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Diaphragm paralysis may occur after traumatic phrenic nerve injury. Here we report three patients in whom right hemi-diaphragmatic paralysis developed after cardiac radiofrequency ablation. We hypothesise that local focused thermal energy at the time of the ablation may have caused direct neuronal damage by axonal coagulation necrosis. The prognosis for this type of injury may be reasonably good; two of the three patients fully recovered diaphragm function by 1 year.

The case is reported of a male track and field athlete with breathing difficulties at rest and during exercise, which were exacerbated in the supine position and during water immersion. Right hemidiaphragmatic paralysis was diagnosed. The cause of this relatively benign disorder is not known and there are no serious clinical implications. There is no treatment, but a continuation of exercise together with interventions to strengthen the subsidiary inspiratory muscles is recommended.

The diaphragm compound-muscle action potential (CMAPdi), elicited by unilateral magnetic stimulation (UMS) of the phrenic nerve can be recorded using surface electrodes. However, there is no consensus on the best positioning of surface electrodes and there are no data on the reproducibility of the signal. Using 36 surface electrode pairs, in five healthy subjects, the CMAPdi elicited by UMS and electrical stimulation (ES) were compared and 12 pairs were identified as providing acceptable signals. The latency and amplitude were measured for each CMAPdi, following UMS at 60-100% of maximal stimulator output, in 12 healthy subjects, on two occasions. Latencies obtained using UMS and ES ranged between 6.1-7.33 and 6.25-7.17 ms, respectively. Optimum CMAPdi were not recorded from the same electrode pair in all subjects, or for both hemidiaphragms in each subject. However, the optimal recording site for a particular individual remained unchanged on subsequent testing. When recorded from the optimal site, latencies and amplitudes of CMAPdi elicited on the two occasions were not significantly different. The current study suggests that the use of multiple chest wall electrodes can identify an optimal electrode pair, from which it is possible to obtain reproducible compound-muscle action potential signals.

Twitch transdiaphragmatic pressure (Tw Pdi) measured with magnetic stimulation of the phrenic nerve is used to follow up patients and to assess the effect of clinical treatments on diaphragm function. However the reproducibility of Tw Pdi on different occasions has been little studied. We investigated 32 normal subjects, measuring Tw Pdi elicited by bilateral magnetic stimulation of the phrenic nerves on two to 14 occasions. Sniff transdiaphragmatic pressure (sniff Pdi) was also measured. The mean value of Tw Pdi and sniff Pdi were 28+/-5 and 134+/-24 cm H(2)O, respectively. The within subjects coefficient of variation was 11% for both Tw Pdi and sniff Pdi. We conclude that there is a variability of Tw Pdi and the variability of Tw Pdi is the same as that of sniff Pdi., (Copyright 2002 Elsevier Science B.V.)

Diaphragm strength can be assessed from twitch gastric (TwPgas), twitch oesophageal (TwPoes), and twitch transdiaphragmatic pressure (TwPdi) in response to phrenic nerve stimulation. This requires the passage of balloon catheters, which may be difficult. Changes in pressure measured at the mouth during phrenic nerve stimulation avoid the need for balloon catheters. We hypothesized that pressures measured at the tracheal tube during phrenic stimulation, could also reflect oesophageal pressure change as a result of isolated diaphragmatic contraction and, therefore, reflect diaphragm strength. We aimed to establish the relationship between twitch tracheal tube pressure (TwPet), TwPoes, and TwPdi in patients in the supine and sitting positions. The phrenic nerves were stimulated magnetically bilaterally, in 14 ICU patients while supine and on another occasion while sitting up at 45 degrees. In the sitting position mean TwPoes was 9.1 cm H2O and TwPet 11.3 cm H2O (mean(SD) difference -2.2 (SD 1.5)). In the supine position mean TwPoes was 8.1 cm H2O and TwPet 9.9 cm H2O (mean difference -1.8 (2.2)). The difference between TwPoes and TwPet was less at low twitch amplitude; less than +/- 1 cm H2O below a mean twitch height of 8 cm H2O supine and 10 cm H2O sitting. Sitting TwPet was related to TwPoes r2=0.93 and TwPdi r2=0.65 (P<0.01). Supine TwPet was related to TwPoes r2=0.84 and TwPdi r2=0.83 (P<0.01). The mean within occasion coefficient of variation while sitting was TwPet=13.3%, TwPoes=13.9%, TwPdi=11.2%, and supine TwPet=11.6%, TwPoes=14.6%, TwPdi=11.8%. We conclude that TwPet reflects TwPoes during diaphragmatic stimulation and is worthy of further study to establish its place as a guide to the presence of respiratory muscle strength and fatigue.

