Diaphragm Compound Muscle Action Potential Research Articles

Effect of lung volume on the oesophageal diaphragm EMG assessed by magnetic phrenic nerve stimulation.

Previous studies have shown conflicting results on the effect of lung volume on the diaphragm compound muscle action potential (CMAP). Consequently, the ability to quantify the oesophageal diaphragm electromyography (EMG) has been questioned. If lung volume changes have little effect on the diaphragm CMAP the accurate measurement of voluntary EMG, as an index of respiratory drive, may be possible. Furthermore, the measurement of CMAP could provide useful clinical information when evaluating patients with neuromuscular disease. To reassess the effect of lung volume on the oesophageal diaphragm CMAP, six normal subjects were studied using an oesophageal catheter incorporating seven electrodes (number one being proximal and seven distal) that were 1 cm in length and 1 cm apart. Electrode number three was positioned at the centre of the electrically active region of the diaphragm (EARdi) at functional residual capacity (FRC). The diaphragm CMAP elicited by bilateral magnetic stimulation of the phrenic nerves was simultaneously recorded from four electrode pairs. Pair one was created from electrodes one and three, pair two from electrodes two and four, pair three from electrodes three and five, and pair four from electrodes five and seven. Phrenic nerve stimulation was at residual volume (RV), FRC, FRC+1.0 L, FRC+2.0 L, and total lung capacity (TLC). The CMAP recorded from pair one was least influenced by changes in lung volume and the amplitude was 2.41+/-0.39 (mean+/-SD), 2.60+/-0.27, 2.64+/-0.29, and 2.71+/-0.45 mV at RV, FRC, FRC+1.0 L and FRC+2.0 L, respectively. At TLC the CMAP was more variable. The CMAP amplitude recorded from pair two increased with increasing lung volume and at FRC+2.0 L was 3.7 times larger than that at FRC. Pair four usually recorded substantially smaller CMAPs at all lung volumes. This study shows that the diaphragm compound muscle action potential recorded from an oesophageal electrode just above the diaphragm is relatively stable over the lung volume range residual volume to functional residual capacity+2.0 L.

Phrenic nerve conduction studies in acute organophosphate poisoning

Phrenic nerve conduction studies were performed within 48 h of admission and subsequently in 29 patients (14 of whom required mechanical ventilation) with acute organophosphate (OP) poisoning. The mean (±SD) amplitude of the diaphragmatic compound muscle action potential (CMAP) in patients requiring mechanical ventilation (119.09 ± 173.85 μV) was significantly lower than in those not requiring mechanical ventilation (461.63 ± 138.69 μV) (P < 0.0001). Diaphragmatic CMAP amplitudes in ventilated patients increased with time during the course of hospitalization and were normal in 5 (36%) patients and only mildly reduced in another 6 (43%) patients prior to discontinuation of mechanical ventilation, which was undertaken 4–18 days (mean 7 ± 3 days) after poisoning. Eleven patients (79%) were successfully weaned from mechanical ventilation at the first attempt. In the 3 (21%) remaining patients, mechanical ventilation had to be reestablished because of weaning failure. The mean (±SD) diaphragmatic CMAP amplitude, prior to discontinuation of ventilatory assistance, was 242.6 ± 94.1 μV in these 3 patients. After ventilatory discontinuation, it fell to 95.5 ± 105.8 μV. Thus, reduced diaphragmatic CMAP amplitudes correlate with the need for mechanical ventilation in acute OP poisoning. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 627–632, 2000.

Phrenic nerve conduction studies in acute organophosphate poisoning.

Phrenic nerve conduction studies were performed within 48 h of admission and subsequently in 29 patients (14 of whom required mechanical ventilation) with acute organophosphate (OP) poisoning. The mean (+/-SD) amplitude of the diaphragmatic compound muscle action potential (CMAP) in patients requiring mechanical ventilation (119.09 +/- 173.85 microV) was significantly lower than in those not requiring mechanical ventilation (461.63 +/- 138.69 microV) (P < 0.0001). Diaphragmatic CMAP amplitudes in ventilated patients increased with time during the course of hospitalization and were normal in 5 (36%) patients and only mildly reduced in another 6 (43%) patients prior to discontinuation of mechanical ventilation, which was undertaken 4-18 days (mean 7 +/- 3 days) after poisoning. Eleven patients (79%) were successfully weaned from mechanical ventilation at the first attempt. In the 3 (21%) remaining patients, mechanical ventilation had to be reestablished because of weaning failure. The mean (+/-SD) diaphragmatic CMAP amplitude, prior to discontinuation of ventilatory assistance, was 242.6 +/- 94.1 microV in these 3 patients. After ventilatory discontinuation, it fell to 95.5 +/- 105.8 microV. Thus, reduced diaphragmatic CMAP amplitudes correlate with the need for mechanical ventilation in acute OP poisoning.

