Journal of the American Academy of Orthopaedic Surgeons
190
Electrodiagnostic evaluation can
be useful in distinguishing among
a variety of causes for numbness,
weakness, and pain. Although
most commonly used in diagnos-
ing entrapment neuropathies, such
as carpal tunnel syndrome and
radiculopathies, electrodiagnostic
evaluation often plays an impor-
tant role in assessing more com-
plex conditions. In individuals
with severe traumatic neuropa-
thies, electromyographic (EMG)
and nerve conduction studies can
establish a prognosis for signifi-
cant functional recovery; those
with severe or complete axon loss
will have a less favorable outcome
than those with evidence of neu-
rapraxia. Radial and sciatic nerve
lesions are two common examples
of this. In patients who present
with diffuse numbness and weak-
ness, it may be difficult to clinical-
ly differentiate central lesions
(such as those of motor neuron dis-
ease) from peripheral neuropathy
or spinal stenosis (cervical and/or
lumbar). In many cases, electrodi-

agnostic evaluation can establish
whether central or peripheral pro-
cesses (or both) contribute to a pa-
tientÕs symptoms.
To provide useful information,
the electrodiagnostic examination
must include a clinical assessment
as well as neurophysiologic testing.
The electrodiagnostic medical con-
sultation should always start with
a directed history and physical
examination and should utilize
electrophysiologic testing to help
answer the diagnostic questions
posed by the differential diagnosis
considered by the referring physi-
cian and the consultant. Diagnoses
should not be made solely on the
basis of electrophysiologic Òabnor-
malities,Ó but rather in the context
of the patientÕs complaints.
Neurophysiology of
Impulse Transmission and
Measurement
The axon membrane is composed of
a lipid bilayer, permeable to water
but not to most ions or larger mole-
cules. This selective permeability,
coupled with the presence of the
Na

+
/K
+
-ATPÐdependent electro-
genic pump, allows for maintenance
of a resting membrane potential of
60 to 90 mV, which is negative
inside the axon membrane. Sodium
ions are accumulated outside the
membrane at a concentration about
12 times greater than inside, and
potassium ions are concentrated
inside the cell, at a concentration
about 30 times greater than outside.
There are also mechanisms pres-
ent to allow the generation of an
action potential. An action poten-
tial is a traveling depolarization
that allows transmission of infor-
mation along the nerve. It is gener-
ated by a specific set of mecha-
Dr. Robinson is Professor of Rehabilitation
Medicine, University of Washington School of
Medicine, Seattle, and Chief of Rehabilitation
Medicine and Director, Electrodiagnostic
Medicine Laboratory, Harborview Medical
Center, Seattle.
Reprint requests: Dr. Robinson, Rehabilitation
Medicine, Harborview Medical Center, Box
359740, 325 Ninth Avenue, Seattle, WA

98104.
Copyright 2000 by the American Academy of
Orthopaedic Surgeons
Abstract
The electrodiagnostic evaluation assesses the integrity of the lower-motor-
neuron unit (i.e., peripheral nerves, neuromuscular junction, and muscle).
Sensory- and motor-nerve conduction studies measure compound action
potentials from nerve or muscle and are useful for assessing possible axon loss
and/or demyelination. Needle electromyography measures electrical activity
directly from muscle and provides information about the integrity of the motor
unit; it can be used to detect loss of axons (denervation) as well as reinnerva-
tion. The electrodiagnostic examination is a useful tool for first detecting
abnormalities and then distinguishing problems that affect the peripheral ner-
vous system. In evaluating the patient with extremity trauma, it can differen-
tiate neurapraxia from axonal transection and can be helpful in following the
clinical course. In patients with complex physical findings, it is a useful
adjunct that can help discriminate motor neuron disease from polyneuropathy
or myeloradiculopathy due to spondylosis.
J Am Acad Orthop Surg 2000;8:190-199
Role of Neurophysiologic Evaluation in Diagnosis
Lawrence R. Robinson, MD
Lawrence R. Robinson, MD
Vol 8, No 3, May/June 2000
191
nisms. Specifically, voltage-gated
Na
+
channels based in the axon
membrane are activated by partial
membrane depolarization; opening

of Na
+
channels allows inflow of
Na
+
ions such that the membrane
becomes further depolarized and
even briefly hyperpolarized (i.e.,
relatively positive inside the mem-
brane [30 to 40 mV]). Closing of
sodium channels and opening of
K
+
channels, with resultant K
+
efflux, then rapidly brings the
membrane back to the resting state
and ready for another wave of
depolarization after an absolute
refractory period (i.e., time during
which the nerve cannot be depolar-
ized again) of about 1 msec.
1
These sequential depolarizations
proceed along the axon membrane.
In the absence of myelin (e.g., on
autonomic fibers and slow pain
fibers), this is a slow process, with a
conduction velocity of about 5 to 15
m/sec, depending on axon diame-