To test the hypothesis that diaphragm fatigue leads to an increase in neural respiratory drive, we measured the esophageal diaphragm electromyogram (EMG) during CO(2) rebreathing before and after diaphragm fatigue in six normal subjects. The electrode catheter was positioned on the basis of the amplitude and polarity of the diaphragm compound muscle action potential recorded simultaneously from four pairs of electrodes during bilateral anterior magnetic phrenic nerve stimulation (BAMPS) at functional residual capacity. Two minutes of maximum isocapnic voluntary ventilation (MIVV) were performed in six subjects to induce diaphragm fatigue. A maximal voluntary breathing against an inspiratory resistive loading (IRL) was also performed in four subjects. The reduction of transdiaphragmatic pressure elicited by BAMPS was 22% (range 13-27%) after 2 min of MIVV and was similar, 20% (range 13-26%), after IRL. There was a linear relationship between minute ventilation (VE) and the root mean square (RMS) of the EMG during CO(2) rebreathing before and after fatigue. The mean slope of the linear regression of RMS on VE was similar before and after diaphragm fatigue: 2.80 +/- 1.31 vs. 3.29 +/- 1.40 for MIVV and 1.51 +/- 0.31 vs 1.55 +/- 0.31 for IRL, respectively. We conclude that the esophageal diaphragm EMG can be used to assess neural drive and that diaphragm fatigue of the intensity observed in this study does not affect respiratory drive.

A nonvolitional test to assess diaphragm strength in neonates has not been previously described. Our aim was to assess the feasibility of cervical (CMS) and anterior (AMS) magnetic stimulation of the phrenic nerves in neonates. Double circular stimulating coils (90-mm) were used. For CMS, one coil was placed over the cervical spine to bilaterally stimulate the phrenic nerve roots, whereas for AMS the coils were placed on the anterolateral aspect of the neck to allow unilateral and bilateral stimulation. Diaphragm contractility was assessed as transdiaphragmatic pressure (Pdi) measured with balloon catheters positioned in the midesophagus and stomach. Stimulus supramaximality was assessed by examining diaphragm twitch Pdi (TwPdi) across a range of stimulator outputs; 85, 90, 95, and 100% of maximum. Pressure signals were measured by differential pressure transducer and displayed in real time on a computer. Patients were studied supine during sleep. CMS was performed on seven neonates (mean gestational age [GA] 38 wk, range 33 to 40 wk) and AMS on 18 neonates (mean GA 37 wk, range 32 to 41 wk). The mean (SD) TwPdi with CMS was 2.5 (0.8) cm H(2)O. CMS was not supramaximal; reducing the stimulator output below 100% caused marked reductions in TwPdi, also the shape of the pressure waveforms suggested that CMS may not have activated the diaphragm alone. Mean (SD) TwPdi with AMS was 4.5 (1.3) cm H(2)O on the left, 4.1 (0.9) cm H(2)O on the right, and 8.7 (3.9) cm H(2)O for bilateral stimulation. The shape of the pressure waveforms suggested that AMS was more specific and a plateau in TwPdi at higher stimulator outputs indicated supramaximality. We conclude that AMS may provide a useful technique to assess diaphragm function in the neonate.

Objective: Anterior magnetic stimulation (aMS) of the phrenic nerves is a new method for the assessment of diaphragm contractility that might have particular applications for the clinical assessment of critically ill patients who are commonly supine., Design: We compared aMS with existing techniques for measurement of diaphragm weakness and fatigue in 10 normal subjects, 27 ambulant patients with suspected diaphragm weakness and 10 critically ill patients., Setting: Laboratory and intensive care unit of two university hospitals., Results: Although aMS was not demonstrably supramaximal in normal subjects, the mean value of twitch transdiaphragmatic pressure (Tw Pdi) obtained at 100% of stimulator output, 23.7 cmH2O, did not differ significantly from that obtained with bilateral supramaximal electrical stimulation (ES), 24.9 cmH2O, or bilateral anterior magnetic phrenic nerve stimulation (BAMPS), 27.3 cmH2O. A fatiguing protocol produced a 20 % fall in aMS-Tw Pdi and a 19% fall in BAMPS-Tw Pdi; the fall in aMS-Tw Pdi correlated with the fall in BAMPS-Tw Pdi (r2 = 0.84, p = 0.03) indicating that aMS can detect diaphragm fatigue. In ambulant patients aMS agreed closely with existing measures of diaphragm strength. The maximal sniff Pdi correlated with both the aMS-Tw Pdi (r2 = 0.60, p < 0.0001) and the BAMPS-Tw Pdi (r2 = 0.65, p < 0.0001) and the aMS-Tw Pdi was a mean (SD) 2.2 (4.3) cmH2O less than BAMPS-Tw Pdi. In addition, aMS correctly identified diaphragm dysfunction in patients studied on the ICU., Conclusions: We conclude that aMS is of clinical value for the investigation of suspected diaphragm weakness.

