Motor and Somatosensory Evoked Potentials in a
Primate Model of Experimental Spinal Cord Injury
M.J. Arunkumar, K.Srinivasa Babu, M.J. Chandy
Department of Neurological Sciences
Christian Medical College and Hospital
Vellore - 632 004, India.
Summary
Motor and somatosensory evoked potentials (MEP and SSEP) were compared after
experimental spinal cord injury in Bonnet monkeys (macaca radiata). The MEP and SSEP
changes following graded injuries were related to clinical outcome. Eight healthy mature
monkeys with a mean weight of 4.2 + 0.9 Kg were chosen for the study. Graded spinal cord
injury was caused using 50, 100, 200, 300 gm-cm force by modified Allens weight drop
device. MEP and SSEP recordings were done before injury and at 0, 2, 4 and 6 hours after
injury and on the 7th postoperative day. Neurological assessment was done at 24 hours and
on the 7th day following injury. 50, 100, 200 gm-cm force caused partial injuries and 300
gm-cm force caused severe spinal cord injury. The predictive value of MEP and SSEP
following partial injuries was 80% and 66.67% respectively. Both MEP and SSEP were
100% predictive in severe injury. MEP and SSEP monitoring can therefore be
complementary to each other in predicting the neurological outcome in partial injuries to
the spinal cord.
Key words : Evoked potentials, Spinal cord injury, Primate model.
Neurol India, 2001; 49 : 219-224
Introduction
Evoked potentials are valuable tools in assessing the
functional status of the nervous system. It is vital to
monitor the motor system as the blood supply and its
anatomical location are different from that of the
sensory system in the spinal cord. Somatosensory
evoked potentials (SSEP) have been used in the past
as an indicator for predicting the outcome following
spinal cord injuries.
1-6
However, some studies have
also demonstrated that the presence of a normal SSEP
may not be associated with normal power,
2,5,7,8
while
others have shown that SSEP changes did not predict
recovery of motor function.
9,10
There have been
various reviews on spinal cord injuries in non-
primates which showed motor evoked potential
(MEP) to be a more sensitive measure of post injury
motor performance.
11-18
We performed graded spinal
219Neurology India, 49, September 2001
Correspondence to : Dr. M.J. Chandy, Department of
Neurosurgery, Indo-American Brain and Spine Centre,
Vaikom - 686 143, Kerala, India.
E-mail : bcf@satyam.net.in
ORIGINAL ARTICLE

cord injury in primate model and analysed the signal
changes in MEP and SSEP to determine their
reliability as predictors of outcome.
Material and Methods
Eight young mature and healthy Bonnet monkeys
(macaca radiata) of either sex were chosen for the
study. Anaesthesia was induced and maintained by Inj.
ketamine hydrochloride 15 mg/kg, intramuscular for
induction, and 10-15 mg/kg/hr, intravenous as
maintenance. Continuous invasive arterial blood
pressure using the femoral artery, pulse rate, rectal
temperature and SaO
2
were monitored.
The animal was placed prone on the operating table.
A mid thoracic laminectomy was performed under
aseptic conditions to expose the dura over the spinal
cord. Bipolar epidural electrodes were placed two
segments cranial and caudal to the proposed site of
injury and the motor evoked potentials (MEP) and
somatosensory evoked potentials (SSEP) prior to
injury were recorded. For obtaining MEPs, the
stimulating electrode was placed at the vertex (anode)
with the reference (cathode) at the forehead.
Transcranial electrical stimulation (Digitimer-185)
was used at 220 V. The recording was done using
bipolar epidural electrode caudal to the proposed site
of the cord injury. For obtaining SSEP, the posterior
tibial nerve was stimulated percutaneously just above
the motor threshold. The recording was done using
bipolar epidural electrodes which were placed cranial
to the proposed site of injury. The stimulus was a
square pulse of 100 microsecond at 7.5 mA at 4.7Hz.
600 responses were averaged using a Nicolect Viking
IV.
The cord injury was produced by Allen s weight drop
method (1911) modified by us using a caliberated
electromagnetic device and galvanometer operated by
a 6 volt battery to provide uniformity of contact time
during injury.
