Kobrine A I, Evans D E, Rizzoli H
Surg Neurol. 1978 Jul;10(1):54-9.
Focal spinal cord blood flow was measured in the left dorsal column of monkeys' spinal cords at T6 during slow balloon compression of the same segment. The physiological integrity of the spinal cord was monitored by the recording of the summated spinal evoked response (SER). In all cases, the evoked response did not disappear until the blood flow in the compressed segment was zero. In four animals, a definite phase of hyperemia occurred during compression, at which time the amplitude of the evoked response was reduced. A post-ischemic hyperemia occurred in seven animals. The evoke response returned in all animals to a varying degree within one-hour post-deflation. The results suggest that mechanical forces of compression, rather than ischemia, are mainly responsible for the loss of neural conduction in such a model. If ischemia plays a role at all in the loss of function in such a model, it appears that focal ischemia secondary to compression in the spinal cord must be profound for loss of physiologic function to occur.
