The influence of regional spinal cord hypothermia on transcranial myogenic motor-evoked potential monitoring and the efficacy of spinal cord ischemia detection.

OBJECTIVE: Myogenic motor-evoked responses to transcranial electrical stimulation (transcranial myogenic motor-evoked potentials) can rapidly detect spinal cord ischemia during thoracoabdominal aortic aneurysm repair. Recent evidence suggests that regional spinal cord hypothermia increases spinal cord ischemia tolerance. We investigated the influence of subdural infusion cooling on transcranial myogenic motor-evoked potential characteristics and the time to detect spinal cord ischemia in 6 pigs.
METHODS: Regional hypothermia was produced by subdural perfusion cooling. A laminectomy and incision of the dura were performed at L2 to advance 2 inflow catheters at L4 and L6, to cool the lumbar subdural space with saline solution. Two temperature probes were advanced at L3 and L5, and 1 cerebrospinal fluid pressure line was advanced at L4. Spontaneous cerebrospinal fluid outflow was allowed. Spinal cord ischemia was produced by clamping a set of critical lumbar arteries, previously identified by transcranial myogenic motor-evoked potentials and lumbar artery clamping. The time between the onset of ischemia and detection with transcranial myogenic motor-evoked potentials (amplitude < 25%) was determined at cerebrospinal fluid temperatures of 37 degrees C and 28 degrees C. Thereafter, the influence of progressive cerebrospinal fluid cooling on transcranial myogenic motor-evoked potential amplitude and latency was determined.
RESULTS: The time necessary to produce ischemic transcranial myogenic motor-evoked potentials, after the clamping of critical lumbar arteries, was not affected at moderate subdural hypothermia (3.8 +/- 0.9 min) compared with subdural normothermia (3.2 +/- 0.5 min; P =.6). Thereafter, progressive cooling resulted in a transcranial myogenic motor-evoked potential amplitude increase at 28 degrees C to 30 degrees C and was followed by a progressive decrease. Response amplitudes decreased below 25% at 14.0 degrees C +/- 1.1 degrees C. The influence of cerebrospinal fluid temperature on transcranial myogenic motor-evoked potential amplitude was best represented by a quadratic regression curve with a maximum at 29.6 degrees C. In contrast, transcranial myogenic motor-evoked potential latencies increased linearly with decreasing subdural temperatures.
CONCLUSIONS: Detection of spinal cord ischemia with transcranial myogenic motor-evoked potentials is not delayed at moderate subdural hypothermia in pigs. At a cerebrospinal fluid temperature of 28 degrees C, transcranial myogenic motor-evoked potential amplitudes are increased. Further cerebrospinal fluid temperature decreases result in progressive amplitude decreases and latency increases.