Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6012_Библиотеки_им_академика_М_И_Перельмана.pdf
Chapter 14 Electrodiagnostic Examination 243
++
Distal latency (ms) Proximal latency (ms)
Distance (cm)
MOTOR NERVE CONDUCTION STUDY
Stimulus
neg. phase
Stimulus
Prox. lat. − Dist. lat. (ms)
R
S
1
Distance
FIG. 14.2 Various components of the motor nerve conduction study
assessing the median nerve. Dist. lat., distal latency; Prox. lat., proximal
latency. (Modied from Isle M, Krauss G, Levin K, et al. Electromyography/
Electroencephalography. Redford, WA: Spacelabs Medical; 1993:40.)
= CV (m/s)
S
2
−−
Peak
latency
Duration
Amplitude (mV):
Baseline to peak
Sensory
Median-index
SECTION
II
Amplitude
Distal
latency
Duration
FIG. 14.3 Compound muscle action potential. Distal latency is measured
from the stimulus to onset of the negative response. Amplitude is measured
from the baseline to the negative peak.
motor NCSs, small muscles of the hand and feet serve as
recording muscles; the nerves supplying them are stimulated
at two separate points along their course. For the upper
extremity, the wrist (distal) and elbow (proximal) are used as
stimulation sites. For the lower extremity, the ankle (distal)
and knee (proximal) are used as stimulation sites.
Numerous parameters are assessed with each CMAP
obtained, including amplitude, latency, and conduction
velocity (Fig. 14.3). e CMAP amplitude represents the
number of nerve bers that responded to the stimulus and
are capable of conducting impulses to the recorded muscle.
1,2
It is measured from baseline to negative peak (negative being
up) and reported in millivolts. e latency is the time interval
between the instant that the nerve was stimulated and the
onset of the CMAP, and is reported in milliseconds. e con-
duction velocity is the speed of transmission over the fastest
FIG. 14.4 Sensory nerve action potential. Peak latency is measured to the
onset of the negative phase. Amplitude is measured from the baseline to
the negative peak.
conducting nerve bers assessed and is reported in meters per
second. Conduction velocities are calculated by dividing the
distance traveled along a nerve segment (as determined by
surface measurements) by the latency dierence between the
responses to proximal and distal stimulation. Normal conduction velocity in the upper limb is greater than 50 m/s; in the
lower limb, it is greater than 40 m/s.
Sensory Nerve Conduction Studies
For sensory NCSs, a sensory nerve or the sensory component
of a mixed nerve is stimulated at one point with recording
electrodes placed distally, usually on the ngers or on the
ankle with routine studies. is stimulation results in a
sensory nerve action potential (SNAP), which is a biphasic
or triphasic waveform that represents summated nerve
action potentials. In contrast to CMAPs, which are generated
by motor units and are measured in millivolts, SNAPs are
generated directly by the nerve bers. SNAPs are 100 times
smaller and are measured in microvolts. Generally, only two
sensory NCS measurements are reported: (1) the amplitude,
which is the height of the response measured from baseline
to negative peak and represents the number of sensory axons
that depolarize; and (2) the peak latency, which is the time
interval between the moment that the nerve was stimulated
and the negative peak of the response, reported in milliseconds
(Fig. 14.4).
1
244 DIAGNOSIS
B
Late Responses (H Responses and F Waves)
Two special studies, the H response and the F wave, are NCSs
used to measure the time in which nerve impulses travel
proximally to the spinal cord along the peripheral nerve trunk
and then back down the limb to the recorded muscle aer
distal stimulation of the nerve. Because the potentials seen
with both of these techniques are much delayed aer nerve
stimulation compared with potentials seen with standard
NCSs, they are referred to as late responses.
e H response is the electrophysiologic correlate of the
Achilles tendon reex and is named aer Homann, who rst
described it in 1918. To obtain the H response, the tibial nerve
is stimulated in the popliteal fossa using low voltage to activate
sensory bers (as opposed to motor bers), which carry the
nerve impulse proximally to the spinal cord (Fig. 14.5). e
bers synapse there with motor neuron cells to complete a
monosynaptic reex arc. e nerve impulse travels down the
motor eerent nerve to the gastrocnemius, where the recording electrode captures the response. Although the amplitude
and the latency of the H response are analyzed, the amplitude
is more reliable for diagnostic purposes in my laboratory.
e F wave was rst described by Magladery and McDou-
gall in 1950 and was named the F wave because it was rst
recorded from muscles in the foot. In contrast to H responses,
F waves are not a component of a reex arc because the nerve
impulses recorded travel only along motor axons. F waves are
produced when, aer distal motor nerve stimulation, some of
the impulses passing antidromically up the motor axons cause
a few of the motor cell bodies in the anterior horns to backre;
the resulting nerve impulses travel back down the motor axons
to produce submaximal muscle activations that are recorded
several milliseconds aer the initial CMAP as F waves. Several
consecutive responses from the same muscle are elicited, and
the shortest latency time usually is used for diagnosis. Also, in
contrast to H responses, F waves can be elicited with any of
the standard motor NCSs.
