Pressure short of producing neuropraxia was applied to the facial nerve in 12 cats. In over half, a neuropraxia promptly developed when the animals were rendered hypotensive with nitroprusside. In six other animals, pressure was applied to the nerve following circulatory collapse. No added effect of the pressure on nerve conduction decay could be demonstrated. Pressure-induced neuropraxia appears to be dependent to some extent on ischemia.
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