:Acta . Ncurochlrurgica

Acta Neurochir (Wien) (1991) 108:140-147

9 Springer-Verlag 1991 Printed in Austria

Motor versus Somatosensory Evoked Potential Changes After Acute Experimental Spinal Cord Injury in Rats* M . Z i l e l i ~ a n d J . Schramm 2 Departments of Neurosurgery, 2University of Erlangen-Nfirnberg, Erlangen, Federal Republic of Germany, 1Faculty of Medicine, Aegean University, Bornova, Izmir, Turkey

Summary

considering

In this study, averaged cortical somatosensory evoked potentials (SEP) after sciatic nerve stimulation, and lower extremity muscle responses after motor cortex stimulation (MEP) were compared in rats. 10 animals served as light (25 g-cm) and 10 animals as severe (80g-em) acute spinal cord injury group after weight dropping trauma. After the initial loss of components, both SEP and MEP recovered in most cases in the light injury group. In the severe injury group, however, no recovery was observed in cortical SEPs, while the muscle MEP recovered in some animals. Light spinal cord injury had little effect on muscle MEPs and caused a paradoxical amplitude increase in some MEP recordings. Latency values of muscle MEPs did not show great changes after either kind of injury, while cortical SEP latency was considerably delayed. In this model cortical SEPs were more sensitive to light spinal cord injury than muscle MEPs after single electrical cortical stimuli. Severe spinal cord injury caused amplitude changes or loss of waves from both SEP and MEP. Keywords: Motor evoked potential; muscle response; somatosensory evoked potential; spinal cord injury; spinal cord monitoring.

stimuli 1. T h e m a j o r a d v a n t a g e o f M E P in i n t r a o p e r -

Introduction In spinal cord monitoring with motor evoked pot e n t i a l s ( M E P ) 2' 8,14,1~20 a n d in e v a l u a t i o n o f the p r o g n o s i s o f s p i n a l c o r d i n j u r y in m a n 6'9' 10,23, it h a s b e e n p o i n t e d o u t t h a t S E P a l o n e has a l i m i t e d v a l u e to s h o w the p r o g n o s i s o f spinal c o r d i n j u r y in m o n i t o r i n g 15. MEP

c o u l d be e v o k e d in m a n a f t e r single s t i m u -

lation using transcranial electrical and magnetic s t i m u l a t o r s 2,18, 20, 24, 31. F o r m o n i t o r i n g this is t h e o r e t ically b e n e f i c i a l , i f t h e t i m e n e e d e d f o r S E P a n a l y s i s is c o n s i d e r e d . Single m o t o r s t i m u l i are also p r e f e r a b l e * This work was partly presented in the poster sections at "39. Jahrestagung der Deutschen Gesellschaft ffir Neurochirurgie, K61n (F. R. G., May 8-1, 1988" and "Congress of the International Medical Society of Motor Disturbances, Rome, Italy, June 2-4, 1988".

the

relative

risks

of multiple

cortical

a t i v e m o n i t o r i n g w o u l d be t h e a d d e d facility to o b s e r v e c o n d u c t i o n in m o t o r p a t h w a y s . T h e r e a r e m a n y d e t a i l e d studies o n s o m a t o s e n s o r y tract function i n j u r y 4'7'1~

changes after experimental cord whereas the time course of

c h a n g e s in m o t o r t r a c t f u n c t i o n is n o t as well known3,8,14,15,28,31. T h i s s t u d y w a s d e s i g n e d to l e a r n the t e m p o r a l c o u r s e o f c h a n g e s o f e v o k e d e n d o r g a n p o t e n t i a l s ( m u s c l e v e r s u s c o r t e x ) in r e s p o n s e to m o t o r a n d s o m a t o s e n s o r y s t i m u l a t i o n a f t e r a light a n d s e v e r e spinal c o r d i n j u r y in rats.

