The electrodiagnostic (EDX) study is an extension of the clinical examination, which means that the clinical features dictate the initial nerve conduction studies (NCS) performed. However, once the EDX study is started, it continues in an independent manner, meaning that the initial NCS findings dictate the subsequent studies performed. Because competent EDX study performance requires considerable knowledge (and special training), it is not possible to convey all of the basic and advanced concepts in a single chapter. Nonetheless, the most important concepts are easily conveyed by a discussion limited to EDX-pertinent anatomical, physiological, pathological, pathophysiological, and basic electrical concepts. The focus of this chapter will be on the standard NCS and needle EMG measurements made during EDX studies and their significance with regard to lesion localization and characterization. Because the most challenging portion of EDX study is motor unit action potential analysis, this topic is more extensively reviewed. The utility of the sensory NCS for identifying focal axon loss, the utility of the motor NCS for screening long nerve segments for focal demyelination and for determining lesion severity, and the utility of the needle EMG for confirming the NCS findings, better defining lesion localization, and identifying the temporal features (e.g., chronicity) and rate of progression of the lesion are also reviewed.

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The goal of the electromyographer is to localize lesions and to characterize them. In order to accomplish these goals, a minimum core of knowledge in neuroscience is required. This book discusses that core of neuroscientific knowledge as a stepping stone to lesion localization and characterization. Following this, it demonstrates how this information is actually utilized in the electromyography (EMG) laboratory using a case study approach. Although several excellent EMG case study-based textbooks are available, the book is unique in that it offers a step-by-step analysis of the nerve conduction studies (NCS) and needle EMG studies as they are collected, including a discussion of the initial studies required based on the presenting clinical features, an interpretation of those initial studies, and the indications for subsequent studies based on that interpretation. This step-by-step analysis continues until the lesion has been fully localized and characterized. The book is extensive and explains the important principles and concepts underlying electrodiagnosis (EDX) medicine. It reviews the anatomy and physiology of the peripheral neuromuscular system, basic principles of NCS, specific concepts pertinent to each type of NCS (motor, sensory, and mixed NCS, as well as repetitive nerve stimulation studies), and the basic principles of needle EMG. Following this, it discusses the NCS and needle EMG measurements made, their meaning, and the EDX manifestations of the various neuromuscular disorders. It also includes a discussion of the various types of nerve injuries and a review of reinnervation. It focuses on lesion localization and the characterization of the lesion, including its pathology, pathophysiology, severity, and temporal features. The book demonstrates the application of the principles and concepts through 60 EDX case studies collected from the authors' EMG laboratories using a step-by-step analysis format.

Purpose of review The purpose of this review is to discuss the therapeutic options available in the treatment of traumatic injuries involving peripheral nerves. Recent findings For nerve gap repair, synthetic nerve tubes are limited to gaps below 3 cm in length and to small-diameter nerve repairs, whereas the dependency on proliferating host Schwann cell limits the size of acellularized autografts. Thus, in most situations, nerve autografts remain superior for nerve gap correction. Summary When conservative treatment is either not indicated or ineffective, surgical intervention may be employed. The ideal timing of surgical intervention is often unclear and determined by a number of factors, including the circumstances surrounding the injury, the timing of the symptoms, the type and severity of the injury, the completeness of the lesion, the required regenerative distance, the degree of fascicular disruption, and the degree of concomitant tissue trauma and contamination, as well as the morbidity and mortality of the procedure, and the age and comorbidities of the patient. The most common nonsurgical error is unnecessary surgical delay. To avoid losing the opportunity to achieve successful motor recovery, it is important to involve a peripheral nerve surgeon early.