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.

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.

Background: Diaphragm 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 from chest wall electrodes with ES is uncertain., Methods: The diaphragm compound muscle action potential (CMAP) was recorded using an oesophageal electrode and lower chest wall electrodes during ES in six normal subjects. Two patients with bilateral diaphragm paralysis were also studied. Stimulations were deliberately given in a manner designed to avoid or incur co-activation of the brachial plexus., Results: For the oesophageal electrode the PNCT was similar with both stimulation techniques with mean (SE) values of 7.1 (0.2) and 6.8 (0.2) ms, respectively (pooled left and right values). However, for surface electrodes the PNCT was substantially shorter when the brachial plexus was activated (4.4 (0.1) ms) than when it was not (7.4 (0.2) ms) (mean difference 3.0 ms, 95% CI 2.7 to 3.4, p<0.0001). A small short latency CMAP was recorded from the lower chest wall electrodes during stimulation of the brachial plexus alone., Conclusions: The results of this study show that lower chest wall electrodes only accurately measure PNCT when care is taken to avoid stimulating the brachial plexus. A false positive CMAP response to phrenic stimulation could be caused by inadvertent stimulation of the brachial plexus. This finding may further explain why the diaphragm CMAP recorded from chest wall electrodes can be unreliable with cervical magnetic stimulation during which brachial plexus activation occurs.

The purpose of the study was to compare electrical stimulation (ES) and cervical magnetic stimulation (CMS) of the phrenic nerves for the measurement of the diaphragm compound muscle action potential (CMAP) and phrenic nerve conduction time. A specially designed esophageal catheter with three pairs of electrodes was used, with control of electrode positioning in 10 normal subjects. Pair A and pair B were close to the diaphragm (pair A lower than pair B); pair C was positioned 10 cm above the diaphragm to detect the electromyogram from extradiaphragmatic muscles. Electromyograms were also recorded from upper and lower chest wall surface electrodes. The shape of the CMAP measured with CMS (CMS-CMAP) usually differed from that of the CMAP measured with ES (ES-CMAP). Moreover, the latency of the CMS-CMAP from pair B (5.3 +/- 0.4 ms) was significantly shorter than that from pair A (7.1 +/- 0.7 ms). The amplitude of the CMS-CMAP (1.00 +/- 0.15 mV) was much higher than that of ES-CMAP (0.26 +/- 0.15 mV) when recorded from pair C. Good-quality CMS-CMAPs could be recorded in some subjects from an electrode positioned very low in the esophagus. The differences between ES-CMAP and CMS-CMAP recorded either from esophageal or chest wall electrodes make CMS unreliable for the measurement of phrenic nerve conduction time.

The transdiaphragmatic pressure (Pdi) elicited by paired bilateral phrenic nerve stimulation may be viewed as the sum of the Pdi values produced by the first (t1) and second (t2) stimulus. The Pdi at t2 (P[di,t2]) is a function of the interstimulus interval. A reduction in the ratio obtained by dividing Pdi,t2 at 10 Hz (P[di,t2,10]) by Pdi at 100 Hz (P[di,t2,100]) (t2(10:100)) has been proposed as a test of low frequency diaphragm fatigue. The aim of the present study was to establish whether this change could also be detected using paired cervical magnetic nerve stimulation (pCMS), and whether t2(10:100) was influenced by lung volume. We studied healthy subjects at functional residual capacity (FRC), at 0.5 and 1.0 L below FRC, and at 0.5, 1.0 and 1.5 L above FRC. The subjects were then subjected to a fatiguing protocol (2 min of maximal isocapnic ventilation (MIV)). Studies were repeated at FRC 20 and 60 min after MIV and between these times at 1.0 L below and 1.5 L above FRC. In the unfatigued state, t2(10:100) had a negative relationship with increasing lung volume (r2=0.98, p=0.002). After MIV there was a fall in the Pdi elicited by a single stimulus (mean fall at 20 min 17.9% and at 60 min 14.6%, p<0.03 for both). t2(10:100) fell by a mean 28.1% after 20 min and mean 22.9% at 60 min (p<0.03 for both). This change was mainly mediated by a fall in the P[di,t2,10]. The t2(10:100) was not able to distinguish between fatigue and acute hyperinflation. We conclude that paired cervical magnetic nerve stimulation may be used to detect low frequency diaphragm fatigue but that it remains important to control for lung volume.

