Abstract
Neurophysiologic reactions of cauda equina nerve roots to intermittently applied compression were assessed for two different modes of compression using a porcine model. To assess the neurophysiologic reactions of cauda equina nerve roots to intermittently applied compression. A number of experimental studies have been presented recently regarding the reaction pattern of spinal nerve roots to compression. These studies have used a continuous pressure level. For studies of pathophysiologic mechanisms behind neurogenic claudication, however, it would be more relevant to study the effects of intermittently applied compression. The cauda equina was exposed and compression was applied by two inflatable balloons. Two different modes of compression were used. Either the two balloons were inflated and deflated simultaneously (intermittent compression), or just the caudal balloon was inflated and deflated while the cranial balloon was kept continuously inflated (continuous/intermittent compression). The experimental series were: intermittent compression at 10 mm Hg (n = 5) and 50 mm Hg (n = 5), and continuous/intermittent compression at 10 mm Hg (n = 5) and 50 mm Hg (n = 5). For both modes of compression the pressure in the balloons with intermittent inflation was maintained for 10 minutes and deflated for 5 minutes. This procedure was repeated in 8 cycles for 2 hours. Muscle action potentials were recorded in the tail muscles. Compression at 10 mm Hg induced similar reductions of muscle action potentials for both compression modes. At 50 mm Hg, the effects were more pronounced at continuous/intermittent compression than at intermittent compression. The reduction of muscle action potentials was slightly more pronounced for 50 than for 10 mm Hg at intermittent compression. However, a statistically significant difference in the results was found only between 10 and 50 mm Hg at the continuous/intermittent compression mode. The established model allows investigation of the effects of intermittent cauda equina compression, which might be clinically more relevant than continuous compression regarding the pathophysiologic mechanisms behind neurogenic claudication.
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