PubMed1985
In cats in which the spinal cord was transected at C-1, the exposed L-7 spinal cord segment was compressed with an electromagnetically driven rod applied to the dorsal surface of the segment. With the magnitude of compression constant at 3 mm, the cord was compressed for durations of 50 msec, 0.5 sec, or 1.0 sec. Polysynaptic reflex discharges integrated in the injured segment and action potentials conducted in dorsal column axons traversing the same region were electrophysiologically measured before, during, and for 41/2 hours after trauma. Structural changes were evaluated on frozen serial sections obtained both from compressed segments and from tissue adjacent to the injury. At a compression duration of 50 msec, the amplitude of evoked reflex activity decreased abruptly, and dorsal column axonal conduction was blocked for 1 minute following compression. This early-phase response was followed by partial recovery of both functions which persisted until the end of the experiment. Prolonging compression to 0.5 sec brought about a further decrease of polysynaptic reflex activity. Axonal conduction was also decreased, but not significantly. With compression lasting 1.0 sec, no significant changes in reflex discharges and axonal conduction occurred compared with those measured at 0.5 sec. Neither function was abolished, even after the longest compression time. Prolongation of compression significantly increased both the intensity and the spread of edema, whereas changes in hemorrhage were not significant. Thus, a plateau rather than a progressive increase in severity of functional and structural posttraumatic changes was reached by increasing the duration of compression. This injury model reduces the sources of variability found in other experimental compression trauma models and permits the quantitative assessment of basic spinal cord mechanisms and correlated histopathological changes in the same preparation following trauma.