Foot drop: where, why and what to do? - Practical Neurology

158 Practical Neurology
REVIEW
Pract Neurol 2008; 8: 158–169
Foot drop: where,
why and what to do?
John D Stewart
Foot drop is a common and distressing problem that can lead to falls and
injury. Although the most frequent cause is a (common) peroneal neuropathy
at the neck of the fibula, other causes include anterior horn cell disease,
lumbar plexopathies, L5 radiculopathy and partial sciatic neuropathy. And
even when the nerve lesion is clearly at the fibular neck there are a variety of
causes that may not be immediately obvious; habitual leg crossing may well
be the most frequent cause and most patients improve when they stop this
habit. A meticulous neurological evaluation goes a long way to ascertain the
site of the lesion. Nerve conduction and electromyographic studies are useful
adjuncts in localising the site of injury, establishing the degree of damage and
predicting the degree of recovery. Imaging is important in establishing the
cause of foot drop be it at the level of the spine, along the course of the
sciatic nerve or in the popliteal fossa; ultrasonography, CT and MR imaging
are all useful. For patients with a severe foot drop of any cause, an ankle foot
orthosis is a helpful device that enables them to walk better and more safely.
he colloquial and medical term ‘‘foot
drop’’ admirably describes weakness of
the dorsiflexor muscles of the foot. It is
to be distinguished from flail foot, in
which all the muscles below the knee are
affected—the plantar flexors as well as the
dorsiflexors. For neurologists, the keen-eyed lot
that we are, the most familiar sighting of a foot
drop is likely to be that of the late John Thaw
who played the part of Inspector Morse in
numerous BBC films; we do not know what the
cause was.1 Although a lesion of the (common)
peroneal nerve is in general the most likely
cause of foot drop, the wary neurologist should
pose the following questions:
T
Consultant Neurologist, Lions Gate
Hospital, North Vancouver, British
Columbia, Canada
Correspondence to:
Dr J D Stewart
145 East 13th Street, #204, North
Vancouver, BC V7L 2L4, Canada;
john.stewart@telus.net
10.1136/jnnp.2008.149393
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is this really a peroneal neuropathy, or
could there be a more proximal lesion?
if it is a peroneal neuropathy, what is the
cause?
what investigations will sort this out?
what can be done to help the patient?
ANATOMY
The tibialis anterior, the main dorsiflexor muscle
of the foot, is innervated by the peroneal nerve.
This is derived from anterior horn cells in the
lower spinal cord. Their axons travel in the L4
and L5 spinal nerve roots (‘‘roots’’), they then
join to form the lumbosacral trunk that
Stewart 159
connects these lumbar plexus structures to the
sacral plexus (fig 1). These nerve fibres then
enter the lateral trunk of the sciatic nerve which
becomes the peroneal nerve when the sciatic
divides just above the knee (fig 2). The lateral
trunk gives off only one branch in the thigh—
that to the short head of the biceps femoris
muscle. All of the other hamstring muscles are
innervated by the medial trunk of the sciatic
nerve; that trunk becomes the tibial nerve.
The peroneal nerve passes laterally through
the popliteal fossa and winds around the head
and neck of the fibula (fig 3). It is closely
applied to the periosteum of that bone for
about 6 cm and, for most of this distance, it is
covered only by skin and subcutaneous tissue.
It then pierces the peroneus longus muscle to
reach the anterior compartment of the lower
leg. At that point, the fibres of the muscle form
a tendinous arch over the nerve, and this has
been termed the fibular tunnel (fig 3). The
nerve supplies the tibialis anterior, the extensors of the toes, and the foot everter (peroneal)
muscles. It also supplies the skin over the
anterolateral aspect of the lower leg from
about midway between the knee and the ankle,
and most of the dorsal aspect of the foot and
toes. This extensive distribution of sensory loss
is seen when the nerve is lacerated at the knee,
However, when it is compressed, the sensory
loss is much more restricted—usually just to
the dorsum of the foot and toes (fig 4). In some
patients there may be no sensory signs or
symptoms at all, presumably because of
sparing of relevant nerve fascicles within the
damaged portion of the nerve.
Therefore, an anatomy-based differential
diagnosis of foot drop includes lesions or
disorders affecting anterior horn cells, L4 or L5
roots, lumbosacral plexus, sciatic nerve and
peroneal nerve. In practice, in many cases, the
cause of the foot drop is clear—that is, a patient
who has fallen and struck the lateral knee, or a
patient with acute low back pain and classic
lumbar radiculopathy symptoms. In many other
patients in whom the diagnosis is less obvious,
a peroneal neuropathy remains the likely
diagnosis, but there are several pitfalls waiting
to confound even the experienced clinician.
