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Preface to the Second Edition
Since the publication of the first edition of this book in
1997, we have been gratified by the overwhelmingly posi-
tive reception it has received from physicians, both in train-
ing and in practice. The goal of the first edition was to create
a textbook that integrated electrodiagnostic studies and
neuromuscular disorders in a practical and concise manner,
always remembering the important principle that nerve con-
duction studies and electromyography (EMG) are an exten-
sion of the clinical examination. As this text is intended to
convey basic and essential information, the question arises,
“why do a second edition?” The authors acknowledge that
no new muscles have been discovered in the human body
over the past six years. Likewise, PCR and genetic tests
have failed to identify any new nerves. Although much of
the basic information in the fields of electrodiagnostic stud-
ies and neuromuscular disorders has not changed, we have
written this second edition to improve and expand on many
topics.
First and most important, needle electromyography
relies upon the proper interpretation of waveforms in real-­
time. While one can read about waveforms until they are
blue in the face, it is very difficult to appreciate the audio
and visual qualities of a waveform unless one can see and
hear it. For the last fifteen years, we have collected video
examples of classic EMG waveforms from a variety of
patients. Two years after the publication of the first edi-
tion of this book, we introduced a companion videotape of
common EMG waveforms. With new digital technology, we
have now been able to digitize these video waveforms and
put them on a companion CD which accompanies this book.
Thus, in this second edition, the reader can view the CD on
any computer, and watch and hear every common and clas-
sic EMG waveform. Because all the waveforms are digital,
the reader can freeze or replay any waveform at any time.
The textbook description and discussion of each waveform
are now greatly enhanced by the companion CD.
Since the publication of the first edition there have been
significant advances in some neuromuscular conditions, and
these are included in the second edition. Some new disor-
ders have been described, among them paralytic poliomyeli-
tis caused by the West Nile virus. In addition, several new
techniques that have been described and validated in the
electrodiagnosis of neuromuscular conditions are included
in this second edition of the book. For instance, the elec-
trodiagnosis of ulnar neuropathy at Guyon’s canal has sig-
nificantly improved over the past few years, and several
new techniques that are useful in making this diagnosis are
included in this second edition.
We spent a considerable amount of time thinking of bet-
ter ways to present complex material in a logical and concise
manner for this second edition of the book. Being strong
believers in “a picture is worth a thousand words,” we have
added many new figures, and others have been updated.
xv
Indeed, we have added or updated more than 175 figures to
the first edition of the book.
We have improved the book in several other ways. First,
we have expanded many of the clinical chapters, and in
some cases separated them into new chapters, including
median neuropathy at the wrist, proximal median neuropa-
thy, ulnar neuropathy at the wrist, ulnar neuropathy at the
elbow, amyotrophic lateral sclerosis, and atypical motor
neuron disorders. All of the clinical chapters follow the
same format that was used in the first edition, first pre-
senting the important anatomic and clinical aspects of the
disorder, followed by a discussion of the relevant electro-
diagnostic studies. Each chapter ends with example cases
based on actual patients, illustrating many important clinical
and electrodiagnostic teaching points. In addition, in section
three we have added a new chapter on basic statistics for
electrodiagnostic studies, discussing several basic statistical
concepts that every electromyographer needs to know in
order to properly interpret a study.
The first edition was divided into six separate sections.
This new edition has been expanded to eight. The first new
section deals with EMG in Special Clinical Settings, includ-
ing the approach to electrodiagnostic studies in the inten-
sive care unit, and the approach to electrodiagnostic studies
in the pediatric patient. In the last several years, electro-
myographers are called upon more frequently to perform
EMG studies in the intensive care unit to evaluate patients
with profound weakness. New clinical disorders and elec-
trodiagnostic techniques to evaluate these disorders have
been extensively reported over the last several years and are
reflected in this new edition. We have included a discussion
of pediatric EMG because of its own unique set of chal-
lenges and techniques that differ from adult studies.
The other new section deals with the basics of elec-
tricity and electronics, in addition to the potential risks
and complications of electrodiagnostic studies. Some
knowledge of electricity and electronics is extremely
helpful in understanding electrodiagnostic studies. From
a practical point of view, this knowledge is also very help-
ful in understanding and correcting many of the technical
problems that arise in the everyday practice of electrodi-
agnostic medicine. The latter chapter arose from a con-
tinuing medical education course which we were asked to
give at an annual meeting of the American Association of
Electrodiagnostic Medicine, which was followed up as a
review article in the journal Muscle and Nerve. Although
nerve conduction studies and EMG are usually well toler-
ated and in most patients have minimal side effects, there
are potential risks and complications, especially in certain
patient populations. It is essential that all physicians per-
forming these studies are aware of these potential risks and
complications, albeit rare, and follow simple protocols to
minimize them.
xvi Preface to the Second Edition
Like the first edition, this text is meant to provide a
single resource for those physicians training in or practicing
electrodiagnostic studies. From our perspective of teaching
for many years, both on a post-­graduate and residency level,
we feel that if one can master the fundamentals in this book,
one should have all the basic concepts and information one
needs to competently understand and interpret electro-
diagnostic studies. Although a great deal of information is
presented regarding the performance of studies, there is no
substitute for hands-­on experience under supervision. How-
ever, it is our hope that with the companion CD as part of
the textbook, the recognition and interpretation of EMG
waveforms will be easier to master.
Finally, the goal of this text is to present material in an
easily understandable and logical manner. The authors have
often commented to their students that with knowledge of
anatomy, physiology, and neurologic localization, the prac-
tice of electrodiagnostic studies makes sense. We hope that
with the information contained in this text, one can sit down
with a patient, take a history, perform a physical examina-
tion, and use the appropriate electrodiagnostic studies to
reach a diagnosis.
DCP
BES

Preface to the First Edition
This text is written primarily for clinicians who perform
and interpret nerve conduction studies and electromyogra-
phy (EMG), as well as for physicians who use the results
of these electrodiagnostic studies to evaluate patients with
peripheral nervous system disorders. Nerve conduction
studies and EMG are best considered an extension of the
clinical examination. Indeed, these studies cannot be prop-
erly planned, performed, or interpreted without knowing
the patient’s symptoms and findings on the clinical exami-
nation. Numerous nerves and literally hundreds of muscles
can be studied. To study them all would be neither practical
for the electromyographer, nor desirable for the patient. In
every case, the study must be individually planned, based
on the clinical differential diagnosis, and then modified as
the study progresses and further information is gained. The
electromyographer needs to perform the studies necessary
to both confirm and exclude certain diagnoses while mini-
mizing the amount of patient discomfort. Most often, nerve
conduction studies and EMG can successfully localize the
lesion, provide further information about the underlying
pathophysiology, and assist in assessing the disorder’s sever-
ity and temporal course.
Although there are many excellent textbooks on electro-
diagnosis and several superb references on clinical neuro-
muscular disorders, few integrate the two in a practical and
concise manner. The approach we take in this text parallels
our teaching program developed for the EMG fellowships
and neurology residencies at the Brigham and Women’s
Hospital and the Massachusetts General Hospital in Boston.
The book is divided into six fundamental sections. Sec-
tion One covers the overall practical approach to a patient
in the EMG laboratory, followed by a review of the basic
anatomy and neurophysiology that every electromyogra-
pher needs to understand. Section Two discusses the fun-
damentals of nerve conductions, including motor, sensory,
and mixed nerve studies, as well as late responses, blink
xvii
reflexes, and repetitive nerve stimulation studies. In Sec-
tion Three, important technical factors and artifacts are
discussed, including the anomalous innervations. Sec-
tion Four discusses the practical details of performing the
most commonly used nerve conduction studies. In Section
Five, the focus changes to needle EMG. After discussing
the overall approach to the needle EMG, the anatomy of
the bulbar, upper extremity, and lower extremity muscles
is reviewed in detail. The last two chapters in this section
cover the approach to the needle EMG examination, includ-
ing the assessment of spontaneous activity and the analysis
of motor unit action potentials.
Section Six, Clinical–Electrophysiologic Correlations,
forms the core of the text. After an overview of the impor-
tant patterns, all of the major peripheral nervous system
conditions are discussed, from both the clinical and the
electrophysiologic points of view. Included are the mono-
neuropathies, polyneuropathies, motor neuron diseases,
radiculopathies, plexopathies, disorders of the neuromus-
cular junction and muscle, and the myotonic and periodic
paralysis disorders. At all times, the text integrates the
important basic clinical and electrophysiologic points. In
Chapters 16–32, clinical cases and their respective nerve
conduction and EMG data are presented. Each case exam-
ple is that of an actual patient taken from our EMG teaching
file during the past 10 years.
The authors appreciate that some specific techniques
and normal values may vary from laboratory to laboratory.
Nevertheless, the goal of this book is to present a logical
approach in the EMG laboratory that combines the clinical
and electrophysiologic evaluations of a patient with a disor-
der of the peripheral nervous system.
DCP
BES
 xix

Dedication

To our daughters, Hannah and Abigail.