Assessment of diaphragm paralysis with oesophageal electromyography and unilateral magnetic phrenic nerve stimulation.

The purpose of this study was to establish a sensitive and reliable method of diagnosing diaphragm paralysis by recording the diaphragm compound muscle action potential (CMAP) using a multipair oesophageal electrode and unilateral magnetic phrenic nerve stimulation. An oesophageal electrode catheter was designed containing six coils (1 cm wide and 3 cm apart), creating an array of four sequential electrode pairs. The oesophageal catheter was taped at the nose with the proximal electrode pair 40 cm from the nares. Eight patients with unilateral (n=5) or bilateral (n=3) diaphragm paralysis were studied. Five to seven phrenic nerve stimulations were performed at 80% of maximum magnetic stimulator output and the CMAPs were recorded simultaneously from the four pairs of electrodes. In the five patients with unilateral diaphragm paralysis, the CMAP amplitudes and latencies were 1.16+/-0.29 mV and 7.6+/-1.5 ms for functioning sides. No diaphragm CMAP could be detected when stimulating nonfunctioning phrenic nerves. This study shows that diaphragm paralysis can be reliably diagnosed by unilateral magnetic stimulation combined with a multipaired oesophageal electrode.

Long-term outcome of critical illness polyneuropathy.

The aim of this study was to describe the outcome of patients with critical illness polyneuropathy (CIP). Twenty-six patients with CIP were studied to determine the clinical and electrophysiological profile 13-24 months after the onset of CIP. Seven patients refused to participate in the study; 6 patients died within the 1st year. Eleven of the 13 survivors showed clinical evidence of polyneuropathy. Five of these patients also had mononeuropathies, including peroneal and ulnar nerves. The quality of life was markedly impaired in all patients. Nerve conduction studies, including limb motor and sensory nerve conductions, bilateral phrenic nerve onset latencies, and bilateral diaphragmatic compound muscle action potentials, were abnormal in all patients. Incomplete recovery within 1-2 years after the onset of disease occurs frequently in patients with CIP.

Quantification of the esophageal diaphragm electromyogram with magnetic phrenic nerve stimulation.

Measurement of the amplitude of the esophageal diaphragm compound muscle action potential (CMAP) could be useful for the diagnosis and monitoring of neuromuscular disease. However, quantification of the diaphragm CMAP has been hampered by difficulty in positioning the esophageal electrode at the diaphragm's electrically active center and many investigators report arbitrary units rather than voltage. To quantify the esophageal diaphragm CMAP we designed a multipair electrode which we evaluated during unilateral magnetic stimulation. The esophageal catheter consisted of four sequential electrode pairs. Overall the electrode spanned 17 cm and covered the entire electrically active region of the diaphragm. The diaphragm CMAP was simultaneously recorded from the four pairs at distances of 40, 39, 38, and 37 cm from the nose to the proximal electrode pair. Studies were undertaken in 10 normal subjects and 10 patients with diaphragm dysfunction. The amplitude of the CMAP (peak to peak) was defined as the average of five twitches recorded from the optimal pair of electrodes. The amplitude of the diaphragm CMAP elicited by unilateral maximal magnetic stimulation was 1.45 +/- 0.35 mV (mean +/- SD) for the right side and 1.68 +/- 0.47 mV for the left. When measured on different occasions the coefficient of variation (CV) was 8.6%. The amplitude of the CMAP measured from dysfunctional hemidiaphragms was much less than that measured from normal subjects. This study suggests that the diaphragm CMAP can be quantified using an appropriate esophageal electrode.

Repetitive phrenic nerve stimulation in myasthenia gravis.