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Neuralgic amyotrophy is a disorder of the peripheral nervous system (PNS) that is associated with a wide range of clinical phenotypes. For this reason, roughly 2 dozen terms have been applied to it, some reflecting the muscle involved (serratus magnus palsy) and others reflecting the presumed lesion site (idiopathic brachial plexitis, idiopathic brachial neuritis). In 1948, Parsonage and Turner recognized that all of these entities represented the same disorder and introduced the term neuralgic amyotrophy to highlight its 2 quintessential features, severe pain and pronounced muscle wasting. In addition to these 2 features, an antecedent event (trigger) is often identified. In the presence of this unifying triad (antecedent event, severe pain, and pronounced muscle wasting), neuralgic amyotrophy is easily recognized. Regarding its localization, although most investigators initially considered neuralgic amyotrophy to be a brachial plexus disorder, many authors have since speculated that at least some of the time it behaves more like an extraplexal disorder. Others, on the basis of both clinical and electrodiagnostic (EDX) findings, have suggested that it rarely involves the brachial plexus and, instead, represents an extraplexal disorder of the forequarter region of the body that presents as either a mononeuropathy or a multiple mononeuropathy, depending on the number of individual nerves involved. We recently evaluated the lesion distribution among 281 patients with sporadic neuralgic amyotrophy. In that study, 699 of 703 lesions were extraplexal nerve lesions; only 4 involved the brachial plexus. The extraplexal lesions had a mononeuropathy (46%) or a multiple mononeuropathy (54%) distribution. Consistent with the belief that neuralgic amyotrophy has a predilection for motor axons, the incidence of nerve involvement in that study reflected the percentage of motor axons composing the nerve as follows: pure motor nerves (e.g., suprascapular, long thoracic, distal motor branch, anterior interosseous)>predominantly motor nerves (e.g., axillary, musculocutaneous)>>mixed nerves (e.g., median, ulnar, radial)>> cutaneous sensory nerves (e.g., lateral antebrachial cutaneous). As a result of this motor axon predilection, nerves innervating the shoulder girdle muscles are frequently involved. Whenever 2 or more such nerves are involved, an upper plexus localization is suggested. However, unlike upper plexopathies, in which nerve conduction study abnormalities are simultaneously present in both the lateral antebrachial cutaneous nerve and the median sensory nerve recording from the thumb 96% of the time, this pattern is unexpected with neuralgic amyotrophy; in our study of 281 patients, it was never observed. In addition to EDX studies, imaging studies are also frequently employed in the evaluation of neuralgic amyotrophy patients, not only to assess the brachial plexus but also to exclude mimicking entities. In this issue of Muscle & Nerve, Sneag et al., having used high-resolution MRI, report the MRI manifestations of neuralgic amyotrophy in 27 patients. Through a retrospective search of the imaging database of their institution, they identified 27 patients with clinically and electrodiagnostically confirmed neuralgic amyotrophy. The clinical and EDX findings in these patients indicated 38 extraplexal (nerve) lesions. None of the clinical or EDX assessments suggested brachial plexus involvement. Among these 38 nerve lesions, 37 were based on both clinical and EDX assessments and 1 was based on clinical assessment alone (this patient had presented with a suprascapular mononeuropathy, the classic triad of neuralgic amyotrophy, and did not undergo EDX assessment). Two radiologists independently assessed the brachial plexus MRI studies, which included the preterminal (e.g., suprascapular) and terminal (e.g., musculocutaneous) nerves of the brachial plexus whenever they were present within the field of view of the study. Correspondence to: M. A. Ferrante; e-mail: mafmd1@gmail.com

ABSTRACTThe thoracic outlet syndromes (TOSs) are a group of etiologically and clinically distinct disorders with 1 feature in common: compression of 1 or more neurovascular elements as they traverse the thoracic outlet. The medical literature reflects 5 TOSs: arterial; venous; traumatic neurovascular; true neurogenic; and disputed. Of these, the first 4 demonstrate all of the features expected of a syndrome, whereas disputed TOS does not, causing many experts to doubt its existence altogether. Thus, some categorize disputed TOS as a cervicoscapular pain syndrome rather than as a type of TOS. To better understand these disorders, their distinctions, and the reasoning underlying the categorical change of disputed TOS from a form of TOS to a cervicoscapular pain syndrome, a thorough understanding of the pertinent anatomy, pathology, pathophysiology, and the electrodiagnostic manifestations of their pathophysiologies is required. This review of the TOSs is provided in 2 parts. In this first part we address information pertinent to all 5 TOSs and reviews true neurogenic TOS. In part 2 we review the other 4 TOSs. Muscle Nerve 55: 782–793, 2017

ABSTRACT The thoracic outlet syndromes (TOSs) are a group of etiologically and clinically distinct disorders with 1 feature in common: compression of 1 or more neurovascular elements as they traverse the thoracic outlet. The medical literature reflects 5 TOSs: arterial; venous; traumatic neurovascular; true neurogenic; and disputed. Of these, the first 4 demonstrate all of the features expected of a syndrome, whereas disputed TOS does not, causing many experts to doubt its existence altogether. Thus, some categorize disputed TOSs as cervicoscapular pain syndrome rather than as a type of TOS. To better understand these disorders, their distinctions, and the reasoning underlying the categorical change of disputed TOS from a form of TOS to a cervicoscapular pain syndrome, a thorough understanding of the pertinent anatomy, pathology, pathophysiology, and electrodiagnostic manifestations of these pathophysiologies is required. This review of the TOSs is provided in 2 parts. In part 1 we covered general information pertinent to all 5 TOSs and reviewed true neurogenic TOS in detail. In part 2, we review the arterial, venous, traumatic neurovascular, and disputed forms of TOS. Muscle Nerve 56 : 663–673, 2017

ABSTRACTIntroductionThe muscles commonly affected by neuralgic amyotrophy (NA) are well known, but the location of the responsible lesions is less clear (plexus versus extraplexus).MethodsWe report the lesion locations in 281 NA patients as determined by extensive electrodiagnostic (EDX) testing.ResultsOur 281 patients had 322 bouts of NA, 57 of which were bilateral, for a total of 379 assessable events. A single nerve was involved in 174 (46%), and 205 (54%) were multifocal. EDX testing identified 703 individual lesions: 699 neuropathies and 4 supraclavicular radiculoplexus lesions.ConclusionsThe frequency of nerve involvement reflects the motor predilection of NA. Involvement of pure motor nerves exceeded that of predominantly motor nerves, both of which far exceeded involvement of more evenly mixed sensorimotor nerves. Cutaneous sensory nerves were least commonly involved. Because of the common C5–C6 innervation, NA often mimics an upper plexus lesion. Extraplexus nerve involvement far exceeded plexus involvement. Distal motor branch involvement explains the severe single‐muscle wasting and weakness often observed. Muscle Nerve 55: 858–861, 2017

An examination of clinical and electrodiagnostic assessments and fully characterized individual hand usage patterns finds a relationship between sustained gripping and the development of carpal tunnel syndrome in the nondominant hand.