SECTION VI • Clinical–Electrophysiologic Correlations
33 
PART IV • Radiculopathy, Plexopathies, and Proximal Neuropathies
Sciatic Neuropathy
Sciatic neuropathies are uncommon in the electromyogra-
phy (EMG) laboratory. When they occur, patients often
present in a manner similar to that of peroneal neuropathy.
Indeed, a footdrop from an early sciatic neuropathy may be
difficult or impossible to distinguish clinically from a foot-
drop from peroneal neuropathy at the fibular neck. It often
falls to the electromyographer to make this differentiation.
Demonstration of a sciatic neuropathy on EMG has impor-
tant diagnostic implications because the differential diag-
nosis is distinctly different from that of other peripheral
nerve entrapment syndromes.
ANATOMY
The sciatic nerve is derived from the L4–S3 roots, carrying
fibers that eventually will become the tibial and common
peroneal nerves. It leaves the pelvis through the sciatic
notch (greater sciatic foramen) under the piriformis muscle
accompanied by the other branches of the lumbosacral
plexus (inferior and superior gluteal nerves and posterior
cutaneous nerve of the thigh). In some individuals, fibers
destined to become the common peroneal nerve run
through the piriformis muscle before joining the sciatic
nerve. Covered by the gluteus maximus, the sciatic nerve
next runs medial and posterior to the hip joint between the
ischial tuberosity and the greater trochanter of the femur
(Figure 33–1). The knee flexors, including the medial ham-
strings (semimembranosus and semitendinosus) and lateral
hamstrings (long and short heads of the biceps femoris), and
the lateral division of the adductor magnus are all supplied
by the sciatic nerve.
Within the sciatic nerve, fibers that eventually form the
common peroneal nerve often are segregated from those
that distally become the tibial nerve. The peroneal division
of the sciatic nerve runs lateral to the tibial division. The
two divisions physically separate from each other in the
mid-thigh to form their respective nerves. All sciatic inner-
vated muscles in the thigh are derived from the tibial divi-
sion of the sciatic nerve, with the important exception
of the short head of the biceps femoris, which is derived
from the peroneal division. In essence, the short head of the
biceps femoris is the only peroneal-innervated muscle above
the level of the fibular neck. This muscle assumes special
importance in the EMG evaluation of peroneal palsy, sciatic
neuropathy, and other more proximal lesions. As the sciatic
©2013 Elsevier Inc
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nerve terminates in the common peroneal and tibial nerves,
it supplies all motor and sensory innervation below the
knee, with the exception of sensation over the medial calf
and foot (saphenous sensory territory).
CLINICAL
Sciatic neuropathies caused by trauma, injection, infarc-
tion, or compression present acutely. Otherwise, most
sciatic neuropathies present in a progressive, subacute
fashion. Patients with a complete sciatic neuropathy have
paralysis of knee flexion and all movements about the ankle
and toes. Sensation is lost in several areas (Figure 33–2),
including the lateral knee (lateral cutaneous nerve of the
knee), lateral calf (superficial peroneal nerve), dorsum of
the foot (superficial peroneal nerve), web space of the great
toe (deep peroneal nerve), posterior calf and lateral foot
(sural nerve), and sole of the foot (distal tibial nerve). Pain
may be perceived in the proximal thigh, radiating posteri-
orly and laterally into the leg, but it usually does not affect
the back. The ankle reflex is depressed or absent on the
involved side.
This complete deficit is seen only in severe lesions or
late in the course of sciatic neuropathy. Initially, the
clinical presentation most often mimics peroneal neuro­
pathy. It has long been recognized that the peroneal fibers are
preferentially affected in most sciatic nerve lesions. Thus, it is
not unusual for a patient with sciatic neuropathy to present
with a footdrop and sensory disturbance over the dorsum of
the foot and lateral calf. Indeed, early sciatic nerve lesions
may be nearly impossible to differentiate clinically from
peroneal nerve lesions at the fibular neck (Table 33–1).
On physical examination, close attention must be paid to
muscles that receive non-peroneal innervation, especially
ankle inversion (tibialis posterior–tibial nerve), toe flexion
(flexor digitorum longus–tibial nerve), and knee flexion
(hamstring muscles–sciatic nerve). Weakness in any of
these muscles in a patient with a footdrop suggests dysfunc-
tion beyond the peroneal nerve distribution. Likewise,
on sensory examination, any sensory disturbance over the
lateral knee, lateral foot, or sole of the foot suggests a lesion
of the sciatic or tibial nerves or more proximally. Isolated
sciatic nerve lesions spare sensation over the medial calf
and foot (saphenous nerve) and posterior thigh (posterior
cutaneous nerve of the thigh). Any involvement of these
 Chapter 33 • Sciatic Neuropathy 519

Sciatic nerve

Hamstring muscles
Semimembranosus
Biceps femoris
Semitendinosus
(short head)
Biceps femoris
(long head) Common peroneal
nerve
Tibial nerve
Gastrocnemius

Plantaris
Distribution of plantar nerves Soleus
Popliteus

Tibial nerve Tibialis posterior

Flexor digitorum longus

Medial calcalneal
nerve Flexor hallucis longus
Lateral plantar
nerve
Medial plantar
nerve
Sural nerve

Plantar digital
nerves Medial and lateral
calcaneal nerves
FIGURE 33–1  Sciatic nerve anatomy.
(From Haymaker, W., Woodhall, B., 1953. Peripheral nerve injuries. WB Saunders, Philadelphia. with permission.)

