From revival to routine: electromyography-based neuromuscular monitoring in contemporary anesthesia practice
Article information
Abstract
Electromyography (EMG)-based neuromuscular monitoring has emerged as a pivotal advancement in anesthesia, offering enhanced precision and reliability in assessing neuromuscular blockade. This review describes the physiological foundations of EMG, the methodologies for quantifying compound muscle action potential, and the comparative utility of EMG over traditional acceleromyography. Clinical applications across various muscle sites—specifically the adductor pollicis, first dorsal interosseous, and abductor digiti minimi—are explored, emphasizing inter-muscle variability and its implications for dosing of reversal agents. EMG-based monitoring is associated with reduced calibration time, improved stability against signal drift, and superior prevention of residual neuromuscular blockade. However, EMG monitoring presents unique challenges, including signal artifacts and device-specific variations in response thresholds. Recent comparative studies have demonstrated the importance of understanding device-specific characteristics to optimize clinical interpretations. Collectively, this evidence supports the use of EMG as a standard modality for perioperative neuromuscular management. Its accurate and reproducible signals, combined with broad clinical compatibility, present a compelling case for widespread adoption in routine anesthetic practice.
INTRODUCTION
Quantitative neuromuscular monitoring is essential for the safe management of patients receiving neuromuscular blocking agents (NMBAs) during general anesthesia [1,2]. Precise neuromuscular monitoring allows anesthesiologists to accurately assess the degree of neuromuscular blockade, optimize the dosing of reversal agents, reliably determine neuromuscular recovery, and enhance patient safety by minimizing residual neuromuscular blockade and its associated complications.
Electromyography (EMG)-based neuromuscular monitors, which assess muscle electrical activity following nerve stimulation, have existed for decades. However, early devices were cumbersome and technically complex, limiting widespread clinical adoption [3]. Instead, despite known limitations—such as overestimation of the train-of-four (TOF) ratio and vulnerability to movement artifacts—acceleromyography (AMG) emerged as the predominant neuromuscular monitoring modality for decades [4].
The interest in EMG monitoring has been renewed in recent years because of significant technological advancements. As described in a previous review article [3], since 2018, several devices, such as TwichView (Blink Device Company) and TetraGraph (Senzime), have become commercially available, facilitating wider clinical adoption of EMG-based neuromuscular monitoring in clinical anesthesiology practice. EMG provides direct and accurate measurements of neuromuscular transmission (NMT) at the neuromuscular junction, offering greater precision and reliability, especially in complex surgical conditions involving restricted patient positioning [5,6]. Moreover, advancements in EMG device technology and simplified electrode application have enhanced its practical accessibility, encouraging broader integration into routine anesthetic practice. These developments align with growing clinical evidence supporting EMG as a superior modality for neuromuscular monitoring, underscoring its potential to become the new standard of care in anesthesia.
Although mechanomyography (MMG), which quantifies the isometric muscle contraction force, has long been regarded as the “gold standard” for neuromuscular monitoring, its cumbersome nature precludes routine clinical practice [7]. Therefore, this review focused on EMG and AMG, the two modalities accessible and practically feasible in contemporary clinical practice.
EMG: BASIC PRINCIPLES
Neuromuscular junction physiology and compound muscle action potential (CMAP)
Fig. 1. illustrates the fundamental electrophysiological basis of NMT. The neuromuscular junction serves as the interface between motor neurons and skeletal muscle fibers. Upon arrival of an action potential at the presynaptic terminal, voltage-gated calcium channels open, facilitating Ca2+ influx. This triggers the fusion of acetylcholine (Ach)-containing vesicles with the presynaptic membrane, releasing Ach into the synaptic cleft.
