Surgical procedures involving the spine require prone positioning and are not devoid
of complications. Perioperative peripheral nerve injury (PPNI) is an important complication
with an incidence of 0.03 to 0.1% and with 0.02% incidence of brachial plexopathy
in noncardiac surgery.[1] Intraoperative neuromonitoring (IONM) used during spine surgery detects peripheral
nerve conduction abnormalities, thus preventing PPNI.[1] Here we report a case of false-negative transcranial motor evoked potential (TcMEP)
leading to transient right upper limb weakness postoperatively.
A 50-year-old woman presented with back pain and difficulty in walking for 3 months.
On examination, sensory deficit was noted below umbilicus. The motor power was 4/5
in both lower limbs according to Medical Research Council (MRC) grading. Magnetic resonance imaging (MRI) spine revealed intradural extramedullary (IDEM) tumor at thoracic vertebra level 7–8 (D7–D8) pushing the spinal cord to left side with significant cord compression; D7–8 laminectomy
and excision of the tumor was planned. Anesthesia was induced with propofol 1.5 mg/kg
and fentanyl 2μg/kg, and maintained with total intravenous anesthesia using propofol
150 µg/kg/min and fentanyl 1µg/kg/h infusions. Muscle relaxants were avoided. TcMEP
were recorded with electrodes inserted in scalp at C3 and C4 (international10–20 system).
Compound muscle action potentials (CMAPs) were recorded from right abductor digiti
minimi in the upper limbs as reference, and tibialis anterior and adductor hallucis
longus in the bilateral lower limbs. The impedance of all electrodes was maintained
below 5 kV. Patient was placed in the prone surrender (superman) position[1] for a total surgical duration of 3 hours. Superman/surrender prone position involves
the patient to be placed prone with head in neutral position, shoulders abducted to
less than 90°, lateral rotation of upper arms and elbows flexed and positioned in
neutral position at or below the mattress level beside the patient’s head. Normothermia
and normocapnia were maintained during the procedure with a total blood loss of 150
mL. A significant drop in power was noted in the right upper limb involving the cervical
(C) 5,6,7 nerve root distribution affecting the muscles like deltoid, biceps, triceps,
and brachioradialis, with MRC grading of 2/5 up on extubation. The intrinsic muscles
of the arm which are innervated by the ulnar nerve were spared. Baseline power was
maintained in rest of the limbs. However, no change in amplitude in TcMEPs was detected
during the procedure ([Fig. 1]).
Fig. 1 Encircled image showing no change in the transcranial motor evoked potentials (TcMEPs)
in the affected right upper limb.
Mechanism of PPNI includes ischemia of nerve fibers due to stretch/compression and
direct trauma. Risk factors for position related brachial plexus injuries include
use of shoulder braces and head-down position, shoulder abduction greater than 90°,
external rotation of the arm, and posterior shoulder displacement.[1] IONM plays a crucial role in detecting PPNI as demonstrated by Luginbuhl et al.[3] The arm was returned to neutral position after evolving plexopathy was detected
with IONM. Tsutsui et al[4] evaluated the effect of spinal cord or root lesioning on 5-pulse TES MEPs from the
hind limb triceps surae muscle in cats and found that CMAPs decreased in amplitude
significantly after the insult to the corticospinal tracts in the spinal cord in all
cats, but the potentials did not always change when the insult was restricted to a
limited area in the anterior horn of the spinal cord or to the single spinal nerve
roots. This might explain the reason for the false-negative findings in our case.
Similar false-negative case was reported by Modi et al[5] where the patient developed paraplegia with intact TcMEP. Another possible explanation
is that the TcMEP was recorded from the intrinsic muscles of the hand which are supplied
by the ulnar nerve (C8, T1) while the actual loss of power happened in the shoulder
abduction which is innervated by the C 5,6,7 nerve roots.
Limitations of our case includes inability to perform nerve conduction studies, which
would have showed slowing of conduction time[6] it would add value in differentiating between the affected nerve roots and nonaffected
nerve roots, and it can help in assessing the progress of the condition. Also, lack
of somatosensory evoked potential (SSEP) monitoring, which would have picked up the
praxia in the early stages.[7]
We conclude that TcMEP, although considered paragon, may not be a foolproof method
to negate postoperative motor deficit, but it can play a significant role in reassuring
the patient regarding the motor recovery. Addition of other modalities like somatosensory
evoked potential and nerve conduction studies would add more value and information
in prognostication of the motor recovery.
