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Fourth Edition

Electromyography
and Neuromuscular
Disorders
CLINICAL-­ELECTROPHYSIOLOGIC-­ULTRASOUND
­CORRELATIONS

David C. Preston, MD
Professor of Neurology
Case Western Reserve University School of Medicine
Program Director, Neurology Residency
Vice Chairman, Department of Neurology
University Hospitals Cleveland Medical Center
Cleveland, Ohio

Barbara E. Shapiro, MD, PhD

Associate Professor of Neurology
Case Western Reserve University School of Medicine
University Hospitals Cleveland Medical Center
Cleveland, Ohio
Elsevier
1600 John F. Kennedy Blvd.
Ste 1600
Philadelphia, PA 19103-­2899

ELECTROMYOGRAPHY AND NEUROMUSCULAR DISORDERS: ISBN: 978-­0-­323-­66180-­5

CLINICAL-­ELECTROPHYSIOLOGIC-­ULTRASOUND CORRELATIONS,
FOURTH EDITION

Copyright © 2021 by Elsevier, Inc. All rights reserved.

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contained in the material herein.

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Printed in Canada

Last digit is the print number: 9 8 7 6 5 4 3 2 1

 ix

Foreword
Electromyography (EMG) is a relatively new test. When although EMG and related tests are a powerful and sensi-
I started my residency training at the Mayo Clinic in tive technology, they are also subject to interpretive error.
1973 with Drs. Ed Lambert and Jasper Daube, it was not As such, they must always be evaluated in light of careful
widely available, and the equipment was rudimentary. The consideration of the clinical findings by an experienced cli-
machines were based on vacuum tube technology, were nician. Improperly interpreted or performed EMG tests can
large and cumbersome, took up most of the room, and had lead to useless diagnostic tests and dangerous treatments.
to be tweaked and calibrated. Filters had to be set manually On virtually a weekly basis, patients are referred to my
for each patient as well as each test. Heating lamps were not clinic because of tests done improperly or misinterpreted
necessary because the heat alone from these machines in a in the light of the clinical findings. Thus there is a need for
small room was enough to keep patients warm and make publications that continue to teach the clinical approach to
the neophyte trainee perspire, especially when the instruc- neurophysiology.
tor entered the room. Although several excellent texts cover the technical and,
Since then, much has changed. New technology has to some extent, clinical aspects of EMG, this book by Pres-
produced compact, microchip-­based, and highly accurate ton and Shapiro is unique in its emphasis on clinical and
and reliable machines. Gains and filters are available at EMG correlation. The book amply and clearly covers the
the touch of a button. Moreover, fostered by the efforts of technical aspects, but its strength lies in its emphasis on
pioneers such as Lambert, Daube, and many others, there clinical/neurophysiologic correlation, a hands-on, interac-
has been an explosion of knowledge in the field of EMG tive approach for the reader, and a style that most closely
and clinical neurophysiology. As a result, we now know a approximates how a clinical neurophysiologist thinks when
great deal about the neurophysiologic findings in many dis- approaching a complicated patient. The authors’ discus-
eases of the peripheral nervous system. Indeed, for those sion of potential pitfalls in testing is also most helpful. The
of us in the day-­to-­day practice of clinical neuromuscular authors’ admonition that, when in doubt, the examiner
diseases and clinical neurophysiology, EMG and related should stop stimulating and needling, retake the history,
electrophysiologic studies can be an enormous help in diag- and repeat the clinical examination bears repeating to every
nosis and management. Most of us regard EMG as the single trainee in every program.
most useful test in clarifying the differential diagnosis of an This text will be a positive and important addition to the
obscure neuromuscular problem, second only to the clinical EMG literature. It will be helpful to trainees in EMG and
examination. should also be useful as a refresher to experienced electro-
We all pay lip service to the concept that the EMG is myographers. I congratulate Drs. Preston and Shapiro on an
an extension of the clinical examination and best used in excellent book. I’m jealous: I wish I had written it.
conjunction with a careful clinical examination. In practice,
however, there are many occasions when this rule is violated, John J. Kelly Jr., MD
and there has been a trend lately to develop “clinical neuro- Chief, Department of Neurology
physiologists” who practice in the laboratory and have little Deputy Director, Cooper Neurological Institute
clinical experience. This is a dangerous approach, because Camden, New Jersey

Dr. Kelly’s most recent position is Chair Emeritus, Department of Neurology, George Washington University, Washington, DC.
 xi

Preface to the Fourth Edition

Since the publication of this book in 1997, followed by the ultrasound has greatly expanded, with several thousand
second and third editions in 2005 and 2012, respectively, peer-­reviewed articles published each year. Neuromus-
we continue to be profoundly gratified by the overwhelm- cular ultrasound workshops are offered by several profes-
ingly positive reception it has received. It has been humbling sional societies and universities. It is being incorporated into
as we have traveled throughout the country and parts of many neuromuscular and EMG fellowships and into some
the world to have so many physicians remark how much residencies.
they have valued the text (not to mention wanting to have Our text is not meant to be a substitute for a compre-
their picture taken with us). The main purpose of the text hensive textbook on neuromuscular ultrasound. Rather, we
remains the same as the previous editions: to create a text- highlight the basics of neuromuscular ultrasound and many
book that integrates electrodiagnostic studies and neuro- of its most useful features as a complement to EDX test-
muscular disorders in a practical and concise manner, always ing. In this edition, we include three new chapters: (1)
remembering the important principle that nerve conduction “Fundamentals of Neuromuscular Ultrasound,” (2) “Neu-
studies and electromyography (EMG) are an extension of romuscular Ultrasound of Mononeuropathies,” and (3)
the clinical examination. “Neuromuscular Ultrasound of Polyneuropathy, Motor
As the intention of this text was, and remains, to convey Neuron Disease, and Myopathy.” In addition, almost all the
basic and essential information and the vast majority of the clinical chapters now include new sections on Ultrasound
basic and essential information has not changed since the Correlations. There are hundreds of new figures in these
third edition, the question arises, why do a fourth edition? chapters and sections. Almost all the ultrasound figures
First, writing a fourth edition has allowed us to update many purposely include the native ultrasound image alongside an
chapters, especially those that deal with clinical disorders, annotated image to facilitate learning of the material. We
with new insights from recent medical literature. Second, refer the reader to several excellent textbooks and manu-
we were able to add additional tables and figures that have scripts on ultrasound and neuromuscular disorders in the
further improved the text. Third, one of the major improve- suggested readings. It is important to emphasize that neu-
ments in the previous edition was the inclusion of cross-­ romuscular ultrasound does not and will not replace EDX
sectional anatomy of the muscles used for needle EMG. testing but is complementary to it. EDX testing assesses the
The idea in that edition was that, to really master the needle physiology of nerve and muscle, which ultrasound cannot
EMG, one needs to be able to think three dimensionally— do, and often localizes the problem. In contrast, ultrasound
not only to know where the muscle is but to also know what is an imaging test that can not only often localize the prob-
other muscles are nearby and, even more importantly, what lem but also add some specific diagnostic information that
other important vascular structures and nerves are nearby EDX studies cannot detect. Once the information from
that one needs to avoid. This addition of the cross-­sectional the EDX study is known, ultrasound can then be used in a
anatomy foreshadowed the major reason for doing a fourth directed manner to obtain important additional structural
edition—the addition of neuromuscular ultrasound correla- and dynamic information.
tions. Since the third edition of this text, much has changed Like the previous editions, this text is meant to provide a
in the field of neuromuscular medicine. The value of neu- single resource for those physicians training in or practicing
romuscular ultrasound has become well-­established, and its electrodiagnostic studies. However, it can now also be used
use will undoubtedly expand in the future. Neuromuscu- to learn the basics of neuromuscular ultrasound and how
lar ultrasound is a natural complement to electrodiagnostic ultrasound can be used to complement the EDX study. In
(EDX) studies. Just as EDX studies are best performed by the future, we expect electromyographers will be referring
neuromuscular physicians, neuromuscular ultrasound stud- more patients for neuromuscular ultrasound or performing
ies are also best performed by neuromuscular physicians, who ultrasound studies themselves. This text will help in both
are very familiar with peripheral nerve and muscle anatomy situations.
and are well acquainted with the associated clinical disor- From our perspective of teaching for more than 30 years
ders. Neuromuscular ultrasound has many advantages. It is on post-­graduate, residency, and fellowship levels, we feel
painless and safe, with no side effects. It is dynamic: one can that if one can master the fundamentals in this book, one
visualize nerves, muscles, and tendons as a limb is moved should have all the basic concepts and information needed
either actively or passively to help understand the relation- to competently understand and interpret electrodiagnostic
ship between the nerves and muscles examined and their studies. Likewise, one will understand the most important
surrounding structures. Knowing neuromuscular ultrasound uses of neuromuscular ultrasound as an adjunct to EDX
improves one’s ability to perform EDX studies; indeed, we studies and how to interpret ultrasound studies. Neverthe-
believe that our knowledge of peripheral nerve and muscle less, with all the information presented in this text regard-
anatomy has more than doubled since starting to perform ing the performance of EDX and ultrasound studies, there
neuromuscular ultrasound. Research in neuromuscular remains no substitute for hands-­on experience guided by
xii Preface to the Fourth Edition

supervision. The continued goal of this text is to present text, one can sit down with a patient, take a history, perform
material in an easily understandable and logical manner. We a physical examination, and use the appropriate electrodi-
have often commented to our students that with knowl- agnostic studies, with ultrasound if indicated, to reach the
edge of anatomy, physiology, and neurologic localization, the most accurate and complete diagnosis.
practice of electrodiagnostic studies makes sense. With the
addition of ultrasound correlation, it now makes even more David C. Preston
sense. We hope that with the information contained in this Barbara E. Shapiro
 xiii

Preface to the Third Edition

Since the publication of this book in 1997, followed by the of them. Most of the photographs are now in color. Being
second edition in 2005, we have been profoundly gratified strong believers in “a picture is worth a thousand words,”
by the continued overwhelmingly positive reception it has we have added over 100 new figures and photos, and others
received from physicians, both in training and in practice. It have been updated. In addition, one of the major improve-
has become one of the key resources for residents and fel- ments in the third edition has been the inclusion of cross-­
lows who are learning electrodiagnostic testing and clinical sectional anatomy of the muscles used for needle EMG.
neuromuscular disorders. The goal of the first edition was to To really master the needle EMG, one needs to be able to
create a textbook that integrated electrodiagnostic studies think three dimensionally – not only where the muscle is,
and neuromuscular disorders in a practical and concise man- but what other muscles are nearby and, even more impor-
ner, always remembering the important principle that nerve tant, what other important vascular structures and nerves
conduction studies and electromyography (EMG) are an are nearby that one needs to avoid. To this end, we adapted
extension of the clinical examination. In the second edition, cross-­sectional line drawings from the outstanding work of
the companion CD of EMG waveforms was added so that Eycleshymer and Schoemaker published in 1911. Each indi-
the reader could have the benefit of being able to see and vidual drawing was scanned and then oriented to the posi-
hear examples of classic EMG waveforms. The second edi- tion used for EMG. The muscle of interest was shaded red
tion was also expanded in the number of chapters and the and, likewise, all major nerves, veins, arteries and tendons
breadth of information, adding chapters on Pediatric EMG, were color coded. Finally, a life size image of a conventional
Electricity and Electronics, EMG in the ICU, Iatrogenic needle EMG was placed in the correct orientation used for
Electrodiagnosis, and Statistics for EMG studies. EMG. Thus, each muscle used for needle EMG now has a
As the intention of this text was, and remains, to convey photo showing its correct insertion point along with its rel-
basic and essential information, and the vast majority of the evant cross-­sectional anatomy at that location.
basic and essential information has not changed, the ques- Like the first and second editions, this text is meant to
tion again arises, “why do a third edition?” The reasons are provide a single resource for those physicians training in
multifactorial. or practicing electrodiagnostic studies. From our perspec-
First, the authors now read many of our neurology jour- tive of teaching for over 20 years, on a post-­graduate, resi-
nals and an increasing number of books on our iPads and dency, and fellowship level, we feel that if one can master
other similar devices. We also now use these devices to the fundamentals in this book, one should have all the basic
connect to our electronic medical record, and look up drug concepts and information one needs to competently under-
information and a host of medical information. It therefore stand and interpret electrodiagnostic studies. Although a
makes sense for a third edition to be both in print and com- great deal of information is presented regarding the perfor-
pletely electronic. Although it is difficult for many of us mance of studies, there remains no substitute for hands-­on
to think about replacing books with electronic media, this experience under supervision. However, for the recognition
is clearly where the world is moving, led by our students, and interpretation of EMG waveforms, the videos now pub-
residents, and fellows in training. lished on the web should make this much easier to master.
Second, writing a third edition gave us the opportunity The continued goal of this text is to present material in
to review the medical literature since 2005 on all the topics an easily understandable and logical manner. The authors
in the text, especially the chapters that deal with clinical have often commented to their students that with knowl-
disorders. Since the publication of the second edition there edge of anatomy, physiology, and neurologic localization,
have been significant advances in understanding the genet- the practice of electrodiagnostic studies makes sense. We
ics, pathophysiology, and treatment of many neuromuscu- hope that with the information contained in this text, one
lar conditions, and these are included in the third edition. can sit down with a patient, take a history, perform a physi-
In addition, some electrodiagnostic techniques have been cal examination, and use the appropriate electrodiagnostic
improved and other new ones described that are included in studies to reach a diagnosis.
this third edition of the book.
Third, with advances in publishing, we have now greatly DCP
improved the figures and color has been added to many BES
 xv

Preface to the Second Edition

Since the publication of the first edition of this book in Indeed, we have added or updated more than 175 figures to
1997, we have been gratified by the overwhelmingly posi- the first edition of the book.
tive reception it has received from physicians, both in train- We have improved the book in several other ways. First,
ing and in practice. The goal of the first edition was to create we have expanded many of the clinical chapters, and in
a textbook that integrated electrodiagnostic studies and some cases separated them into new chapters, including
neuromuscular disorders in a practical and concise manner, median neuropathy at the wrist, proximal median neuropa-
always remembering the important principle that nerve con- thy, ulnar neuropathy at the wrist, ulnar neuropathy at the
duction studies and electromyography (EMG) are an exten- elbow, amyotrophic lateral sclerosis, and atypical motor
sion of the clinical examination. As this text is intended to neuron disorders. All of the clinical chapters follow the
convey basic and essential information, the question arises, same format that was used in the first edition, first pre-
“why do a second edition?” The authors acknowledge that senting the important anatomic and clinical aspects of the
no new muscles have been discovered in the human body disorder, followed by a discussion of the relevant electro-
over the past six years. Likewise, PCR and genetic tests diagnostic studies. Each chapter ends with example cases
have failed to identify any new nerves. Although much of based on actual patients, illustrating many important clinical
the basic information in the fields of electrodiagnostic stud- and electrodiagnostic teaching points. In addition, in section
ies and neuromuscular disorders has not changed, we have three we have added a new chapter on basic statistics for
written this second edition to improve and expand on many electrodiagnostic studies, discussing several basic statistical
topics. concepts that every electromyographer needs to know in
First and most important, needle electromyography order to properly interpret a study.
relies upon the proper interpretation of waveforms in real-­ The first edition was divided into six separate sections.
time. While one can read about waveforms until they are This new edition has been expanded to eight. The first new
blue in the face, it is very difficult to appreciate the audio section deals with EMG in Special Clinical Settings, includ-
and visual qualities of a waveform unless one can see and ing the approach to electrodiagnostic studies in the inten-
hear it. For the last fifteen years, we have collected video sive care unit, and the approach to electrodiagnostic studies
examples of classic EMG waveforms from a variety of in the pediatric patient. In the last several years, electro-
patients. Two years after the publication of the first edi- myographers are called upon more frequently to perform
tion of this book, we introduced a companion videotape of EMG studies in the intensive care unit to evaluate patients
common EMG waveforms. With new digital technology, we with profound weakness. New clinical disorders and elec-
have now been able to digitize these video waveforms and trodiagnostic techniques to evaluate these disorders have
put them on a companion CD which accompanies this book. been extensively reported over the last several years and are
Thus, in this second edition, the reader can view the CD on reflected in this new edition. We have included a discussion
any computer, and watch and hear every common and clas- of pediatric EMG because of its own unique set of chal-
sic EMG waveform. Because all the waveforms are digital, lenges and techniques that differ from adult studies.
the reader can freeze or replay any waveform at any time. The other new section deals with the basics of elec-
The textbook description and discussion of each waveform tricity and electronics, in addition to the potential risks
are now greatly enhanced by the companion CD. and complications of electrodiagnostic studies. Some
Since the publication of the first edition there have been knowledge of electricity and electronics is extremely
significant advances in some neuromuscular conditions, and helpful in understanding electrodiagnostic studies. From
these are included in the second edition. Some new disor- a practical point of view, this knowledge is also very help-
ders have been described, among them paralytic poliomyeli- ful in understanding and correcting many of the technical
tis caused by the West Nile virus. In addition, several new problems that arise in the everyday practice of electrodi-
techniques that have been described and validated in the agnostic medicine. The latter chapter arose from a con-
electrodiagnosis of neuromuscular conditions are included tinuing medical education course which we were asked to
in this second edition of the book. For instance, the elec- give at an annual meeting of the American Association of
trodiagnosis of ulnar neuropathy at Guyon’s canal has sig- Electrodiagnostic Medicine, which was followed up as a
nificantly improved over the past few years, and several review article in the journal Muscle and Nerve. Although
new techniques that are useful in making this diagnosis are nerve conduction studies and EMG are usually well toler-
included in this second edition. ated and in most patients have minimal side effects, there
We spent a considerable amount of time thinking of bet- are potential risks and complications, especially in certain
ter ways to present complex material in a logical and concise patient populations. It is essential that all physicians per-
manner for this second edition of the book. Being strong forming these studies are aware of these potential risks and
believers in “a picture is worth a thousand words,” we have complications, albeit rare, and follow simple protocols to
added many new figures, and others have been updated. minimize them.
xvi Preface to the Second Edition

Like the first edition, this text is meant to provide a Finally, the goal of this text is to present material in an
single resource for those physicians training in or practicing easily understandable and logical manner. The authors have
electrodiagnostic studies. From our perspective of teaching often commented to their students that with knowledge of
for many years, both on a post-­graduate and residency level, anatomy, physiology, and neurologic localization, the prac-
we feel that if one can master the fundamentals in this book, tice of electrodiagnostic studies makes sense. We hope that
one should have all the basic concepts and information one with the information contained in this text, one can sit down
needs to competently understand and interpret electro- with a patient, take a history, perform a physical examina-
diagnostic studies. Although a great deal of information is tion, and use the appropriate electrodiagnostic studies to
presented regarding the performance of studies, there is no reach a diagnosis.
substitute for hands-­on experience under supervision. How-
ever, it is our hope that with the companion CD as part of DCP
the textbook, the recognition and interpretation of EMG BES
waveforms will be easier to master.
 xvii