The authors are indebted to their mentors in clinical neuro-
physiology: Drs. John J. Kelly, Jr., Eric L. Logigian, and Bhag-
wan T. Shahani. Dr. Bashar Katirji, our friend and colleague
for more than 20 years, has been an inspiration and a great
partner in teaching, research, and patient care in clinical neu-
romuscular disorders and electrophysiology. In addition, the
authors wish to thank their colleagues, technologists, and
present and former Neuromuscular and EMG fellows at the
University Hospitals Cleveland Medical Center, the Brigham
and Women’s Hospital, and the Massachusetts General Hos-
pital. The contributions of Dale Preston, Thayer Preston,
and Richard (Zack) Zydek to the photography are greatly
appreciated. A special thanks to our friend, colleague, and
mentor, Dr. Martin A. Samuels, who was instrumental in
xxi
Acknowledgments
the early parts of our academic and publishing careers. Then
there are a host of individuals whose books, presentations,
courses, and research ignited our passion in neuromuscular
ultrasound. Among them are Drs. Francis O. Walker, Michael
S. Cartwright, Lisa D. Hobson-­Webb, Jeff Strakowski, Lucia
Padua, Stefano Bianchi, Carlo Martinoli, Andrea J. Boon,
Leo Visser, Craig M. Zaidman, Antonios Kerasnoudis, H.
Stephan Goedee, James B. Caress, and Joon Shik Yoon. At
Elsevier, Melanie Tucker, Lisa Barnes, and Doug Turner were
instrumental in bringing the fourth edition into print and
electronic forms. And of course we will always be grateful
to our dear friend, Susan Pioli, who has been there since the
inception of this book and was instrumental in bringing the
first and second editions to publication.
 SECTION I • Overview of Nerve Conduction Studies and Electromyography
Approach to Nerve Conduction
Studies, Electromyography, and
Neuromuscular Ultrasound
Electrodiagnostic (EDX) studies play a key role in the eval-
uation of patients with neuromuscular disorders. In selected
cases, the additional use of neuromuscular ultrasound (U/S)
can add key complementary anatomical and diagnostic
information.
EDX studies include nerve conduction studies (NCSs),
repetitive nerve stimulation, late responses, blink reflexes,
and needle electromyography (EMG), in addition to a vari-
ety of other specialized examinations. NCSs and needle
EMG form the core of the EDX study. They are performed
first and usually yield the greatest diagnostic information.
NCSs and needle EMG are complementary and, therefore,
are always performed together and in the same setting.
Performed and interpreted correctly, EDX studies yield
critical information about the underlying neuromuscular
disorder and allow other laboratory and diagnostic tests,
including neuromuscular U/S, to be used in an appropriate
and efficient manner. Sometimes, the information gained
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
studies, most often has a potentially treatable condition.
Indeed, the value of EDX studies has been validated in
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-
cal examination and should always be considered as such.
Accordingly, a directed neurologic examination should always
be performed before EDX studies to identify key clinical
abnormalities and establish a differential diagnosis. With
numerous nerves and literally hundreds of muscles available,
it is neither desirable for the patient nor practical for the elec-
tromyographer to study them all. In each case, the study must
be individualized, based on the neurologic examination and
differential diagnosis, and modified in real time as the study
progresses and further information is gained.
NCSs and EMG are most often used to diagnose disor-
ders of the peripheral nervous system (Fig. 1.1, Box 1.1).
These include disorders affecting the primary motor neu-
rons (anterior horn cells), primary sensory neurons (dorsal
root ganglia), nerve roots, brachial and lumbosacral plexuses,
1
peripheral nerves, neuromuscular junctions (NMJs), and
muscles. In addition, these studies may provide useful diag-
nostic information when the disorder arises in the central
nervous system (CNS) (e.g., tremor or upper motor neu-
ron weakness). Occasionally, information from the EDX
study is so specific that it suggests a precise etiology. In
most cases, however, the exact etiology cannot be defined
based on EDX studies alone. It is in some of these cases that
neuromuscular U/S is most useful. Neuromuscular U/S,
the use of U/S to study the peripheral nerves and muscles,
is often able to suggest the precise etiology of the disease,
such as chronic inflammatory demyelinating polyneuropa-
thy (CIDP) when a particular pattern of nerve enlargement
is seen or inclusion body myositis when a particular pattern
of muscle involvement is present. EDX studies provide an
initial aid in defining the disorder, giving several key pieces
of information, which in some cases can be further refined
with neuromuscular U/S.
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Fig. 1.1 Elements of the peripheral nervous system. Note that the
primary motor neuron resides within the spinal cord, whereas the
primary sensory neuron, the dorsal root ganglion, lies outside the
spinal cord. The dorsal root ganglion is a bipolar cell. Its proximal
process forms the sensory nerve root; the distal process becomes the
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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 Chapter 1 • Approach to Nerve Conduction Studies, Electromyography, and Neuromuscular Ultrasound 3
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imaging (MRI) scan of the cervical spine to assess a pos-
sible cervical radiculopathy because the EDX studies dem-
onstrated an ulnar neuropathy at the elbow as the source
of the patient’s symptoms. This is a situation where neuro-
muscular U/S may be particularly useful, able to precisely
localize the lesion and help assess for anatomic etiologies.
In a patient with a CNS disorder who is mistaken as hav-
ing a peripheral disorder, the EDX study often correctly sug-
gests that the localization is central. For example, transverse
myelitis may mimic Guillain-­Barré syndrome, or a small
acute cortical stroke may occasionally mimic the pattern of
a brachial plexopathy or mononeuropathy. In settings such
as these, the EDX study is often the first test to suggest that
the correct localization is central rather than peripheral.
Neuropathic Localization
Neuropathic is probably the most common localization made
on EDX studies. Neuropathic literally means a disorder of
the peripheral nerves. However, in common usage, it includes
the primary sensory and motor neurons as well. EDX stud-
ies are particularly helpful in neuropathic conditions. First, in
conjunction with the history and examination, they can usu-
ally further localize the disorder to the neurons, roots, plexus,
or peripheral nerve. In the case of peripheral nerves, further
localization is usually possible to a single nerve (mononeu-
ropathy), multiple individual nerves (mononeuropathy mul-
tiplex), or all nerves (polyneuropathy). In the case of a single
nerve, the exact segment of nerve responsible for the prob-
lem may be localized in some cases.
In the case of neuropathic lesions, EDX studies often
yield further key information, including the fiber types
involved, the underlying pathophysiology, and the temporal
course of the disorder (Fig. 1.3).
Information About the Fiber Types Involved and the
Underlying Nerve Pathophysiology can be Gained,
Which Then Further Narrows the Differential Diagnosis
In the case of neuropathic disorders, the involved fiber types
and the underlying pathology can usually be determined. First,
EDX studies are more sensitive than the clinical examination
in determining which fiber types are involved: motor, sen-
sory, or a combination of the two. Sensorimotor polyneurop-
athies are common and suggest a large differential diagnosis.
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Fig. 1.3 Key electrodiagnostic findings in a neuro-
&KURQLF pathic localization.
Conversely, predominantly motor or predominantly sensory
neuropathies are rare and suggest a much more limited set of
disorders. For instance, a patient with numbness in the hands
and feet and diminished reflexes may be diagnosed with a
peripheral neuropathy. However, if EDX studies demon-
strate abnormal sensory nerve conductions with completely
normal motor nerve conductions and needle EMG, then the
differential diagnosis changes from a peripheral neuropathy
to a pure sensory neuropathy or neuronopathy, which has a
much more limited differential diagnosis.
Second, EDX studies often can define whether the
underlying pathophysiology is demyelination or axonal loss.
Although most demyelinating neuropathies have some sec-
ondary axonal loss and many axonal loss neuropathies have
some secondary demyelination, EDX studies usually can
differentiate between a primary demyelinating and a pri-
mary axonal neuropathy. Because EDX studies usually can
make this differentiation quickly and noninvasively, nerve
biopsy is essentially never required to make this determi-
nation. Furthermore, the differentiation between primary
axonal and primary demyelinating pathology is of consid-
erable diagnostic and prognostic importance, especially in
the case of polyneuropathies. Most polyneuropathies are
associated with primary axonal degeneration, which has an
extensive differential diagnosis. In contrast, the number
of true electrophysiologic primary demyelinating neuropa-
thies is extremely small. They are generally subdivided into
those that are inherited and those that are acquired (e.g.,
Charcot Marie Tooth [CMT] vs. CIDP). EDX studies can
typically make that determination as well. The finding of
an unequivocal primary demyelinating polyneuropathy on
EDX studies often leads quickly to the correct diagnosis
and, in the case of an acquired demyelinating polyneuropa-
thy, often suggests a potentially treatable disorder.
Assessing the Degree of Axonal Loss Versus
Demyelination has Implications for Severity and
Prognosis
A nerve that has sustained a demyelinating injury often can
remyelinate in a very short time, usually weeks. However, if
there has been substantial axonal loss, whether primary or
secondary, the prognosis is much more guarded. The rate of
axonal regrowth is limited by the rate of slow axonal trans-
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
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similarly placed lesion that is predominantly demyelinating
in nature. EDX studies can readily differentiate axonal loss &UDQLREXOEDU
from demyelinating lesions.
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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.
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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,
myasthenia gravis preferentially affects oculobulbar muscles
and then proximal muscles on EDX studies, whereas myas-
thenic syndrome is a generalized disorder on EDX studies,
although clinically it has a predilection for proximal muscles.
Broadly speaking, the underlying pathology can be
divided into presynaptic and postsynaptic disorders. EDX
studies are usually very good at making this determination.
Myasthenia gravis is the prototypic postsynaptic disorder,
whereas myasthenic syndrome and botulism target the pre-
synaptic junction.
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
disorders. In some of these, there may be unique findings on
EDX testing that suggest one of these rare disorders.
PATIENT ENCOUNTER
Every EDX study begins with a brief history and directed
physical examination (Box 1.2). This point cannot be overem-
phasized! Some may (incorrectly) argue that the history and
clinical examinations are not part of the EDX examination and
that the EDX study needs to stand on its own. Nothing could
be further from the truth. One is not expected to perform the
same detailed history and physical examination that is done in
the office consultation setting. However, before starting every
study, the EDX physician must know some basic facts:
• What are the patient’s symptoms?
• How long have they been going on?
• Is there any important past medical history (e.g., diabe-
tes, history of chemotherapy, etc.)?
• Is there muscle atrophy?
• What is the muscle tone (normal, decreased, or in-
creased)?
• Is there weakness, and, if so, where is it and how severe
is it?
• What do the reflexes show (normal, decreased, or
increased)?
• Is there any loss of sensation, and, if so, what is the dis-
tribution; what modalities are disturbed (e.g., tempera-
ture, pain, vibration, etc.)?
  
The duration, type, and distribution of symptoms, along
with the physical examination, help determine the differen-
tial diagnosis, which in turn is used to plan the EDX stud-
ies. The EDX study is planned only after the differential
diagnosis is determined. For instance, the EDX evaluation
of a patient with slowly progressive proximal weakness is
very different from that of a patient with numbness and
tingling of the fourth and fifth fingers. In the former case,
the differential diagnosis includes disorders of the anterior
horn cell, motor nerve, NMJ, or muscle. In the latter case,
the differential diagnosis includes an ulnar neuropathy at its
various entrapment sites, a lower brachial plexus lesion, or
cervical radiculopathy. The EDX plan includes which nerves
and muscles to study and whether specialized tests, such as
repetitive nerve stimulation, may be helpful. The study can
Box 1.2 Patient Encounter
1. Take a brief history and perform a directed physical
examination.
2. Formulate a differential diagnosis.
3. Formulate a study based on the differential diagnosis.
4. Explain the test to the patient.
5. Perform the nerve conduction studies and modify which
nerve conduction studies to add, based on the findings as
the test proceeds.
6. Perform the needle electromyography study and modify
which additional muscles to sample, based on the findings
as the test proceeds.
always be amended as the testing proceeds. Before begin-
ning, however, one should first explain to the patient in
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-
tions, both before the test begins and while it is ongoing, can
greatly reduce a patient’s anxiety.
After the test is explained to the patient, the NCSs are
performed first, followed by the needle EMG. Indeed, one
needs the findings on the NCSs to adapt the needle EMG
strategy accordingly and to interpret the needle EMG find-
ings correctly. For instance, active denervation in the abduc-
tor digiti minimi (an ulnar, C8–T1 innervated muscle) has a
completely different interpretation depending on whether
the ulnar motor and sensory NCSs are abnormal or not
(ulnar neuropathy in the former, a radiculopathy or motor
neuron disease in the latter).
A proper balance must be maintained among obtain-
ing a thorough study, collecting the necessary information
to answer the clinical question, and minimizing patient dis-
comfort. If performed correctly, nearly all NCSs and needle
EMG can be completed within 1–1.5 hours. Rarely, a longer
study is needed if specialized tests such as repetitive nerve
stimulation are performed in addition to the standard stud-
ies. There clearly is a limit to what most patients can tolerate.
The electromyographer should always remember the Willy
Sutton rule concerning robbing banks: “Go where the money
is.” If there is any question as to whether a patient will toler-
ate the entire examination, the study should begin with the
area of interest. For instance, in the patient with numbness
and tingling of the fourth and fifth fingers, ulnar motor and
sensory studies should be done first. Likewise, needle EMG
examination of the ulnar-­innervated muscles, as well as the
C8–T1 non-­ulnar–innervated muscles, are of most interest
in such a patient. Plan and consider which NCSs and needle
examination of which muscles should be performed first, in
case the patient can tolerate only one or two nerve conduc-
tions or examination of only a few muscles by EMG.
CARDINAL RULES OF NERVE
CONDUCTION STUDIES AND
ELECTROMYOGRAPHY
EDX studies rely on the physician’s ability to pay meticu-
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
and electromyography. EDX, Electrodiagnostic; EMG,
electromyography; NCS, nerve conduction study.
keeping in mind the bigger picture of why the study is being
performed. As more data are obtained, the study must be
analyzed in real time and the test altered as needed. Analy-
sis of online results gives the electromyographer the oppor-
tunity to modify the strategy as the testing proceeds, an
opportunity that is lost once the patient has left the labo-
ratory. The following cardinal rules of EDX studies should
always be kept in mind while an EDX study is being per-
formed (Fig. 1.6):
1. NCSs and EMG are an extension of the clinical
examination. NCSs and EMG cannot be performed
without a good directed clinical examination. Every
examination must be individualized based on the
patient’s symptoms and signs and the resulting
differential diagnosis. If marked abnormalities are found
on electrophysiologic testing in the same distribution
where the clinical examination is normal, either the
clinical examination or the electrophysiologic testing
must be called into question. One usually finds that
the better the clinical examination, the better the
differential diagnosis, and thus, the more clearly
directed the EDX studies will be.
2. When in doubt, always think about technical factors.
EDX studies rely upon collecting and amplifying
very small bioelectric signals in the millivolt and
microvolt range. Accomplishing this is technically
demanding; many physiologic and nonphysiologic
factors can significantly interfere with the accuracy
of the data. Accurate NCSs and EMG depend on
intact equipment (e.g., EMG machine, electrodes,
and stimulator), and on correct performance of the
study by the electromyographer. Technical problems
can easily lead to absent or abnormal findings. Failure
to recognize technical factors that influence the EDX
study can result in type I errors (i.e., diagnosing an
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abnormality when none is present) and type II errors
(i.e., failing to recognize an abnormality when one is
present). Although both are important, type I errors
are potentially more serious (e.g., the patient is labeled
with an abnormal EDX study result, such as neuropathy,
when the “abnormality” on the EDX testing is simply
due to unrecognized technical errors). Such faulty
diagnoses can lead to further inappropriate testing
and treatment. If there is an unexpected abnormal
EDX finding that does not fit the clinical examination,
the lack of a clinical-­electrophysiologic correlation
should suggest a technical problem. For instance, if a
routine sural nerve sensory conduction study shows an
absent potential but the patient has a normal sensory
examination of the lateral foot (i.e., sural territory),
one should suspect a technical problem (e.g., improper
electrode or stimulator placement or too low of a
stimulus intensity). If the data are not technically
accurate, then correct data interpretation can never
occur, either at the time of the study or later by the
treating physician.
3. When in doubt, reexamine the patient. This is essentially
an extension of cardinal rule number 1. In the example
given with rule number 2, if the sural sensory response
is absent after all possible technical factors have been
corrected, the clinician should reexamine the patient.
If the patient has clear loss of vibration at the ankles,
there is less concern about an absent sural sensory
response. If the patient’s sensory examination is normal
on reexamination, the absent sensory response does not
fit the clinical findings, and technical factors should be
investigated further.
4. EDX findings should be reported in the context of
the clinical symptoms and the referring diagnosis. In
every study, electrophysiologic abnormalities must be
correlated with the clinical deficit.
 Chapter 1 • Approach to Nerve Conduction Studies, Electromyography, and Neuromuscular Ultrasound 7
Because electrophysiologic studies are quite sensitive, it
is not uncommon for the electromyographer to discover
mild, subclinical deficits of which the patient may not
be aware. For example, a diabetic patient referred to
the EMG laboratory for polyneuropathy may show
electrophysiologic evidence of a superimposed ulnar
neuropathy but have no symptoms of such. Accordingly,
the electromyographer should always report any
electrophysiologic abnormality in the context of its
clinical relevance so that it can be properly interpreted.
5. When in doubt, do not overcall a diagnosis. Because
electrophysiologic tests are very sensitive, mild,
subclinical, and sometimes clinically insignificant
findings often appear on EDX testing. This occurs
partly because of the wide range of normal values,
which vary with the nerve and muscle being tested.
In addition, there are a variety of physiologic and
nonphysiologic factors that may alter the results of both
NCSs and EMG, despite attempts to control for them.
These factors, often when combined, may create minor
abnormalities. Such minor abnormalities should not
be deemed relevant unless they correlate with other
electrophysiologic findings and, most importantly, with
the clinical history and examination. It is a mistake to
overcall an electrophysiologic diagnosis based on minor
abnormalities or on findings that do not fit together
well. Sometimes, the clinical or electrophysiologic
diagnosis is not clear-­cut and a definite diagnosis
cannot be reached. Occasionally, NCSs and EMG are
clearly and definitely abnormal, but a precise diagnosis
still cannot be determined. For example, consider
the patient whose clinical history and examination
suggest an ulnar neuropathy at the elbow. The EDX
study often demonstrates abnormalities of the ulnar
nerve in the absence of any localizing findings, such as
conduction block or slowing across the elbow. Although
the referring surgeon usually wants to know whether
the ulnar neuropathy is at the elbow, often, the only
accurate impression that the electromyographer can
give is one of a non-­localizable ulnar neuropathy that is
at, or proximal to, the most proximal abnormal ulnar-­
innervated muscle found on EMG.
6. Always think about the clinical-­electrophysiologic
correlation. This rule combines all of the earlier rules.
One usually can be certain of a diagnosis when the
clinical findings, NCSs, and EMG abnormalities all
correlate well. Consider again the example of the
patient with weakness of the hand and tingling and
numbness of the fourth and fifth fingers. If NCSs
demonstrate abnormal ulnar motor and sensory
potentials associated with slowing across the elbow,
and the needle EMG shows denervation and reduced
numbers of motor unit potentials in all ulnar-­
innervated muscles and a normal EMG of all non-­
ulnar–innervated muscles, there is a high degree of
certainty that the patient truly has an ulnar neuropathy
at the elbow, and the electrophysiologic abnormalities
are indeed relevant.
If all three results fit together, the diagnosis is secure.
However, if the NCSs and EMG findings do not fit together
and, more importantly, if they do not correlate with the
clinical findings, the significance of any electrical abnormali-
ties should be seriously questioned. Consider a patient with
pain in the arm who has an otherwise normal history and
examination. If the NCSs are normal except for a low ulnar
sensory potential and the EMG demonstrates only mild rein-
nervation of the biceps, one should be reluctant to interpret
the study as showing a combination of an ulnar neuropathy
and a C5 radiculopathy. These mild abnormalities, which
are not substantiated by other electrophysiologic findings
and do not have clear clinical correlates, may have little to
do with the patient’s pain. In such a case, the patient should
be reexamined. If no clinical correlate is found, the studies
should be rechecked. If the abnormalities persist, they may
be noted as part of the impression but interpreted as being
of uncertain clinical significance.
When performed properly, NCSs and EMG can be very
helpful to the referring physician. However, the limitations
of EDX studies must be appreciated, technical factors well
controlled, and a good differential diagnosis established
before each study. Otherwise, the study may actually do a
disservice to the patient and to the referring physician by
leading them astray by way of minor, irrelevant, or techni-
cally induced “abnormalities.” If the cardinal rules of NCSs
and EMG are kept in mind, EDX studies are far more likely
to be of help to the referring clinician and the patient with
a neuromuscular disorder.
NEUROMUSCULAR ULTRASOUND
Over the last several years, neuromuscular U/S has increas-
ingly been used along with EDX studies in the evaluation
of patients with various neuromuscular conditions. The use
of neuromuscular U/S has grown due to a combination of
several factors, including the marked improvement of the
resolution and software of U/S machines while the physi-
cal size and cost of the machines have gone down. These
smaller, portable machines can easily be used and shared
among EDX laboratory rooms. Indeed, some manufacturers
are working on combined EDX and U/S machines housed in
one unit. Hundreds of peer-­reviewed articles on the useful-
ness of neuromuscular U/S are published each year. Thus,
neuromuscular U/S has become a validated, reliable, and
important tool in the evaluation of many neuromuscular
disorders.
Physicians who perform EDX studies are best suited to
learn and perform neuromuscular U/S, which is the study
of peripheral nerves and muscles. Neuromuscular U/S dif-
fers from vascular U/S and musculoskeletal U/S, although
there is some overlap. It is essential to emphasize that neuro-
muscular U/S is complementary to EDX studies; it does not
replace EDX studies. The situation is similar to the role that
EDX studies and MRI have in the evaluation of radiculopa-
thy. EDX studies are physiologic tests and, as such, yield
information about the function of the nerves, nerve roots,
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-
tion on the functioning. Thus, for example, whereas EDX
studies give information about how well the nerve root is
functioning, an MRI can show the nerve roots and whether
they appear impinged by a disk, spondylosis, or other struc-
tural causes. Likewise, whereas EDX studies may be able
to identify an ulnar neuropathy at the elbow, they cannot
discern what is causing it. This is where neuromuscular U/S
may add critical complementary information to the EDX
studies. For example, it may reveal bony spurs and excess
callus in the ulnar groove from tardy ulnar palsy, compres-
sion of the ulnar nerve in the true cubital tunnel under
the humeral-­ulnar aponeurosis, or in some cases a synovial
cyst compressing the ulnar nerve, among many possible
etiologies.
Best used, neuromuscular U/S serves as an extension of
the clinical examination and most often of the EDX studies,
and should be used as such. Chapters 17, 18, and 19 discuss
neuromuscular U/S in greater detail. In addition, many of
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-
ples of neuromuscular U/S. Each neuromuscular U/S study
must be individualized, based on the neurologic examina-
tion, the EDX study, and the differential diagnosis, and
modified as the study progresses and further information
is gained. Its primary use is to add anatomic and pathologic
information that complements the EDX study. Among neu-
romuscular U/S’s many potential uses, the major ones are
described in the following sections.
Peripheral Nerve: Mononeuropathy
In general, U/S is particularly helpful in many mononeu-
ropathies. Mononeuropathies are commonly caused by
entrapment, trauma, and in some cases other structural
causes. When the EDX study has localized the problem to
one segment of one peripheral nerve (e.g., the median nerve
at the carpal tunnel), U/S can confirm the localization by
revealing structural changes in the nerve at the involved site.
In the case of carpal tunnel syndrome, U/S usually simply
adds additional confirmatory evidence of the nerve loca-
tion, although as we will see later in Chapter 20 on Median
Neuropathy at the Wrist, U/S may add more information,
especially in postoperative cases or when symptoms recur.
In other cases of mononeuropathy, when the EDX study
localizes the problem to one nerve but is not able to local-
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
localize the lesion more precisely than EDX studies. Take
the example of the patient with a weak grip and numbness
involving digit 5. An ulnar neuropathy is considered most
likely. The EDX study might show abnormalities limited to
the ulnar nerve, but there is no slowing or conduction block
across the elbow. Is the lesion at the elbow? Or is it as the
wrist, in the forearm, upper arm, or in the lower brachial
plexus? U/S can visualize the ulnar nerve from the wrist to
its origin in the lower brachial plexus and assess for struc-
tural abnormalities to localize the lesion.
Regardless of whether the EDX study can definitely
localize the mononeuropathy or not, it is important to know
what is causing it. Is it an entrapment from wear and tear?
Or from tenosynovitis? Or from compression from a gan-
glion cyst? Or from a nerve sheath tumor? And the list con-
tinues. This is also where U/S may add critical anatomic
information about what is causing the mononeuropathy.
Performing U/S after EDX studies for a mononeuropa-
thy may result in three different outcomes:
1. It may add no useful information, or
2. It may add important complementary information, or
3. It may be the key to the case.
  