Schematic of neuromuscular transmission and the associated ionic currents at the neuromuscular junction. Upon arrival of an action potential at the presynaptic terminal, voltage-gated calcium channels open, allowing Ca2+ influx into the nerve terminal (⓪). This triggers the fusion of acetylcholine-containing vesicles with the presynaptic membrane and the subsequent release of acetylcholine into the synaptic cleft. Acetylcholine then binds to ligand-gated sodium channels (nicotinic acetylcholine receptors) on the postsynaptic muscle membrane, allowing the influx of Na+ ions (①), which initiates depolarization. If the threshold potential is reached, voltage-gated sodium channels open (②), propagating an action potential along the muscle fiber. Repolarization follows via the efflux of K⁺ through voltage-gated potassium channels (③). The figure illustrates the corresponding phases of membrane potential change during an action potential: resting potential (− 90 mV), threshold (− 50 mV), depolarization (①,②), and repolarization (③). These electrochemical events generate a compound muscle action potential that can be measured via electromyography.
Ach subsequently binds to nicotinic acetylcholine receptors on the postsynaptic membrane, inducing conformational changes that permit Na+ influx through ligand-gated ion channels. This initial ionic current generates an endplate potential (EPP). When the EPP reaches the threshold potential (approximately – 50 mV), voltage-gated sodium channels in the adjacent sarcolemma activate, precipitating a rapid and massive influx of Na+ ions. This explosive increase in Na+ permeability causes a sharp upstroke (depolarization phase) in the muscle fiber action potential, during which the membrane potential reverses polarity, becoming transiently positive (approximately + 50 mV).
The depolarization phase is promptly followed by the inactivation of voltage-gated Na+ channels, concurrent with the delayed activation of voltage-gated K+ channels. This leads to a significant efflux of K+ ions from the muscle fibers, resulting in a downstroke (repolarization phase) of the muscle fiber action potential, thereby restoring the resting membrane potential. This electrical activity manifests as a single muscle fiber action potential.
The synchronous generation of such action potentials in multiple muscle fibers within a motor unit and the summation of these electrical activities from numerous motor units produce the CMAP [8].
EMG signal measurement and analysis
EMG signals are recorded using surface electrodes placed over the target muscles. After amplification and filtering, the EMG signals are analyzed to quantify the twitch height. Epstein et al. [9] recently described two methodologies for quantifying twitch height from the CMAP: (1) measurement of the CMAP amplitude and (2) calculation of the area under the curve (AUC) of the CMAP waveform (Fig. 2).
Two approaches for quantifying twitch height from the compound muscle action potential (CMAP) waveform. After nerve stimulation, the evoked EMG signal is captured and processed to extract the CMAP waveform. (A) The amplitude method quantifies the twitch height as the peak-to-peak voltage difference, measured from the maximum positive deflection to the maximum negative deflection of the CMAP waveform. (B) The area under the curve method quantifies the twitch height by integrating the total area enclosed within the CMAP waveform (① + ②).
The CMAP amplitude is defined as the vertical distance between the waveform’s highest peak and lowest trough, representing the maximal voltage change recorded during the stimulation response.
The AUC is calculated by integrating the area enclosed by the CMAP waveform. The AUC value represents the overall electrical displacement during the response to stimulation.
Epstein et al. [9] also reviewed five commercially available EMG devices, noting that two (NMT Pod, Nihon Kohden; TetraGraph, Senzime) employed amplitude-based measurements, while three (E-NMT, GE HealthCare; Stimpod, Xavant Technology; TwitchView, Blink Device Company) utilized AUC-based methods. Their comparative analysis demonstrated a strong correlation between the amplitude and AUC measurements with minimal bias and narrow limits of agreement, suggesting that both approaches are reliable and clinically interchangeable.