ter. Myelin, however, allows for
faster conduction, as currents jump
from one node of Ranvier to the
next; saltatory (node-to-node) con-
duction speeds of 40 to 70 m/sec
are achieved. Most motor and sen-
sory fibers in human peripheral
nerves are myelinated; the largest-
diameter and most heavily myelin-
ated fibers are spindle afferents and
alpha motor neurons.
When a nerve is electrically
stimulated, the propagation of
these action potentials can be re-
corded by using surface electrodes.
The voltage at the skin surface for
these action potentials ranges from
a few microvolts to a few hundred
microvolts. A recording from
nerve is usually referred to as a
compound nerve action potential
(CNAP). If the action potential is
recorded from a pure sensory
nerve, it is referred to as a sensory
nerve action potential (SNAP).
When motor nerves are stimulated,
potentials can be recorded directly
from muscle. Because each axon
synapses with many muscle fibers,
a much larger response is usually

produced at the muscle level. The
amplitude of the resulting com-
pound muscle action potential
(CMAP) is typically a few millivolts.
If mixed axons are involved (e.g.,
motor and sensory), the response is
best referred to as a CNAP.
Principles of Nerve
Conduction Studies
Sensory- and Mixed-Nerve
Conduction Studies
Typically, CNAPs and SNAPs
are measured by electrically stimu-
lating a peripheral nerve and re-
cording the response a known dis-
tance away. Recording that reflects
propagation along the nerve in a
physiologic direction (e.g., after
stimulating a digital sensory nerve
and recording from the wrist) is
referred to as Òorthodromic record-
ing.Ó However, stimulation of a
nerve usually activates the nerve in
both directions from the point of
stimulation. If recordings are from
a nonphysiologic direction (e.g.,
stimulation of the median sensory
nerve at the wrist and recording
from a digital nerve), this is re-
ferred to as Òantidromic recording.Ó

The speed of conduction is the
same in either direction.
For clinical purposes, there are, in
broad terms, usually two measures
one makes of CNAPs or SNAPs:
(1) speed of conduction (i.e., latency
or velocity) and (2) size of the
response (i.e., amplitude) (Fig. 1).
Traditionally, the speed of conduc-
tion for CNAPs and SNAPs has
been measured in terms of latency
(i.e., the time between the onset of
stimulation and either the onset or
the peak of the potential). Peak
latency is easier to measure, particu-
larly when the potential is small or
the baseline is noisy. Onset latency,
although more difficult to measure,
has the physiologic significance of
representing the arrival of the
impulse via the fastest-conducting
nerve fibers at the recording elec-
trode. Conduction velocity for
CNAPs can be derived by dividing
the distance between the stimulation
site and the active (G1) electrode by
the onset latency, represented by the
equation CV = d/t, where CV = con-
duction velocity in meters per sec-
ond, d = distance between stimula-

tion site and recording electrode in
millimeters, and t = onset latency in
milliseconds.
Latency and conduction velocity
can be affected by a number of
physiologic and pathologic factors.
In healthy control subjects, slowed
conduction can be a result of fac-
tors such as the temperature of the
extremity or even normal aging.
Pathologically, demyelination pro-
duces slowing. Conditions that
result in loss of axons, particularly
faster-conducting axons, also pro-
duce slowing of nerve conduction
or prolongation of latency.
The amplitude of the CNAP can
be measured from baseline to peak
or from peak to peak. In general,
the size of the CNAP and the SNAP
is roughly proportional to the num-
ber of axons depolarizing under the
active electrode. It can be affected
Figure 1 Measures of the SNAP or
CNAP. Latency is the time between stimu-
lus and the onset or peak of the potential.
Amplitude is measured from peak to peak.
Conduction velocity (CV) is calculated as
distance divided by onset latency.
peak latency

amplitude
onset
latency
distance
onset latency
CV =
Neurophysiologic Evaluation
Journal of the American Academy of Orthopaedic Surgeons
192
by a number of physiologic and
pathologic factors. Cold increases
the amplitude of both the CNAP
and the SNAP. Aging produces
smaller-amplitude SNAPs, probably
as a result of gradual loss of large
myelinated axons.
Pathologically, loss of axons will
reduce the amplitude of the CNAP.
Distal lesions between the sites of
stimulation and recording will de-
crease the amplitude of the CNAP
immediately, as conduction cannot
traverse the lesion. Proximal le-
sions (e.g., brachial plexus lesions)
that separate sensory axons from
their cell bodies (in the dorsal root
ganglion) will produce distal axon
loss due to axonal (wallerian) de-
generation over time (usually 7 to
10 days after injury).

2
Thus, a
reduced-amplitude SNAP can be
due to an axonal lesion anywhere
distal to the dorsal root ganglion.
Motor-Nerve Conduction Studies
The principles of stimulation and
recording for motor-nerve conduc-
tion studies are similar to those
used for sensory-nerve conduction
studies with several exceptions.
The primary difference is that
motor-nerve conduction studies
involve recording a CMAP over
muscle rather than recording direct-
ly from nerve. Therefore, the distal
latency involves not only conduc-
tion along the nerve from the point
of stimulation (proceeding at about
50 m/sec), but also includes neuro-
muscular junction transmission
time (which takes about 1 msec) and
conduction along muscle fibers
(about 3 to 5 m/sec). Although la-
tency from a distal stimulation site
can be measured, it cannot be con-
verted into a nerve conduction
velocity in the same way as a SNAP
can be, because of this additional
time for neuromuscular junction

