Treatment of Nerve Injury and Entrapment Neuropathy PDF
Preview Treatment of Nerve Injury and Entrapment Neuropathy
Springer Japan KK Y. Hirasawa (Ed.) Treatment of Nerve Injury and Entrapment Neuropathy With 365 Figures t Springer YASUSUKE HIRASAWA, M.D., Ph.D. Professor Emeritus, Kyoto Prefectural University of Medicine Professor, Graduate School, Meiji University of Orient al Medicine Kyoto, Japan This book is based on the Japanese original, Y. Hirasawa (Ed), Treatment for Peripheral Nerve Injury and Neuropathy, Kanehara & Co., Tokyo, 2000. Many figures are reproduced with permission of Kanehara & Co., Ltd. ISBN 978-4-431-70326-6 ISBN 978-4-431-67883-0 (eBook) DOI 10.1007/978-4-431-67883-0 Printed on acid-free paper © Springer Japan 2002 Corrected second printing 200S Originally published by Springer Japan in 2002 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustra tions, recitation, broadcasting, reproduction on microfilms or in other ways, and storage in data banks. The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protec tive laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. In every individual case the respective user must check its accuracy by consulting other pharmaceuticalliterature. Typesetting: SNP Best-set Typesetter Ltd., Hong Kong SPIN: 11395935 Preface Many patients visit hospitals due to numbness, tingling, weakness, and muscle atrophy of the extremities. Peripheral nerve injury and entrapment neuro pathy are often complicated by injury to adjacent tissue such as bone, joints, blood vessels, and tendons. Clinicians who provide primary care should have broad knowledge of wound and nerve injury treatment techniques. In par ticular, the treatment of fractures and lacerations without knowledge of con comitant peripheral nerve injury may result in adverse outcomes. With knowledge of the extent of peripheral nerve involvement, the injury can be systematically evaluated and appropriate treatment initiated in specific clin ical cases. Recently, the diagnosis of peripheral nerve injury has improved with the clinical application of various diagnostic imaging modalities in addition to electrophysiological methods. Marked advances have also been made in recent years in basic research on peripheral nerve regeneration, triggered by studies on nerve growth factors. In particular, further clarification of the elongation mechanism of the growth cone and advances in molecular biology such as the elucidation of cytoskeleton components, trophic factors, and adhe sion molecules have led to progress in functional reconstruction after nerve injury. On the other hand, the use of microsurgery techniques has markedly improved the surgical results in the treatment of peripheral nerve injury, particularly allowing accurate microscopic nerve suturing and neurolysis with minimal vascular injury inside and outside the nerve fascicles. Those advances in surgical procedures have improved the results of nerve repair. However, difficult problems remain, including misdirection at the time of neural regeneration, large nerve injury, and repair of old and neglected nerve injury. The most important element in the treatment of peripheral nerve injury is accurate surgical repair or functional reconstruction techniques, such as muscle-tendon transfer for residual functional disturbance that cannot be treated by nerve repair, to permit return of function of the affected extremity. Postoperative physical and occupational therapy is also necessary. This book summarizes current topics in the field of surgical nerve repair, the selection of treatment methods for peripheral nerve paralysis with some personal viewpoints, practical issues in surgery, and aspects of postoperative care for areadership including clinical trainees, general clinicians, and allied health care workers. The importance of evidence-based medicine is currently emphasized, and treatment methods are selected based on objective data. We are now entering the era of medical record release to determine whether treatment appears appropriate from the viewpoint of a third party. At the dawn of this new era in medicine, we hope that this book will be consulted by clinicians involved in first-line treatment. Professor Chizuka Ide kindly contributed to the descriptions of recent advances in basic research, described mainly in Chapter 1. Professor Takao v VI Preface Tokioka cooperated by allowing the inclusion of his results from morpholog ical studies on entrapment points. The other clinical sections were summa rized through the concerted efforts of the peripheral nerve group of our department and the rehabilitation staff of our institution. Here, I take the liberty of adding a personal note. I was in my first year of residency at the Department of Orthopaedic Surgery when the Chairman, Professor Takefumi Morotomi, suggested a research theme of peripheral nerve injury, saying that while research on bone and joints was of course important, research about the neuromuscular system which controls them would soon become distinguished. I then wrote to Professor Leonard Marmor at VCLA, renowned for his work in irradiated nerve grafts, and I was accepted by his laboratory. I spent two years at VCLA as a research fellow from my second year of residency. I have been researching this field for almost 40 years since then. I also have had valuable clinical experience through acquaintances with many prominent doctors while I was a clinical fellow under Professor C.B. Sledge at Harvard Medical School, and while I was a visiting professor working