J Neurosurg 99:575–578, 2003

Neurophysiological criteria for intraoperative prediction of

pure motor hemiplegia during aneurysm surgery

Case report

ANDREA SZELÉNYI, M.D., ADAURI BUENO DE CAMARGO, M.D., EUGENE FLAMM, M.D.,
AND VEDRAN DELETIS, M.D., PH.D.

Division of Intraoperative Neurophysiology, Adult Neurosurgery, Hyman–Newman Institute for

Neurology and Neurosurgery, Beth Israel Medical Center, New York, New York

The value of motor evoked potentials (MEPs) as an intraoperative neurophysiological monitoring tool for detect-
ing selective subcortical ischemia of the motor pathways during intracerebral aneurysm repair is described and the use
of such measures to predict postoperative motor status is discussed.
The authors present the case of a 64-year-old woman in whom there was an incidental finding of two right middle
cerebral artery (MCA) aneurysms. During the aneurysm clipping procedure, an intraoperative MEP loss in the left ab-
ductor pollicis brevis and tibial anterior muscles occurred during an attempt at permanent clip placement. There were
no concurrent changes in somatosensory evoked potentials. Postoperatively, the patient demonstrated a left hemiple-
gia with intact sensation. A computerized tomography scan revealed an infarct in the anterior division of the MCA ter-
ritory, including the posterior limb of the internal capsule.
In this patient, intraoperative neurophysiological monitoring with MEPs has been shown to be a sensitive tool for
indicating subcortical ischemia affecting selective motor pathways in the internal capsule. Therefore, intraoperative
loss of MEPs can be used to predict postoperative motor deficits.

KEY WORDS • cerebral aneurysm • direct cortical stimulation •

intraoperative monitoring • motor evoked potential • transcranial electrical stimulation

URING cerebrovascular procedures, intraoperative Case Report

D neurophysiological monitoring commonly uses

SSEPs, which provide real-time data to forewarn
the surgeon of imminent ischemia.8,18 This SSEP monitor-
ing is limited in its ability to assess ischemia in cortical ar-
eas outside the vascular supply of the somatosensory cortex
or its pathways. This limitation has led to several reports
of false-negative results in which—despite intraoperative-
ly unchanged SSEPs—the postoperative motor status had
deteriorated.3,8,9,14 The term “pure motor hemiplegia” was
coined by Fisher and Curry7 who defined it “as a total or
severe hemiplegia affecting face, arm and leg, unaccompa-
nied by somatosensory signs, visual field defect, dysphasia,
dyspraxia, or nondominant apractognosia.”
The advent of intraoperative MEP monitoring, which us-
es a multipulse stimulation method, allows for intraopera-
tive assessment of the functional integrity of the motor cor-
tex and the motor pathways.3,16,19 The intraoperative use of
MEPs might be the monitoring modality of choice in pa-
tients who undergo procedures for which there is a risk of
developing a lesion that could cause a pure motor hemiple-
gia.15
Abbreviations used in this paper: CT = computerized tomogra-
phy; DCS = direct cortical stimulation; MCA = middle cerebral
artery; MEP = motor evoked potential; SSEP = somatosensory
evoked potential; TES = transcranial electrical stimulation.
Clinical Presentation. This 64-year-old woman with no
neurological deficits presented with an incidental finding of
two right MCA aneurysms. The first aneurysm was located
at the proximal M1 segment in front of the MCA bifurcation
(15 mm in diameter) and the second was found at the right
MCA bifurcation (6 mm in diameter). The patient’s medical
history was remarkable for noninsulin-dependent diabetes
mellitus during the 3 years before admission. Elective sur-
gical treatment for clip occlusion of the aneurysms was per-
formed after a condition of mild hypothermia had been in-
duced (the patient’s lowest body temperature was 32.8˚C).
Anesthesia. Anesthesia was induced with bolus doses of
propofol (200 g/kg), fentanyl (250 g), midazolam (2
mg), and the short-acting muscle relaxant Cisatracurium
(20 mg) for intubation purposes, and was further main-
tained with propofol (100 g/kg/min) and fentanyl (0.5 g/
kg/hr).
Neurophysiological Monitoring Methods. For stimulation
and recording of evoked responses, a modified Axon Senti-
nel 4 EP Analyzer (Axon Systems, Inc., Hauppauge, NY)
was used. For cortical and subcortical median and posterior
tibial nerve SSEP recordings, corkscrewlike needle elec-
trodes (model CS; Nicolet Co., Madison, WI) were subcu-
taneously placed at FZ (reference), C3, C4, Cz, and at
Cv1 (International 10–20 EEG System). Stimulation pa-

