spinal shortening did not cause injury if the amount of shortening was less than the mean segmental height of the entire spinal column (27.7 ± 1.6 mm for T1-L6). The spinal cord blood flow increased slightly (by 11.6% ± 20.6%) during phase 2, but decreased by 43.1% ± 11.4% during phase 3. The wake-up test performed after thirty minutes revealed no movement in the lower limbs. Conclusions: Spinal shortening of ≥104.2% of one vertebral body height at the thoracolumbar level caused spinal cord injury, but shortening of ≤73.8% did not result in injury. Clinical Relevance: This study provides guidelines for the mean amount of spinal shortening that will result in spinal cord injury in swine.

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