PERONEAL NEUROPATHIES
The many causes of this common focal
neuropathy are listed in the table.
Figure 1
The sacral plexus and the origin of the
sciatic nerve. (Reproduced with
permission from Stewart JD. Focal
peripheral neuropathies. Third edition.
Philadelphia: Lippincott Williams &
Wilkins, 2000.)
Figure 2
Posterior view of the course and branches of the right sciatic nerve. (Reproduced with permission from
Stewart JD. Focal peripheral neuropathies. Third edition. Philadelphia: Lippincott Williams & Wilkins, 2000.)
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160 Practical Neurology
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Acute trauma is a frequent cause and
includes direct blows and lacerations,
severe adduction injuries and dislocations
of the knee, fractures of the head or neck
of the fibula, and bullet wounds. The
common peroneal nerve can also be
inadvertently injured during knee operations, including total knee replacement
and arthroscopic surgery. A specific type
of injury results from acute plantar
flexion and inversion injuries at the ankle,
usually severe sprains or fractures of the
distal tibia and fibula;2, 3 the foot drop is
usually immediate, but may not appear
for several days. It seems that extreme
and sudden ankle inversion exerts enough
traction on the peroneal nerve in the
popliteal fossa to tear the vasa nervorum
where they enter the nerve sheath.
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External pressure is probably the most
frequent cause of peroneal neuropathy
and occurs for several reasons. 4 , 5
Symptoms of a peroneal neuropathy are
often noticed first on wakening from a
normal night’s sleep, probably the result
of sleeping in an abnormal position
causing nerve compression. During long
aeroplane, train and car journeys, the
traveller may sleep or sit in such a
position that the nerve becomes compressed. Bedridden patients often develop
this neuropathy, probably due to a
combination of weight loss and pressure
on hard hospital mattresses or bed
railings. Comatose patients can also lie
in such a way as to compress the nerve.
Plaster casts unfortunately remain a
common cause of peroneal neuropathy.
These include below knee casts with a
hard upper edge that compresses the
nerve as it crosses the fibular neck, and
also above knee casts. Leg braces with the
upper edge just below the knee, and tight
bandages around the knee are other
causes of compression at the fibular neck.
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Crossing the legs has long been alleged to
cause peroneal neuropathy by compressing the nerve between the head of the
fibula and the patella or lateral femoral
condyle of the opposite leg (fig 5).5–7 Leg
crossing is such an ubiquitous habit that
its role in causing peroneal palsy is
difficult to assess, but I believe it to be
the most common cause of otherwise
unexplained peroneal neuropathy. This is
based on the fact that many of these
patients admit to being habitual leg
Figure 3
Anterolateral view of the right leg showing the course, clinically relevant anatomical relations, and major
branches of the common peroneal nerve. (Reproduced with permission from Stewart JD. Focal peripheral
neuropathies. Third edition. Philadelphia: Lippincott Williams & Wilkins, 2000.)
Figure 4
Patient with a right foot drop and sensory abnormality in the territory of the distal superficial peroneal
nerve (dorsum of the foot) and the deep peroneal nerve (web space between first and second toes and a
small area in the adjacent dorsum of the foot). This is the same patient as in figure 5. Informed consent
was obtained for publication of this figure.
10.1136/jnnp.2008.149393
Stewart 161
crossers; the nerve involved is in the leg
they habitually cross over the top of the
other; and they invariably recover when
they stop leg crossing. Sometimes the
patient recounts an episode of unusual
pressure; for example, an episode of
sitting (or falling asleep) for a long period
with the legs crossed and wedged under a
table top, or of another person sitting on
the patient’s knee when the legs were
crossed. Some people, when sitting crosslegged, may either ignore the resulting
paraesthesias or are unaware of them
because of alcohol, drugs, illness or sleep.
Perhaps some do not have warning
paraesthesias, or these are not enough
to wake them. Recent weight loss is
sometimes very clearly associated with
the development of a peroneal neuropathy (‘‘slimmer’s palsy’’). Although a
metabolic cause for this condition has
been propounded, it is caused by the
reduction in the protective padding over
the nerve and the satisfaction of once
again being able to cross the legs (which
obese persons cannot do).8–10
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Farm labourers and other workers such
as carpet layers who squat or kneel for
long periods are particularly at risk of
developing peroneal palsies (‘‘strawberry
pickers’ palsy’’) (figs 6 and 7).5, 7, 11 When
the fully flexed knee is bearing the whole
weight of the body, the peroneal nerve is
probably compressed between the biceps
tendon above and the lateral head of the
gastrocnemius and the head of the fibula
below or, possibly, this position kinks and
compresses the nerve within the fibular
tunnel (fig 3). Compression at this site
has been found on surgical exploration in
affected farm workers. In other related
postures there may be additional direct
pressure against the nerve when the knee
is both flexed and pressed against the
ground.