Needle Electrode Examination
NEE is the second and oldest component of the basic electrodiagnostic examination. During this procedure, a recording
needle electrode is inserted into various muscles, and the
electrical activity being generated in them is evaluated on a
visual and audio display system via a dierential amplier.
NEE records activity in muscle (1) at rest during needle insertion, (2) at rest without needle movement, and (3) during
voluntary muscle activation.
Insertional Phase
During the insertional phase, the electrical activity resulting
from needle movement in a relaxed muscle is evaluated. In a
normal muscle, each needle insertion and advancement
S1 root
(tibial nerve)
A
Increasing stimulus strength
2 mV
10 ms
M-wave
R
M-waveH-wave H-wave
FIG. 14.5 Standard lower limb H response. (A) With minimal stimulus strength, only the H wave is elicited. (B)
As stimulation strength increases, the M wave appears and becomes progressively larger, while the H wave
progressively loses amplitude.
Chapter 14 Electrodiagnostic Examination 245
injures a few individual muscle bers, which generate a small
burst of electrical potentials called insertional activity. ese
electrical potentials prove that the needle electrode is in a
viable muscle because they are not seen if it is in subcutaneous
tissue, fat, or severely brotic muscle. In the context of periph-
eral nerve ber lesions, if the NEE is performed on a partially
denervated muscle a few days before spontaneous brillation
potentials appear (discussed later), the insertional activity is
abnormal in that unsustained trains of insertional positive
sharp waves are seen.
At-Rest Phase
During the at-rest phase, electrical silence ordinarily is noted.
With neuromuscular pathology, various types of spontaneous
activity may be discernible. Only three of these are relevant to
spine-related nerve disease: brillation potentials, fasciculation potentials, and complex repetitive discharges.
Fibrillation potentials are spontaneous, usually regularly
ring action potentials of individual muscle bers. Although
nonspecic in that they can be seen with neuropathic and
myopathic disorders, their presence indicates denervation.
Fibrillation potentials typically appear in the form of a biphasic
spike if the tip of the recording needle electrode is near the
denervated muscle ber. Alternatively, they may appear as a
positive sharp wave if the needle has injured the abnormal
muscle ber. In the setting of nerve lesions, brillation potentials are not present at the onset of motor axon loss. Instead,
they are rst seen 14 to 35 days aer axon degeneration has
been initiated; the most widely cited average time is 21 days.
When established, brillation potentials persist until the
denervated muscle bers generating them either reinnervate
or degenerate for lack of a nerve supply. e latter usually
occurs 18 to 24 months aer the initial nerve ber injury.
Fibrillation potentials are the most reliable and objective
manifestation of active or recent motor axon loss. ey can be
neither produced nor abolished voluntarily by the patient. ey
are very sensitive indicators of such loss because the degeneration
of a single motor axon can result in hundreds of individual
muscle bers brillating within a given muscle, depending
on the innervation ratio of the latter. Fibrillation potentials
objectively can show that motor axon loss has occurred when
the lesion is far too mild in degree to produce clinical muscle
weakness, atrophy, or loss of CMAP amplitude on motor NCS.3
Showing brillation potentials in a myotome distribution has
been the principal method of identifying root lesions in the
electrodiagnostic laboratory for more than half a century.
Fasciculation potentials are spontaneous action potentials
of an individual motor unit. Unlike brillation potentials, they
are indicative of motor unit irritation rather than denervation;
only intact motor unit potentials (MUPs) can generate them.
ey are encountered far less oen than brillation potentials,
being restricted essentially to radiculopathies, anterior horn
cell disorders, radiation-induced plexopathies, a few entrapment neuropathies, polyneuropathies, and, most oen, the
syndrome of generalized benign fasciculations.
Complex repetitive discharges are produced when a single
muscle ber is depolarized and that depolarization is spread
by ephaptic transmission to adjacent muscle bers, which
2–4
5,6
reactivate the initial muscle ber. A recurrent cycle of ring is
established. ese potentials have a bizarre conguration and
re at high frequency. For many years, they were known as
bizarre high-frequency discharges. Although they are abnormal,
they are nonspecic, being seen with neuropathic and myopathic disorders. Generally, they appear when there is grouped
atrophy (i.e., denervation, reinnervation, and subsequent
denervation) and are evidence of chronicity. Although these
potentials are not helpful in localization, they are frequently
encountered on NEE of the cervical paraspinal muscles in
patients with chronic cervical root lesions.
3
Activation Phase
Aer the muscle is evaluated at rest, the patient is asked to
contract the muscle. is contraction results in the generation
of MUPs, which represent the summated electrical activity
produced by contracting muscle bers of a single motor unit.
