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1
J, Robinson William. The effects of skill level on EMG activity during internal and external imagery. Eugene: Microform Publications, College of Human Development and Performance, University of Oregon, 1985.
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2
K, Silver Julie, and Weiss Jay, eds. Easy EMG: A guide to performing nerve conduction studies and electromyography. Edinburgh: Butterworth-Heinemann, 2004.
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3
Rembrandt Harmenszoon van Rijn, 1606-1669., Rodari Florian, and Musée Jenisch. Cabinet cantonal des estampes., eds. Rembrandt, les collections du Cabinet des estampes de Vevey. Vevey: Fonds Pierre Decker et Cabinet cantonal des estampes, Musée Jenisch, 1997.
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4
Misra, V. Peter, and 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.
5
Headley, Barbara J. Muscle scanning: Interpreting EMG scans. Pain Resources, 1990.
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6
Ramdass, Ranjit. Neurophysiology in the assessment of inflammatory myopathies. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0015.
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Clinical neurophysiology (electrodiagnosis) includes the assessment of peripheral nerves by electrical stimulation (nerve conduction studies, NCS) and needle examination of muscles (electromyography, EMG). Electrodiagnostic assessment is a functional extension of clinical examination into the laboratory. It plays an important role in the investigation of a patient suspected of having myositis, providing valuable information regarding peripheral nerve, neuromuscular junction and muscle functions, to better characterize clinical syndromes. NCS can establish the presence and quantify the severity of a primary or co-existing peripheral neuropathy, while EMG examination can help discriminate between primary myogenic and primary neurogenic disorders. EMG is potentially more sensitive than clinical examination, as abnormalities can be detected in muscles apparently unaffected on clinical examination. Additionally, a number of muscles can be sampled to help target an optimal muscle biopsy site. Neurophysiology can also assist in monitoring treatment responses and detecting emerging problems, such steroid myopathy or drug-induced neuropathy.
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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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EMG Methods for Evaluating Muscle and Nerve Function. InTech, 2012.
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9
Schwartz, Mark, ed. EMG Methods for Evaluating Muscle and Nerve Function. InTech, 2012. http://dx.doi.org/10.5772/1465.
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10
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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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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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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Kennett, Robin P., and 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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Gunjan, Vinit Kumar, and Bita Mokhlesabadifarahani. EMG Signals Characterization in Three States of Contraction by Fuzzy Network and Feature Extraction. Springer, 2015.
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15
Gunjan, Vinit Kumar, and Bita Mokhlesabadifarahani. EMG Signals Characterization in Three States of Contraction by Fuzzy Network and Feature Extraction. Springer London, Limited, 2015.
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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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Katirji, Bashar. The Scope of the EMG Examination. Edited by 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.
18
Maximum speed of forearm flexion practice effects upon surface EMG signal characteristics. 1985.
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19
The effect of short term EMG biofeedback on neck muscle relaxation for rotary pursuit performance. 1990.
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20
Li, Chien-min. The effect of short term EMG biofeedback on neck muscle relaxation for rotary pursuit performance. 1990.
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21
Fuglsang-Frederiksen, Anders, Kirsten Pugdahl, and Hatice Tankisi. Quantitative electromyography. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0008.
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Several quantitative electromyography (QEMG) methods are used for diagnosing and monitoring in patients with neuromuscular disorders. At weak effort of the muscle, motor unit potential (MUP) analyses as individual MUP, multi-MUP, and macro-EMG are diagnostically sensitive and well tested. At higher effort of the muscle, interference pattern analyses such as the turns amplitude analysis are also diagnostically sensitive. Other potential diagnostic methods are power spectrum analysis, muscle fibre conduction velocity analysis, and some surface EMG methods. In patients with myopathy, QEMG has an important role in the diagnosis as a supplement to blood tests, muscle biopsy, and genetic testing. In patients with neurogenic disorders such as anterior horn cell disorders, peripheral nerve lesions, or polyneuropathy, QEMG has important roles in characterizing the lesion and differential diagnosis. Furthermore, QEMG may be useful in the examination of patients with neuromuscular transmission failure, critical illness disorders, and in treatment of dystonic muscle with botulinum toxin.
22
The effects of skill level on EMG activity during internal and external imagery. 1985.
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23
Robinson, William J. The effects of skill level on EMG activity during internal and external imagery. 1985.
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24
Silver, Julie K., Lyn D. Weiss, and Jay M. Weiss. Easy EMG: A Guide to Performing Nerve Conduction Studies and Electromyography. Elsevier, 2022.
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25
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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26
Sella, Gabriel E., and G. E. Sella. Muscles in Motion: S-Emg Analysis of the Range of Motion of the Human Body. Gabriel E. Sella, 1993.