with Professor A. Rütt at the Vniversity of Würzburg in Germany. My research work and the clinical reports, which have been published previously in journals, are integrated here. This is something I have long desired to do, and I greatly appreciate those journals giving me permission to reprint these articles. Sincere gratitude is expressed for the partial financial support received from the Memorial Committee for the 50th Anniversary of the Department of Orthopaedic Surgery, Kyoto Prefectural Vniversity of Medicine, for the English translation work. We also acknowledge partial support by a Grant in-Aid for Scientific Research from the Japanese Ministry of Education, Science and Culture, for the basic research section. We are also deeply grate ful to the staff of Springer-Verlag, Tokyo, for their assistance throughout the preparation of this volume. Y ASUSUKE HIRASAWA Editor Contents v Preface .................................. Chapter 1 Basic Research on Peripheral Nerve Injury and Regeneration .................. . Chapter 2 Diagnosis of Peripheral Nerve Injury and Entrapment Neuropathy ....................... . 13 Chapter 3 Electrophysiological Study of Peripheral Nerve Injury 21 Chapter 4 Treatment of Peripheral Nerve Injury and Entrapment Neuropathy ......................... . 33 Chapter 5 Nerve Injury and Entrapment Neuropathy Around the Shoulder ......................... . 47 Chapter 6 Median Nerve Injury and Entrapment 65 Chapter 7 Ulnar Nerve Injury and Entrapment 81 Chapter 8 Radial Nerve Injury and Entrapment 93 Chapter 9 Nerve Injury in the Hand 103 Chapter 10 Nerve Injury and Entrapment in the Lower Extremity 115 Chapter 11 Causalgia and Reflex Sympathetic Dystrophy 137 Chapter 12 Nerve Injury Due to Compartment Syndrome 141 VII VIII Contents Chapter 13 Tumors of Peripheral Nerves 145 Chapter 14 Differential Diagnosis from Spinal and Brain Disorders . . . . . 151 Chapter 15 Rehabilitation 161 References ..... 171 Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 177 Chapter 1 Basic Research on Peripheral Nerve Injury and Regeneration The Italian histologist Golgi [57] developed a method fibers. Many fascicles of nerve fibers are covered by to stain nerve cells in 1894. Cajal [23] in Spain per epineurium to form a nerve trunk. formed histological analysis of the central nervous Seddon [181] classified nerve injury into three types system using Golgi stain and established the basis of from the histopathological point of view: neurapraxia neurological investigations. (non-action), axonotmesis, and neuro tmesis (cutting). The nerve cell body in the CNS is specially differen Sunderland classified nerve injury into five grades from tiated and developed to receive information and trans the first to the fifth, according to whether continuity is mit it to the periphery. One nerve cell body has a single preserved in the axon, myelin sheath, endoneurium, long axon and several short processes with multiple perineurium, fascicles of nerve fibers, epineurium, or ramifications called dendrites, which together form nerve trunk. Axonometosis according to Seddon's clas one neuron. In the cytoplasm of the nerve cell body, sification has no damage in the myelin sheath, so that there are a large nucleus; distinct nucleoli; Nissl bodies, the regenerated axon can reach the original target including ribosomes to synthesize proteins; the Golgi organ. In that case, pathologically and functionally apparatus, which concentrates synthesized proteins; better regeneration can be expected, because myelina and mitochondria, which produce energy by intracellu tion and maturation are better than in neurotmesis. lar respiration. Proteins, including neuropeptides and When the peripheral nerve trunk is cut, degeneration enzymes, and various neurotransmitters are synthe of all the components occurs, including the axons and sized in the nerve cell, and these products are carried to myelin sheath in the segment distal to the damaged site the periphery by axonal transport. (Wallerian degeneration). [222] On the central (proxi There are two kinds of nerve fibers (axons): myeli mal) side, retrograde degeneration occurs in one to nated and unmyelinated. The myelinated nerve fiber several myelomeres. Therefore, the regenerated axon rapidly transmits excitatory impulse by saltatory con starts growing out from the proximal stump of the duction. When the excitatory impulse reaches the nerve Schwann tube. Synthesis of ribosomes and mRNA terminal, neurotransmitters are secreted to transmit the begins to increase several hours after cutting of nerve impulse to the synapse or the end organ. Thus, the axon cells in the CNS. Delivery of nutrient substances via ret has the ability not only to transmit impulses, but also to rograde transport is stopped, which causes abnormal transport substances. RNA metabolism leading to chromatolysis (disappear Peripheral nerves are supplied by vascular networks ance of Nissl bodies), one of the features of retrograde (Fig. la and 1b ) Relatively large arteries are innervated regeneration. When the nerve cell body recovers, Nissl by monoaminergic fibers (Fig. lc). The length of the bodies reappear. On the other hand, Schwann cells pro axon is usually several millimeters to one centimeter, liferate at the broken site in the degenerative process, but the longest axon, the motor axon derived from the forming a cordlike structure wrapped with basement spinal cord and traveling to the foot, reaches about one membrane called the Schwann cell funiculus. New meter. The axon can grow to that