SPINAL NERVE ROOT COMPRESSION - NUTRITION AND FUNCTION OF THE PORCINE CAUDA-EQUINA COMPRESSED INVIVO

A model for experimental studies of acute, graded compression of the cauda equina in pigs was presented (Olmarker et al. 1991a). Detailed analyses of the neural and vascular anatomy demonstrated a close resemblance to the human cauda equina. There were structural and vascular differences between spinal nerve roots and peripheral nerves that could contribute to differences in compression susceptibility between these two parts of the nervous system. The pressure transmission from the balloon to the nerve roots showed to have a high accuracy. The occlusion-pressures for the arterioles, capillaries and venules of the cauda equina were determined (Olmarker et al. 1989a). Arteriolar blood flow was stopped at a pressure close to the mean arterial blood pressure. Capillary blood flow was found to be dependent upon flow in the connected venules. The blood flow in some venules was found to be stopped at 5-10 mm Hg. However, venular occlusion pressures ranged from 5 to 60 mm Hg. Compression up to 200 mm Hg for 2 hours did not induce a "no-reflow" phenomenon when the compression was ended. However, a transient hyperemia was noted at all pressure/time relations studied, indicating nutritional deficit in the compressed segment during compression. Signs of edema were seen in nerve roots exposed to compression for 2 hours at either 50 or 200 mm Hg. The nutritional supply to the cauda equina was found to be impaired at low pressure levels (less than 10 mm Hg; Olmarker et al. 1990a). Diffusion from adjacent tissues with a better nutritional supply, including the cerebrospinal fluid, could thus not compensate completely for compression-induced effects on the transport of nutrients. However, a certain nutritional supply to the compressed segment was present even at 200 mm Hg compression. There were more pronounced effects on the nutritional supply induced by a rapid (0.05-0.1 sec.) than a slow (20 sec.) compression onset rate. Nutritional impairment was noted both within and outside the compressed nerve segment. An increase in vascular permeability was induced by compression at 50 mm Hg for 2 minutes (Olmarker et al. 1989b). The magnitude of this permeability increase was dependant on both the magnitude and the duration of compression. The permeability increase was more pronounced for the rapid than for the slow compression onset rate at all pressure/time relations studied. Reduction of muscle action potential (MAP) amplitude in tail muscles, after stimulation cranial to the compression zone, was induced by compression at 100 and 200 mm Hg for 2 hours (Olmarker et al. 1990b). The reduction was more pronounced at 200 than 100 mm Hg. The recovery after compression was also slower at 200 than 100 mm Hg. Sham compression and compression at 50 mm Hg induce no or only minor reduction of MAP-amplitude. The reduction of MAP-amplitude was more pronounced for the rapid than for the slow compression onset rate, and was statistically significant at 100 and 200 mm Hg compression.