Unfortunately, one does not know before doing the U/S
study which of these three outcomes will be the result.
Thus, one can make a strong argument that U/S is a reason-
able adjunct to EDX studies for most mononeuropathies.
Peripheral Nerve: Polyneuropathy
The role of neuromuscular U/S in polyneuropathy is most
useful when looking for evidence of a hypertrophic (usu-
ally meaning demyelinating) polyneuropathy. As will be dis-
cussed in Chapter 29 on Polyneuropathy, the vast majority
of polyneuropathies display an axonal loss pattern on EDX
studies. Very few are primarily demyelinating. However,
the presence of demyelination on EDX studies of a poly-
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
inflammatory (autoimmune) and potentially very treatable.
The U/S picture of a chronic demyelinating polyneu-
ropathy is usually that of a hypertrophic neuropathy (from
repeated demyelination and remyelination, Schwann cell
proliferation, and onion blub formation). EDX studies may
be indeterminate in some chronic demyelinating neuropa-
thies. Sometimes, this is due to responses being absent. In
others, the EDX criteria for demyelination are not fully
met, or the conduction velocities are in the borderline range
between axon loss and demyelination. In these cases, pre-
sumably the demyelination is not marked enough to call,
or the segments of nerve that are demyelinated are not eas-
ily assessed by standard EDX studies (e.g., very proximal
nerves, plexus, and/or roots). Hence, U/S can be extremely
useful in establishing a polyneuropathy as demyelinating.
Motor Neuron Disease
EDX studies in conjunction with the history and physi-
cal examination are the cornerstones of diagnosing motor
neuron disease. U/S has a limited role in the diagnosis of
motor neuron disease, with a couple of notable exceptions.
First, U/S is extremely good at detecting fasciculations—
better than the clinical examination and needle EMG. The
research criteria for the diagnosis of motor neuron disease
(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,
more recent criteria accept the presence of fasciculations
along with reinnervation as evidence of ongoing lower motor
neuron loss. Thus, U/S can be very helpful in more easily
detecting fasciculations.
Second, a diagnostic dilemma often arises in patients with
suspected motor neuron disease when they present with
a pure lower motor neuron syndrome without any definite
upper motor neuron signs. This syndrome is typically desig-
nated as the progressive muscular atrophy (PMA) form of
motor neuron disease. However, in such patients, the ques-
tion often remains whether the patient has a motor neuron
disorder, such as PMA, or a motor nerve disorder. True motor
nerve disorders are rare, but when they occur, they typically
mimic PMA. Oftentimes, EDX studies cannot distinguish
between these two, especially when conduction blocks are
very proximal or motor NCSs are in the borderline range.
Motor neuropathies are most often inflammatory and treat-
able. Variants of CIDP, but more often, multifocal motor
neuropathy with conduction block (MMNCB) may present
as pure lower motor neuron weakness. In these conditions,
U/S may demonstrate hypertrophic nerves, whereas in amyo-
trophic lateral sclerosis (ALS), PMA, and other motor neu-
ron disorders, nerve size is normal or even small. Thus, U/S
should be strongly considered in all patients presenting as a
pure lower motor neuron syndrome.
Myopathy
The original reports of using U/S in neuromuscular disorders
come from evaluation of young boys with Duchenne mus-
cular dystrophy. Like motor neuron disease, the use of U/S
in myopathies is limited, but with a few notable exceptions.
First, U/S can easily screen many muscles at one sitting. The
pattern formed by which muscles are abnormal and which are
spared is increasingly used to help limit the differential diag-
nosis in myopathies. U/S is much quicker and less expensive
than MRI in establishing the pattern of muscle involvement
and can screen all four limbs, proximally and distally, in one
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-
ceps muscles and the involvement of the forearm finger flex-
ors are both highly suggestive of the diagnosis, in the proper
clinical context.
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-
cle that is abnormal but not end stage. Needle EMG is often
used in this regard, but one then needs to biopsy the muscle
on the contralateral side to the muscle identified on needle
EMG as the optimal site. If one biopsied the muscle sampled
with needle EMG, the biopsy might include the area where
the needle had been placed, which could result in inflamma-
tion and other injury along the needle track and carries the
inherent risk of diagnosing an inflammatory myopathy incor-
rectly. Using U/S, one can biopsy the specific muscle that was
examined and determined to be optimal, without the need to
choose the contralateral side.
CARDINAL RULES OF
NEUROMUSCULAR ULTRASOUND
Similar to EDX studies, neuromuscular U/S relies on the
physician’s ability to perform and interpret the study cor-
rectly and analyze the findings in real time, altering the
study as needed. The following cardinal rules of neuromus-
cular U/S should always be kept in mind when performing
a study (Fig. 1.7):
  