In patients with MG it may be difficult to determine whether respiratory insufficiency is due to a defect in neuromuscular transmission. We therefore studied the clinical value of repetitive electrical stimulation of the phrenic nerve. Repetitive phrenic nerve stimulation at 3 Hz was performed in 25 patients with MG. We recorded from the ipsilateral hemidiaphragm with surface electrodes before and after exercising the diaphragm for 10 and 90 seconds. The percent decrement of the negative peak (NP) area between the first and the fifth or sixth diaphragmatic compound muscle action potential (DCMAP) was analyzed and results compared with those from 10 healthy individuals. The mean +/- standard deviation percent change of the NP area in healthy individuals was -2.1 +/- 4.2%, with a normal cutoff of > or = 11%. Twelve patients (48%) had an abnormal decrement of DCMAP--9 had a decrement when the diaphragm was rested, 3 only after fatiguing of the diaphragm. The mean percent change in the 12 patients was 20% at rest, -18% after 10 seconds of exercise, and -23% after 90 seconds of exercise-a pattern consistent with MG. Repetitive stimulation of the accessory nerve with recording of the trapezius CMAP (TCMAP) was abnormal in nine patients (36%). The three patients with abnormal decrement of the DCMAP despite normal TCMAP had symptoms of dyspnea. Repetitive phrenic nerve stimulation studies are a promising tool in the diagnosis of respiratory muscle weakness in MG and should be part of electrophysiologic studies in patients with undiagnosed respiratory failure.

Effect of brachial plexus co-activation on phrenic nerve conduction time

BACKGROUNDDiaphragm function can be assessed by electromyography of the diaphragm during electrical phrenic nerve stimulation (ES). Whether phrenic nerve conduction time (PNCT) and diaphragm electrical activity can be reliably measured...

Diaphragm electromyogram measured with unilateral magnetic stimulation.

The purpose of this study was to establish the phrenic nerve conduction time (PNCT) for magnetic stimulation and further assess the relatively new technique of anterior unilateral magnetic stimulation (UMS) of the phrenic nerves in evaluating the diaphragm electromyogram (EMG). An oesophageal electrode was used to record the diaphragm compound muscle action potential (CMAP) elicited by supramaximal percutaneous electrical phrenic nerve stimulation (ES) and UMS from eight normal subjects. The oesophageal electrode used for recording the CMAP was positioned at the level of the hiatus and 3 cm below. The diaphragm CMAP was also recorded from chest wall surface electrodes in five subjects. All of the phrenic nerves could be maximally stimulated with UMS. A clear plateau of the amplitude of the CMAP was achieved for the right and left phrenic nerves. The mean amplitudes of the CMAP recorded from the oesophageal electrode were, for the right side, 0.74+/-0.29 mV (mean+SD) for ES and 0.76+/-0.30 mV for UMS with maximal power output, and for the left side 0.88+/-0.33 mV for ES and 0.80+/-0.24 mV for UMS. PNCT measured by the oesophageal electrode with ES and UMS with maximal output were, for the right side, 7.0+/-0.8 ms and 6.9+/-0.8 ms, respectively, and for the left side 7.8+/-1.2 ms and 7.7+/-1.3 ms, respectively. However, the CMAP recorded from chest wall surface electrodes with UMS was unsuitable for the measurement of PNCT. The results suggest that unilateral magnetic stimulation of the phrenic nerves combined with an oesophageal electrode can be used to assess diaphragmatic electrical activity and measure the phrenic nerve conduction time.

Repetitive phrenic nerve stimulation study in normal subjects.

In patients with myasthenia gravis (MG), it may be difficult to determine by clinical methods if respiratory insufficiency is due to a defect in neuromuscular transmission. We therefore studied the technique of repetitive electrical stimulation of the phrenic nerve in 6 healthy subjects. It was easily performed and quite reproducible. Responses at 3-Hz stimulation were recorded from surface electrodes of the ipsilateral hemidiaphragm, before and after exercise. We analyzed the percent decrement of the negative peak (NP) amplitude, area, and duration of the diaphragmatic compound muscle action potential (CMAP) between the first and the fifth or sixth potentials. The mean percentage change of the area was -2.2% (+/-4.3), and in all tests the change was <10.6%, yielding a normal range of <11%. The change in the NP amplitude was 12.1% (+/-8.3); in duration, the change was -8.7% (+/-9.6). Producing diaphragm fatigue did not change these results. The increase in amplitude and decrease in duration with little change in area, termed pseudofacilitation, may be due to shifts in the position of the diaphragm affecting volume conduction. The technique is a promising tool in the diagnosis of respiratory involvement from neuromuscular transmission disorders.

Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration.

The effect of chest wall configuration on the diaphragm electromyogram (EMGdi) was evaluated in five healthy subjects with an esophageal electrode for both interference pattern EMGdi (voluntary contractions) and electrically evoked diaphragm compound muscle action potentials (CMAPs). Diaphragm CMAPs (both unilateral and bilateral) were evaluated for the baseline-to-peak amplitude (Ampl), the time from the onset of the CMAP to first peak (T1), root mean square (RMS), and center frequency (CF) values of the CMAP power spectrum. CF values from the interference pattern EMGdi power spectrum were also calculated. For CMAPs obtained at an electrode position least influenced by variations induced by electrode positioning, Ampl increased with diaphragm shortening from functional residual capacity (FRC) to total lung capacity (TLC) by 101 and 98% (unilateral and bilateral, respectively). Bilateral CMAP RMS values increased 116% from FRC to TLC. CMAP T1 values decreased with diaphragm shortening from FRC to TLC by 1.1 and 2.1 ms for the unilateral and bilateral stimulations, respectively, and CF increased for the bilateral diaphragm CMAPs with diaphragm shortening. CF values from the interference pattern EMGdi did not show any consistent change with chest wall configuration. Thus CF values of the interference pattern EMGdi obtained with an esophageal electrode can be considered reliable for physiological interpretation, at any diaphragm length (if electrode positioning and signal contamination are controlled for), contrary to the diaphragm CMAPs, which are sensitive to changes in chest wall configuration. It is speculated that the different results (over the effects of chest wall configuration on interference pattern EMGdi and diaphragm CMAPs) amy be because of summation properties of the signals and how these influence the EMG power spectrum.

Respiratory electrophysiological studies in Guillain-Barré syndrome.

Respiratory failure is a common and potentially life threatening complication in patients with Guillain-Barré syndrome. The incidence of phrenic nerve involvement and the predictive value of phrenic nerve conduction and diaphragmatic needle EMG were studied in 40 patients with Guillain-Barré syndrome within the first three days of admission to hospital. The negative peak onset latency of the diaphragmatic compound muscle action potential (CMAP), and its amplitude, duration, and area were abnormal in 83%. The need for ventilation was correlated with diaphragmatic CMAP amplitude (P = 0.005), and area (P = 0.001), but not with latency or duration. Abnormalities in diaphragmatic needle EMG were found in 45%, mainly a decreased number of motor unit potentials. The abnormalities correlated with the need for ventilation (P = 0.013). Of the 40% who required ventilation, all had either abnormal phrenic conduction, abnormal diaphragmatic needle EMG, or both. Eighty one per cent of the ventilated patients had abnormal forced vital capacity on the day of the electrophysiological examination. The results indicate that phrenic nerve conduction studies and diaphragmatic EMG are useful in detecting respiratory involvement in patients with Guillain-Barré syndrome and in identifying those at risk of respiratory failure.

Central and peripheral respiratory electrophysiological studies in myotonic dystrophy.

Acute and chronic respiratory failure is a common and potentially life-threatening feature in patients with myotonic dystrophy (MD). The causes may be varied, and can involve both the central and peripheral nervous system. To evaluate the incidence of respiratory muscle involvement and the function of the central motor inspiratory pathway to phrenic motor neurons we performed magnetic stimulation of the cortex and cervical spinal cord, phrenic nerve conduction studies and needle EMG of diaphragm and intercostal muscles in 25 patients with MD. The results were compared with those from 35 healthy subjects. In addition, pulmonary function tests, blood gas analyses and static mouth pressures were evaluated. Abnormalities in response to magnetic stimulation, including a reduced compound muscle action potential (CMAP) from the diaphragm and increased excitability threshold, indicated impaired central inspiratory drive in 20% of cases. Phrenic nerve conduction showed a reduced diaphragmatic CMAP amplitude in 20%, and a delayed negative peak onset latency in 4% of cases. Abnormalities in diaphragm and intercostal muscle needle EMG were found in 76% of cases, these were mainly myotonic discharges (68%) and a decrease in the number of active motor units (36%). Patients with abnormal respiratory electrophysiological parameters had a significantly lower functional vital capacity (FVC; P = 0.005). The duration of the disease correlated negatively with diaphragmatic CMAP amplitude to phrenic nerve, but not magnetic, stimulation. Our results demonstrate that the involvement of the central inspiratory pathway is common in MD patients. Central and peripheral electrophysiological studies of the diaphragm should be considered in the diagnosis and management of patients with MD and dyspnoea.

