failure of motor evoked potentials to predict neurologic outcome in experimental thoracic aortic...

ORIGINAL ARTICLES

Failure of motor evoked potentials to predict neurologic outcome in experimental thoracic aortic occlusion James R. Elmore, MD, Peter Gloviczki, MD, C. Michel Harper , MD, Peter C. Pairolero, MD, Michael J. Murray, MD, Russell G. Born.chief, MB, ChB, Thomas C. Bower, MD, and Jasper R. Daube, MD, Rochester, Minn.

Motor evoked potential monitoring was tested as an alternative to somatosensory evoked potential monitoring in evaluating spinal cord fimction during thoracic aortic occlusion indogs. Twenty-seven animals underwent 60 minutes of cross-clamping of the proximal descending thoracic aorta with (n = 18) or without (n = 9) cerebrospinal fluid drainage. Spinal cord blood flow was measured with microspheres, and neurologic outcome was evaluated at 24 hours with Tarlov's scoring system. Cerebrospinal fluid drainage improved neurologic outcome (p < 0.05). Motor evoked potentials recorded over the lumbar spinal cord were lost in 9 of 20 dogs with ischemic cord injury and were not lost in any of the 7 dogs that were neurologically normal. Somatosensory evoked potential were lost in 19 of 20 paraplegic/paraparetic dogs and lost in 3 of 7 normal dogs (p < 0.01). After reperfusion, motor evoked potentials returned in all nine neurologically injured dogs that lost the potentials and were still present at 24 hours. Changes in amplitude, latency, or time until loss or return of motor evoked potentials or somatosensory evoked potentials did not predict neurologic injury. Loss of somatosensory evoked potentials had a high sensitivity (95%) but had low specificity (67%) because of peripheral nerve ~schemia. Loss of motor evoked potentials recorded from the spinal cord had high specificity (100%) but a low sensitivity (46%) and was therefore not a reliable predictor of neurologic injury. Ke~rn of motor evoked potentials during reperfusion did not correlate with functional recovery. Motor evoked potentials stimulated in the cortex and recorded from the spinal cord had low overall accuracy (59%). Alternative techniques to improve sensitivity and accuracy of motor evoked potentials must be developed. (J VAsc SuR~ 1991;14:131-9.)

The ability to monitor spinal cord function during operations on the thoracic and thoracoabdominal aorta may provide insight into the patho- physiology of spinal cord ischemic injury and guide therapeutic decisions. Paraplegia was first observed by Carrel ~ after thoracic aortic occlusion in dogs. The reported incidence of paraplegia has varied between 0.4% and 40% depending on the urgency of the operation, the presence of aortic dissection, hypoten-

From the Section of Vascular Surgery (Drs. Elmore, Gloviczki, Pairolero, Bourchier, and Bower), Department of Neurology (Drs. Harper and Daube), and Department of Anesthesiology (Dr. Murray), Mayo Clinic and Foundation, Rochester.

Reprint requests: Peter Gloviczki, MD, Mayo Clinic, 200 1st St. SW, Rochester, MN 55905.

24/1/29237

sion, the age of the patient, and the extent and duration of aortic cross-clamping. 2-1' Numerous methods have been used to decrease the incidence of neurologic injury, but none have consistently pre- vented the development of neurologic compli- cations. 2-i

Further development of adjuncts to prevent neurologic injury have been hampered, in part, by the lack of a reliable method to monitor spinal cord peffusion during operation. Somatosensory evoked potential (SEP) monitoring has been used both experimentally and clinically to monitor spinal cord function perioperatively. 4"~2-~6 Somatosensory evoked potentials rely primarily on transmission of impulses through the posterior column pathways of the spinal cord after stimulation of a peripheral nerve.

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Somatosensory evoked potentials are limited by the fact that (1) impulses are not traveling in the motor pathways and may therefore not reflect ischemic injury to the motor system and (2) peripheral nerve ischemia may block the transmission of the potentials.

Because of the limitations of SEPs, motor evoked potential (MEP) monitoring has been proposed as a method to directly monitor the motor tracts of the spinal cord27"18 These electrical impulses are gener- ated at the level of the cerebral cortex and travel down to the lower motor neurons of the spinal gray matter. Motor evoked potential recordings from the spinal cord would not be hampered by peripheral nerve ischemia and in theory would be more representative of ischemic injury to the motor tracts.