1. Neuromuscular U/S is complementary to the EDX study.
As emphasized earlier, EDX assesses the physiologic
function of nerve and muscle, whereas U/S imaging
of nerve and muscle is used to provide anatomic and,
possibly, pathologic etiologic information. These are
complementary pieces of information that, when used
together, allow more accurate and complete information
on the nature of the neuromuscular disorder.
2. Each U/S study should be tailored for the individual
patient. Each study must be tailored to the individual
patient and differential diagnosis. Properly used,
neuromuscular U/S is used after the EDX study is
completed to answer specific questions. It is not
desirable or practical to image all nerves and all muscles.
The specific neuromuscular U/S study done will be
different for each patient.
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
abnormality in at least two planes. Just like MRI, when
an “abnormality” is seen on a sagittal image but not on
the axial image, it is probably an artifact. Use the color
Doppler to look for increased blood flow, which may
occur with inflammation, infection, or neoplasia. Check
for compressibility and mobility. Note the echogencity
(i.e., how bright or how dark the lesion is). Look for the
classic U/S findings of posterior acoustic enhancement
or shadowing. Then, look closely at the nearby
structures: bone, tendon, ligament, and blood vessel. If
possible, do a dynamic evaluation and see what happens
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Fig. 1.7 Cardinal rules of neuromuscular ultrasound. EDX,
­Electrodiagnostic; U/S, ultrasound.
10 SECTION I Overview of Nerve Conduction Studies and Electromyography
to the lesion with passive range of motion, or during
voluntary contraction of nearby muscles. Take lots of
still pictures and movie clips, all of which will help you
later in making your determination.
4. When in doubt, think about technical factors, artifacts,
and anomalies. U/S has its own set of artifacts and
technical factors (see Chapter 17). If not recognized,
these can lead to the mistaken impression of pathology
when none actually exists. Similar to EDX studies, such
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,
muscle, and blood vessel. One quickly appreciates that
every patient’s anatomy does not necessarily follow the
textbook. Sometimes, these anatomic anomalies are
actually the cause of the patient’s problem; in other
cases, they are simply incidental findings.
5. When in doubt, do not overcall a diagnosis. This general
rule is equally applicable to EDX studies and all other
laboratory and radiographic tests. It is not uncommon
to find minor abnormalities of unclear significance or to
misinterpret technical issues as findings. It is a mistake
to overcall any diagnosis based on minor abnormalities
or findings that do not fit together with the clinical
presentation.
6. Always think about the clinical-­electrophysiologic-­
ultrasound correlation. This is simply an extension
of the final cardinal rule of EDX. One usually can
be certain of a diagnosis when the clinical findings,
NCSs, EMG, and U/S abnormalities all correlate
well. Consider again the example of the patient with
weakness of the hand and tingling and numbness of
the fourth and fifth fingers. If NCSs demonstrate
abnormal ulnar motor and sensory potentials associated
with slowing across the elbow, the needle EMG
shows denervation and a reduced number of motor
unit potentials in all ulnar-­innervated muscles and a
normal EMG of all non-ulnar–innervated muscles,
and the U/S shows an enlarged, hypoechoic ulnar
nerve under the humeral-­ulnar aponeurosis at the true
cubital tunnel without any other pathology; there is
a very high degree of certainty that the patient truly
has an ulnar neuropathy at the elbow. In this case, the
electrophysiological abnormalities are indeed relevant,
with the U/S demonstrating the etiology of the ulnar
nerve entrapment at the cubital tunnel.
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Mondelli M, Aretini A, Greco G. Requests of
electrodiagnostic testing: consistency and agreement of
referral diagnosis. What is changed in a primary outpatient
EDX lab 16 years later? Neurol Sci. 2014;35(5):669–675.
Mondelli M, Giacchi M, Federico A. Requests for
electromyography from general practitioners and specialists:
critical evaluation. Ital J Neurol Sci. 1998;19(4):195–203.
 SECTION I • Overview of Nerve Conduction Studies and Electromyography
Anatomy and Neurophysiology for
Electrodiagnostic Studies
The electromyographer need not have detailed knowl-
edge of all the electrical and chemical events that occur at
a molecular level to perform an electrodiagnostic (EDX)
study. However, one must have a basic understanding of
anatomy and physiology to plan, perform, and properly
interpret an EDX study.
In the everyday evaluation of patients with neuromus-
cular disorders, nerve conduction studies (NCSs) and elec-
tromyography (EMG) serve primarily as extensions of the
clinical examination. For NCSs, one needs to know the
location of the various peripheral nerves and muscles so
that the stimulating and recording electrodes are properly
positioned. For the needle EMG study, knowledge of gross
muscle anatomy is crucial for inserting the needle electrode
correctly into the muscle being sampled.
On the microscopic level, knowledge of nerve and muscle
anatomy and basic neurophysiology is required to appreciate
and interpret the EDX findings both in normal individu-
als and in patients with various neuromuscular disorders. In
addition, knowledge of anatomy and physiology is crucial to
understanding the technical aspects of the EDX study and
appreciating its limitations and potential pitfalls.
ANATOMY
The strict definition of the peripheral nervous system
includes that part of the nervous system in which the
Schwann cell is the major supporting cell, as opposed to the
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central nervous system in which the glial cells are the major
supporting cells. The peripheral nervous system includes
the nerve roots, peripheral nerves, primary sensory neurons,
neuromuscular junctions (NMJs), and muscles (Fig. 2.1).
Although not technically part of the peripheral nervous sys-
tem, the primary motor neurons (i.e., anterior horn cells),
which are located in the spinal cord, are usually included as
part of the peripheral nervous system as well. In addition,
cranial nerves III through XII are also considered to be part
of the peripheral nervous system, being essentially the same
as peripheral nerves, except that their primary motor neu-
rons are located in the brainstem rather than the spinal cord.
The primary motor neurons, the anterior horn cells, are
located in the ventral gray matter of the spinal cord. The
axons of these cells ultimately become the motor fibers in
peripheral nerves. Their projections first run through the
white matter of the anterior spinal cord before exiting ven-
trally as the motor roots. In contrast to the anterior horn cell,
the primary sensory neuron, also known as the dorsal root
ganglion (DRG), is not found within the substance of the
spinal cord itself but rather lies outside the spinal cord, near
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-
nal cord on the dorsal side to ascend in either the posterior
columns or synapse with sensory neurons in the dorsal horn.
The peripheral projections of the DRGs ultimately become
the sensory fibers in peripheral nerves. Because the DRGs
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Fig. 2.1 Elements of the peripheral nervous
system. The peripheral nervous system includes
the peripheral motor and sensory nerves; their
primary neurons, the anterior horn cells, and
dorsal root ganglia; the neuromuscular junctions
(NMJs); and muscle. The dorsal root ganglion, a
bipolar cell located distal to the sensory root, is
anatomically different from the anterior horn cell.
Consequently, lesions of the nerve roots result in
10- abnormalities of motor nerve conduction studies
but do not affect the sensory conduction studies,
as the dorsal root ganglion and its peripheral
0XVFOH nerve remain intact.
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
 ,;
,9  innervation to underlying deep structures. Because of this
 ;
9   arrangement, motor fibers from the same nerve root sup-
;,
9,   ply muscles innervated by different peripheral nerves, and
7 ;,,
9,,  sensory fibers from the same nerve root supply cutane-
7
 7
 7 ous sensation in the distribution of different peripheral
,,
,,   nerves. For instance, the C5 motor root supplies the biceps
,,,
  (musculocutaneous nerve), deltoid (axillary nerve), and
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  brachioradialis (radial nerve), among other muscles (Fig.
9
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 2.6). Similarly, C5 sensory fibers innervate the lateral arm
9, (axillary nerve) and forearm (lateral antebrachial cutaneous
9 
 9,, sensory nerve), in addition to other nerves.

9,  9,,, All muscles supplied by one spinal segment (i.e., one
 nerve root) are known as a myotome, whereas all cutaneous
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Fig. 2.2 Spinal cord and nerve roots. The spinal cord is divided into
31 segments (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccy-
geal). At each segment, motor and sensory fibers leave the spinal cord
as nerve roots before exiting the bony spinal column. In the adult, the
spinal cord usually ends at the level of the L1 vertebra. Consequently,
below this level, only the lumbosacral nerve roots, known as the
cauda equina, are present within the spinal column. (From Haymaker
W, Woodhall B. Peripheral Nerve Injuries. Philadelphia: WB Saun-
ders; 1953, with permission.)
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Fig. 2.3 Nerve roots and rami. The motor root, originating from
anterior horn cells, leaves the cord ventrally, whereas the sensory root
enters the cord on the dorsal side. Immediately distal to the dorsal root
ganglion, the motor and sensory roots come together to form the spinal
nerve. Each spinal nerve quickly divides into a dorsal and ventral
ramus. Each ramus contains both motor and sensory fibers. The dorsal
rami supply sensation to the skin over the spine and muscular innerva-
tion to the paraspinal muscles. The ventral rami continue as intercostal
nerves in the thoracic region. In the lower cervical region, the ventral
rami fuse to form the brachial plexus. In the mid-­lumbar through sacral
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
dermatome (Fig. 2.7). For both myotomes and dermatomes,
there is considerable overlap between adjacent segments.
Because of the high degree of overlap between spinal seg-
ments, a single root lesion seldom results in significant sen-
sory loss and never in anesthesia. Likewise, on the motor
side, even a severe single nerve root lesion usually results
in only mild or moderate weakness and never in paralysis.
For instance, a severe lesion of the C6 motor root causes
weakness of the biceps; however, paralysis would not
occur because C5 motor fibers also innervate the biceps.
In contrast, a severe peripheral nerve lesion usually results
in marked sensory and motor deficits because contribu-
tions from several myotomes and dermatomes are affected
simultaneously.
At the microscopic level, nerve fibers are protected by
three different layers of connective tissue: the epineurium,
perineurium, and endoneurium (Fig. 2.8). The thick epineu-
rium surrounds the entire nerve and is in continuity with the
dura mater at the spinal cord level. Within the epineurium,
axons are grouped into fascicles, surrounded by perineu-
rium. A final layer of connective tissue, the endoneurium, is
present between individual axons. Effectively, a blood-­nerve
barrier is formed by the combination of vascular endothe-
lium supplying the nerve and the connective tissue of the
perineurium. Together, the three layers of connective tissue
give peripheral nerve considerable tensile strength, usually
in the range of 20–30 kg. However, the weakest point of a
nerve occurs where the nerve roots meet the spinal cord,
where the nerve can sustain only 2–3 kg of force. For this
reason, nerve root avulsion may occur after a significant
trauma and especially after a stretch injury.
Analogous to nerve fibers, muscle fibers have a very
similar arrangement at the microscopic level with three
layers of connective tissue: the epimysium, perimysium,
and endomysium (Fig. 2.9). The epimysium surrounds
the entire muscle. Within the epimysium, muscle fibers
(which are the actual muscle cells) are grouped into fas-
cicles surrounded by the perimysium. The final layer of
connective tissue, the endomysium, is present between
individual muscle fibers. Muscle fibers are cylindrical and
contain the actual muscle fibrils: the structural proteins
that are responsible for muscle contraction. When muscle
contraction occurs, the force is transmitted most often to
a bone to move a joint (occasionally, muscle is connected
to other connective tissue or the skin). This connection
is most often made by way of a tendon, which is a thick
rope-­like piece of connective tissue that is in continuity
with the epimysium of the muscle. In some muscles, the
contraction is by way of an aponeurosis, which is a large,
sheet-­like piece of connective tissue. Most muscles have
two tendons, one at their origin (typically proximal and
more static) and one at their insertion (typically more
distal and more mobile). In some muscles, the tendon
originates from inside the muscle, known as an internal or
central tendon.

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14 SECTION I Overview of Nerve Conduction Studies and Electromyography

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

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Fig. 2.9 Internal muscle anatomy. The endomysium is present
between muscle fibers. Muscle fibers are grouped into fascicles,
surrounded by perimysium. Surrounding the entire muscle is the last
layer of connective tissue, the epimysium.

Fig. 2.10 Resting membrane potential. At rest, the axonal mem-
brane is negatively polarized inside compared to outside. This
resting potential results from the combination of a membrane that is
semipermeable to charged particles and an active Na+/K+ pump. At
rest, the concentration of Na+ and Cl− is higher in the extracellular
space, with the concentration of K+ and large anions (A−) greater
inside the axon.

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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
into the axon, driven both by concentration and by electrical
gradients. Every time a depolarization of 10–30 mV above
the resting membrane potential occurs (i.e., threshold), it
creates an action potential and a cycle of positive feedback;
further depolarization occurs and more sodium channels
open (Fig. 2.12). Action potentials are always all-­or-­none
responses that then propagate away from the initial site of
depolarization. The axon does not remain depolarized for
long, however, because the opening of the sodium channels
is time limited. Sodium channels have a second gate, known
as the inactivation gate. Inactivation of the sodium channel
occurs within 1–2 ms. During this time, the membrane is
not excitable and cannot be opened (i.e., refractory period).
The inactivation gate of the sodium channel has been mod-
eled as a “hinged lid.” From a practical point of view, the
refractory period limits the frequency that nerves can con-
duct impulses. It also ensures that the action potential con-
tinues to propagate in the same direction (i.e., the area of
nerve behind the depolarization is refractory when the area
ahead is not so that the impulse will continue forward and
will not return backward).
In addition to sodium channel inactivation, depolariza-
tion also results in the opening of potassium channels, which
also then drives the membrane voltage in a more negative
direction. These factors, along with the Na+/K+ pump,
then reestablish the resting membrane potential.
The conduction velocity of the action potential depends
on the diameter of the axon: the larger the axon, the less
resistance and the faster the conduction velocity. For typi-
cal unmyelinated axons, the conduction velocity of an
action potential is very slow, typically in the range of 0.2–
1.5 m/s. Conduction velocity can be greatly increased with
the addition of myelin. Myelin insulation is present on all
fast-­conducting fibers and is derived from Schwann cells,
the major supporting cells in the peripheral nervous sys-
tem. Myelin is composed of concentric spirals of Schwann
cell membrane (Fig. 2.13). For every myelinated fiber,
 Chapter 2 • Anatomy and Neurophysiology for Electrodiagnostic Studies 17
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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.
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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
present on all fast-­conducting fibers, both motor and sensory. Myelin
is composed of concentric spirals of Schwann cell membrane, with
each Schwann cell supporting a single myelinated axon.
successive segments are myelinated by single Schwann
cells. Each segment of the axon covered by myelin is
termed the “internode.” At small gaps between successive
internodes, the axon is exposed; these areas are known as
the nodes of Ranvier. They are very small, in the range of
1–2 μm in length.
Most of the nerve is effectively insulated with myelin,
and depolarization occurs by way of saltatory conduction,
whereby depolarization occurs only at the nodes of Ranvier.
After one node depolarizes, the current essentially jumps
to the next adjacent node, and the cycle continues (Fig.
2.14). The physiology of normal saltatory conduction was
first shown in a series of elegant experiments on normal
animal myelinated nerve fibers, recording along the motor
root in very small increments and measuring the current
as a function of distance and latency (Fig. 2.15). From an
electrical point of view, myelin insulates the internode and
reduces the capacitance. A lower capacitance results in
less current lost as the action potential travels from node
to node. Although more current is needed for saltatory
conduction than for continuous conduction, much less






