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Electromyographic facial nerve monitoring during resection for acoustic neurinoma under moderate to profound levels of peripheral neuromuscular blockade

Brauer, M.*; Knuettgen, D.; Quester, R.; Doehn, M.

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European Journal of Anaesthesiology: November 1996 - Volume 13 - Issue 6 - p 612-615



Post-operative facial nerve dysfunction is a common complication following resection of an acoustic neurinoma. Devices have therefore been designed to monitor facial nerve function intra-operatively. One of these devices is the Nerve Integrity Monitor 2 (NIM-2), manufactured by XOMED (Xomed Inc., Jacksonville, FL). Stimulation of the facial nerve can result from inadvertent surgical manipulation of the nerve or the intentional use of a stimulation electrode in the surgical field. The evoked electromyographic response is obtained using bipolar recording electrodes placed intramuscularly (i.m.) in the orbicularis oculi and oris muscle [1]. Preservation of facial nerve function can be enhanced by electrical monitoring of facial pathways [2,3].

Unfortunately, the use of such a monitoring unit is in conflict with the demand for absolute immobility of the patient during cerebellopontine angle surgery. Close proximity of the trigeminal nerve and brainstem structures may result in unintentional stimulation of these structures by the surgeon, producing rapid motor reflexes with deleterious outcome. As these motor reflexes cannot be excluded even under deep levels of anaesthesia the use of muscle relaxants is indicated. On the other hand, the monitoring unit needs a functional intact facial nerve muscle junction to enable an electromyogram (EMG) to be recorded.

The aim of this study is to examine the possibility of using controlled levels of peripheral neuromuscular blockade while preserving the ability to monitor adequately facial EMGs.


Eleven patients (four male, seven female, ASA-I-II, 24-73-years-old, 57-113 kg body weight) undergoing acoustic neurinoma resection with standard facial and ulnar nerve EMG monitoring were studied. Four patients showed pre-operative clinical signs of facial nerve injury whereas seven did not. Written informed consent was obtained from all patients.

All patients were premedicated with midazolam, 7.5 mg orally. Anaesthesia was induced with thiopentone (3-5 mg kg−1), fentanyl (0.3-0.5 mg) and flunitrazepam (0.5 mg) and maintained with fentanyl (0.005-0.017 mg kg−1 h−1), flunitrazepam (0.003-0.008 mg kg−1 h−1), Droperidol (0.33 mg kg−1 single dose) and N2O/O2 1:1. This was the standard anaesthetic procedure for intracranial surgery in this hospital. Tracheal intubation was facilitated with atracurium, 0.6 mg kg−1. After partial recovery of neuromuscular function, atracurium infusion was started at a rate of 0.33 mg kg−1 h−1. The infusion rate was adjusted if necessary to achieve the desired level of neuromuscular blockade. Ease of administration, rapid titrability and reversibility made atracurium a suitable choice for this study [4]. Arterial pH and arterial PaCO2 were measured hourly, arterial PaCO2 was kept between 4.0 and 7.3 kPa. Core temperature was kept above 35.5°C using warming blankets.

The level of peripheral neuromuscular blockade was determined using the integrated EMG relaxograph NMT 100 (Datex Corp., Helsinki, Finland). Stimulation of the ulnar nerve was performed using surface electrodes placed over the ulnar nerve 2 and 9 cm proximal to the distal end of the ulna. The ulnar nerve was stimulated every 20 s with four 2 Hz supramaximal stimuli with a square wave monophasic pulse (Train-of-four (TOF)). The electrically evoked muscle potentials (EEMPs) were obtained from surface electrodes placed on the hypothenar eminence and at the base of the dorsum of the fifth finger. As a precaution against electrical drift these surface electrodes were used for no more than 3 h. Prolonged use of surface electrodes may result in electrode electrolyte depletion because of a small leakage current delivered by the monitor (Wissing, personal communication). This may explain the reason why a small base-line drift was detected in only two cases.

The EEMP magnitude was measured by integrating the area under the wave. The first integrated TOF response was compared with a mean reference integral obtained during the prerelaxant automatic calibration procedure. The percentage decrement of the first integrated TOF response from prerelaxant baseline EEMP (T1%) was used to determine the level of peripheral neuromuscular blockade. By adapting the dosage of atracurium, the T1 value was varied between 0 and 30% in each patient.