MUPs are assessed in regard to their recruitment pattern and
appearance.
Recruitment
Recruitment of MUPs refers to the orderly increase in number
and ring rate of activated motor units as force is increased
during contraction of muscle. On initial activation of the
muscle with minimal force, a single motor unit res at its basal
rate of 5 to 10 Hz. As the force is increased, additional units
are recruited, and the ring rate gradually increases by 5 Hz
with each additional unit—up to 20 to 30 Hz. With progressively increasing force, spatial and temporal recruitment
occurs, resulting in a full interference pattern in which the
screen is obscured by the ring patterns of several MUPs.
Reduced MUP recruitment, also known as a neurogenic MUP
ring pattern, is observed whenever numerous motor units in
the muscle being sampled cannot be activated on maximal
eort because either conduction block or axon loss aects their
axons. e fewer MUPs seen on maximal eort, the weaker
the muscle is clinically. MUPs that are capable of ring are
noted to do so in decreased numbers and oen faster than their
basal ring rate of 5 to 10 Hz.
still functioning motor units is important because, similar to
brillation potentials, it is unequivocal evidence of involuntary
interruption of motor axon impulse transmission. Conversely,
if the muscle was weak because of an upper motor neuron
lesion or because voluntary eort was simply submaximal (e.g.,
because of malingering or pain on activation), incomplete MUP
activation would be seen—that is, MUPs would re in equally
decreased numbers but at a slow to moderate rate.
Morphology
e amplitude, duration, and conguration of MUPs are
important morphologic characteristics that are assessed during
the activation phase. Together, these features reect the number
and size of muscle bers within a motor unit and their ability
to re in synchrony. Patient age, technical details (e.g., lter
setting, type of needle used), and the specic muscle being
examined are some of the factors that aect the appearance
of MUPs. Based on quantitative analyses, normal ranges for
MUP morphology are available for comparison, which vary
3,7
e rapid rate of ring of the
SECTION
II
246 DIAGNOSIS
depending on the patient age and proximity of the muscle to the
trunk. A normal MUP has a triphasic waveform appearance.
With chronic nerve lesions, the process of reinnervation of
denervated muscle bers can occur as the result of regeneration of the nerve trunk from the point of nerve transection or
(when the nerve transection is not total) by collateral nerve
branch sprouting from remaining intact nerve bers close to
the denervated muscle bers. e latter process is much faster
because nerve ber regeneration occurs at the rate of about
1 mm/day. On NEE, manifestations of reinnervation include
resolution of brillation potentials; return of activation of
motor unit action potentials with voluntary muscle contraction; and appearance of polyphasic, enlarged (so-called neurogenic) motor unit action potentials, reecting the increased
number of muscle bers attached to surviving nerve bers
owing to collateral sprouting.
Chronic neurogenic MUP changes generally develop about
4 to 6 months aer an axon loss injury has occurred because
it takes this much time for such congurational remodeling to
occur. Aer chronic neurogenic MUP changes develop, they
can persist indenitely. With many remote, proximal neurogenic lesions (e.g., radiculopathies and, particularly, poliomyelitis), they are the sole electrical residuals detected during the
entire electrodiagnostic examination.
3,7,8
*
A
Electrodiagnostic Findings in Radiculopathy
e electrodiagnostic examination has been used to assess
patients with possible radiculopathies for more than 50 years.
Root lesions were one of the rst focal peripheral nerve ber
disorders for which the diagnostic utility of NEE was shown.
For many years, lumbosacral radiculopathies were the most
common reason for referral to the electrodiagnostic labora-
9,10
tor y.
Although several other electrodiagnostic procedures
have been introduced over the past half-century, NEE remains
the mainstay for diagnosing radiculopathies. e amplitudes
of motor NCS are also helpful when root damage is severe,
extensive, or both.
8,9
Radiculopathies are most commonly caused by nerve root
compression secondary to degenerative spine changes, disc
herniation, or rupture. e type of nerve pathology at the lesion
site depends on the nature of the injury and degree of nerve
compression. When the injury results in signicant motor
axon loss, NEE shows numerous abnormalities, including the
presence of brillation potentials in corresponding myotomes.
Demyelinating conduction block may also be inferred by
ndings on the electrodiagnostic examination. In many cases
of nerve root disease, the electrodiagnostic examination can
provide invaluable information regarding localization, severity, age of the lesion, and nerve pathophysiology.