transmission and muscle fiber con-
duction. Therefore, to evaluate con-
duction velocities, motor nerves are
typically stimulated in two places,
and the distance between the two
stimulation sites is divided by the dif-
ference in latency; neuromuscular-
junction transmission time and
muscle-fiber conduction velocity are
canceled out in the process (Fig. 2).
Many of the same factors affect
motor-nerve conduction studies as
affect sensory-nerve conduction
studies.
3
There are, however, two
important differences. First, be-
cause motor-neuron cell bodies
reside in the anterior horn of the
spinal cord rather than in the dor-
sal root ganglion, the amplitude of
the response is diminished by axon
loss at the anterior horn cell or dis-
tally (i.e., not at the dorsal root gan-
glion). A root lesion proximal to
the dorsal root ganglion, for exam-
ple, would diminish the amplitude
of the CMAP but not that of the
SNAP. Second, because recording
is from muscle, neuromuscular-

junction transmission defects or
primary myopathies may reduce
the amplitude of the CMAP.
Late Responses
There are two ÒlateÓ responses
(i.e., occurring late after the CMAP
or M wave), which sometimes pro-
vide useful information: the F wave
and the H wave.
4
The F wave (so
named because it was first recorded
in foot muscles) is a late response
usually recorded from distal mus-
cles. Physiologically, when a motor
nerve is stimulated distally, axons
are depolarized in both directionsÑ
distally (orthodromically) and proxi-
mally (antidromically). The ortho-
dromic volley activates the muscle
distally, and the antidromic volley
proceeds proximally to the anterior
horn cell. It is thought that the F
wave occurs when a small percent-
age (3% to 5%) of antidromically
activated motor cell bodies dis-
charge and produce orthodromic
activation of their motor axons. This
is noted as a small-amplitude (about
100 to 200 µV) late (about 30 msec in

the distal upper limb) potential.
F-wave measurements usually
find their greatest applicability in
the assessment of multifocal or dif-
fuse processes, especially those af-
fecting proximal areas of the periph-
eral nervous system. Acquired or
inherited demyelinating polyneu-
ropathies that produce multifocal
or diffuse slowing are clinical set-
tings in which F waves can provide
additional useful information.
Although it would seem appealing
to use F waves for the diagnosis of
brachial plexopathy or some en-
trapment neuropathies, they are
usually not of significant help in
these applications, nor do they
offer unique information not ob-
tained by conventional nerve con-
duction studies. Because the F
wave is produced by only a small
percentage of the motor axons, the
presence of just a few normally
conducting fibers will result in nor-
mal latencies. Moreover, the F-
wave volley traverses such a long
distance of peripheral nerve that a
focal lesion, unless there is severe
demyelination, would not be ex-

pected to produce marked abnor-
malities in F-wave latencies.
The H wave (named after Hoff-
man) involves synaptic transmis-
amplitude
amplitude
latency1
latency2
Wrist
Elbow
∆ distance
lat2 − lat1
CV =
Figure 2 Measures of the CMAP. Latency
is the time between stimulus and the onset
of the potential. Amplitude is measured
from baseline to peak. Conduction velocity
(CV) can be calculated as the distance be-
tween two points divided by the latency
difference between two points.
Lawrence R. Robinson, MD
Vol 8, No 3, May/June 2000
193
sion at the spinal cord level and is
in many ways analogous to the
muscle stretch reflex. However,
instead of activating stretch recep-
tors within the muscle mechanical-
ly, the large-diameter afferent
nerve fibers are activated electrical-

ly. After the afferent volley reaches
the spinal cord, a monosynaptic
reflex excites alpha motor neurons,
and a late response is produced in
the muscle. The H reflex can usual-
ly be elicited only in the soleus
muscle in adults.
The most useful application of
the H wave is in the detection of S1
radiculopathy.
5
It has been shown
that the H wave is more sensitive
than needle electromyography in
the assessment of S1 radiculopathy,
probably related to the fact that the
H wave can depict conduction
block and demyelination, whereas
needle electromyography can be
used to detect only motor axon loss.
Principles of Needle
Electromyography
Needle electromyography assesses
the function of the motor unitÑthe
combination of an anterior horn
cell, an axon, and all the muscle
fibers supplied by the single axon.
It is very sensitive for detection of
axon loss at any level along the
lower motor neuron once sufficient

time has elapsed for fibrillations
and other abnormalities to develop
(usually 2 to 3 weeks).
6
There are
usually four distinct steps in the
needle EMG examination for each
muscle: (1) insertional activity, (2)
spontaneous activity, (3) examina-
tion of motor-unit potentials, and
(4) assessment of recruitment.
Insertional Activity
Insertional activity is examined
by moving the needle through the
muscle briefly and observing the
amount and duration of the electri-
cal potentials produced. Insertional
activity may be decreased or may be
prolonged in duration. Decreased
insertional activity can result if the
needle is not positioned in muscle
or is in a muscle that has marginal
viability. Muscles that have become
atrophied and fibrotic will have
reduced insertional activity, as will
muscles that have become necrotic
due to compartment syndrome.
Prolonged or increased insertional
activity, as an isolated finding, is a
very ÒsoftÓ abnormality. No diag-

