This study determined normal values for motor evoked potentials (MEPs) and compound muscle action potentials (CMAPs) of the diaphragm following cortical and cervical magnetic stimulation (COMS and CEMS) of the phrenic nerves in healthy adults.
Using surface electrodes, diaphragmatic MEP and CMAP were recorded in 70 subjects (34 ± 13 years, 25 men) following supramaximal cortical magnetic stimulation and CEMS at functional residual capacity and using a standardized inspiratory pressure trigger (−0.5 kPa). All healthy volunteers underwent standard spirometry and measurement of maximum inspiratory and expiratory pressure.
At functional residual capacity, upper limit of normal for MEP latency was 25 ms in men and 23 ms in women (p < 0.05), and upper limit of normal for CMAP latency was 6 ms. In contrast to MEP and CMAP amplitude, corresponding latencies showed little interindividual and intraindividual variability. Use of an inspiratory pressure trigger enhanced reproducibility and amplitude of diaphragm MEP. Diaphragm responses to both cortical and cervical magnetic stimulation were symmetrical and independent of age (in our cohort), with higher values for latency and amplitude in men (each p < 0.05). Diaphragm CMAP amplitude showed weak–moderate correlations with forced vital capacity (r = 0.47; p < 0.01), maximum inspiratory pressure (r = 0.39; p < 0.01), and maximum expiratory pressure (r = 0.32; p < 0.01).
Combination of cortical magnetic stimulation and CEMS of the phrenic nerves is feasible and allows noninvasive assessment of both central and peripheral conductivity of the diaphragm and the inspiratory pathway.
*Respiratory Physiology Laboratory, Department of Neurology with Institute for Translational Neurology, University of Muenster, Muenster, Germany;
†Bethanien Hospital GmbH Solingen, Solingen, Germany;
‡Institute for Pneumology at the University of Cologne, Solingen, Germany;
§Medical Park Klinik Reithofpark, Bad Feilnbach, Germany; and
‖Institute for Medical Informatics, University of Muenster, Muenster, Germany.
Address correspondence and reprint requests to Matthias Boentert, MD, University Hospital of Muenster, Respiratory Physiology Laboratory, Department of Neurology with Institute for Translational Neurology, University of Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany; e-mail: matthias.boentert.@ukmuenster.de.
J. Spiesshoefer has been supported by the ´Else-Kröner-Fresenius Stiftung´ (Grant A109) and by ´Kommission für Innovative Medizinische Forschung an der Medizinischen Fakultät Muenster´ (IMF Grant SP 11 18 15) outside this work. M. Boentert and P. Young have received speaker honoraria and financial research support outside this work by Sanofi-Genzyme, Neu-Isenburg, Germany, Löwenstein Medical and the Löwenstein Foundation, Bad Ems, Germany. W. Randerath has received travel grants and speaking fees outside the submitted work from Löwenstein Medical, Weinmann, Philips Respironics, Novartis, Inspire, and Boehringer Ingelheim. C. Henke, M. Schneppe, T. Brix, and S. Herkenrath declare no conflicts of interest.
This study was supported by Sanofi-Genzyme, Neu-Isenburg, Germany. The funders had no role in study design, data collection and analysis, preparation of the manuscript, or the submission process.
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