Direct noninvasive monitoring of spinal cord motor function during thoracic aortic occlusion: use of motor evoked potentials

Spinal cord monitoring during thoracic aneurysmectomy by somatosensory evoked potentials has been criticized for its failure to measure anterior (motor) spinal cord function. We have developed a clinically applicable, noninvasive technique for intraoperative monitoring of motor evoked potentials (MEP), which allows direct functional assessment of spinal cord motor tracts during thoracic aortic occlusion. Twelve dogs underwent continuous intraoperative monitoring of MEP before, during, and after thoracic aortic cross-clamping. Motor tract response to noninvasive cord stimulation (5 to 10 mA, 0.02 msec, 4.3 H2) was recorded by subcutaneous electrodes placed along the length of the spine (T-10, L-1, and L-4). Six animals (group I) subjected to aortic cross-clamping alone demonstrated a characteristic time- and level-dependent deterioration and loss of MEP. Ischemic cord dysfunction (as determined by time from clamping to loss of MEP) progressed from the distal to the proximal cord (L-4 = 11.3 +/- 1.5 minutes; L-1 = 14.9 +/- 2.3 minutes; T-10 = 16.9 +/- 2.3 minutes; p less than 0.05 between all levels). Reperfusion of the distal aorta 20 minutes after clamping resulted in MEP return that progressed from the proximal (T-10) to distal (L-1 and L-4) cord. In another six animals (group II), distal perfusion (mean blood pressure = 95 mm Hg) was maintained for 1 hour after cross-clamping by left atrial-femoral artery bypass. Normal configuration and amplitude of MEP was maintained throughout the cross-clamping period. These data suggest that distinctive changes in MEP indicative of reversible ischemia of spinal cord motor tracts occur after aortic cross-clamping. Such ischemia begins in the most distal cord, exhibits upward progression with time, and can be prevented by maintenance of adequate distal aortic perfusion. Clinical use of MEP monitoring during thoracic aneurysmectomy may provide a method for intraoperative assessment of the adequacy of motor tract perfusion.     

Myogenic transcranial motor evoked potentials monitoring cannot always predict neurologic outcome after spinal cord ischemia in rats

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.     

The role of transcranial motor evoked potentials in predicting neurologic and histopathologic outcome after experimental spinal cord ischemia

BACKGROUND: Monitoring of myogenic motor evoked potentials to transcranial stimulation (tcMEPs) is clinically used to assess motor pathway function during aortic and spinal procedures that carry a risk of spinal cord ischemia (SCI). Although tcMEPs presumably detect SCI before irreversible neuronal deficit occurs, and prolonged reduction of tcMEP signals is thought to be associated with impending spinal cord damage, experimental evidence to support this concept has not been provided. In this study, histopathologic and neurologic outcome was examined in a porcine model of SCI after different durations of intraoperative loss of tcMEP signals. METHODS: In 15 ketamine-sufentanil-anesthetized pigs (weight, 35-45 kg) the spinal cord feeding lumbar arteries were exposed. tcMEP were recorded from the upper and lower limbs. Under normothermic conditions, animals were randomly allocated to undergo short-term tcMEP reduction (group A, < 10 min, n = 5) or prolonged tcMEP reduction (group B, 60 min, n = 10), resulting from temporary or permanent clamping of lumbar segmental arteries. Neurologic function was evaluated every 24 h, and infarction volume and the number of eosinophilic neurons and viable motoneurons in the lumbosacral spinal cord was evaluated 72 h after induction of SCI. RESULTS: In all animals except one, segmental artery clamping reduced tcMEP to below 25% of baseline. All but one animal in group A had reduced tcMEP for less than 10 min and had normal motor function and no infarction at 72 h after the initial tcMEP reduction. Seven animals in group B (70%) had reduced tcMEP signals for more than 60 min and were paraplegic with massive spinal cord infarction at 72 h. Two animals (one in both groups) had tcMEP loss for 40 min, with moderate infarction and normal function. In general, histopathologic damage and neurologic dysfunction did not occur when tcMEP amplitude recovered within 10 and 40 min after the initial decline, respectively. CONCLUSION: 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.     