CLINICAL APPLICATION AND UTILIZATION STRATEGIES OF RECENT EMG-BASED MONITORS
Recommended monitoring sites: three muscles
Current guideline [7] recommends three primary muscles for EMG monitoring: the adductor pollicis (AP), first dorsal interosseous (FDI), and abductor digiti minimi (ADM). Phillips et al. [10] investigated EMG responses using the E-NMT system (GE HealthCare) in these muscles during recovery from neuromuscular blockade and observed differences in recovery rates among the AP, FDI, and ADM. They reported that a TOF ratio of 0.8 at the AP and FDI muscles corresponds to a TOF ratio of 0.9 at the ADM, suggesting that the ADM recovers more quickly to a TOF ratio of 0.9 compared to the AP and FDI. The authors attributed these differences to the inherent resistance of the ADM to NMBAs. However, some studies have reported inconsistent findings. Iwasaki et al. [11] conducted a prospective comparative study between the AP and ADM muscles using an EMG AF-201P (Nihon Koden) monitor during rocuronium-induced blockade. The authors observed a time-to-TOF ratio of 0.9 and concluded that EMG monitoring of both the AP and ADM muscles can effectively guide appropriate sugammadex dosing for the reversal of moderate neuromuscular blockade and verification of adequate neuromuscular recovery.
Sensor attachment methods
Accurate electrode placement is required for reliable EMG monitoring because measurement outcomes can vary significantly depending on electrode positioning. According to current guideline [7], the skin at both stimulating and recording electrode sites should be cleaned to ensure supramaximal stimulation and improve EMG signal quality. Stimulating electrodes should be placed over the course of the target nerve, with the negative electrode positioned distally. For recording electrodes, the active electrode should be placed over the muscle belly and the reference electrode over the muscle tendon [7]. Variations in electrode placement may require different stimulus currents and can introduce inconsistencies in monitoring results [12,13]. In a study utilizing the TwitchView (Blink Device Company), Ebert et al. [14] described optimal stimulating electrode placement as directly over the ulnar nerve within the ulnar tunnel and within 2 cm of the wrist crease (Fig. 3), emphasizing that deviations from these positions can compromise the consistency and reliability of monitoring results.
CLINICAL ADVANTAGES OF EMG-BASED MONITORING OVER AMG-BASED MONITORING
Faster calibration time
Jung et al. [15] conducted a randomized trial in pediatric patients receiving rocuronium, comparing EMG (E-NMT, GE HealthCare) with AMG (TOF-Watch SX, Organon) in terms of calibration times and intubation conditions. The study demonstrated that the calibration time was significantly shorter with EMG monitoring (16.7 ± 11.0 s vs. 28.1 ± 13.4 s; P = 0.012). Furthermore, when tracheal intubation was performed at the point of maximal neuromuscular blockade as determined by each device, intubation condition scores (1 = poor, 2 = good, 3 = excellent) were significantly higher in the EMG group than in the AMG group (2.27 ± 0.65 vs. 1.86 ± 0.50; P = 0.007). These findings indicate that EMG monitoring facilitates a more rapid calibration process and provides a more reliable indication of optimal intubation timing, resulting in improved intubation conditions.
Stabilization period
Effective neuromuscular monitoring requires signal stabilization prior to administration of NMBAs to minimize twitch height variability [7]. AMG typically requires a stabilization period ranging from 5 min to 20 min or 2 min to 5 min after tetanic stimulation. This requirement arises because of the staircase phenomenon [16], wherein repeated stimulation progressively enhances mechanical muscle responses. Conversely, EMG exhibits significantly less susceptibility to baseline drift because repetitive stimuli do not substantially enhance the CMAP size [17]. Current guideline [7] recommends maintaining a stable control response for at least 2 min for all monitoring methods. Although EMG does not completely eliminate the need for stabilization, it may be more robust in signal stabilization and requires fewer special interventions, such as tetanic stimulation, thereby facilitating a more efficient induction process.
