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-

+
/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

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-

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

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

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

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

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-

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-

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

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-

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

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.

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

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.

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-

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

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

(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

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

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

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10. Seddon H: Surgical Disorders of the
Peripheral Nerves, 2nd ed. New York:
Churchill-Livingstone, 1975, pp 21-23.
11. Robinson LR, Micklesen PJ, Wang L:
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