Obturator nerve Lateral femoral cutaneous

nerve of thigh
Lateral femoral cutaneous Obturator nerve
nerve of thigh Posterior cutaneous
nerve of thigh
Intermediate and medial
cutaneous nerves of thigh Medial cutaneous
(from femoral nerve) Lateral cutaneous nerve of the knee nerve of thigh
(from common peroneal nerve) (from femoral nerve)
Saphenous nerve Lateral cutaneous nerve of calf
(from femoral nerve) (from common peroneal nerve) Saphenous nerve
(from femoral nerve)
Superficial peroneal nerve
Superficial peroneal nerve
Deep peroneal nerve (from common peroneal nerve)
(from common peroneal nerve) Sural nerve
(from common peroneal nerve)
(from tibial nerve)
Sural nerve
Medial and lateral plantar nerves
(from tibial nerve) Calcanean branches of
(from posterior tibial nerve)
sural and tibial nerves
FIGURE 33–2  Sensory loss in sciatic neuropathy (in green).
(Adapted from Haymaker, W., Woodhall, B., 1953. Peripheral nerve injuries. WB Saunders, Philadelphia, with permission.)

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520 SECTION VI Clinical–Electrophysiologic Correlations

Table 33–1.  Clinical Differentiating Factors in Suspected Sciatic Neuropathy

Deep Peroneal Common Sciatic Lumbosacral
Nerve Peroneal Nerve Nerve Plexus L5
Weakness of foot dorsiflexion X X X X X
Weakness of foot eversion X X X X
Weakness of foot inversion X X X
Weakness of knee flexion X X X
Weakness of glutei X X
Decreased ankle tendon reflex X† X† X†
Sensory loss in webspace great toe X X X X X
Sensory loss in dorsum of foot X X X X
Sensory loss in lateral calf X X X X
Sensory loss in lateral knee X X X
Sensory loss in sole foot X† X† X†
Sensory loss in posterior thigh X† X†
Tinel’s sign at fibular neck X X
Hip and thigh pain X X X
Back pain X
Positive straight-leg raise test X
X = may be present; †May be present if lesion involves S1 fibers as well; CMAP = compound muscle action potential; SNAP = sensory nerve action potential.

territories in a patient with a footdrop suggests a more Box 33–1.  Etiology of Sciatic Neuropathy
widespread lesion, either in the lumbosacral plexus or
Hip (Gluteal) Region
proximally. Hip replacement surgery (retraction, stretch,
It is important to remember that in addition to sciatic methylmethacrylate cement)
neuropathy and peroneal neuropathy, a footdrop with Hip dislocation/fracture
sensory disturbance over the lateral calf and dorsum of the Acute, external compression (coma, anesthesia, drug
foot may occur in lumbosacral plexopathy, radiculopathy overdose, prolonged sitting)
Gluteal compartment syndrome
(especially L5), or even a central lesion, such as a frontal
Gluteal contusion
meningioma or anterior cerebral artery infarct. Gluteal injection
Piriformis syndrome
Thigh Region
ETIOLOGY Femur fracture
Acute, external compression
Sciatic neuropathy is distinctly uncommon and is associated Posterior thigh compartment syndrome
with a limited differential diagnosis (Box 33–1). As the Entrapment (myofascial band)
sciatic nerve runs posterior to the hip joint, one of the most Laceration
common presentations occurs following hip or femur frac- Baker’s cyst
Hip or Thigh Region
ture (especially posterior dislocation) or as a complication
Gunshot wound
of the subsequent surgery to repair the fracture. As a com- Nerve infarction
plication of surgery, sciatic neuropathy may occur due to Vasculitis
retraction or stretch, as well as a result of methylmetha­ Arterial thrombosis
crylate cement forming spurs and then eroding into the Arterial bypass surgery
nerve months to years later, which has been well docu- Diabetes mellitus
Postradiation therapy
mented in several case reports.
Mass Lesions
Another common cause of sciatic neuropathy is tumor Benign tumors
(neurofibroma, schwannoma, neurofibrosarcoma, lipoma, Malignant cancers/lymphoma
and lymphoma). Tumors affecting the sciatic nerve usually Endometriosis
can be imaged quite well as a mass lesion on computed Arterial aneurysm
tomography or magnetic resonance imaging (MRI) scanning Arteriovenous malformations
Persistent sciatic artery
(Figure 33–3). Other rare mass lesions also may affect the Myositis ossificans
sciatic nerve. An enlarged Baker’s cyst in the popliteal fossa Abscess
may compress the distal sciatic nerve as it bifurcates into
Modified from Yuen, E.C., So, Y.T., 1999. Sciatic neuropathy. Neurol Clin
the tibial and common peroneal nerves. Several unusual 17, 617–631.
vascular abnormalities, including aneurysms of the inferior

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 Chapter 33 • Sciatic Neuropathy 521

