The influence of regional spinal cord hypothermia on transcranial myogenicmotor-evoked potential monitoring and the efficacy of spinal cord ischemiadetection

Objective: Myogenic motor-evoked responses to transcranial electrical stimu lation (transcranial myogenic motor-evoked potentials) can rapidly detect s pinal cord ischemia during thoracoabdominal aortic aneurysm repair. Recent evidence suggests that regional spinal cord hypothermia increases spinal co rd ischemia tolerance. We investigated the influence of subdural infusion c ooling on transcranial myogenic motor-evoked potential characteristics and the time to detect spinal cord ischemia in 6 pigs, Methods: Regional hypoth ermia was produced by subdural perfusion cooling. A laminectomy and incisio n 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. S pinal cord ischemia was produced by clamping a set of critical lumbar arter ies, previously identified by transcranial myogenic motor-evoked potentials and lumbar artery clamping. The time between the onset of ischemia and det ection 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 coo ling on transcranial myogenic motor-evoked potential amplitude and latency was determined. Results: The time necessary to produce ischemic transcrania l myogenic motor-evoked potentials, after the clamping of critical lumbar a rteries, 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 poten tial 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 d egrees C +/- 1.1 degrees C. The influence of cerebrospinal fluid temperatur e on transcranial myogenic motor-evoked potential amplitude was best repres ented by a quadratic regression curve crith 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 fl uid temperature of 28 degrees C, transcranial myogenic motor-evoked potenti al amplitudes are increased. Further cerebrospinal fluid temperature decrea ses result in progressive amplitude decreases and latency increases.