“… - To elicit abnormally propagated electromyographic (EMG) polysynaptic current spreading, three to four segments surrounding the stimulated L4 nerve and the creation of an upper motor lesion (14,15) that is not present in the normal central nervous system of either animals (5) or humans (7).
- To investigate if there are differences of threshold between both damaged and nondamaged sides.
- To compare the latencies of motor‐evoked potentials (MEP) in normal specimens and both sides of the brain in damaged specimen preparations.
- Because latencies of MEPs are strongly dependent on conduction speed that is roughly the same in pigs and humans, we felt that the pig model was a good experimental approach that would closely mimic human clinical conditions (16).
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