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Journal Article
Research Support, Non-U.S. Gov't
A model for acute, chronic, and delayed graded compression of the dog cauda equina. Neurophysiologic and histologic changes induced by acute, graded compression.
Spine 1995 November 16
STUDY DESIGN: The results of acute compression on nerve function and morphology were analyzed in a recently developed model for graded cauda equina compression in the dog.
OBJECTIVES: The model was developed to better mimic the clinical situation of cauda equina compression in association with spinal canal stenosis.
SUMMARY OF BACKGROUND DATA: The compression of the cauda equina has been induced by metal clips, plastic bands, constrictors, and inflatable balloons. No model has used the intact spinal canal and induced compression by increasing the pressure per se in the canal.
METHODS: An inflatable balloon with a diameter exceeding the diameter of the spinal canal was placed under the lamina of the L7 vertebra in the dog. The balloon was inflated to various pressures, and muscle action potential area and nerve conduction velocity were monitored during 2 hours of compression and 1.5 hours of recovery. Nerve root specimens were processed for light microscopic examination.
RESULTS: There was a progressive reduction of muscle action potential area and nerve conduction velocity that was proportional to the applied pressure. Histologic evaluation revealed no nerve fiber damage but a slight intraneural edema after compression at 200 mg Hg.
CONCLUSIONS: The presented model may provide reproducible results regarding neurophysiologic and morphologic effects after acute, graded compression of the dog cauda equina. Two additional conclusions can be made from this study. First, the area measurement of the MAP is probably well suited for recordings and analyses of changes in muscle action potentials. Second, the specific onset rate of this study, in relation to previous studies, indicates that there is a threshold for the compression onset rate for inducing additional nerve injury located in the interval 0.1-0.8 seconds. The results from the present study provides important baseline data for the continued studies on chronic and intermittent compression with the compression model.
OBJECTIVES: The model was developed to better mimic the clinical situation of cauda equina compression in association with spinal canal stenosis.
SUMMARY OF BACKGROUND DATA: The compression of the cauda equina has been induced by metal clips, plastic bands, constrictors, and inflatable balloons. No model has used the intact spinal canal and induced compression by increasing the pressure per se in the canal.
METHODS: An inflatable balloon with a diameter exceeding the diameter of the spinal canal was placed under the lamina of the L7 vertebra in the dog. The balloon was inflated to various pressures, and muscle action potential area and nerve conduction velocity were monitored during 2 hours of compression and 1.5 hours of recovery. Nerve root specimens were processed for light microscopic examination.
RESULTS: There was a progressive reduction of muscle action potential area and nerve conduction velocity that was proportional to the applied pressure. Histologic evaluation revealed no nerve fiber damage but a slight intraneural edema after compression at 200 mg Hg.
CONCLUSIONS: The presented model may provide reproducible results regarding neurophysiologic and morphologic effects after acute, graded compression of the dog cauda equina. Two additional conclusions can be made from this study. First, the area measurement of the MAP is probably well suited for recordings and analyses of changes in muscle action potentials. Second, the specific onset rate of this study, in relation to previous studies, indicates that there is a threshold for the compression onset rate for inducing additional nerve injury located in the interval 0.1-0.8 seconds. The results from the present study provides important baseline data for the continued studies on chronic and intermittent compression with the compression model.
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