19
After a midthoracic laminectomy, 25
gm weight which was held by a electromagnet was
dropped from a predetermined height on to the cord
through a caliberated tube. The galvanometer was
used to lift the weight from the cord after a contact
time of 50 msec. The weight dropped from a height of
2, 4, 8 and 12 cm, gave a 50, 100, 200 and 300 gm-cm
force respectively. Two monkeys were used for each
of these above mentioned categories. MEPs and
SSEPs were recorded at 0, 2, 4 and 6 hours after injury
and on the 7th post operative day. The 7th day
recordings were done by reanaesthetising the animal
with Inj. ketamine hydrochloride, 15mg/kg
intramuscularly, after assessing the neurological status
or muscle power in the lower limbs.
Motor power in the lower limbs was graded using
Tarlov scale modified by Ducker et al in 1978.
20
Grade 0 : Paraplegia
Grade 1 : Minor movements at the joints.
Grade 2 : Major movements at the joints but inability
to stand.
Grade 3 : Animal can stand and possibly walk.
Grade 4 : Animal can run and has a normal motor
system with no obvious weakness.
Statistical Analysis
Predictive value was calculated using the formula:
True positive/ (true positive + false positive) x 100. In
partial injuries true positives were those where the
waveforms became normal (+) at 6 hours following
injury and motor status corresponded to grade 3 or
above. False positives were those in which the
waveforms were normal (+) at 6 hours after injury, but
motor power was grade 2 or less on the 7th post
operative day (Table I). For uniformity in analysis, the
value which indicated less than 5% change over the
baseline value in either latency or amplitude in
MEPs and SSEPs were taken as Normal
(Table II A - D). In severe injuries true positive
corresponded to recordings of waveform being
negative at 6 hours following injury and the motor
power grade 0 or plegic at the end of one week.
Results
Neurological Outcome
50 to 200 gm-cm force (n=6) caused partial injuries
(paretic or grade 1 - 4). 300 gm-cm force (n=2) caused
severe injury (plegic or grade 0), which remained so at
the end of one week. The motor power was grade 3 or
more in 4 out of the 6 monkeys, and grade 2 in the
remaining two monkeys with partial cord injuries
(n=6) on assessment at the end of one week.
Partial Injuries
(a) Motor evoked potentials : Latency (Table IIA) :
Percentage changes in MEP latency was prominent
(prolonged latency) at the end of the second hour after
injury with 50 and 100 gm-cm force. 200 gm-cm force
produced notable changes soon after injury. Signal
changes in one primate (case 6) failed to recover at the
sixth hour, and remained so at the end of one week
following injury with a 200 gm-cm force.
Amplitude (Table IIB) : Marked changes in MEP
220
MEP and SSEP in Experimental Spinal Cord Injury
Neurology India, 49, September 2001

amplitude (a decrease in amplitude) were seen in the
initial hours with partial injuries to the cord (ie. at
zero and 2 hours). This indicated that in almost
every case of partial injury a distinct change in the
amplitude can be expected. The reversal of the MEP
amplitude was seen from four to six hours after injury,
except for one case (no. 6), which did not recover to
the baseline values even at the end of one week.
(b) Somatosensory evoked potentials : Latency
(Table IIC) : A uniform change in the SSEP latencies
(an increase in latent period) was observed with
partial injuries in all cases, irrespective of the force
used. Reversal of the latency changes was seen in only
50% of the cases (3/6 primates) towards the end of 6
hours. In the 200 gm-cm force group (cases 5 and 6),
there was no recovery of the latency at the sixth hour
or even at one week following injury. The SSEP
waveforms seemed to be susceptible to greater
magnitude of force within partial injuries, though the
animals were only paretic (and not plegic ) on
clinical assessment done at the end of one week
(Table I).
Amplitude (Table IID) : Uniform decrease in SSEP
amplitude was noticed irrespective of the force used.
Similar to the changes in SSEP latencies with 200 gm-
cm force (cases 5 and 6), there was no recovery in the
amplitude inspite of some motor response seen at 6
hours and one week following injury.
An illustrated example of a partial injury : (50 gm-cm
force) : The changes in MEP and SSEP signals with
50 gm-cm force (case 1) have been reviewed (Fig. 1).
The baseline (before injury) latency value obtained in
SSEP for the PlN1 complex was 7.2 msec. Soon
221
Arunkumar et al
Neurology India, 49, September 2001
Table I
MEP, SSEP and Neurological Status Following Partial Spinal Cord Injuries (50,100 and 200 gm-cm force).