Perioperative peroneal neuropathy not
due to direct surgical injury (see above)
has been recognised for decades, but is
infrequent compared to ulnar neuropathies and brachial plexopathies.12 The
incidence of peroneal neuropathy related
to operations remote from the leg can be
judged from the report of 421 patients
undergoing cardiac bypass surgery: 8
(2%) developed peroneal neuropathies.13
Compression from leg positioning or leg
supports may be the cause, but nerve
Figure 5
This patient sat like this through most of the history taking and denied that he habitually crossed his
legs! His foot drop is shown in figure 4. Informed consent was obtained for publication of this figure.
compression pre- and postoperatively can
also occur, as with perioperative ulnar
neuropathies, because bedridden patients
may lie in such a way to compress
peripheral nerves. Some perioperative
peroneal neuropathies are associated
with the lithotomy position. In a prospective study of 991 adults undergoing
general anaesthesia and surgery while
positioned in lithotomy, 15 (1.5%) developed lower limb neuropathies.14 The
peroneal nerve was involved in 3 patients
(0.3%). The symptoms were sensory only,
and in 2 patients the neuropathy was
bilateral; they all recovered well.
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Postpartum foot drop is usually due to
a common peroneal neuropathy, but
other causes include an L5 radiculopathy
Crossing the legs
has long been
alleged to cause
peroneal
neuropathy
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162 Practical Neurology
cause, but also point to pressure from
the patient’s hands against the nerves
while prolonged hip and knee flexion is
maintained by the patient herself during
labour.17, 18
TABLE Causes of peroneal neuropathy
External compression
During anaesthesia, coma, sleep, bed rest
Plaster casts, braces
Habitual leg crossing
Sitting cross-legged
Prolonged squatting, kneeling
Direct trauma
Blunt injuries, lacerations
Fractures of the fibula
Adduction injuries and dislocations of the knee
Surgery and arthroscopy in popliteal fossa and knee
Traction injuries
Acute ankle injuries
Masses
Ganglia, Baker’s cysts, callus, fibular tumours, osteomas, haematomas
Tumours
Nerve sheath tumours
Nerve sheath ganglia
Lipomas
Entrapment
In the fibular tunnel
Anterior (tibial) compartment syndrome
Vascular
Vasculitis, local vascular disease
Diabetes mellitus: susceptibility to compression, ischaemic damage
Leprosy
Idiopathic
and damage to the lumbosacral trunk
(see below). Pressure on the nerve at
the neck of the fibula by knee supports
is one likely cause.15 In countries where
prolonged natural childbirth is common,
such neuropathies are often bilateral
and may be due to prolonged squatting.16
Other reports confirm squatting as a
Figure 6
This young man worked all day tiling a
bathroom floor (A), and at the end of
the job had a marked left foot drop (B).
External compression and kinking of the
peroneal nerve was the cause of his
peroneal neuropathy. Informed consent
was obtained for publication of this
figure.
10.1136/jnnp.2008.149393
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Masses: the most common of these is a
ganglion arising from the superior tibiofibular joint. Although benign, they are
infiltrative and can compress or invade
the nerve.19–21 Baker’s cysts may also
compress the common peroneal nerve,
and sometimes also the tibial nerve.22
Schwannomas and neurofibromas can
arise anywhere along the course of
the common peroneal nerve, or its two
major branches, but are most common
in the popliteal fossa.23 Other rare mass
lesions are listed in the table. Callus
from old fibular fractures, osteomas,
and malignant tumours arising from the
head or neck of the fibula are all
possibilities.
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Several cases of true entrapment of the
common peroneal nerve in the fibular
tunnel have been confirmed surgically.4, 24–26 The characteristic operative
findings have been described as a ‘‘tight
crescentic band at the origin of the
peroneus longus ... constricting the nerve
which was swollen proximally’’.25 Division
of these bands is effective in relieving the
symptoms. Such true peroneal entrapment is rare: Sidey explored 26 common
peroneal nerves in 23 patients, and of the
8 with no apparent cause for the
neuropathy, he found evidence of entrapment in only one.26 One other report of
allegedly surgically proven peroneal nerve
entrapments lacks credibility.27 Cadaver
dissection studies have shown that few
people have a firm fibrous arch as part of
Stewart 163
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the fibular tunnel; this may explain the
rarity of nerve entrapment at this site.24
Spontaneous entrapment of the peroneal
nerve should be considered when there is
absolutely no identifiable cause, when
other more proximal lesions have been
excluded, and when symptoms and signs
worsen progressively, and imaging studies (see below) are normal.
