[Clinical application of the evoked spinal cord potentials. Part 1. Neurophysiological assessment of the evoked spinal cord potentials in experimental cord trauma - with reference to cord compression and ischemia (author's transl)].

Numerous investigators endeavored to make clear pathophysiological changes in a traumatic spinal cord lesion. The development of neuroscience contributed to have an influence on methods of these researches. This study was undertaken to assess electrophysiological changes resulting from variable periods of experimental spinal cord compression or ischemia by using the evoked spinal cord potentials. Experiments were performed on dogs. Following laminectomies at Th7-9 and L3-4 levels under anesthesia, cord injuries were produced at the lower thoracic level by inflation of an extradurally placed balloon which produced slow graded compression of cord dorsum. Evoked spinal cord potentials to sciatic nerve stimulation were recorded from bipolar electrodes in the midline dorsal subdural space at the operative sites. The normal wave forms of two responses consisted of initially positive triphasic potentials (P1, N1, P2). The conduction velocity of the ascending afferent from the leg was found on the average to be 54.8 +/- 9.7 m/sec between lumbar and dorsal cord. On the basis of the conduction velocities and the responses to stimulus intensities, the afferent volley recorded in the present experiments might reflect synaptic cord afferent pathways originated without Group I fibers in the cord dorsum which were situated ipsilateral to the stimulated nerve. After inflation of the balloon with 0.1 cc of water, spinal canal narrowing rate increased to 14.3 +/- 2.9%. The evoked spinal cord potentials in the lead rostral to the site of compression began to decrease in amplitude. When more water was added into the balloon up to 0.4 - 0.6 cc, spinal canal narrowing rate was enhanced to 42.5 - 77.7% in which potentials were abolished. P2 wave was the first to be abolished and subsequently N1, P1 disappeared in order. On the other hand, the potentials reappeared after decompression in the reverse of their disappearance in order. Responses in dogs with complete recovery from paraplegia returned to the precompression wave pattern both in the amplitude and in latency. On the contrary, in dogs with spastic paraparesis, the recovery of wave form was shown as P1, N1 or P1, N1 with depressed P2. Despite this variability, the evoked response from animals with reversible cord injury were discernible in the early period of spinal shock phase. The degree of recovery varied and had no linear relationship to the recovery grade of clinical symptoms. The experimental cord ischemia was made by inflation of a balloon catheter which was inserted from femoral artery into the upper thoracic aorta. The evoked spinal cord potentials were recorded at the midthoracic and lumbar level. Changes of wave form resulting from the ischemic period of 30 minutes were first the amplitude loss of N1 and subsequently that of P2, P1. On the other hand, the responses gradually returned to their pre-ischemic characteristic about 30 minutes after circulatory reestablishment...