FIGURE 33–3  Mass lesion of the sciatic

nerve. This patient presented with a slowly
progressive, painful sciatic neuropathy over
several months. Axial magnetic resonance
imaging scan of the mid-thigh shows
a large mass lesion in the region of the
left sciatic nerve (large arrow). A normal-
appearing sciatic nerve is seen on the
contralateral side (small arrow). Biopsy
demonstrated large cell lymphoma
infiltrating and expanding the sciatic nerve.
(Adapted from Preston, D.C., Shapiro, B.E.,
2001. Lymphoma of the sciatic nerve. J Clin
Neuromuscul Dis 2, 227–228.)

gluteal, iliac, or persistent sciatic arteries and arteriovenous M. piriformis

malformations near the piriformis muscle, have been asso-
ciated with sciatic neuropathy.
Damage to the sciatic nerve can occur from trauma or as 90%
a result of a penetrating injury, such as gunshot and knife
wounds. Sciatic neuropathy also may occur as a complica-
tion of immobilization and external compression, such as
during anesthesia, coma, or intoxication. In the hospital
setting, damage to the sciatic nerve may occur iatrogeni-
cally from misplaced intramuscular buttock injections,
especially in thin patients.
Disorders that result in a mononeuritis multiplex syn-
Sciatic Nerve
drome (see Chapter 26) may affect the sciatic nerve. For
example, vasculitic neuropathy commonly results in in­
farction of the sciatic nerve in the proximal thigh, which 7.1% 2.1% 0.8%
is a watershed area for nerve ischemia. The neuropathy
often is acute and begins with prominent pain. Until
additional nerve lesions develop, recognition of the un-
derlying mono­neuritis multiplex pattern is difficult or
impossible.
FIGURE 33–4  Anatomic relationships of the sciatic nerve to the
piriformis muscle. As the sciatic nerve leaves the pelvis, it most
Piriformis Syndrome often runs under the piriformis muscle. However, there are other less
As the sciatic nerve leaves the pelvis, it runs under common anatomic variations. The proximity of the sciatic nerve to
the piriformis muscle puts it at theoretic risk of entrapment.
or through the piriformis muscle (Figure 33–4). The piri- (Adapted from Beaton, L.E., Anson, B.J., 1938. The sciatic nerve and the
formis muscle originates from the sacrum, the sciatic notch piriformis muscle: their interrelation as possible cause of coccygodynia. J Bone J
and the sacrotuberous ligament, and then runs through the Surg 20, 686–688.)

greater sciatic foramen to attach to the greater trochanter

of the femur. The main action of the piriformis is to exter-
nally rotate the hip. When the hip is in a flexed position, it
also acts as a partial hip abductor. Theoretically, a hypertro-
phied piriformis muscle could compress the sciatic nerve
(piriformis syndrome), somewhat comparable to compres-
sion of the median nerve by the pronator teres muscle in
pronator teres syndrome. In the past, many cases of “sciat-
ica” were attributed to piriformis syndrome. However,
most, if not all, cases of sciatica are due to lumbo­sacral
radiculopathy and not sciatic neuropathy from piriformis
syndrome. Piriformis syndrome is considered by many to be
a controversial entity. There are very few reported cases of
patients who meet the criteria for definite piriformis syn-
drome, which include (1) sciatic neuropathy clinically, (2)
electrophysiologic evidence of sciatic neuro­pathy, (3) surgi-
cal exploration showing entrapment of the sciatic nerve
within a hypertrophied piriformis muscle, and (4) subse-
quent improvement following surgical decompression.
Clinically, piriformis syndrome should be suspected
when a patient has more pain while sitting than standing;
worsening of symptoms with flexion, adduction, and

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522 SECTION VI Clinical–Electrophysiologic Correlations

Table 33–2.  Electromyographic and Nerve Conduction Study Abnormalities Localizing the Lesion Site in Sciatic Neuropathy
Deep Peroneal Common Sciatic Lumbosacral
Nerve Peroneal Nerve Nerve Plexus L5
Electromyographic Findings
Tibialis anterior X X X X X
Extensor hallucis longus X X X X X
Peroneus longus X X X X
Tibialis posterior X X X
Flexor digitorum longus X X X
Short head of biceps femoris X X X
Gluteus medius X X
Tensor fascia latae X X
Paraspinal muscles X
Nerve Conduction Study Findings
Abnormal peroneal SNAP (if axonal) X X X
Abnormal sural SNAP (if axonal) X X
Low peroneal CMAP (if axonal) X X X X X
Low tibial CMAP (if axonal) X† X† X†
Abnormal H reflex X† X† X†
Conduction slowing/block at fibular X X
neck (if demyelinating)
X = may be abnormal; †May be abnormal if lesion involves S1 fibers as well; CMAP = compound muscle action potential; SNAP = sensory nerve
action potential.