Mononeuropathy multiplex syndromes
may involve the common peroneal nerve.
These disorders include diabetes, vasculitis, and hereditary neuropathy with
liability to pressure palsies. In tuberculoid
and borderline leprosy, the peroneal nerve
is one of the most frequently involved
major peripheral nerves.
Idiopathic peroneal neuropathy is the
frustrating appellation for those patients
in whom no specific cause can be found. I
believe that with the increasing recognition of leg crossing (including recent
weight loss) as a cause, and that with
improved imaging techniques, this group
is shrinking. Some of these patients may
have had an unnoticed episode of
external compression, or pressure on the
nerve during sleep.
Deep peroneal nerve
When a patient has neurological deficits
restricted to the deep peroneal nerve, the
lesion may lie in that major terminal branch
of the common peroneal nerve, or there may
be a partial lesion of the common peroneal
nerve that only damages the fascicles going
to form the deep peroneal nerve.
The anterior (tibial) compartment syndrome
results from raised pressure within the fascial
compartment that contains the deep peroneal
nerve and the muscles it supplies. Causes
include excessive exercise, soft tissue trauma,
fractures, haemorrhage, occlusion of the
anterior tibial artery or its parent trunk, or
restoration of blood flow after acute arterial
insufficiency in the leg.28 Severe anterior
lower leg pain, swelling and redness are
associated with motor and sensory dysfunction of the deep peroneal nerve. The neuropathy is caused by compression by the
swollen muscles, and improves rapidly following urgent surgical decompression of the
anterior compartment.
Chronic deep peroneal neuropathy can result
from compression by ganglia, osteochondromas
Figure 7
This young woman was in the habit of putting on her make-up sitting like this. She would also often
read in the same position. After one particularly long period spent putting on make-up she developed
asymmetrical peroneal neuropathies. The mechanism is likely to be kinking of the nerves during
prolonged knee flexion. Informed consent was obtained for publication of this figure.
and aneurysms. A chronic compartment syndrome has been described, but the involvement
of the peroneal nerve is uncertain.29
EXAMINATION OF THE PATIENT
WITH FOOT DROP
A patient with a complete lesion of the
common peroneal nerve has the classical
clinical picture of paralysis of dorsiflexion and
eversion of the foot, and of extension of the
toes, resulting in a foot drop and a
characteristic slapping gait. Weakness is
present in the foot and toe dorsiflexors, the
foot everter muscles, but nowhere else. The
important other muscles to test in a patient
with foot drop are those supplied by the L4–
S1 roots, lumbosacral plexus, and sciatic
nerve: the gluteal and hamstring muscles,
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164 Practical Neurology
Foot drop following hip arthroplasty is much more
likely to be due to sciatic nerve damage than to
pressure on the peroneal nerve at the fibular head
gastrocnemius, and the tibialis posterior. This
last muscle is the foot inverter and is
innervated by the same roots as the tibialis
anterior (L4, 5), but via the tibial nerve.
The sensory loss of a peroneal neuropathy
classically extends over the anterolateral surface
of the lower leg and the dorsum of the foot and
toes. However, except in total nerve lacerations,
the sensory loss is often less widespread than
the textbook description and is usually restricted
to the dorsum of the foot and some toes, as
discussed above (fig 4). Sometimes there are
no sensory symptoms or signs. The knee and
ankle reflexes should be normal in a peroneal
neuropathy. If the ankle reflex is abnormal,
then an L5 radiculopathy with involvement of
the adjacent S1 root, or a plexus or sciatic
nerve lesion are to be considered.
Case 1
A 69-year-old retired nurse was out for a vigorous walk when she realised that
her right foot was slapping the ground. There was also tingling on the dorsum
of the foot and ankle. Over the next several days she tripped on the toes of that
foot. She had been dieting and exercising and had lost 22 kg. She sat during
the consultation with her right leg crossed over the left, and when this was
commented on, she said she had been doing this ‘‘all the time’’ since she had
lost weight and was able to cross her legs again. Examination showed weakness
of the right tibialis anterior (2/5), extensor hallucis longus (3/5), and the
peroneal muscles (3/5). The tibialis posterior and all other muscles in both legs
were normal. There was no sensory loss. The peroneal nerve was tender to
palpation at the fibular neck. Motor nerve conduction studies showed
conduction blocking and slowing at the neck of the fibula; the peroneal sensory
response was very small compared to that on the left. The patient refused an
ankle foot orthosis. She was counselled not to cross her knees. In two months,
her strength was somewhat better, and by four months, it was back to normal
Take home messages
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Peroneal neuropathy can result from habitual leg crossing and, in this
patient, illustrates the phenomenon of ‘‘slimmer’s palsy’’.