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27
Pillarella, Debbie Ban. Dino-Muscles & City KidZ Step: A comprehensive fitness, wellness & edu-tainment program for today's youth. BodyWorks, 1993.
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28
Pitt, Matthew. Paediatric Electromyography. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754596.001.0001.
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Paediatric Electromyography is a single-author textbook which covers the full range of applications of the techniques of nerve conduction and electromyography (EMG) in children from the neonatal period to the late teenage years. It comprises five sections. Section 1 in its first chapter, gives a detailed introduction to the different skills that are needed to effect successful interventions in paediatric EMG. The emphasis here is that paediatric EMG is not simply adult EMG applied to younger subjects. Its second chapter is an introduction to the basic physiology which is common to any practice of nerve and muscle study. The next three sections (2–4), each comprised of three chapters, are structured anatomically covering in order, nerves, muscles, and neuromuscular junctions. All follow a similar pattern with the first chapter of the section dedicated to the underlying physiology needed for interpretation of the techniques used in the investigation of that particular part of the nervous system. The second chapter gives the pathophysiological associations and the final chapter covers any aspect not covered in the previous two chapters. In section 5 the techniques needed to deal with the more unusual clinical requests, such as investigation of facial palsy, swallowing abnormalities, brachial plexus injuries, and diaphragmatic problems are brought together in a final chapter. The book is concluded with three appendices. Appendix 1 describes protocols devised to cover the differing clinical request sent to any laboratory. Appendix 2 gives a comprehensive database of normative data, often derived from e-norm methodology, and intending to cover every measure recorded. Appendix 3 is an illustrated description of electrode placements for all the common nerve studies.
29
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.
30
EMG activity and kinematics of cycling movements at different pedal shaft widths. 1995.
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31
Mills, Kerry R., ed. Oxford Textbook of Clinical Neurophysiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.001.0001.
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The Oxford Textbook of Clinical Neurophysiology provides a comprehensive account from world experts of the modern practice of the specialty. It deals with the full range of techniques giving the underpinning basic science and clinical use. The importance of clinical skills, as well as technical expertise are emphasized. Section I reviews the physiology of nerve, muscle, and cortex, and the digital techniques used to study them. Section II discusses the techniques for nerve conduction, electromyography (EMG), electroencephalography (EEG), magnetoencephalography, evoked potentials, and transcranial magnetic stimulation, including axonal excitability measurement, reflex studies, sleep studies pelvic floor neurophysiology and intracranial EEG. Section III reviews focal and generalized neuropathy, nerve, root, and plexus lesions, neuromuscular junction disorders, muscle disease, paediatric conditions, neurodegenerations, such as amyotrophic lateral sclerosis and EMG-guided botulinum toxin therapy. Section IV reviews generalized and focal epilepsy, status epilepticus, coma, presurgical evaluation for epilepsy, syncope, paediatric conditions, sleep disorders and intraoperative monitoring. This title incudes video content and is written for trainees and trainers in clinical neurophysiology.
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Katirji, Bashar. Routine Clinical Electromyography. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0002.
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Nerve conduction studies and needle EMG represent the two essential parts of the clinical EMG study. In almost all patients, both studies need to be completed before a final conclusion is made. This chapter outlines the basic concepts of nerve conduction studies including stimulations, recordings, variables and sources of errors. This is followed by detailed discussions of basic pathophysiological changes that accompany peripheral nerve disorders. The chapter then covers the normal needle EMG findings including normal insertional activity, motor unit action potential morphology and recruitment. This is followed by details on abnormal spontaneous activity findings and changes in motor unit action potential morphology and recruitment seen on needle EMG with peripheral nerve and muscle disorders.
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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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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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Shaibani, Aziz. Proximal Leg Weakness. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0013.
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Proximal leg weakness is a common presentation in neuromuscular clinics. Hips flexion, abduction, adduction, and rotation are mainly achieved by iliopsoas, glutei, and obturator muscles. Hip pathology, especially when painless, may lead to diagnostic confusion that needs a good EMG of these muscles to be cleared. Most myopathies present with painless proximal leg weakness (difficulty climbing stairs and arising out of a deep chair). CIDP, diabetic amyotrophy, motor neuron diseases, and lumbar plexitis may all present similarly. Severe pain is typical of plexus pathology and is rarein myopathies. Students should be taught to avoid the assumption that proximal weakness is only caused by myopathies.
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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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Shaibani, Aziz. Proximal Leg Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0013.
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Proximal leg weakness is a common presentation to neuromuscular clinics. Hip flexion, abduction, adduction, and rotation is mainly achieved by the iliopsoas, glutei, and obturator muscles. Hip pathology, especially when painless, may lead to diagnostic confusion that needs a good electromyogram (EMG) of these muscles to be cleared. Most myopathies present with painless proximal leg weakness (difficulty climbing stairs and arising out of a deep chair). chronic inflammatory demyelinating polyneuropathy (CIDP), diabetic amyotrophy, motor neuron diseases (MNDs), and lumbar plexitis may all present similarly. Pain is more typical of these conditions that myopathies. Students should be taught to avoid the assumption that proximal weakness is caused only by myopathies.