length because of the axons grow and spread along the Schwann cell funicu cytoskeleton in the axon. In the axon, there are mito lus toward the peripheral organ and eventually make chondria, endoplasmic reticulum, neuro filaments, and functional connection with the target organ while microtubles forming the cytoskeleton. The axon is maturing. [144] The rate of regeneration seems to be supported by its connection to microtrabeculae. Each 1-2 mm/day. Figure 2 shows sprouting nerve fibers. The axon is covered by endoneurium, and many axons are theory ofaxonal regeneration is illustrated in Fig. 3. covered by perineurium to form a fascicle of nerve 2 1. Basic Research on Peripheral Nerve Injury and Regeneration a b FIG. 1. Blood supply to the peripheral nerve (femoral nerve of the rabbit). a Blood vessel network in the normal periph eral nerves (light microscopic photograph of acryl plastic cast of the vessel). b Blood vessels inside and outside a nerve regenerated after being cut (light microscopic photograph of the transverse section by injection of red acryl plastic into the vessels). c Monoaminergic nerve fibers. White arrow, in the nerve trunk; black arrows, to the perivascular tissue c (fluorescent microscope) a b FIG. 2. Axonal regeneration at sutured site. a Sprouting of regenerating axons (Badian stain, x160). b Regenerating axons by fluorescent microscope (X200) (from [79]). c c magnified view of b (x400) Axonal Transport 3 (1928) in the axon. In slow anterograde transport, structural Cajal proteins, including tublin, neurofilament, and actin, are ~ : neurotrophism earried to grow and maintain the axon. The regenera -c::::> : contact guidance tion rate is related to the transport ofaxoskeletal pro teins necessary for regeneration. It is interesting that the speed of anterograde transport is almost the same as that of regeneration. In fast retrograde transport, movement of the inter nal membrane system is generaUy observed. Vesicles of Levi Montalcini the lysosomal system, such as multivesicular bodies, (1966) are earried by this fast retrograde transport. They are thought to have a funetion to eonvey waste matter pro 1980 duced by the nerve terminals to the nerve ceU body to process them. In addition, many exogenous proteins, FIG.3. Mechanism of neural regeneration including neurotrophic factors, are carried though this transport path. When ligated peripheral nerve is observed with Falck-Hillarp's fluorescent teehnique, [46] mild aceu Axonal Transport mulation of catecholamine is seen 3 hours after ligation, and significant aecumulation is observed 4h after Although the axon arising from the nerve ceU body is ligation. If the proximal side of the nerve is ligated 1 h more than 1000 times longer than the 50-11m ceU body, before the distal side is ligated, decreased fluorescenee is it has no ability to synthesize high-molecular-weight observed on the distal side. If the proximal side of the substances such as proteins. Consequently, the axon nerve is ligated lOh urs before the distal side is ligated, receives aU the necessary substances via axonal trans no catecholamine accumulation is observed on the distal port (axonal flow). As described above, ligation, agents side. Lysosomes, mitochondria, and vesicles are found in such as colchicine, and cooling are used to stop axonal the segment proximal to the ligated site (Fig. 4). flow at a certain part of the nerve, and its composition Recently, Skene and Virag [187] found that proteins, is biochemicaUy and morphologicaUy examined to whieh are produced at low levels under normal eon prove axonal transport. ditions, are produeed in large amounts as a result of gene Recently, a method to label the nerve eeU body regulation when axons grow or regenerate. They sug with radioisotopes and to observe the movement of gested that these proteins might be earried to axonal labeled substances has often been used to prove ax endings by axonal transport and incorporated into on al flow. According to the analysis, three kinds of the membrane. They eaUed these proteins growth axonal transport can be observed: fast anterograde associated pro teins (GAPs). They reported that the transport (50-500 mm/day), slow anterograde transport synthesis of four types of proteins inereased fourfold (0.2-1 mm/day, 5-30mm/day), and fast retrograde after erush injury of the optic nerve. These proteins transport (l0-300 mm/day). The smooth endoplasmie were caUed GAP-24, -33, -43, and -50 according to their reticulum (SER) in the internal membrane system is molecular weights. GAP-24, -43, and -50 are membrane selectively carried by this fast anterograde transport proteins and are earried by fast axon al flow. The increase along with glycoprotein and phospholipid. It has been and decrease of GAP-43 are especiaUy closely related to reported that neurotransmitters and related substances, the growth ofaxons. This is a major structural protein neuropeptides, synaptic vesicles, glycoprotein, phos in the nerve growth cone and changes with development pholipids, and enzymes used for renewal of the synap as weU as regeneration. Reeent studies have demon tic membrane are also earried by fast anterograde strated that GAP-43 appears in glial ceUs in apart of the transport. [103] central nerve and Schwann eeUs of unmyelinated Mitochondria are transported at an intermediate peripheral nerve fibers. However, the role of GAP-43 in speed, and they provide ATP and regulate calcium levels peripheral nerve regeneration is still unknown.
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