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
range of 35–75 m/s.
nerve membrane must be depolarized. For unmyelinated
fibers, depolarization must occur over the entire length of
the nerve (i.e., continuous conduction), which takes much
more time than in myelinated fibers. In myelinated fibers,
the axonal membrane only needs to depolarize at the nodes
of Ranvier; the internodes do not depolarize, but rather
the action potential jumps over them. As the internode
is approximately 1 mm in length and the node of Ranvier
is only 1–2 μm in length, markedly less axonal membrane
needs to depolarize to propagate an action potential. The
lower the total depolarization time, the faster the conduc-
tion velocity. In myelinated axons, the density of sodium
channels is highest in nodal areas, the areas undergoing
depolarization. Myelinated human peripheral nerve fibers
typically conduct in the range of 35–75 m/s, far faster
than could ever be achieved by increasing the diameter
of unmyelinated fibers. Not all human peripheral nerve
fibers are myelinated. Unmyelinated fibers, which con-
duct very slowly (typically 0.2–1.5 m/s), primarily medi-
ate pain, temperature, and autonomic functions. Schwann
cells also support these unmyelinated fibers; however, one
Schwann cell typically surrounds several unmyelinated
fibers, but without the formation of concentric spirals of
myelin.
When an individual axon is depolarized, an action poten-
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
fiber. An axon, along with its anterior horn cell and all mus-
cle fibers with which it is connected, is known as a motor
unit (Fig. 2.16). Depolarization of all the muscle fibers in
a motor unit creates an electrical potential known as the
motor unit action potential (MUAP). Analysis of MUAPs
is an important part of every needle EMG examination.
When an action potential is generated, all muscle fibers in
the motor unit are normally activated, again an all-­or-­none
response.
However, before a muscle fiber can be activated, the
nerve action potential must be carried across the NMJ. The
NMJ is essentially an electrical-­ chemical-­
electrical link
from nerve to muscle. It is formed from two specialized
membranes, one on nerve and one on muscle, separated by
a thin synaptic cleft (Fig. 2.17). As a nerve action poten-
tial travels to the presynaptic side of the NMJ, voltage-­
gated calcium channels are activated, allowing an influx
of calcium (Ca+). Increasing Ca+ concentration results in
a series of enzymatic steps that ultimately results in the
release of acetylcholine, the neurotransmitter at the NMJ.
Acetylcholine diffuses across the synaptic cleft to bind to
specialized acetylcholine receptors on the muscle mem-
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
case with nerve, once threshold is reached, a muscle fiber
action potential is created that spreads throughout the
muscle fiber. Following the muscle fiber action potential,
a complex set of molecular interactions occurs within the
muscle fiber, resulting in increasing overlap of the major
muscle fiber filaments: actin and myosin, with the final
result of muscle shortening, contraction, and generation of
force (Fig. 2.18).
CLASSIFICATION
Multiple peripheral nerve classification schemes exist
(Table 2.1). Peripheral nerves can be classified based on
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Fig. 2.17 Neuromuscular junction. The neuromuscular junction is
a specialized junction between the terminal axon and muscle fiber.
When the nerve action potential invades the presynaptic terminal,
acetylcholine is released and diffuses across the synaptic cleft to
bind to acetylcholine receptors on the muscle membrane. This bind-
ing results in a muscle endplate potential, which, once threshold is
reached, causes the generation of a muscle fiber action potential.
Z Myosin
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.
the following attributes: (1) myelinated or unmyelinated,
(2) somatic or autonomic, (3) motor or sensory, and (4)
diameter.
There are several important points to glean from
Table 2.1, some of which are directly relevant to clinical
EDX testing. First is the direct relationship between fiber
diameter and conduction velocity: the larger the diameter,
the faster the conduction velocity. The large myelinated
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-
est fibers of the particular peripheral nerve that is being
studied. Large-­diameter fibers have the most myelin and
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
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
skin follicles. Note that the size and conduction velocities
of these fibers are similar to those of the muscle efferent
fibers from the anterior horn cells that are recorded during
routine motor studies. These myelinated fibers have veloci-
ties in the range of 35–75 m/s.
Third, the largest and fastest fibers in the peripheral
nervous system are not recorded during either routine
motor or sensory NCSs. These are the muscle afferents,
the Aα fibers (also known as Ia fibers), which originate
from muscle spindles and mediate the afferent arc of
the muscle stretch reflex. These fibers are recorded only
during mixed nerve studies in which the entire mixed
nerve is stimulated and recorded. Therefore mixed
nerve conduction velocities usually are faster than either
routine motor or cutaneous sensory conduction veloci-
ties because they contain these Ia fibers. Because the
Ia fibers have the largest diameter and accordingly the
Z
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
by demyelinating lesions such as those found in entrap-
ment neuropathies. For example, in the EDX evaluation
of carpal tunnel syndrome, the mixed nerve study from
the palm to the wrist often is more sensitive in detecting
abnormalities than either the routine motor or sensory
conduction study.
RECORDING
All potentials obtained during NCSs and needle EMG
result from the extracellular recording of intracellular
events from either nerve or muscle. NCSs usually are per-
formed by recording with surface electrodes over the skin,
and EMG potentials by recording with a needle electrode
placed within the muscle. In both procedures, intracellu-
lar electrical potentials are transmitted through tissue to
the recording electrodes. The process of an intracellular
electrical potential being transmitted through extracellular
fluid and tissue is known as volume conduction. Although
the theory of volume conduction is complex and beyond
the scope of this text, volume-­conducted potentials can be
modeled as either near-­field or far-­field potentials. Near-­
field potentials can be recorded only close to their source,
and the characteristics of the potential depend on the dis-
tance between the recording electrodes and the electrical
source (i.e., the action potential). With near-­field poten-
tials, a response generally is not seen until the source is
close to the recording electrodes. The closer the recording
electrodes are to the current source, the higher the ampli-
tude. Compound muscle action potentials, sensory nerve
action potentials, and MUAPs recorded during routine
motor conduction, sensory conduction, and needle EMG
studies, respectively, are essentially all volume-­conducted
near-­field potentials.
Volume-­ conducted, near-­ field potentials produce a
characteristic triphasic waveform as an advancing action
potential approaches and then passes beneath and away
from a recording electrode (Fig. 2.19, top). In practice,
most sensory and mixed nerve studies display this tri-
phasic waveform morphology, as do fibrillation potentials
and most MUAPs. The electrical correlate of an action
potential traveling toward, under, and then away from the
recording electrode is an initial positive phase, followed by
a negative phase, and then a trailing positive phase, respec-
tively. The first positive peak represents the time that the
action potential is first beneath the active electrode; this is
the point at which the onset latency should be measured
for nerve action potentials. The initial positive peak may
be very small or absent with some sensory responses. In
that case, the initial negative deflection best marks the
true onset of the potential.
 Chapter 2 • Anatomy and Neurophysiology for Electrodiagnostic Studies 21
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B

Fig. 2.19 Volume conduction and waveform morphology. Top, An
advancing action potential recorded by volume conduction will result
in a triphasic potential that initially is positive, then is negative, and
finally is positive again. Bottom, If the depolarization occurs directly
beneath the recording electrode, the initial positive phase will be
absent, and a biphasic, initially negative potential will be seen. Note
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
begins directly under the recording electrode, the initial
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-
cally only a positive deflection will occur (Fig. 2.20, bot-
tom). For example, this pattern is seen when stimulating
the median nerve and recording a hypothenar muscle, as
might be done during routine motor studies looking for
an anomalous innervation. The muscle action potential of
the median-­innervated thenar muscles occurs at a distance
but never travels under the recording electrodes located
over the hypothenar muscles. The result is a small positive
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.
Two recording electrodes, one closer and the other far-
ther from the source, essentially see the source at the
same time. Although far-­field potentials are more often
of concern in evoked-­potential studies, they occasionally
are important in NCSs. The stimulus artifact seen at the
P9
PV
î

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
then travels under and past the active electrode, resulting in an initial
positive deflection (middle trace). If the depolarization occurs at a
distance and never travels under the recording electrode, only a small
positive potential will be seen (bottom trace). Note that, by conven-
tion, negative is up and positive is down in all nerve conduction and
electromyographic traces.
P9
PV
Fig. 2.21 Near-­field and far-­field potentials. Median motor study,
recording the abductor pollicis brevis muscle, stimulating at the
wrist (top trace) and antecubital fossa (bottom trace). At each site,
a compound muscle action potential is present, representing a near-­
field recording of the underlying muscle fiber action potentials. The
compound muscle action potential latencies occur at different times,
reflecting their different arrival times at the recording electrode. At the
start of each trace is the stimulus artifact (blue arrow). The stimu-
lus artifact is an example of a far-­field potential being transmitted
instantaneously and seen at the same time, despite the difference in
distances between the two stimulation sites.
onset of all NCSs is a good example of a far-­field poten-
tial (Fig. 2.21). The shock artifact is instantly transmit-
ted and is seen at the same time at distal and proximal
recording sites. Those potentials whose latencies do not
vary with distance from the stimulation site usually are
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
After the history is taken and a directed physical examina-
tion is performed, every study begins with nerve conduc-
tion studies (NCSs). The needle electromyography (EMG)
examination is performed after the NCSs are completed
because the findings on the NCSs are used in the planning
and interpretation of the needle EMG examination that
follows.
Peripheral nerves usually can be easily stimulated
and brought to action potential with a brief electrical
pulse applied to the overlying skin. Techniques have been
described for studying most peripheral nerves. In the upper
extremity, the median, ulnar, and radial nerves are the most
easily studied; in the lower extremity, the peroneal, tibial,
and sural nerves are the most easily studied (see Chapters
10 and 11). Of course, the nerves selected for study depend
on the patient’s symptoms and signs and the differential
diagnosis. Motor, sensory, or mixed nerve studies can be
performed by stimulating the nerve and placing the record-
ing electrodes over a distal muscle, a cutaneous sensory
nerve, or the entire mixed nerve, respectively. The findings
from motor, sensory, and mixed nerve studies often comple-
ment one another and yield different types of information
based on distinct patterns of abnormalities, depending on
the underlying pathology.
MOTOR CONDUCTION STUDIES
Motor conduction studies are technically less demanding
than sensory and mixed nerve studies; thus, they usually are
performed first. Performing the motor studies first also has
other major advantages. It is not uncommon for the sensory
responses to be very low in amplitude or absent in many
neuropathies. Performing the motor studies first allows one
to know where the nerve runs, where it should be stimu-
lated, and how much current is needed and also gives some
information about whether the nerve is normal or abnor-
mal. On the other hand, if the sensory study is done before
the motor study, one might spend a lot of unnecessary time
stimulating and trying to record a sensory response that is
not present. For example, imagine a patient with a moder-
ately severe median neuropathy at the wrist who is sent for
an electrodiagnostic (EDX) evaluation. If the median motor
study is performed first, the correct stimulation site can be
confirmed, the amount of current needed to stimulate the
median nerve will be known, and one will also know that the
3
median nerve is abnormal before doing the median sensory
study. Then, when performing the median sensory study,
one is confident of where to stimulate the nerve and how
much current is needed. In this case, if no sensory response
is present, one can have a high degree of certainty that the
response is truly absent and move along to the next nerve
to be studied. However, if the sensory conduction study
is done first and is absent, it will not be as obvious if the
absent response is due to a technical problem or is truly
absent. One can waste a lot of time unnecessarily trying to
figure this out. Do the motor conduction study first; your
study will be more efficient, and the patient will tolerate
the study much better.
Motor responses typically are in the range of several
millivolts (mV), as opposed to sensory and mixed nerve
responses, which are in the microvolt (μV) range. Thus,
motor responses are less affected by electrical noise and
other technical factors. For motor conduction studies, the
gain usually is set at 2–5 mV per division. Recording elec-
trodes are placed over the muscle of interest. In general,
the belly-­tendon montage is used. The active recording
electrode (also known as G1) is placed on the center of
the muscle belly (over the motor endplate), and the refer-
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
when electrodes were attached to grids (hence the G) of
an oscilloscope. The stimulator then is placed over the
nerve that supplies the muscle, with the cathode placed
closest to the recording electrode. It is helpful to remem-
ber “black to black,” indicating that the black electrode of
the stimulator (the cathode) should be facing the black
recording electrode (the active recording electrode). For
motor studies, the duration of the electrical pulse usually
is set to 200 ms. Most normal nerves require a current in
the range of 20–50 mA to achieve supramaximal stimula-
tion. As current is slowly increased from a baseline 0 mA,
usually by 5–10 mA increments, more of the underlying
nerve fibers are brought to action potential and, subse-
quently, more muscle fiber action potentials are generated.
The recorded potential, known as the compound muscle
action potential (CMAP), represents the summation of all
underlying individual muscle fiber action potentials. When
the current is increased to the point that the CMAP no
longer increases in size, one presumes that all nerve fibers
23
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 DANCE ON STILTS AT THE GIRLS’ UNYAGO, NIUCHI