The motor deficits are perfectly in keeping with the distribution of the
peroneal nerve, but there was no sensory loss presumably because the
sensory fascicles within the nerve were not sufficiently damaged. The
tingling was probably due to nerve irritation and abnormal impulse
generation.
Focal nerve tenderness at the knee is a simple but valuable localising sign.
Merely avoiding leg crossing can be curative.
The course of the common peroneal nerve
should be examined carefully. When present,
local tenderness of the nerve and a Tinel’s sign
at the fibular head and neck are valuable
indicators of a nerve lesion there; however, one
sometimes sees patients with L5 radiculopathies and tenderness of the peroneal nerve. The
simple straight leg raising test, when abnormal,
is always useful in indicating a root or other
proximal nerve lesion. Cysts or other masses in
the popliteal fossa or lateral to the knee may be
found on careful palpation. Thickening of the
nerve occurs in leprosy.
Patients with foot drop sometimes pose a
difficult diagnostic challenge for two reasons:
first, partial involvement of the common
peroneal nerve may produce highly variable
degrees of weakness and sensory loss in the
muscles and skin supplied by the nerve, and
second the nerve lesion lies more proximally
than the common peroneal nerve.
Partial peroneal neuropathies
Variable involvement of the muscles and skin
supplied by the common peroneal nerve is
frequent in all but complete lacerations of the
nerve.5, 30, 31 Patients often have sensory only or
motor only symptoms and signs. The former
may involve the superficial or deep sensory
branches only. Likewise, the weakness may be
confined mainly to the muscles supplied by the
deep or the superficial peroneal nerves. This
variable motor and sensory involvement is
explained by the microscopic anatomy of the
nerve. At the knee, the fibres that form the deep
and superficial peroneal nerves clearly lie in
separate fascicles.32 Damage to the common
peroneal nerve from whatever cause can
produce differing involvement of individual
fascicles in the nerve similar to the partial
deficits seen in radial ‘‘Saturday night’’ neuropathies, and ulnar neuropathies at the elbow.
DIFFERENTIAL DIAGNOSIS OF
FOOT DROP
The more proximal focal neuropathies that
produce foot drop and masquerade as
common peroneal neuropathies are:
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L5 radiculopathies
Lumbar plexopathies
Lesions of the lumbosacral trunk of the
lumbosacral plexus
Sciatic neuropathies
Stewart 165
The cause may be clear from the history—
for example, a patient with characteristic
symptoms of lumbar radiculopathy, a hip
fracture, a difficult labour that may have
involved the use of forceps or a clear episode
of compression or trauma to the sciatic or
common peroneal nerve. However, in other
situations, it may not be so obvious. Lumbar
radiculopathy can occur without low back
pain that radiates down the leg. Foot drop
following hip arthroplasty is much more likely
to be due to sciatic nerve damage than to
pressure on the common peroneal nerve at
the fibular head. Foot drop following delivery
of a child may be due to a disc herniation and
L5 radiculopathy, compression of the lumbosacral trunk33 or pressure on the peroneal
nerve by knee supports.
An L5 radiculopathy, lumbar plexopathy
and a lumbosacral trunk lesion will all
produce weakness in muscles not supplied
by the common peroneal nerve, notably the
gluteal, hamstring and, particularly, the
tibialis posterior muscle. However, damage
to the lateral trunk of the sciatic nerve can
exactly mimic a peroneal neuropathy because
this trunk becomes the peroneal nerve.
Although a trunk lesion involves the innervation to the short head of the biceps femoris,
this muscle cannot be clinically examined
separately from the other hamstring muscles,
so electromyographic examination is required
to sort this out. Fortunately, in many cases of
lateral trunk lesions, there are often signs of
mild involvement of the medial trunk, and
these can be revealed by careful clinical and
electrophysiological examination.