internal rotation of the hip; a history of trauma or unusual ELECTROPHYSIOLOGIC

body habitus (especially very thin); and tenderness in the
mid-buttock that reproduces the pain and paresthesias.
Several physical examination maneuvers are reported to be
useful in suspected piriformis syndrome. In each, the piri-
formis muscle is either stretched or voluntarily contracted.
Pain from the buttock down the sciatic nerve, but without
any back pain, is said to be consistent with piriformis syn-
drome. These maneuvers include:
• The Freiberg maneuver: with the patient lying supine,
the examiner forcefully internally rotates the leg,
stretching the piriformis muscle.
• The Pace maneuver: in the seated position, the
patient abducts the hip against resistance, activating
the piriformis muscle.
• The Beatty maneuver: lying on their side, the
patient abducts the hip, activating the piriformis
muscle.
• The FAIR (flexion, adduction, internal rotation)
maneuver: with the patient lying supine, the examiner
passively flexes, adducts, and internally rotates the
hip, stretching the piriformis muscle. This maneuver
is also reported to be useful in the EDX of piriformis
syndrome (see below).
EVALUATION
The electrophysiologic evaluation plays a key role in the
assessment of a possible sciatic neuropathy. The electro-
physiologic approach is similar to the clinical approach:
evaluate and exclude disorders that can mimic sciatic neu-
ropathy, including peroneal palsy at the fibular neck,
lumbosacral plexopathy, and lumbosacral radiculopathy
(Table 33–2).
Nerve Conduction Studies
The nerve conduction evaluation of sciatic neuropathy is
straightforward (Box 33–2). Routine peroneal and tibial
motor studies should be performed bilaterally, recording
the extensor digitorum brevis (EDB) and abductor hallucis
brevis, respectively. Careful attention must be paid to the
peroneal motor study, with the electromyographer looking
for evidence of peroneal palsy at the fibular neck (either
focal slowing or conduction block). In this regard, it is
useful to perform peroneal motor studies recording the
tibialis anterior as well as the extensor digitorum brevis. In
sciatic nerve lesions with axonal loss, the amplitude of the
peroneal or tibial compound muscle action potentials

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Box 33–2.  Recommended Nerve Conduction Study
Protocol for Sciatic Neuropathy
Routine studies:
1. Tibial motor study, recording abductor hallucis brevis and
stimulating medial ankle and popliteal fossa; bilateral
studies
2. Peroneal motor study, recording extensor digitorum brevis
and stimulating ankle, below fibular neck and lateral
popliteal fossa; bilateral studies. In patients with an
isolated footdrop and clinical findings limited to the
distribution of the peroneal nerve, the study should be
performed, recording the tibialis anterior and stimulating
below fibular neck and lateral popliteal fossa, to increase
the yield of demonstrating conduction block or focal
slowing across the fibular neck.
3. Sural sensory study, stimulating posterior lateral calf,
recording posterior ankle; bilateral studies
4. Superficial peroneal sensory study, stimulating lateral calf,
recording lateral ankle; bilateral studies
5. Tibial and peroneal F responses; bilateral studies
6. H reflex; bilateral studies
Special consideration:
• In patients with suspected piriformis syndrome, consider
comparing the H reflex latency between the normal
anatomic and hip FAIR positions.
FAIR, flexion, adduction, and internal rotation.
(CMAPs) may be reduced on the symptomatic side com-
pared with normal control values or, more importantly,
when compared with the contralateral asymptomatic leg.
The peroneal fibers often are affected out of proportion to
the tibial fibers. If there has been loss of the fastest con-
ducting axons, there may be mild prolongation of the distal
motor latency and some slowing of conduction velocity, but
never into the demyelinating range.
Bilateral peroneal and tibial F responses and H reflexes
should be obtained. In sciatic neuropathy, ipsilateral F wave
responses may be prolonged compared with the contralat-
eral side. In a sciatic nerve lesion, the H reflex may be
prolonged or more difficult to elicit on the involved side.
Although abnormal late responses place the lesion some-
where along the course of the nerve fibers being studied,
the finding of prolonged or absent F and H responses
cannot help in differentiating among a sciatic neuropathy,
lumbosacral plexopathy, or radiculopathy. A proximal lesion
is implied only if the distal conductions are normal.
Likewise, sensory nerve conduction studies must be per-
formed bilaterally, comparing the superficial peroneal
and sural sensory responses to the contralateral side. In
sciatic neuropathy, both responses are expected to be
abnormal, reflecting dysfunction of both the peroneal and
tibial nerves. However, as noted earlier, the peroneal fibers
are often the most affected.
Special Studies in Suspected Piriformis Syndrome
Most often, standard nerve conduction studies and needle
EMG are normal in patients who are clinically diagnosed
with piriformis syndrome. The one electrophysiologic test
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Chapter 33 • Sciatic Neuropathy 523
FAIR (Flexion - Adduction - Internal Rotation)
a
FIGURE 33–5  Flexion, adduction, and internal rotation (FAIR)
position. Simultaneous downward pressure of the flexed knee and
passive superolateral movement of the shin, with both acetabula
oriented vertically, maximize adduction and internal rotation at the
flexed thigh. The angle between the ground and flexed leg (a) should
be 20 to 35 degrees.
(From Fishman, L.M., Zybert, P.A., 1992. Electrophysiological evidence of
piriformis syndrome. Arch Phys Med Rehabil 73, 359–364.)
proposed to be of value is a modification of the H reflex.
In piriformis syndrome, the H reflex is reported to be
prolonged when performed with the hip in flexion, adduc-
tion, and internal rotation (FAIR test) compared to the
normal anatomic position (Figure 33–5). This position
stretches the piriformis muscle and theoretically may put
pressure on the sciatic nerve.
In the largest reported study of this test, in patients with
clinical criteria suggestive of piriformis syndrome, the mean
prolongation of the H reflex in the FAIR position was
3.39 ms, which is equivalent to 5.45 standard deviations
above the mean for a normal population. Compare this to
the mean delay of the H reflex in 88 normal persons in the
FAIR position compared to the anatomic position, which
was 0.01 ms, with a standard deviation of 0.62 ms (Figure
33–6). However, the asymptomatic population was not
normally distributed. Using a cutoff of 3 standard devia-
tions (1.86) resulted in a specificity of 83% (i.e., 17% of a
normal control population would be misidentified as abnor-
mal). In addition, the contralateral, asymptomatic limbs
of the patient group often demonstrated abnormalities,
although they were less marked than in the symptomatic
limbs.
The authors have little personal experience with the
FAIR test. Other so-called dynamic nerve conduction tests
generally fail to increase the yield of abnormalities in
entrapment neuropathies (e.g., flexing the wrist in carpal
tunnel syndrome while performing median nerve conduc-
tion studies), although this is not always true. In addition,
the H reflex is well known to be affected by a variety
of variables, including body and especially head position.
Because the circuitry of the H reflex traverses the spinal
cord, it can be modified by a variety of suprasegmental
facilitatory and inhibitory inputs. For instance, the Jen-
drassik (reinforcement) maneuver is commonly used to
“prime” the anterior horn cells and is of use in the EMG
laboratory to elicit H reflexes. Presumably, head position
can modify the H reflex by activating the vestibulospinal
tracts. The take-home message is the following: if the FAIR
test is used in patients with suspected piriformis syndrome,
ensure that other variables are held constant, especially the
head and body positions; and remember the possibility of
false-positive results, given the distribution of the values
from a control population.
524 SECTION VI Clinical–Electrophysiologic Correlations