Newala, too, suffers from the distance of its water-supply—at least

the Newala of to-day does; there was once another Newala in a lovely
valley at the foot of the plateau. I visited it and found scarcely a trace
of houses, only a Christian cemetery, with the graves of several
missionaries and their converts, remaining as a monument of its
former glories. But the surroundings are wonderfully beautiful. A
thick grove of splendid mango-trees closes in the weather-worn
crosses and headstones; behind them, combining the useful and the
agreeable, is a whole plantation of lemon-trees covered with ripe
fruit; not the small African kind, but a much larger and also juicier
imported variety, which drops into the hands of the passing traveller,
without calling for any exertion on his part. Old Newala is now under
the jurisdiction of the native pastor, Daudi, at Chingulungulu, who,
as I am on very friendly terms with him, allows me, as a matter of
course, the use of this lemon-grove during my stay at Newala.
 FEET MUTILATED BY THE RAVAGES OF THE “JIGGER”
(Sarcopsylla penetrans)

The water-supply of New Newala is in the bottom of the valley,

some 1,600 feet lower down. The way is not only long and fatiguing,
but the water, when we get it, is thoroughly bad. We are suffering not
only from this, but from the fact that the arrangements at Newala are
nothing short of luxurious. We have a separate kitchen—a hut built
against the boma palisade on the right of the baraza, the interior of
which is not visible from our usual position. Our two cooks were not
long in finding this out, and they consequently do—or rather neglect
to do—what they please. In any case they do not seem to be very
particular about the boiling of our drinking-water—at least I can
attribute to no other cause certain attacks of a dysenteric nature,
from which both Knudsen and I have suffered for some time. If a
man like Omari has to be left unwatched for a moment, he is capable
of anything. Besides this complaint, we are inconvenienced by the
state of our nails, which have become as hard as glass, and crack on
the slightest provocation, and I have the additional infliction of
pimples all over me. As if all this were not enough, we have also, for
the last week been waging war against the jigger, who has found his
Eldorado in the hot sand of the Makonde plateau. Our men are seen
all day long—whenever their chronic colds and the dysentery likewise
raging among them permit—occupied in removing this scourge of
Africa from their feet and trying to prevent the disastrous
consequences of its presence. It is quite common to see natives of
this place with one or two toes missing; many have lost all their toes,
or even the whole front part of the foot, so that a well-formed leg
ends in a shapeless stump. These ravages are caused by the female of
Sarcopsylla penetrans, which bores its way under the skin and there
develops an egg-sac the size of a pea. In all books on the subject, it is
stated that one’s attention is called to the presence of this parasite by
an intolerable itching. This agrees very well with my experience, so
far as the softer parts of the sole, the spaces between and under the
toes, and the side of the foot are concerned, but if the creature
penetrates through the harder parts of the heel or ball of the foot, it
may escape even the most careful search till it has reached maturity.
Then there is no time to be lost, if the horrible ulceration, of which
we see cases by the dozen every day, is to be prevented. It is much
easier, by the way, to discover the insect on the white skin of a
European than on that of a native, on which the dark speck scarcely
shows. The four or five jiggers which, in spite of the fact that I
constantly wore high laced boots, chose my feet to settle in, were
taken out for me by the all-accomplished Knudsen, after which I
thought it advisable to wash out the cavities with corrosive
sublimate. The natives have a different sort of disinfectant—they fill
the hole with scraped roots. In a tiny Makua village on the slope of
the plateau south of Newala, we saw an old woman who had filled all
the spaces under her toe-nails with powdered roots by way of
prophylactic treatment. What will be the result, if any, who can say?
The rest of the many trifling ills which trouble our existence are
really more comic than serious. In the absence of anything else to
smoke, Knudsen and I at last opened a box of cigars procured from
the Indian store-keeper at Lindi, and tried them, with the most
distressing results. Whether they contain opium or some other
narcotic, neither of us can say, but after the tenth puff we were both
“off,” three-quarters stupefied and unspeakably wretched. Slowly we
recovered—and what happened next? Half-an-hour later we were
once more smoking these poisonous concoctions—so insatiable is the
craving for tobacco in the tropics.
Even my present attacks of fever scarcely deserve to be taken
seriously. I have had no less than three here at Newala, all of which
have run their course in an incredibly short time. In the early
afternoon, I am busy with my old natives, asking questions and
making notes. The strong midday coffee has stimulated my spirits to
an extraordinary degree, the brain is active and vigorous, and work
progresses rapidly, while a pleasant warmth pervades the whole
body. Suddenly this gives place to a violent chill, forcing me to put on
my overcoat, though it is only half-past three and the afternoon sun
is at its hottest. Now the brain no longer works with such acuteness
and logical precision; more especially does it fail me in trying to
establish the syntax of the difficult Makua language on which I have
ventured, as if I had not enough to do without it. Under the
circumstances it seems advisable to take my temperature, and I do
so, to save trouble, without leaving my seat, and while going on with
my work. On examination, I find it to be 101·48°. My tutors are
abruptly dismissed and my bed set up in the baraza; a few minutes
later I am in it and treating myself internally with hot water and
lemon-juice.
Three hours later, the thermometer marks nearly 104°, and I make
them carry me back into the tent, bed and all, as I am now perspiring
heavily, and exposure to the cold wind just beginning to blow might
mean a fatal chill. I lie still for a little while, and then find, to my
great relief, that the temperature is not rising, but rather falling. This
is about 7.30 p.m. At 8 p.m. I find, to my unbounded astonishment,
that it has fallen below 98·6°, and I feel perfectly well. I read for an
hour or two, and could very well enjoy a smoke, if I had the
wherewithal—Indian cigars being out of the question.
Having no medical training, I am at a loss to account for this state
of things. It is impossible that these transitory attacks of high fever
should be malarial; it seems more probable that they are due to a
kind of sunstroke. On consulting my note-book, I become more and
more inclined to think this is the case, for these attacks regularly
follow extreme fatigue and long exposure to strong sunshine. They at
least have the advantage of being only short interruptions to my
work, as on the following morning I am always quite fresh and fit.
My treasure of a cook is suffering from an enormous hydrocele which
makes it difficult for him to get up, and Moritz is obliged to keep in
the dark on account of his inflamed eyes. Knudsen’s cook, a raw boy
from somewhere in the bush, knows still less of cooking than Omari;
consequently Nils Knudsen himself has been promoted to the vacant
post. Finding that we had come to the end of our supplies, he began
by sending to Chingulungulu for the four sucking-pigs which we had
bought from Matola and temporarily left in his charge; and when
they came up, neatly packed in a large crate, he callously slaughtered
the biggest of them. The first joint we were thoughtless enough to
entrust for roasting to Knudsen’s mshenzi cook, and it was
consequently uneatable; but we made the rest of the animal into a
jelly which we ate with great relish after weeks of underfeeding,
consuming incredible helpings of it at both midday and evening
meals. The only drawback is a certain want of variety in the tinned
vegetables. Dr. Jäger, to whom the Geographical Commission
entrusted the provisioning of the expeditions—mine as well as his
own—because he had more time on his hands than the rest of us,
seems to have laid in a huge stock of Teltow turnips,[46] an article of
food which is all very well for occasional use, but which quickly palls
when set before one every day; and we seem to have no other tins
left. There is no help for it—we must put up with the turnips; but I
am certain that, once I am home again, I shall not touch them for ten
years to come.
Amid all these minor evils, which, after all, go to make up the
genuine flavour of Africa, there is at least one cheering touch:
Knudsen has, with the dexterity of a skilled mechanic, repaired my 9
× 12 cm. camera, at least so far that I can use it with a little care.
How, in the absence of finger-nails, he was able to accomplish such a
ticklish piece of work, having no tool but a clumsy screw-driver for
taking to pieces and putting together again the complicated
mechanism of the instantaneous shutter, is still a mystery to me; but
he did it successfully. The loss of his finger-nails shows him in a light
contrasting curiously enough with the intelligence evinced by the
above operation; though, after all, it is scarcely surprising after his
ten years’ residence in the bush. One day, at Lindi, he had occasion
to wash a dog, which must have been in need of very thorough
cleansing, for the bottle handed to our friend for the purpose had an
extremely strong smell. Having performed his task in the most
conscientious manner, he perceived with some surprise that the dog
did not appear much the better for it, and was further surprised by
finding his own nails ulcerating away in the course of the next few
days. “How was I to know that carbolic acid has to be diluted?” he
mutters indignantly, from time to time, with a troubled gaze at his
mutilated finger-tips.
 Since we came to Newala we have been making excursions in all
directions through the surrounding country, in accordance with old
habit, and also because the akida Sefu did not get together the tribal
elders from whom I wanted information so speedily as he had
promised. There is, however, no harm done, as, even if seen only
from the outside, the country and people are interesting enough.
The Makonde plateau is like a large rectangular table rounded off
at the corners. Measured from the Indian Ocean to Newala, it is
about seventy-five miles long, and between the Rovuma and the
Lukuledi it averages fifty miles in breadth, so that its superficial area
is about two-thirds of that of the kingdom of Saxony. The surface,
however, is not level, but uniformly inclined from its south-western
edge to the ocean. From the upper edge, on which Newala lies, the
eye ranges for many miles east and north-east, without encountering
any obstacle, over the Makonde bush. It is a green sea, from which
here and there thick clouds of smoke rise, to show that it, too, is
inhabited by men who carry on their tillage like so many other
primitive peoples, by cutting down and burning the bush, and
manuring with the ashes. Even in the radiant light of a tropical day
such a fire is a grand sight.
Much less effective is the impression produced just now by the
great western plain as seen from the edge of the plateau. As often as
time permits, I stroll along this edge, sometimes in one direction,
sometimes in another, in the hope of finding the air clear enough to
let me enjoy the view; but I have always been disappointed.
Wherever one looks, clouds of smoke rise from the burning bush,
and the air is full of smoke and vapour. It is a pity, for under more
favourable circumstances the panorama of the whole country up to
the distant Majeje hills must be truly magnificent. It is of little use
taking photographs now, and an outline sketch gives a very poor idea
of the scenery. In one of these excursions I went out of my way to
make a personal attempt on the Makonde bush. The present edge of
the plateau is the result of a far-reaching process of destruction
through erosion and denudation. The Makonde strata are
everywhere cut into by ravines, which, though short, are hundreds of
yards in depth. In consequence of the loose stratification of these
beds, not only are the walls of these ravines nearly vertical, but their
upper end is closed by an equally steep escarpment, so that the
western edge of the Makonde plateau is hemmed in by a series of
deep, basin-like valleys. In order to get from one side of such a ravine
to the other, I cut my way through the bush with a dozen of my men.
It was a very open part, with more grass than scrub, but even so the
short stretch of less than two hundred yards was very hard work; at
the end of it the men’s calicoes were in rags and they themselves
bleeding from hundreds of scratches, while even our strong khaki
suits had not escaped scatheless.