Sometimes a generalised peripheral neuropathy appears superficially like bilateral peroneal neuropathies because foot drop is more
obvious than plantar flexor weakness. In
Case 2
A 33-year-old, very athletic man competed in a long distance run and cycle
ride. Two days later, he realised he had started to limp and when he ran, he
tripped over his left foot. He also had a foot drop and numbness over the
anterolateral aspect of his lower left leg and dorsum of the foot. He denied any
low back or leg pain, and habitual leg crossing. On examination two weeks later,
the left tibialis anterior and extensor hallucis muscles were weak (42/5);
however, tibialis posterior, gastrocnemius, hamstring, and gluteal muscles were
also weak at 4–4+/5. There was sensory loss over the anterolateral aspect of
the lower leg and dorsum of the foot. The left ankle reflex was less brisk than
the right. Straight leg raising was normal, and the peroneal nerve was not
tender at the fibular neck. Nerve conduction studies showed no evidence of a
peroneal neuropathy. Needle electromyographic studies showed fibrillation
potentials and polyphasic motor unit potentials in the left tibialis anterior, tibialis
posterior, and gluteus medius muscles. A CT scan of the lumbosacral spine showed
a large L5/S1 disc herniation on the left compressing the L5 and S1 nerve roots.
The patient underwent a discectomy and made a complete recovery.
Take home messages
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The patient had symptoms that strongly suggested peroneal neuropathy,
but the examination clearly showed deficits best explained by L5 and S1
radiculopathies.
In spite of having a large disc herniation, he had no low back pain or
‘‘sciatica’’.
Because of the athletic event preceding the symptoms, an anterior
compartment syndrome was an important consideration but the absence
of shin pain, swelling and hyperaemia argued strongly against that
diagnosis.
amyotrophic lateral sclerosis, an early feature
may be foot drop. And patients with myopathies, particularly the rare distal ones, will often
have foot drop. Patients with upper motor
neuron weakness of the leg generally have more
weakness of foot dorsiflexion than plantar
flexion. In all of these, a careful examination
will usually show that there are signs beyond
the innervation of the common peroneal nerve.
Finally, focal dystonia of the foot may present
with apparent weakness in dorsiflexion.
Figure 8
(A) Longitudinal ultrasonographic view
of a normal peroneal nerve (PN) and
the adjacent fibula (F). (B) Similar view
of a peroneal nerve with an intraneural
ganglion. (Reproduced with permission
from Visser LH. High-resolution
sonography of the common peroneal
nerve: detection of intraneural ganglia.
Neurology 2006;67:1473–5.)
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166 Practical Neurology
Case 3
A 35-year-old primigravida had marked low back pain in the last three months
of her pregnancy. She was admitted at 41 weeks gestation and labour was
induced under epidural anaesthesia. The fetus was in the right occipital lie. The
second stage of labour was prolonged. Forceps were used to rotate the fetus to
an occiput anterior position and then to assist in delivery. Throughout labour
the mother experienced considerable pain down the left leg. This persisted and
developed into burning paraesthesia over the anterolateral lower leg and
dorsum of the foot. She had a marked left foot drop. Examination three weeks
later showed marked weakness of the tibialis anterior, extensor hallucis longus,
the peroneal muscles, and tibialis posterior muscle. There was mild weakness of
the left gluteal muscles and hamstrings. There was decreased light touch over
the dorsum of the foot. Reflexes were normal. Electrophysiological studies
showed no peroneal motor conduction abnormalities at the knee. The peroneal
and sural sensory amplitudes were both reduced in size. Needle EMG showed
fibrillations and neurogenic motor unit potentials in the clinically weak
muscles, but not in lumbar paraspinal muscles. A CT scan of the lumbar spine
was normal. A diagnosis of damage to the lumbosacral trunk of the left
lumbosacral plexus was made.33 She was fitted with an ankle foot orthosis, and
made a slow but nearly complete recovery.
Take home messages
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The differential diagnosis here includes L5 radiculopathy from an L4/5 disc
herniation, root damage from misplaced epidural injections, and peroneal
neuropathy at the knee due to compression against stirrups, or prolonged
knee flexion during delivery. Less frequent than all of these is crush
damage to the lumbosacral trunk against the ala of the sacrum (fig 1) from
the fetal head and/or forceps.
Careful clinical examination and electrodiagnostic studies can usually
localise the lesion.
Imaging of the lumbar spine is helpful when disc herniation is suspected.
INVESTIGATIONS
Nerve conduction and
electromyographic studies
These are a valuable extension of the clinical
examination in evaluating patients with foot
drop. They should be done whenever there is
the slightest concern, following a careful
examination, that the foot drop may be due
to something other than a peroneal neuropathy. Conduction abnormalities at the level
of the fibular neck/head are often found, and
electromyographic (EMG) abnormalities are
restricted to muscles supplied by that nerve.
When more proximal lesions are suspected,
then a very useful strategy is to do needle
EMG examinations of lumbar paraspinal,
gluteal and hamstring muscles. Often the
two most important muscles to test are the
short head of the biceps femoris and the
tibialis posterior, for reasons explained above.