Accuracy and precision
A recent study by Wedemeyer et al. [18] compared three AMG monitors (TOFscan, Dräger; Stimpod NMS450, Xavant Technology; Philips NMT, Philips), three EMG monitors (TwitchView, Blink Device Company; Stimpod NMS450X, Xavant Technology; TetraGraph, Senzime), and a laboratory MMG monitor in 28 patients who did not receive NMBAs. Across 3,567 measurements, all AMG monitors significantly overestimated the TOF ratio, with mean values ranging from 1.10 to 1.13 and substantial variability ranging from 0.07 to 0.18. The authors found that even after normalization, 27–51% of the AMG-measured TOF ratios deviated beyond the clinically acceptable range of 0.9–1.1, whereas only 0.3% of the EMG- and MMG-measured TOF ratios were out of this range. This persistent lack of accuracy and precision in AMG, despite normalization, can lead to a clinically significant misinterpretation of recovery and provide constructive evidence for the adoption of EMG as a more reliable standard for quantitative monitoring.
Prevention of postoperative residual neuromuscular blockade (PRNB)
PRNB is a common complication associated with NMBA use and can lead to adverse respiratory compromise [19]. AMG, while widely used for quantitative monitoring [4], presents challenges in reliably preventing PRNB, primarily owing to its inherent tendency to overestimate the degree of neuromuscular recovery compared to MMG or EMG. This overestimation means that a TOF ratio of 0.9, measured by AMG, may not consistently signify adequate recovery. In an exploratory analysis of the POPULAR study data [20], postoperative pulmonary complications occurred in 11.3% of patients with a TOF ratio > 0.9. Although increasing the extubation criterion to a TOF ratio of 0.95 resulted in an adjusted absolute risk reduction of 4.9% for pulmonary complications, complete prevention was not achieved.
Therefore, current guidelines emphasize the importance of normalization (dividing the measured TOF ratio by the baseline TOF ratio) when using AMG [1,2,7]. If normalization is not performed, a non-normalized TOF ratio of 1.0 is recommended as a more reliable endpoint to minimize PRNB. However, understanding that a non-normalized TOF ratio of 1.0 does not guarantee a recovery equivalent to a normalized TOF ratio of 0.9 is crucial, especially if the baseline TOF ratio exceeds approximately 1.11 (1.0/1.11 ≒ 0.9).
Conversely, EMG-guided neuromuscular management has demonstrated superior efficacy in preventing PRNB. In a prospective study involving 189 patients, Thilen et al. [21] reported a 0% incidence of PRNB—defined as TOF ratio < 0.9 at extubation—when a quantitative EMG-based monitoring protocol (TwitchView, Blink Device Company) targeting a TOF ratio ≥ 0.9 was implemented. The effectiveness of this EMG-guided approach is attributed to its more accurate and direct measurement of electrical activity at the neuromuscular junction, which is less susceptible to the overestimation issues inherent in AMG. This precision in EMG monitoring allows for more accurate detection of residual blockade, facilitates better informed decisions regarding the selection and timing of reversal agents (such as neostigmine or sugammadex), and enables reliable confirmation that a TOF ratio ≥ 0.9 has been achieved before extubation. Notably, this protocol also resulted in a significant reduction (43%) in the overall cost of reversal agents because of the selective utilization of sugammadex. Collectively, these findings demonstrate that the use of EMG for a more reliable assessment of neuromuscular function enhances patient safety by minimizing PRNB, thereby justifying its adoption in routine clinical practice.
PRACTICAL CHALLENGES IN EMG MONITORING
Despite its advantages, EMG-based neuromuscular monitoring presents practical challenges. One major issue is the presence of electrical artifacts during signal processing. Artifacts can arise from various sources, including surgical cautery and direct muscle stimulation [22]. These artifacts can distort EMG signals, leading to an inaccurate assessment of neuromuscular function.
