Contributor Information and Disclosures

Author

James W Pritchett, MD Chief of Orthopedic Surgery, Swedish Orthopedic Institute; Active Staff,
Swedish Medical Center

James W Pritchett, MD is a member of the following medical societies: American Academy of

Orthopaedic Surgeons, American College of Surgeons, Washington State Medical Association,
Association of Bone and Joint Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Margaret A Porembski, MD Attending Physician, Oklahoma Hand Fellowship

Margaret A Porembski, MD is a member of the following medical societies: American College of

Surgeons, American Medical Association, American Society for Surgery of the Hand

Disclosure: Nothing to disclose.

Chief Editor

Jason H Calhoun, MD, FACS Department Chief, Musculoskeletal Sciences, Spectrum Health
Medical Group

Jason H Calhoun, MD, FACS is a member of the following medical societies: American
Academy of Orthopaedic Surgeons, American College of Surgeons, American Diabetes
Association, American Medical Association, American Orthopaedic Association, American
Orthopaedic Foot and Ankle Society, Michigan State Medical Society, Missouri State Medical

Association, Southern Medical Association, Southern Orthopaedic Association, Texas Medical

Association, Texas Orthopaedic Association, Musculoskeletal Infection Society

Disclosure: Received grant/research funds from Biocomposite for other.

Acknowledgements

John S Early, MD Foot/Ankle Specialist, Texas Orthopaedic Associates, LLP; Co-Director, North
Texas Foot and Ankle Fellowship, Baylor University Medical Center

John S Early, MD is a member of the following medical societies: American Academy of

Orthopaedic Surgeons, American Medical Association, American Orthopaedic Foot and Ankle
Society, Orthopaedic Trauma Association, and Texas Medical Association

Disclosure: AO North America Honoraria Speaking and teaching; Stryker Consulting fee
Consulting; Biomet Consulting fee Consulting; AO North America Grant/research funds
fellowship funding; MMI inc Honoraria Speaking and teaching; Osteomed Consulting fee
Consulting; MedHab Inc Management position

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical
Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Updated: Sep 16, 2015

Background

Foot drop is a deceptively simple name for a potentially complex problem. It can be defined as a
significant weakness of ankle and toe dorsiflexion. The foot and ankle dorsiflexors include the
tibialis anterior, the extensor hallucis longus, and the extensor digitorum longus. These muscles
help the body clear the foot during swing phase and control plantarflexion of the foot on heel
strike.

Weakness in this group of muscles results in an equinovarus deformity. This is sometimes

referred to as steppage gait, because the patient tends to walk with an exaggerated flexion of the
hip and knee to prevent the toes from catching on the ground during swing phase. During gait,
the force of heel strike exceeds body weight, and the direction of the ground reaction vector
passes behind the ankle and knee center (see the image below).

Diagram of ground reaction vector during heel stri

Diagram of ground reaction vector during heel strike.

This causes the foot to plantarflex and, if uncontrolled, to slap the ground. Ordinarily, eccentric
lengthening of the tibialis anterior, which controls plantar flexion, absorbs the shock of heel
strike. Foot drop can result if there is injury to the dorsiflexors or to any point along the neural
pathways that supply them.

Foot drop can be associated with a variety of conditions, including dorsiflexor injuries,
peripheral nerve injuries, stroke, neuropathies, drug toxicities, or diabetes. The causes of foot
drop may be divided into three general categories: neurologic, muscular, and anatomic. These
causes may overlap. Treatment is variable and is directed at the specific cause (see Treatment).

Anatomy

Fibers from the dorsal branches of the ventral rami of L4-S1 are found in the peroneal nerve,
which is paired with the tibial nerve to constitute the sciatic nerve. The sciatic nerve leaves the
pelvic cavity at the greater sciatic foramen, just inferior to the piriformis. It bifurcates to form the
peroneal and tibial nerves either in the distal third of the thigh or at the midthigh level.

The peroneal nerve crosses laterally to curve over the posterior rim of the fibular neck to the
anterior compartment of the lower leg, dividing into superficial and deep branches. The
superficial branch travels between the two heads of the peronei and continues down the lower leg
to lie between the peroneal tendon and the lateral edge of the gastrocnemius. It then branches to
the ankle anterolaterally to supply sensation to the dorsum of the foot (see the image below).

Common and superficial peroneal nerves, branches,

Common and superficial peroneal nerves, branches, and cutaneous innervation.

The deep branch divides just after rounding the fibular neck. Its initial branch supplies the tibialis
anterior, and the remaining branches supply the extensor digitorum longus, the extensor hallucis
longus, and a small sensory patch at the first dorsal web space (see the image below).

Deep peroneal nerve, branches, and cutaneous inner

Deep peroneal nerve, branches, and cutaneous innervation.

The peroneal nerve is susceptible to injury all along its course. In that it is part of the sciatic
nerve, its funiculi are relatively isolated from those of the tibial nerve. Therefore, trauma to the
sciatic nerve may affect only one of its divisions. The funiculi of the peroneal nerve also are
larger and have less protective connective tissue than those of the tibial nerve, making the
peroneal nerve more susceptible to trauma. In addition, the peroneal nerve has fewer autonomic
fibers; thus, in any injury, motor and sensory fibers bear the brunt of the trauma.

The peroneal nerve runs a more superficial course than the tibial nerve does, especially at the
fibular neck, and this relatively exposed position makes it vulnerable to direct insult. Its close
adherence to the periosteum of the proximal fibula renders it susceptible to injury during surgical
procedures in this area.