Material and Method Thirty adult albino rats (weight 225-450 g) were anaesthetized by intraperitoneal injection of 80 mg/kg thiobutobarbital-Na. After a midline scalp incision a burr-hole 2mm posterior to the right coronal suture and 2 mm lateral to the sagittal suture, and a second burr hole 6 mm posterior to the first one were performed. Two steel screws 1,5 mm in diameter in these burr-holes served as electrodes. A thoracic laminectomy (T 10-12) with a diamond burr was done. The rectal temperature was monitored and kept between 35 ~ and 38 ~ with an infrared lamp. The injury was achieved by dropping a 5 g weight from 5 or 16cm height onto a metal impounder with 2 x 5 mm diameter. The impounder was placed directly on the dura. As a result, 10 animals were lightly injured (25 g-cm), 10 were severely injured (80 g-cm) and 10 were used as controls. Electrical stimulation of the motor cortex was done via the cranial screw electrodes, the rostral screw as anode, the caudal as cathode. 50-100 gsec square waves, intensity between 33-10mA were used. Muscle responses (muscle MEP) were recorded from two unipolar needle electrodes ((Pt-Ir, Nicolet) inserted into the left femoral muscle (cathode) and patellar tendon (anode). A needle electrode inserted into the back muscles was used as earth (Fig. I). Stimulation of the left sciatic nerve was done with two needle electrodes inserted near to nerve. Cortical recording of somatosensory evoked potentials

M. ZiMi and J. Schramm: M E P versus SEP in Experimental Cord Injury

141

Results

SEP recording

Normal MEP:

I'

cortical

trauma

stimulation

n

9

ii

stimulation

-

muscle 4, recording

MEP Fig. 1. Experimental set-up

(cortical SEP) was done from rostral screw electrode and a reference needle electrode inserted into the nasion. All MEP responses were recorded simultaneously using the channels of a Nicolet CA 1000 averaged after single stimuli. Only rarely 2~4 responses were averaged. For the cortical SEP 100 200 responses were averaged. 20 an 50 msec analysis times, 30-3000 Hz bandpass were used. All recordings were duplicated to confirm the reproducibility (Figs. 2 and 3). All animals were monitored for 4 hours after spinal cord injury and regular measurements were done before injury, immediately after (1 minute) and 15, 60, 120, 180, 240 minutes after injury (Figs. 5 and 6). For the SEP, the latencies of the first positive (P 1) and negative (N 1) peaks from cortical electrodes were measured. The onset latency of the muscle MEP response was also measured. Only the amplitudes between the maximal negativity and postivity was measured for both EP modalities. Latency and amplitude values of MEP and SEP were qualitatively scored. The score for amplitude values: 0 = no response; 1 = amplitude reduced more than 50% of initial value; 2 = amplitude reduced less than 50% or normal. The score for latency values: 0 = no response; 1 = latency delay greater than + 2 SD, 2 = latency delay less than + 2 SD or normal. M E P versus SEP, and also light injury versus severe injury were compared with chi-square analysis of these qualitative scores. Other than this, the latency and amplitude changes of both potentials in both injury groups were plotted in a percent ratio after considering the initial control measurement as 100% (Figs. 7 and 8). Additionally, the number of animals which have an M E P or SEP either normal or pathological were plotted against time after injury (Fig. 9). At the end o f the monitoring period the animals were killed with intracardiac KC1 injections. The injured segments of the spinal cord were removed, and fixed in 10% formaline solution. Longitudinal sections of the injured spinal cords and haematoxylene eosine stained cross sections showed that all animals with 80 g-cm injury had widespread central haemorrhages and petechial white matter haemorrhages. Animals with 25 g-cm injury had cord oedema and mild haemorrhages in the central cord.

A muscle response from contralateral hindlimb was observed in all animals (Fig. 2). In a few cases 2-4 averaging runs had to be used. Test-retest variability was very low. The latencies and amplitudes tended to be stable (Fig. 4). The observation period of the control animals was also 4 hours on average. Figure 4 shows minor changes in MEP and SEP data before and after laminectomy in control animals. The normal values and variablity of MEP in 30 animals were extensively described in another paper 32, the main results are briefly summarized here: Latency of first muscle MEP response: 6.1 4-0.9ms, amplitude 51.9 • 42gV. Latency of late muscle response 16 + 1.9ms (13/30 animals). Due to some evidence (response to tendon vi-

