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3. Standards of instrumentation of EMG

Author

Tankisi, Hatice, Burke, David, Cui, Liying, de Carvalho, Mamede, Kuwabara, Satoshi, Nandedkar, Sanjeev D., Rutkove, Seward, Stålberg, Erik, van Putten, Michel J.A.M., and Fuglsang-Frederiksen, Anders

Published
2020
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5. Guidelines for single fiber EMG

Author

Sanders, Donald B., Arimura, Kimiyoshi, Cui, LiYing, Ertaş, Mustafa, Farrugia, Maria Elena, Gilchrist, James, Kouyoumdjian, João Aris, Padua, Luca, Pitt, Matthew, and Stålberg, Erik

Published
2019
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6. Assessment of the reliability of the motor unit size index (MUSIX) in single subject “round-robin” and multi-centre settings

Author

Alix, James J.P., Neuwirth, Christoph, Gelder, Lucy, Burkhardt, Christian, Castro, José, de Carvalho, Mamede, Gawel, Malgorzata, Goedee, Stephan, Grosskreutz, Julian, Lenglet, Timothée, Moglia, Cristina, Omer, Taha, Schrooten, Maarten, Nandedkar, Sanjeev, Stalberg, Erik, Barkhaus, Paul E., Furtula, Jasna, van Dijk, Johannes P., Baldinger, Reto, Costa, Joao, Otto, Marit, Sandberg, Arne, and Weber, Markus

Published
2019
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24. Reinnervation as measured by the motor unit size index is associated with preservation of muscle strength in amyotrophic lateral sclerosis, but not all muscles reinnervate

Author

Chan, Young, primary, Alix, James J. P., additional, Neuwirth, Christoph, additional, Barkhaus, Paul E., additional, Castro, José, additional, Jenkins, Thomas M., additional, McDermott, Christopher J., additional, Shaw, Pamela J., additional, Carvalho, Mamede, additional, Nandedkar, Sanjeev, additional, Stålberg, Erik, additional, and Weber, Markus, additional

Published
2021
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32. Neurogenic vs. Myogenic Origin of Acquired Muscle Paralysis in Intensive Care Unit (ICU) Patients: Evaluation of Different Diagnostic Methods

Author

Marrero, Humberto D. J. Gonzalez, Stålberg, Erik, Cooray, Gerald, Corpeno Kalamgi, Rebeca, Hedstrom, Yvette, Bellander, Bo-Michael, Nennesmo, Inger, and Larsson, Lars

Subjects
critical care, lcsh:R5-920, EMG, Neurology, Neurologi, CMAP, ENeG, myosin, muscle biopsy, lcsh:Medicine (General), Article, myopathy
Abstract

Introduction. The acquired muscle paralysis associated with modern critical care can be of neurogenic or myogenic origin, yet the distinction between these origins is hampered by the precision of current diagnostic methods. This has resulted in the pooling of all acquired muscle paralyses, independent of their origin, into the term Intensive Care Unit Acquired Muscle Weakness (ICUAW). This is unfortunate since the acquired neuropathy (critical illness polyneuropathy, CIP) has a slower recovery than the myopathy (critical illness myopathy, CIM), therapies need to target underlying mechanisms and every patient deserves as accurate a diagnosis as possible. This study aims at evaluating different diagnostic methods in the diagnosis of CIP and CIM in critically ill, immobilized and mechanically ventilated intensive care unit (ICU) patients. Methods. ICU patients with acquired quadriplegia in response to critical care were included in the study. A total of 142 patients were examined with routine electrophysiological methods, together with biochemical analyses of myosin:actin (M:A) ratios of muscle biopsies. In addition, comparisons of evoked electromyographic (EMG) responses in direct vs. indirect muscle stimulation and histopathological analyses of muscle biopsies were performed in a subset of the patients. Results. ICU patients with quadriplegia were stratified into five groups based on the hallmark of CIM, i.e., preferential myosin loss (myosin:actin ratio, M:A) and classified as severe (M:A &lt, 0.5, n = 12), moderate (0.5 &le, M:A &lt, 1, n = 40), mildly moderate (1 &le, 1.5, n = 49), mild (1.5 &le, 1.7, n = 24) and normal (1.7 &le, M:A, n = 19). Identical M:A ratios were obtained in the small (4&ndash, 15 mg) muscle samples, using a disposable semiautomatic microbiopsy needle instrument, and the larger (&gt, 80 mg) samples, obtained with a conchotome instrument. Compound muscle action potential (CMAP) duration was increased and amplitude decreased in patients with preferential myosin loss, but deviations from this relationship were observed in numerous patients, resulting in only weak correlations between CMAP properties and M:A. Advanced electrophysiological methods measuring refractoriness and comparing CMAP amplitude after indirect nerve vs. direct muscle stimulation are time consuming and did not increase precision compared with conventional electrophysiological measurements in the diagnosis of CIM. Low CMAP amplitude upon indirect vs. direct stimulation strongly suggest a neurogenic lesion, i.e., CIP, but this was rarely observed among the patients in this study. Histopathological diagnosis of CIM/CIP based on enzyme histochemical mATPase stainings were hampered by poor quantitative precision of myosin loss and the impact of pathological findings unrelated to acute quadriplegia. Conclusion. Conventional electrophysiological methods are valuable in identifying the peripheral origin of quadriplegia in ICU patients, but do not reliably separate between neurogenic vs. myogenic origins of paralysis. The hallmark of CIM, preferential myosin loss, can be reliably evaluated in the small samples obtained with the microbiopsy instrument. The major advantage of this method is that it is less invasive than conventional muscle biopsies, reducing the risk of bleeding in ICU patients, who are frequently receiving anticoagulant treatment, and it can be repeated multiple times during follow up for monitoring purposes.