Preface to the First Edition

This text is written primarily for clinicians who perform reflexes, and repetitive nerve stimulation studies. In Sec-
and interpret nerve conduction studies and electromyogra- tion Three, important technical factors and artifacts are
phy (EMG), as well as for physicians who use the results discussed, including the anomalous innervations. Sec-
of these electrodiagnostic studies to evaluate patients with tion Four discusses the practical details of performing the
peripheral nervous system disorders. Nerve conduction most commonly used nerve conduction studies. In Section
studies and EMG are best considered an extension of the Five, the focus changes to needle EMG. After discussing
clinical examination. Indeed, these studies cannot be prop- the overall approach to the needle EMG, the anatomy of
erly planned, performed, or interpreted without knowing the bulbar, upper extremity, and lower extremity muscles
the patient’s symptoms and findings on the clinical exami- is reviewed in detail. The last two chapters in this section
nation. Numerous nerves and literally hundreds of muscles cover the approach to the needle EMG examination, includ-
can be studied. To study them all would be neither practical ing the assessment of spontaneous activity and the analysis
for the electromyographer, nor desirable for the patient. In of motor unit action potentials.
every case, the study must be individually planned, based Section Six, Clinical–Electrophysiologic Correlations,
on the clinical differential diagnosis, and then modified as forms the core of the text. After an overview of the impor-
the study progresses and further information is gained. The tant patterns, all of the major peripheral nervous system
electromyographer needs to perform the studies necessary conditions are discussed, from both the clinical and the
to both confirm and exclude certain diagnoses while mini- electrophysiologic points of view. Included are the mono-
mizing the amount of patient discomfort. Most often, nerve neuropathies, polyneuropathies, motor neuron diseases,
conduction studies and EMG can successfully localize the radiculopathies, plexopathies, disorders of the neuromus-
lesion, provide further information about the underlying cular junction and muscle, and the myotonic and periodic
pathophysiology, and assist in assessing the disorder’s sever- paralysis disorders. At all times, the text integrates the
ity and temporal course. important basic clinical and electrophysiologic points. In
Although there are many excellent textbooks on electro- Chapters 16–32, clinical cases and their respective nerve
diagnosis and several superb references on clinical neuro- conduction and EMG data are presented. Each case exam-
muscular disorders, few integrate the two in a practical and ple is that of an actual patient taken from our EMG teaching
concise manner. The approach we take in this text parallels file during the past 10 years.
our teaching program developed for the EMG fellowships The authors appreciate that some specific techniques
and neurology residencies at the Brigham and Women’s and normal values may vary from laboratory to laboratory.
Hospital and the Massachusetts General Hospital in Boston. Nevertheless, the goal of this book is to present a logical
The book is divided into six fundamental sections. Sec- approach in the EMG laboratory that combines the clinical
tion One covers the overall practical approach to a patient and electrophysiologic evaluations of a patient with a disor-
in the EMG laboratory, followed by a review of the basic der of the peripheral nervous system.
anatomy and neurophysiology that every electromyogra-
pher needs to understand. Section Two discusses the fun- DCP
damentals of nerve conductions, including motor, sensory, BES
and mixed nerve studies, as well as late responses, blink
 xix

Dedication

To our daughters, Hannah and Abigail.

 xxi

Acknowledgments
The authors are indebted to their mentors in clinical neuro- the early parts of our academic and publishing careers. Then
physiology: Drs. John J. Kelly, Jr., Eric L. Logigian, and Bhag- there are a host of individuals whose books, presentations,
wan T. Shahani. Dr. Bashar Katirji, our friend and colleague courses, and research ignited our passion in neuromuscular
for more than 20 years, has been an inspiration and a great ultrasound. Among them are Drs. Francis O. Walker, Michael
partner in teaching, research, and patient care in clinical neu- S. Cartwright, Lisa D. Hobson-­Webb, Jeff Strakowski, Lucia
romuscular disorders and electrophysiology. In addition, the Padua, Stefano Bianchi, Carlo Martinoli, Andrea J. Boon,
authors wish to thank their colleagues, technologists, and Leo Visser, Craig M. Zaidman, Antonios Kerasnoudis, H.
present and former Neuromuscular and EMG fellows at the Stephan Goedee, James B. Caress, and Joon Shik Yoon. At
University Hospitals Cleveland Medical Center, the Brigham Elsevier, Melanie Tucker, Lisa Barnes, and Doug Turner were
and Women’s Hospital, and the Massachusetts General Hos- instrumental in bringing the fourth edition into print and
pital. The contributions of Dale Preston, Thayer Preston, electronic forms. And of course we will always be grateful
and Richard (Zack) Zydek to the photography are greatly to our dear friend, Susan Pioli, who has been there since the
appreciated. A special thanks to our friend, colleague, and inception of this book and was instrumental in bringing the
mentor, Dr. Martin A. Samuels, who was instrumental in first and second editions to publication.
 SECTION I • Overview of Nerve Conduction Studies and Electromyography

Approach to Nerve Conduction

Studies, Electromyography, and
Neuromuscular Ultrasound
1
Electrodiagnostic (EDX) studies play a key role in the eval- peripheral nerves, neuromuscular junctions (NMJs), and
uation of patients with neuromuscular disorders. In selected muscles. In addition, these studies may provide useful diag-
cases, the additional use of neuromuscular ultrasound (U/S) nostic information when the disorder arises in the central
can add key complementary anatomical and diagnostic nervous system (CNS) (e.g., tremor or upper motor neu-
information. ron weakness). Occasionally, information from the EDX
EDX studies include nerve conduction studies (NCSs), study is so specific that it suggests a precise etiology. In
repetitive nerve stimulation, late responses, blink reflexes, most cases, however, the exact etiology cannot be defined
and needle electromyography (EMG), in addition to a vari- based on EDX studies alone. It is in some of these cases that
ety of other specialized examinations. NCSs and needle neuromuscular U/S is most useful. Neuromuscular U/S,
EMG form the core of the EDX study. They are performed the use of U/S to study the peripheral nerves and muscles,
first and usually yield the greatest diagnostic information. is often able to suggest the precise etiology of the disease,
NCSs and needle EMG are complementary and, therefore, such as chronic inflammatory demyelinating polyneuropa-
are always performed together and in the same setting. thy (CIDP) when a particular pattern of nerve enlargement
Performed and interpreted correctly, EDX studies yield is seen or inclusion body myositis when a particular pattern
critical information about the underlying neuromuscular of muscle involvement is present. EDX studies provide an
disorder and allow other laboratory and diagnostic tests, initial aid in defining the disorder, giving several key pieces
including neuromuscular U/S, to be used in an appropriate of information, which in some cases can be further refined
and efficient manner. Sometimes, the information gained with neuromuscular U/S.
from EDX studies leads to specific medical or surgical ther-
apy. For example, a patient with a peripheral neuropathy
clinically, who is subsequently found to have an acquired
demyelinating neuropathy with conduction blocks on EDX 6HQVRU\QHUYH
studies, most often has a potentially treatable condition. 'RUVDOURRW URRW
Indeed, the value of EDX studies has been validated in JDQJOLRQ
several large case studies. In the most recent study by Lind-
strom and colleagues, they analyzed data from 1414 consec-
utive patients and found that EDX studies either changed
or confirmed the diagnosis in 52% and 47% of cases, respec-
tively. Even more impressive was that EDX studies resulted
in a change in patient management in 63% of patients.
In practice, EDX studies serve as an extension of the clini- 0RWRUQHXURQ
cal examination and should always be considered as such. 0RWRUQHUYH
3HULSKHUDO
Accordingly, a directed neurologic examination should always QHUYH URRW
be performed before EDX studies to identify key clinical
abnormalities and establish a differential diagnosis. With 6HQVRU\ 0RWRU
numerous nerves and literally hundreds of muscles available, QHUYH QHUYH
it is neither desirable for the patient nor practical for the elec-
1HXURPXVFXODU
tromyographer to study them all. In each case, the study must MXQFWLRQ
be individualized, based on the neurologic examination and
differential diagnosis, and modified in real time as the study
progresses and further information is gained. 0XVFOH
NCSs and EMG are most often used to diagnose disor- Fig. 1.1 Elements of the peripheral nervous system. Note that the
ders of the peripheral nervous system (Fig. 1.1, Box 1.1). primary motor neuron resides within the spinal cord, whereas the
primary sensory neuron, the dorsal root ganglion, lies outside the
These include disorders affecting the primary motor neu- spinal cord. The dorsal root ganglion is a bipolar cell. Its proximal
rons (anterior horn cells), primary sensory neurons (dorsal process forms the sensory nerve root; the distal process becomes the
root ganglia), nerve roots, brachial and lumbosacral plexuses, peripheral sensory nerve.

1
2 SECTION I Overview of Nerve Conduction Studies and Electromyography

Box 1.1 Peripheral Nervous System Disorders: LOCALIZATION OF THE DISORDER

Localization and Major Categories
IS THE MAJOR AIM OF THE
Motor Neuronopathy Neuropathy ELECTRODIAGNOSTIC STUDY
Amyotrophic lateral Pattern The principal goal of every EDX study is to localize the
sclerosis and its variants Mononeuropathy disorder. The differential diagnosis is often dramatically
Spinal muscular atrophy • Entrapment
narrowed once the disorder has been localized. Broadly
Infectious (poliomyelitis, • Trauma
West Nile virus) Mononeuritis multiplex speaking, the first order of localization is whether the dis-
Focal motor neuron disease Polyneuropathy order is neuropathic, myopathic, a disorder of neuromuscu-
(monomelic amyotrophy) Primary nerve pathology lar transmission, or a disorder of the CNS. For example, in
Demyelinating patients with pure weakness, EDX studies can be used to
Sensory Neuronopathy Axonal localize whether the disorder is caused by dysfunction of
Autoimmune Primary fiber type
Paraneoplastic involvement
the motor neurons/axons, NMJs, or muscles or if it has a
Toxic Sensorimotor central etiology. The pattern of nerve conduction and espe-
Infectious Motor cially EMG abnormalities usually can differentiate among
Sensory these possibilities and guide subsequent laboratory investi-
Radiculopathy gations. For example, a patient with proximal muscle weak-
Macroscopic Neuromuscular
­Junction Disorders ness may have spinal muscular atrophy (i.e., a motor neuron
Disk herniation
Spondylosis Postsynaptic disorder), myasthenic syndrome (i.e., a NMJ disorder), or
Neoplasia Myasthenia gravis polymyositis (i.e., a muscle disorder) among other condi-
Hemorrhage Toxic tions, including those with central etiologies (e.g., a para-
Abscess Congenital sagittal frontal lesion). EDX studies can easily differentiate
Microscopic Presynaptic among these conditions, providing key information to guide
Infarction Lambert-­Eaton
subsequent evaluation and treatment, which differ mark-
Infectious myasthenic syndrome
Inflammatory Botulism edly among these diseases.
Neoplastic Toxic Once the localization is determined to be neuropathic,
Demyelinating Congenital myopathic, or a disorder of the NMJ or of the CNS, EDX
studies can usually add other important pieces of informa-
Plexopathy Myopathy
tion to localize the problem further (Fig. 1.2). For instance,
Radiation induced Inherited
Neoplastic Muscular dystrophy
the differential diagnosis of a patient with weakness of the
Entrapment Congenital hand and numbness of the fourth and fifth fingers includes
Diabetic Metabolic lesions affecting the ulnar nerve, lower brachial plexus, or
Hemorrhagic Acquired C8-­T1 nerve roots. If EDX studies demonstrate an ulnar
Inflammatory Inflammatory neuropathy at the elbow, the differential diagnosis is limited
Toxic
to a few conditions, and further diagnostic studies can be
Endocrine
Infectious directed in a more intelligent manner. In this situation, for
instance, there is no need to obtain a magnetic resonance

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Fig. 1.2 Possible localizations determined from PRQRQHXURSDWKLHV
the electrodiagnostic study. CNS, Central nervous
system; NMJ, neuromuscular junction. 3RO\QHXURSDWK\
 Chapter 1 • Approach to Nerve Conduction Studies, Electromyography, and Neuromuscular Ultrasound 3

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0L[HG 6XEDFXWH
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&KURQLF pathic localization.

imaging (MRI) scan of the cervical spine to assess a pos- Conversely, predominantly motor or predominantly sensory
sible cervical radiculopathy because the EDX studies dem- neuropathies are rare and suggest a much more limited set of
onstrated an ulnar neuropathy at the elbow as the source disorders. For instance, a patient with numbness in the hands
of the patient’s symptoms. This is a situation where neuro- and feet and diminished reflexes may be diagnosed with a
muscular U/S may be particularly useful, able to precisely peripheral neuropathy. However, if EDX studies demon-
localize the lesion and help assess for anatomic etiologies. strate abnormal sensory nerve conductions with completely
In a patient with a CNS disorder who is mistaken as hav- normal motor nerve conductions and needle EMG, then the
ing a peripheral disorder, the EDX study often correctly sug- differential diagnosis changes from a peripheral neuropathy
gests that the localization is central. For example, transverse to a pure sensory neuropathy or neuronopathy, which has a
myelitis may mimic Guillain-­Barré syndrome, or a small much more limited differential diagnosis.
acute cortical stroke may occasionally mimic the pattern of Second, EDX studies often can define whether the
a brachial plexopathy or mononeuropathy. In settings such underlying pathophysiology is demyelination or axonal loss.
as these, the EDX study is often the first test to suggest that Although most demyelinating neuropathies have some sec-
the correct localization is central rather than peripheral. ondary axonal loss and many axonal loss neuropathies have
some secondary demyelination, EDX studies usually can
differentiate between a primary demyelinating and a pri-
Neuropathic Localization mary axonal neuropathy. Because EDX studies usually can
Neuropathic is probably the most common localization made make this differentiation quickly and noninvasively, nerve
on EDX studies. Neuropathic literally means a disorder of biopsy is essentially never required to make this determi-
the peripheral nerves. However, in common usage, it includes nation. Furthermore, the differentiation between primary
the primary sensory and motor neurons as well. EDX stud- axonal and primary demyelinating pathology is of consid-
ies are particularly helpful in neuropathic conditions. First, in erable diagnostic and prognostic importance, especially in
conjunction with the history and examination, they can usu- the case of polyneuropathies. Most polyneuropathies are
ally further localize the disorder to the neurons, roots, plexus, associated with primary axonal degeneration, which has an
or peripheral nerve. In the case of peripheral nerves, further extensive differential diagnosis. In contrast, the number
localization is usually possible to a single nerve (mononeu- of true electrophysiologic primary demyelinating neuropa-
ropathy), multiple individual nerves (mononeuropathy mul- thies is extremely small. They are generally subdivided into
tiplex), or all nerves (polyneuropathy). In the case of a single those that are inherited and those that are acquired (e.g.,
nerve, the exact segment of nerve responsible for the prob- Charcot Marie Tooth [CMT] vs. CIDP). EDX studies can
lem may be localized in some cases. typically make that determination as well. The finding of
In the case of neuropathic lesions, EDX studies often an unequivocal primary demyelinating polyneuropathy on
yield further key information, including the fiber types EDX studies often leads quickly to the correct diagnosis
involved, the underlying pathophysiology, and the temporal and, in the case of an acquired demyelinating polyneuropa-
course of the disorder (Fig. 1.3). thy, often suggests a potentially treatable disorder.

Information About the Fiber Types Involved and the Assessing the Degree of Axonal Loss Versus
Underlying Nerve Pathophysiology can be Gained, Demyelination has Implications for Severity and
Which Then Further Narrows the Differential Diagnosis Prognosis
In the case of neuropathic disorders, the involved fiber types A nerve that has sustained a demyelinating injury often can
and the underlying pathology can usually be determined. First, remyelinate in a very short time, usually weeks. However, if
EDX studies are more sensitive than the clinical examination there has been substantial axonal loss, whether primary or
in determining which fiber types are involved: motor, sen- secondary, the prognosis is much more guarded. The rate of
sory, or a combination of the two. Sensorimotor polyneurop- axonal regrowth is limited by the rate of slow axonal trans-
athies are common and suggest a large differential diagnosis. port, approximately 1 mm per day. Clinically, axonal loss
4 SECTION I Overview of Nerve Conduction Studies and Electromyography

lesions can rarely be differentiated from demyelinating ones, 0\RSDWKLF

especially in the acute setting. For example, in a patient who
awakens with a complete wrist and finger drop, the etiology
usually is compression of the radial nerve against the spiral 'LVWULEXWLRQ 3DWKRORJ\ 7HPSRUDOFRXUVH
groove of the humerus. However, the paralysis could result
from either conduction block (i.e., demyelination) or axonal
loss, depending on the severity and duration of the compres- 3UR[LPDO %ODQG $FXWH
sion. Clinically, both conditions appear the same. Neverthe-
less, if the injury is due to axonal loss, it has a much worse 'LVWDO $FWLYHGHQHUYDWLRQ 6XEDFXWH
prognosis and a longer rehabilitation time to recovery than a
*HQHUDOL]HG 0\RWRQLFGLVFKDUJHV &KURQLF
similarly placed lesion that is predominantly demyelinating
in nature. EDX studies can readily differentiate axonal loss &UDQLREXOEDU
from demyelinating lesions.
6\PPHWULF$V\PPHWULF
Assessment of the Temporal Course can Often be Made
For neuropathic conditions, there is an orderly, temporal 6HYHULW\RILQYROYHPHQW
progression of abnormalities that occurs in NCSs and nee- Fig. 1.4 Key electrodiagnostic findings in a myopathic localization.
dle EMG. A combination of findings often allows differ-
entiation among hyperacute (less than 1 week), acute (up
to a few weeks), subacute (weeks to a few months), and
chronic (more than a few months) lesions. The time course 10-
suggested by the EDX findings may alter the impression
and differential diagnosis. For example, it is not uncommon
for a patient to report an acute time course to his or her 'LVWULEXWLRQ 3DWKRORJ\ (WLRORJ\
symptoms, whereas the EDX studies clearly indicate that
the process has been present for a longer period of time than 3UR[LPDO
the patient has been aware of.
Conversely, the temporal course described by the patient *HQHUDOL]HG 3UHV\QDSWLF $FTXLUHG
may impact the interpretation of the EDX findings. For
instance, the finding of a normal ulnar sensory nerve action &UDQLREXOEDU 3RVWV\QDSWLF ,QKHULWHG
potential recording the little finger, in a patient with numb- Fig. 1.5 Key electrodiagnostic findings in a neuromuscular junction
ness of the little finger, has very different implications localization. NMJ, Neuromuscular junction.
depending on the time course of the symptoms. If the symp-
toms are truly less than 1 week in duration, the normal ulnar can be very helpful in narrowing the differential diagnosis. For
sensory response could indicate an ulnar neuropathy (with example, inclusion body myositis may present asymmetrically,
wallerian degeneration yet to have been completed), a proxi- whereas polymyositis and dermatomyositis do not.
mal demyelinating lesion, or a lesion at the level of the nerve Second, the presence of spontaneous activity on needle
root or above. On the other hand, if the symptoms have EMG is helpful in limiting the differential diagnosis and
been present for several weeks or longer, the same finding suggesting certain underlying pathologies. Most myopathies
would indicate either a proximal demyelinating lesion or a are bland, with little or no spontaneous activity. However,
lesion at the level of the nerve root or above. These temporal myopathies that are inflammatory, necrotic, and some that
changes underscore the electromyographer’s need to know the are toxic or dystrophic may be associated with active dener-
clinical time course of symptoms and signs to ensure an accu- vation. In addition, other myopathies may have prominent
rate interpretation of any electrophysiologic abnormalities. myotonic discharges at rest. The presence of myotonic dis-
charges in a myopathy markedly narrows the differential
diagnosis to only a few possible disorders.
Myopathic Localization Last is the issue of the temporal course. Although this
In the case of myopathic (i.e., muscle) disease, EDX studies can determination is more challenging than with neuropathic
also add key information to further define the condition (Fig. lesions, in some myopathies, a determination can be made if
1.4). First, the distribution of the abnormalities may suggest a the myopathy is acute, subacute, or chronic, a finding that
diagnosis: are they proximal, distal, or generalized? Most myopa- again narrows the differential diagnosis.
thies preferentially affect the proximal muscles. Few myopathies,
such as myotonic dystrophy type I, affect distal muscles. Some
very severe myopathies (e.g., critical illness myopathy) can be Neuromuscular Junction Localization
generalized. In rare myopathies, there is prominent bulbar weak- Disorders of the NMJ are distinctly uncommon. However,
ness; accordingly, EDX abnormalities may be most prominent in when they occur, EDX studies not only help in identifying
the bulbar muscles. Most myopathies are fairly symmetric; the them but can also add other key pieces of information (Fig.
finding of asymmetry either clinically and/or on EDX studies 1.5). First is the distribution of the abnormalities on EDX
 Chapter 1 • Approach to Nerve Conduction Studies, Electromyography, and Neuromuscular Ultrasound 5

testing: are they proximal, bulbar, or generalized? For instance, Box 1.2 Patient Encounter
myasthenia gravis preferentially affects oculobulbar muscles
1. Take a brief history and perform a directed physical
and then proximal muscles on EDX studies, whereas myas- examination.
thenic syndrome is a generalized disorder on EDX studies, 2. Formulate a differential diagnosis.
although clinically it has a predilection for proximal muscles. 3. Formulate a study based on the differential diagnosis.
Broadly speaking, the underlying pathology can be 4. Explain the test to the patient.
divided into presynaptic and postsynaptic disorders. EDX 5. Perform the nerve conduction studies and modify which
nerve conduction studies to add, based on the findings as
studies are usually very good at making this determination. the test proceeds.
Myasthenia gravis is the prototypic postsynaptic disorder, 6. Perform the needle electromyography study and modify
whereas myasthenic syndrome and botulism target the pre- which additional muscles to sample, based on the findings
synaptic junction. as the test proceeds.
Last is the issue of the etiology of the NMJ disorder,
whether it is acquired or inherited. Almost all NMJ disor-
ders are acquired. However, there are rare inherited NMJ always be amended as the testing proceeds. Before begin-
disorders. In some of these, there may be unique findings on ning, however, one should first explain to the patient in
EDX testing that suggest one of these rare disorders. simple terms what the test involves. Many patients are very
anxious about the examination and may have slept poorly or
not at all the night before the EDX study. Simple explana-
PATIENT ENCOUNTER tions, both before the test begins and while it is ongoing, can
Every EDX study begins with a brief history and directed greatly reduce a patient’s anxiety.
physical examination (Box 1.2). This point cannot be overem- After the test is explained to the patient, the NCSs are
phasized! Some may (incorrectly) argue that the history and performed first, followed by the needle EMG. Indeed, one
clinical examinations are not part of the EDX examination and needs the findings on the NCSs to adapt the needle EMG
that the EDX study needs to stand on its own. Nothing could strategy accordingly and to interpret the needle EMG find-
be further from the truth. One is not expected to perform the ings correctly. For instance, active denervation in the abduc-
same detailed history and physical examination that is done in tor digiti minimi (an ulnar, C8–T1 innervated muscle) has a
the office consultation setting. However, before starting every completely different interpretation depending on whether
study, the EDX physician must know some basic facts: the ulnar motor and sensory NCSs are abnormal or not
  
