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Bücher zum Thema „Signal EMG du muscle“

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Autor: Grafiati
Veröffentlicht am 8. Juni 2024

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1

B, Bolton T., und Tomita T, Hrsg. Smooth muscle excitation. London: Harcourt Brace, 1996.

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2

Raeburn, David, und Mark A. Giembycz, Hrsg. Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7504-2.

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3

Raeburn, David, und Mark A. Giembycz, Hrsg. Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7362-8.

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4

Kelly, James Anthony. Aspects of signal transduction in bovine lymphatic smooth muscle cells. Dublin: University College Dublin, 1996.

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5

1953, Raeburn D., und Giembycz M. A. 1961-, Hrsg. Airways smooth muscle: Neurotransmitters, amines, lipid mediators, and signal transduction. Basel: Birkhauser Verlag, 1995.

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6

Yamada Conference on Calcium as Cell Signal (1994 Tokyo, Japan). Calcium as cell signal: Proceedings of the Yamada Conference XXXIX on Calcium as Cell Signal, April 26-28, 1994, Tokyo, Japan. Tokyo: Igaku-Shoin, 1996.

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7

Kazuhiro, Kohama, und Sasaki Yasuharu, Hrsg. Molecular mechanisms of smooth muscle contraction. Austin, Tex: R.G. Landes Co., 1999.

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8

Oldenhof, Alexandra Dianne. Effects of mechanical stretch on signal transduction and gene expression in myometrial smooth muscle cells. Ottawa: National Library of Canada, 2001.

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9

A, Sassoon D., Hrsg. Stem cells and cell signalling in skeletel myogenesis. Amsterdam: Elsevier, 2002.

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10

Haruhiro, Higashida, Yoshioka Tohru, Mikoshiba Katsuhiko 1945- und Numa Shōsaku 1929-, Hrsg. Molecular basis of ion channels and receptors involved in nerve excitation, synaptic transmission and muscle contraction: In memory of Professor Shosaku Numa. New York, N.Y: New York Academy of Sciences, 1993.

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11

Maximum speed of forearm flexion practice effects upon surface EMG signal characteristics. 1985.

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12

Gunjan, Vinit Kumar, und Bita Mokhlesabadifarahani. EMG Signals Characterization in Three States of Contraction by Fuzzy Network and Feature Extraction. Springer, 2015.

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13

Gunjan, Vinit Kumar, und Bita Mokhlesabadifarahani. EMG Signals Characterization in Three States of Contraction by Fuzzy Network and Feature Extraction. Springer London, Limited, 2015.

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14

Stålberg, Erik. Electromyography. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0007.

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Electromyography (EMG) has been used since the 1940s in the diagnosis of neuromuscular disorders. It has particularly developed with the advent of computers and recording equipment with integrated software. This has made methods of analysis fast, robust, and precise, helping to deal with increasing numbers of patients. Indications have changed dynamically over the years, with the development of new EMG methods themselves and complementary methods used in this field for diagnosis such as histochemistry, genetics, and imaging techniques. This chapter focuses mainly on the routine methods based on recordings with concentric or monopolar needle electrodes, but will also briefly review some of the other EMG methods. There is an increasing understanding of the relationship between the generators (muscle fibres) and the recorded signal that helps interpretation of the recordings. The parameters used for quantitation of the EMG signal are discussed. The findings in pathological conditions are discussed and some practical hints on EMG studies given.
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15

Headley, Barbara J. Muscle scanning: Interpreting EMG scans. Pain Resources, 1990.

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16

Shaibani, Aziz. Myotonia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0021.

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Myotonia is a slow relaxation phase after normal contraction. Patients report dystonia as muscle stiffness and sometimes pain. They usually adapt to it well. Falls due to myotonia may lead to accidents. Examination for percussion myotonia should be part of neuromuscular examination. Percussion of the thenar muscles with the reflex hammer is the most productive method. Electrically silent myotonia is a sign of Brody myopathy. Myotonia may be incidentally discovered during electromyography (EMG). The most important task is to differentiate between myotonia from paramyotonia clinically and electrically. There has been a significant understanding of the underlying channelopathies lately. Severe myotonia respond well to mexiletine.
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17

Shaibani, Aziz. Myotonia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0021.