Nerve Conduction Studies
Routine Studies
Axon loss occurs when the axon is disconnected from its cell
body. e motor cell body (anterior horn cell) resides in the
5,6
*
B
FIG. 14.6 Cross-sectional views of cervical region, showing (A) relationship
of dorsal root ganglia (asterisk) to surrounding structures and (B) usual site
of disc herniation (arrow). Preganglionic sensory root bers usually are
compromised.
anterior zone of the spinal cord; the sensory cell body (DRG)
resides outside the spinal cord, either within individual intervertebral foramina or within the spinal canal (intradural and
intraarachnoid) (Fig. 14.6). A disc protrusion causing severe
compression of a motor and sensory nerve root within the
spinal canal disconnects the anterior horn cell from its motor
axon, but if the DRG is distal to the point of compression, the
extraspinal sensory axons remain connected to their DRG and
do not undergo degeneration (see Fig. 14.6). In that setting,
motor NCSs show amplitude loss, but sensory NCSs are
normal despite marked clinical sensory impairment with few
exceptions.
One exception is seen with nerve root pathology that
extends beyond the intraspinal canal. A mass lesion (e.g.,
meningioma) or inltrative process (e.g., malignancy, inam-
matory cause, or infection) that progresses distally along the
nerve root to involve the DRG can result in decreased SNAP
amplitudes. e other exception is when the DRG resides
inside the intraspinal canal, proximal to the intervertebral
foramina; this has been found to occur in the lumbosacral
region. Based on cadaveric, radiographic, and magnetic
Chapter 14 Electrodiagnostic Examination 247
resonance imaging (MRI) studies, 3% of L3 and L4 DRG are
intraspinal, about 11% to 38% of L5 DRG are intraspinal, and
71% of S1 DRG are intraspinal.11 As a result, root lesions in
the lower spine, particularly lesions involving the L5 root, can
aect the corresponding SNAP amplitude, which in the case
of an L5 lesion is the supercial peroneal SNAP (discussed
later). SNAP peak latency and nerve conduction velocity are
never involved in radiculopathy, however.
e CMAP amplitude is the only portion of motor NCS
that may be signicantly aected in radiculopathy. Because it
is a measure of the number of viable, conducting nerve bers,
the CMAP amplitude can be decreased with severe motor
axon-loss lesions. e ulnar CMAP amplitude would be
reduced in a severe C8 radiculopathy. In chronic lesions, reinnervation changes, such as collateral sprouting, can contribute
to the CMAP amplitude and may lead to normal or nearnormal values over time.
In many cases, motor NCSs remain relatively unaected in
radiculopathies for two reasons. First, most radiculopathies
result in only partial nerve injuries. For the CMAP amplitude
to be signicantly reduced on motor NCS, about half of the
motor axons within the peripheral nerve trunk need to be
lost or injured. Second, the myotomes of the aected nerve
root must be accessible to stimulation and recording. e
ulnar-innervated hand muscles may be examined for a C8
radiculopathy, and the biceps and deltoids are available for
assessing a C5 radiculopathy. Muscles innervated by C6 and
C7 nerve roots cannot be reliably examined with routine
motor NCSs, however, owing to technical factors and overlap
in innervation.
Late Responses
Although the H response and F wave are theoretically helpful
in the evaluation of the damaged proximal nerve root segment,
there are technical limitations to each procedure that can
hamper their utility in the evaluation of a radiculopathy.
Because the H response is elicited by stimulating the tibial
nerve in the popliteal fossa while recording from the
gastrocnemius/soleus muscle group, as described previously,
it is highly sensitive and very useful in the evaluation of S1
radiculopathy. In axon loss lesions aecting the S1 nerve root,
the amplitude may be either reduced or absent. e normal
value of the H amplitude, as dened by my electrodiagnostic
laboratory, is 1 mV, with abnormal values being either less
than 1 mV or reduced by 50% compared with the contralateral
response. Additionally, the H response may become abnormal
at the onset of nerve root injury and remain so until the injury
is resolved or may remain abnormal despite resolution of
clinical symptoms.
7
A major limitation of the H responses is that they are frequently absent bilaterally in patients older than 60 years, in
patients with polyneuropathies, and in patients who have had
lumbar laminectomies even when the S1 roots reportedly were
not within the operative eld. Also, when the H responses are
abnormal, they do not localize to the S1 root because the
lesion could be at many other points along the extended
neural pathway that the impulses traverse (e.g., S1 spinal cord
7,9
segment, sacral plexus, sciatic nerve, and proximal tibial
nerve). When H responses are abnormal, they remain so
indenitely in many cases.
8,9
Despite these limiting and confounding factors, H responses
are very helpful in the evaluation of a possible lumbosacral
radiculopathy because they are seldom normal with S1 root
lesions. Part of their high sensitivity may be because, in contrast to all other constituents of the electrodiagnostic examination, they evaluate the preganglionic components of the S1
sensory root bers.
8,9
Although most electrodiagnostic physicians agree on the value of H responses, they disagree regarding which component (amplitude or latency) of the H response
is likely to be abnormal.
9,12–14
Ideally, F waves should be able to detect demyelinating
conduction slowing along the motor bers at the root level.