(ulnar neuropathy in the former, a radiculopathy or motor
• What are the patient’s symptoms?
neuron disease in the latter).
• How long have they been going on?
A proper balance must be maintained among obtain-
• Is there any important past medical history (e.g., diabe-
ing a thorough study, collecting the necessary information
tes, history of chemotherapy, etc.)?
to answer the clinical question, and minimizing patient dis-
• Is there muscle atrophy?
comfort. If performed correctly, nearly all NCSs and needle
• What is the muscle tone (normal, decreased, or in-
EMG can be completed within 1–1.5 hours. Rarely, a longer
creased)?
study is needed if specialized tests such as repetitive nerve
• Is there weakness, and, if so, where is it and how severe
stimulation are performed in addition to the standard stud-
is it?
ies. There clearly is a limit to what most patients can tolerate.
• What do the reflexes show (normal, decreased, or
The electromyographer should always remember the Willy
increased)?
Sutton rule concerning robbing banks: “Go where the money
• Is there any loss of sensation, and, if so, what is the dis-
is.” If there is any question as to whether a patient will toler-
tribution; what modalities are disturbed (e.g., tempera-
ate the entire examination, the study should begin with the
ture, pain, vibration, etc.)?
   area of interest. For instance, in the patient with numbness
The duration, type, and distribution of symptoms, along and tingling of the fourth and fifth fingers, ulnar motor and
with the physical examination, help determine the differen- sensory studies should be done first. Likewise, needle EMG
tial diagnosis, which in turn is used to plan the EDX stud- examination of the ulnar-­innervated muscles, as well as the
ies. The EDX study is planned only after the differential C8–T1 non-­ulnar–innervated muscles, are of most interest
diagnosis is determined. For instance, the EDX evaluation in such a patient. Plan and consider which NCSs and needle
of a patient with slowly progressive proximal weakness is examination of which muscles should be performed first, in
very different from that of a patient with numbness and case the patient can tolerate only one or two nerve conduc-
tingling of the fourth and fifth fingers. In the former case, tions or examination of only a few muscles by EMG.
the differential diagnosis includes disorders of the anterior
horn cell, motor nerve, NMJ, or muscle. In the latter case, CARDINAL RULES OF NERVE
the differential diagnosis includes an ulnar neuropathy at its
various entrapment sites, a lower brachial plexus lesion, or CONDUCTION STUDIES AND
cervical radiculopathy. The EDX plan includes which nerves ELECTROMYOGRAPHY
and muscles to study and whether specialized tests, such as EDX studies rely on the physician’s ability to pay meticu-
repetitive nerve stimulation, may be helpful. The study can lous attention to technical details during the study while
6 SECTION I Overview of Nerve Conduction Studies and Electromyography

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Fig. 1.6 Cardinal rules of nerve conduction studies

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and electromyography. EDX, Electrodiagnostic; EMG,
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electromyography; NCS, nerve conduction study.

keeping in mind the bigger picture of why the study is being abnormality when none is present) and type II errors
performed. As more data are obtained, the study must be (i.e., failing to recognize an abnormality when one is
analyzed in real time and the test altered as needed. Analy- present). Although both are important, type I errors
sis of online results gives the electromyographer the oppor- are potentially more serious (e.g., the patient is labeled
tunity to modify the strategy as the testing proceeds, an with an abnormal EDX study result, such as neuropathy,
opportunity that is lost once the patient has left the labo- when the “abnormality” on the EDX testing is simply
ratory. The following cardinal rules of EDX studies should due to unrecognized technical errors). Such faulty
always be kept in mind while an EDX study is being per- diagnoses can lead to further inappropriate testing
formed (Fig. 1.6): and treatment. If there is an unexpected abnormal
  
EDX finding that does not fit the clinical examination,
1. NCSs and EMG are an extension of the clinical the lack of a clinical-­electrophysiologic correlation
examination. NCSs and EMG cannot be performed should suggest a technical problem. For instance, if a
without a good directed clinical examination. Every routine sural nerve sensory conduction study shows an
examination must be individualized based on the absent potential but the patient has a normal sensory
patient’s symptoms and signs and the resulting examination of the lateral foot (i.e., sural territory),
differential diagnosis. If marked abnormalities are found one should suspect a technical problem (e.g., improper
on electrophysiologic testing in the same distribution electrode or stimulator placement or too low of a
where the clinical examination is normal, either the stimulus intensity). If the data are not technically
clinical examination or the electrophysiologic testing accurate, then correct data interpretation can never
must be called into question. One usually finds that occur, either at the time of the study or later by the
the better the clinical examination, the better the treating physician.
differential diagnosis, and thus, the more clearly 3. When in doubt, reexamine the patient. This is essentially
directed the EDX studies will be. an extension of cardinal rule number 1. In the example
2. When in doubt, always think about technical factors. given with rule number 2, if the sural sensory response
EDX studies rely upon collecting and amplifying is absent after all possible technical factors have been
very small bioelectric signals in the millivolt and corrected, the clinician should reexamine the patient.
microvolt range. Accomplishing this is technically If the patient has clear loss of vibration at the ankles,
demanding; many physiologic and nonphysiologic there is less concern about an absent sural sensory
factors can significantly interfere with the accuracy response. If the patient’s sensory examination is normal
of the data. Accurate NCSs and EMG depend on on reexamination, the absent sensory response does not
intact equipment (e.g., EMG machine, electrodes, fit the clinical findings, and technical factors should be
and stimulator), and on correct performance of the investigated further.
study by the electromyographer. Technical problems 4. EDX findings should be reported in the context of
can easily lead to absent or abnormal findings. Failure the clinical symptoms and the referring diagnosis. In
to recognize technical factors that influence the EDX every study, electrophysiologic abnormalities must be
study can result in type I errors (i.e., diagnosing an correlated with the clinical deficit.
 Chapter 1 • Approach to Nerve Conduction Studies, Electromyography, and Neuromuscular Ultrasound 7

Because electrophysiologic studies are quite sensitive, it If all three results fit together, the diagnosis is secure.
is not uncommon for the electromyographer to discover However, if the NCSs and EMG findings do not fit together
mild, subclinical deficits of which the patient may not and, more importantly, if they do not correlate with the
be aware. For example, a diabetic patient referred to clinical findings, the significance of any electrical abnormali-
the EMG laboratory for polyneuropathy may show ties should be seriously questioned. Consider a patient with
electrophysiologic evidence of a superimposed ulnar pain in the arm who has an otherwise normal history and
neuropathy but have no symptoms of such. Accordingly, examination. If the NCSs are normal except for a low ulnar
the electromyographer should always report any sensory potential and the EMG demonstrates only mild rein-
electrophysiologic abnormality in the context of its nervation of the biceps, one should be reluctant to interpret
clinical relevance so that it can be properly interpreted. the study as showing a combination of an ulnar neuropathy
5. When in doubt, do not overcall a diagnosis. Because and a C5 radiculopathy. These mild abnormalities, which
electrophysiologic tests are very sensitive, mild, are not substantiated by other electrophysiologic findings
subclinical, and sometimes clinically insignificant and do not have clear clinical correlates, may have little to
findings often appear on EDX testing. This occurs do with the patient’s pain. In such a case, the patient should
partly because of the wide range of normal values, be reexamined. If no clinical correlate is found, the studies
which vary with the nerve and muscle being tested. should be rechecked. If the abnormalities persist, they may
In addition, there are a variety of physiologic and be noted as part of the impression but interpreted as being
nonphysiologic factors that may alter the results of both of uncertain clinical significance.
NCSs and EMG, despite attempts to control for them. When performed properly, NCSs and EMG can be very
These factors, often when combined, may create minor helpful to the referring physician. However, the limitations
abnormalities. Such minor abnormalities should not of EDX studies must be appreciated, technical factors well
be deemed relevant unless they correlate with other controlled, and a good differential diagnosis established
electrophysiologic findings and, most importantly, with before each study. Otherwise, the study may actually do a
the clinical history and examination. It is a mistake to disservice to the patient and to the referring physician by
overcall an electrophysiologic diagnosis based on minor leading them astray by way of minor, irrelevant, or techni-
abnormalities or on findings that do not fit together cally induced “abnormalities.” If the cardinal rules of NCSs
well. Sometimes, the clinical or electrophysiologic and EMG are kept in mind, EDX studies are far more likely
diagnosis is not clear-­cut and a definite diagnosis to be of help to the referring clinician and the patient with
cannot be reached. Occasionally, NCSs and EMG are a neuromuscular disorder.
clearly and definitely abnormal, but a precise diagnosis
still cannot be determined. For example, consider
the patient whose clinical history and examination NEUROMUSCULAR ULTRASOUND
suggest an ulnar neuropathy at the elbow. The EDX Over the last several years, neuromuscular U/S has increas-
study often demonstrates abnormalities of the ulnar ingly been used along with EDX studies in the evaluation
nerve in the absence of any localizing findings, such as of patients with various neuromuscular conditions. The use
conduction block or slowing across the elbow. Although of neuromuscular U/S has grown due to a combination of
the referring surgeon usually wants to know whether several factors, including the marked improvement of the
the ulnar neuropathy is at the elbow, often, the only resolution and software of U/S machines while the physi-
accurate impression that the electromyographer can cal size and cost of the machines have gone down. These
give is one of a non-­localizable ulnar neuropathy that is smaller, portable machines can easily be used and shared
at, or proximal to, the most proximal abnormal ulnar-­ among EDX laboratory rooms. Indeed, some manufacturers
innervated muscle found on EMG. are working on combined EDX and U/S machines housed in
6. Always think about the clinical-­electrophysiologic one unit. Hundreds of peer-­reviewed articles on the useful-
correlation. This rule combines all of the earlier rules. ness of neuromuscular U/S are published each year. Thus,
One usually can be certain of a diagnosis when the neuromuscular U/S has become a validated, reliable, and
clinical findings, NCSs, and EMG abnormalities all important tool in the evaluation of many neuromuscular
correlate well. Consider again the example of the disorders.
patient with weakness of the hand and tingling and Physicians who perform EDX studies are best suited to
numbness of the fourth and fifth fingers. If NCSs learn and perform neuromuscular U/S, which is the study
demonstrate abnormal ulnar motor and sensory of peripheral nerves and muscles. Neuromuscular U/S dif-
potentials associated with slowing across the elbow, fers from vascular U/S and musculoskeletal U/S, although
and the needle EMG shows denervation and reduced there is some overlap. It is essential to emphasize that neuro-
numbers of motor unit potentials in all ulnar-­ muscular U/S is complementary to EDX studies; it does not
innervated muscles and a normal EMG of all non-­ replace EDX studies. The situation is similar to the role that
ulnar–innervated muscles, there is a high degree of EDX studies and MRI have in the evaluation of radiculopa-
certainty that the patient truly has an ulnar neuropathy thy. EDX studies are physiologic tests and, as such, yield
at the elbow, and the electrophysiologic abnormalities information about the function of the nerves, nerve roots,
are indeed relevant. and muscles. In contrast, imaging studies show a picture of
  
8 SECTION I Overview of Nerve Conduction Studies and Electromyography

the nerves, nerve roots, and muscles, but yield no informa- its origin in the lower brachial plexus and assess for struc-
tion on the functioning. Thus, for example, whereas EDX tural abnormalities to localize the lesion.
studies give information about how well the nerve root is Regardless of whether the EDX study can definitely
functioning, an MRI can show the nerve roots and whether localize the mononeuropathy or not, it is important to know
they appear impinged by a disk, spondylosis, or other struc- what is causing it. Is it an entrapment from wear and tear?
tural causes. Likewise, whereas EDX studies may be able Or from tenosynovitis? Or from compression from a gan-
to identify an ulnar neuropathy at the elbow, they cannot glion cyst? Or from a nerve sheath tumor? And the list con-
discern what is causing it. This is where neuromuscular U/S tinues. This is also where U/S may add critical anatomic
may add critical complementary information to the EDX information about what is causing the mononeuropathy.
studies. For example, it may reveal bony spurs and excess Performing U/S after EDX studies for a mononeuropa-
callus in the ulnar groove from tardy ulnar palsy, compres- thy may result in three different outcomes:
  
sion of the ulnar nerve in the true cubital tunnel under
1. It may add no useful information, or
the humeral-­ulnar aponeurosis, or in some cases a synovial
2. It may add important complementary information, or
cyst compressing the ulnar nerve, among many possible
3. It may be the key to the case.
etiologies.   
Best used, neuromuscular U/S serves as an extension of Unfortunately, one does not know before doing the U/S
the clinical examination and most often of the EDX studies, study which of these three outcomes will be the result.
and should be used as such. Chapters 17, 18, and 19 discuss Thus, one can make a strong argument that U/S is a reason-
neuromuscular U/S in greater detail. In addition, many of able adjunct to EDX studies for most mononeuropathies.
the later clinical chapters expand on the usefulness of neu-
romuscular U/S in specific conditions.
Similar to EDX studies, there are several general princi- Peripheral Nerve: Polyneuropathy
ples of neuromuscular U/S. Each neuromuscular U/S study The role of neuromuscular U/S in polyneuropathy is most
must be individualized, based on the neurologic examina- useful when looking for evidence of a hypertrophic (usu-
tion, the EDX study, and the differential diagnosis, and ally meaning demyelinating) polyneuropathy. As will be dis-
modified as the study progresses and further information cussed in Chapter 29 on Polyneuropathy, the vast majority
is gained. Its primary use is to add anatomic and pathologic of polyneuropathies display an axonal loss pattern on EDX
information that complements the EDX study. Among neu- studies. Very few are primarily demyelinating. However,
romuscular U/S’s many potential uses, the major ones are the presence of demyelination on EDX studies of a poly-
described in the following sections. neuropathy is a critical piece of information, as it mark-
edly narrows the differential diagnosis. Furthermore, in the
case of acquired demyelinating polyneuropathies, most are
Peripheral Nerve: Mononeuropathy inflammatory (autoimmune) and potentially very treatable.
In general, U/S is particularly helpful in many mononeu- The U/S picture of a chronic demyelinating polyneu-
ropathies. Mononeuropathies are commonly caused by ropathy is usually that of a hypertrophic neuropathy (from
entrapment, trauma, and in some cases other structural repeated demyelination and remyelination, Schwann cell
causes. When the EDX study has localized the problem to proliferation, and onion blub formation). EDX studies may
one segment of one peripheral nerve (e.g., the median nerve be indeterminate in some chronic demyelinating neuropa-
at the carpal tunnel), U/S can confirm the localization by thies. Sometimes, this is due to responses being absent. In
revealing structural changes in the nerve at the involved site. others, the EDX criteria for demyelination are not fully
In the case of carpal tunnel syndrome, U/S usually simply met, or the conduction velocities are in the borderline range
adds additional confirmatory evidence of the nerve loca- between axon loss and demyelination. In these cases, pre-
tion, although as we will see later in Chapter 20 on Median sumably the demyelination is not marked enough to call,
Neuropathy at the Wrist, U/S may add more information, or the segments of nerve that are demyelinated are not eas-
especially in postoperative cases or when symptoms recur. ily assessed by standard EDX studies (e.g., very proximal
In other cases of mononeuropathy, when the EDX study nerves, plexus, and/or roots). Hence, U/S can be extremely
localizes the problem to one nerve but is not able to local- useful in establishing a polyneuropathy as demyelinating.
ize a specific segment, U/S can be particularly useful. This
occurs when the pathophysiology is that of axonal loss. In
this situation, U/S is particularly helpful as it can often Motor Neuron Disease
localize the lesion more precisely than EDX studies. Take EDX studies in conjunction with the history and physi-
the example of the patient with a weak grip and numbness cal examination are the cornerstones of diagnosing motor
involving digit 5. An ulnar neuropathy is considered most neuron disease. U/S has a limited role in the diagnosis of
likely. The EDX study might show abnormalities limited to motor neuron disease, with a couple of notable exceptions.
the ulnar nerve, but there is no slowing or conduction block First, U/S is extremely good at detecting fasciculations—
across the elbow. Is the lesion at the elbow? Or is it as the better than the clinical examination and needle EMG. The
wrist, in the forearm, upper arm, or in the lower brachial research criteria for the diagnosis of motor neuron disease
plexus? U/S can visualize the ulnar nerve from the wrist to (and qualification for clinical studies) requires evidence of
 Chapter 1 • Approach to Nerve Conduction Studies, Electromyography, and Neuromuscular Ultrasound 9