18.9

1 140 pV

! 20 ms 1 1.0

SEP- Cortical o

8.0

I

] 4gV 50 ms

Fig. 2. Typical examples of normal MEP and SEP. Late muscle response with 17.2 ms onset latency could well be observed. Positivity is downward in this and all other figures 8.8 17,:6

p~

] 125 ;V 20 ms

Fig. 3. An example of three early and late muscle MEP responses following single electrical cortical stimulation obtained shortly after another in the same animal

142

M. Zileliand J. Schramm: MEP versus SEP in ExperimentalCord Injury ms

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There was no significant latency delay of MEPs in both injury groups if MEP were preserved after injury (Fig. 7). Severe injury caused loss of SEPs in all animals, thus demonstrating the adequacy of the 80 g-cm injury. Light injury, however, caused a mean latency delay of cortical SEP reaching 190% of the initial values. MEP latencies, in contrast, did only show some fluctuations about the pre-injury levels. Analysis of the qualitative score of the latencies showed that MEP latency scores were significanlty higher, i.e. showed less affection of MEP by light trauma than SEP. Comparing severe and light injury latency scores showed that MEP scores were significantly higher, i.e. showed much less trauma effects in the light injury group than the severe injury group. Late muscle MEP scores suggest that they start to recover, but small numbers do not allow one to prove such a conclusion. Cortical SEP latency scores were also higher as with MEP scores, because there was no animal with preserved cortical SEP in the severe injury group.

1 D

Fig. 4. Graphic displayof MEP and SEP valuesin 10controlanimals during the 4 hours monitoringperiod

bration and increasing stimulus intensity) it was suggested in that same paper ... "that this is the result of a reflex response caused by the first/early descending volley and similar to the mechanism in the H-reflex ''32.

Normal SEP: Cortical SEP had a first positivity (P1) at 9.1 4- 1.2ms and a first negativity (N 1) at 13 4- 1.6ms (Fig. 2). The amplitude of the cortical SEP between P 1 and N 1 was 4.2 + 3.7 gV. A typical example of the monitoring series in both modalities from the respective end organs in the same animal after light (25g-cm) cord injury is shown in Fig. 5. Early muscle MEP persisted throughout the observation period after injury. An amplitude increase of MEP after injury could also be seen. Cortical SEP was deformed after injury, lost the normal " W " configuration, and no response could be recorded at 240 minutes. In one animal with severe (80 g-cm) spinal cord injury, cortical SEPs were lost immediately after injury and never recovered (Fig. 6). MEP, however, recorded after the 60th minute interval with some latency delay.

Amplitude analysis: Figure 8 compares the changes of amplitude of muscle MEPs and cortical SEPs in both injury groups. MEP amplitudes in the light injury group reached about 200% of the initial value at the 2rid hour interval after injury. The SEP amplitudes in the same group were also increased in the last hours. The light injury group, i.e. the incomplete lesion, thus showed a surprising increase of end organ EP amplitudes especially with MEPs. Comparing MEP versus SEP, amplitude scores showed that MEP amplitudes recovered better than SEP amplitudes in the light injury group (p < 0.05 at 60, 120 and 240th minutes). In the severe injury group, however, since all cortical SEPs were lost; it was impossible to make a comparison with MEPs. Of the animals with light injury, MEP amplitude changes alone were seen in seven animals, amplitude plus latency changes in one. There were two animals which had latency changes alone. Among the severely injured animals four had only amplitude changes, one had only latency changes and none had both parameters changed.

Presence of waves." Plotting the number of animals having a preserved MEP or SEP (either normal or pathological), the cortical SEP of the severe injury group have the poorest

M. Zileli and J. Schramm: MEP versus SEP in Experimental Cord Injury MEP - muscle

143

SEP - cortical Preinjury

~r~d~tely alter injury

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240minutes Fig. 5. Muscle MEP (left) and cortical SEP (right) after subjecting the spinal cord to a 25 g*cm impact injury

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Preinjury

Immediately after injury

15minutes 60minutes 120minutes 180minutes 240 minutes

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record and the muscle MEP of the light injury group have the best record (Fig. 9). This means that severe spinal cord injury depresses all cortical SEPs. Light spinal cord injury, however, causes disappearance of a large part of SEPs, while almost all of the MEPs remain. In the severe injury group, five animals were dead by the 4th post-injury hour. Figure 10 compares MEP

Fig. 6. Muscle MEP (left) and cortical SEP (right) after subjecting the spinal cord to a 80g-cm impact injury

data between those five animals which survived till the end of the experiment and those which did not. The lines showing the numbers of animals with preserved MEPs have identical curves. Despite the difficulty of making a statistical comparison because of small numbers, it can be said that MEPs of five surviving animals did not look different from those which did not survive.

