Table Of ContentSpringer 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
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© Springer Japan 2002
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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.
