JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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A model for acute, chronic, and delayed graded compression of the dog cauda equina. Presentation of the gross, microscopic, and vascular anatomy of the dog cauda equina and accuracy in pressure transmission of the compression model.

Spine 1995 December 16
STUDY DESIGN: A new model for controlled, graded compression of the dog cauda equina was developed using the dog lumbar spine. The model was defined regarding macroscopic, microscopic, and vascular anatomy and regarding accuracy in pressure transmission.

OBJECTIVES: The study was performed to develop a model for controlled, graded compression that would allow for acute, chronic, and delayed compression.

SUMMARY OF BACKGROUND DATA: There has been an increasing interest for the reactions of the spinal nerve roots to mechanical deformation. The previously used models have had limitations regarding the duration and the onset of the compression and possibilities for a controlled variation of the compression pressure on chronically compressed nerve roots.

METHODS: Macroscopic examination, light microscopy, and ink injection of the vasculature was used to assess the anatomic characteristics of the nerve tissue and the vasculature of the cauda equina in the dog lower lumbar spine. The relation between known pressures in the compression balloon used to compress the cauda equina and the pressure in the central thecal sac was assessed by measuring the pressure in an artificial thecal sac with a pressure transducer. RESULTS. The neural and vascular anatomy was found to have a close resemblance to the human cauda equina. The pressure in the thecal sac was within 5% of the pressure in the compression balloon at various pressures between 0-200 mm Hg.

CONCLUSION: The presented model provides a good pressure transmission to the dog cauda equina, which has an anatomy that closely resembles the human cauda equina. The model may be well suited for physiologic studies of cauda equina compression. A double-balloon system may provide unique opportunities to induce chronic compression and delayed compression, i.e., additional compression after a certain time of chronic compression to resemble the changes in pressure that are characteristic for neurogenic claudication.

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