The purpose of these experiments was to deter- mine the response of MEPs to spinal cord ischemia during occlusion of the thoracic aorta in terms of (a) changes in amplitude and latency of MEPs, (b) ischemic time necessary to produce loss of MEPs and subsequent reperfusion time for return of MEPs, and (c) correlation with SEPs and neurologic outcome.

MATERIAL AND METHODS Experimental protocol

Twenty-seven mongrel dogs of either sex weigh- ing between 20 and 25 kg were divided into three groups. All animals underwent cross-clamping of the proximal descending thoracic aorta for 60 minutes with or without cerebrospinal fluid (CSF) drainage. Cerebrospinal fluid drainage was used to vary neurologic outcome without having to vary other parameters (such as clamp time or the use of shunts) that could affect the evoked potentials. In group A, 14 animals underwent thoracic aortic cross-clamping without CSF drainage. In group B, nine animals had CSF drainage before aortic occlusion. Four animals in group C underwent aortic occlusion followed by CSF drainage at the time of the loss of MEPs. Five additional animals that were to have been in group C did not have loss of MEPs. These dogs, therefore, did not undergo CSF drainage and are included in group A. Animals in experimental groups were studied in a sequential fashion and were not randomized.

Operative procedure Anesthesia was induced with intravenous meth-

ohexital sodium (10 mg/kg), and the dogs had their tracheas intubated. Ventilation was controlled with a Mark 7 (Bird Products Corp., Palm Springs, Calif.) ventilator, and anesthesia was maintained with halothane (1.0% to 1.5% concentration). Glucose-

free crystalloid (1500 ml) was administered intravenously. Operative procedures were done with sterile technique by use of a model described previously in work from our laboratory. 1° In brief, indwelling catheters consisted of (1) right carotid and femoral arterial cannulas, (2) pulmonary artery catheter, and (3) an intrathecal catheter placed by direct cut down on the cisterna magna to record pressure and drain CSF. Cerebrospinal fluid drainage, once instituted, was continued throughout the cross-clamp period. A left fourth intercostal space thoracotomy was performed with dissection of the thoracic aorta i cm distal to the origin of the left subclavian artery. A left atrial line was inserted for injection of microspheres.

Baseline data samples of temperature, blood glucose, arterial blood gases, cardiac output, pulmonary artery pressures, and proximal and distal aortic pressures were recorded. Spinal cord perfusion pressure was calculated as the difference between the mean distal aortic pressure and the CSF pressure. Baseline MEPs, SEPs, and measurement of spinal cord blood flow (SCBF) were done as detailed below.

Intravenous heparin (100 units/kg) was given, and the proximal thoracic aorta was cross-clamped just distal to the left subclavian artery for 60 minutes. Data sampling and microsphere injection were performed during cross-clamping at 30 minutes and 60 minutes. Repeat measurements were made 30 minutes after reperfusion. After injection of the last microsphere sample, the thoracotomy was closed in layers, and air was aspirated from the pleural space. Animals were maintained in a postoperative recovery room and received butorphanol tartrate (10 mg/dose) intramuscularly as an analgesic. After 24 hours neurologic function was evaluated. Evoked potentials were measured at 24 hours in paraplegic dogs by use of a similar anesthetic technique as described above. The dogs were killed with an intravenous overdose of sodium pentobarbital. The animal care complied with the "Principles of Labo- ratory Animal Care" (formulated by the National Society for Medical Research) and the "Guide for the Care and Use of Laboratory Animals" (NIH publication No. 80-23, revised 1985).

MEP and SEP measurements Spinal cord potentials were stimulated and re-

corded with an evoked potential system by use of constant voltage stimulator (TECA TD20; Teca Corp., Pleasantville, N.Y.). The stimulator delivered a square-wave pulse of 300 volts at a rate of 10 impulses per second for SEPs and 20 impulses per second for MEPs. Duration of each pulse was 500

Volume 14 Number 2 August 1991 Motor evoked potentials 133

Cortical stimulator

MEP SEP

Spinal cord recording electrodes

CFS pressure stimulator

Fig. 1. Canine model used to evaluate MEP and SEP monitoring during thoracic aortic occlusion.

~sec. Recorded potentials were filtered (20 to 2000 Hz) and averaged for a minimum of 200 impulses per recording. For MEPs, two small burr holes 2 cm apart were made 1 cm lateral to the midline of the skull just posterior to the frontal sinuses without entering the dura. The stimulating electrodes consisted of two stainless steel screws placed through the burr holes onto the dura. The posterior screw served as the anode. For SEPs the left sciatic nerve was exposed and encircled with a nerve stimulator ori- ented with the cathode proximally.

