OBJECTIVES: A day after undergoing an operation of the thoracic aorta, a patient showed signs of spastic paraplegia, but on myogenic transcranial motor evoked potential monitoring, the myogenic transcranial motor evoked potentials recorded from the left anterior tibial muscle appeared normal. We sought to confirm these observations by using a rat spinal ischemia model to define the possibility of false-negative results in myogenic transcranial motor evoked potential monitoring by motor function behavior and spinal histopathology. METHODS: Spinal ischemia was induced for 6 minutes (group A, n = 6) or 10 minutes (group B, n = 6) with an intra-aortic balloon. After ischemia, motor function was assessed periodically by using the motor deficit index (0, complete recovery; 6, complete paraplegia). Myogenic transcranial motor evoked potentials were recorded from the right soleus muscle before ischemia, 2 and 6 minutes after the start of spinal ischemia, and at 30 minutes, 24 hours, and 72 hours of reperfusion. RESULTS: All group A rats showed normal motor function at 72 hours of reperfusion, whereas all group B rats displayed complete spastic paraplegia (motor deficit index = 6) at 72 hours of reperfusion. However, transcranial motor evoked potential was preserved in both group B and group A. Histopathologic analysis in group B revealed the presence of extensive necrotic changes of the gray matter distributed between laminae V through VII in the L3 to L5 segments but normal appearance of alpha motor neurons. CONCLUSION: According to our data, in using myogenic transcranial motor evoked potential monitoring during thoracic or thoracoabdominal aneurysm repair, we should be aware that transcranial motor evoked potentials cannot always be used to predict neurologic outcome after the operation.
OBJECTIVES: A day after undergoing an operation of the thoracic aorta, a patient showed signs of spastic paraplegia, but on myogenic transcranial motor evoked potential monitoring, the myogenic transcranial motor evoked potentials recorded from the left anterior tibial muscle appeared normal. We sought to confirm these observations by using a ratspinal ischemia model to define the possibility of false-negative results in myogenic transcranial motor evoked potential monitoring by motor function behavior and spinal histopathology. METHODS:Spinal ischemia was induced for 6 minutes (group A, n = 6) or 10 minutes (group B, n = 6) with an intra-aortic balloon. After ischemia, motor function was assessed periodically by using the motor deficit index (0, complete recovery; 6, complete paraplegia). Myogenic transcranial motor evoked potentials were recorded from the right soleus muscle before ischemia, 2 and 6 minutes after the start of spinal ischemia, and at 30 minutes, 24 hours, and 72 hours of reperfusion. RESULTS: All group A rats showed normal motor function at 72 hours of reperfusion, whereas all group B rats displayed complete spastic paraplegia (motor deficit index = 6) at 72 hours of reperfusion. However, transcranial motor evoked potential was preserved in both group B and group A. Histopathologic analysis in group B revealed the presence of extensive necrotic changes of the gray matter distributed between laminae V through VII in the L3 to L5 segments but normal appearance of alpha motor neurons. CONCLUSION: According to our data, in using myogenic transcranial motor evoked potential monitoring during thoracic or thoracoabdominal aneurysm repair, we should be aware that transcranial motor evoked potentials cannot always be used to predict neurologic outcome after the operation.