J. Neurosurg. / Volume 99 / September, 2003 575


FIG. 1. Tracings showing results of intraoperative monitoring of
MEPs and SSEPs (SEP). Bilateral median nerve SSEPs and MEPs
elicited by DCS were performed for intraoperative monitoring dur-
ing the clip occlusion of the right MCA aneurysm. L APB = left ab-
ductor pollicis brevis muscle; L Med = left median nerve SSEPs;
PC = permanent clip application; R Med = right median nerve
SSEPs; SuDe = clipping of the aneurysm in a modified suction de-
compression technique; TC = temporary vessel occlusion of the
right MCA.
rameters consisted of constant-current, square- wave pulses
(median nerve stimulation 40 mA [max], 0.2-msec pulse
duration, 8.1-Hz stimulation rate; tibial nerve stimulation
40 mA [max], 0.5-msec pulse duration, 4.3-Hz stimulation
rate). Signals were amplified
40,000, recorded within a
100-msec epoch length, and filtered (bandpass 30–300 Hz).
A mean of 200 sweeps was completed per response.4 A re-
duction in cortical SSEP amplitudes of more than 50% from
baseline responses was considered to be a significant warn-
ing sign.
For TES, corkscrewlike electrodes were placed subcuta-
neously at C1()/C2() for left and at C2()/C1() for
right hemispheric stimulation. For DCS, a strip electrode
with eight contacts (each 0.5 cm in diameter) was placed
subdurally perpendicular to the central sulcus. The contact
with the lowest stimulation intensity to elicit a contralateral
muscle response was chosen for continuous stimulation.
For eliciting MEPs, multipulse (train of five stimuli, sin-
gle-pulse duration 0.5 msec, interstimulus interval 4 msec)
anodal stimulation (200 mA [max] for TES; 20 mA [max]
576
A. Szelényi, et al.
for DCS) was applied at a repetition rate of 2 Hz. The MEPs
were recorded using needle electrodes inserted bilaterally
in the abductor pollicis brevis and tibialis anterior muscles
as well as in the left extensor digitorum communis and left
biceps brachii muscles. The signals were recorded within a
100-msec epoch, filtered (bandpass 1.5–853 Hz), and am-
plified
10,000. The loss of the MEP response was con-
sidered to be a warning sign.
All SSEP and TES–MEP recordings were present at
baseline. After opening the dura mater and placing the strip
electrode, a repeatable response from the left abductor pol-
licis brevis muscle with an amplitude of 400 V was elicit-
ed with DCS by using a stimulation intensity of 20 mA.
This intensity was then used for continuous monitoring, and
MEPs elicited by TES were intermittently performed for
control assessment of the unaffected hemisphere and for the
left tibialis anterior muscle.
Neurosurgical Treatment. A right frontopterional ap-
proach was performed. After 6 minutes of uneventful tem-
porary vessel occlusion of the right MCA, a permanent clip
was placed on the larger, proximal aneurysm. A decrease
in the MEP amplitude of the left anterior pollicis brevis
muscle followed. When we replaced the permanent clip, a
loss of the left anterior pollicis brevis muscle response for
approximately 3 minutes occurred; SSEP amplitudes re-
mained unchanged throughout. The MEP response did not
recover with the removal of the temporary clip (total occlu-
sion time 15 minutes), but the response improved with the
removal of the permanent one (Fig. 1). After allowing for
reperfusion of the right MCA, a second temporary clip
placement (total occlusion time 17 minutes) was performed
and an attempt to place a permanent clip resulted in MEP
loss from the left anterior pollicis brevis muscle. While
MEPs from the right anterior pollicis brevis and tibialis an-
terior muscles remained, MEPs could not be elicited with
DCS or TES for the muscles of the left upper and lower ex-
tremities.
Because the arteriosclerotic aneurysm wall prevented the
clip from closing completely, a modified suction decom-
pression procedure was performed in combination with
temporary clip placement. This resulted in complete oc-
clusion of the aneurysm neck. After the final permanent clip
placement, a temporary decrease in both the left median
and right median SSEP amplitudes was observed (13 and 5
minutes, respectively). A Doppler signal was obtained from
the proximal and distal M1 branches as well as all of the M2
branches. Inspection of the permanent clip position and the
back wall of the aneurysm showed no compromised per-
forating vessels. During the clipping procedure, vital signs
were unchanged; the blood pressure was 130/60 mm Hg,
which was increased to 160/80 mm Hg after the MEP loss.
The second, smaller aneurysm was occluded without fur-
ther SSEP changes.
Postoperative Course. Postoperatively, the patient imme-
diately presented with a left hemiplegia and reacted with
eye opening to painful stimuli applied to her left side. The
postoperative CT scan (performed immediately postsur-
gery) demonstrated a loss of normal gray-white matter dis-
tinction within the anterior division of the right MCA ter-
