Rigidity of hind limbs of cats produced by occlusion of spinal cord blood supply

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Abstract
Permanent hind-limb rigidity in cats was produced by temporary occlusion of the blood supply to the lumbar spinal cord. The optimal technique evolved was the clamping of both Internal mammary arteries and the arch of the aorta Just above the 1st intercostal branches for 47 minutes. Of all cats surviving postoperatively, 37% exhibited permanent rigidity, 33% permanent flaccidity, and 29% no effect. The animals exhibiting rigidity had active stretch reflexes, moderate "spontaneous" motoneuron activity, and no grossly detectable spinal reflexes other than those due to stretch. There was usually no sensitivity to vigorous skin stimulation, but a pain reaction could be elicited by forceful manipulation of the muscles or Joints. Rigidity in extension was the rule: only 4 of 55 cats with rigidity exhibited any form of flexor rigidity. Muscle spindle afferent receptors, intra-fusal muscle fibers, and fusimotor neurons were functionally intact and did not exhibit grossly abnormal behavior. Tonic efferent fusimotor neuron activity was present and might account for at least a portion of the hyperactive stretch reflex activity. The monosynaptic reflex recorded from ventral roots was either normal or increased in magnitude in the rigid preparations. Motoneuron responses to dorsal root stimulation were significantly less depressed by repetitive stimulation in the rigid preparations than in normal cats. Posttetanic potentiation was prolonged in the rigid preparations. Excitation of muscle spindle afferents by succinylcholine was associated with an increased monosynaptic reflex response. A variety of polysynaptic reflex responses were either decreased or absent. It is postulated that, among other effects, spinal cord ischemia causes a decrease in presynaptic inhibition, most probably as a result of interneuron destruction.

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