However, this is not the case in practical application. ey are
oen normal in unequivocal cases of radiculopathy, and even
when abnormal, they do not provide any additional information because the abnormalities are already clearly seen on
4,7
NEE.
erefore, F waves are of no signicant value in the
evaluation of root lesions.
Needle Electrode Examination
Because NCSs and the late responses generally are normal
with isolated root lesions (except for the H response with S1
radiculopathies), NEE usually is the sole component of the
electrodiagnostic examination that is benecial in detecting a
radiculopathy. e diagnosis depends on nding abnormali-
ties on NEE in a root or myotome (all the muscles that receive
innervation from a single spinal cord segment or root). ese
abnormalities include insertional positive sharp waves, brillation potentials, a reduced or neurogenic recruitment of
motor units, and changes in the motor unit morphology (e.g.,
increased duration, amplitude, and polyphasia).
e most widely used criterion for diagnosing radiculopathies by NEE is that abnormalities should be found in two, and
preferably more, limb muscles innervated by the same root but
dierent peripheral nerves. In addition, muscles in the limb
not innervated by the damaged root, but rather by the roots
contiguous to it, should appear normal. For instance, a patient
with a C7 radiculopathy should have brillation potentials or
other signs of denervation in the triceps (radial nerve) and
pronator teres (median nerve), but not the abductor digiti
minimi or deltoid muscles. Needle electromyography (EMG)
not only should be tailored to the clinical question and the
survey of a sucient number of muscles (proximal and distal
when possible) to make a reliable diagnosis of a radiculopathy.
Numerous myotome charts derived from radiographic,
cadaveric, and electrodiagnostic studies have been established
to help guide the electrodiagnostic physician in choosing the
best muscles to examine for each patient (Figs. 14.7 through
14.9). A radiculopathy screen in my laboratory consists of an
examination of at least seven muscles, including the paraspinals, to help with localization in the upper extremity (Table
14.3) and lower extremity (Table 14.4). e presence of bril-
lation potentials in the paraspinals is typically indicative of an
9,15,16
SECTION
II
248 DIAGNOSIS
ANTERIOR PRIMARY RAMI C5 C6 C7 C8 T1
PROXIMAL NERVES
RHOMBOID MAJOR/MINOR (DORSAL SCAPULAR)
SUPRA/INFRASPINATUS (SUPRASCAPULAR)
DELTOID (AXILLARY)
BICEPS BRACHII (MUSCULOCUTANEOUS)
RADIAL NERVES
TRICEPS
ANCONEUS
BRACHIORADIALIS
EXTENSOR CARPI RADIALIS
EXTENSOR DIGITORUM COMMUNIS
EXTENSOR CARPI ULNARIS
EXTENSOR POLLICIS BREVIS
EXTENSOR INDICIS PROPRIUS
MEDIAN NERVES
PRONATOR TERES
FLEXOR CARPI RADIALIS
FLEXOR POLLICIS LONGUS
PRONATOR QUADRATUS
ABDUCTOR POLLICIS BREVIS
ULNAR NERVES
FLEXOR CARPI ULNARIS
FLEXOR DIGITORUM PROFUNDUS (MED)
ABDUCTOR DIGITI MINIMI
ADDUCTOR POLLICIS
FIRS
T DORSAL INTEROSSEOUS
POSTERIOR PRIMARY RAMI L2 L3 L4 L5 SI S2
PROXIMAL NERVES
ILIACUS
ADDUCTOR LONGUS (OBTURATOR)
VASTUS LATERALIS/MEDIALIS (FEMORAL)
RECTUS FEMORIS (FEMORAL)
TENSOR FASCIA LATA (GLUTEAL)
GLUTEUS MEDIUS (GLUTEAL)
GLUTEUS MAXIMUS (GLUTEAL)
SCIATIC NERVES
SEMITENDINOSUS/MEMBRANOSUS (TIBIAL)
BICEPS FEMORIS (SHT. HD) (PERONEAL)
BICEPS FEMORIS (LONG HD) (TIBIAL)
PERONEAL NERVES
TIBIALIS ANTERIOR
EXTENSOR HALLUCIS
PERONEAL LONGUS
EXTENSOR DIGITORUM BREVIS
TIBIAL NERVES
TIBIALIS POSTERIOR
FLEXOR DIGITORUM LONGUS
GASTROCNEMIUS LATERAL
GASTROCNEMIUS MEDIAL
SOLEUS
ABDUCTOR HALLUCIS
ABDUCTOR DIGITI QUINTI PEDIS
POSTERIOR PRIMARY RAMI C5 C6 C7 C8 T1
CERVICAL PARASPINALIS
HIGH THORACIC PARASPINALIS
Main innervation
Partial innervation
FIG. 14.7 Traditional myotome chart. (From Wilbourn AJ, Amino MF. Radiculopathies. In Brown WF, Bolton CF,
eds. Clinical Electromyography. 2nd ed. Boston: Butterworth-Heinemann; 1993:192.)