Recordings of spinal cord potentials were made from tetrafluoroethylene (Teflon) coated monopolar electromyography needles (50 mm length) placed percutaneously against the bony lamina at the T-2 and T- 13 levels. The T- 13 bony landmark correlates approximately with the T-13 to L-1 spinal cord level. Recordings were made at both levels with results reported for MEPs at the low thoracic position and for SEPs at the high thoracic level (Fig. 1). Needle electrodes placed in the subcutaneous tissue 4 cm lateral to the recording electrode served as the reference. A ground electrode was placed in the soft tissue of the neck. Complete neuromuscular blockade was achieved after thoracotomy with succinylcholine (1 mg/kg, intravenously) with repeated doses as necessary. Recorded data were analyzed for peak-to- peak amplitude, onset latency, and time until loss of

the signal with ischemia and time until return with reperfusion. Recordings were made throughout the experiment every 60 to 90 seconds. Measurements are reported at baseline, 30 minutes, 60 minutes (or last measurable curve ;after 30 minutes), and again after reperfusion.

Spinal cord blood flow

Spinal cord blood flow measurements were made with isotope tagged microspheres by use of a method developed by Heymann et al. Iv and previously reported in work from our laboratory. ~° Micro- spheres (15 ± 3 Ixm) were labeled with either cobalt (SyCo), tin (~a3Sn), st:rontium (SSSr), or scandium (46Sc) obtained from New England Nuclear (Boston, Mass.). Approximately 1.6 × 106 microspheres were suspended in a well-mixed solution of 10% dextran and polyoxyethylenc sorbitan mono-oleate (Tween- 80, Sigma Chemical Co., St. Louis, Mo.). Before injection, the microspheres were agitated in a soni- cator and then mixed to a total volume of 10 ml with saline. The microspheres were injected in the left atrial line over 10 seconds. A simultaneous reference sample was withdrawn from the carotid arterial line by a withdrawal pump at a constant rate of 8.82 ml/min for 60 seconds. The injection ofmicrospheres was random to prevent ordering bias.

At necropsy the spinal cord was removed and

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Baseline

Low Thoracic MEP

Occlusion-60 min

Reperfusion-30 rain

4,v

Baseline

High Thoracic SEP

Occlusion-60 rain ~ _ _

Reperfusion-30 min

t~J 2 ms

~1 pV

Fig. 2. Motor evoked potential and SEP sample recordings in a control animal without CSF drainage and resultant paraplegia. Note persistence of MEPs with loss of SEPs. Somatosensory evoked potentials return after reperfusion with prolonged latencies.

divided into cervical, upper thoracic, middle thoracic, lower thoracic, and lumbar regions. Each region was divided into gray and white matter and weighed to the nearest 0.01 gm. Samples were placed in a gamma counter (Beckman 310; Beckman Instruments Inc., Fullerton, Calif.), and counts were made with reference to each of the four microspheres after setting the appropriate window for the energy spectra of each microsphere.

Neurologic assessment Functional outcome was assessed at 24 hours and

graded according to the method of Tarlova°: (0) - no movement of hind limbs; (1) - perceptible movement of the joints of the hind limbs; (2) - good movement but unable to stand; (3) - able to stand and walk; (4) - complete recovery. Animals with scores of 0 are paraplegic and animals with scores of 1 to 3 are paraparetic.

Histologic analysis Small sections of each segment of the spinal cord

were submitted for hematoxylin and eosin staining. Sections were taken after the cord had been kept in

tbrmaiin for a minimum of 48 hours. The pathologist reviewing the specimens was blinded to each animal's neurologic outcome.

Statistical analysis

All statistical calculations used two-tailed proba- bility tests with statistical significance based on p <- 0.05. The Wilcoxon rank sum test or two-sample t tests were used for SCBF and the hemodynamic and metabolic parameters. The Fisher's exact test was used for comparison of neurologic outcome. The chi-square test was used for analysis of evoked potential data in relationship to neurologic outcome. In addition, paired t tests or paired signed rank tests were performed within groups to assess changes in measures at selected times in the experiment.

R E S U L T S Neurologic outcome

Sixty minutes of cross-clamp (group A) resulted in nine paraplegic (Tarlov 0), four paraparetic (Tarlov 1-3), and one normal dog (Tarlov 4). When CSF was drained before cross-clamping (group B) there were no paraplegic, four paraparetic, and five normal dogs (p < 0.05, when compared to group A). In the four group C dogs with CSF drainage at the loss of MEPs, two were paraplegic, one was paraparetic, and one was normal.