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If searching for evidence of medial trunk of
sciatic nerve damage when a sciatic neuropathy with predominant lateral trunk damage
is suspected, sural and tibial nerve conduction
studies are helpful.
The electrophysiological findings are also
useful in predicting recovery. Patients with
conduction blocking and little or no axonal
damage as determined by EMG study of the
tibialis anterior muscle often recover in a few
weeks if further pressure on the nerve is
avoided. Severe axonal damage neuropathies
recover slowly and partially over many
months. Patients with mixed axonal and
conduction block neuropathies will often
have a biphasic recovery: improvement within
weeks is due to recovery of those fibres that
have been affected by demyelination, while
the much slower process of axonal regeneration takes many months—up to a year.
Imaging
Imaging of the knee should be done when a
patient with a peroneal neuropathy of no
apparent cause is not improving, or is
worsening. Plain radiographs sometimes
reveal a soft tissue mass or bone lesion.
Ultrasonography is effective in outlining
Baker’s cysts, aneurysms and ganglia (fig 8).34
CT scanning is excellent for detecting large
soft tissue masses in this area. MRI is even
more effective for demonstrating the range of
intrinsic and extrinsic mass lesions involving
the peroneal nerve (fig 9).35, 36
MANAGEMENT OF THE PATIENT
WITH FOOT DROP
Most patients with a peroneal neuropathy fall
into one of three main groups:
N
N
N
acute trauma
a recognisable compressive episode, or
recurrent episodes
progressive neuropathy of uncertain
cause.
If the type of trauma—for example, a
laceration, suggests a complete transection,
immediate nerve repair is indicated.
Incomplete traumatic neuropathies are followed clinically, and spontaneous improvement is expected. If this does not occur within
several months, surgical exploration of the
nerve may be warranted because scar tissue
and neuroma formation can impede axonal
Stewart 167
regeneration; careful surgical resection of
these, combined with cable nerve grafting can
often bring about some degree of recovery.
For blunt injuries that appear to be complete,
waiting for spontaneous improvement to
occur over a period of several months is
probably the best approach. Stretch injuries of
the peroneal nerve are often associated with
long areas of damage. Even when they are
repaired with nerve grafts, the results are
poor.37 The acute compartment syndromes of
the lower leg are surgical emergencies.
Prompt fasciotomy is important for good
recovery of nerves and muscles.
When a definite compressive episode can
be identified I re-evaluate the patient in two
months. When leg crossing or other postural
habits that may repetitively compress the
nerve are suspected, I instruct the patient to
avoid these and re-evaluate in two months.
Extensive investigations are usually not
necessary. If a patient does not show signs
of improving at this time, or if they worsen,
they are categorised in the progressive group.
Patients with progressive peroneal neuropathies should have imaging studies. The
choice between ultrasonography, CT scanning
and MR imaging depends on local availability,
expertise, and cost considerations. I usually
do ultrasound first, then CT if the diagnosis is
still uncertain, and then MRI if necessary. If a
mass is discovered, it should be surgically
removed unless it is a bony metastasis. If no
mass is found, surgical exploration is still
warranted. Some soft tissue lesions may not
be visible on imaging (with improved imaging
this is becoming less likely). If the patient has
a true entrapment of the nerve within the
Figure 9
Proton density-weighted MR axial image of the leg below the knee. The tibia lies superiorly and to the
left, the fibula lower and to the right. Lateral to the neck of the fibula is a large mass (arrow) exactly
where the common peroneal nerve lies. The patient had a peroneal neuropathy. The lesion was excised
and was a neuroma arising from a branch of the nerve. Reproduced with permission from Loredo R,
Hodler J, Pedowitz R, et al. MRI of the common peroneal nerve: normal anatomy and evaluation of
masses associated with nerve entrapment. J Comput Assist Tomogr 1998;22:925–31.
fibular tunnel, this can only be confirmed
surgically.
Patients in whom a popliteal mass is
palpated when they first present with foot
drop should be sent for imaging. For patients
with suspected radiculopathy, imaging with
CT or MR should be undertaken and further
management then decided. If a lumbosacral
Figure 10
(A) Foot drop caused by a severe L5
radiculopathy. (B, C) Ankle foot orthosis
in place. Informed consent was
obtained for publication of this figure.