nosis should be made on the basis
of this ÒabnormalityÓ when it is an
isolated finding, as it may be seen in
some asymptomatic individuals. In-
creased insertional activity can also
be seen in association with fibril-
lations or positive sharp waves and
thus may be an indicator of either
denervation or a primary muscle
disorder.
Spontaneous Activity
Spontaneous activity consists of
electrical discharges that are seen
without needle movement or vol-
untary contraction. Fibrillation
potentials represent abnormal
spontaneous single muscle-fiber
discharges. Fibrillation potentials
are essentially always abnormal,
but they are a nonspecific finding.
Fibrillation potentials are often seen
in denervated muscles. Myopathies
may be associated with fibrillation
potentials. Disorders characterized
by upper-motor-neuron lesions,
such as stroke and spinal cord
injury, have been shown to produce
fibrillation potentials; these are usu-
ally seen early after onset of the
lesion and can be confusing when

trying to diagnose a peripheral-
nerve lesion superimposed on an
upper-motor-neuron lesion.
Fibrillation potentials are usually
graded on a scale from 1+ to 4+,
with 1+ representing a repro-
ducibly observed fibrillation in an
isolated area and 4+ representing
sustained fibrillation potentials
(which often obscure the baseline)
throughout the muscle. The size of
fibrillation potentials has been cor-
related with the time since onset of
denervation. Large-amplitude fi-
brillation potentials (>100 µV) are
seen within the first year after onset
of denervation; smaller amplitudes
(<100 µV) are seen later.
7
It has
been postulated that this relation-
ship reflects muscle fiber atrophy
over time, with smaller-diameter
fibers producing smaller-amplitude
fibrillations. Consequently, large-
amplitude fibrillations in the pres-
ence of a neuropathic lesion suggest
recent denervation.
Positive sharp waves can be
thought of in much the same way

as fibrillation potentials. They also
represent abnormal spontaneous
single-muscle-fiber discharges.
Positive sharp waves can be seen in
essentially all the same disorders as
fibrillation potentials. In some
cases of muscle trauma, positive
sharp waves may be seen in isola-
tion without associated fibrilla-
tions. Positive sharp waves are
thought to have the same patho-
physiologic characteristics as fibril-
lation potentials and can be graded
by using the same scheme.
Complex repetitive discharges,
formally known as Òbizarre high-
frequency discharges,Ó probably
represent groups of muscle fibers
firing in near synchrony. They are
usually seen in chronic neuropathic
and myopathic conditions. When
seen in isolation, they are a nonspe-
cific but usually abnormal finding,
similar to positive sharp waves and
fibrillations.
Fasciculation potentials repre-
sent spontaneous discharges of a
single motor unit. As opposed to a
fibrillation potential (in which only
a single muscle fiber fires), a fascic-

ulation potential involves the entire
motor unit (the axon and all the
muscle fibers that it supplies).
Unlike fibrillation potentials, fasci-
culations produce enough force
that they can be seen on the skin
Neurophysiologic Evaluation
Journal of the American Academy of Orthopaedic Surgeons
194
clinically. Fasciculation potentials
are often generated at the anterior
horn cell, as in motor neuron dis-
eases, but they may also be ectopi-
cally generated distally along the
axon, possibly even in intramuscu-
lar axons.
Fasciculation potentials can be
seen in a variety of neuromuscular
disorders. In addition to motor
neuron disease and the syndrome of
benign fasciculations, fasciculation
potentials can be seen in chronic
radiculopathies, peripheral polyneu-
ropathies, thyrotoxicosis, and over-
dosage of anticholinesterase med-
ications.
Motor-Unit Analysis
A great deal of information can be
obtained from analysis of voluntarily
activated motor-unit action poten-

tials (MUAPs) (Fig. 3). The MUAP
represents the electrical potential cre-
ated by the synchronous discharge
of all the muscle fibers supplied by a
single motor axon.
Theoretically, in neuropathic
conditions in which there has been
partial denervation and reinnerva-
tion, one will see changes represen-
tative of the underlying process of
axonal sprouting (Fig. 4). Within
days after partial denervation, intra-
muscular axons that remain unaf-
fected will send sprouts, usually
emanating from distal nodes of
Ranvier, to reinnervate nearby
denervated muscle fibers. These
sprouts, particularly early on, are
not yet well myelinated and, there-
fore, conduct slowly. Consequently,
in the early phases of reinnervation,
one will note increased polyphasici-
ty and increased duration of the
MUAP as a result of temporal dis-
persion in newly formed sprouts
and poor synchronization of muscle-
fiber discharges. As these sprouts
mature, synchronization of muscle-
fiber discharges improves; the
polyphasicity tends to be reduced,

and one is left with large-amplitude,
long-duration MUAPs. The in-
crease in amplitude is a result of the
increased number of muscle fibers
belonging to the same motor unit
within the recording area of the tip
of the EMG needle.
Myopathic changes in the MUAP
result from loss of individual mus-
cle fibers. In myopathic conditions,
the MUAPs are typically small in
amplitude and short in duration.
Furthermore, fewer muscle fibers
from the same motor unit fire with-
in the recording area of the needle
electrode.
Recruitment
Evaluation of motor unit recruit-
ment can assess whether reduced
strength is due to a reduction in the
lower-motor-neuron pool or to
poor central effort. In distinguish-
ing between these two possibilities,
the primary feature that is mea-
sured is the motor-unit firing rate.
Central recruitment implies that
there are reduced numbers of mo-
tor units firing but that they are fir-
ing at normal or slow speed. This
1