Thoracic aortic occlusion: somatosensory evoked potential monitoring and neurologic outcome in a canine model

Somatosensory evoked potentials (SEPs) were monitored in 17 canines during spinal cord ischemia induced by balloon occlusion of the thoracic aorta. Graded distal aortic hypotension to 40 mmHg in seven animals had no significant effect upon the evoked potential. A significant alteration in the SEP did result in 21 +/- 9.8 minutes when distal aortic pressures were reduced in a graded fashion below 30 mmHg. Acute occlusion of the thoracic aorta (10 animals, distal pressure 15-25 mmHg) was associated with a change in the SEP in 8.4 +/- 4.3 minutes. Continuation of aortic occlusion for 30 minutes beyond an evoked potential change resulted in a moderate to severe motor deficit in all cases. Somatosensory evoked potentials obtained 72-96 hours after the ischemic injury were closely correlated with sensory deficits, but were not predictive of motor examination. Histologic examination of the spinal cords demonstrated central gray necrosis of the lumbar region in all animals with a severe deficit, and a variable degree of neuronal loss in the intermediate and dorsal gray matter zones in animals with moderate deficits. This balloon occlusion method is relevant as a model of spinal cord injury during aortic occlusion, such as may occur during aortic surgery.     

Intraoperative unilateral changes in myogenic motor evoked potentials in patients undergoing thoracic aortic surgery

Motor evoked potentials (MEPs) can be employed for monitoring the functional integrity of the descending motor pathways during thoracic aortic surgery. Since MEPs can be affected by a variety of intraoperative factors, intraoperative MEP changes have to be carefully interpreted. In this report, we describe two patients undergoing thoracic aortic surgery, in whom MEPs from the unilateral lower limb disappeared after femoral artery cannulation, and MEPs' recovered by modifying the position or removing the cannula. MEPs in the contralateral side remained unchanged. Neither patients showed postoperative neurologic dysfunction in the lower limbs. These observations suggest that regional ischemia of the lower limbs caused by femoral artery cannulation can affect intraoperative MEP finding.     

Assessment of intraoperative motor evoked potentials for predicting postoperative paraplegia in thoracic and thoracoabdominal aortic aneurysm repair

Purpose  

Monitoring motor evoked potentials (MEPs) has been recognized as a highly reliable method to detect intraoperative spinal cord ischemia (SCI) in aortic repair. However, the data regarding the sensitivity and specificity of MEPs for predicting postoperative paraplegia are limited. We retrospectively assessed the value of intraoperative MEP amplitudes for predicting postoperative paraplegia.     

Comparison of transcranial motor evoked potentials and somatosensory evoked potentials during thoracoabdominal aortic aneurysm repair

OBJECTIVE: To compare transcranial motor evoked potentials (tc-MEPs) and somatosensory evoked potentials (SSEPs) as indicators of spinal cord function during thoracoabdominal aortic aneurysm repair. SUMMARY BACKGROUND DATA: Somatosensory evoked potentials reflect conduction in dorsal columns. tc-MEPs represent anterior horn motor neuron function. This is the first study to compare the techniques directly during thoracoabdominal aortic aneurysm repair. METHODS: In 38 patients, thoracoabdominal aortic aneurysm repair (type I, n = 10, type II, n = 14, type III, n = 6, type IV, n = 8) was performed using left heart bypass and segmental artery reimplantation. tc-MEP amplitudes <25% and SSEP amplitudes <50% and/or latencies >110% were considered indicators of cord ischemia. The authors compared the response of both methods to interventions and correlated the responses at the end of surgery to neurologic outcomes. RESULTS: Ischemic tc-MEP changes occurred in 18/38 patients and could be restored by segmental artery reperfusion (n = 12) or by increasing blood pressure (n = 6). Significant SSEP changes accompanied these tc-MEP events in only 5/18 patients, with a delay of 2 to 34 minutes. SSEPs recovered in only two patients. In another 11 patients, SSEP amplitudes fell progressively to <50% of control without parallel tc-MEP changes or association with cross-clamp events or pressure decreases. At the end of the procedure, tc-MEP amplitudes were 84 +/- 46% of control. In contrast, SSEP amplitudes were <50% of control in 15 patients (39%). No paraplegia occurred. CONCLUSION: In all patients, tc-MEP events could be corrected by applying protective strategies. No patient awoke paraplegic. SSEPs showed delayed ischemia detection and a high rate of false-positive results.     