Motor evoked potentials Motor evoked potentials were lost during the

cross-clamp period in 9 of 20 paraplegic/paraparetic dogs. This loss was not significantly related to outcome. The MEPs were not lost in the seven normal dogs. In groups A and B all dogs that lost the MEPs were paraplegic. However, the MEPs persisted in 3 of the 11 paraplegic animals. The sensitivity, specificity, and overall accuracy for the ability to predict neurologic injury by the loss of MEPs were 46%, 100%, and 59%, respectively. In calculating the sensitivity, specificity and overall accuracy, animals that were drained at the loss of MEPs (group C) were counted as Tarlov 0 (paraplegia) to prevent any bias against the MEPs. Typical MEP tracings are dis- played in Fig. 2.

During reperfusion, return of MEPs did not correlate with neurologic recovery. These potentials continued to be present at 24 hours in the dogs with paraplegia. The MEPs returned immediately after CSF drainage in the four group C animals that underwent drainage when the MEPs were lost. Overall, changes in amplitudes and latencies of MEPs did not correlate statistically with neurologic out-


MEP

100

80

60

40

20

0

Amplitude

[-i-- NS-- I F-NS-- I [-- NS'-] i

Occlusion 30 min

g X3

8 o

Latency I--NS-] 1.0 F F Ns- ]

0.8

0,6

0,4

0.2

0

[-- NS--]

Occlusion Reperfusion Occlusion Occlusion Reperfusion 60 min 30 min 30 rain 60 rain 30 rain

[P] Normal (Tarlov 4) Ef~ Paraplegia/paraparesis (Tarlov 0-3)

Fig. 3. Amplitude and latency of MEPs. Amplitude data expressed as a percentage of baseline (mean-+ SEM). Latency data expressed as a prolongation over baseline in milliseconds (mean _+_ SEM). No significant difference between neurologically injured and normal dogs.

come (Fig. 3). The mean change in MEPs amplitude was greater in injured than in normal dogs at 30 minutes after aortic clamping (Fig. 3). However, this difference was not statistically significant and nar- rowed drastically by 60 and 90 minutes. At 60 minutes, even normal dogs had nearly a 50% drop in MEPs amplitude (Fig. 3). The average time until loss of MEPs and time until return during reperfusion are listed in Table I. Data in Table I related to time until loss of MEPs after aortic occlusion are available only for neurologically injured dogs since none of the normal animals lost the MEPs.

Table I. Time until loss/return of potentials

MEP SEP

(minutes) (minuteO

Loss of potential Normal N/A 17 +_ 9 Neurologic injury 25 ± 4 9 -+ 1.5

Return of potential Normal N/A 9 + 7 Neurologic injury 12 _+ 5 12 _+ 3

Data expressed as mean -+ SEM. Note, no normal dog lost MEPs. No significant difference between normal and neurologic injury for SEP data.

Somatosensory evoked potentials

Somatosensory evoked potentials were lost in 19 of 20 paraplegic/paraparetic dogs. Somatosensory evoked potentials were also lost in three of seven normal dogs. The loss of SEPs did correlate with neurologic injury GO < 0.01). The ability to predict neurologic injury by the loss of SEPs had a sensitivity of 95%, specificity of 67%, and overall accuracy of 89%. Somatosensory evoked potentials return were not significantly different between injured dogs (79%) and normal dogs (100%). In Fig. 2 are examples of typical SEP tracings.

Changes in the amplitudes and latencies of the SEPs at 30 minutes did not predict neurologic injury (Fig. 4). Since all but one neurologically injured dog lost the SEPs by 60 minutes, comparisons could not be made at this time point between the two groups. During reperfusion the latencies of SEPs were

significantly prolonged in injured dogs as compared to normal dogs, but no difference was observed in the amplitudes of SEPs (Fig. 4). The average time until loss of SEPs and time until return were not signifi- candy related to neurologic injury (Table I).