2
3
duration
amplitude
Figure 3 Measures of the MUAP include
duration (from onset to termination),
amplitude (from peak to peak), and num-
ber of phases (numbered, as shown).
Figure 4 Top, Normal MUAP, recorded by a needle electrode from muscle fibers within
its recording area. Middle, After denervation, single muscle fibers spontaneously dis-
charge, producing fibrillations and positive sharp waves. Bottom, When reinnervation by
axon sprouting has occurred, the newly formed sprouts will conduct slowly, producing
temporal dispersion (i.e., prolonged MUAP duration) and MUAP polyphasicity. The high-
er density of muscle fibers within the recording area of the needle belonging to the enlarg-
ing second motor unit results in an increased-amplitude MUAP.
Normal
Denervation
Reinnervation
Lawrence R. Robinson, MD
Vol 8, No 3, May/June 2000
195
is by far the most common Òabnor-
malityÓ in recruitment, but in isola-
tion it is completely nondiagnostic.
Central recruitment can be reflec-
tive of upper-motor-neuron le-
sions, pain, or poor voluntary ef-
fort. Reduced recruitment (noted
in less severe conditions) and dis-
crete recruitment (noted in more

severe conditions) are pathologically
significant and imply that there are
reduced numbers of motor units
firing rapidly.
Interpretation of the
Electrodiagnostic
Examination
Principles of Localization
Needle electromyography is con-
ventionally used for evaluation of
lesions that are primarily axonal or
so proximal that it is not possible to
stimulate both proximal and distal
to an entrapment site. Muscles that
are supplied by multiple peripheral
nerves, roots, or areas of the plexus
are examined, and a localization is
made on the basis of the distribu-
tion of abnormalities. A sciatic
nerve lesion in the thigh can be dis-
tinguished from L5 radiculopathy,
for example, if there is evidence of
denervation in muscles supplied by
the superficial and deep branches
of the peroneal nerve but not the
tensor fasciae latae or paraspinal
muscles. Thus, localization is based
on finding abnormalities distal to a
branch point but normal findings
proximally.

8,9
Nerve conduction studies are
best at localizing the site of patho-
logic change when there is demye-
lination. As mentioned previously,
demyelination causes focal slowing
and conduction block; the presence
of these findings can precisely lo-
calize a focal entrapment. Conduc-
tion block and slowing is observed
only in demyelination and neura-
praxia. It is not present in lesions
with axon loss once wallerian de-
generation has occurred (about 7
days after onset); therefore, localiza-
tion of purely axonal lesions de-
pends primarily on EMG findings.
Deducing the Pathophysiology
Neurapraxia and demyelination
are best demonstrated when there
is focal conduction block and slow-
ing on nerve conduction studies
but a large-amplitude CMAP or
SNAP is elicited distal to the site of
the lesion. Purely neurapraxic
injuries have no electrophysiologic
evidence of axon loss (fibrillation
potentials or positive sharp waves)
or reinnervation.
Axon-loss lesions (e.g., axonot-

mesis and neurotmesis
10
) are usually
demonstrated by evidence of de-
nervation on needle EMG examina-
tion as well as small-amplitude
CMAP and SNAP responses with
stimulation and recording distal to
the site of the lesion. While needle
electromyography is a more sensi-
tive indicator for motor-axon loss,
measurement of CMAP or SNAP
amplitude is a better measure of the
degree of axon loss and of prognosis.
Axonotmesis and neurotmesis can-
not usually be distinguished on elec-
trodiagnostic studies, because the
primary difference between the two
conditions is integrity of the support-
ing structures (which have no elec-
trophysiologic function) (Table 1).
Timing of Electrophysiologic
Changes
The time course of electrodiag-
nostic changes after the onset of a
neuropathic lesion is an important
consideration that influences the
interpretation of the electrophysio-
logic examination. Neurapraxia,
demyelination, and severe axon

loss produce electrophysiologic
changes immediately at onset if the
nerve can be stimulated both proxi-
mal and distal to the lesion. How-
ever, proximal lesions, in which it
is not possible to get proximal and
distal to the lesion, do not immedi-
ately produce changes on distal
nerve conduction studies or elec-
tromyography. Moreover, distinc-
tion between neurapraxia and ax-
onotmesis cannot be made until 7
days have passed, allowing time
for wallerian degeneration to have
progressed to the point that stimu-
lation of motor axons elicits no
Table 1
Electrodiagnostic Findings in Various Peripheral Nerve Disorders
Root Plexus Focal Axonal Demyelinating
Finding Lesion Lesion Entrapment Polyneuropathy Polyneuropathy
Motor nerve amplitude +/− (focal) +/− (diffuse) +/−
Sensory nerve amplitude Normal (focal) +/− (diffuse) +/−
Distal latency Normal Normal (focal) Normal (diffuse)
Conduction velocity Normal Normal (focal) Normal (diffuse)
Fibrillations + (acute) + (acute) +/− (severe) + +/−
Large polyphasic MUAPs + (chronic) + (chronic) +/− (severe) + +/−
Neurophysiologic Evaluation
Journal of the American Academy of Orthopaedic Surgeons
196
motor responses.