NATIVE PATH THROUGH THE MAKONDE BUSH, NEAR

MAHUTA

I see increasing reason to believe that the view formed some time
back as to the origin of the Makonde bush is the correct one. I have
no doubt that it is not a natural product, but the result of human
occupation. Those parts of the high country where man—as a very
slight amount of practice enables the eye to perceive at once—has not
yet penetrated with axe and hoe, are still occupied by a splendid
timber forest quite able to sustain a comparison with our mixed
forests in Germany. But wherever man has once built his hut or tilled
his field, this horrible bush springs up. Every phase of this process
may be seen in the course of a couple of hours’ walk along the main
road. From the bush to right or left, one hears the sound of the axe—
not from one spot only, but from several directions at once. A few
steps further on, we can see what is taking place. The brush has been
cut down and piled up in heaps to the height of a yard or more,
between which the trunks of the large trees stand up like the last
pillars of a magnificent ruined building. These, too, present a
melancholy spectacle: the destructive Makonde have ringed them—
cut a broad strip of bark all round to ensure their dying off—and also
piled up pyramids of brush round them. Father and son, mother and
son-in-law, are chopping away perseveringly in the background—too
busy, almost, to look round at the white stranger, who usually excites
so much interest. If you pass by the same place a week later, the piles
of brushwood have disappeared and a thick layer of ashes has taken
the place of the green forest. The large trees stretch their
smouldering trunks and branches in dumb accusation to heaven—if
they have not already fallen and been more or less reduced to ashes,
perhaps only showing as a white stripe on the dark ground.
This work of destruction is carried out by the Makonde alike on the
virgin forest and on the bush which has sprung up on sites already
cultivated and deserted. In the second case they are saved the trouble
of burning the large trees, these being entirely absent in the
secondary bush.
After burning this piece of forest ground and loosening it with the
hoe, the native sows his corn and plants his vegetables. All over the
country, he goes in for bed-culture, which requires, and, in fact,
receives, the most careful attention. Weeds are nowhere tolerated in
the south of German East Africa. The crops may fail on the plains,
where droughts are frequent, but never on the plateau with its
abundant rains and heavy dews. Its fortunate inhabitants even have
the satisfaction of seeing the proud Wayao and Wamakua working
for them as labourers, driven by hunger to serve where they were
accustomed to rule.
But the light, sandy soil is soon exhausted, and would yield no
harvest the second year if cultivated twice running. This fact has
been familiar to the native for ages; consequently he provides in
time, and, while his crop is growing, prepares the next plot with axe
and firebrand. Next year he plants this with his various crops and
lets the first piece lie fallow. For a short time it remains waste and
desolate; then nature steps in to repair the destruction wrought by
man; a thousand new growths spring out of the exhausted soil, and
even the old stumps put forth fresh shoots. Next year the new growth
is up to one’s knees, and in a few years more it is that terrible,
impenetrable bush, which maintains its position till the black
occupier of the land has made the round of all the available sites and
come back to his starting point.
The Makonde are, body and soul, so to speak, one with this bush.
According to my Yao informants, indeed, their name means nothing
else but “bush people.” Their own tradition says that they have been
settled up here for a very long time, but to my surprise they laid great
stress on an original immigration. Their old homes were in the
south-east, near Mikindani and the mouth of the Rovuma, whence
their peaceful forefathers were driven by the continual raids of the
Sakalavas from Madagascar and the warlike Shirazis[47] of the coast,
to take refuge on the almost inaccessible plateau. I have studied
African ethnology for twenty years, but the fact that changes of
population in this apparently quiet and peaceable corner of the earth
could have been occasioned by outside enterprises taking place on
the high seas, was completely new to me. It is, no doubt, however,
correct.
The charming tribal legend of the Makonde—besides informing us
of other interesting matters—explains why they have to live in the
thickest of the bush and a long way from the edge of the plateau,
instead of making their permanent homes beside the purling brooks
and springs of the low country.
“The place where the tribe originated is Mahuta, on the southern
side of the plateau towards the Rovuma, where of old time there was
nothing but thick bush. Out of this bush came a man who never
washed himself or shaved his head, and who ate and drank but little.
He went out and made a human figure from the wood of a tree
growing in the open country, which he took home to his abode in the
bush and there set it upright. In the night this image came to life and
was a woman. The man and woman went down together to the
Rovuma to wash themselves. Here the woman gave birth to a still-
born child. They left that place and passed over the high land into the
valley of the Mbemkuru, where the woman had another child, which
was also born dead. Then they returned to the high bush country of
Mahuta, where the third child was born, which lived and grew up. In
course of time, the couple had many more children, and called
themselves Wamatanda. These were the ancestral stock of the
Makonde, also called Wamakonde,[48] i.e., aborigines. Their
forefather, the man from the bush, gave his children the command to
bury their dead upright, in memory of the mother of their race who
was cut out of wood and awoke to life when standing upright. He also
warned them against settling in the valleys and near large streams,
for sickness and death dwelt there. They were to make it a rule to
have their huts at least an hour’s walk from the nearest watering-
place; then their children would thrive and escape illness.”
The explanation of the name Makonde given by my informants is
somewhat different from that contained in the above legend, which I
extract from a little book (small, but packed with information), by
Pater Adams, entitled Lindi und sein Hinterland. Otherwise, my
results agree exactly with the statements of the legend. Washing?
Hapana—there is no such thing. Why should they do so? As it is, the
supply of water scarcely suffices for cooking and drinking; other
people do not wash, so why should the Makonde distinguish himself
by such needless eccentricity? As for shaving the head, the short,
woolly crop scarcely needs it,[49] so the second ancestral precept is
likewise easy enough to follow. Beyond this, however, there is
nothing ridiculous in the ancestor’s advice. I have obtained from
various local artists a fairly large number of figures carved in wood,
ranging from fifteen to twenty-three inches in height, and
representing women belonging to the great group of the Mavia,
Makonde, and Matambwe tribes. The carving is remarkably well
done and renders the female type with great accuracy, especially the
keloid ornamentation, to be described later on. As to the object and
meaning of their works the sculptors either could or (more probably)
would tell me nothing, and I was forced to content myself with the
scanty information vouchsafed by one man, who said that the figures
were merely intended to represent the nembo—the artificial
deformations of pelele, ear-discs, and keloids. The legend recorded
by Pater Adams places these figures in a new light. They must surely
be more than mere dolls; and we may even venture to assume that
they are—though the majority of present-day Makonde are probably
unaware of the fact—representations of the tribal ancestress.
 The references in the legend to the descent from Mahuta to the
Rovuma, and to a journey across the highlands into the Mbekuru
valley, undoubtedly indicate the previous history of the tribe, the
travels of the ancestral pair typifying the migrations of their
descendants. The descent to the neighbouring Rovuma valley, with
its extraordinary fertility and great abundance of game, is intelligible
at a glance—but the crossing of the Lukuledi depression, the ascent
to the Rondo Plateau and the descent to the Mbemkuru, also lie
within the bounds of probability, for all these districts have exactly
the same character as the extreme south. Now, however, comes a
point of especial interest for our bacteriological age. The primitive
Makonde did not enjoy their lives in the marshy river-valleys.
Disease raged among them, and many died. It was only after they
had returned to their original home near Mahuta, that the health
conditions of these people improved. We are very apt to think of the
African as a stupid person whose ignorance of nature is only equalled
by his fear of it, and who looks on all mishaps as caused by evil
spirits and malignant natural powers. It is much more correct to
assume in this case that the people very early learnt to distinguish
districts infested with malaria from those where it is absent.
This knowledge is crystallized in the
ancestral warning against settling in the
valleys and near the great waters, the
dwelling-places of disease and death. At the
same time, for security against the hostile
Mavia south of the Rovuma, it was enacted
that every settlement must be not less than a
certain distance from the southern edge of the
plateau. Such in fact is their mode of life at the
present day. It is not such a bad one, and
certainly they are both safer and more
comfortable than the Makua, the recent
intruders from the south, who have made USUAL METHOD OF
good their footing on the western edge of the CLOSING HUT-DOOR
plateau, extending over a fairly wide belt of
country. Neither Makua nor Makonde show in their dwellings
anything of the size and comeliness of the Yao houses in the plain,
especially at Masasi, Chingulungulu and Zuza’s. Jumbe Chauro, a
Makonde hamlet not far from Newala, on the road to Mahuta, is the
most important settlement of the tribe I have yet seen, and has fairly
spacious huts. But how slovenly is their construction compared with
the palatial residences of the elephant-hunters living in the plain.
The roofs are still more untidy than in the general run of huts during
the dry season, the walls show here and there the scanty beginnings
or the lamentable remains of the mud plastering, and the interior is a
veritable dog-kennel; dirt, dust and disorder everywhere. A few huts
only show any attempt at division into rooms, and this consists
merely of very roughly-made bamboo partitions. In one point alone
have I noticed any indication of progress—in the method of fastening
the door. Houses all over the south are secured in a simple but
ingenious manner. The door consists of a set of stout pieces of wood
or bamboo, tied with bark-string to two cross-pieces, and moving in
two grooves round one of the door-posts, so as to open inwards. If
the owner wishes to leave home, he takes two logs as thick as a man’s
upper arm and about a yard long. One of these is placed obliquely
against the middle of the door from the inside, so as to form an angle
of from 60° to 75° with the ground. He then places the second piece
horizontally across the first, pressing it downward with all his might.
It is kept in place by two strong posts planted in the ground a few
inches inside the door. This fastening is absolutely safe, but of course
cannot be applied to both doors at once, otherwise how could the
owner leave or enter his house? I have not yet succeeded in finding
out how the back door is fastened.

MAKONDE LOCK AND KEY AT JUMBE CHAURO

 This is the general way of closing a house. The Makonde at Jumbe
Chauro, however, have a much more complicated, solid and original
one. Here, too, the door is as already described, except that there is
only one post on the inside, standing by itself about six inches from
one side of the doorway. Opposite this post is a hole in the wall just
large enough to admit a man’s arm. The door is closed inside by a
large wooden bolt passing through a hole in this post and pressing
with its free end against the door. The other end has three holes into
which fit three pegs running in vertical grooves inside the post. The
door is opened with a wooden key about a foot long, somewhat
curved and sloped off at the butt; the other end has three pegs
corresponding to the holes, in the bolt, so that, when it is thrust
through the hole in the wall and inserted into the rectangular
opening in the post, the pegs can be lifted and the bolt drawn out.[50]

MODE OF INSERTING THE KEY

With no small pride first one householder and then a second

showed me on the spot the action of this greatest invention of the
Makonde Highlands. To both with an admiring exclamation of
“Vizuri sana!” (“Very fine!”). I expressed the wish to take back these
marvels with me to Ulaya, to show the Wazungu what clever fellows
the Makonde are. Scarcely five minutes after my return to camp at
Newala, the two men came up sweating under the weight of two
heavy logs which they laid down at my feet, handing over at the same
time the keys of the fallen fortress. Arguing, logically enough, that if
the key was wanted, the lock would be wanted with it, they had taken
their axes and chopped down the posts—as it never occurred to them
to dig them out of the ground and so bring them intact. Thus I have
two badly damaged specimens, and the owners, instead of praise,
come in for a blowing-up.
The Makua huts in the environs of Newala are especially
miserable; their more than slovenly construction reminds one of the
temporary erections of the Makua at Hatia’s, though the people here
have not been concerned in a war. It must therefore be due to
congenital idleness, or else to the absence of a powerful chief. Even
the baraza at Mlipa’s, a short hour’s walk south-east of Newala,
shares in this general neglect. While public buildings in this country
are usually looked after more or less carefully, this is in evident
danger of being blown over by the first strong easterly gale. The only
attractive object in this whole district is the grave of the late chief
Mlipa. I visited it in the morning, while the sun was still trying with
partial success to break through the rolling mists, and the circular
grove of tall euphorbias, which, with a broken pot, is all that marks
the old king’s resting-place, impressed one with a touch of pathos.
Even my very materially-minded carriers seemed to feel something
of the sort, for instead of their usual ribald songs, they chanted
solemnly, as we marched on through the dense green of the Makonde
bush:—
 “We shall arrive with the great master; we stand in a row and have
no fear about getting our food and our money from the Serkali (the
Government). We are not afraid; we are going along with the great
master, the lion; we are going down to the coast and back.”
With regard to the characteristic features of the various tribes here
on the western edge of the plateau, I can arrive at no other
conclusion than the one already come to in the plain, viz., that it is
impossible for anyone but a trained anthropologist to assign any
given individual at once to his proper tribe. In fact, I think that even
an anthropological specialist, after the most careful examination,
might find it a difficult task to decide. The whole congeries of peoples
collected in the region bounded on the west by the great Central
African rift, Tanganyika and Nyasa, and on the east by the Indian
Ocean, are closely related to each other—some of their languages are
only distinguished from one another as dialects of the same speech,
and no doubt all the tribes present the same shape of skull and
structure of skeleton. Thus, surely, there can be no very striking
differences in outward appearance.
 Even did such exist, I should have no time
to concern myself with them, for day after day,
I have to see or hear, as the case may be—in
any case to grasp and record—an
extraordinary number of ethnographic
phenomena. I am almost disposed to think it
fortunate that some departments of inquiry, at
least, are barred by external circumstances.
Chief among these is the subject of iron-
working. We are apt to think of Africa as a
country where iron ore is everywhere, so to
speak, to be picked up by the roadside, and
where it would be quite surprising if the
inhabitants had not learnt to smelt the
material ready to their hand. In fact, the
knowledge of this art ranges all over the
continent, from the Kabyles in the north to the
Kafirs in the south. Here between the Rovuma
and the Lukuledi the conditions are not so
favourable. According to the statements of the
Makonde, neither ironstone nor any other
form of iron ore is known to them. They have
not therefore advanced to the art of smelting
the metal, but have hitherto bought all their
THE ANCESTRESS OF
THE MAKONDE
iron implements from neighbouring tribes.
Even in the plain the inhabitants are not much
better off. Only one man now living is said to
understand the art of smelting iron. This old fundi lives close to
Huwe, that isolated, steep-sided block of granite which rises out of
the green solitude between Masasi and Chingulungulu, and whose
jagged and splintered top meets the traveller’s eye everywhere. While
still at Masasi I wished to see this man at work, but was told that,
frightened by the rising, he had retired across the Rovuma, though
he would soon return. All subsequent inquiries as to whether the
fundi had come back met with the genuine African answer, “Bado”
(“Not yet”).
 BRAZIER

Some consolation was afforded me by a brassfounder, whom I

came across in the bush near Akundonde’s. This man is the favourite
of women, and therefore no doubt of the gods; he welds the glittering
brass rods purchased at the coast into those massive, heavy rings
which, on the wrists and ankles of the local fair ones, continually give
me fresh food for admiration. Like every decent master-craftsman he
had all his tools with him, consisting of a pair of bellows, three
crucibles and a hammer—nothing more, apparently. He was quite
willing to show his skill, and in a twinkling had fixed his bellows on
the ground. They are simply two goat-skins, taken off whole, the four
legs being closed by knots, while the upper opening, intended to
admit the air, is kept stretched by two pieces of wood. At the lower
end of the skin a smaller opening is left into which a wooden tube is
stuck. The fundi has quickly borrowed a heap of wood-embers from
the nearest hut; he then fixes the free ends of the two tubes into an
earthen pipe, and clamps them to the ground by means of a bent
piece of wood. Now he fills one of his small clay crucibles, the dross
on which shows that they have been long in use, with the yellow
material, places it in the midst of the embers, which, at present are
only faintly glimmering, and begins his work. In quick alternation
the smith’s two hands move up and down with the open ends of the
bellows; as he raises his hand he holds the slit wide open, so as to let
the air enter the skin bag unhindered. In pressing it down he closes
the bag, and the air puffs through the bamboo tube and clay pipe into
the fire, which quickly burns up. The smith, however, does not keep
on with this work, but beckons to another man, who relieves him at
the bellows, while he takes some more tools out of a large skin pouch
carried on his back. I look on in wonder as, with a smooth round
stick about the thickness of a finger, he bores a few vertical holes into
the clean sand of the soil. This should not be difficult, yet the man
seems to be taking great pains over it. Then he fastens down to the
ground, with a couple of wooden clamps, a neat little trough made by
splitting a joint of bamboo in half, so that the ends are closed by the
two knots. At last the yellow metal has attained the right consistency,
and the fundi lifts the crucible from the fire by means of two sticks
split at the end to serve as tongs. A short swift turn to the left—a
tilting of the crucible—and the molten brass, hissing and giving forth
clouds of smoke, flows first into the bamboo mould and then into the
holes in the ground.
The technique of this backwoods craftsman may not be very far
advanced, but it cannot be denied that he knows how to obtain an
adequate result by the simplest means. The ladies of highest rank in
this country—that is to say, those who can afford it, wear two kinds
of these massive brass rings, one cylindrical, the other semicircular
in section. The latter are cast in the most ingenious way in the
bamboo mould, the former in the circular hole in the sand. It is quite
a simple matter for the fundi to fit these bars to the limbs of his fair
customers; with a few light strokes of his hammer he bends the
pliable brass round arm or ankle without further inconvenience to
the wearer.
SHAPING THE POT