Spinal cord blood flow

Spinal cord blood flow was significantly decreased in paraplcgic/paraparetic dogs as compared to normal dogs (p < 0.05) in the low thoracic and lumbar gray matter regions during 30 and 60 minutes of cross-clamping. Fig. 5 displays the median blood flows obtained at the different time periods for the low thoracic and lumbar gray matter in these dogs. Cerebrospinal fluid drainage significantly improved distal SCBF in group B (CSF drainage before damp) as compared to dogs without drainage. This differ-

136 Elmore et al.

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SEP

100

80

60 c~

~6 o~ 40

20

Amplitude Latency 1.50 ,---- N:q ..----, ,-P < n n~,-~

g,

1.25

1.00

0.75

0,50

0.25

0 0 Occlusion Reperfusion Occlusion Reperfusion

30 rain 30 min 30 min 30 min

[~ Normal (Tartov 4) [] Paraplegia/paraparesis (Tarlov 0-3) [ ~ CG 129404X-2B

Fig. 4. Amplitude and latency of SEPs. Amplitude data expressed as a percentage of baseline (mean -+ SEM). Latency data expressed as a prolongation over baseline in milliseconds (mean -+ SEM). No significant difference between neurologically injured and normal dogs at 30 minutes of occlusion. Ninety-five percent of injured dogs lost SEPs by 60 minutes so no data analysis at that time interval. Note significant prolongation in latencies of SEPs during reperfusion.

o c g,g OB, 0 5 g ~ - 80

80 Low Thoracic Gray Matter

60 IA ~ ~_~ Normal (n = 7) 40 Paraplegia/paraparesis

(n =20) 20 : *

ol t l r emove

40

20

Lumbar Gray Matter

Baseline 30 60 90 Minutes

Fig. 5. Spinal cord blood flow in low thoracic and lumbar gray matter. Data expressed as median blood flow in ml/100 gm/min. Significantly decreased flow in neurologically injured dogs during the cross-clamp time.

ence was statistically significant in the low thoracic and lumbar gray matter at 30 and 60 minutes of cross-clamping.

Hemodynamic and metabolic parameters

Pulmonary artery pressures, cardiac index, and proximal aortic pressures were not significantly different between the dogs with ischemic cord injury and the normal dogs. The mean distal aortic pressure

was significantly less in the injured dogs (30 rain, 21 mm Hg; 60 min, 21 mm Hg) as compared to the normal dogs (30 min, 25 mm Hg; 60 min, 27 mm Hg) at 30 and 60 minutes.

Blood glucose levels were not significantly different between paraplegic/paraparetic dogs (base, 85 mg/dl; 90 min, 104 mg/dl) and normal dogs (base, 84 mg/dl; 90 min, i06 mg/dl). Core temperatures were not significantly different between neurologi-


Fig. 6. Light micrograph of proximal lumbar spinal cord gray matter of paraplegic control animal. Histologically there is anterior horn cell degeneration with ischemia of surrounding neural tissue. The three anterior horn cells in the top right corner are normal, whereas the three anterior horn cells in the center exhibit features of ischemic necrosis. (Hematoxylin-eosin stain; original magnification x400.)

cally injured dogs (base, 36 ° C; 90 min, 35 ° C) and normal dogs (base, 35 ° C; 90 min, 35 ° C). Arterial blood gases were identical between the paraplegic/paraparetic and normal dogs at each time interval except for the Pco2 at 30 minutes of cross-clamp, which was lower in the injured group (mean Pco2, 35 mm Hg) as compared to the normal dogs (mean Pco2, 40 mm Hg).

There was a significant difference in CSF pressure between normal dogs and those with ischemic cord injury, which was due in a large part to the effect of the CSF drainage. However, CSF pressure significantly increased during cross-clamping in paralyzed dogs without CSF drainage from a baseline of 4.7-+ 0.8 mm Hg to 10.2_+ 1.5 mm Hg 30 minutes after cross-clamping. This increase persisted to the 60-minute time point. Spinal cord perfusion pressure was significantly greater in the normal compared to the neurologically injured dogs.

Histology Histologic examination revealed anterior horn

cell degeneration with degeneration of surrounding neural tissue in the gray matter in paraplegic animals (Fig, 6). These changes were seen in the proximal segment of the lumbar cord of 5 of the 11 paraplegic dogs but were not seen in the paraparetic animals.

DISCUSSION Motor evoked potentials have been proposed as

an alternative to SEPs in monitoring spinal cord fimc-

tion during thoracic aortic occlusion.~8 One potential advantage of MEPs is that peripheral nerve ischemia does not affect the measurement as it does with SEPs. Motor evoked potentials also have the benefit of monitoring anterior and lateral column ischemia in the area of the motor tracts, whereas the SEPs prefer- entially monitor posterior and lateral columns. 2>2. Interpretation of SEPs can therefore give the false impression of spinal cord injury caused by peripheral nerve ischemia or may fail to detect spinal cord injury by monitoring the wrong pathways.