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Myotonia is a slow relaxation phase of a muscle after normal contraction. Patients report myotonia as muscle stiffness and sometimes pain. They usually adapt to it well. Falls due to myotonia may lead to accidents. Checking for percussion and action myotonia should be part of neuromuscular examination. Electrically silent myotonia is a sign of Brody’s syndrome. Myotonia may be incidentally discovered during EMG. The most important task is to differentiate between myotonia and paramyotonia clinically and electromyographically. Most myotonic disorders are caused by mutations of sodium, and chloride channels. There has been a significant understanding of the underlying channelopathies recently. Severe myotonia respond well to Mexiletine.
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18

Schwartz, Mark, Hrsg. EMG Methods for Evaluating Muscle and Nerve Function. InTech, 2012. http://dx.doi.org/10.5772/1465.

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19

EMG Methods for Evaluating Muscle and Nerve Function. InTech, 2012.

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20

Trebak, Mohamed, und Scott Earley. Signal Transduction and Smooth Muscle. Taylor & Francis Group, 2021.

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21

Trebak, Mohamed, und Scott Earley. Signal Transduction and Smooth Muscle. Taylor & Francis Group, 2018.

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22

Trebak, Mohamed. Signal Transduction and Smooth Muscle. Taylor & Francis Group, 2018.

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23

Trebak, Mohamed, und Scott Earley. Signal Transduction and Smooth Muscle. Taylor & Francis Group, 2018.

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24

Trebak, Mohamed, und Scott Earley. Signal Transduction and Smooth Muscle. Taylor & Francis Group, 2018.

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25

Kennett, Robin P., und Sidra Aurangzeb. Primary muscle diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0024.

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This chapter on primary muscle diseases explains how analysis of compound muscle action potential (CMAP) amplitude, abnormal spontaneous activity on needle electromyography (EMG), and motor unit action potentials (MUAP) characteristics may be used to give an indication of pathophysiological processes, and goes on to describe the combination and distribution of abnormalities that may be expected in the more commonly encountered myopathies. The conditions considered in detail are inflammatory myopathy (including myositis), critical illness myopathy, disorders with myotonia, inherited myopathy (including muscular dystrophy), and endocrine, metabolic and toxic disorders. Each of these has a characteristic combination of CMAP, spontaneous EMG, and MUAP findings, but the systematic approach to clinical neurophysiology as a way of understanding muscle pathophysiology can be used to investigate the myriad of rare myopathies that may be encountered in clinical practice.
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26

Shaibani, Aziz. Muscle Atrophy and Hypertrophy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0017.

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Muscle atrophy is usually caused by interruption of axonal flow [axonal neuropathies, motor neuron diseases (MNDs), etc.]. If weakness is out of proportion to atrophy, demyelinating neuropathy should be suspected. Chronic myopathies and immobility also may cause atrophy, but no electromyography (EMG) evidence of denervation or myopathy is found. The pattern of atrophy is often helpful to localize the lesions. Atrophy of the interossi and preservation of the bulk of the thenar muscles suggest ulnar neuropathy, but atrophy of both would suggest a C8 or plexus pathology. Muscle enlargement may be due to fatty replacement, which can be confirmed by EMG and magnetic resonance imaging (MRI), or due to real muscle hypertrophy from excessive discharges (neuromyotonia).
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27

Shaibani, Aziz. Muscle Atrophy and Hypertrophy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0017.

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Muscle atrophy is usually caused by interruption of axonal flow (axonal neuropathies, motor neuron diseases, etc.). If weakness is out of proportion to atrophy, conduction block due to demyelinating neuropathy should be suspected. Chronic myopathies and immobility may also cause atrophy, but no EMG evidence of denervation or myopathy is respectively found. The pattern of atrophy is often helpful to localize the lesion. Atrophy of the interossi and preservation of the bulk of the thenar muscles suggest ulnar neuropathy, but atrophy of both would suggest a C8 or plexus pathology. Muscle enlargement may be due to tissue replacement (fatt, amyloid), which can be confirmed by EMG and MRI, or may be due to real muscle hypertrophy from excessive discharges (neuromyotonia).
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28

Shaibani, Aziz. Muscle Twitching. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0019.

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Muscle twitching is a pianless involuntary movement of muscles, usually focal short lived. Patients may confuse it with restlessness of the legs and jerking of extremities unless specifically asked. Tremor,especially of the tongue, is also commonly confused with twitching, but its regular nature should be noticed. Fasciculations and rippling are the most important neuromuscular causes of twitching. Reproduction of the symptoms in the clinic, if possible, is very useful for the diagnosis. Otherwise, a video taken by the patient or family members showing these twitchings is equally good. Fasciculations may be enhanced by tapping the affected muscle group and hyperventilation. Surprisingly, EMG evidence of fasciculations may be scarce despite their clinical predominance.
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29

Pitt, Matthew. Needle EMG findings in different pathologies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754596.003.0007.