SMOOTHING WITH MAIZE-COB

CUTTING THE EDGE

 FINISHING THE BOTTOM

LAST SMOOTHING BEFORE

BURNING

FIRING THE BRUSH-PILE

 LIGHTING THE FARTHER SIDE OF
THE PILE

TURNING THE RED-HOT VESSEL

NYASA WOMAN MAKING POTS AT MASASI

Pottery is an art which must always and everywhere excite the
interest of the student, just because it is so intimately connected with
the development of human culture, and because its relics are one of
the principal factors in the reconstruction of our own condition in
prehistoric times. I shall always remember with pleasure the two or
three afternoons at Masasi when Salim Matola’s mother, a slightly-
built, graceful, pleasant-looking woman, explained to me with
touching patience, by means of concrete illustrations, the ceramic art
of her people. The only implements for this primitive process were a
lump of clay in her left hand, and in the right a calabash containing
the following valuables: the fragment of a maize-cob stripped of all
its grains, a smooth, oval pebble, about the size of a pigeon’s egg, a
few chips of gourd-shell, a bamboo splinter about the length of one’s
hand, a small shell, and a bunch of some herb resembling spinach.
 Nothing more. The woman scraped with the
shell a round, shallow hole in the soft, fine
sand of the soil, and, when an active young
girl had filled the calabash with water for her,
she began to knead the clay. As if by magic it
gradually assumed the shape of a rough but
already well-shaped vessel, which only wanted
a little touching up with the instruments
before mentioned. I looked out with the
MAKUA WOMAN closest attention for any indication of the use
MAKING A POT. of the potter’s wheel, in however rudimentary
SHOWS THE a form, but no—hapana (there is none). The
BEGINNINGS OF THE embryo pot stood firmly in its little
POTTER’S WHEEL
depression, and the woman walked round it in
a stooping posture, whether she was removing
small stones or similar foreign bodies with the maize-cob, smoothing
the inner or outer surface with the splinter of bamboo, or later, after
letting it dry for a day, pricking in the ornamentation with a pointed
bit of gourd-shell, or working out the bottom, or cutting the edge
with a sharp bamboo knife, or giving the last touches to the finished
vessel. This occupation of the women is infinitely toilsome, but it is
without doubt an accurate reproduction of the process in use among
our ancestors of the Neolithic and Bronze ages.
There is no doubt that the invention of pottery, an item in human
progress whose importance cannot be over-estimated, is due to
women. Rough, coarse and unfeeling, the men of the horde range
over the countryside. When the united cunning of the hunters has
succeeded in killing the game; not one of them thinks of carrying
home the spoil. A bright fire, kindled by a vigorous wielding of the
drill, is crackling beside them; the animal has been cleaned and cut
up secundum artem, and, after a slight singeing, will soon disappear
under their sharp teeth; no one all this time giving a single thought
to wife or child.
To what shifts, on the other hand, the primitive wife, and still more
the primitive mother, was put! Not even prehistoric stomachs could
endure an unvarying diet of raw food. Something or other suggested
the beneficial effect of hot water on the majority of approved but
indigestible dishes. Perhaps a neighbour had tried holding the hard
roots or tubers over the fire in a calabash filled with water—or maybe
an ostrich-egg-shell, or a hastily improvised vessel of bark. They
became much softer and more palatable than they had previously
been; but, unfortunately, the vessel could not stand the fire and got
charred on the outside. That can be remedied, thought our
ancestress, and plastered a layer of wet clay round a similar vessel.
This is an improvement; the cooking utensil remains uninjured, but
the heat of the fire has shrunk it, so that it is loose in its shell. The
next step is to detach it, so, with a firm grip and a jerk, shell and
kernel are separated, and pottery is invented. Perhaps, however, the
discovery which led to an intelligent use of the burnt-clay shell, was
made in a slightly different way. Ostrich-eggs and calabashes are not
to be found in every part of the world, but everywhere mankind has
arrived at the art of making baskets out of pliant materials, such as
bark, bast, strips of palm-leaf, supple twigs, etc. Our inventor has no
water-tight vessel provided by nature. “Never mind, let us line the
basket with clay.” This answers the purpose, but alas! the basket gets
burnt over the blazing fire, the woman watches the process of
cooking with increasing uneasiness, fearing a leak, but no leak
appears. The food, done to a turn, is eaten with peculiar relish; and
the cooking-vessel is examined, half in curiosity, half in satisfaction
at the result. The plastic clay is now hard as stone, and at the same
time looks exceedingly well, for the neat plaiting of the burnt basket
is traced all over it in a pretty pattern. Thus, simultaneously with
pottery, its ornamentation was invented.
Primitive woman has another claim to respect. It was the man,
roving abroad, who invented the art of producing fire at will, but the
woman, unable to imitate him in this, has been a Vestal from the
earliest times. Nothing gives so much trouble as the keeping alight of
the smouldering brand, and, above all, when all the men are absent
from the camp. Heavy rain-clouds gather, already the first large
drops are falling, the first gusts of the storm rage over the plain. The
little flame, a greater anxiety to the woman than her own children,
flickers unsteadily in the blast. What is to be done? A sudden thought
occurs to her, and in an instant she has constructed a primitive hut
out of strips of bark, to protect the flame against rain and wind.
This, or something very like it, was the way in which the principle
of the house was discovered; and even the most hardened misogynist
cannot fairly refuse a woman the credit of it. The protection of the
hearth-fire from the weather is the germ from which the human
dwelling was evolved. Men had little, if any share, in this forward
step, and that only at a late stage. Even at the present day, the
plastering of the housewall with clay and the manufacture of pottery
are exclusively the women’s business. These are two very significant
survivals. Our European kitchen-garden, too, is originally a woman’s
invention, and the hoe, the primitive instrument of agriculture, is,
characteristically enough, still used in this department. But the
noblest achievement which we owe to the other sex is unquestionably
the art of cookery. Roasting alone—the oldest process—is one for
which men took the hint (a very obvious one) from nature. It must
have been suggested by the scorched carcase of some animal
overtaken by the destructive forest-fires. But boiling—the process of
improving organic substances by the help of water heated to boiling-
point—is a much later discovery. It is so recent that it has not even
yet penetrated to all parts of the world. The Polynesians understand
how to steam food, that is, to cook it, neatly wrapped in leaves, in a
hole in the earth between hot stones, the air being excluded, and
(sometimes) a few drops of water sprinkled on the stones; but they
do not understand boiling.
To come back from this digression, we find that the slender Nyasa
woman has, after once more carefully examining the finished pot,
put it aside in the shade to dry. On the following day she sends me
word by her son, Salim Matola, who is always on hand, that she is
going to do the burning, and, on coming out of my house, I find her
already hard at work. She has spread on the ground a layer of very
dry sticks, about as thick as one’s thumb, has laid the pot (now of a
yellowish-grey colour) on them, and is piling brushwood round it.
My faithful Pesa mbili, the mnyampara, who has been standing by,
most obligingly, with a lighted stick, now hands it to her. Both of
them, blowing steadily, light the pile on the lee side, and, when the
flame begins to catch, on the weather side also. Soon the whole is in a
blaze, but the dry fuel is quickly consumed and the fire dies down, so
that we see the red-hot vessel rising from the ashes. The woman
turns it continually with a long stick, sometimes one way and
sometimes another, so that it may be evenly heated all over. In
twenty minutes she rolls it out of the ash-heap, takes up the bundle
of spinach, which has been lying for two days in a jar of water, and
sprinkles the red-hot clay with it. The places where the drops fall are
marked by black spots on the uniform reddish-brown surface. With a
sigh of relief, and with visible satisfaction, the woman rises to an
erect position; she is standing just in a line between me and the fire,
from which a cloud of smoke is just rising: I press the ball of my
camera, the shutter clicks—the apotheosis is achieved! Like a
priestess, representative of her inventive sex, the graceful woman
stands: at her feet the hearth-fire she has given us beside her the
invention she has devised for us, in the background the home she has
built for us.
At Newala, also, I have had the manufacture of pottery carried on
in my presence. Technically the process is better than that already
described, for here we find the beginnings of the potter’s wheel,
which does not seem to exist in the plains; at least I have seen
nothing of the sort. The artist, a frightfully stupid Makua woman, did
not make a depression in the ground to receive the pot she was about
to shape, but used instead a large potsherd. Otherwise, she went to
work in much the same way as Salim’s mother, except that she saved
herself the trouble of walking round and round her work by squatting
at her ease and letting the pot and potsherd rotate round her; this is
surely the first step towards a machine. But it does not follow that
the pot was improved by the process. It is true that it was beautifully
rounded and presented a very creditable appearance when finished,
but the numerous large and small vessels which I have seen, and, in
part, collected, in the “less advanced” districts, are no less so. We
moderns imagine that instruments of precision are necessary to
produce excellent results. Go to the prehistoric collections of our
museums and look at the pots, urns and bowls of our ancestors in the
dim ages of the past, and you will at once perceive your error.
MAKING LONGITUDINAL CUT IN
BARK

DRAWING THE BARK OFF THE LOG

REMOVING THE OUTER BARK

 BEATING THE BARK

WORKING THE BARK-CLOTH AFTER BEATING, TO MAKE IT

SOFT

MANUFACTURE OF BARK-CLOTH AT NEWALA

To-day, nearly the whole population of German East Africa is
clothed in imported calico. This was not always the case; even now in
some parts of the north dressed skins are still the prevailing wear,
and in the north-western districts—east and north of Lake
Tanganyika—lies a zone where bark-cloth has not yet been
superseded. Probably not many generations have passed since such
bark fabrics and kilts of skins were the only clothing even in the
south. Even to-day, large quantities of this bright-red or drab
material are still to be found; but if we wish to see it, we must look in
the granaries and on the drying stages inside the native huts, where
it serves less ambitious uses as wrappings for those seeds and fruits
which require to be packed with special care. The salt produced at
Masasi, too, is packed for transport to a distance in large sheets of
bark-cloth. Wherever I found it in any degree possible, I studied the
process of making this cloth. The native requisitioned for the
purpose arrived, carrying a log between two and three yards long and
as thick as his thigh, and nothing else except a curiously-shaped
mallet and the usual long, sharp and pointed knife which all men and
boys wear in a belt at their backs without a sheath—horribile dictu!
[51]
Silently he squats down before me, and with two rapid cuts has
drawn a couple of circles round the log some two yards apart, and
slits the bark lengthwise between them with the point of his knife.
With evident care, he then scrapes off the outer rind all round the
log, so that in a quarter of an hour the inner red layer of the bark
shows up brightly-coloured between the two untouched ends. With
some trouble and much caution, he now loosens the bark at one end,
and opens the cylinder. He then stands up, takes hold of the free
edge with both hands, and turning it inside out, slowly but steadily
pulls it off in one piece. Now comes the troublesome work of
scraping all superfluous particles of outer bark from the outside of
the long, narrow piece of material, while the inner side is carefully
scrutinised for defective spots. At last it is ready for beating. Having
signalled to a friend, who immediately places a bowl of water beside
him, the artificer damps his sheet of bark all over, seizes his mallet,
lays one end of the stuff on the smoothest spot of the log, and
hammers away slowly but continuously. “Very simple!” I think to
myself. “Why, I could do that, too!”—but I am forced to change my
opinions a little later on; for the beating is quite an art, if the fabric is
not to be beaten to pieces. To prevent the breaking of the fibres, the
stuff is several times folded across, so as to interpose several
thicknesses between the mallet and the block. At last the required
state is reached, and the fundi seizes the sheet, still folded, by both
ends, and wrings it out, or calls an assistant to take one end while he
holds the other. The cloth produced in this way is not nearly so fine
and uniform in texture as the famous Uganda bark-cloth, but it is
quite soft, and, above all, cheap.
Now, too, I examine the mallet. My craftsman has been using the
simpler but better form of this implement, a conical block of some
hard wood, its base—the striking surface—being scored across and
across with more or less deeply-cut grooves, and the handle stuck
into a hole in the middle. The other and earlier form of mallet is
shaped in the same way, but the head is fastened by an ingenious
network of bark strips into the split bamboo serving as a handle. The
observation so often made, that ancient customs persist longest in
connection with religious ceremonies and in the life of children, here
finds confirmation. As we shall soon see, bark-cloth is still worn
during the unyago,[52] having been prepared with special solemn
ceremonies; and many a mother, if she has no other garment handy,
will still put her little one into a kilt of bark-cloth, which, after all,
looks better, besides being more in keeping with its African
surroundings, than the ridiculous bit of print from Ulaya.
MAKUA WOMEN