144

M. Zileli and J, Schramm: M E P versus SEP in Experimental Cord Injury amplitude

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Fig. 7. Latencies plotted versus time post-injury for muscle M E P and cortical SEP. Pre-injury values were used as 100%. The numbers in parentheses give the number of animals which had an evoked response at this time. In severe injury group 3 animals at 3rd hour and 5 animals at 4th hour were dead. Dotted line represents the light injury, straight line the severe injury

b-on. after

9 80 gm-cmmean

15'

60

120'

9 25 gm~cmmean

180'

240" minutes after trauma

Fig. 8. Amplitudes plotted versus time post-injury for muscle M E P and cortical SEP. Pre-injury values were used as 100%. The numbers in parentheses give the number of animals which had an evoked response at this time point

TRAUMA ~'

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Fig. 9. N u m b e r of animals with preserved muscle M E P (early answer) and cortical SEP (either normal or pathological). The numbers in parentheses show the total number of animals which could be monitored at this time point

M. Zileli and J. Schramm: MEP versus SEP in Experimental Cord Injury

No of animals with

H

animals which survived

o----.o

animals which did not survive

3

2

i

immed. after trauma

15"

60"

120"

180"

0

240"

Fig. 10. Graph comparing MEPs of animals which died before the end of experiment (n = 5) and those which did not (n = 5). The numbers in parentheses show the total number of animals which was monitored at this time point

Discussion

Considering the experimental model, it is well known that 80 g-cm impact injury causes paraplegia or severe paraparesis in rats, while 20 40g-cm injury causes transient paraparesis lasting 12-24 hours 22'25. Since examination of the pathological specimens confirmed that 80 g-cm impact is a severe injury, no postinjury clinical examination was done. Comparison of both EP modalities shows that with a severe degree of injury cortical SEP was more sensitive (i.e. was lost more frequently and earlier) than muscle MEP. In mild injury MEP gave an even increased amplitude, i.e. as judged by the score MEP tolerated the injury better than SEP. Concerning the value of EP changes for clinical monitoring, it is at first glance not easy to describe the time course and degree of changes which would serve the purpose of intra-operative monitoring best. If an EP modality is lost rapidly or persists too long compared to the degree of injury, it would not be very helpful. The background of this study was not to evaluate MEP as a substitute for SEP in monitoring, but to delineate the time course of typical MEP changes with regard to monitoring, since in the clinical setting using both modalities would be preferable to using only one.

MEP was introduced as an additional monitoring tool in spinal cord injuries clinically and intra-

145

operatively, following several laboratory studies 3' 8,14--16,24,28,31, Levy etal. (1986) have compared SEP and MEP in a cat spinal cord injury model and have reported that both sciatic nerve and spinal cord MEP responses were more sensitive to injury than SEP responses 15. They have, however, recorded MEP with averaging methods and not single stimuli, and have used different recording and stimulation methods. Baskin and Simpson (1987) have compared SEP and MEP in a rat model 3 with two recordings only in the first hour after injury and averaging 50 responses. They suggested that muscle MEP was more sensitive to spinal cord injury than cortical SEP. We found, contrary to these two studies 3'15, that cortical SEPs are more sensitive to light spinal cord injury in rats than muscle MEPs elecited with single electrical cortical stimulation. But these contradictory findings do not mean that MEPs are of no value for monitoring. Some different features of MEPs should not be forgotten; unimportance of latency measurements, amplitude increase after inury, and a relatively high frequency of false positive responses. One of the common features of the other studies is the use of averaging techniques 3' 15.28. Levy et al. (1984) have shown that averaging may cause attenuation of MEP 16. The assumption that with non-averaging techniques MEP is a less sensitive technique for monitoring purposes, should be further investigated. "Less sensitive" does not mean useless: 1) MEP represents another, even more important pathway, 2) Even if SEPs are lost, the persisting MEPs may still be used as monitor, 3) During SEP monitoring in neurosurgery, a relatively high proportion of cases showed such poor quality SEP (due to the presence of a cord lesion) that useful monitoring could not be applied 26. If MEP in such a situation would be available, monitoring could be done. Zentner (1988) has reported that during intra-operative MEP monitoring with single stimulus technique about 20% false positive results (i.e. MEP loss without clinical deficit) were found ~1. Our results cannot be compared directly with those obtained from humans, because the motor tract in the rat is located in the center of the cord 3~ The wellknown central location of cord necrosis after the weight-dropping injury makes it even more remarkable that in this rat study the MEPs were better preserved than SEP. Slight fluctation of MEP amplitudes during the observation period of control animals might either be due to decreasing level of anaesthesia or metabolic factors. But the amplitude increase of more than 50% seen in