denervation and reinnervation on EDX studies. However, CARDINAL RULES OF

more recent criteria accept the presence of fasciculations
along with reinnervation as evidence of ongoing lower motor
NEUROMUSCULAR ULTRASOUND
Similar to EDX studies, neuromuscular U/S relies on the
neuron loss. Thus, U/S can be very helpful in more easily
physician’s ability to perform and interpret the study cor-
detecting fasciculations.
rectly and analyze the findings in real time, altering the
Second, a diagnostic dilemma often arises in patients with
study as needed. The following cardinal rules of neuromus-
suspected motor neuron disease when they present with
cular U/S should always be kept in mind when performing
a pure lower motor neuron syndrome without any definite
a study (Fig. 1.7):
upper motor neuron signs. This syndrome is typically desig-   
nated as the progressive muscular atrophy (PMA) form of 1. Neuromuscular U/S is complementary to the EDX study.
motor neuron disease. However, in such patients, the ques- As emphasized earlier, EDX assesses the physiologic
tion often remains whether the patient has a motor neuron function of nerve and muscle, whereas U/S imaging
disorder, such as PMA, or a motor nerve disorder. True motor of nerve and muscle is used to provide anatomic and,
nerve disorders are rare, but when they occur, they typically possibly, pathologic etiologic information. These are
mimic PMA. Oftentimes, EDX studies cannot distinguish complementary pieces of information that, when used
between these two, especially when conduction blocks are together, allow more accurate and complete information
very proximal or motor NCSs are in the borderline range. on the nature of the neuromuscular disorder.
Motor neuropathies are most often inflammatory and treat- 2. Each U/S study should be tailored for the individual
able. Variants of CIDP, but more often, multifocal motor patient. Each study must be tailored to the individual
neuropathy with conduction block (MMNCB) may present patient and differential diagnosis. Properly used,
as pure lower motor neuron weakness. In these conditions, neuromuscular U/S is used after the EDX study is
U/S may demonstrate hypertrophic nerves, whereas in amyo- completed to answer specific questions. It is not
trophic lateral sclerosis (ALS), PMA, and other motor neu- desirable or practical to image all nerves and all muscles.
ron disorders, nerve size is normal or even small. Thus, U/S The specific neuromuscular U/S study done will be
should be strongly considered in all patients presenting as a different for each patient.
pure lower motor neuron syndrome. 3. Fully evaluate any abnormalities. When any
“abnormality” is seen on U/S, one must define it
to the fullest extent possible. Always look at the
Myopathy abnormality in at least two planes. Just like MRI, when
The original reports of using U/S in neuromuscular disorders an “abnormality” is seen on a sagittal image but not on
come from evaluation of young boys with Duchenne mus- the axial image, it is probably an artifact. Use the color
cular dystrophy. Like motor neuron disease, the use of U/S Doppler to look for increased blood flow, which may
in myopathies is limited, but with a few notable exceptions. occur with inflammation, infection, or neoplasia. Check
First, U/S can easily screen many muscles at one sitting. The for compressibility and mobility. Note the echogencity
pattern formed by which muscles are abnormal and which are (i.e., how bright or how dark the lesion is). Look for the
spared is increasingly used to help limit the differential diag- classic U/S findings of posterior acoustic enhancement
nosis in myopathies. U/S is much quicker and less expensive or shadowing. Then, look closely at the nearby
than MRI in establishing the pattern of muscle involvement structures: bone, tendon, ligament, and blood vessel. If
and can screen all four limbs, proximally and distally, in one possible, do a dynamic evaluation and see what happens
sitting. Certain myopathies have a characteristic pattern of
muscle involvement. For instance, in inclusion body myositis,
sparing of the rectus femoris compared to the other quadri- &DUGLQDOUXOHVRI
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ceps muscles and the involvement of the forearm finger flex-
ors are both highly suggestive of the diagnosis, in the proper 1HXURPXVFXODU86LV
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clinical context. VWXGLHV
Second, U/S may be useful in identifying a muscle site for
biopsy. The best yield of a muscle biopsy is in choosing a mus-
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cle that is abnormal but not end stage. Needle EMG is often WDLORUHG
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used in this regard, but one then needs to biopsy the muscle DOODEQRUPDOLWLHV
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on the contralateral side to the muscle identified on needle
EMG as the optimal site. If one biopsied the muscle sampled
$OZD\VWKLQNDERXWWKH
with needle EMG, the biopsy might include the area where FOLQLFDO(';86
the needle had been placed, which could result in inflamma- FRUUHODWLRQ
tion and other injury along the needle track and carries the
inherent risk of diagnosing an inflammatory myopathy incor- :KHQLQGRXEW
rectly. Using U/S, one can biopsy the specific muscle that was GRQRWRYHUFDOODGLDJQRVLV
examined and determined to be optimal, without the need to Fig. 1.7 Cardinal rules of neuromuscular ultrasound. EDX,
choose the contralateral side. ­Electrodiagnostic; U/S, ultrasound.
10 SECTION I Overview of Nerve Conduction Studies and Electromyography

to the lesion with passive range of motion, or during normal EMG of all non-ulnar–innervated muscles,
voluntary contraction of nearby muscles. Take lots of and the U/S shows an enlarged, hypoechoic ulnar
still pictures and movie clips, all of which will help you nerve under the humeral-­ulnar aponeurosis at the true
later in making your determination. cubital tunnel without any other pathology; there is
4. When in doubt, think about technical factors, artifacts, a very high degree of certainty that the patient truly
and anomalies. U/S has its own set of artifacts and has an ulnar neuropathy at the elbow. In this case, the
technical factors (see Chapter 17). If not recognized, electrophysiological abnormalities are indeed relevant,
these can lead to the mistaken impression of pathology with the U/S demonstrating the etiology of the ulnar
when none actually exists. Similar to EDX studies, such nerve entrapment at the cubital tunnel.
faulty diagnoses can lead to inappropriate testing and
treatment. In addition, when performing U/S, it is not
uncommon to encounter anatomic anomalies of nerve, Suggested Readings
muscle, and blood vessel. One quickly appreciates that Cocito D, Tavella A, Ciaramitaro P, Costa P, Poglio
every patient’s anatomy does not necessarily follow the F, Paolasso I, et al. A further critical evaluation of
textbook. Sometimes, these anatomic anomalies are requests for electrodiagnostic examinations. Neurol Sci.
2006;26(6):419–422.
actually the cause of the patient’s problem; in other
Haig AJ, Tzeng HM, LeBreck DB. The value of
cases, they are simply incidental findings.
electrodiagnostic consultation for patients with upper
5. When in doubt, do not overcall a diagnosis. This general extremity nerve complaints: a prospective comparison
rule is equally applicable to EDX studies and all other with the history and physical examination. Arch Phys Med
laboratory and radiographic tests. It is not uncommon Rehabil. 1999;80(10):1273–1281.
to find minor abnormalities of unclear significance or to Kothari MJ, Blakeslee MA, Reichwein R, Simmons Z, Logigian
misinterpret technical issues as findings. It is a mistake EL. Electrodiagnostic studies: are they useful in clinical
to overcall any diagnosis based on minor abnormalities practice? Arch Phys Med Rehabil. 1998;79(12):1510–1511.
or findings that do not fit together with the clinical Kothari MJ, Preston DC, Plotkin GM, Venkatesh S,
presentation. Shefner JM, Logigian EL. Electromyography: do the
6. Always think about the clinical-­electrophysiologic-­ diagnostic ends justify the means? Arch Phys Med Rehabil.
1995;76(10):947–949.
ultrasound correlation. This is simply an extension
Lindstrom H, Ashworth NL. The usefulness of
of the final cardinal rule of EDX. One usually can electrodiagnostic studies in the diagnosis and
be certain of a diagnosis when the clinical findings, management of neuromuscular disorders. Muscle Nerve.
NCSs, EMG, and U/S abnormalities all correlate 2018;58(2):191–196.
well. Consider again the example of the patient with Mondelli M, Aretini A, Greco G. Requests of
weakness of the hand and tingling and numbness of electrodiagnostic testing: consistency and agreement of
the fourth and fifth fingers. If NCSs demonstrate referral diagnosis. What is changed in a primary outpatient
abnormal ulnar motor and sensory potentials associated EDX lab 16 years later? Neurol Sci. 2014;35(5):669–675.
with slowing across the elbow, the needle EMG Mondelli M, Giacchi M, Federico A. Requests for
shows denervation and a reduced number of motor electromyography from general practitioners and specialists:
critical evaluation. Ital J Neurol Sci. 1998;19(4):195–203.
unit potentials in all ulnar-­innervated muscles and a
 SECTION I • Overview of Nerve Conduction Studies and Electromyography

Anatomy and Neurophysiology for

Electrodiagnostic Studies 2
The electromyographer need not have detailed knowl- central nervous system in which the glial cells are the major
edge of all the electrical and chemical events that occur at supporting cells. The peripheral nervous system includes
a molecular level to perform an electrodiagnostic (EDX) the nerve roots, peripheral nerves, primary sensory neurons,
study. However, one must have a basic understanding of neuromuscular junctions (NMJs), and muscles (Fig. 2.1).
anatomy and physiology to plan, perform, and properly Although not technically part of the peripheral nervous sys-
interpret an EDX study. tem, the primary motor neurons (i.e., anterior horn cells),
In the everyday evaluation of patients with neuromus- which are located in the spinal cord, are usually included as
cular disorders, nerve conduction studies (NCSs) and elec- part of the peripheral nervous system as well. In addition,
tromyography (EMG) serve primarily as extensions of the cranial nerves III through XII are also considered to be part
clinical examination. For NCSs, one needs to know the of the peripheral nervous system, being essentially the same
location of the various peripheral nerves and muscles so as peripheral nerves, except that their primary motor neu-
that the stimulating and recording electrodes are properly rons are located in the brainstem rather than the spinal cord.
positioned. For the needle EMG study, knowledge of gross The primary motor neurons, the anterior horn cells, are
muscle anatomy is crucial for inserting the needle electrode located in the ventral gray matter of the spinal cord. The
correctly into the muscle being sampled. axons of these cells ultimately become the motor fibers in
On the microscopic level, knowledge of nerve and muscle peripheral nerves. Their projections first run through the
anatomy and basic neurophysiology is required to appreciate white matter of the anterior spinal cord before exiting ven-
and interpret the EDX findings both in normal individu- trally as the motor roots. In contrast to the anterior horn cell,
als and in patients with various neuromuscular disorders. In the primary sensory neuron, also known as the dorsal root
addition, knowledge of anatomy and physiology is crucial to ganglion (DRG), is not found within the substance of the
understanding the technical aspects of the EDX study and spinal cord itself but rather lies outside the spinal cord, near
appreciating its limitations and potential pitfalls. the intervertebral foramen. The DRG are bipolar cells with
two separate axonal projections. Their central projections
form the sensory nerve roots. The sensory roots enter the spi-
ANATOMY nal cord on the dorsal side to ascend in either the posterior
The strict definition of the peripheral nervous system columns or synapse with sensory neurons in the dorsal horn.
includes that part of the nervous system in which the The peripheral projections of the DRGs ultimately become
Schwann cell is the major supporting cell, as opposed to the the sensory fibers in peripheral nerves. Because the DRGs

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11
12 SECTION I Overview of Nerve Conduction Studies and Electromyography

lie outside the spinal cord, this results in a different pattern motor and sensory fibers. The dorsal ramus runs posteriorly
of sensory nerve conduction abnormalities, depending on to supply sensory innervation to the skin over the spine and
whether the lesion is in the peripheral nerve or proximal to muscular innervation to the paraspinal muscles at that seg-
the DRG at the root level (see Chapter 3). ment. The ventral ramus differs, depending on the segment
Motor and sensory roots at each spinal level unite distal within the body. In the thoracic region, each ventral ramus
to the DRG to become a mixed spinal nerve. There are 31 continues as an intercostal nerve. In the lower cervical to
pairs of spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 upper thoracic (C5–T1) region, the ventral rami unite to
sacral, 1 coccygeal; Fig. 2.2). Each spinal nerve divides into form the brachial plexus (Fig. 2.4). In the mid-­lumbar to
a dorsal and ventral ramus (Fig. 2.3). Unlike the dorsal and sacral regions, the ventral rami intermix to form the lumbo-
ventral nerve roots, the dorsal and ventral rami both contain sacral plexus (Fig. 2.5).
Within each plexus, motor and sensory fibers from dif-
& ferent nerve roots intermix to ultimately form individual
, & ,  peripheral nerves. Each peripheral nerve generally sup-
,,  ,,
  plies muscular innervation to several muscles and cutane-
,,,
,,,   ous sensation to a specific area of skin, as well as sensory
 ,;
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 ;
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7 ;,,
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 7
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,,,
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,,, ,9
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9
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 2.6). Similarly, C5 sensory fibers innervate the lateral arm
9, (axillary nerve) and forearm (lateral antebrachial cutaneous
9 
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9,  9,,, All muscles supplied by one spinal segment (i.e., one
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&RF Fig. 2.3 Nerve roots and rami. The motor root, originating from
anterior horn cells, leaves the cord ventrally, whereas the sensory root
Fig. 2.2 Spinal cord and nerve roots. The spinal cord is divided into enters the cord on the dorsal side. Immediately distal to the dorsal root
31 segments (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccy- ganglion, the motor and sensory roots come together to form the spinal
geal). At each segment, motor and sensory fibers leave the spinal cord nerve. Each spinal nerve quickly divides into a dorsal and ventral
as nerve roots before exiting the bony spinal column. In the adult, the ramus. Each ramus contains both motor and sensory fibers. The dorsal
spinal cord usually ends at the level of the L1 vertebra. Consequently, rami supply sensation to the skin over the spine and muscular innerva-
below this level, only the lumbosacral nerve roots, known as the tion to the paraspinal muscles. The ventral rami continue as intercostal
cauda equina, are present within the spinal column. (From Haymaker nerves in the thoracic region. In the lower cervical region, the ventral
W, Woodhall B. Peripheral Nerve Injuries. Philadelphia: WB Saun- rami fuse to form the brachial plexus. In the mid-­lumbar through sacral
ders; 1953, with permission.) segments, the ventral rami intermix to form the lumbosacral plexus.
 Chapter 2 • Anatomy and Neurophysiology for Electrodiagnostic Studies 13

areas supplied by a single spinal segment are known as a nerve occurs where the nerve roots meet the spinal cord,
dermatome (Fig. 2.7). For both myotomes and dermatomes, where the nerve can sustain only 2–3 kg of force. For this
there is considerable overlap between adjacent segments. reason, nerve root avulsion may occur after a significant
Because of the high degree of overlap between spinal seg- trauma and especially after a stretch injury.
ments, a single root lesion seldom results in significant sen- Analogous to nerve fibers, muscle fibers have a very
sory loss and never in anesthesia. Likewise, on the motor similar arrangement at the microscopic level with three
side, even a severe single nerve root lesion usually results layers of connective tissue: the epimysium, perimysium,
in only mild or moderate weakness and never in paralysis. and endomysium (Fig. 2.9). The epimysium surrounds
For instance, a severe lesion of the C6 motor root causes the entire muscle. Within the epimysium, muscle fibers
weakness of the biceps; however, paralysis would not (which are the actual muscle cells) are grouped into fas-
occur because C5 motor fibers also innervate the biceps. cicles surrounded by the perimysium. The final layer of
In contrast, a severe peripheral nerve lesion usually results connective tissue, the endomysium, is present between
in marked sensory and motor deficits because contribu- individual muscle fibers. Muscle fibers are cylindrical and
tions from several myotomes and dermatomes are affected contain the actual muscle fibrils: the structural proteins
simultaneously. that are responsible for muscle contraction. When muscle
At the microscopic level, nerve fibers are protected by contraction occurs, the force is transmitted most often to
three different layers of connective tissue: the epineurium, a bone to move a joint (occasionally, muscle is connected
perineurium, and endoneurium (Fig. 2.8). The thick epineu- to other connective tissue or the skin). This connection
rium surrounds the entire nerve and is in continuity with the is most often made by way of a tendon, which is a thick
dura mater at the spinal cord level. Within the epineurium, rope-­like piece of connective tissue that is in continuity
axons are grouped into fascicles, surrounded by perineu- with the epimysium of the muscle. In some muscles, the
rium. A final layer of connective tissue, the endoneurium, is contraction is by way of an aponeurosis, which is a large,
present between individual axons. Effectively, a blood-­nerve sheet-­like piece of connective tissue. Most muscles have
barrier is formed by the combination of vascular endothe- two tendons, one at their origin (typically proximal and
lium supplying the nerve and the connective tissue of the more static) and one at their insertion (typically more
perineurium. Together, the three layers of connective tissue distal and more mobile). In some muscles, the tendon
give peripheral nerve considerable tensile strength, usually originates from inside the muscle, known as an internal or
in the range of 20–30 kg. However, the weakest point of a central tendon.

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8OQDU the C5–T1 nerve roots intermix to form the
0HGLDO brachial plexus between the neck and shoul-
EUDFKLDO 7KRUDFRGRUVDO der. From the brachial plexus, the major upper
FXWDQHRXV extremity peripheral nerves are derived. (From
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14 SECTION I Overview of Nerve Conduction Studies and Electromyography

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Fig. 2.6 Myotomal and peripheral nerve innervation. Motor fibers
from one nerve root, a myotome, supply muscles innervated by
3XGHQGDOQHUYH
different peripheral nerves. For example, the C5 motor root supplies
the biceps (musculocutaneous nerve), deltoid (axillary nerve), and
6FLDWLFQHUYH brachioradialis (radial nerve), among other muscles. (Adapted from
Haymaker W, Woodhall B. Peripheral Nerve Injuries. Philadelphia:
WB Saunders; 1953, with permission.)
3RVWHULRUFXWDQHRXV
QHUYHRIWKLJK
and cations). The membrane is always impermeable to large
negatively charged anions, and it is relatively impermeable
to sodium in the resting state. This semipermeable mem-
Fig. 2.5 Lumbosacral plexus. The L1–S4 nerve roots intermix in
brane, in conjunction with an active Na+/K+ pump that
the pelvis to form the lumbosacral plexus. From this plexus, the moves sodium outside in exchange for potassium, leads to
individual major peripheral nerves of the lower extremity are derived. concentration gradients across the membrane. The concen-
(From Mayo Clinic and Mayo Foundation. Clinical Examinations in tration of sodium is larger outside the membrane, whereas
Neurology. Philadelphia: WB Saunders; 1956, with permission.) the concentration of potassium and larger anions is greater
inside. The combination of these electrical and chemical
gradients results in forces that create a resting equilibrium
PHYSIOLOGY potential. At the nerve cell soma, this resting membrane
The primary role of nerve is to transmit information reli- potential is approximately 70 mV negative inside compared
ably from the anterior horn cells to muscles for the motor with the outside; distally in the axon it is approximately 90
system and from the sensory receptors to the spinal cord mV negative.
for the sensory system. Although functionally nerves may The membrane of the axon is lined with voltage-­gated
seem similar to electrical wires, there are vast differences sodium channels (Fig. 2.11). These structures are essen-
between the two. At the molecular level, a complex set of tially molecular pores with gates that open and close. For
chemical and electrical events allows nerve to propagate an many ion channels, gates open in response to molecules
electrical signal. that bind to the channel. In the case of the voltage-­gated
The axonal membrane of every nerve is electrically sodium channel, the gate is controlled by a voltage sensor
active. This property results from a combination of a spe- that responds to the level of the membrane potential. If cur-
cialized membrane and the sodium/potassium (Na+/K+) rent is injected into the axon, depolarization occurs (i.e.,
pump (Fig. 2.10). The specialized axonal membrane is the axon becomes more positive internally). Voltage sensors
semipermeable to electrically charged molecules (anions within the sodium channel respond to the depolarization by
 Chapter 2 • Anatomy and Neurophysiology for Electrodiagnostic Studies 15

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Fig. 2.7 Dermatomes. The cutaneous area supplied from one spinal segment (i.e., one sensory nerve root) is known as a dermatome. Despite
the apparent simplicity of dermatomal charts, in actuality there is a wide overlap of adjacent dermatomes. Consequently, a nerve root lesion,
even if severe, never results in anesthesia but rather results in altered or decreased sensation. (From O’Brien MD. Aids to the Examination of the
Peripheral Nervous System. London: Baillière Tindall; 1986.)

Fig. 2.8 Internal peripheral nerve anatomy. Myelinated

fibers are recognized as small dark rings (myelin) with a
central clearing (axon) in this 1-­micron thick, semi-­thin
section of plastic embedded nerve tissue. The endoneu-
rium is present between axons. Axons are grouped into
fascicles, surrounded by perineurium (small arrows). Sur-
rounding the entire nerve is the last layer of connective
tissue, the epineurium (large arrow).
16 SECTION I Overview of Nerve Conduction Studies and Electromyography

Fascicle Muscle 1D.

fiber 3XPS 1D &, .
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Fig. 2.10 Resting membrane potential. At rest, the axonal mem-
brane is negatively polarized inside compared to outside. This
Epimysium Perimysium Endomysium resting potential results from the combination of a membrane that is
semipermeable to charged particles and an active Na+/K+ pump. At
Fig. 2.9 Internal muscle anatomy. The endomysium is present rest, the concentration of Na+ and Cl− is higher in the extracellular
between muscle fibers. Muscle fibers are grouped into fascicles, space, with the concentration of K+ and large anions (A−) greater
surrounded by perimysium. Surrounding the entire muscle is the last inside the axon.
layer of connective tissue, the epimysium.