Our study showed a relatively high overall accuracy of SEPs in predicting ischemic cord injury. This is in agreement with the experience of others using similar animal models of spinal cord ischemia.12'~4'24 Our data suggest that the main limitation of SEP monitoring in thoracic aortic occlusion is its lack of specificity. It is of interest to note that in this study the mean time until loss of SEPs (Table I) was shorter in neurologically injured dogs (9 minutes) than in normal dogs (17 minutes). This difference was not statistically different, but the trend suggests that the loss of SEPs in .animals that are normal after operation is likely due to peripheral nerve ischemia caused by aortic cross-clamping.

Unfortunately, the clinical experience with SEP monitoring in human studies has been disappointing. Cunningham et al. 2s reported on 33 patients undergoing thoracic aortic occlusion in whom 15% developed paraplegia. 'The SEPs were lost in all 5 patients with paraplegia but were also lost in 11

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other patients who did not become paraplegic. Crawford et al. 4 subsequently reported on 198 patients and reported a false-positive rate of 67% and false-negative rate of 13% for the loss of SEPs in predicting neurologic deficits. Distal perfusion may improve the overall accuracy of SEP monitoring, but there can still be limitations. 4

Motor evoked potential monitoring usually in- volves stimulation of the cerebral cortex with recordings made from the spinal cord, peripheral nerve, or muscle. Merton and Morton 26 were the first to report a method of transcranial, high voltage electrical stimulation to generate MEPs. Motor evoked poten- rials have subsequently been used to monitor patients during spinal cord surgery. 27 Transcranial magnetic stimulation of the cortex has also been used to record MEPs in awake humans. 28 In vascular surgery, experimental work by Laschinger et al.la has shown loss of MEPs in dogs undergoing 20 minutes of thoracic aortic cross-clamping.

In our study MEPs recorded over the spinal cord after transcranial electrical stimulation were lost in only 45% of animals with neurologic injury, indicat- ing a low sensitivity. The specificity was, however, 100% because none of the normal dogs lost the MEPs. Overall accuracy for the loss of MEPs as a predictor of ischemic cord injury was only 59%. The amplitude, latency, or return of the signal did not correlate with neurologic outcome. Indeed MEPs were still present 24 hours after the ischemic injury in all paraplegic dogs.

The low sensitivity of MEPs in our study may be related to several factors. First, the MEP signal recorded over the spinal cord has a complex poly- phasic morphology. This makes simplified quantita- tive analysis of changes in amplitude, configuration, and latency difficult. There may well be changes occurring in these and other parameters of the MEPs that would correlate with neurologic injury if more sophisticated analysis was possible.

Second, we hypothesize that the MEPs recorded over the lower spinal canal are produced by electrical activity transmitted in the myelinated axons of descending corticospinal tracts. These white matter fibers, with cell bodies in the cerebral cortex, are likely to be more resistant to ischemia than anterior horn cells and interneurons whose cell bodies lie within the ischemic cord. Postmortem histologic examination in this study supports the view that ischemic injury to motor neurons within the spinal gray matter accounts for a significant degree of the neurologic deficit after aortic occlusion.

In this study recordings of MEPs were made at the T-13 bony landmark, which correlates approximately with the T-13 to L-1 spinal cord level.

Changes in MEPs should therefore reflect ischemia of the thoracic and the most proximal lumbar cord. Indeed, histology and SCBF data are consistent with ischemia in these segments of the cord but MEPs were still relatively inaccurate. These results suggest that future attempts at recording MEPs should be directed distal to the levels of our measurements (such as, lumbosacral cord, cauda equina, peripheral nerve, or muscle) to improve sensitivity. This conclusion is supported by recent work by Svensson et al. 29 suggesting that MEPs are highly sensitive in predicting paraplegia when stimulations are elicited with an intrathecal electrode and recordings are made from lower extremity muscles. These data support our conclusion that it is important to measure these potentials distal to the anterior horn cell. Motor evoked potential monitoring may be clinically useful in vascular surgery if the sensitivity of the test can be improved. More distal recording of the signals, improvements in stimulation techniques, and more sophisticated analysis of the MEPs may all help to improve the sensitivity.

The authors thank H a m o Okazaki, MD, for reviewing the histology, Peter C. O'Brien, PhD, and James M. Naessens for the statistical calculations, O. Arian Hildestad for technical expertise, and Marcia A. Simonson for manuscript preparation.

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Submitted Dec. 5, 1990; accepted Mar. 4, 1991.

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failure of motor evoked potentials to predict neurologic outcome in experimental thoracic aortic...

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