S.No Force Evoked BI Time after injury Power
(gm-cm) Potential 0 2 4 6 1 24 1
Hr Hr Hr Hr Week Hr. Week
1. 50 MEP + A A + + + 3 4
SSEP + A A A A +
2. 50 MEP + A A A + + 2 4
SSEP + A A A + +
3. 100 MEP + A A + + + 1 2
SSEP + A A A + +
4. 100 MEP + A A A + + 2 3
SSEP + A A A + +
5. 200 MEP + A A A + + 2 3
SSEP + A A A A A
6. 200 MEP + A A A A A 1 2
SSEP + A A A A A
+ : Normal wave form A : Abnormal wave form BI : Before Injury
Table IIA
MEP Latency (Percentage Changes) in
Partial Injuries, n = 6
Force Time after injury
(gm-cm) 0 2 4 6 1
Hr. Hr. Hr. Hr. Week
50 3.6 9.0 1.8 0 0
50 4.3 13.8 7.2 2.2 1.4
100 9.2 12.4 3.9 3.3 2.6
100 3.1 10.2 5.5 2.4 1.6
200 19.6 13.0 10.9 1.4 0.7
200 11.5 14.1 24.4 26.9 23.0
Table IIB
MEP Amplitude (Percentage Changes) in
Partial Injuries, n = 6
Force Time after injury
(gm-cm) 0 2 4 6 1
Hr. Hr. Hr. Hr. Week
50 77.7 83.0 2.7 1.8 0.9
50 37.5 21.7 17.2 2.4 2.1
100 29.8 22.1 3.8 2.8 0.3
100 24.7 28.9 12.0 3.2 1.4
200 80.0 63.8 33.6 2.5 3.6
200 58.1 22.3 33.2 34.1 33.6

after the injury (0 hour) it increased to 7.7 msec
(6.9% change). At 2, 4 and 6 hours following the
injury, the latency prolonged to 8.4, 8.9 and 9.2 msec
(ie. a 16.7%, 23.6% and 27.8% change) respectively.
The amplitude of the P1N1 complex decreased to a
certain extent. It was 8.9 µ V before injury. At 0 hour
after injury the amplitude was 8.1µ V (9% change or
decrease in amplitude); at 2, 4 and 6 hours the
amplitude remained low at 7.5 uV (a 15.7% change or
decrease), but reversed to normal only at the end of
one week.
The baseline (before injury) latency of the D wave in
MEP recording was 5.5 msec. At 0 and 2 hours
following injury, it prolonged to 5.7 and 6.0 msec
(3.6% and 9% change) respectively. At the end of 6
hours, the latency reversed to normal. Nevertheless,
the changes in MEP amplitude was well established.
Before injury, the amplitude of the D wave was 11.2
µ V. The amplitude at 0 and 2 hours decreased to 2.5
µ V and 1.9 µ V (a 77.7% and 83% change or decrease
in amplitude) respectively. At the end of 4 hours, it
reversed to 10.9 µ V (a 1.8% change or decrease) and
became almost normal (11.0 µ V) at 6 hour time
intervel (0.9% change). A change in percentage to less
than 5% of the baseline values (latency or amplitude)
were considered normal.
Severe Injury
300 gm-cm force weight drop (n=2) caused severe
injury. The motor power was grade 0 at 24 hours
following injury and remained so even on the 7th post
operative day. Both MEPs and SSEPs did not reappear
at the end of one week.
Predictive Value
In partial injuries, the predictive value of MEP was
80% and SSEP was 66.67%. In severe injury, the
predictive value of both the MEP and SSEP were
100%.
Discussion
Activation of the motor system either by direct
stimulation of the brain or spinal cord with recording
from either the spinal cord or the peripheral nerve
produce reproducible and reliable waveforms (MEP),
which indicates the degree of dysfunction of the
nervous system.
13,14
It is known that the D wave in
MEP signifies direct stimulation of the pyramidal tract
neurons which is much more consistent and recovers
faster, both in amplitude and latency than the I wave,
which are generated by relayed excitation of
pyramidal neurons through cortical interneurons .