2
Ten days after
the onset of a complete lesion,
SNAPs will be absent as well.
Therefore, 7 to 10 days after onset,
a neurapraxic injury (in which the
distal amplitudes will be normal)
can be differentiated by nerve con-
duction studies from an axonot-
metic lesion (in which the distal
amplitudes will be reduced).
Two to three weeks after the
onset of injury, the needle EMG
study starts to show fibrillation
potentials and positive sharp
waves.
6
Proximal muscles demon-
strate these abnormalities first;
more distal muscles, later. Radicu-
lopathies, for example, may show
paraspinal abnormalities at day 10
to 14 after onset, but distal-limb
muscle changes may not be appar-
ent for 3 to 4 weeks after onset.
Fibrillations and positive sharp
waves may persist for several
months or even many years after a
single injury, depending on the
extent of reinnervation.

The timing and type of electro-
physiologic changes consequent to
reinnervation will depend in part
on the mechanism of reinnervation.
When reinnervation is a result of
axonal regrowth from the site of the
lesion (usually in complete injuries),
the appearance of new MUAPs will
not occur until motor axons have
had sufficient time to regenerate
across the distance between the
lesion site and the muscle (usually
proceeding at a rate of a few mil-
limeters a day). When these new
axons first reach the muscle, they
will innervate only a few muscle
fibers, producing short-duration,
small-amplitude potentials, some-
times referred to as Ònascent poten-
tials.Ó With time, as more muscle
fibers join the motor unit, the
MUAPs will become larger, more
polyphasic, and longer in duration.
Motor-unit potential changes
will also develop when reinnerva-
tion occurs by axonal sprouting.
Polyphasicity and increased dura-
tion develop first as newly formed,
poorly demyelinated sprouts sup-
ply the recently denervated muscle

fibers. As the sprouts mature, large-
amplitude, long-duration MUAPs
develop and persist indefinitely.
Evaluation of Common
Clinical Entities
Hand Numbness (Case 1)
A 50-year-old woman presents
with a 3-month history of progres-
sive right-hand numbness. The
numbness involves all digits of the
hand but is restricted to the palmar
aspect. She reports mild chronic
neck pain but denies symptoms in
the feet. Physical examination
demonstrates normal strength and
muscle stretch reflexes; sensation is
normal to pin prick and light touch.
There is a positive Tinel sign over
the median nerve at the wrist and
at the ulnar groove bilaterally, but
no Phalen sign.
The differential diagnosis in this
case includes median neuropathy
at the wrist (e.g., carpal tunnel syn-
drome), cervical radiculopathy,
and ulnar neuropathy. Electrodiag-
nostic studies are therefore oriented
toward looking for evidence of
slowing in peripheral nerves or evi-
dence of denervation in the mus-

cles of the upper limb. A notable
finding is slowing in the median
nerve at the wrist, with prolonged
latencies compared with both radial
and ulnar nerves (Fig. 5). It has
recently been shown that it is better
(in terms of sensitivity, specificity,
and reliability) to perform the three
comparisons of median and ulnar
nerves illustrated and then to add
the median-ulnar and median-radial
nerve latency differences, rather
than looking at individual tests
alone (Fig. 6).
11
There is no evi-
dence of slowing in the ulnar
nerve, nor is there evidence of de-
nervation in the C5 to T1 myotomes
of the upper limb; thus, the find-
Nerve Conduction Studies
Stimulate Record Latency (msec) Amplitude Velocity (m/sec)
Median nerve (sensory) Wrist Ring finger 4.8 12 µV
Ulnar nerve (sensory) Wrist Ring finger 3.5 8 µV
Median nerve (sensory) Wrist Thumb 4.1 21 µV
Radial nerve (sensory) Wrist Thumb 2.8 11 µV
Median nerve (sensory) Palm Wrist 3.1 20 µV
Ulnar nerve (sensory) Palm Wrist 2.1 22 µV
Median nerve (motor) Wrist APB 4.5 (<4.3) 6.7 (³5.0) mV
Elbow APB 6.1 (³5.0) mV 51 (³50)

Ulnar nerve (motor) Wrist ADM 3.6 (<3.8) 8.3 (³5.0) mV
Below elbow ADM 8.1 (³5.0) mV 57 (³50)
Above elbow ADM 7.7 (³5.0) mV 61 (³50)
Needle EMG
Spontaneous Activity Motor Unit Action Potentials
Muscle Myotome Ins. Act. Fibs/PSWs Amplitude Duration Phasicity Recruitment
Deltoid C5,6 Normal None Normal Normal Normal Full
Biceps C5,6 Normal None Normal Normal Normal Full
Pronator teres C6,7 Normal None Normal Normal Normal Full
ECR C6,7 Normal None Normal Normal Normal Full
FCR C6-8 Normal None Normal Normal Normal Full
Triceps C7,8 Normal None Normal Normal Normal Full
APB C8,T1 Normal None Normal Normal Normal Full
FDI C8,T1 Normal None Normal Normal Normal Full
Cervical paraspinals C5-T1 Normal None
Figure 5 Findings from nerve conduction and needle EMG studies in case 1. Normal val-
ues are shown in parentheses. Abbreviations: ADM = abductor digiti minimi; APB = abduc-
tor pollicis brevis; ECR = extensor carpi radialis; FCR = flexor carpi radialis; FDI = first dorsal
interosseous; Fibs/PSWs = fibrillations/positive sharp waves; Ins. Act. = insertional activity.
Lawrence R. Robinson, MD
Vol 8, No 3, May/June 2000
197
ings are consistent with carpal tun-
nel syndrome but are not sugges-
tive of ulnar neuropathy or cervical
radiculopathy.
Pain in the Low Back and Lower
Limb (Case 2)
A 45-year-old man reports low
back pain extending into the left