Na+

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Na+
Fig. 2.11 Voltage-­gated sodium channel. The axonal membrane is lined with voltage-­gated sodium channels. These channels are molecular
pores with gates that open and close; when open, gates are selective for sodium. (A) There are two gates: an activation gate (large arrow) and an
inactivation gate (small arrow). (B) If current is injected into the axon, depolarization occurs and the voltage-­gated activation gate opens, allow-
ing the influx of sodium into the axon, driven both by concentration and electrical gradients. However, the opening of the sodium channels is
time limited. Inactivation of the sodium channel occurs within 1–2 ms. (C) The inactivation gate of the sodium channel has been modeled as a
“hinged lid,” which closes the end of the channel within 1–2 ms of depolarization, preventing further depolarization.

opening the gate to the channel and allowing sodium to rush nerve behind the depolarization is refractory when the area
into the axon, driven both by concentration and by electrical ahead is not so that the impulse will continue forward and
gradients. Every time a depolarization of 10–30 mV above will not return backward).
the resting membrane potential occurs (i.e., threshold), it In addition to sodium channel inactivation, depolariza-
creates an action potential and a cycle of positive feedback; tion also results in the opening of potassium channels, which
further depolarization occurs and more sodium channels also then drives the membrane voltage in a more negative
open (Fig. 2.12). Action potentials are always all-­or-­none direction. These factors, along with the Na+/K+ pump,
responses that then propagate away from the initial site of then reestablish the resting membrane potential.
depolarization. The axon does not remain depolarized for The conduction velocity of the action potential depends
long, however, because the opening of the sodium channels on the diameter of the axon: the larger the axon, the less
is time limited. Sodium channels have a second gate, known resistance and the faster the conduction velocity. For typi-
as the inactivation gate. Inactivation of the sodium channel cal unmyelinated axons, the conduction velocity of an
occurs within 1–2 ms. During this time, the membrane is action potential is very slow, typically in the range of 0.2–
not excitable and cannot be opened (i.e., refractory period). 1.5 m/s. Conduction velocity can be greatly increased with
The inactivation gate of the sodium channel has been mod- the addition of myelin. Myelin insulation is present on all
eled as a “hinged lid.” From a practical point of view, the fast-­conducting fibers and is derived from Schwann cells,
refractory period limits the frequency that nerves can con- the major supporting cells in the peripheral nervous sys-
duct impulses. It also ensures that the action potential con- tem. Myelin is composed of concentric spirals of Schwann
tinues to propagate in the same direction (i.e., the area of cell membrane (Fig. 2.13). For every myelinated fiber,
 Chapter 2 • Anatomy and Neurophysiology for Electrodiagnostic Studies 17

9P

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Fig. 2.12 Action potential. When the resting membrane voltage (Vm)
is depolarized to threshold, voltage-­gated sodium channels are opened,



increasing Na+ conductance (gNa), resulting in an influx of sodium and
further depolarization. The action potential, however, is short lived,
due to the inactivation of the sodium channels within 1–2 ms and an
increase in K+ conductance (gK). These changes, along with the Na+/K+
pump, allow the axon to reestablish the resting membrane potential.

0\HOLQ

Fig. 2.14 Saltatory conduction. Myelinated fibers propagate ac-

tion potentials by way of saltatory conduction. Depolarization
only occurs at the small uninsulated areas of membrane between
internodes, with the action potential essentially jumping from node
to node. Thus, less membrane needs to be depolarized, less time
is required, and, consequently, conduction velocity dramatically
increases. Most human peripheral myelinated fibers conduct in the
6FKZDQQFHOO range of 35–75 m/s.
Fig. 2.13 Schwann cell and the myelin sheath. Left, Electron micro-
graph of a single Schwann cell and myelinated axon. Right, Schemat-
ic of the same. Myelin insulation is derived from Schwann cells and is nerve membrane must be depolarized. For unmyelinated
present on all fast-­conducting fibers, both motor and sensory. Myelin fibers, depolarization must occur over the entire length of
is composed of concentric spirals of Schwann cell membrane, with the nerve (i.e., continuous conduction), which takes much
each Schwann cell supporting a single myelinated axon.
more time than in myelinated fibers. In myelinated fibers,
the axonal membrane only needs to depolarize at the nodes
successive segments are myelinated by single Schwann of Ranvier; the internodes do not depolarize, but rather
cells. Each segment of the axon covered by myelin is the action potential jumps over them. As the internode
termed the “internode.” At small gaps between successive is approximately 1 mm in length and the node of Ranvier
internodes, the axon is exposed; these areas are known as is only 1–2 μm in length, markedly less axonal membrane
the nodes of Ranvier. They are very small, in the range of needs to depolarize to propagate an action potential. The
1–2 μm in length. lower the total depolarization time, the faster the conduc-
Most of the nerve is effectively insulated with myelin, tion velocity. In myelinated axons, the density of sodium
and depolarization occurs by way of saltatory conduction, channels is highest in nodal areas, the areas undergoing
whereby depolarization occurs only at the nodes of Ranvier. depolarization. Myelinated human peripheral nerve fibers
After one node depolarizes, the current essentially jumps typically conduct in the range of 35–75 m/s, far faster
to the next adjacent node, and the cycle continues (Fig. than could ever be achieved by increasing the diameter
2.14). The physiology of normal saltatory conduction was of unmyelinated fibers. Not all human peripheral nerve
first shown in a series of elegant experiments on normal fibers are myelinated. Unmyelinated fibers, which con-
animal myelinated nerve fibers, recording along the motor duct very slowly (typically 0.2–1.5 m/s), primarily medi-
root in very small increments and measuring the current ate pain, temperature, and autonomic functions. Schwann
as a function of distance and latency (Fig. 2.15). From an cells also support these unmyelinated fibers; however, one
electrical point of view, myelin insulates the internode and Schwann cell typically surrounds several unmyelinated
reduces the capacitance. A lower capacitance results in fibers, but without the formation of concentric spirals of
less current lost as the action potential travels from node myelin.
to node. Although more current is needed for saltatory When an individual axon is depolarized, an action poten-
conduction than for continuous conduction, much less tial propagates down the nerve. Distally, the axon divides
18 SECTION I Overview of Nerve Conduction Studies and Electromyography

into many twigs, each of which goes to an individual muscle NMJ is essentially an electrical-­ chemical-­
electrical link
fiber. An axon, along with its anterior horn cell and all mus- from nerve to muscle. It is formed from two specialized
cle fibers with which it is connected, is known as a motor membranes, one on nerve and one on muscle, separated by
unit (Fig. 2.16). Depolarization of all the muscle fibers in a thin synaptic cleft (Fig. 2.17). As a nerve action poten-
a motor unit creates an electrical potential known as the tial travels to the presynaptic side of the NMJ, voltage-­
motor unit action potential (MUAP). Analysis of MUAPs gated calcium channels are activated, allowing an influx
is an important part of every needle EMG examination. of calcium (Ca+). Increasing Ca+ concentration results in
When an action potential is generated, all muscle fibers in a series of enzymatic steps that ultimately results in the
the motor unit are normally activated, again an all-­or-­none release of acetylcholine, the neurotransmitter at the NMJ.
response. Acetylcholine diffuses across the synaptic cleft to bind to
However, before a muscle fiber can be activated, the specialized acetylcholine receptors on the muscle mem-
nerve action potential must be carried across the NMJ. The brane. These receptors, when activated, allow an influx of

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Fig. 2.15 Demonstration of saltatory conduction. Recording of a normal single fiber from an intact ventral root in a rat. (A) Successive records
of external longitudinal current recorded from a single fiber as electrodes were moved along a ventral root in steps of 0–2 mm. (B) Lines from
each record indicate positions of electrodes with respect to underlying nodes and internodes. (C) Latency to peak of external longitudinal current
as a function of distance. Note how the distance/latency graph is a “staircase” configuration. As current proceeds down a normal myelinated
axon, the latency (i.e., the conduction time) abruptly increases approximately every 1.0–1.5 mm. This is the depolarization time at the nodes of
Ranvier. Conversely, note the flat part of the staircase graph; here the latency stays almost exactly the same despite a change in distance. This is
the saltatory conduction jumping from node to node. (From Rasminsky M, Sears TA. Internodal conduction in undissected demyelinated nerve
fibres. J Physiol. 1972;227:323–350, with permission.)

MUAP

Fig. 2.16 Motor unit. The motor unit is defined as one axon, its anterior horn cell, and all connected muscle fibers and neuromuscular junc-
tions. A nerve fiber action potential normally always results in depolarization of all the muscle fibers of the motor unit, creating an electrical
potential known as the motor unit action potential (MUAP). Analysis of MUAPs is a large part of the needle electromyographic examination.
 Chapter 2 • Anatomy and Neurophysiology for Electrodiagnostic Studies 19

sodium and depolarization of the muscle fiber. As is the the following attributes: (1) myelinated or unmyelinated,
case with nerve, once threshold is reached, a muscle fiber (2) somatic or autonomic, (3) motor or sensory, and (4)
action potential is created that spreads throughout the diameter.
muscle fiber. Following the muscle fiber action potential, There are several important points to glean from
a complex set of molecular interactions occurs within the Table 2.1, some of which are directly relevant to clinical
muscle fiber, resulting in increasing overlap of the major EDX testing. First is the direct relationship between fiber
muscle fiber filaments: actin and myosin, with the final diameter and conduction velocity: the larger the diameter,
result of muscle shortening, contraction, and generation of the faster the conduction velocity. The large myelinated
force (Fig. 2.18). fibers are the fibers that are measured in clinical NCSs.
Indeed, all routine motor and sensory conduction velocity
and latency measurements are from the largest and fast-
CLASSIFICATION est fibers of the particular peripheral nerve that is being
Multiple peripheral nerve classification schemes exist studied. Large-­diameter fibers have the most myelin and
(Table 2.1). Peripheral nerves can be classified based on the least electrical resistance, both of which result in faster
conduction velocities. The small myelinated (Aδ, B) and
unmyelinated (C) fibers carry autonomic information
(afferent and efferent) and somatic pain and temperature
sensations. These fibers are not recorded with standard
nerve conduction techniques. Thus, neuropathies that
'LVWDOQHUYH preferentially affect only small fibers may not reveal any
abnormalities on NCSs.
Second, routine sensory conduction studies typically
record cutaneous nerves innervating skin. The largest and
fastest cutaneous fibers are the Aβ fibers from hair and
3UHV\QDSWLFWHUPLQDO
skin follicles. Note that the size and conduction velocities
of these fibers are similar to those of the muscle efferent
0LWRFKRQGULD fibers from the anterior horn cells that are recorded during
routine motor studies. These myelinated fibers have veloci-
$FHW\OFKROLQHTXDQWD ties in the range of 35–75 m/s.
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Third, the largest and fastest fibers in the peripheral
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nervous system are not recorded during either routine
motor or sensory NCSs. These are the muscle afferents,
-XQFWLRQDOIROGV the Aα fibers (also known as Ia fibers), which originate
from muscle spindles and mediate the afferent arc of
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the muscle stretch reflex. These fibers are recorded only
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during mixed nerve studies in which the entire mixed
Fig. 2.17 Neuromuscular junction. The neuromuscular junction is
a specialized junction between the terminal axon and muscle fiber. nerve is stimulated and recorded. Therefore mixed
When the nerve action potential invades the presynaptic terminal, nerve conduction velocities usually are faster than either
acetylcholine is released and diffuses across the synaptic cleft to routine motor or cutaneous sensory conduction veloci-
bind to acetylcholine receptors on the muscle membrane. This bind- ties because they contain these Ia fibers. Because the
ing results in a muscle endplate potential, which, once threshold is
reached, causes the generation of a muscle fiber action potential.
Ia fibers have the largest diameter and accordingly the

Z Myosin Z
Actin

Cross bridging

Fig. 2.18 Actin and myosin. Following a muscle fiber action potential, muscle contraction results from a complex set of molecular interactions,
ultimately ending with the overlapping of two interlacing muscle proteins, actin and myosin. This overlap, which occurs along with the forma-
tion of energy-­dependent cross-­bridges, effectively results in shortening of the muscle and the generation of force. Actin filaments are connected
by Z lines (Z). The sarcomere, a unit of muscle, is defined from one Z line to the next. The overlapping pattern of actin and myosin filaments
gives muscle its striated appearance.
20 SECTION I Overview of Nerve Conduction Studies and Electromyography

Table 2.1 Peripheral Nerve Classification Schemes.

Diameter Conduction Alternative
Fiber Type(s) Name Subtype (mm) Velocity (m/s) Classification
Myelinated Somatic Afferent/Efferent
Cutaneous afferent A β 6–12 35–75 α
δ 1–5 5–30

Muscle afferent A α 12–21 80–120 I Ia, Ib

β 6–12 35–75 II
δ 1–5 5–30 III
Muscle efferent A 6–12 35–75
   Anterior horn cells (α and γ motor neurons)
Myelinated Autonomic Efferent
Preganglionic efferent B 3 3–15
Unmyelinated Somatic/Autonomic Afferent/Efferent
Postganglionic efferent C 0.2–1.5 1–2
Afferent to dorsal root ganglion (pain) C 0.2–1.5 1–2 IV
Sensory receptor Fiber type
Hair follicle Aβ
Skin follicle Aβ
Muscle spindle Aa
Joint receptor Aβ
Pain, temperature Aδ, C

greatest amount of myelin, they often are affected early source (i.e., the action potential). With near-­field poten-
by demyelinating lesions such as those found in entrap- tials, a response generally is not seen until the source is
ment neuropathies. For example, in the EDX evaluation close to the recording electrodes. The closer the recording
of carpal tunnel syndrome, the mixed nerve study from electrodes are to the current source, the higher the ampli-
the palm to the wrist often is more sensitive in detecting tude. Compound muscle action potentials, sensory nerve
abnormalities than either the routine motor or sensory action potentials, and MUAPs recorded during routine
conduction study. motor conduction, sensory conduction, and needle EMG
studies, respectively, are essentially all volume-­conducted
near-­field potentials.
RECORDING Volume-­ conducted, near-­ field potentials produce a
All potentials obtained during NCSs and needle EMG characteristic triphasic waveform as an advancing action
result from the extracellular recording of intracellular potential approaches and then passes beneath and away
events from either nerve or muscle. NCSs usually are per- from a recording electrode (Fig. 2.19, top). In practice,
formed by recording with surface electrodes over the skin, most sensory and mixed nerve studies display this tri-
and EMG potentials by recording with a needle electrode phasic waveform morphology, as do fibrillation potentials
placed within the muscle. In both procedures, intracellu- and most MUAPs. The electrical correlate of an action
lar electrical potentials are transmitted through tissue to potential traveling toward, under, and then away from the
the recording electrodes. The process of an intracellular recording electrode is an initial positive phase, followed by
electrical potential being transmitted through extracellular a negative phase, and then a trailing positive phase, respec-
fluid and tissue is known as volume conduction. Although tively. The first positive peak represents the time that the
the theory of volume conduction is complex and beyond action potential is first beneath the active electrode; this is
the scope of this text, volume-­conducted potentials can be the point at which the onset latency should be measured
modeled as either near-­field or far-­field potentials. Near-­ for nerve action potentials. The initial positive peak may
field potentials can be recorded only close to their source, be very small or absent with some sensory responses. In
and the characteristics of the potential depend on the dis- that case, the initial negative deflection best marks the
tance between the recording electrodes and the electrical true onset of the potential.
 Chapter 2 • Anatomy and Neurophysiology for Electrodiagnostic Studies 21

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B
Fig. 2.20 Volume conduction and motor potentials. With the active
recording electrode (G1) over the motor point, depolarization first
occurs at that site, with the depolarization subsequently spreading

away. The corresponding waveform has an initial negative deflec-
tion without any initial positivity (top trace). If the active recording
electrode is off the motor point, depolarization begins distally and
Fig. 2.19 Volume conduction and waveform morphology. Top, An then travels under and past the active electrode, resulting in an initial
advancing action potential recorded by volume conduction will result positive deflection (middle trace). If the depolarization occurs at a
in a triphasic potential that initially is positive, then is negative, and distance and never travels under the recording electrode, only a small
finally is positive again. Bottom, If the depolarization occurs directly positive potential will be seen (bottom trace). Note that, by conven-
beneath the recording electrode, the initial positive phase will be tion, negative is up and positive is down in all nerve conduction and
absent, and a biphasic, initially negative potential will be seen. Note electromyographic traces.
that, by convention, negative is up and positive is down in all nerve
conduction and electromyographic traces.

If a volume-­ conducted, near-­ field action potential P9

begins directly under the recording electrode, the initial PV
deflection will be negative (Fig. 2.19, bottom). During
routine motor NCSs, this is the expected compound mus-
cle action–potential morphology if the active electrode is
correctly placed over the motor point (i.e., endplate) of
the muscle. There is no advancing action potential, as mus-
cle fiber depolarization begins at the endplate; hence, the
waveform has no initial positive deflection. This results
in a characteristic biphasic potential with an initial nega-
tive deflection (Fig. 2.20, top). If the electrode is inad-
vertently placed off the motor point, a triphasic potential
with an initial positive deflection will be seen (Fig. 2.20
middle). If the depolarization occurs at a distance but
never passes under the recording electrode, characteristi- Fig. 2.21 Near-­field and far-­field potentials. Median motor study,
cally only a positive deflection will occur (Fig. 2.20, bot- recording the abductor pollicis brevis muscle, stimulating at the
tom). For example, this pattern is seen when stimulating wrist (top trace) and antecubital fossa (bottom trace). At each site,
the median nerve and recording a hypothenar muscle, as a compound muscle action potential is present, representing a near-­
field recording of the underlying muscle fiber action potentials. The
might be done during routine motor studies looking for compound muscle action potential latencies occur at different times,
an anomalous innervation. The muscle action potential of reflecting their different arrival times at the recording electrode. At the
the median-­innervated thenar muscles occurs at a distance start of each trace is the stimulus artifact (blue arrow). The stimu-
but never travels under the recording electrodes located lus artifact is an example of a far-­field potential being transmitted
over the hypothenar muscles. The result is a small positive instantaneously and seen at the same time, despite the difference in
distances between the two stimulation sites.
deflection, volume-­conducted potential.
The other type of volume-­ conducted potential is
the far-­field potential. Far-­
field potentials are electri-
cal potentials that are distributed widely and instantly. onset of all NCSs is a good example of a far-­field poten-
Two recording electrodes, one closer and the other far- tial (Fig. 2.21). The shock artifact is instantly transmit-
ther from the source, essentially see the source at the ted and is seen at the same time at distal and proximal
same time. Although far-­field potentials are more often recording sites. Those potentials whose latencies do not
of concern in evoked-­potential studies, they occasionally vary with distance from the stimulation site usually are
are important in NCSs. The stimulus artifact seen at the all far-­field potentials.
22 SECTION I Overview of Nerve Conduction Studies and Electromyography

Suggested Readings Hollinshead WH. Anatomy for Surgeons, Volume 2: The Back
and Limbs. New York: Harper & Row; 1969.
Brown WF. The Physiological and Technical Basis of
Mayo Clinic and Mayo Foundation. Clinical Examinations in
Electromyography. Boston: Butterworth-­Heinemann; 1984.
Neurology. Philadelphia: WB Saunders; 1956.
Dumitru D, Delisa JA. AAEM Minimonograph #10: Volume
O’Brien MD. Aids to the Examination of the Peripheral
Conduction. Rochester, MN: American Association of
Nervous System. London: Baillière Tindall; 1986.
Electrodiagnostic Medicine; 1991.
Rasminsky M, Sears TA. Internodal conduction in undissected
Haymaker W, Woodhall B. Peripheral Nerve Injuries.
demyelinated nerve fibres. J Physiol. 1972;227:323–350.
Philadelphia: WB Saunders; 1953.
 SECTION II • Fundamentals of Nerve Conduction Studies