Percutaneous magnetic coil stimulation of the phrenic nerve roots and trunk

We describe a technique of percutaneous magnetic coil NO stimulation of the phrenic nerve trunk on one side of the neck and phrenic roots over the upper cervical vertebral column in 10 normal subjects and 2 patients. We were able to obtain compound muscle action potentials (CMAPs) from the diaphragm at two sites (xiphoid process and 7th intercostal space) after stimulation of the phrenic nerve trunk and roots. We noted that the onset latencies after phrenic root stimulation remained fixed despite increasing the stimulus intensity from 50% to 100% and on moving the MC vertically or laterally, suggesting that stimulation of the fastest conducting fibers was occurring at a fixed site, most likely at the intervertebral foramina. Absent responses unilaterally in one and prolonged latencies to diaphragmatic CMAPs in another patient confirmed phrenic neuropathy in these patients.

Application of a cervical stimulating apparatus for bilateral transcutaneous phrenic nerve stimulation

Transcutaneous bilateral phrenic nerve stimulation (tPNS) is frequently used to assess diaphragmatic function in humans. Commonly, stimulation is performed with hand-held electrodes; however, these are unsuitable for studies requiring repeated PNS and where recruitment of rib cage and neck muscles may shift the probes in relation to the nerves. In this study we describe the design of a cervical neck brace and electrode probes that maintain stimulating electrodes in constant position relative to the phrenic nerves and facilitates studies requiring repeated maximal PNS. The effectiveness of the apparatus was examined by 1) reviewing the reproducibility of the transdiaphragmatic pressure response to 0.1 ms tPNS (PdiT) at relaxed functional residual capacity in four subjects studied on 25 +/- 8 (SD) occasions (> or = 24 h apart) over a 4-yr period, and 2) measuring peak-to-peak amplitude of the left and right diaphragmatic compound muscle action potentials (surface electrodes) during two prolonged studies (38 +/- 9 min) in each subject, when tPNS was performed during repeated submaximal and maximal inspiratory efforts. PdiT was reproducible in each subject when measured repeatedly within a single study [coefficient of variation (CV) of 3.8 +/- 0.8%] and over separate days (CV of 11.5 +/- 3.5%). The peak-to-peak amplitudes of the left and right compound muscle action potentials were also reproducible (CV of 8.4 +/- 4.3 and 8.4 +/- 2.9%, respectively) and independent of the degree of effort. The apparatus appears effective for the maintenance of maximal stimulation under varied conditions for long periods and provides reproducible measurements of PdiT both within and between studies.

Peripheral Nerve Function in Sepsis and Multiple Organ Failure

Forty-three patients who had sepsis and multiple organ failure (critical illness) were studied prospectively to determine the incidence and severity of peripheral nerve function and to correlate such function with a number of variables. Electrophysiologic studies indicated a primary axonal degeneration of motor and sensory fibers in 30 (70 percent). Fifteen (30 percent) had the clinical signs of difficulty in weaning from assisted ventilation, weakness of limb muscles, and reduced or absent deep tendon reflexes. Full recovery from the polyneuropathy occurred among the 23 (53 percent) who survived, except three who had a very severe polyneuropathy. A peripheral nerve function index, computed from electrophysiologic measurements, showed statistically significant (p less than 0.01) negative correlations with the time in the critical care unit, and the serum glucose value; the serum albumin level showed a positive correlation. Multiple regression analyses indicated all three factors accounted for 47 percent (r2 = 0.4678) of all potential variables. In a separate analysis, the nerve function index correlated with the amplitude of the diaphragm compound muscle action potential (p less than 0.01). The results were consistent with the polyneuropathy being due to the same mechanisms that are currently postulated to cause dysfunction in this syndrome of other organ systems (including the neuromuscular respiratory system).