Changes of motor evoked potentials during descending thoracic and thoracoabdominal aortic surgery with deep hypothermic circulatory arrest

Background  

Paraplegia is a serious complication of descending and thoracoabdominal aortic aneurysms (dTAAs and TAAAs) surgery. Motor evoked potentials (MEPs) enable monitoring the functional integrity of motor pathways during dTAA and TAAA surgery. Although MEPs are sensitive to temperature changes, there are few human data on changes of MEPs during mild and deep hypothermia. Therefore, we investigated changes of MEPs in deep hypothermic circulatory arrest (DHCA) in dTAA and TAAA surgery.     

Effects of thoracic aortic occlusion and cerebrospinal fluid drainage on regional spinal cord blood flow in dogs: correlation with neurologic outcome

We studied the effect of thoracic aortic occlusion and cerebrospinal fluid (CSF) drainage on regional spinal cord blood flow and its correlation with neurologic outcome. Using isotope-tagged microspheres, we determined blood flow to the gray and white matter of five regions of the spinal cord in dogs: group I (control), group II (cross-clamp only), group III (cross-clamp plus CSF drainage). At 60 minutes after thoracic aortic occlusion in group II, median gray matter blood flow (GMBF) in the lower thoracic and lumbar cord decreased from 23.1 and 27.0 ml/100 gm/min at baseline to 4.0 and 2.5 ml/100 gm/min, respectively. The addition of CSF drainage improved GMBF during aortic cross-clamping in the lower thoracic and lumbar cord to 11.3 (p less than 0.05) and 15.1 ml/100 gm/min (p less than 0.03), respectively. After removal of the aortic cross-clamp, median blood flow more than tripled from baseline blood flow in group II, whereas CSF drainage prevented significant reperfusion hyperemia. Both low GMBF during cross-clamping and reperfusion hyperemia were associated with a worse neurologic outcome. In group II, no dog was neurologically normal, and more than 60% of the dogs had spastic paraplegia. In contrast, almost 60% of dogs in group III were normal, and none had spastic paraplegia (p less than 0.001). We conclude that CSF drainage in dogs during thoracic aortic occlusion maintained spinal cord perfusion above critical levels, diminished reperfusion hyperemia, and improved neurologic outcome.     

Influence of low proximal aortic pressure on spinal cord oxygenation in experimental thoracic aortic occlusion

BACKGROUND: To evaluate the effect of low proximal aortic pressure on cerebrospinal fluid (CSF) oxygenation in an experimental thoracic occlusion model. METHODS: In nine pigs, continuous intrathecal pO(2), pCO(2) and pH monitoring was used during double descending thoracic aortic clamping following insertion of an aorto-aortic shunt. In five pigs, the shunt was connected to a citrated bag adjusted at approximately 40-45 cm above the heart for partial exsanguination in order to decrease mean proximal aortic pressure (MPAP) to below 50 mmHg. In four animals, sodium nitroprusside infusion was used for this purpose. RESULTS: Intrathecal pO(2) demonstrated a significant decrease from 4.9+/-2.1 to 2.9+/-2.4 kPa after 10 minutes of aortic cross-clamping. Lowering proximal aortic pressure caused a further significant decrease to 1.2+/-1.7 kPa (p<0.05). In seven pigs (5 in the exsanguination and 2 in the vasodilator group), restoration of mean proximal aortic pressure to 94.0+/-27.7 caused a recovery of CSF pO(2) from 1.2+/-1.9 to 2.8+/-3.0 (p<0.05). CONCLUSIONS: The results of this study demonstrate that MPAP which provides spinal cord perfusion through subclavian-vertebral arteries are crucial for maintenance of spinal cord oxygenation during thoracic aortic occlusion in this pig model.