Physiological and Technical Basis of Electromyography (eBook)

William F. Brown (Autor)

eBook Download: PDF | EPUB

2013 | 1. Auflage
524 Seiten
Elsevier Science (Verlag)
978-1-4831-6329-1 (ISBN)

Infos

The Physiological and Technical Basis of Electromyography aims to help the clinician involved in the study of diseases of the peripheral nervous system and muscle to better understand the pathophysiological basis for many of the observations derived from electromyography and nerve conduction studies. The book begins with basic background information to enable the reader to understand the pathophysiological mechanisms covered in the remainder of the text. This is followed by separate chapters on the physiological consequences of the main patterns of injury and repair affecting the peripheral nervous system; the general principles of stimulation and recording techniques as applied to man; and techniques employed to record somatosensory evoked potentials. Subsequent chapters cover the motor unit; priorities and objectives of needle electromyography; abnormal spontaneous and provoked activity originating in motoneurons or their axons; neuromuscular transmission; and the important aspects of the anatomy and physiology of cranial nerves and the electrophysiological methods available for testing them. This book is intended not only for practicing electromyographers but also for those neurologists and physiatrists who, although they may not practice electromyography, have an interest in neuromuscular diseases and the place of electromyography in the analysis of these disorders.

Textauszug

INTRODUCTION: THE LIMITATIONS OF ELECTROPHYSIOLOGICAL TESTING

The considerable progress of recent years in understanding and treating many of the neuromuscular diseases has broadened the range of clinical possibilities for the physician. With the increased capacity for managing patients afflicted with these disorders has come stronger emphasis on rapid and accurate diagnosis. Present electrophysiological methods have established an important place in the diagnostic workup for diseases of muscle and nerve. If these tests are to be used to best advantage, however, their role and their limitations must be understood.

Despite the many conceptual and methodological advances of recent years, the clinical examination remains the best single tool for analysis of neuromuscular diseases. In the case of peripheral neuropathies, for example, it should be possible to establish whether the basic pattern of the peripheral neuropathy is primarily distal or proximal, is symmetrical or asymmetrical, or is best explained by multiple local lesions affecting peripheral nerve. The examination should also predict the likely types of nerve fibers involved (motor, sensory, autonomic) and even give some indication of whether demyelination, axonal degeneration, or both are prominent characteristics of the neuropathy. Moreover, only the history can tell us about the presence or absence of abnormal spontaneous activity in sensory nerve fibers. The presence of such activity, reported as paresthesias, dysesthesias, or pain, often provides the earliest clue to the nature and localization of a lesion in the peripheral or root compression syndromes.

The place of electrophysiological testing in the assessment of neuromuscular diseases is to act as an extension of the neurological examination. Specifically, the pattern of the pathophysiological changes seen in the electromyogram (EMG) and on nerve conduction studies (NCS) can shed light on the location of the lesion and on the nature of the underlying processes in the nerve or muscle (or both). These electrophysiological techniques provide evidence as to whether neuronal (or axonal) degeneration has taken place, whether any substantial degree of demyelination is present, and whether there is a disorder affecting neuromuscular transmission or one primarily affecting the muscle fibers. Additionally, the tests can provide important clues to the localization of lesions affecting the peripheral nerves and an indication of the severity of the lesions. Electrophysiological tests thus provide a sort of physiological biopsy of the peripheral nervous system and muscle. For example, degeneration of neurones or axons may be indicated by a number of alterations in the NCS and EMG, as outlined in Table 1 and discussed in detail in Chapters 2, 3, 6, 8 and 10. Table 2 lists the alterations to be expected in an established primary demyelinating neuropathy and Table 3, the indications of a focal nerve lesion.

TABLE 1

Indicators of Neuronal-Axonal Degeneration *

*See Chapter 2, 3, 6, 8, and 10.

TABLE 2

Indicators of Demyelination *

Substantial reduction in conduction velocities of motor/sensory nerve fibers

Desynchronization of compound nerve and muscle action potentials

Conduction block

*See Chapter 2 and 3.

TABLE 3

Indication of a Focal Nerve Lesion*

*See Chapter 2.

As any neurological clinician or experienced electromyographer knows, all abnormalities observed in NCS and the EMG must be interpreted in the light of the history and findings on examination. For example, increases in fiber density, the appearance of fibrillation potentials, and abnormalities in neuromuscular transmission may all be seen in primary muscle diseases. In these disorders,

portions of muscle fibers may become denervated and collateral reinnervation may later take place, with concomitant alteration in the innervation patterns of muscle fibers and formation of new neuromuscular junctions. Likewise, characteristic features such as conduction slowing and desynchronization of nerve and muscle potentials, ordinarily seen in demyelinating neuropathies, may be absent, for example, early in the course of Guillain-Barré polyneuropathy. At the same time, conduction block may not be apparent unless the very proximal portions of the peripheral nervous system are included in the study.