Cervical magnetic stimulation (CMS) produces a greater twitch transdiaphragmatic pressure (TwPdi) than electrical stimulation. This may be because CMS produces rib cage muscle activation, thus producing an inspiratory action independent of the diaphragm. Alternatively, CMS could merely stiffen the rib cage, allowing the diaphragm to act efficiently, by contracting against a stable rib cage. To examine these two hypotheses we studied five patients with isolated bilateral diaphragm paralysis using CMS and bilateral electrical phrenic stimulation (BES). TwPdi, twitch esophageal pressure (TwPes), and twitch gastric pressure (TwPgas) were measured. We also assessed maximal sniff esophageal and transdiaphragmatic pressures (SnPes) (SnPdi), maximal inspiratory and expiratory mouth pressures (MIP) (MEP), and fall in VC on moving from an upright to a supine position. Respiratory muscle strength tests were consistent with bilateral diaphragm paralysis, and the MEPs confirmed normal expiratory muscle function. The patients were able to generate a mean SnPes of -30 cm H2O, mainly because of inspiratory activity of rib cage and neck muscles. However, TwPdi and TwPes during both CMS and BES were close to zero. We conclude that in our patients with diaphragm paralysis caused by neuralgic amyotrophy, CMS stiffens the rib cage but does not have an inspiratory action independent of the diaphragm.

Background: Accurate assessment of diaphragm strength can be difficult. Transdiaphragmatic pressure (PDI) measurements during volitional manoeuvres are useful but it may be difficult to ensure maximum patient effort. Magnetic stimulation of the phrenic nerves is easy to perform and the results are reproducible in normal subjects. The purpose of the present study was to evaluate the usefulness of magnetic stimulation of the phrenic nerves in the assessment of diaphragm weakness in patients., Methods: Sixty-six patients referred for assessment of respiratory muscle strength and 23 normal subjects were studied. Twitch PDI (TwPDI) following magnetic stimulation of the phrenic nerves and sniffPDI were obtained in all individuals. TWPDI following bilateral electrical stimulation of the phrenic nerves was also obtained in eight patients., Results: Mean (SD) TwPdi for the normal subjects was 31 (6) cm H2O and 18 (11) cm H2O for the patients. TwPDI and sniffPDI were correlated (r = 0.77). Seven of the 37 patients (19%) with a reduced sniffPDI had a TwPDI within the normal range whereas two of the 32 patients (6%) with a reduced TwPDI had a normal sniffPDI. TwPDI was similar with magnetic and electrical stimulation., Conclusions: TwPDI following magnetic stimulation of the phrenic nerves is a clinically useful measurement when assessing diaphragm weakness.

We investigated whether bilateral magnetic stimulation of the phrenic nerves from an anterolateral approach (BAMPS) could combine the reproducibility and ease of use of cervical magnetic stimulation (CMS) with the specificity of bilateral electrical stimulation (BES) and whether it could be used in supine subjects. We placed two double 43-mm coils over the phrenic nerves in the neck. BAMPS produced supramaximal phrenic stimulation by electromyogram (EMG) assessment in six of seven subjects. There was no significant difference in the twitch gastric pressure/twitch esophageal pressure ratio (twitch Pgas/Pes) between BAMPS (1.2) and BES (1.3). Both differed from CMS (0.9, p < 0.001). The effect of a change in posture on twitch transdiaphragmatic pressure (TwPdi) and Pgas/Pes ratio was the same for BAMPS and BES. In normal subjects and patients BAMPS correlated significantly with BES (r = 0.97), maximal sniffs (r = 0.85), and CMS (r = 0.92). The mean difference between BAMPS and BES was 0.3 cm H2O (SD = 2.3). Two-minute maximal isocapnic ventilation produced a 19% fall in TwPdi elicited by BAMPS. BAMPS is easy, well tolerated and can be used in the supine subject. TwPdi and partitioning of Pes and Pgas were very close for BAMPS and BES, suggesting similar specificity for the diaphragm.