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In this chapter, the inability of electromyography (EMG) to be able to further progress the diagnosis of myopathy on its own—requiring muscle biopsy and other modalities such as genetics to complete this process—is emphasized. The role of EMG particularly in the era of genetics is discussed. Findings in neurogenic abnormality are next described and the important hereditary conditions such as spinal muscular atrophy (SMA), distal SMA, Brown–Vialetto–Van Laere syndrome, segmental anterior horn cell disease, conditions with progressive bulbar palsy, SMARD1, and pontocerebellar hypoplasia with spinal muscle are discussed in detail. The differential diagnosis of 5q SMA type 1 is specifically outlined. Acquired forms of anterior horn disease, including Hirayama disease, poliomyelitis and enteropathic motor neuropathy, Hopkins syndrome, tumours, and vascular lesions are covered. There is discussion of the use of physiological tests to monitor progress in SMA, with tests including compound muscle action potential amplitude and motor unit number estimation. Finally, the important correlation between muscle biopsy and EMG is highlighted.
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30

Misra, V. Peter, und Santiago Catania. EMG-guided botulinum toxin therapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0026.

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This chapter explains the mechanism by which botulinum neurotoxin (BoNT) causes its neuromuscular paralytic effects, and reviews the developments that led these effects to be harnessed therapeutically. It specifically focuses upon the conditions of dystonia and spasticity. Within the spectrum of these diseases, it discusses those situations where BoNT injections are the treatment of choice. The very accurate targeting of BoNT into specific muscles in many situations is both desirable and crucial in some situations BoNT’s therapeutic neuroparalytic effect may need to be restricted to a single muscle fascicle.. In some cases, an inaccurately placed injection may be associated with unacceptable side effects. In order to achieve accuracy of BoNT injection delivery, intramuscular injections of BoNT aided by electromyography (EMG) guidance allows the very accurate targeting of specific muscles. The practical aspects related to the preparation of BoNT for injection and the methodology and techniques for injecting using EMG guidance are discussed. The importance of good anatomical knowledge and the relevant EMG techniques to target individual muscles are highlighted and applied to injection of muscles in different body areas. Finally, certain diagnostic neurophysiological tests, which may be useful for the management of some neurological conditions that are treated by BoNT are briefly discussed.
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31

Pfurtscheller, Gert, Clemens Brunner und Christa Neuper. EEG-Based Brain–Computer Interfaces. Herausgegeben von Donald L. Schomer und Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0047.

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A brain–computer interface (BCI) offers an alternative to natural communication and control by recording brain activity, processing it online, and producing control signals that reflect the user’s intent or the current user state. Therefore, a BCI provides a non-muscular communication channel that can be used to convey messages and commands without any muscle activity. This chapter presents information on the use of different electroencephalographic (EEG) features such as steady-state visual evoked potentials, P300 components, event-related desynchronization, or a combination of different EEG features and other physiological signals for EEG-based BCIs. This chapter also reviews motor imagery as a control strategy, discusses various training paradigms, and highlights the importance of feedback. It also discusses important clinical applications such as spelling systems, neuroprostheses, and rehabilitation after stroke. The chapter concludes with a discussion on different perspectives for the future of BCIs.
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32

Katirji, Bashar. The Scope of the EMG Examination. Herausgegeben von Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0001.

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Clinical electromyography (EMG) refers to the diagnostic tool in the electrophysiological evaluation of disorders of peripheral nerve and muscle. This introductory chapter defines the terms of the discipline and its scope. Clinical EMG used in the evaluation of Clinical EMG is utilized by a variety of physicians, including specialists in the field of neurology, physical medicine and rehabilitation, orthopedics, hand surgery, neurosurgery, spine, rheumatology and pain management. The scope of the EMG Examination includes nerve conduction studies and needle EMG. It also includes other specialized testing such as late responses, repetitive nerve stimulation and single fiber EMG. This chapter discusses the referral process to the EMG laboratory and guides the readers to the best practice in the EMG evaluation of patients with neuromuscular disease. Special attention to testing young children and testing patients in the intensive care unit is given. The generation, format and final layout of the EMG report is also advised.
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33

The effect of short term EMG biofeedback on neck muscle relaxation for rotary pursuit performance. 1990.