TABLE 14.3 Screening Needle Electrode Examination for the Arm
Muscle Root Level Nerve Trunk
First dorsal interosseous C8 Ulnar
Extensor indicis proprius C8 Posterior interosseous (radial)
Flexor pollicis longus C8 Anterior interosseous (median)
Pronator teres C6–C7 Median
Triceps C6–C7 Radial
Biceps C5–C6 Musculocutaneous
Deltoids C5–C6 Axillary
C7 paraspinal Overlap
axon-loss lesion localized to or near the intraspinal canal,
excluding the possibility of a plexopathy or more distal lesion.
Paraspinal brillation potentials are most valuable for the
support of radiculopathy when they are present at only one or
two contiguous segmental levels and absent at levels above,
below, and contralaterally.
Many limitations can reduce the value of the paraspinal
examination. First, there is overlapping innervation of most
POSTERIOR PRIMARY RAMI L2 L3 L4 L5 SI S2
CERVICAL PA RASPINALIS
HIGH THORACIC PARASPINALIS
TABLE 14.4 Screening Needle Electrode Examination for the Leg
Muscle Root Level Nerve Trunk
Abductor hallucis S1 Tibial
Medial gastrocnemius S1 Tibial
Biceps femoris (short head) S1 Peroneal
Extensor digitorum brevis L5–S1 Peroneal
Flexor digitorum longus L5 Tibial
Gluteus medius L5 Superior gluteal
Tibialis anterior L4–L5 Peroneal
Rectus femoris L2–L4 Femoral
S1 paraspinal Overlap
paraspinals, which prevents accurate localization of brillation potentials to one specic segment or root. Second, even
in proven radiculopathies, brillation potentials may be absent
owing to reinnervation or sampling error. ird, paraspinal
brillation potentials may be seen in diabetic patients, in
patients with a prior history of spine surgery, or in some
asymptomatic elderly patients. Finally, paraspinal denervation
L2
L3
L4
L5
S1
AL IL VL RF VM PT TA EDB PL EHL GM ST TFL MG LG AD BFBF GM AH PSP
ED SH LH
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
SECTION
II
34
35
36
37
38
39
40
41
42
43
44
45
Fibrillation potentials
Neurogenic recruitment changes only
Normal examination
FIG. 14.8 Lower limb myotome chart. Needle electrode examination results grouped by surgically dened
root level of involvement. Numbers in the left column represent patients. Blue circle, positive waves or
brillation, with or without neurogenic recruitment and motor unit changes; red circle, neurogenic recruitment
changes only; green circle, normal examination. (From Tsao BE, Levin KH, Bodner RA. Comparison of surgical and
electrodiagnostic ndings in single root lumbosacral radiculopathies. Muscle Nerve. 2003;27:61.)
C5
C6
C7
C8
NEEDLE ELECTRODE EXAMINATION RESULTS GROUPED BY
THE SURGICALLY DEFINED ROOT LEVEL OF INVOLVEMENT
SUP INF DEL BRAC BC PT FCR TRC ANC EDC EIP FPL APB FDI ADM PSP
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
Fibrillation potentials
Neurogenic recruitment changes only
Normal examination
FIG. 14.9 Upper limb myotome chart. Needle electrode examination results grouped by surgically dened
root level of involvement. Numbers in the left column represent patients. Blue circle, positive waves or
brillation, with or without neurogenic recruitment and motor unit changes; red circle, neurogenic recruitment
changes only; green circle, normal examination. (From Levin KH, Maggiano HJ, Wilbourn AJ. Cervical
radiculopathies: comparison of surgical and EMG localization of single-root lesions. Neurology. 1996;46:1023.)
Chapter 14 Electrodiagnostic Examination 251
BOX 14.1 Appropriate Timing of the Electrodiagnostic Examination
interpretations can be made from nerve conduction studies (NCSs)
and needle electrode examination (NEE) obtained any time after
3 wk from onset of symptoms.
interpretations can be made from NCSs obtained after 10 days from
onset of symptoms.
block lesion (neurapraxia), such as might be the case for
perioperative peroneal or ulnar neuropathy owing to positioning on
the operating table, reliable interpretations can be made from NCSs
obtained any time after onset of symptoms
such as diabetic polyneuropathy, it is reasonable to consider
baseline electrodiagnostic examination (NCS and NEE) immediately
after the onset of new symptoms of a potential iatrogenic cause.
This study is to assess the nature of preexisting abnormalities before
acute changes from new symptoms are visible on electrodiagnostic
examination. This is especially useful if a medicolegal issue may arise
from new symptoms, because it would be valuable to dierentiate
preexisting nerve pathology from any procedure-related changes.