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Mills, Kerry R. Disorders of single nerves, roots, and plexuses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0021.
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The role of electromyography (EMG) and nerve conduction studies in disorders of single nerve, root, and plexus lesions are discussed. The motor and sensory anatomy underpinning diagnosis is described and a scheme presented showing the key muscles to be examined using EMG to differentiate nerve, plexus, and root lesions. The main causes of mononeuritis multiplex, of either axonal degeneration or demyelinative pathology, are covered, including diabetic neuropathy, vasculitic neuropathy, multifocal motor neuropathy with block, and the Lewis–Sumner syndrome. The confirmatory role of EMG and nerve conduction studies in the investigation of cervical and lumbar radiculopathies is highlighted as is the use of transcranial magnetic stimulation to differentiate cervical radiculopathy with myelopathy from amyotrophic lateral sclerosis. The neurophysiological hallmarks of traumatic cervical plexus lesions, including obstetric causes, inherited and acquired brachial neuritis, hereditary liability to pressure palsies, the cervical rib syndrome, and radiation plexopathy are also covered.
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(Contributor), Roxana Adams, ed. Museums: Places of Learning (Professional Practice Series). American Association of Museums, 1998.
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40
Shaibani, Aziz. Pseudoneurologic Syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0022.
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The term functional has almost replaced psychogenic in the neuromuscular literature for two reasons. It implies a disturbance of function, not structural damage; therefore, it defies laboratory testing such as MRIS, electromyography (EMG), and nerve conduction study (NCS). It is convenient to draw a parallel to the patients between migraine and brain tumors, as both cause headache, but brain MRI is negative in the former without minimizing the suffering of the patient. It is a “software” and not a “hardware” problem. It avoids irritating the patient by misunderstanding the word psychogenic which to many means “madness.”The cause of this functional impairment may fall into one of the following categories:• Conversion reaction: conversion of psychological stress to physical symptoms. This may include paralysis, hemisensory or distal sensory loss, or conversion spasms. It affects younger age groups.• Somatization: chronic multiple physical and cognitive symptoms due to chronic stress. It affects older age groups.• Factions disorder: induced real physical symptoms due to the need to be cared for, such as injecting oneself with insulin to produce hypoglycemia.• Hypochondriasis: overconcern about body functions such as suspicion of ALS due to the presence of rare fasciclutations that are normal during stress and after ingestion of a large amount of coffee. Medical students in particular are targets for this disorder.The following points are to be made on this topic. FNMD should be diagnosed by neuromuscular specialists who are trained to recognize actual syndrome whether typical or atypical. Presentations that fall out of the recognition pattern of a neuromuscular specialist, after the investigations are negative, they should be considered as FNMDs. Sometimes serial examinations are useful to confirm this suspicion. Psychatrists or psychologists are to be consulted to formulate a plan to discover the underlying stress and to treat any associated psychiatric disorder or psychological aberration. Most patients think that they are stressed due to the illness and they fail to connect the neuromuscular manifestations and the underlying stress. They offer shop around due to lack of satisfaction, especially those with somatization disorders. Some patients learn how to imitate certain conditions well, and they can deceive health care professionals. EMG and NCS are invaluable in revealing FNMD. A normal needle EMG of a weak muscles mostly indicates a central etiology (organic or functional). Normal sensory responses of a severely numb limb mean that a lesion is preganglionic (like roots avulsion, CISP, etc.) or the cause is central (a doral column lesion or functional). Management of FNMD is difficult, and many patients end up being chronic cases that wander into clinics and hospitals seeking solutions and exhausting the health care system with unnecessary expenses.It is time for these disorders to be studied in detail and be classified and have criteria set for their diagnosis so that they will not remain diagnosed only by exclusion. This chapter will describe some examples of these disorders. A video clip can tell the story better than many pages of writing. Improvement of digital cameras and electronic media has improved the diagnosis of these conditions, and it is advisable that patients record some of their symptoms when they happen. It is not uncommon for some Neuromuscular disorders (NMDs), such as myasthenia gravis (MG), small fiber neuropathy, and CISP, to be diagnosed as functional due to the lack of solid physical findings during the time of the examination. Therefore, a neuromuscular evaluation is important before these disorders are labeled as such. Some patients have genuine NMDs, but the majority of their symptoms are related to what Joseph Marsden called “sickness behavior.” A patient with carpal tunnel syndrome (CTS) may unconsciously develop numbness of the entire side of the body because he thinks that he may have a stroke.