Pathophysiology

The pathophysiology of nerve damage that commonly causes foot drop is as follows. The
functional integrity of an axon and its target depends on the continued supply of trophic
substances synthesized in the neuronal perikaryon and transported down the axon (axoplasmic
flow). A laceration interrupts axoplasmic flow; a crush injury may compromise it as well. A
double-crush phenomenon occurs when a proximal insult in a nerve root diminishes axoplasmic
flow, making it more susceptible to injury.

A distal lesion further compromises axoplasmic flow, and clinical palsy results. This is the
phenomenon thought to be responsible for the increased risk of foot drop after hip replacement in
a patient with preexisting spinal stenosis. The spinal stenosis causes the proximal compromise,
and intraoperative stretch of the sciatic nerve provides the distal insult.

Etiology

Foot drop may follow direct injury to the dorsiflexors. A few cases of rupture of the anterior
tibial tendon leading to foot drop and suspicion of peroneal nerve palsy have been reported. This
subcutaneous tendon rupture usually occurs after a minor trauma with the foot in plantar flexion.

Compartment syndromes also may lead to foot drop. These are surgical emergencies and are not
associated only with fracture or acute trauma. March gangrene, a form of anterior compartment
syndrome, is thought to be due to edema and small hemorrhages in the muscles of the anterior
compartment occurring after strenuous activity in individuals not accustomed to it. Deep
posterior compartment syndrome also may result in foot drop as a late sequela due to contracture
formation.

Neurologic causes of foot drop include mononeuropathies of the deep peroneal nerve, the
common peroneal nerve, or the sciatic nerve. Lumbosacral plexopathy, lumbar radiculopathy,
motor neuron disease, or parasagittal cortical or subcortical cerebral lesions also can manifest as
foot drop. These lesions can be differentiated by means of clinical and electrodiagnostic
examinations.

A common behavioral cause of foot drop is habitual crossing of the legs.[1] These cases typically
resolve with discontinuance of the habit.

Foot drop also may be seen as a combination of neurologic, muscular, and anatomic dysfunction.
Charcot foot is one example.

Epidemiology
. All age groups are affected equally, but the condition is more common in males (male-to-female
ratio, 2.8:1). About 90% of peroneal lesions are unilateral, and they can affect the right or the left
side with equal frequency.

Peroneal neuropathy caused by compression at the fibular head is the most common compressive
neuropathy in the lower extremity. Foot drop is its most notable symptom. All age groups are
affected equally, but the condition is more common in males (male-to-female ratio, 2.8:1). About
90% of peroneal lesions are unilateral, and they can affect the right or the left side with equal
frequency.

A foot drop of particular concern to orthopedic surgeons is the peroneal nerve palsy seen after
total knee arthroplasty (TKA; 0.3-4% of cases) or proximal tibial osteotomy (3-13% of cases).
Ischemia, mechanical irritation, traction, crush injury, and laceration can cause intraoperative
injury to the peroneal nerve. It has also been suggested that correction of a severe valgus or
flexion deformity can stretch the peroneal nerve and lead to palsy. Postoperative causes of
peroneal nerve palsy include hematomas and constrictive dressings.

In a study by Cohen et al, the relative risk of palsy was 2.8 times higher with epidural anesthesia
for TKA than with general or spinal anesthesia.[2] Epidural anesthesia probably decreased

proprioception and sensation (intraoperatively and, to some extent, postoperatively), allowing the
limb to rest in an unprotected state susceptible to local compression. In addition, intraoperative
neurologic damage may not have been readily apparent in the immediate postoperative period,
because of ongoing effects of epidural anesthesia.

In the same study, the relative risk of palsy was 6.5 times greater in patients who had a prior
lumbar laminectomy.[2]

A series of patients who developed foot drop after primary hip arthroplasty were carefully
examined and found to have spinal stenosis.[3] As many as 70% of patients undergoing hip
arthroplasty have electromyographic (EMG) evidence of nerve injury, but they rarely have
clinical symptoms.[4] Patients with preexisting spinal stenosis are believed to be at increased risk
for foot drop after hip arthroplasty because of this proximal compromise; this is the double-crush
phenomenon.

Prognosis

Prognosis and outcome vary according to the cause of the foot drop. In a peripheral compressive
neuropathy, recovery can be expected in up to 3 months, provided that further compression is
avoided. A partial peroneal nerve palsy after total knee replacement has a uniformly good
prognosis.[5] A variable amount of recovery is seen with a complete postoperative palsy. Followup EMG and nerve conduction studies may be useful for assessing recovery.

A partial palsy recovers faster because of local sprouting. With complete axonal loss,
reinnervation is achieved solely through proximal-to-distal axonal growth, which usually
proceeds at a rate of 1 mm/day. Thus, injuries of a nerve close to its target muscle also have a
more favorable outcome. In a nerve root compressive neuropathy, one study concluded that
severe motor weakness lasting longer than 6 months, a negative straight leg-raising test, and old
age were poor prognostic factors for recovery of dorsiflexion.[6]

When there is direct injury to the peroneal nerve, the outcome is more favorable for penetrating
trauma than for blunt trauma; a traction or stretch injury to the nerve has an intermediate

outcome. When nerve grafting is performed, functional recovery depends on the severity of
injury and thus on the length of the graft used. With grafts longer than 12 cm, good functional
recovery is rare.

Wound infection may occur after surgical treatment, as may nerve graft failure. In tendon transfer
procedures, recurrent deformity has been reported. In arthrodeses or fusion procedures,
pseudoarthrosis, delayed union, or nonunion may be noted.

Clinical Presentation