A second study is necessary when sucient time has elapsed to
assess a new lesion.
is not specic to radiculopathy and is seen in other disorders,
including diseases of the muscle (e.g., inammatory myopa-
thy) and the anterior horn cell (e.g., amyotrophic lateral
sclerosis). Nonetheless, NEE of the paraspinal muscles is an
integral portion of the electrodiagnostic examination and
should be routinely performed in all patients with suspected
nerve root disease.
e timing of needle EMG is also crucial. Fibrillation
potentials do not appear in a denervated muscle until 2 to 3
weeks aer the onset of the initial injury and in some patients
may require 4 to 6 weeks to develop.11 Consequently, the
ndings on NEE performed earlier than 3 weeks aer onset
of a radiculopathy are likely to be false-negative or, at best,
indeterminate, even if subsequently they would be positive
for a root lesion. It is optimal to wait at least 3 weeks aer
the onset of symptoms before performing NEE. Guidelines
that help the clinician decide the best timing of a study to
obtain maximal information are provided in Box 14.1. ese
are based on the neurophysiologic concepts of axon loss as
described in Box 14.2.
Determining Duration of Radiculopathy: Acute Versus Chronic
Information regarding the duration of a radiculopathy is oen
derived by ndings on NEE. Whenever evidence of an isolated
compressive root disorder of recent onset is detected on the
electrodiagnostic examination, the typical combination of
ndings is as follows: (1) motor NCSs are normal (unless the
degree of axon loss is severe); (2) sensory NCSs are normal;
(3) with S1 root involvement, the H response usually is
abnormal; and (4) NEE discloses brillation potentials in
several muscles that are innervated by the compromised root
unaccompanied by changes in the size and conguration of
the MUP.
BOX 14.2 Timing of Nerve Pathology: Neurophysiologic Concepts
response amplitude from electrical stimulation distal to the
transection point decreases from day 3 through days 5 to 8 after
transection. For sensory nerve bers, response amplitude decreases
progressively from day 5 through days 9 to 11, coinciding with
evolution of wallerian degeneration of nerve bers. For this reason,
identifying maximum axon loss cannot be assessed by nerve
conduction studies until at least 11 days have elapsed since the date
of nerve injury or onset of symptoms.
completion, the attached muscle ber becomes denervated, leading
to breakdown of the neuromuscular junction. Over 2 to 3 weeks,
membrane changes occur along the muscle ber, resulting in
spontaneous, continuous action potential propagation along the
muscle ber, recognized during needle electrode examination (NEE)
as brillation potentials. About 3 weeks must elapse after an acute
axon-loss event before brillation potentials can be reliably
visualized on NEE.
as the result of regeneration of the nerve trunk from the point of the
nerve transection, or (when nerve transection is not total) by the
collateral nerve branch sprouting from the remaining intact nerve
bers close to the denervated muscle bers. The latter process is
much faster because nerve ber regeneration occurs at rate of
about 1 mm/day. On NEE, manifestations of reinnervation include
resolution of brillation potentials, return of activation of motor unit
action potentials with voluntary muscle contraction, and the
appearance of polyphasic motor unit potential changes.
In contrast, when chronic neurogenic MUP changes (poly-
phasic conguration with increased duration and amplitude)
are the prominent nding on NEE with only a few brillation
potentials, the lesion is likely to be chronic. When the chronic
neurogenic MUP changes are limited to distal muscles within
a myotome in the absence of brillation potentials, the radiculopathy is likely to be static and remote.
Finally, when brillation potentials and chronic neurogenic
MUP changes are found in a myotome distribution, the diagnostic possibilities include a chronic, progressive radiculopathy or an acute root lesion superimposed on a remote lesion.
e latter possibility is the more likely choice if brillation
potentials are found in proximal muscles (e.g., the glutei and
hamstrings with L5 or S1 root lesions), in addition to more
distal muscles in the same myotome.
7–9
When the previous factors are considered, it is apparent
that whenever the classic NEE presentation of a radiculopathy
is encountered—brillation potentials in most or all of the
muscles constituting the myotome—the root lesion in question
usually is of more recent onset, and motor root axon loss has
been substantial. Whenever other circumstances prevail, as
is far more commonly the case, brillation potentials usually
are found in only some, if any, of the muscles of the myotome.
ey are typically seen in the more distal muscles. Fibrillation
potentials generally are important only if they are present; their
absence in any specic muscle does not exclude the diagnosis.
8,9
Determining Severity of Radiculopathy
e severity of a nerve root lesion is based on motor NCSs
and NEE. e degree of reduced MUP recruitment seen on
SECTION
II
252 DIAGNOSIS
NEE correlates with the degree of muscle weakness and, in
combination with the CMAP amplitude reduction (in muscles
that can be assessed with NCS), the degree of axon loss. e
amount of brillation potentials seen in a muscle is a subjec-
tive measure and does not correlate as well with the degree of
axon loss.