EMG vs. EMG
Different EMG devices utilize distinct signal-processing algorithms that influence the measurement accuracy. Bussey et al. [23] compared two commercial EMG devices, TwitchView (Blink Device Company) and GE NMT (E-NMT, GE HealthCare), and found that they yielded different TOF ratios and counts. For instance, in 11% of the measurement pairs, GE NMT showed a TOF count of 4, while TwitchView showed a TOF count of 0. The authors attributed this discrepancy to the GE NMT’s signal processing algorithm misinterpreting electrical artifacts as valid CMAP signals. This misinterpretation of artifacts can lead to falsely reassuring TOF count or TOF ratio, potentially masking deep neuromuscular blockade and compromising patient safety. Similarly, Sato et al. [24] compared the AF-201P (Nihon Kohden) and TetraGraph (Senzime) monitors and observed a shorter time to the first post-tetanic count (PTC) appearance and TOF counts of 1 and 2 with the AF-201P during recovery, emphasizing the need to understand device-specific characteristics. The authors attributed this difference to the lower noise filter threshold of AF-201P compared to that of TetraGraph (0.7 mV vs. 1 mV). This lower threshold in AF-201P may enable the detection of smaller CMAPs, potentially explaining the earlier appearance of PTC and TOF counts. However, the authors also cautioned that noise filter threshold setting is critical; a threshold set too low might lead to misinterpretation of noise as a valid CMAP, while a threshold set too high could result in missed CMAP and underestimation of twitch height. Table 1 summarizes the device-specific characteristics of the four EMG monitors [9,23,24].
EMG vs. AMG
Nemes et al. [25] conducted a simultaneous ipsilateral comparison of EMG (Tetragraph, Senzime) and AMG (TOF-Watch SX, Organon) responses in patients from the induction of a neuromuscular block to recovery. In their study, TOF measurements were performed every 15 s, and PTC measurements were performed every 3–5 min. Their findings revealed that during deep and moderate neuromuscular blockade, the EMG monitor generally displayed fewer TOF counts than did the AMG monitor, with an average difference of approximately one response. Specifically, during deep neuromuscular blockade, the mean PTC recorded by EMG was significantly lower than that recorded by AMG (mean 4.3 ± standard error 0.7 for EMG vs. 8.6 ± 0.7 for AMG; P < 0.0001). The authors suggested that these discrepancies, where EMG indicated a deeper level of block, might be partly attributable to the high threshold of the EMG monitor, which may have disregarded the low-amplitude responses as subthreshold signals during deep or moderate blocks. Joo et al. [26] further supported this finding by demonstrating that EMG (TwitchView, Blink Device Company) measured fewer PTCs than did AMG (Philips IntelliVue NMT Module, Philips Healthcare) during deep neuromuscular blockade. Iwasaki et al. [27] observed that when an EMG (Tetragraph, Senzime) indicated a TOF count of 2, an AMG (TOF-Watch SX, Schering-Plough, USA) concurrently showed a TOF count of 4. This study suggests that an EMG-indicated moderate blockade may correspond to a shallower level of neuromuscular blockade than that conventionally interpreted using AMG monitoring. While established guidelines recommend 2 mg/kg sugammadex for moderate blockade, Iwasaki et al. [27] cited the study by Pongrácz et al. [28] using AMG (TOF-Watch SX, Organon), which demonstrated effective reversal of shallow neuromuscular blockade (TOF count of 4) with 1 mg/kg sugammadex. Based on this evidence, Iwasaki et al. [27] cautiously proposed that if EMG indicates a TOF count of 2, a reduced dose of sugammadex might be considered as an alternative, warranting further investigation into EMG-guided dosing strategies.
CONCLUSION
EMG-based neuromuscular monitoring provides distinct advantages over AMG-based methods and is increasingly recognized as a reliable tool for managing neuromuscular blockade. Its accuracy, efficiency, and clinical applicability make it a valuable option in routine practice. However, device-specific limitations and vulnerability to artifacts underscore the importance of understanding the characteristics of each monitor. EMG is a recommended modality for improving the safety and precision of neuromuscular monitoring; however, thoughtful interpretation remains essential for optimal clinical application.
Notes
FUNDING
None.
CONFLICTS OF INTEREST
No potential conflict of interest relevant to this article was reported.
DATA AVAILABILITY STATEMENT
Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