Published
2020

34. Agrin mutations lead to a congenital myasthenic syndrome with distal muscle weakness and atrophy

Author

Nicole, Sophie, Chaouch, Amina, Torbergsen, Torberg, Bauché, Stéphanie, de Bruyckere, Elodie, Fontenille, Marie-Joséphine, Horn, Morten A., van Ghelue, Marijke, Løseth, Sissel, Issop, Yasmin, Cox, Daniel, Müller, Juliane S., Evangelista, Teresinha, Stålberg, Erik, Ioos, Christine, Barois, Annie, Brochier, Guy, Sternberg, Damien, Fournier, Emmanuel, Hantaï, Daniel, Abicht, Angela, Dusl, Marina, Laval, Steven H., Griffin, Helen, Eymard, Bruno, and Lochmüller, Hanns

Published
2014
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45. Marching band model for simulating a single muscle fiber action potential.

Author

Nandedkar, Sanjeev D. and Stålberg, Erik V.

Subjects
*MARCHING bands, *FIBERS, *TENDONS
Abstract

• A modification to previously described line source model for calculating a single muscle fiber action potential is described. • Change in action potential waveform at different sites from end-plate to tendon is demonstrated and discussed. • The conceptually simple model simulated waveforms seen in clinical recordings, and using complex volume conductor models. We describe a mathematical model to calculate a single muscle fiber action potential (AP). Based on a marching band pattern, it is an enhancement to our previously described "modified line source" model. Calculations were performed using an Excel spread sheet. AP was simulated for a 200 mm long muscle fiber with 60 µm diameter, propagation velocity of 4 m/s, and end-plate located at the center. Several different electrode locations were used to calculate the AP. The AP amplitude was highest at the end-plate where the waveform was biphasic with initial negativity. When the electrode was moved towards the tendon, the amplitude decreased for the first 1.5 mm. The AP was triphasic and its waveform was relatively constant at electrode positions beyond 1.5 mm from the end-plate. It matched the calculations using the modified line source model. When the electrode was near the tendon, the AP amplitude decreased asymmetrically and waveform became biphasic resembling a positive sharp wave. The model is conceptually and computationally simple. It simulated the expected AP shape at different electrode positions along the muscle fiber. The waveforms are similar to those obtained from mathematically complex volume conductor models. The revised model can be useful for teaching and future simulation studies. [ABSTRACT FROM AUTHOR]

Published
2022
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46. Reinnervation as measured by the motor unit size index is associated with preservation of muscle strength in amyotrophic lateral sclerosis, but not all muscles reinnervate.

Author

Chan, Young, Alix, James J. P., Neuwirth, Christoph, Barkhaus, Paul E., Castro, José, Jenkins, Thomas M., McDermott, Christopher J., Shaw, Pamela J., de Carvalho, Mamede, Nandedkar, Sanjeev, Stålberg, Erik, and Weber, Markus

Abstract

Introduction/Aims: The motor unit size index (MUSIX) may provide insight into reinnervation patterns in diseases such as amyotrophic lateral sclerosis (ALS). However, it is not known whether MUSIX detects clinically relevant changes in reinnervation, or if all muscles manifest changes in MUSIX in response to reinnervation after motor unit loss. Methods: Fifty‐seven patients with ALS were assessed at 3‐month intervals for 12 months in four centers. Muscles examined were abductor pollicis brevis, abductor digiti minimi, biceps brachii, and tibialis anterior. Results were split into two groups: muscles with increases in MUSIX and those without increases. Longitudinal changes in MUSIX, motor unit number index (MUNIX), compound muscle action potential amplitude, and Medical Research Council strength score were investigated. Results: One hundred thirty‐three muscles were examined. Fifty‐nine percent of the muscles exhibited an increase in MUSIX during the study. Muscles with MUSIX increases lost more motor units (58% decline in MUNIX at 12 months, P <.001) than muscles that did not increase MUSIX (34.6% decline in MUNIX at 12 months, P <.001). However, longitudinal changes in muscle strength were similar. When motor unit loss was similar, the absence of a MUSIX increase was associated with a significantly greater loss of muscle strength (P =.002). Discussion MUSIX increases are associated with greater motor unit loss but relative preservation of muscle strength. Thus, MUSIX appears to be measuring a clinically relevant response that can provide a quantitative outcome measure of reinnervation in clinical trials. Furthermore, MUSIX suggests that reinnervation may play a major role in determining the progression of weakness. [ABSTRACT FROM AUTHOR]

Published
2022
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