The facial nerve was directly stimulated by square wave constant current pulses (0.4-0.6 mA, to ensure that the extent of current spread was about 1 mm from the electrode frequency 4 Hz) delivered by special monopolar surgical instruments, connected to the NIM-2, or mechanically by surgical manipulation. The evoked ongoing muscle potentials (EMPs) were obtained by needle electrodes, placed in the orbicularis oris and oculi muscles and the heights of the EMPs were recorded.


Intra-operative facial nerve monitoring was possible in all patients in the presence of moderate to profound peripheral neuromuscular blockade. Even complete peripheral neuromuscular blockade with T1=0% and no palpable hypothenar muscle response, EMPs from the facial nerve were obtained during electrical stimulation and inadvertent mechanical manipulation. At all tested levels of peripheral neuromuscular blockade, the height of the corresponding facial EMPs varied greatly. A correlation was not found between the degree of peripheral neuromuscular blockade and the facial EMP amplitude. It was not possible to distinguish between patients with clinical signs of facial nerve injury and patients without clinical signs of facial nerve injury by the height of the facial EMP amplitude. The range of the facial EMPs at different T1-classes in all 11 patients are summarized in Table 1.

Table 1
Table 1:
Peak mechanically or electrically evoked facial muscle potential (in μV) at different levels of peripheral neuromuscular blockade, expressed as T1% value, summary of all data from the 11 examined patients. Missing values indicate that no data has been measured at this T1% class


Anatomical preservation of the facial nerve and the degree of functional improvement 3 months after surgery increase if the facial nerve has been monitored during primary removal of an acoustic neurinoma [2,3]. So far, an anaesthetic technique that does not require the use of muscle relaxants to maintain the proper level of anaesthesia has been recommended because the use of muscle relaxants was thought to adversely affect the EMG response [1-3]. Lennon et al. showed that it is possible to obtain a facial EMG intra-operatively under a moderate level of peripheral neuromuscular blockade [5]. But the chosen level of peripheral neuromuscular blockade (T1=50%) is not sufficient to prevent all movements of great muscle groups [6]. Ho et al. reported that the facial muscles are less sensitive to atracurium than the hypothenar muscles [7] but their study differed methodologically from this study. First, they assessed facial and hypothenar function mechanomyographically by means of accelerometry. This technique seems to overestimate the degree of neuromuscular blockade by at least 15% [8]. Second, a single large bolus dose of atracurium was administered to abolish even the facial muscle response, and recovery of the facial and hypothenar muscle responses were compared. A stable level of neuromuscular blockade with a facial EMG, but with no hypothenar muscle response, was not achieved [7].

The result of the present study demonstrate the possibility of obtaining a facial EMG by direct electrical or mechanical stimulation of the facial nerve under moderate to profound levels of peripheral neuromuscular blockade.

Facial monitoring was possible even when the hypothenar muscles were completely blocked (T1=0%, no palpable hypothenar muscle response). The facial muscles are known to be relatively insensitive to neuromuscular blocking agents [9-12]. The explanation for this relative insensitivity remains unclear. A different type of innervation is found in some muscles of expression in the face and neck. These muscles have a greater number of neuromuscular junctions than have other muscles in the body [9]. So far, it is unknown, whether a different affinity of the facial acetylcholine-receptor for acetylcholine or nondepolarizing muscle relaxants plays an additional role.

Moreover the facial nerve was stimulated directly whereas the ulnar nerve was stimulated by surface electrodes. Concurrent measurements showed that stimulation by surface electrodes is less effective than stimulation by direct contact [12].

We could not demonstrate a relation between the level of peripheral neuromuscular blockade and the magnitude of the facial action potential. Nor could we find evidence for pre-operative or intra-operative partial facial nerve injury by comparing the amplitude of the action potential during an operation or between different patients. At any given measuring point the differences between single action potentials were great. A phenomenon probably explained by the impossibility of standardizing the conditions for stimulation. An additional reason might be because the facial EMG response was not calculated. A reduction in the accuracy of the electromyographic unit used to monitor the magnitude of hypothenar neuromuscular blockade (for instance a small base-line drift observed in two cases) might be an additional reason for missing the relation between the level of relaxation and the amplitude of the action potential.

Further studies are necessary to determine, whether complete neuromuscular blockade diminishes the sensitivity or even the effectiveness of facial nerve monitoring during acoustic neurinoma resection.


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© 1996 European Academy of Anaesthesiology