100

90 Piriformis

80

70
Normals
60
Frequency

50
Contralaterals
40

30

20

10

0
-4.5 -3.5 -2.5 -1.5 -0.5 0.5 1.5 2.5 3.5 4.5 5.5 6.5 7.5 8.5 9.5
H Latency difference (FAIR - Anatomic position)
FIGURE 33–6  H latency differences (ms) between the flexion, adduction, and internal rotation (FAIR) and anatomic positions. H
latency differences between the FAIR and anatomic positions in patients with clinical piriformis syndrome, in limbs contralateral to the clinical
piriformis syndrome legs, and in normals are compared.
(From Fishman, L.M., Dombi, G.W., Michaelsen, C., et al., 2002. Piriformis syndrome: diagnosis, treatment, and outcome – a 10-year study. Arch Phys Med Rehabil 83,
295–301.)

Electromyographic Approach Box 33–3.  Recommended Electromyographic

After the nerve conduction studies are completed, EMG is
used to further localize the lesion and assess its severity
(Box 33–3). First, muscles innervated by the deep and
superficial peroneal nerves should be sampled (e.g., tibialis
anterior, extensor hallucis longus, peroneus longus). Abnor-
malities in these muscles are consistent with a lesion of the
peroneal nerve, sciatic nerve, lumbosacral plexus, or L5–S1
nerve roots. Next, tibial-innervated muscles in the calf
should be sampled, including the medial gastrocnemius and
especially the tibialis posterior or flexor digitorum longus.
If abnormalities are found in any of these muscles, as well
as in the peroneal-innervated muscles, an isolated lesion of
the peroneal nerve has been excluded. The differential at
this point includes a lesion of both the tibial and peroneal
nerves versus a lesion of either the sciatic nerve, lumbo­
sacral plexus, or L5–S1 nerve roots.
Next, the hamstring muscles need to be sampled. The
short head of the biceps femoris has an important role,
being the only muscle supplied by the peroneal division of
the sciatic nerve that originates above the fibular neck. The
short head of the biceps can easily be sampled four finger-
breadths above the lateral knee, just medial to the long
head of the biceps femoris tendon. Abnormalities found in
the short head of the biceps femoris muscle exclude an
isolated lesion of the peroneal nerve at the fibular neck and
imply a more proximal lesion. After examination of the
hamstring muscles, the gluteal muscles should be checked.
Both the gluteus maximus (inferior gluteal nerve) and
either the gluteus medius or tensor fascia latae (superior
gluteal nerve) should be checked. If abnormalities are
Protocol for Sciatic Neuropathy
Routine muscles:
1. At least two peroneal-innervated muscles (tibialis anterior,
extensor hallucis longus, peroneus longus)
2. At least two tibial-innervated muscles (medial
gastrocnemius, tibialis posterior, flexor digitorum longus)
3. Short and long heads of the biceps femoris
4. At least one superior gluteal-innervated muscle (gluteus
medius, tensor fascia latae)
5. At least one inferior gluteal-innervated muscle (gluteus
maximus)
6. L5 and S1 paraspinal muscles
7. At least two non-sciatic, non-L5–S1-innervated muscles
(vastus lateralis, iliacus, thigh adductors) to exclude a
more widespread lesion
Special consideration:
• If motor unit action potential abnormalities are borderline
or equivocal, comparison should be made to the
contralateral side.
found in any of these muscles, an isolated sciatic neuropa-
thy is excluded, and the differential diagnosis at this point
is restricted to a lesion of the lumbosacral plexus or the
L5–S1 nerve roots. Next, the L5 and S1 paraspinal muscles
must be sampled to look for abnormalities at or proximal
to the root level. Lastly, if any of the muscles studied during
the needle EMG examination show borderline or equivocal
abnormalities, comparison to the contralateral side is
indicated.

