Experimental acute balloon compression of the spinal cord

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Abstract
Acute balloon compression of the thoracic spinal cord for 15, 7, 5, 3 and 1 min in macaque monkeys caused immediate disappearance of the spinal evoked response and complete focal ischemia of the compressed segment in all animals. Only the animals in the 1-min group demonstrated return of the evoked response. These data, coupled with data from previous experiments of slow balloon compression of the spinal cord and spinal cord ischemia, suggest that the major pathological substrate for neural dysfunction after balloon compression of the spinal cord, be it acute or slow, is physical injury of the neural membrane, irrespective of blood flow changes. The ability of that membrane to recover is related to rapidity and length of time of compression. Focal changes in blood flow do not appear to be significant in this mechanism.

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