Even in diseases in which axons undergo degeneration, fibrillation may be difficult to detect or even absent if the degeneration has been very recent or the disease is progressing slowly. Furthermore, in some severe late-stage neuronopathies such as the neuronal type of Charcot-Marie-Tooth disease (HMSN type II), so few motor axons may remain that a motor conduction velocity determination is based on less than 5 percent of the normal number of motor axons. In the extreme, it could represent only the last surviving motor axon and could fall well below the 2 standard deviation lower limit for healthy maximum motor conduction velocities. Such a result could indicate abnormally slow conduction in a normally faster conducting nerve fiber because of associated demyelination, axonal shrinkage, or both; or, theoretically at least, it could represent normal conduction in a motor axon that ordinarily conducts more slowly. In such a case, the conduction velocity may be so low as to mistakenly suggest a primary demyelinating neuropathy. More normal conduction velocities in less affected motor nerves, as well as electromyographic signs of denervation and reinnervation, help to establish the predominant pathological alteration in the nerve fibers to give a more accurate picture of the clinical situation.

Critical to a proper appreciation of the role of EMG and NCS is a clear understanding of what these studies do not tell us and the biases inherent in many of the techniques. For example, conduction velocities as conventionally measured assess conduction in the fastest-conducting motor axons, while there is known to be a 30 to 50 percent range in the conduction velocities of alpha motor axons in man. Inherent in studies of sensory conduction is a similar bias toward the faster-conducting nerve fibers. In these studies, the compound nerve action potential is generated primarily by fibers with conduction velocities between 30 and 65 meters per second, more slowly conducting and numerous smaller-diameter fibers making relatively little contribution except to the later components of the compound nerve action potential.

On the other hand, needle electromyographic studies, whether utilizing conventional concentric needle electrodes or the more recently introduced macro or single-fiber needle electrodes (see Chapter 7) are biased as well. In these studies, the bias is toward the lowest-threshold motor units recruited in muscle contractions. From earlier investigations in normal human subjects, it is known that such lower-threshold motor units generate the least tensions and that the conduction velocities of their axons are slower compared with higher-tension, higher-recruitment-threshold motor units having faster-conducting motor axons and larger-amplitude motor unit potentials as recorded with surface electrodes (Chapter 5). Thus, while maximum motor conduction velocity determinations probably reflect primarily the contributions of the higher-tension, larger-amplitude motor units, studies of motor unit potentials based on the first few potentials recruited at each recording site in the course of a voluntary contraction are probably weighted toward the smaller motor units with slower-conducting motor axons (Fig. 1). It seems likely too, based on the range of motor unit tensions and amplitudes in normal subjects, that the maximum M-potential primarily reflects the contributions of the larger-amplitude motor unit potentials. The fastest-conducting motor axons, however, probably constitute a minority of the whole population of motor unit potentials.

FIGURE 1 Relationship between the size of a motor unit as measured by the tension or voltage it generates and the threshold at which motor units are recruited. In all studies carried out to date in humans, the lowest-threshold motor units are those generating the least tension. These same motor units have slower conduction velocities compared to the larger-tension, larger-voltage motor units recruited only in stronger contractions. The latter are precisely those motor units which, because of their faster conduction velocities, are responsible for the maximum motor conduction velocities (MCV) measured throughout the various somatic motor nerves in the body; they are probably not the same motor units whose potentials (MUPs) are recruited in weak voluntary contractions and studied by electromyography. (see Chapter 5)

Needle electromyographic studies share yet another bias: they reflect the activities of only those muscle fibers in motor units lying within the pickup territory of the recording electrode. While the size of this pickup zone varies appreciably with the surface area and shape of the recording electrode, all conventional concentric needle electrodes see but a part of the whole motor unit at least in respect to the spike components of the motor unit potential. The amplitude of the potentials recorded is determined predominantly by the number of muscle fibers sharing the same innervation within the spike...

Produkt-Details

• Erscheint lt. Verlag: 22.10.2013
• Sprache: englisch
• Themenwelt: Sachbuch/Ratgeber ► Gesundheit / Leben / Psychologie ► Krankheiten / Heilverfahren
• Themenwelt: Medizin / Pharmazie ► Allgemeines / Lexika
• Themenwelt: Medizin / Pharmazie ► Medizinische Fachgebiete
• ISBN-10: 1-4831-6329-6 / 1483163296
• ISBN-13: 978-1-4831-6329-1 / 9781483163291