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34

Li, Chien-min. The effect of short term EMG biofeedback on neck muscle relaxation for rotary pursuit performance. 1990.

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35

Raeburn, D. Ed. Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators & Signal Transduction (Exs). Birkhauser, 1996.

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36

Raeburn, David, und Mark A. Giembycz. Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction. Birkhauser Verlag, 2012.

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37

1953-, Raeburn D., und Giembycz M. A. 1961-, Hrsg. Airways smooth muscle: Peptide receptors, ion channels, and signal transduction. Basel: Birkhäuser Verlag, 1995.

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38

Raeburn, David, und Mark A. Giembycz. Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction. Birkhauser Verlag, 2012.

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39

Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction. Birkhäuser, 2012.

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40

Raeburn, David. Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators And Signal Transduction. Birkhäuser, 2012.

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41

Raeburn, David. "Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction". Springer, 2012.

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42

Calcium as cell signal: Proceedings of the Yamada Conference XXXIX on Calcium as Cell Signal, April 26-28, 1994, Tokyo, Japan. Igaku-Shoin, 1995.

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43

Fashanu, Billy. Exploring EMG-Torque relationship in the quadriceps femoris and the hamstring muscle group and muscle activity duringthe sit-to-stand movement in female subjects: A methodological study. UEL, 1994.

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44

Raeburn, D. Airways Smooth Muscle: Peptide Receptors, Ion Channels, and Signal Transduction (Agents and Actions Supplements). Birkhauser, 1995.

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45

(Editor), E. Raeburn, und M. A. Giembycz (Editor), Hrsg. Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction (Respiratory Pharmacology and Pharmacotherapy). Birkhauser Boston, 1995.

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46

Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction (Respiratory Pharmacology and Pharmacotherapy). Birkhauser Boston, 1995.

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47

Nuwer, Marc R., Ronald G. Emerson und Cecil D. Hahn. Principles and Techniques for Long-Term EEG Recording (Epilepsy Monitoring Unit, Intensive Care Unit, Ambulatory). Herausgegeben von Donald L. Schomer und Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0031.

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Long-term monitoring is a set of methods for recording electroencephalographic (EEG) signals over a period of 24 hours or longer. Patient video recording is often synchronized to the EEG. Interpretation aids help physicians to identify events, which include automated spike and seizure detection and various trending displays of frequency EEG content. These techniques are used in epilepsy monitoring units for presurgical evaluations and differential diagnosis of seizures versus nonepileptic events. They are used in intensive care units to identify nonconvulsive seizures, to measure the effectiveness of therapy, to assess depth and prognosis in coma, and other applications. The patient can be monitored at home with ambulatory monitoring equipment. Specialized training is needed for competent interpretation of long-term monitoring EEGs. Problems include false-positive events flagged by automated spike and seizure detection software, and muscle and movement artifact contamination during seizures.
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48

Shaibani, Aziz. Proximal Arm Weakness. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0012.

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Proximal arm muscles include supra and infra spinatii, pectoralis major and minor, teres major and minor, rhomboids, serratus anterior, deltoids, biceps, and triceps. The main function of these muscles is to lift the arms. The first sign of proximal weakness is difficulty in raising the arms above a horizontal level. Shoulder conditions like supraspinatus tendonitis are often confused as proximal weakness. In myopathies, usually proximal arm weakness is associated with proximal leg weakness. Motor neuron diseases like ALS and SMA and neuropathies like CIDP may present with symmetrical proximal weakness. For differentiation, EMG/NCS is crucial.
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49

Sassoon, D. A. Stem Cells and Cell Signalling in Skeletal Myogenesis (Advances in Developmental Biology and Biochemistry, V. 11). Elsevier Science, 2002.

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50

Shaibani, Aziz. Proximal Arm Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0012.

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Proximal arm muscles include supra and infra spinatii, pectoralis major and minor, teres major and minor, rhomboids, serratus anterior, deltoids, biceps, and triceps. The main function of these muscles is to abduct the arms. The first sign of proximal weakness is difficulty raising arms above the horizontal level. Shoulder conditions like supraspinatus tendonitis are often confused as proximal weakness. In myopathies, usually proximal arm weakness is associated with proximal leg weakness. Motor neuron diseases (MNDs) like amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) and neuropathies like chronic inflammatory demyelinating polyneuropathy (CIDP) may present with symmetrical proximal weakness. For differentiation, electromyography/nerve conduction study (EMG/NCS) is crucial.
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