Basic Nerve Conduction Studies

3
After the history is taken and a directed physical examina- median nerve is abnormal before doing the median sensory
tion is performed, every study begins with nerve conduc- study. Then, when performing the median sensory study,
tion studies (NCSs). The needle electromyography (EMG) one is confident of where to stimulate the nerve and how
examination is performed after the NCSs are completed much current is needed. In this case, if no sensory response
because the findings on the NCSs are used in the planning is present, one can have a high degree of certainty that the
and interpretation of the needle EMG examination that response is truly absent and move along to the next nerve
follows. to be studied. However, if the sensory conduction study
Peripheral nerves usually can be easily stimulated is done first and is absent, it will not be as obvious if the
and brought to action potential with a brief electrical absent response is due to a technical problem or is truly
pulse applied to the overlying skin. Techniques have been absent. One can waste a lot of time unnecessarily trying to
described for studying most peripheral nerves. In the upper figure this out. Do the motor conduction study first; your
extremity, the median, ulnar, and radial nerves are the most study will be more efficient, and the patient will tolerate
easily studied; in the lower extremity, the peroneal, tibial, the study much better.
and sural nerves are the most easily studied (see Chapters Motor responses typically are in the range of several
10 and 11). Of course, the nerves selected for study depend millivolts (mV), as opposed to sensory and mixed nerve
on the patient’s symptoms and signs and the differential responses, which are in the microvolt (μV) range. Thus,
diagnosis. Motor, sensory, or mixed nerve studies can be motor responses are less affected by electrical noise and
performed by stimulating the nerve and placing the record- other technical factors. For motor conduction studies, the
ing electrodes over a distal muscle, a cutaneous sensory gain usually is set at 2–5 mV per division. Recording elec-
nerve, or the entire mixed nerve, respectively. The findings trodes are placed over the muscle of interest. In general,
from motor, sensory, and mixed nerve studies often comple- the belly-­tendon montage is used. The active recording
ment one another and yield different types of information electrode (also known as G1) is placed on the center of
based on distinct patterns of abnormalities, depending on the muscle belly (over the motor endplate), and the refer-
the underlying pathology. ence electrode (also known as G2) is placed distally, over
the tendon to the muscle (Fig. 3.1). The designations G1
and G2 remain in the EMG vernacular, referring to a time
MOTOR CONDUCTION STUDIES when electrodes were attached to grids (hence the G) of
Motor conduction studies are technically less demanding an oscilloscope. The stimulator then is placed over the
than sensory and mixed nerve studies; thus, they usually are nerve that supplies the muscle, with the cathode placed
performed first. Performing the motor studies first also has closest to the recording electrode. It is helpful to remem-
other major advantages. It is not uncommon for the sensory ber “black to black,” indicating that the black electrode of
responses to be very low in amplitude or absent in many the stimulator (the cathode) should be facing the black
neuropathies. Performing the motor studies first allows one recording electrode (the active recording electrode). For
to know where the nerve runs, where it should be stimu- motor studies, the duration of the electrical pulse usually
lated, and how much current is needed and also gives some is set to 200 ms. Most normal nerves require a current in
information about whether the nerve is normal or abnor- the range of 20–50 mA to achieve supramaximal stimula-
mal. On the other hand, if the sensory study is done before tion. As current is slowly increased from a baseline 0 mA,
the motor study, one might spend a lot of unnecessary time usually by 5–10 mA increments, more of the underlying
stimulating and trying to record a sensory response that is nerve fibers are brought to action potential and, subse-
not present. For example, imagine a patient with a moder- quently, more muscle fiber action potentials are generated.
ately severe median neuropathy at the wrist who is sent for The recorded potential, known as the compound muscle
an electrodiagnostic (EDX) evaluation. If the median motor action potential (CMAP), represents the summation of all
study is performed first, the correct stimulation site can be underlying individual muscle fiber action potentials. When
confirmed, the amount of current needed to stimulate the the current is increased to the point that the CMAP no
median nerve will be known, and one will also know that the longer increases in size, one presumes that all nerve fibers

23
24 SECTION II Fundamentals of Nerve Conduction Studies

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Fig. 3.1 Motor conduction study setup. Median motor study,

recording the abductor pollicis brevis muscle, stimulating the median
nerve at the wrist. In motor studies, the “belly-­tendon” method is Fig. 3.2 Compound muscle action potential (CMAP). The CMAP
used for recording. The active recording electrode (G1) is placed on represents the summation of all the underlying muscle fiber action
the center of the muscle, with the reference electrode (G2) placed potentials. With recording electrodes properly placed, the CMAP is
distally over the tendon. a biphasic potential with an initial negative deflection. Latency is the
time from the stimulus to the initial negative deflection from baseline.
Amplitude is most commonly measured from baseline to negative
peak. Duration is measured from the initial deflection from baseline
have been excited and that supramaximal stimulation has to the first baseline crossing (i.e., negative peak duration). In addition,
been achieved. The current is then increased by another negative CMAP area (i.e., the area above the baseline) is calculated
20% to ensure supramaximal stimulation. by most modern computerized electromyographic machines. Latency
The CMAP is a biphasic potential with an initial negativ- reflects only the fastest conducting motor fibers. All fibers contribute
to amplitude and area. Duration is primarily a measure of synchrony.
ity, or upward deflection from the baseline, if the record-
ing electrodes have been properly placed with G1 over
the motor endplate. For each stimulation site, the latency,
amplitude, duration, and area of the CMAP are measured
(Fig. 3.2). A motor conduction velocity can only be calcu-
Area
lated after two sites, one distal and one proximal, have been CMAP area also is conventionally measured as the area
stimulated. above the baseline to the negative peak. Although the area
cannot be determined manually, the calculation is readily
performed by most modern computerized EMG machines.
Latency A negative peak CMAP area is another measure reflecting
Latency is the time from the stimulus to the initial CMAP the number of muscle fibers that depolarize. Differences
deflection from baseline. Latency represents three separate in CMAP area between the distal and proximal stimula-
processes: (1) the nerve conduction time from the stimu- tion sites take on special significance in the determination
lus site to the neuromuscular junction (NMJ), (2) the time of conduction block from a demyelinating lesion (see the
delay across the NMJ, and (3) the depolarization time “Conduction Block” section).
across the muscle. Latency measurements usually are made
in milliseconds (ms) and reflect only the fastest conducting
motor fibers.
Duration
CMAP duration usually is measured from the initial deflec-
tion from baseline to the first baseline crossing (i.e., nega-
Amplitude tive peak duration), but it also can be measured from the
CMAP amplitude is most commonly measured from base- initial to the terminal deflection back to baseline. The for-
line to the negative peak and less commonly from the first mer is preferred as a measure of CMAP duration because
negative peak to the next positive peak. CMAP ampli- when CMAP duration is measured from the initial to termi-
tude reflects the number of muscle fibers that depolarize. nal deflection back to baseline, the terminal CMAP returns
Although low CMAP amplitudes most often result from to baseline very slowly and can be difficult to mark pre-
loss of axons (as in a typical axonal neuropathy), other cisely. Duration is primarily a measure of synchrony (i.e.,
causes of a low CMAP amplitude include conduction block the extent to which each of the individual muscle fibers fire
from demyelination located between the stimulation site at the same time). Duration characteristically increases in
and the recorded muscle, as well as some NMJ disorders conditions that result in slowing of some motor fibers but
and myopathies. not others (e.g., in a demyelinating lesion).
 Chapter 3 • Basic Nerve Conduction Studies 25

'/ 3/
& % $ '

'LVWDO 3UR[LPDO
Fig. 3.3 Motor conduction velocity (CV) calculation. Top, Median motor study, recording abductor pollicis brevis, stimulating wrist and elbow.
The only difference between distal and proximal stimulations is the latency, with PL being longer than DL. Bottom, DL represents three separate
times: the nerve conduction time from the distal stimulation site to the neuromuscular junction (NMJ) (A), the NMJ transmission time (B), and
the muscle depolarization time (C). Accordingly, DL cannot be used alone to calculate a motor CV. Two stimulations are necessary. PL includes
the nerve conduction time from the distal stimulation site to the NMJ (A), the NMJ transmission time (B), and the muscle depolarization time (C),
as well as the nerve conduction time between the proximal and distal stimulation sites (D). If DL (A + B + C) is subtracted from PL (A + B + C + D),
only the nerve conduction time between the distal and proximal stimulation sites (D) remains. The distance between those two sites can be
measured, and a CV can be calculated (distance/time). CV reflects only the fastest conducting fibers in the nerve being studied. DL, Distal motor
latency; PL, proximal motor latency.

Conduction Velocity in the distal motor latency measurement. In addition to

Motor conduction velocity is a measure of the speed of (A) the nerve conduction time between the distal site and
the fastest conducting motor axons in the nerve being the NMJ, (B) the NMJ transmission time, and (C) the
studied, which is calculated by dividing the distance muscle depolarization time, the proximal motor latency
traveled by the nerve conduction time. However, motor also includes (D) the nerve conduction time between the
conduction velocity cannot be calculated by performing proximal and distal stimulation sites (Fig. 3.3). There-
a single stimulation. The distal motor latency is more fore, if the distal motor latency (containing compo-
than simply a conduction time along the motor axon; it nents A + B + C) is subtracted from the proximal motor
includes not only (A) the conduction time along the dis- latency (containing components A + B + C + D), the first
tal motor axon to the NMJ, but also (B) the NMJ trans- three components will cancel out. This leaves only com-
mission time and (C) the muscle depolarization time. ponent D, the nerve conduction time between the proxi-
Therefore, to calculate a true motor conduction velocity mal and distal stimulation sites, without the distal nerve
without including NMJ transmission and muscle depo- conduction, NMJ transmission, and muscle depolariza-
larization times, two stimulation sites must be used, one tion times. The distance between these two sites can be
distal and one proximal. approximated by measuring the surface distance with a
When the nerve is stimulated proximally, the result- tape measure. A conduction velocity then can be calcu-
ing CMAP area, amplitude, and duration are, in general, lated along this segment: (distance between the proximal
similar to those of the distal stimulation waveform. The and distal stimulation sites) divided by (proximal latency
only major difference between CMAPs produced by minus distal latency). Conduction velocities usually are
proximal and distal stimulations is the latency. The proxi- measured in meters per second (m/s).
mal latency is longer than the distal latency, reflecting the It is essential to note that both latency and conduction
longer time and distance needed for the action potential velocity reflect only the fastest conducting fibers in the
to travel. The proximal motor latency reflects four sepa- nerve being studied. By definition, conduction along these
rate times, as opposed to the three components reflected fibers arrives first and thus it is these fibers that are the
26 SECTION II Fundamentals of Nerve Conduction Studies

ones measured. The many other normal slower conducting

—9
fibers participate in the CMAP area and amplitude but are
not reflected in either the latency or conduction velocity PV
measurements.

$PSOLWXGH
SENSORY CONDUCTION STUDIES
In contrast to motor conduction studies, in which the
CMAP reflects conduction along the motor nerve, NMJ, 'XUDWLRQ
and muscle fibers, in sensory conduction studies, only nerve
fibers are assessed. Because most sensory responses are very
small (usually in the range of 1–50 μV), technical factors 3HDNODWHQF\
and electrical noise assume more importance. For sensory 2QVHWODWHQF\
conduction studies, the gain usually is set at 10–20 μV per Fig. 3.5 Sensory nerve action potential (SNAP). The SNAP rep-
division. A pair of recording electrodes (G1 and G2) are resents the summation of all the underlying sensory fiber action
placed in line over the nerve being studied, at an interelec- potentials. The SNAP usually is biphasic or triphasic in configuration.
trode distance of 2.5–4 cm, with the active electrode (G1) Onset latency is measured from the stimulus to the initial negative de-
flection for biphasic SNAPs (as in the waveform here) or to the initial
placed closest to the stimulator. Recording ring electrodes positive peak for triphasic SNAPs. Onset latency represents nerve
are conventionally used to test the sensory nerves in the conduction time from the stimulus site to the recording electrodes
fingers (Fig. 3.4). For sensory studies, an electrical pulse of for the largest cutaneous sensory fibers in the nerve being studied.
either 100 or 200 ms in duration is used, and most nor- Peak latency is measured at the midpoint of the first negative peak.
Amplitude most commonly is measured from baseline to negative
mal sensory nerves require a current in the range of 5–30
peak. Duration is measured from the initial deflection from baseline
mA to achieve supramaximal stimulation. This is less cur- to the first baseline crossing (i.e., negative peak duration). Only one
rent than what is usually required for motor conduction stimulation site is required to calculate a sensory conduction velocity,
studies. Thus, sensory fibers usually have a lower thresh- as sensory onset latency represents only nerve conduction time.
old to stimulation than do motor fibers. This can easily
be demonstrated on yourself; when slowly increasing the
stimulus intensity, you will feel the paresthesias (sensory) latency, peak latency, duration, and amplitude are measured
before you feel or see the muscle starts to twitch (motor). (Fig. 3.5). Unlike motor studies, a sensory conduction
As in motor studies, the current is slowly increased from a velocity can be calculated with one stimulation site alone,
baseline of 0 mA, usually in 3–5-­mA increments, until the by taking the measured distance between the stimulator and
recorded sensory potential is maximized. This potential, active recording electrode and dividing by the onset latency.
the sensory nerve action potential (SNAP), is a compound No NMJ or muscle time needs to be subtracted out by using
potential that represents the summation of all the individual two stimulation sites.
sensory fiber action potentials. SNAPs usually are biphasic
or triphasic potentials. For each stimulation site, the onset
Onset Latency
The onset latency is the time from the stimulus to the initial
negative deflection from baseline for biphasic SNAPs or to
the initial positive peak for triphasic SNAPs. Sensory onset
latency represents nerve conduction time from the stimulus
site to the recording electrodes for the largest cutaneous
sensory fibers in the nerve being studied.

Cathode Peak Latency

The peak latency is the time from the stimulus to the mid-
point of the first negative peak. When sensory NCSs were
first developed, peak latencies were classically used instead
G1 of onset latencies. In the past, peak latencies offered several
G2
advantages, some of which are still as valid today as when
they were first developed. The peak latency can be ascer-
Ground tained in a straightforward manner; there is practically no
interindividual variation in its determination. In contrast, the
Fig. 3.4 Sensory conduction study setup. Median sensory study, onset latency can be obscured by noise or by the stimulus
antidromic technique. Ring electrodes are placed over the index artifact, making it difficult to determine precisely. In addi-
finger, 3–4 cm apart. The active recording electrode (G1) is placed tion, for some potentials, especially small ones, it may be dif-
more proximally, closest to the stimulator. Although the entire median
ficult to determine the precise point of deflection from the
nerve is stimulated at the wrist, only the cutaneous sensory fibers are
recorded over the finger. baseline (Fig. 3.6). These problems do not occur in marking
 Chapter 3 • Basic Nerve Conduction Studies 27

P9
PV
—9
PV

Fig. 3.6 Sensory nerve action potential onset and peak laten-
cies. Onset and peak latency measurements each have their own
advantages and disadvantages. Onset latency represents the fastest
conducting fibers and can be used to calculate a conduction velocity.
However, for many potentials, especially small ones, it is difficult to
precisely place the latency marker on the initial deflection from base-
—9
line (blue arrows: possible onset latencies). Marking the peak latency
is straightforward, with nearly no interexaminer variation. However, PV
the population of fibers represented by peak latency is unknown; it
cannot be used to calculate a conduction velocity.

the peak latency. Normal values exist for peak latencies for
the most commonly performed sensory studies.
However, peak latencies have two distinct disadvan-
tages. Most important, the peak latency cannot be used to
calculate a conduction velocity. The population of sensory Fig. 3.7 Compound muscle action potential (CMAP) and sensory
fibers represented by the peak latency is not known, in nerve action potential (SNAP) comparison. CMAPs (top) and
contrast to the onset latency, which represents the fast- SNAPs (bottom) are both compound potentials but are quite different
est conducting fibers in the nerve being studied. Second, in terms of size and duration. CMAP amplitude usually is measured
in millivolts, whereas SNAPs are small potentials measured in the
normal values for peak latencies are dependent on using microvolt range (note different gains between the traces). CMAP
standard distances. This can be problematic especially in negative peak duration usually is 5–6 ms, whereas SNAP negative
the upper extremities in patients with particularly large or peak duration is much shorter, typically 1–2 ms. When both sensory
small hands. and motor fibers are stimulated (such as when performing antidromic
sensory or mixed studies), these differences (especially duration) usu-
Both onset and peak latencies can be used in the analy-
ally allow an unknown potential to be recognized as either a nerve or
sis of sensory NCSs. In the examples given in this text in muscle potential.
the later clinical chapters, both values are measured and
reported. If the potential has an abrupt, consistent, and eas-
ily marked onset latency, the onset latency is the preferred
measurement. However, in cases where the onset latency is baseline. The former is preferred given that the SNAP dura-
obscured, or not precise, peak latency is better used. tion measured from the initial to terminal deflection back to
baseline is difficult to mark precisely because the terminal
SNAP returns to baseline very slowly. The SNAP duration
Amplitude typically is much shorter than the CMAP duration (typi-
The SNAP amplitude is most commonly measured from cally 1.5 vs. 5–6 ms, respectively). Thus, duration is often a
baseline to negative peak, but it can also be measured from useful parameter to help identify a potential as a true nerve
the first negative peak to the next positive peak. The SNAP potential rather than a muscle potential (Fig. 3.7).
amplitude reflects the sum of all the individual sensory
fibers that depolarize. Low SNAP amplitudes indicate a
definite disorder of peripheral nerve. Conduction Velocity
Unlike the calculation of a motor conduction velocity, which
requires two stimulation sites, sensory conduction velocity
Duration can be determined with one stimulation, simply by dividing
Like the CMAP duration, SNAP duration is usually mea- the distance traveled by the onset latency. Essentially, distal
sured from the onset of the potential to the first baseline conduction velocity and onset latency are the same mea-
crossing (i.e., negative peak duration), but it also can be surement; they differ only by a multiplication factor (i.e.,
measured from the initial to the terminal deflection back to the distance). Sensory conduction velocity represents the
28 SECTION II Fundamentals of Nerve Conduction Studies