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 Chapter 33 • Sciatic Neuropathy 525

It is important to emphasize that the EMG study can EXAMPLE CASE

only localize a lesion at or proximal to the most proximal
abnormal muscle sampled. For instance, in examining the
hamstring muscles, if the semitendinosus muscle is abnor-
mal and the semimembranosus muscle is normal, one
would be tempted to assume that the sciatic nerve lesion
lies between these two sites. The situation is not that
simple, however. It is well known from evaluation of various
compressive neuropathies that fascicles to certain muscles
can be preferentially affected, whereas others are prefer-
entially spared. Thus, in the earlier example, the lesion
could even be at the level of the nerve roots, sparing fasci-
cles to the semimembranosus. Accordingly, EMG can be
used only to identify a lesion at or proximal to the most
proximal muscle involved.
The classic electrophysiologic picture of sciatic neuropa-
thy is reduced tibial and peroneal motor amplitudes com-
pared with the contralateral side, with normal or slightly
prolonged distal motor latencies and normal or slightly
slowed conduction velocities. The tibial and peroneal F
responses are prolonged or absent on the symptomatic side,
with similar findings for the H reflex. Both the sural and
superficial peroneal sensory nerves are reduced in ampli-
tude or absent with normal potentials on the contralateral
asymptomatic side. Needle EMG findings show active den-
ervation or reinnervation with reduced recruitment of
motor unit action potentials (MUAPs) in muscles supplied
by (1) the sciatic nerve in the thigh, (2) the peroneal nerve,
and (3) the tibial nerve, but with sparing of the gluteal,
tensor fascia latae, and lumbosacral paraspinal muscles. In
both the nerve conduction and needle EMG studies, the
peroneal fibers are involved more often than the tibial fibers.
Case 33–1
History and Physical Examination
A 52-year-old woman was referred for further evaluation
of a persistent left footdrop. She described her condition
as having begun slowly 6 months previously. She initially
noted a sensation of numbness over the top of the foot
and the lateral calf. This was followed shortly thereafter
by her left foot dropping. During the last 2 months,
symptoms slowly progressed to a nearly complete foot-
drop. More recently, she noted a sensation of tightness
and pain from her hip down to her knee and into her calf.
An orthopedic consultant advised MRI scanning of
the knee to evaluate the peroneal nerve. The scan was
obtained and was unremarkable. She subsequently under-
went MRI scanning of the lumbar spine to look for a
possible L5 radiculopathy as the cause of her footdrop.
The scan was obtained and was unremarkable. Past
history was notable for a left hip fracture with surgical
repair 3 years previously.
On examination, there was atrophy of the anterior
compartment of the left leg and wasting of the left EDB
muscle. In the left lower extremity there was a complete
footdrop. Toe and ankle dorsiflexion were 1/5, as was
ankle eversion. Ankle inversion also was weak (4/5). In
addition, toe flexion was slightly but definitely weak,
as was knee flexion. Knee extension was normal. Hip
flexion, extension, abduction, and adduction were com-
pletely normal. Strength testing was completely normal
in the right lower extremity. Deep tendon reflexes were

CASE 33–1.  Nerve Conduction Studies

Amplitude
Motor = mV; Conduction F-wave
Sensory = µV Latency (ms) Velocity (m/s) Latency (ms)
Nerve
Stimulated Stimulation Site Recording Site RT LT NL RT LT NL RT LT NL RT LT NL
Peroneal (m) Ankle EDB 5.3 2.2 ≥2 5.4 5.8 ≤6.5 52 55 ≤56
Below fibula EDB 4.9 2.1 11.4 12.6 50 44 ≥44
Lateral popliteal fossa EDB 4.8 2.1 13.5 14.8 48 45 ≥44
Peroneal (m) Below fibula TA 6.7 3.1 ≥3 4.5 4.7
Lateral popliteal fossa TA 6.5 2.9 7.4 7.7 49 46 ≥44
Tibial (m) Ankle AHB 6.2 3.7 ≥4 4.8 5.8 ≤5.8 51 56 ≤56
Popliteal fossa AHB 5.4 3.1 11.3 13.1 46 41 ≥41
Sural (s) Calf Posterior ankle 13 6 ≥6 4.1 4.3 ≤4.4 50 48 ≥40
Peroneal (s) Lateral calf Lateral ankle 9 NR ≥6 4.1 NR ≤4.4 52 NR ≥40
H reflex Popliteal fossa Soleus 29.4 NR ≤34
m = motor study; s = sensory study; RT = right; LT = left; NL = normal; NR = no response; EDB = extensor digitorum brevis; TA = tibialis anterior;
AHB = abductor hallucis brevis.
Note: All sensory latencies are peak latencies. All sensory conduction velocities are calculated using onset latencies. The reported F-wave latency represents
the minimum F-wave latency.