16
In experimental spinal cord injury, it has been proven
that MEP obtained from the spinal cord below the
lesion was found to be a significant correlate of the
ambulation recovery , though signals obtained from
222 Neurology India, 49, September 2001
MEP and SSEP in Experimental Spinal Cord Injury
Table IIC
SSEP Latency (Percentage Changes) in
Partial Injuries, n = 6
Force Time after injury
(gm-cm) 0 2 4 6 1
Hr. Hr. Hr. Hr. Week
50 6.9 16.7 23.6 27.8 1.4
50 4.2 21.1 18.3 4.2 2.8
100 2.4 6.4 5.6 3.2 2.4
100 2.8 5.7 7.5 1.8 13.2
200 2.4 7.3 11.0 29.3 25.6
200 2.1 10.6 17.0 42.6 36.2
Table IID
SSEP Amplitude (Percentage Changes) in
Partial Injuries, n = 6
Force Time after injury
(gm-cm) 0 2 4 6 1
Hr. Hr. Hr. Hr. Week
50 9.0 15.7 15.7 15.7 1.1
50 3.1 15.6 10.4 2.1 1.0
100 4.0 10.0 8.0 2.0 4.0
100 5.1 14.1 12.8 3.8 23.1
200 9.8 22.0 41.5 58.5 70.7
200 11.5 17.3 28.9 38.5 42.3
Fig. 1 : SSEPs and MEPs in case 1 showing EP signal
changes following injury with 50 gm-cm force. Note the
recovery of the latency in SSEP seen on 7th day following the
injury; recovery of latency and amplitude in MEP were seen
at 4 hour time interval.

the peripheral nerve (EMG) were equally sensitive. In
motor evoked potentials, changes in amplitude were
gross and therefore these were found to correlate well
with the degree of neurological dysfunction and
histological damage.
12,15,17,18, 21
On the other hand, somatosensory evoked potentials
are being used for predicting outcome in experimental
studies and in humans.
1-4,12,22
It is known that
somatosensory evoked potentials can be of limited use
in predicting spinal cord injury, as they are transmitted
primarily by the dorsal columns, and hence do not
reflect the integrity of the important ventral motor
pathways. The blood supply and the location of the
dorsal column are also different from that of the
corticospinal tract, and therefore ischaemic changes
do vary in these tracts.
2,5,7-10
However, it is interesting to note that there is a set of
second order fibers that send collaterals to the dorsal
column nuclei. This pathway has been located outside
the dorsal column in the dorsolateral fasciculus of the
spinal cord. They consist of axons arising from the
region of the spinal cord above the lumbar
enlargement.
23-25
These dorsolateral fibres transmit
more or less the same information as the ascending
dorsal column pathway, but end in the reticular region
of the dorsal column nuclei.
23,25,26
The presence of
this pathway indicates that the dorsal column nuclei
are not totally deafferented by sectioning the dorsal
columns or injury to it, as there is an alternate pathway
carried by the dorsolateral fasciculus.
27
Therefore, if
an injury to the spinal cord is mild or if it occurs in the
midline with relatively less force transmitted to the
lateral fasciculus, there is a possibility that the cortico
spinal tract be damaged relatively more when
compared to the ascending dorsal column tracts,
which is found in the outer aspect of the dorsolateral
fasciculus. This perhaps provides an explanation, why
SSEP signals are not completely lost sometimes,
though, there is a significant impairment in motor
power.
In the present study, we found that partial injuries
produce changes in both amplitude and latency of the
MEPs. However, the amplitude changes were very
marked as compared to changes in latency, especially
at zero and 2 hours following injury. Both latency and
amplitude of the MEPs had a significant correlation
with the recovery in partial injuries, but were not
100% predictive. MEPs reversed almost in all except
one (l/6) at the end of 6 hours, thus having a predictive
value of 80% at the end of one week. It was also seen
that the predictive value of SSEP was about 66.67%.
The latency of the SSEP in partial injuries was
prolonged more than MEP, though the latency had
reversed at the end of one week following the injury.
Nevertheless, MEP and SSEP monitoring could still
be ideal prognostic indicators of post injury
neurological recovery, as long as they are used
complementary to one another, because the MEP
signals by itself were 100% predictive with partial
injuries in primates. Not much significance was
achieved in motor and sensory evoked potential
monitoring in the case of severe cord injuries as both
of them were 100% predictive of the clinical outcome.
Conclusions
In a primate model of spinal cord injury, the predictive
value of MEP was 80% and SSEP 66.67% (partial
injuries); MEP and SSEP signals were cent percent
predictive of the outcome in severe injuries. MEP
signals, especially the amplitude were found to be
highly sensitive to changes in the cord following
partial injuries to the spinal cord. Percentage changes
of both MEP and SSEP must be precisely monitored
as they can be complementary to each other in
predicting the final neurological outcome.
Acknowledgement
The authors would like to thank the FLUID Research
Committee of the Christian Medical College, Vellore
for financial assistance to carry out this study.
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Accepted for publication : 20th July, 2000.