speed of the fastest, myelinated cutaneous sensory fibers in sensory receptor) techniques. For instance, when studying
the nerve being studied. median sensory fibers to the index finger, one can stimulate
Sensory conduction velocity along proximal segments the median nerve at the wrist and record the potential with
of nerve can be determined by performing proximal stim- ring electrodes over the index finger (antidromic study).
ulation and calculating the conduction velocity between Conversely, the same ring electrodes can be used for stimu-
proximal and distal sites, in a manner similar to the calcula- lation, and the potential recorded over the median nerve
tion for motor conduction velocity: (distance between the at the wrist (orthodromic study). Latencies and conduction
proximal and distal stimulation sites) divided by (proximal velocities should be identical with either method (Fig. 3.8),
latency minus distal latency). However, proximal sensory although the amplitude generally is higher in antidromically
studies result in smaller amplitude potentials and often are conducted potentials.
more difficult to perform, even in normal subjects, because In general, the antidromic technique is superior for sev-
of the normal processes of phase cancellation and temporal eral reasons, but each method has its advantages and dis-
dispersion (see later). Note that one can also determine the advantages. Most important, the amplitude is higher with
sensory conduction velocity from the proximal site to the antidromic than with orthodromic recordings, which makes
recording electrode by simply dividing the total distance it easier to identify the potential. The SNAP amplitude
traveled by the proximal onset latency. is directly proportional to the proximity of the recording
electrode to the underlying nerve. For most antidromically
conducted potentials, the recording electrodes are closer
Special Considerations in Sensory
to the nerve. For example, in the antidromically conducted
Conduction Studies: Antidromic Versus median sensory response, the recording ring electrodes are
Orthodromic Recording placed on the finger, very close to the underlying digital
When a nerve is depolarized, conduction occurs equally nerves just beneath the skin from which the potential is
well in both directions away from the stimulation site. Con- recorded. When the montage is reversed for orthodromic
sequently, sensory conduction studies may be performed recording, there is more tissue (e.g., the transverse carpal
using either antidromic (stimulating toward the sensory ligament and other connective tissues) at the wrist separat-
receptor) or orthodromic (stimulating away from the ing the nerve from the recording electrodes. This results
in attenuation of the recorded sensory response, resulting
in a much lower amplitude. The higher SNAP amplitude
obtained with antidromic recordings is the major advantage
—9 of using this method. The antidromic technique is espe-
PV cially helpful when recording very small potentials, which
often occur in pathologic conditions. Furthermore, because
the antidromic potential generally is larger than the ortho-
—9
dromic potential, it is less subject to noise or other artifacts.
PV However, the antidromic method has some disadvantages
(Fig. 3.9). Because the entire nerve is often stimulated, includ-
ing the motor fibers, this frequently results in the SNAP being
followed by a volume-­ conducted motor potential. It usu-
ally is not difficult to differentiate between the two because
the SNAP latency typically occurs earlier than the volume-­
conducted motor potential. However, problems occur if the
two potentials have a similar latency or, more importantly, if
—9
PV the sensory potential is absent. When the latter occurs, one
can mistake the first component of the volume conducted
motor potential for the SNAP, where none truly exists. It is in
this situation that measuring the duration of the potential can
be helpful in distinguishing a sensory from a motor potential.
If one is still not sure, performing an orthodromic study will
Fig. 3.8 Antidromic and orthodromic sensory studies. Median settle the issue, as no volume conducted motor response will
sensory nerve action potential (SNAPs). Top trace, Antidromic study, occur with an orthodromic study. In this case, the antidromic
stimulating wrist, recording index finger. Bottom trace, Orthodro-
mic study, stimulating index finger, recording wrist. Latencies and
and orthodromic potentials should have the same onset latency.
conduction velocities are identical for both. The antidromic method
has the advantage of a higher-­amplitude SNAP but is followed by
a large volume-­conducted motor potential. If the SNAP is absent
Lesions Proximal to the Dorsal Root
in an antidromic study, care must be taken not to confuse the ­Ganglion Result in Normal Sensory Nerve
volume-­conducted motor potential as the sensory potential. Note Action Potentials
the difference in duration between SNAP and compound muscle
action potential, which helps discriminate between the SNAP and the Peripheral sensory fibers are all derived from the dor-
volume-­conducted motor potential that follows. sal root ganglia cells, the primary sensory neurons. These
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 Il lui toucha le bras, du bout de son doigt :
— Regardez-moi bien !
Elle le regarda, d’un regard neutre, où tout semblait mort.
Il dit :
— Vous comprenez, nous devons prendre quelques petits
arrangements. Voici donc ce que je vous impose : l’hypocrisie. Ça ne
vous sera pas difficile… J’aime ma mère plus que tout au monde, et
aujourd’hui plus que jamais. Il faut qu’elle soit heureuse… Si elle
savait ce qui se passe en ce moment dans la maison de son fils, elle
en mourrait !… Elle n’en saura rien. Je le veux… je vous impose de
la rendre heureuse, à force de ruse habile, et de mensonge…
J’entends que vous trompiez tout le monde, — excepté moi. C’est
bien clair, n’est-ce pas ?
Elle se taisait.
— Mais répondez donc !
Elle se taisait toujours, l’air hautain et dur.
Une fureur inouïe le secoua. Il crispa ses poings et serra les
dents ; et, terrible, il gronda :
— Ça sera comme ça, — ou j’étrangle !
Il lui montrait ses deux mains ouvertes, crispées en crochets,
pareilles à des serres.
— Oh ! je n’ai jamais peur ! fit-elle.
Et après avoir cherché et pesé son mot :
— J’obéirai, dit-elle tout sec.
Elle était sans crainte, mais elle préparait les lendemains ; et,
pour cela, cette promesse d’obéir, faite sur ce ton d’insolence et de
révolte, fut la seule concession qu’elle trouva.
— Vous obéirez ? C’est heureux ! fit-il. Allons, bonsoir ; je vous
souhaite le doux repos que donne une conscience pure. A demain !
Il la quitta.
 « C’est bien cela, songeait-il : ruse, mensonge, orgueil, orgueil
surtout !… Il me faudra un gant de fer. »
A peine hors de sa présence, il se sentit défaillir, sous
l’écroulement de son bonheur, mais il marcha jusqu’à sa chambre et
se jeta, tout vêtu, sur son lit. Au milieu du pêle-mêle de ses pensées
affreuses, celle-ci reparaissait toujours dans un demi-rêve : « Si elle
pouvait avoir l’idée d’aller se noyer, est-ce qu’il ne faudrait pas la
laisser faire ?… Allons, allons, c’est une autre que j’aimais. Voilà ce
que je dois me dire. Il y a erreur sur la personne, répétait-il… Mais
comment peut-on se laisser aveugler à ce point ? — Oh ! la
passion ! »
Quant à elle, elle se déshabilla lentement, et tout de suite, se mit
au lit.
Elle renonçait à penser. Tout cela était fatal, et trop fort,
décidément, trop compliqué… « Non ! quelle affaire, mes amis ! et
que de bruit pour trois chiffons de papier !… Qu’est-ce que dira cette
folle de Berthe ?… Elle n’en reviendra pas !… Je suis sûre qu’il n’y a,
en France, qu’un seul homme comme ça. Et j’ai eu la veine de
tomber dessus ! Vrai, c’était fait pour moi !… Était-il beau tout à
l’heure ! C’est un homme, un vrai, ça, et crâne, encore !… Bah ! je le
ramènerai. C’est ça qui sera amusant !… Le bonheur de la mère,
c’est la planche de salut, — et solide ; il faut s’y tenir… Je ne peux
pourtant pas songer… aux inscrits, avant d’avoir fait la conquête de
mon époux… C’est bien drôle !… »
Et comme il arrive après les morts, après les désespoirs, les
grandes épreuves, lasse de tant d’émotions et d’aventures, — elle
dormit, cette nuit-là, d’un sommeil d’enfant. D’ailleurs, il fallait ça,
pour être jolie dès le lendemain, et engager la bataille.
 IV

Le comte Paul, à son réveil, après un somme pesant et court, eut

toutes les peines du monde à reprendre conscience de la vie… Que
tout cela fût vrai, c’était impossible. Et de même que certains rêves
impressionnent l’âme plus fortement que la réalité, de même, aussi
fortement, cette réalité l’impressionnait comme un rêve.
Il alla s’accouder à sa fenêtre ouverte. Septembre rayonnait.
L’éternelle verdure des pins, des eucalyptus, des palmiers donne
aux automnes de Provence des gaîtés de printemps. Aucune
mélancolie ne venait des choses. Le soleil, levé depuis une heure,
resplendissait sur la mer et sur les salins. Le paysage familier parla
tendrement au cœur du jeune homme. De quoi ? de son enfance,
écoulée parmi ces arbres et ces rochers, dans cette nature paisible
et câline. Il se revit courant avec Pauline, parmi les bruyères ;
cherchant, dans les touffes du thym et du romarin, le prie-dieu et la
sauterelle, ou, sur le tronc rugueux des pins, la cigale, toute dorée
comme les perles de la résine.
Pauvre petite Pauline ! il revit ce doux visage mélancolique. La
veille encore, il l’avait vue, triste comme toujours… plus triste peut-
être… Et il secoua la tête, en songeant : « C’était une affection sûre,
celle-là ! Qu’est-ce donc que nos cœurs et nos destinées ? Pourquoi
ne l’ai-je pas aimée, cette noble créature, cette chère sœur de mon
ami ? N’avais-je pas pour elle de la tendresse ? Oui, certes… Et, —
chose affreuse ! — cette tendresse même m’a empêché d’avoir pour
elle de l’amour ! Quelle idée singulière avais-je donc de l’amour ?
Elle m’aimait peut-être… et c’eût été le bonheur, le mien, celui de ma
mère… Tandis que maintenant… maintenant…, l’autre est là ! quelle
autre ?… une étrangère, vraiment, puisqu’elle n’a rien de nos cœurs,
de nos éducations, de nos âmes ! »
 Il revit en pensée celle qu’il ne pouvait s’empêcher d’appeler
Rita, — et, aussitôt tout le charme du jour commençant, du paysage
aimé, s’attrista, s’enveloppa d’une mélancolie que la saison ne lui
donnait point.
A ce moment, le landau sortit des remises. Paul se rappela que
sa mère et sa sœur s’étaient promis de partir de très bonne heure
pour Hyères, malgré les fatigues de la veille. Il les vit en effet,
monter en voiture… s’éloigner… « Pauvre chère maman ! si elle
savait !… » A cette idée, il sentit son cœur défaillir, mais il se roidit, et
reprit le cours de ses réflexions, en les dirigeant, cette fois : if refit le
procès de Marie Déperrier et, de nouveau, il la condamna. Il conclut
en dernier ressort qu’il devait avant tout, maintenir l’attitude qu’il
avait prise. Certainement, elle essaierait de le reconquérir. « Mais,
se dit-il, si j’avais le malheur de céder, je serais perdu ! Je me
mépriserais, et elle me mépriserait elle-même. La lutte deviendrait
entre nous une lutte d’égaux ; je perdrais sur elle l’autorité morale ;
ce serait l’âpre querelle quotidienne installée chez moi. Je dois
garder ma supériorité, c’est-à-dire ma liberté ; il le faut. Il faut, à tout
prix, qu’elle me demeure étrangère ! »
Et comprenant que, malgré tout, cette lutte serait, par moments,
difficile, il se donna à lui-même sa parole d’honneur de rester libre
de cette femme ; de résister à tout désir de pardon, à toute
suggestion d’indulgence, même devant les apparences du repentir ;
il alla jusqu’à admettre d’avance qu’il serait injuste, au cours de la
vie quotidienne, plutôt que de se laisser vaincre. Il arma pour
toujours de parti-pris sa dure volonté.
Il se déshabilla, passa sous la douche, mit un costume
d’intérieur, et, une cigarette d’Orient entre les doigts, il se dirigea
vers la chambre de sa femme. D’un mouvement instinctif, il
s’apprêtait à jeter sa cigarette. Il la garda. Il fumait, à l’ordinaire,
devant elle. Eh bien ! il fumerait dans sa chambre, comme il le faisait
en sa présence au salon. C’était une contenance, et dédaigneuse.
— Entrez ! dit-elle au coup léger qu’il avait frappé.
Elle était au lit, parmi les dentelles.
 — Vous avez bien dormi, j’espère ?
Elle ne répondit point.
— Moi, pas, reprit-il. J’étais nerveux. J’ai dû réfléchir, régler en
esprit beaucoup de choses.
Et, voulant trancher dans le vif :
— Pour commencer, — la question d’argent… Voici le premier
semestre…
Il déposa sur la cheminée un petit portefeuille.
— Vous trouverez là quelques billets… vos appointements.
Sur ce mot elle tressaillit, intérieurement, et n’en laissa rien
paraître.
Elle était déroutée par l’attitude de cet homme. Que devait-elle
faire ? Elle aussi croyait avoir rêvé. Mais non, tout était bien vrai.
L’impossible lui était arrivé. Le hasard, le destin, du premier coup
l’avait livrée, et désarmée. Maintenant, elle appartenait en esclave à
cet homme qui entrait chez elle, méprisant, la cigarette aux doigts,
dans sa chambre à coucher… De ses droits de mari, il n’acceptait
que ce droit outrageant d’être là ; et, seul entre tous les hommes
qu’elle connaissait, il n’implorait plus rien d’elle, ni regard, ni sourire,
— mais il exigeait, il imposait l’obéissance.
Avoir été ainsi vaincue du premier coup, — c’était bien
surprenant et c’était bien dur. Incertaine du parti à prendre, elle
s’abandonnait à l’étonnement, attendait qu’une circonstance lui
indiquât la voie à choisir.
Il fumait, réfléchissant, assis près de la fenêtre ; il ne la regardait
pas ; il suivait de l’œil la fumée légère ou regardait, à travers les
vitres claires, les oiseaux qui voletaient, piailleurs, dans les platanes,
les hirondelles qui passaient, de temps à autre, en flèches… et la
mer bleue, là-bas, tachetée d’écumes blanches.
Un abîme séparait ces deux êtres jeunes qui avaient cru se
rapprocher, jusqu’à mêler, pour toujours, leurs vies.
L’idée vint à Rita que peut-être ?… Car enfin…
 Elle s’accouda, laissant à dessein glisser un bout d’épaule hors
des dentelles, et prononça lentement :
— Je n’ai rien dit encore depuis cet affreux moment où vous avez
voulu voir ces lettres… qui n’appartenaient qu’à moi.
Il releva la tête. Une réplique violente et amère lui vint aux lèvres.
Il s’ordonna à lui-même de se taire, d’écouter.
— Vous avez voulu voir ces lettres. Vous les avez vues. Où est
mon crime ? J’ai vingt-quatre ans : je ne vous ai pas attendu, c’est
vrai, — avant de savoir même que vous existiez — pour rêver, pour
désirer l’amour. Il y a huit ou neuf ans que j’ai ce droit-là. Vous auriez
pu vous le dire. Mais non… Il vous plaît mieux de me reprocher
d’avoir eu un cœur, comme toutes les jeunes filles, à l’âge même où
le cœur s’éveille, où les rêves commencent. Est-ce là mon crime ?…
Non. Est-ce alors d’avoir gardé ces lettres ? C’est une faiblesse, j’en
conviens, mais c’est une faiblesse d’enfant, — oui, un enfantillage.
Ne vous avais-je pas promis de vous les montrer un jour ou l’autre ?
Je l’aurais fait à coup sûr, mais seulement après des confidences qui
vous auraient préparé à tout connaître, sans colère et sans mépris,
tout mon passé. M’accusez-vous de ne pas vous l’avoir dit, ce passé
où il y a des douleurs, pénibles à avouer, mais non pas une seule
faute ? Je vous réponds : Me l’avez-vous seulement demandé ? Et
comme je savais que bien des choses, dont je ne suis point
responsable, vous déplairaient pourtant, ne trouvez-vous pas naturel
et même légitime mon silence ? C’est de l’héroïsme qu’il eût fallu
avoir, pour courir, spontanément, le risque de vous éloigner de moi ?
Eh bien ! je l’avoue, je me suis consultée un moment. Je n’ai pas su
pousser la sincérité jusqu’à dire, au risque de vous perdre, ce que
vous ne demandiez pas…
Elle s’arrêta ; puis, la main sur ses yeux où montaient des
larmes, elle acheva, d’une voix pénétrée et basse : — Je vous
aimais trop pour cela !…
Il se taisait, immobile, l’œil sur le vide ouvert devant eux.
Elle le regarda entre ses doigts légèrement écartés :
 — Vous ne savez pas ce qu’il m’en coûte, de vous parler ainsi,
en ce moment, si tôt après vos insultes ! Car, j’en conviens, — j’ai
une nature rebelle, un peu sauvage. Je n’ai jamais plié devant
personne… Tout mon orgueil, depuis hier au soir, est en révolte.
C’est pour cela que je me suis tue. Mais maintenant, voyez, je parle,
vaincue, soumise, parce que je comprends votre douleur… et je ne
veux pas que vous souffriez plus longtemps !
Il regardait toujours dans le vide, avec cet œil vitreux de ceux qui
ont tout perdu — et dont le songe voit par delà la vie. Les paroles
qu’elle murmurait arrivaient tardivement à son intelligence. Il les
comprit un moment après qu’elle eut fait silence. Et déjà il se
demandait si, en effet, elle n’avait pas raison, s’il n’avait pas des
exigences trop hautes, s’il avait le droit de condamner si vite, si
absolument. Ah ! qu’il est difficile d’être juste ! Et il voulait l’être.
N’avait-il pas obéi à un coup de passion rageuse, jalouse ? Oh ! s’il
pouvait retrouver, en elle, une excuse ; et, en lui, le pardon ! S’il
pouvait retrouver le bonheur entrevu la veille, le même, ou
seulement quelque chose de ce bonheur, rêvé durant deux années.
Il jeta dans la cheminée la cigarette qu’il avait apportée avec un
parti pris de désinvolture et même d’impertinence.
Le souvenir de sa mère lui traversa le cœur. Si les choses
restaient ainsi, pourrait-il lui cacher longtemps le malheur de sa vie ?
Certes, pour la malheureuse mère, c’est la réconciliation qu’il fallait.
Dans son cerveau, lassé par l’insomnie, les détails de la scène
affreuse de cette nuit s’estompaient, affaiblis. Il n’avait plus l’énergie
physique nécessaire pour interpréter les faits, les rapprocher, les
presser, en faire jaillir tout le sens.
Elle devina que son silence disait une hésitation.
Que devait-elle faire, pour influencer son juge ?
Elle cachait toujours son visage avec ses mains. Elle comprit que
Paul la regardait. Alors, pour jouer mieux son rôle, elle plongea tout
à coup son visage dans les coussins, entre ses deux bras nus, avec
un sanglot volontaire. Elle sentit avec joie que de vraies larmes
coulaient sur ses joues et que ses épaules s’étaient découvertes.
« Car enfin, songeait-elle, il n’est pas en bois, le bonhomme ! » Ses
grands cheveux cendrés serpentaient de tous côtés autour de sa
tête. Un rayon vint toucher sa nuque, les changea çà et là en or
flamboyant. Sa chair prit les transparences exquises de la vie jeune,
mystérieuse, attirante. Il la regardait toujours et elle le sentait bien.
Les tentations qui étaient en lui, elle les savait. On n’attend pas,
durant deux années, une jeune fille, on ne l’aime pas jusqu’au
mariage, pour renoncer à elle subitement, à tout jamais, dès le
contrat signé, sans quelque révolte de l’égoïsme physique. La
passion grondait, dans ce mari pris au piège. Et quand bien même il
voudrait la chasser demain, ne devait-il pas désirer encore, —
comme tous les autres hommes, — avoir fait d’elle sa maîtresse
d’une heure ? Mais comme il était naïf et bon, — cela l’engagerait,
celui-là ! Et si ?… Oui !… Pourquoi pas ? — Elle était bien sûre d’une
chose, c’est qu’il ne chasserait jamais plus la mère d’un
d’Aiguebelle… Dans l’émouvante idée de maternité, elle ne voyait
qu’un moyen de défense et d’ambition.
Elle cria, la voix étouffée dans les coussins : — Paul ! Paul, ayez
pitié ! pitié de moi… et pitié de vous-même !… Ayez pitié !… Ne me
rejetez pas, du haut d’un ciel, dans l’abîme !
Et, comme poussée par un irrésistible élan, elle se leva alors, se
jeta hors de son lit, demi-nue, les cheveux enflammés de soleil, et se
précipita à ses genoux… Il s’était levé, le cœur bondissant… Il allait
tout oublier. Il oubliait tout, puisqu’il ne songeait pas à s’étonner de
voir une jeune fille aussi prompte à se montrer ainsi…
La beauté l’attirait à lui, triomphante, d’une invincible puissance.
Dans la débâcle de sa volonté, de ses idées, il voulut, pour se rejeter
loin d’elle, invoquer en lui son mépris de la veille. Mais les raisons de
ce mépris se faisaient toujours en lui plus éparpillées, plus diffuses,
plus impossibles à ressaisir… Il ne les voyait plus. Mais il savait
encore qu’elles existaient. Alors il se dit :
« Eh bien ! qu’importe ? Pourquoi pas ? Pourquoi ne pas la traiter
en courtisane ? Pourquoi ?… N’est-ce pas la pire vengeance ? N’est-
ce pas lui infliger la dernière des hontes, que de profiter de mes
droits, tout en restant dégagé d’elle ? »
 Ainsi la bête commandait l’esprit qui, n’avouant pas sa défaite, se
répétait les suprêmes sophismes de la dignité et de la liberté
expirantes.
Rita leva vers son mari ses yeux bleus, noyés de larmes, lui
montra ses joues ruisselantes. Il regardait cette femme courbée à
ses pieds, — si belle, si touchante à la fin ! Les larmes lui allaient
bien. « Je me suis trompé, songea-t-il. — Tant de beauté, de
charme, la clarté d’expression de ce visage, ne peuvent pas cacher
les noirceurs que j’ai cru deviner. C’est impossible. » Il s’inclina pour
la relever. Elle tendit les bras vers lui. Ces beaux bras nus, il les prit
dans ses mains, et se sentit frémir de la tête aux pieds.
Alors, pour l’achever, elle cria :
— Au nom de ta mère, Paul ! au nom de ta mère !
C’était la note fausse, puisque, sur ce mot, il s’aperçut qu’elle
était à moitié nue. Il conçut qu’elle voulait s’aider d’un nom sacré,
cacher sous ce nom un essai de séduction impudique. Une jeune
fille pure, injustement accusée, se serait-elle défendue ainsi, comme
une Phryné ?
Il était redevenu froid.
Elle sentit se desserrer sur ses bras, les doigts qui l’étreignaient.
— Ah ! fit-il d’un ton glacial.
Le nom de sa mère, invoqué dans un tel moment, avait produit
un effet tout contraire à celui qu’elle attendait. Il se rappela les
pressentiments de la comtesse. Il regarda instinctivement le petit
meuble recéleur des lettres maudites. Il revit cette femme qui était là,
sa femme, lançant par la fenêtre, pour le tromper, cette bourse
vide… Ah ! oui, il se souvenait, à présent. Il croyait assister encore à
cet acte de mensonge qui la lui avait révélée à fond. Et il tressaillit,
comme si cette révélation lui était faite dans l’instant même.
— Ces lettres, dit-il alors, donnez-les-moi.
— Je les ai brûlées.
— Allons, dit-il, c’est complet. Et je conclus : Comme ma mère,
— c’est entendu, — doit ignorer mon malheur, et qu’il serait difficile
de simuler l’accord entre nous assez parfaitement pour la tromper
chaque jour à toute minute, nous partirons ce soir pour Nice. C’est
un caprice de ma femme, — votre premier caprice, — auquel j’obéis.
J’ai même, à Nice, quelque affaire. Vous comprenez. De Nice, nous
partirons pour Paris. Cela nous donnera un peu de temps pour
préparer la suite de notre misérable existence à deux. Encore un
mot : j’avais congédié, pour cette nuit, notre vieille femme de
chambre. Vous allez l’appeler. Je veux qu’elle nous voie ici, en ce
moment, réunis, et, tout à l’heure, déjeunant ensemble. Ma mère et
ma sœur viennent de partir ce matin pour Toulon où elles ont
quelques emplettes à faire. Elles rentreront vers quatre heures.
Nous partirons à six. Habillez-vous. Et, après le déjeuner, nous
irons, avec la charrette anglaise, seuls tous deux, à Hyères. Il faut se
donner du mouvement, chercher la distraction, ne pas rester face à
face avec notre misère, — et nous montrer le moins possible,
aujourd’hui, aux braves serviteurs de ma maison.
Ce programme fut exécuté.
 V