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526 SECTION VI Clinical–Electrophysiologic Correlations

CASE 33–1.  Electromyography

Spontaneous Activity Voluntary Motor Unit Action Potentials

Configuration
Insertional Fibrillation
Muscle Activity Potentials Fasciculations Activation Recruitment Duration Amplitude Polyphasia
Left tibialis ↑ +2 0 NL ↓↓ +2 +1 +2
anterior
Left extensor ↑ +2 0 NL ↓↓ +2 +2 +1
hallucis longus
Left peroneus ↑ +1 0 NL ↓↓ +1 +1 +1
longus
Left medial NL 0 0 NL NL NL NL NL
gastrocnemius
Left tibialis ↑ +2 0 NL ↓↓ +2 +1 +1
posterior
Left biceps ↑ +2 0 NL ↓ +2 +2 +1
femoris (short
head)
Left biceps ↑ 0 0 NL ↓ NL/+1 NL/+1 +1
femoris (long
head)
Left NL 0 0 NL NL NL NL NL
semitendinosus
Left gluteus NL 0 0 NL NL NL NL NL
medius
Left gluteus NL 0 0 NL NL NL NL NL
maximus
Left vastus NL 0 0 NL NL NL NL NL
lateralis
Left iliacus NL 0 0 NL NL NL NL NL
Left L5 paraspinal NL 0 0 NL NL NL NL NL
Left S1 paraspinal NL 0 0 NL NL NL NL NL
↑ = increased; ↓ = slightly reduced; ↓↓ = moderately reduced; NL = normal.

2+ and symmetric in the upper extremities and 2+ at the
knees and right ankle. The left ankle jerk was absent. Toes
were downgoing. There was a clear sensory disturbance
to light touch on the top of the foot, lateral foot and calf,
lateral knee, and posterior calf on the left side. Sensation
over the medial calf, anterior thigh, lateral thigh, poste-
rior thigh, and sole of the foot was intact. There was a
well-healed surgical scar over the left lateral thigh.
Summary
The initial clinical presentation is that of a footdrop with
numbness over the dorsum of the foot and lateral calf.
Most often, this clinical picture is the result of a peroneal
neuropathy at the fibular neck. However, an early sciatic
neuropathy, lumbosacral plexopathy, or lumbosacral
radiculopathy (especially L5) can present in a similar
fashion. The slowly progressive nature of the symptoms
suggests a slowly expanding or infiltrating structural
lesion. As the symptoms progressed, the patient noted a
sensation of tightness and pain from the hip toward the
knee into the calf. These additional symptoms would be
unusual for a peroneal palsy at the fibular neck and are
suggestive of a more proximal lesion. MRI scanning
obtained at the usual sites of compression causing a foot-
drop (the fibular neck and lumbar spine) did not demon-
strate any abnormality and led to further evaluation and
eventually an EMG study.
Neurologic examination showed severe weakness and
atrophy in the distribution of the deep and superficial
peroneal nerves (ankle and toe dorsiflexion, ankle ever-
sion). Ankle inversion (tibialis posterior) and toe flexion
(flexor digitorum longus), both of which are subserved
by non-peroneal-innervated L5 muscles, were also weak.
In addition, there was weakness of knee flexion, which
is subserved by the sciatic nerve. These findings place the
lesion at or proximal to the sciatic nerve. Further testing