146

M. ZiMi and J. Schramm: MEP versus SEP in Experimental Cord Injury

traumatized animals is difficult to explain by these two factors. Although at different time points and with different characteristics, the amplitude increase of MEPs following injury was, nevertheless, prominent. The amplitude increase after injury in animal experiments was also described for spinal MEP 14, for spinal SEPs from the distal isolated cord segment 4, and also for spinal MEPs after middle cerebral artery occlusion 29. This phenomenon might be due to; 1) the development of an "evoked injured potential", 2) increase in excitability of axons as a result of hypoxia or hypoperfusion, 3) selective suppression of an inhibitory system by hypotension, hypoxia or anaesthetics 14. Konrad etal. have reported an increase in amplitude during the critical first two minutes ofischaemia 13. It might also occur as a result of the injury MEP modulating system in anterior horn neurones. Despite these suggestions, to explain the amplitude increase of muscle MEPs seems to be more difficult. This amplitude increase after injury may be a disadvantage, because it can cause misinterpretation as an "improvement", whereas in fact usually a deterioration occurs therafter. It was suggested that the latency changes in the cord and peripheral nerve response are not as useful as amplitude changes in terms of providing adequate detection of injury ~3. This seems also true in the light of MEP findings of this study.

Acknowledgements This work was supported by a grant from the Deutsche Forschungsgemeinschaft (Schr 285/1-2) and Dr. M. ZiMi was supported by Alexander yon Humboldt Foundation, Bonn, Federal Republic of Germany.

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M. Zileli and J. Schramm: MEP versus SEP in Experimental Cbrd Injury 26. Schramm J: Spinal cord monitoring (1985) Current status and new developments. CNS Trauma 2:207-227 27. Schramm J, Krause R, Shigeno T, Brock M (1983) Experimental investigation on the spinal cord evoked injury potential. J Neurosurg 59:485-492 28. Simpson RK, Baskin DS (1987 a) Corticomotor evoked potentials in acute and chronic blunt spinal cord injury in the rat: correlation with neurological outcome and histological damage. Neurosurgery 20:131-137 29. Simpson RK, Baskin DS (1987 b) Early component changes in corticomotor evoked potentials following experimental stroke. Stroke 18:1141-1147 30. Zeman W, Innes JRM (1963) Chraigie's neuroanatomy of the rat. Academic Press, New York 3 I. Zentner J (1988) Intra- und perioperatives Monitoring mit too-

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torisch evozierten Potentialen nach transkranieller elektrischer Cortexstimulation bei neurochirurgischen Eingriffen am R/ikkenmark. Poster Presentation, 39. Jahrestagung der Deutschen Gesellschaft ffir Neurochirurgie, K61n, May 8-11 32. ZiMi M, Schramm J (1989 a) Spinale und muskul6se Reizantwort nach Einzelreizung des motorischen Cortex der Ratte. Z EEG-EMG, 20:106-111 33. Zileli M, Taniguchi M, Cedzich C, Schramm J (1989 b) Vestibulospinal evoked potential versus motor evoked potential monitoring in experimental cord injuries of cats. Acta Neurochir (Wien) I01:141-148 Correspondence and Reprints: Johannes Schramm, M.D., Neurosurgical Clinic, University of Bonn, Sigmund-Freud-Strasse 25, D-W-5300 Bonn-Venusberg, Federal Republic of Germany.