Electrodiagnostic Findings
at Specic Root Levels
Cervical Radiculopathy
Lesions of the cervical nerve roots account for 36% of all
radiculopathies.9 In clinical and radiographic studies, the most
common root aected is at the C7 level (70% of the time)
followed by C6 (19% to 25%), C8 (4% to 10%), and C5
9,16–18
(2%).
with C5 radiculopathies are typically manifested as abnormalities in the spinati, deltoid, biceps, and brachioradialis
muscles. NCSs are typically unhelpful because proximal
muscles are not assessed during routine studies, although the
biceps and deltoid muscles are amenable to NCS and may
show reduced CMAP amplitudes when axon loss is suciently
severe.
ance. Rather, they have two very dierent ones, which imitate
those of C5 and C7 root lesions. Manifestations of C5 root
lesions may also be seen with some C6 radiculopathies.19 C7
lesions are diagnosed by the presence of abnormalities in some
muscles innervated by radial and median nerves: the triceps
and anconeus (radial) and the pronator teres and exor carpi
radialis (median). As stated before, NEE abnormalities sometimes are seen in the same combination of upper limb muscles
with C6 root lesions as well.
electrodiagnostic presentation, manifesting as abnormalities
in ulnar-innervated muscles, the extensor indicis proprius,
and the exor pollicis longus.19 Nonetheless, they can sometimes be confused with combined axon-loss lesions of the
posterior interosseous nerve and the ulnar nerve whenever the
ipsilateral ulnar SNAP is of low amplitude or cannot be elicited
(e.g., because of advanced age or a coexisting polyneuropathy).
For uncertain reasons, the axon loss that occurs with many C8
radiculopathies is exceptionally severe, so much so that the
CMAPs recorded from the ulnar nerve–innervated hand
muscles, particularly the hypothenar, are low in amplitude.
Some of these patients never regain normal hand strength.
Dierential Diagnoses
Findings on NEE of cervical radiculopathies can look identical
to brachial plexopathies (Table 14.5). In particular, lesions
aecting the C5 and C6 roots may resemble upper trunk
plexus lesions, whereas lesions of the C8 and T1 roots can
mimic lower trunk lesions. ere are two critical parameters
on the electrodiagnostic examination that can discern the two
types of lesions. e rst parameter is NEE ndings in the
paraspinals. With nerve root lesions, the paraspinal muscles
e electrodiagnostic examination presentations
C6 radiculopathies do not have a single, discrete appear-
In contrast, C8 radiculopathies have a very characteristic
TABLE 14.5 Disorders Commonly Confused With Compressive
Radiculopathies
Roots Entity
Cervical
C5, C6 Upper trunk brachial plexopathy
Neuralgic amyotrophy
Axillary/suprascapular neuropathies
Motor neuron disease
Rotator cu tear
C6, C7 Carpal tunnel syndrome
C8, T1 Lower trunk brachial plexopathy
Ulnar neuropathy
Motor neuron disease
Thoracic
T1 Neurogenic thoracic outlet syndrome
Lumbosacral
L2–L4 Diabetic amyotrophy
Lumbar plexopathy
Femoral neuropathy
L5 Sacral plexopathy
Peroneal neuropathy
Motor neuron disease
S1, S2 Sacral plexopathy
Sciatic neuropathy
Tibial neuropathy
Bilateral (L5), S1, S2 Polyneuropathy
show brillation potentials but are spared in a lesion of the
brachial plexus. e second parameter is the assessment of
the SNAPs. In radiculopathies, the lesion is located within the
intraspinal canal and proximal to the DRG, which results in
normal SNAPs. In plexopathies, the lesion is distal to the
DRG, producing reduced amplitude or absent SNAPs.
Clinically, this second parameter is especially important
when distinguishing a radiculopathy from neuralgic amyotrophy, which commonly aects proximal shoulder girdle muscles
(e.g., the spinati and the deltoids) derived from C5 and C6
roots. Abnormally reduced or absent SNAP amplitudes of the
lateral antebrachial cutaneous sensory nerve and median
sensory branch recording from the thumb and index nger
point to a plexus lesion.
Likewise, carpal tunnel syndrome can resemble C6 and C7
radiculopathies clinically but are easily distinguished by the
presence of abnormalities seen in the triceps and pronator
teres and other muscles proximal to the hand or outside of the
median nerve territory. In contrast, C8 radiculopathies may
be dicult to discern from an ulnar mononeuropathy, espe-
cially in the setting of partial lesions in which the ulnar SNAP
is unaected. Finding abnormalities in C8-innervated radial
muscles is important in this setting. Finally, unless a rotator
cu injury results in entrapment of a nerve innervating proximal muscles located in the shoulder girdle (e.g., suprascapular
nerve), the electrodiagnostic examination would show no
abnormalities.
Thoracic Radiculopathy
Radiculopathies in this region are dicult to assess by electrodiagnostic examination because there are relatively few