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of muscles innervated by the femoral, superior gluteal,
inferior gluteal, and obturator nerves were normal. The
absence of abnormalities in these muscles on clinical
examination suggested that a more widespread lesion of
the lumbosacral plexus or nerve roots was unlikely. Of
course, early in any lesion, it may be difficult to demon-
strate subtle weakness of the proximal limb muscles.
Moving on with the clinical examination, the left ankle
reflex was absent, signifying a lesion somewhere along
that reflex loop, in the tibial nerve, sciatic nerve, lum-
bosacral plexus, or lumbosacral nerve roots. Lastly, the
sensory disturbance involved not only the distribution of
the peroneal nerve but also the territories of the sural
nerve and the lateral cutaneous nerve of the knee. Normal
sensation was found in the medial calf, innervated by the
saphenous nerve, the anterior thigh, innervated by the
femoral nerve, the lateral thigh, innervated by the lateral
cutaneous nerve of the thigh, and the posterior thigh,
innervated by the posterior cutaneous nerve of the thigh.
This distribution of sensory abnormalities again suggests
a lesion at or proximal to the sciatic nerve. However, note
that the entire sciatic sensory territory was not involved
because sensation on the sole of the foot was spared
(innervated by the plantar nerves).
Before proceeding to the nerve conduction study
and EMG findings, the clinical history of a slowly
progressive deficit, along with the neurologic examina-
tion as described, should suggest a slowly expanding
or infiltrating structural lesion affecting the sciatic nerve,
the lumbosacral plexus, or the lumbosacral roots. The
history of prior hip surgery should suggest a likely
connection between the surgery and a possible sciatic
nerve palsy.
Reviewing the nerve conduction studies first, the motor
nerve conduction studies in the left leg are abnormal,
with borderline low CMAP amplitudes for both the pero-
neal and tibial motor studies. Furthermore, a clear asym-
metry is seen when the potentials are compared with
those from the contralateral, asymptomatic side. The
tibial distal motor latency, minimum F response latency,
and tibial and peroneal conduction velocities are slightly
slowed. However, the amount of slowing is mild, within
the range of axonal loss. Of note, there is no focal drop
in amplitude or focal conduction velocity slowing in the
peroneal nerve around the fibular neck. Note that for the
peroneal motor studies, both the extensor digitorum
brevis and tibialis anterior muscles were recorded. There
are some cases of peroneal neuropathy at the fibular neck
wherein conduction block and/or slowing is only seen
when recording the tibialis anterior.
Moving next to the sensory nerve conduction studies,
both the sural and superficial peroneal sensory studies are
abnormal on the symptomatic side compared with the
normal findings on the contralateral side. The superficial
peroneal response is absent, whereas the sural response
is only borderline low, reflecting greater involvement of
peroneal, compared to tibial, nerve fibers. Finally, on the
nerve conduction studies, the H reflex is absent on the
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Chapter 33 • Sciatic Neuropathy 527
ipsilateral side, corresponding to the absent ankle reflex
on the clinical examination.
Thus, at the conclusion of the nerve conduction studies,
there is a good clinical–electrophysiologic correlation.
The muscle atrophy and weakness seen on clinical exami-
nation correspond to the low CMAP amplitudes on the
peroneal and tibial motor studies. Likewise, the areas of
sensory loss on clinical examination correspond to the
distribution of reduced sensory nerve action potentials.
Both clinical examination and electrophysiologic studies
demonstrate that the peroneal nerve fibers are more
involved than the tibial.
Moving next to the needle EMG study, there is marked
active denervation and reinnervation in muscles inner-
vated by the superficial and deep peroneal nerves. These
prominent abnormalities correspond to the patient’s
clinical symptoms of footdrop. In contrast, the medial
gastrocnemius (tibial nerve innervated) is normal.
However, the tibialis posterior, another tibial-innervated
muscle, shows fibrillation potentials and large polyphasic
MUAPs with decreased recruitment. These findings
provide further evidence that the abnormalities are
beyond the peroneal nerve territory and must be due to
either separate lesions of the tibial and peroneal nerves
or a more proximal lesion.
Next, the short head of the biceps femoris is sampled.
This muscle assumes special significance on the EMG
examination because it is the only peroneal-innervated
muscle that originates above the fibular neck. This muscle
is normal in peroneal palsy at the fibular neck, but it may
be abnormal in lesions at or proximal to the sciatic nerve.
In this case, the short head of the biceps femoris has
fibrillation potentials with reduced recruitment of large
polyphasic MUAPs. Similar but less marked findings are
found in the long head of the biceps femoris. The semi-
tendinosus muscle, which is also innervated by the sciatic
nerve, is normal. No abnormalities are found in the more
proximal hip girdle muscles, which are innervated by the
superior and inferior gluteal nerves (gluteus medius and
maximus). Similarly, muscles innervated by the femoral
nerve (vastus lateralis and iliacus) and the L5 and S1
paraspinal muscles are normal. At this point, we are ready
to formulate our electrophysiologic impression.
IMPRESSION: The electrophysiologic findings are
consistent with a severe sciatic neuropathy at or
proximal to the takeoff to the biceps femoris.
Although the patient’s initial symptoms suggested a
simple peroneal palsy at the fibular neck, the subsequent
clinical findings suggested a more proximal lesion, which
was then confirmed with nerve conduction study and
EMG findings. The abnormal sensory conduction studies
mark the lesion as at or distal to the dorsal root ganglion,
which is inconsistent with a disorder of the L5 or S1 nerve
roots. Because both the superficial peroneal and sural
sensory responses were abnormal, the lesion must be in
the tibial and peroneal nerves, the sciatic nerve, or the
528 SECTION VI Clinical–Electrophysiologic Correlations
lumbosacral plexus. The needle EMG findings also dem-
onstrated abnormalities outside the peroneal distribution,
involving the tibial and distal sciatic nerves. Several
important questions can be addressed at this point.
Can the Lesion be Localized between the Biceps
Femoris and the Semitendinosus?
The most proximal abnormal muscle is the biceps femoris
(short and long heads). Although one may be tempted to
definitely state that the sciatic nerve lesion is between
the semitendinosus, which was normal on the needle
examination, and the biceps femoris, which was abnor-
mal, such a conclusion cannot be reached. It is well
known from studying other compressive neuropathies
that individual fascicles to certain muscles can be prefer-
entially affected, whereas others are spared. In this case,
one cannot exclude a sciatic nerve lesion proximal to,
although sparing, the fibers to the semitendinosus. Fur-
thermore, although the present study is most consistent
with a sciatic nerve lesion, one cannot definitively exclude
an unusual lumbosacral plexopathy, which may spare the
gluteal muscles or may not yet be severe enough to show
axonal loss in the gluteal muscles.
What is the Most Likely Clinical Diagnosis
Although the prior hip surgery suggests a possible sciatic
lesion adjacent to the site of the surgery, the slowly pro-
gressive nature of the clinical presentation is worrisome
for an expanding or infiltrating mass lesion, such as a
tumor. Of course, the possibility of methylmethacrylate
cement from the hip replacement forming spurs and then
slowly eroding into the nerve must be considered in this
context. The combination of the clinical history, neuro-
logic examination, and electrodiagnostic studies provides
a basis for imaging studies that now can be done in a
more intelligent manner. In this case, subsequent MRI
scanning of the left thigh showed a large enhancing lesion
of the sciatic nerve in the mid-thigh. A subsequent biopsy
revealed large cell lymphoma (see Figure 33–3).
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