lower limb, with pain and numb-
ness in the posterolateral thigh
and leg and the lateral aspect of
the foot. This started after an
injury at work when he was lifting
and rotating a heavy object. He
had a similar episode 4 years pre-
viously, which resolved with con-
servative management. Physical
examination demonstrates normal
strength and sensation but a de-
creased left ankle jerk. The diag-
nostic questions in this case are
whether a radiculopathy is present
and, if so, at what level and of
what duration.
Needle electromyography was
performed on the muscles of the
left lower limb, evaluating com-
monly affected myotomes (L3 to
S2) to look for evidence of either
acute denervation or prior dener-
vation and reinnervation. The
findings shown in Figure 7 indicate
both recent denervation (fibrilla-
tions and positive sharp waves)
and reinnervation (large, long-
duration MUAPs) in the left S1 dis-
tribution. These findings allow one
to infer that there is both a new-

onset S1 radiculopathy and a pre-
existing radiculopathy at the same
level. Asymmetry of the H waves
(smaller amplitude and longer
latency on the left) confirms the
presence of an abnormality at the
S1 level.
Combined Upper- and Lower-
Motor-Neuron Findings (Case 3)
A 70-year-old retired cardiac sur-
geon complains of progressive
weakness in the upper and lower
limbs and muscle atrophy in the
upper limbs. He has only vague
sensory symptoms of numbness in
the upper limbs. He denies bowel
or bladder dysfunction. There is a
history of chronic mild neck pain
with no difficulty speaking or swal-
lowing. He reports intermittent
muscle twitching in the pectoral
muscles, worse with cold (he is not
sure if this is shivering). On physi-
cal examination, there is marked
muscle atrophy in the upper limbs
but normal muscle bulk in the lower
limbs. Strength is diffusely weak
(4/5 on MRC scale) in the upper
and lower limbs. Sensation is nor-
mal. Muscle stretch reflexes are

hyperactive in the upper and lower
limbs. Cervical spine radiographs
reveal marked degenerative changes
(spondylosis).
The diagnostic question in this
case is whether cervical myelopathy
or motor neuron disease is the
cause of the patientÕs symptoms.
Although the clinical features could
be consistent with either diagnosis,
the electrodiagnostic features are
usually different. Cervical spondy-
Figure 6 Nerve conduction studies in
case 1. Note prolongation of peak latencies
(values in parentheses) in median nerves
compared with ulnar and radial nerves.
The combined sensory index is calculated
by adding the peak latency differences
between median and ulnar nerves to the
ring finger (4.8 Ð 3.5 = 1.3 msec), the median
and radial latency differences to the thumb
(4.1 Ð 2.8 = 1.3 msec), and the median and
ulnar latencies with stimulation in the
palm and recording over the wrist (3.1 - 2.1
= 1.0 msec); this difference totals 3.6 msec.
Values of 1.0 msec or above are considered
abnormal and consistent with median neu-
ropathy at the wrist.
Median
ring

(4.8)
Ulnar
ring
(3.5)
Median
thumb
(4.1)
Radial
thumb
(2.8)
Median
palm
(3.1)
Ulnar
palm
(2.1)
Nerve Conduction Studies
Stimulate Record Latency, msec Amplitude, mV
Left H wave Knee Soleus 35.1 1.7
Right H wave Knee Soleus 32.8 4.9
(Normal side-to-side difference for latency is 1.2 msec, with normal amplitude difference up to 40%.)
Needle EMG
Spontaneous Activity Motor Unit Action Potentials
Muscle Myotome Ins. Act. Fibs/PSWs Amplitude Duration Phasicity Recruitment
Vastus medialis L3,4 Normal None Normal Normal Normal Full
Adductor longus L3,4 Normal None Normal Normal Normal Full
Tibialis anterior L4,5 Normal None Normal Normal Normal Full
Tensor fasciae latae L4-S1 Normal None Normal Normal Normal Full
Biceps femoris L5,S1 Increased 1+/2+ Increased Increased Normal Full
Peroneus longus L5,S1 Increased 1+/1+ Increased Increased Normal Full