ritory, including the posterior limb of the internal capsule.
The follow-up CT scans confirmed the presence of an
infarct within this distribution (Fig. 2). The patient still suf-
J. Neurosurg. / Volume 99 / September, 2003
Intraoperative MEP loss as predictor of postoperative hemiplegia
FIG. 2. Head CT scans obtained on the 1st postoperative day. The CT scans demonstrate an ischemia within the anteri-
or division of the right MCA including the internal capsule.
fered from left hemiplegia with a dysarthria and maintained
intact sensation when she was discharged to a rehabilitation
unit 1 month postoperatively.
Discussion
During supratentorial vascular surgery, our ability to use
MEP loss to predict subcortical, ischemia-induced pure mo-
tor sequelae has been clearly demonstrated. Our patient suf-
fered a pure motor hemiplegia predicted by intraoperative
loss of MEPs. The use of MEPs and their ability to predict
postoperative motor status has been demonstrated in a large
series of patients with intramedullary spinal cord tumors.12,13
Also, MEPs have been shown to be useful in intravascular
procedures for the treatment of spinal arteriovenous malfor-
mations.17 Reports concerning the use of MEPs in supraten-
torial surgery predominantly describe mapping techniques
for localization of the motor cortex in tumor surgery.1,15
Nevertheless, the sensitivity of MEPs for predicting motor
outcome is a common feature of all the aforementioned
studies. In contrast to the N20/P27 SSEP generator’s pure-
ly cortical location, MEPs elicited using electrical stimula-
tion in patients who are in a state of general anesthesia are
generated at different depths below the motor cortex. Short,
weak, focal anodal pulses are thought to activate the corti-
cospinal tract neurons at their axons located in the white
matter.10 This explains the increased sensitivity of MEPs to
subcortical rather than cortical ischemia. Unlike TES, the
weak current intensity used for DCS activates the cortico-
spinal tract at its most superficial location below the gray
matter.
Interestingly, in our patient the final clip placement (11
minutes after the MEP loss) resulted in a temporary decre-
ment of bilateral SSEP amplitudes. Studies of patients with
a pure motor hemiplegia involving parts of the internal cap-
sule or prerolandic areas indicate that these individuals
might have delayed cortical SSEPs.2,11 Because the genera-
tor of the primary cortical SSEP complex (N20/P27) is ro-
bust, purely contralateral to the stimulation, and relatively
insensitive to influences of anesthesia and environmental
noise, it is used for intraoperative SSEP recordings.6 In con-
trast, the P22/N30 complex can be recorded at the contra-
lateral prerolandic area and also spreads to the ipsilateral
parietal region.5,6 The temporary decrease of the bilateral
median nerve SSEP amplitudes might have been a decrease
J. Neurosurg. / Volume 99 / September, 2003
of the P22/N30 complex induced by ischemia in the anteri-
or MCA branch. Because the N20/P27 response being gen-
erated at the postrolandic region was not affected, it might
have masked changes in the P22/N30 complex.
After MEPs were lost (during permanent clip placement)
an inspection of the aneurysm wall showed no compro-
mised perforating vessels. The Doppler signal from the M1
and M2 branches was present. Because the aneurysm wall
was arteriosclerotic, its manipulation during the clip place-
ment might have loosened a plaque, which could have
caused the embolic occlusion of the anterior M2 branch that
was also supplying the internal capsule. Only the involve-
ment of the internal capsule can explain the motor deficit in
the upper and lower extremities.
Conclusions
Intraoperative neurophysiological monitoring with
MEPs and SSEPs is a sensitive tool that can be used to
reach beyond the scope of SSEP monitoring alone to indi-
cate subcortical ischemia affecting only those perforating
branches that supply the motor pathways exclusively. The
combination of preserved SSEPs and the loss of MEPs for
the upper and lower extremities is an intraoperative neuro-
physiological marker for induced pure motor hemiplegia.
As has been demonstrated in this patient, the intraoperative
loss of MEPs is predictive of the postoperative motor sta-
tus. Thus, the intraoperative recording of MEPs should be
encouraged during vascular neurosurgical procedures.
Acknowledgment
We thank David Hershberger, B.S., for his help in editing the
manuscript.
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Manuscript received December 18, 2002.
Accepted in final form May 20, 2003.
Address reprint requests to: Andrea Szelényi, M.D., Klinikum der
Johann Wolfgang Goethe Universität, Klinik und Poliklinik für Neu-
rochirurgie, Haus 95, Am Schleusenweg 2-16, D-60528 Frankfurt,
Germany. email: A.Szelenyi@em.uni-frankfurt.de.
J. Neurosurg. / Volume 99 / September, 2003