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Experimental spinal cord injury produced by slow, graded compression

Alterations of cortical and spinal evoked potentials

Johannes Schramm, Keizo Hashizume, Takanori Fukushima and Hiroshi Takahashi

✓ A new model of experimental spinal cord injury produced by slow, graded compression in cats is described. The extent of cord compression was evaluated by monitoring somatosensory evoked potentials (SEP's). The compression was exerted by means of a special screw-plate assembly with stepwise advancement of the compression plate at different time intervals and was completed when cortical SEP had disappeared. Every stage in the total course of gradual compression was expressed as a percentage of the total. Cortical and spinal SEP's were recorded at each increment. The SEP pattern was analyzed in terms of latency, amplitude, and wave form. It was noteworthy that SEP's were remarkably resistant to gradual compression. The amplitude of cortical SEP's began decreasing at a late stage of compression, usually at about 80% of total compression, and that of spinal SEP's some time earlier, at about 60% of total compression. They both then rapidly fell to zero. Cortical SEP's showed a slight increase in latency concurrent with the reduction of amplitude, while the latency of spinal SEP's was constant. Mid-thoracic SEP's showed considerable individual variation in wave form. Their changes were similar to those of cortical SEP. Thoracolumbar SEP's, recorded immediately rostral to the compression, showed little individual variation, and did not show flat recordings even with maximum compression. A small monophasic positive wave was present in all animals even after the cortical SEP's became flat. This “final potential” was assumed to be caused by electrotonic volume conduction from the activities of the dorsal white matter caudal to the compression site. The reversibility of SEP's after the release of compression was remarkable. Both cortical and spinal SEP's could show complete recovery even when histological examination demonstrated hemorrhagic necrosis. The present data show no linear correlation between SEP changes and degree of compression. There are no changes with slight or moderate degree of compression. Alterations of SEP's in slow compression models should suggest the presence of a severe degree of compression.