www.practical-neurology.com
168 Practical Neurology
Case 4
A 74-year-old man underwent a right total hip replacement for advanced
osteoarthritis. When mobilised by the physiotherapist two days later, it was
apparent that he had a right foot drop, with paraesthesia and numbness over
the anterolateral aspect of the lower leg and dorsum of the foot. He went on to
develop allodynia in this area and neuropathic pain in the lower leg. The
anaesthetist was blamed for poorly positioning the leg and causing a peroneal
neuropathy and the orthopaedic surgeon was contemplating exploring the
peroneal nerve at the knee. However, although careful neurological
examination confirmed major weakness of the peroneal innervated muscles,
and the gluteal, hamstring and tibialis posterior muscles were not weak, the
gastrocnemius was mildly weak and the ankle reflex was absent. Also, the
sensory abnormality was not only mainly in the peroneal nerve distribution, but
there was some impairment in the lateral border and sole of the foot. Nerve
conduction studies showed no evidence for a peroneal motor conduction
abnormality at the knee. Both the peroneal and sural sensory potentials were
abnormally small. Needle EMG studies showed fibrillations and neurogenic
abnormalities in the tibialis anterior, the short head of the biceps femoris and,
to a lesser degree, in the gastrocnemius. A diagnosis of a lesion of the sciatic
nerve in which the predominant damage was to the lateral trunk, was made.
The patient was fitted with an ankle foot orthosis, given medications for
neuropathic pain, and eventually regained considerable strength.
and prevent tripping. The most satisfactory is
a lightweight plastic ankle foot orthosis that
fits inside the shoe and up the back of the
calf (fig 10). In cold climates, a pair of boots
often suffices. If the foot drop is permanent,
surgical treatment with tendon transfers
should be considered.
ACKNOWLEDGEMENTS
This article was reviewed by David HiltonJones, Oxford, UK.
REFERENCES
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2.
3.
4.
5.
Take home messages
l
l
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A lesion of the sciatic nerve involving exclusively or predominantly the
lateral trunk closely mimics a peroneal neuropathy.
Many traumatic lesions of the proximal sciatic nerve preferentially or
exclusively damage the lateral trunk.
Careful examination of the muscles and skin supplied by the medial trunk
of the sciatic nerve often reveals some damage to that trunk as well.
Electrodiagnostic studies are a valuable tool in diagnosing the site of the
lesion. Needle EMG of the short head of the biceps femoris muscle,
innervated by the only branch of the lateral trunk, is particularly useful.
Nerve conduction studies of the tibial nerve and EMG of muscles
innervated by it are helpful in confirming some damage to the medial trunk
of the sciatic nerve.
6.
7.
8.
9.
10.
11.
12.
plexus lesion is suspected, then CT or MR
imaging of the lower lumbar retroperitoneal
area and the pelvis should be done. For sciatic
nerve lesions with foot drop, it may not be
necessary to perform imaging studies—for
example, the post-hip surgery patient.
However, if there is no apparent cause, then
the main trunk of the sciatic nerve from the
sciatic notch to the popliteal fossa should be
imaged with MR using gadolinium enhancement searching for tumours of the nerve, or
other lesions that may be impinging on it.
Regardless of the cause of the peroneal
palsy, patients with foot drop benefit greatly
from a brace to support the foot, aid walking
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PRACTICE POINTS
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34.
35.
36.
37.
The most common cause of a unilateral foot drop is peroneal nerve injury.
Most of these patients have had a single episode of pressure to the nerve
such as during a long aeroplane journey, are habitual leg crossers, or have
an occupational cause for the neuropathy.
When such causes are identified, the patient should be advised to avoid
such risks, and good recovery is to be expected.
Proximal nerve lesions mimicking a peroneal neuropathy include L5
radiculopathy, lumbosacral plexopathy and sciatic neuropathy; these
produce weakness in muscles outside of the peroneal territory—for
example, the hamstring and the foot invertor (tibialis posterior) muscles,
and sensory loss in the tibial nerve territory.
EMG and nerve conduction studies are helpful in differentiating proximal
lesions from peroneal neuropathy.
Footdrop due to an L5 radiculopathy sometimes occurs without any low
back or radicular pain.
Imaging is helpful in diagnosing the cause of foot drop, be it a more
proximal nerve lesion or a progressive peroneal neuropathy at the knee.
Whatever the cause of the foot drop, it is important to prescribe an ankle
foot orthosis to improve gait and help prevent falls.
Visser LH. High-resolution sonography of the
common peroneal nerve: detection of intraneural
ganglia. Neurology 2006;67:1473–5.
Loredo R, Hodler J, Pedowitz R, et al. MRI of the
common peroneal nerve: normal anatomy and
evaluation of masses associated with nerve
entrapment. J Comput Assist Tomogr 1998;22:925–31.
Iverson, DJ. MRI detection of cysts of the knee
causing common peroneal neuropathy. Neurology
2005;65:1829–31.
Kim DH, Kline DG. Management and results of
peroneal nerve lesions. Neurosurgery
1996;39:312–19.
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