Soleus S1,2 Increased 2+/2+ Increased Increased Normal
Lumbar paraspinals L3-S1 Normal None
Figure 7 Findings from nerve conduction and needle EMG studies in case 2.
Abbreviations: Fibs/PSWs = fibrillations/positive short waves; Ins. Act. = insertional
activity.
Neurophysiologic Evaluation
Journal of the American Academy of Orthopaedic Surgeons
198
losis may produce lower-motor-
neuron loss in the upper limbs due
to root or anterior horn cell involve-
ment, but it should not cause lower-
motor-neuron loss in other regions
of the body. In contrast, motor neu-
ron disease produces widespread
evidence of upper- and lower-
motor-neuron loss and fascicula-
tions. Electromyographic diagnosis
of amyotrophic lateral sclerosis re-
quires evidence of denervation in
three of the following four ÒregionsÓ:
bulbar, cervical, thoracic, and lum-
bosacral.
The needle EMG findings in this
case (Fig. 8) demonstrate evidence of
denervation in the upper limbs, con-
sistent with two processes. There is
denervation of C6-innervated mus-
cles, consistent with a C6 radicu-
lopathy. Additionally, the distal

muscles of the upper and lower
limbs demonstrate denervation,
suggesting a distal peripheral poly-
neuropathy. However, extensive
evaluation of other body regions
(including the tongue, thoracic
paraspinal muscles, and proximal
lower limbs) did not show evidence
of denervation. Fasciculations were
limited to two distal hand muscles
and were not widespread.
Nerve conduction studies dem-
onstrate slowing of conduction dif-
fusely (in the sural, peroneal, and
ulnar nerves) but more severe ab-
normalities in the median nerve
(with absent sensory response and
very prolonged motor latency).
These findings confirm the pres-
ence of a peripheral polyneuropa-
thy and also suggest a superim-
posed median neuropathy at the
wrist.
Thus, the findings are more con-
sistent with cervical spondylosis
and myeloradiculopathy than with
motor neuron disease. A peripheral
polyneuropathy with focal median
neuropathy is also present. Surgi-
cal decompression of the cervical

spine resulted in rapid improve-
ment.
Summary
The electrodiagnostic examination is
a useful tool for detecting problems
affecting the peripheral nervous sys-
tem. Clinical assessment and defini-
tion of the questions to be answered
are essential to tailor the electrodiag-
nostic examination for each patient.
Potential pitfalls include performing
tests in a standardized manner with-
out examining the patient, not form-
ing a differential diagnosis, technical
errors, examining too few areas, and
overinterpretation of minor devia-
tions from Ònormal.Ó However,
when performed appropriately, elec-
trodiagnostic studies contribute sig-
nificantly to the evaluation of patients
with peripheral nervous system com-
plaints.
Nerve Conduction Studies
Stimulate Record Latency, msec Amplitude Velocity, msec
Median nerve (sensory) Wrist Thumb Absent response
Radial nerve (sensory) Wrist Thumb 3.7 (²2.7) 3 µV (³5)
Sural nerve (sensory) Leg Ankle 6.0 (²4.0) 1 µV (³5)
Median nerve (motor) Wrist APB 5.1 (<4.3) 8.8 mV (³5.0)
Elbow APB 7.5 mV (³5.0) 49 (³50)
Ulnar nerve (motor) Wrist ADM 3.6 (<3.8) 8.3 mV (³5.0)

Below elbow ADM 8.1 mV (³5.0) 50 (³50)
Above elbow ADM 7.7 mV (³5.0) 49 (³50)
Peroneal nerve (motor) Ankle EDB 8.6 (²6.0) 2.5 mV (³2.0)
Knee EDB 2.5 mV (³2.0) 35 (³40)
Needle EMG
Spontaneous Activity Motor Unit Action Potentials
Muscle Myotome Ins. Act. Fibs/PSWs Fasc Amplitude Duration Phasicity Recruitment
Deltoid C5,6 Normal None None Normal Normal Normal Full
Biceps C5,6 Normal None None Normal Normal Normal Full
Extensor carpi radialis C6,7 Increased 2+/2+ None Normal Normal Normal Central
Pronator teres C6,7 Increased 1+/1+ None Normal Normal Normal Full
Triceps C7,8 Normal None None Increased Increased Normal Reduced
APB C8,T1 Increased 1+/1+ 1+ Increased Increased Normal Reduced
FDI C8,T1 Increased 1+/1+ 1+ Increased Increased Normal Reduced
Pectoralis major C5-T1 Normal None None Normal Normal Normal Full
Cervical paraspinals C5-T1 Normal None None
Vastus medialis L3,4 Normal None None Normal Normal Normal Full
Adductor longus L3,4 Normal None None Normal Normal Normal Full
Tibialis anterior L4,5 Normal None None Normal Normal Normal Full
Tensor fasciae latae L4-S1 Normal None None Normal Normal Normal Full
Biceps femoris L5,S1 Normal None None Normal Normal Normal Full
Soleus S1,2 Increased 2+/2+ None Increased Increased Normal
Lumbar paraspinals L3-S1 Normal None None
Tongue XII Normal None None
Figure 8 Findings from nerve conduction and needle EMG studies in case 3. Normal val-
ues are shown in parentheses. Abbreviations: ADM = abductor digiti minimi; APB =
abductor pollicis brevis; EDB = extensor digitorum brevis; Fasc = fasciculations; FDI = first
dorsal interosseous; Fibs/PSWs = fibrillations/positive short waves; Ins. Act. = insertional
activity.
Lawrence R. Robinson, MD

Vol 8, No 3, May/June 2000
199
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