Maintenant, ils étaient à Paris. Paul n’avait eu aucune peine à

faire accepter par sa mère son brusque départ. La bonne dame, en
mariant son fils, avait consommé un grand sacrifice. Elle n’était pas
femme à se démentir en détail, à reprendre à l’étrangère des bribes
de son bonheur.
Désormais « ces enfants » s’appartenaient à eux-mêmes. Bien
plus, elle trouvait juste et bon qu’ils fussent là-bas, libres, hors des
atteintes de son égoïsme, disait-elle, éloignés du spectacle de son
déclin… C’était un peu triste pour Annette, par exemple ! mais la
chère enfant adorait sa mère ; ils avaient de bons voisins, au
château des Bormettes, et puis cet isolement ne devait pas durer.
Elles iraient, dans quelques mois, voir les nouveaux mariés à Paris.
Après cela, ils viendraient passer le printemps aux Bormettes.
Rassuré pour le moment du côté de sa mère, le comte Paul
arrangea sa vie à Paris, de façon à ne rien laisser deviner de son
malheur.
D’ailleurs, ce n’était guère qu’en présence d’Albert, de sa sœur
Pauline et de Madame de Barjols qu’il lui était difficile de dissimuler.
Il présenta sa femme à peu de personnes, préférant les
interprétations mauvaises de cette attitude, à ce qu’on dirait, si l’on
venait à entrevoir la vérité. Aux yeux du monde, c’étaient deux
époux corrects, qui s’isolaient dans leur bonheur, et semblaient
désirer beaucoup qu’on ne les dérangeât point.
De la part du comte Paul, le contraire eût paru surprenant.
— Ah ! disait Berthe, — la pauvre jeune femme ne s’amusera pas
tous les jours avec ce gentilhomme de trumeau ; mais enfin, pour les
débuts, ça paraît lui convenir, et puisqu’elle ne se plaint pas…
 Marie, en effet, n’avait rien dit à Berthe, sans trop s’expliquer
pourquoi. C’est que, pour l’instant, l’aveu l’eût humiliée.
Vis-à-vis des de Barjols, Paul avait pris une double précaution.
La première, c’était de répéter à tout propos qu’il avait horreur de
ces gens qui affichent leur bonheur conjugal. Pour lui il préférait
tomber dans l’excès contraire, et paraître un mari désagréable. La
seconde précaution, la meilleure, avait été de voir moins souvent
ses amis.
Albert, cédant aux supplications de sa mère, avait obtenu la
résidence libre. Il habitait Paris pour un temps inconnu. Mais comme
de son côté il avait résolu de voir Paul et Marie le moins souvent
possible, il croyait être lui-même la seule cause de la rareté des
entrevues. Les sentiments de Pauline la poussaient également à
éviter les rencontres jadis si désirées. Madame de Barjols disait :
« On ne le voit plus, ce Paul… C’est bien naturel ! » Tout allait donc
pour le mieux dans la pire des situations.
Marie et Paul adressaient, presque tous les jours, à la comtesse
des lettres pleines de gaîté. Paul racontait toutes les pièces de
théâtre nouvelles, et, en effet, il conduisait sa femme au théâtre à
peu près tous les soirs. C’était le moyen d’éviter le tête-à-tête sous
la lampe, et aussi de fuir les réunions, les bals, où le comte Paul
redoutait de rencontrer celui qu’il désignait ainsi dans sa pensée de
philosophe : « Un homme assez sot pour s’imaginer qu’elle en vaut
la peine ! »
La jeune comtesse d’Aiguebelle ne voyait guère que des
connaissances de son mari. Léon Terral, à sa grande joie, lui avait
écrit, quinze jours après leur entrevue à Aiguebelle, qu’il partait pour
l’Amérique. Il avait donné sa démission. On l’avait intéressé dans
une affaire grosse d’espérances. Marie avait pensé : « Bon voyage !
Et si c’est possible, bon retour ! Mais, pour l’instant, m’en voilà
débarrassée, ça n’est pas malheureux ! J’ai assez de complications
comme ça. »
Lérin de La Berne s’était vainement présenté chez elle. Elle lui
avait fait refuser sa porte. « Encore un gêneur. Dans la situation où
je suis, des imbéciles pareils, c’est trop dangereux ! »
Elle revit Berthe une ou deux fois, continua à ne rien lui dire du
fond des choses, mais elle lui donna à entendre que certaines
difficultés exigeaient la plus grande prudence, la plus grande
discrétion.
— Un jour je te conterai tout, ma chérie. Il y a quelque chose,
quelque chose de grave. Que veux-tu ? C’est un jaloux, il est jaloux
de tout… de toi comme des autres.
— De moi, bon Dieu !
— De toi et de tous ; il le serait de mon petit chien et de mon
perroquet, si j’avais un perroquet et un petit chien.
— Et cela s’est déclaré à quel propos ?
— Le soir même de mon mariage. Pour une conversation…
Tiens, justement, avec Lérin… Tu ne te rappelles pas ? Tu vins me
dire, par deux fois : Comme ton mari te regarde !
— Oui, en effet.
— Eh bien, ça le travaillait. C’est un homme comme ça. Il a du
sombre dans le caractère ; il faut que je prenne garde…
— Oui, en effet, dans les commencements il faut les ménager…
Ça me fait de la peine pour Lérin… Il y comptait, tu sais ?
— Sur quoi donc ?
— Sur son numéro d’ordre.
— Cette bêtise ! Non ! Pas possible !
— Comme j’ai l’honneur… Et vrai, j’aurais voulu le voir à
l’échéance. C’est à crever… Car tu sais, son lorgnon…
— Son lorgnon ?
— C’était, dans toute sa personne, la seule chose qui tenait
encore…
— Eh bien ?
— Eh bien ! figure-toi ! il ne tient plus !
 Cette plaisanterie les fit mourir de rire toutes les deux, même
elles en revinrent et de nouveau moururent deux ou trois fois, dans
les spasmes d’une gaîté inquiétante.
— Bref, conclut Berthe, je comprends : tu veux décidément qu’on
te fiche la paix pendant quelques semaines ? Tu dois avoir tes
raisons. Tu manigances quelque chose, et tu ne veux pas qu’on
sache, de peur qu’on fasse rater tes petits projets. Soit, c’est sacré,
ça. C’est ton affaire, on obéira. Mais, au premier signe, j’accours. Tu
me diras tout, hein, plus tard ? C’est convenu ? A propos, tu ne sais
pas ce qu’on dit partout ? Que Monsieur de Barjols, le grand ami de
ton mari, le Pylade de cet Oreste, — était tombé amoureux de toi, à
cette soirée des Russes, en même temps que son cher ami. Ce
serait pour ça qu’il aurait demandé son commandement au Tonkin…
Mais j’y pense, ton prince russe, plus de nouvelles ?
Marie, très intéressée, avait dressé l’oreille.
— Il s’agit bien des Russes !… Qu’est-ce que tu me dis là, de
Monsieur de Barjols ?
— Tu ne t’en étais pas doutée ? Vrai de vrai ?
— Ça m’avait passé par l’esprit, comme une idée de roman. Mais
non, je ne savais pas… Voyons, tu veux rire. Comment aurait-on pu
savoir ?
— Comment ? C’est bien simple : figure-toi ; il veut partir encore,
malgré sa mère. Il paraît que ça lui a repris ! Pour obtenir cette
faveur de repartir, il a cru pouvoir se confesser, à mots couverts,
sans te nommer, au commandant Ripert, du ministère, un homme
sûr, — mais qui a en sa femme — ma meilleure amie, après toi, —
une confiance… bien mal placée. Le commandant s’est laissé tirer
par elle les vers du nez ; — et je tiens l’histoire… d’elle-même, —
parce qu’elle a en moi une confiance… également mal placée ! Ça
peut servir, ce que je t’annonce ! Je ne sais pas à quoi… Mais ça
sert toujours, tôt ou tard, de savoir ces machines-là.
Berthe était partie, laissant Rita très songeuse.
La jeune comtesse d’Aiguebelle avait donc déblayé son terrain
d’opération. Elle avait éloigné de chez elle toutes les personnes qui
pouvaient rappeler au comte son passé bohème, révélé par les
lettres de Léon Terral.
Cela lui avait semblé la plus nécessaire de toutes les prudences.
Elle s’était arrêtée à l’idée de reconquérir son mari ; mais avant tout,
il fallait l’apaiser. On verrait ensuite.
Cette tâche ne s’annonçait pas comme des plus faciles.
Le comte Paul était de ces cœurs droits, fanatiques de droiture,
qui, trompés une fois par l’être en qui ils avaient confiance,
demeurent incapables à tout jamais de croire en cet être, même
redevenu sincère.
La moindre défaillance de la sincérité leur paraît si monstrueuse
qu’elle développe en eux une faculté, également monstrueuse, de
soupçon, de supposition ou de divination du mal. Ces croyants-là se
retournent tout d’une pièce : ils passent de la foi aveugle au doute
non moins aveugle.
En expiation d’un mensonge unique et véniel, un innocent peut
paraître à leurs yeux le pire coupable, et devenir la pitoyable victime
de leurs soupçons forcenés.
Mais si leur scepticisme déchaîné se mêle de traquer une âme
de mensonge, s’obstine à la poursuivre dans tous ses détours, à la
précéder pour l’arrêter dans ses ruses, ils deviennent des justiciers
effroyables. Supposez Desdémone coupable, tous les soupçons
d’Othello, jaloux sans preuve suffisante, sont divinateurs, et chacune
de ses paroles inflige à la malheureuse le supplice mérité !
Le comte Paul, dans un seul mensonge de Rita, avait vu une
âme habituée au mensonge, une âme de malignité. En lui prêtant
toujours toutes les pensées mauvaises, il se croyait sûr de deviner
juste, et il était rare qu’il se trompât.
Naturellement, elle se piquait d’être du troupeau des sphinx, et
elle s’affolait de se voir devinée. C’était s’étonner de peu. Comme il
avait contre elle tous les soupçons, il tombait toujours juste, parce
qu’elle avait, elle, tous les mauvais instincts. Il était certes plus
passionné que judicieux. Mais ses aveuglements même paraissaient
être de la clairvoyance.
 Tout en ne perdant aucune occasion de lui prouver qu’elle était
pénétrée à fond, Paul s’efforçait de montrer la plus grande froideur.
Avoir des scènes avec sa femme, cela semblait au comte Paul
misérable et indigne de lui.
Il lui arrivait pourtant, malgré sa volonté, de formuler un blâme à
propos de telle attitude qu’elle avait prise, de telle phrase qu’elle
avait prononcée. De son côté elle répondait le plus patiemment
qu’elle pouvait, rusant, se dérobant, pour s’insinuer de nouveau, peu
à peu, si c’était possible, dans ce cœur armé contre elle. Mais ses
moindres feintes, il les suivait, il les dénonçait d’une parole. Ainsi elle
pouvait juger de la perspicacité de son adversaire, et elle
commençait à craindre de ne plus jamais la trouver en défaut.
Elle ne pouvait plus, d’ailleurs, cacher si bien son âme vraie
qu’elle n’en trahît çà et là quelque chose. Souvent, après des
prodiges d’adresse, elle finissait par laisser échapper un mot de trop,
un mot malheureux, une phrase qui sonnait faux comme son rire, et
qui rendait au comte Paul toute la fermeté de ses résolutions.
Un jour, par exemple, qu’elle lui parlait de sa douleur, de son
désespoir profond :
— Cela ne vous a point empêchée, lui dit-il, de danser hier soir, à
ce bal, où vingt hommes vous entouraient, vous accablaient de
compliments indécents, dont vous avez ri !
Elle répondit ingénument :
— Faut-il donc ne plus aller au bal sous prétexte qu’on est
désespérée ?
En des mots semblables, qui partaient tout à coup, —
inexplicablement, car elle avait une intelligence aiguë, — il
entrevoyait des abîmes d’inconscience.
Une autre fois, sous un trait d’ironie poignante qu’il lui lança, elle
ne put retenir des larmes de rage. Elle voulut profiter de ces larmes
pour l’attendrir, pour faire appel une fois encore à sa pitié. Il
l’interrompit sèchement :
 — Vous ne me séduirez plus, pas plus avec vos pleurs
d’aujourd’hui, qu’avec vos sourires d’autrefois. Les uns valent les
autres. Tout cela, c’est la même chose. Tout cela — ment toujours !
Alors, elle s’écria parmi les sanglots, en secouant entre ses deux
mains sa tête échevelée :
— Mais comment faut-il donc pleurer ?
C’étaient ses façons à elle d’être naïve.
 VI

Quatre mois s’étaient écoulés. Le comte Paul avait pu cacher à

tous ceux qui l’aimaient, le malheur de sa vie, quand sa mère
annonça l’intention de venir le rejoindre à Paris.
On était en janvier. Le plus dur de l’hiver était passé. Annette, là-
bas aux Bormettes, ne tenait plus en place. Elle voulait revoir son
frère, sa jolie belle-sœur, ses amies. La comtesse d’Aiguebelle
cédait aux instances de sa fille, « car pour moi, écrivait-elle, pour
moi, mes chers enfants, j’ai peur avant tout de déranger votre
bonheur. Mais l’hôtel est vaste. Nous resterons dans notre coin,
Annette et moi. Nous nous ferons très petites et très silencieuses,
vous verrez ! »
La chère femme ajoutait que, toujours plus vieille, elle sentait
s’aggraver sa maladie de cœur, et qu’elle obéissait aussi à un désir
impérieux de ne pas mourir sans avoir revu son Paul…, « et même
Paris », répétait-elle gaiement. — C’était rendre impossible à Paul
toute idée nouvelle de voyage.
Il prévint sa femme de l’arrivée prochaine de sa mère. — « Le
plus difficile commence, lui dit-il. Je ne peux vraiment pas m’opposer
à son projet. Je prévois que ma mère fera un séjour de trois mois au
plus. Vers le premier mai, elle repartira pour notre pays de Provence.
Si je le jugeais absolument nécessaire d’ailleurs, nous quitterions
brusquement Paris, vous et moi. Plutôt que laisser croire à ma mère
que je la néglige, mieux vaudrait lui avouer la vérité !… Si nous
étions dans la nécessité de partir, nous irions voir l’Algérie, car vous
êtes une personne pleine de caprices et moi un mari très obéissant.
Mais tâchons de ne pas en arriver à cette extrémité. Ces départs,
s’ils se renouvelaient, donneraient l’éveil. Apprêtez-vous donc à
jouer pour le mieux votre rôle de femme heureuse et, en même
temps, soucieuse du bonheur de toute sa famille… Il faudra, le soir,
nous faire beaucoup de musique. Vous chantez à ravir ; et, quand
vous chantez, vous ressemblez à sainte Cécile. Il faudra nous
charmer… comme avant. Vous nous lirez aussi de beaux vers, de
belle prose…
L’amertume lui venait, en faisant le tableau de ces soirées de
famille, en ordonnant ce simulacre de vie heureuse.
Il ajouta donc :
— Ce sera délicieux, n’est-ce pas ?
Elle éleva vers lui un regard suppliant. Elle eut dans les yeux une
prière vraie. Il venait de lui dépeindre un paradis perdu. Elle venait
de concevoir, à l’entendre, tout ce qu’elle ne connaîtrait jamais, — et
de le désirer.
Ils se regardaient. Il la trouva belle. Une chaude émotion lui
gonfla la poitrine, — et il pensa que peut-être elle avait assez
expié… Expié, quoi ? Ah ! oui, — ce mensonge !… Il s’aperçut que
s’il n’avait plus pour elle la tendresse qu’on a pour l’épouse, pour les
mères, pour les femmes faibles, pures, désarmées, il avait encore
pour cette violente, pour cette rusée, — ce qu’on appelle de l’amour,
afin sans doute de rester poli.
Il désira le plaisir âpre, mauvais, mortel peut-être, qu’il
éprouverait à l’avoir à lui comme une conquête, en maître absolu,
tout en la maintenant dans l’impuissance de nuire.
Tout ce trouble, elle l’aperçut très bien dans ses yeux, mais, une
fois encore, elle se perdit avec une parole, avec un geste.
Elle tendit les bras et cria :
— Je ne suis pas celle que vous croyez ! Sur les cendres de ma
mère, Paul, je vous le jure !
Le geste était théâtral. Et quant « aux cendres de la mère », oh
cela ! c’était le comble du banal à la fois et de l’inouï !
Elles jurent toutes, les femmes menteuses, avec une facilité
surprenante, sur la tête de leur nourrisson ou sur les cendres d’un
pauvre mort qui ne proteste jamais.
 Les sincères n’ont pas besoin de s’appuyer si fortement et si vite
sur des témoins muets, ni même sur d’autres. Ils imaginent
fièrement que leur parole suffit.
Le comte se rappela que, sur cette remarque générale faite un
jour par lui, Albert lui avait conté un authentique et bien curieux
souvenir de voyage.
A Smyrne, où il était allé avec l’escadre, il se trouva admis dans
la familiarité d’une veuve mûre et de sa jeune fille, qui gardaient
chez elles, selon l’usage du pays, les ossements du mari, du père,
— non pas tous, mais quelques restes, — précieusement recueillis
dans une urne.
Une querelle, très orientale, c’est-à-dire tout de suite exaspérée
et criarde, s’étant élevée entre la fille et la mère, celle-ci jura ses
grands dieux, la main étendue au-dessus de l’urne sacrée, que,
dans cette discussion dont le sujet importe peu, elle disait la vérité,
rien que la vérité, toute la vérité.
La fille résistant à cette preuve suprême, la mère était entrée
dans une violente colère, et s’excitant toujours davantage, affolée
par les insolences de sa délicieuse enfant, elle lui lança à la tête,
tout d’un coup, l’urne elle-même, qui dans sa chute s’ouvrit,
répandant tout ce qu’elle contenait !
— Oh ! ma mère ! les os sacrés de mon père ! — cria, — en grec
bien entendu, — la jeune smyrniote indignée.
Et la mère de répliquer, sans reprendre haleine :
— Si encore c’était ton père, petite sotte !
A peine Rita eut-elle prononcé : « sur les cendres de ma mère »,
que ce souvenir revint positivement à la mémoire du comte Paul, et
un sourire plissa ses lèvres tristes.
« Paul ! Paul ! » répéta Marie, prête à se jeter à ses genoux, car
elle aimait ces manifestations suprêmes. Sans s’en douter, elle les
copiait du théâtre. Il vit ce mouvement à peine indiqué ; il l’arrêta
court, en répondant à sa prière muette par ce mot qui tomba en coup
de hache : « Jamais ! »