The data indicate that treatment with riluzole can increase the tolerance of spinal cord motoneurons to a period of normothermic ischemia. Intraischemic ketamine did not provide neuroprotection in this model.

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.

Prolonged reduction of intraoperative tcMEP amplitude is predictive for postoperative neurologic dysfunction, while recovery of the tcMEP signal within 10 min after the initial decline corresponds with normal histopathology and motor function in this experimental model. This finding confirms that intraoperative tcMEPs have a good prognostic value for neurologic outcome during procedures in which the spinal cord is at risk for ischemia.