Foot Drop

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).

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

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.

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.

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 plantarflexion.

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 may be of iatrogenic origin (eg, resulting from traction applied during treatment of a fracture[2] ). 

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

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.[3] 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.[3]

A series of patients who developed foot drop after primary hip arthroplasty were carefully examined and found to have spinal stenosis.[4] As many as 70% of patients undergoing hip arthroplasty have electromyographic (EMG) evidence of nerve injury, but they rarely have clinical symptoms.[5] 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 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.[6] A variable amount of recovery is seen with a complete postoperative palsy. Follow-up 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.[7]

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.

In a study evaluating factors predictive of short- and long-term recovery outcomes after surgery for foot drop secondary to lumbar degenerative disease, Berger et al determined that whereas early surgery may improve the recovery rate in these patients, the strongest predictor of the extent of recovery was the severity of preoperative tibialis anterior muscle weakness.[8] Maximal recovery in the short-term postoperative period was associated with sustained long-term functional improvement and independence.

Direct injury to dorsiflexors

With dorsiflexor injury due to laceration or contusion, both cause and effect are readily apparent on clinical examination. (See the video below.) A young healthy patient or an active healthy elderly patient usually benefits from surgical repair of the injury.

If the patient develops a degenerative rupture of the tibialis anterior, foot drop may be observed, but the cause may not be immediately apparent. Such a patient is often an elderly man who suffers a minor trauma with the foot in plantarflexion. The patient stands with the foot everted and has some loss of dorsiflexion when attempting to heel-walk. The degree of foot drop varies, depending on the time elapsed since the rupture.

Active function in the other muscles innervated by the deep and superficial branches of the peroneal nerve essentially rules out the possibility of a peripheral neuropathy. Functional recovery is achieved over time and is aided by bracing of the affected ankle. Surgery may not be required in this situation.

Compartment syndromes

Increased pain with passive stretch of the involved muscles is a consistent diagnostic indicator of a compartment syndrome. The usual initial presenting symptom is pain that is out of proportion to the injury. Paresthesias follow, but at this point, irreversible myoneural injury is likely to have occurred. Foot drop also may be noted; the time of presentation varies with the compartment involved.

Anterior compartment syndrome

Clinical presentation of an acute anterior compartment syndrome includes pain with passive toe flexion, some weakness of toe extension, and diminished sensation in the first web space because of deep peroneal nerve compression. The extensor hallucis longus (EHL) usually is the first muscle to show weakness. Anterior compartment syndrome may follow trauma to the extremity but also can be observed in march gangrene (ie, ischemic myositis of leg muscles following exercise[9] ). In march gangrene, local erythema, heat, and brawny edema over the anterior compartment are present.

Regardless of the cause, wide fasciotomy of the anterior compartment must be performed to salvage the ischemic muscles.

Deep posterior compartment syndrome

An acute deep posterior compartment syndrome presents as pain and some weakness of toe flexion and ankle inversion. Pain on passive toe extension is referred to the calf. Diminished sensation over the sole of the foot, especially on the medial side, is noted, resulting from posterior tibial nerve compression. Foot drop develops because of ischemic contracture of the posterior compartment and is seen if the acute syndrome is not treated.

Once again, wide fasciotomy of the involved compartment is mandatory at the time of acute presentation.

Chronic compartment syndrome

Chronic compartment syndrome occurs in athletes in their third or fourth decade who have exercise-induced pain in the lower leg or foot within 20-30 minutes after beginning to exercise. Often, this occurs after a recent increase in intensity or duration of training or after a change in the training routine. The symptoms resolve after 15-30 minutes of rest; however, as the syndrome progresses, pain occurs earlier and takes longer to resolve. The anterior compartment is the one that is most commonly involved.

Unless the patient has been exercising just before being examined, the physical examination may yield nonspecific or normal results. Patients with a chronic anterior compartment syndrome may have diminished sensation in the first dorsal web space.

Recording of intracompartmental pressures before, during, and after exercise can provide useful diagnostic information as to which compartments may be involved. The following, individually or in combination, are believed to be indicative of the syndrome:

• Resting pressure of 15 mm Hg or higher
• Pressure of 30 mm Hg or higher 1 minute after exercise
• Pressure of 20 mm Hg or higher 5 minutes after exercise

A slit catheter may be used to measure these pressures, with the understanding that the accuracy of the readings is influenced by the depth of needle insertion; the positioning of the leg, ankle, and foot; and the force of muscle contraction.

Some preliminary investigation has been completed into the use of magnetic resonance imaging (MRI) as a potential test for chronic compartment syndrome.

Nonsurgical treatment of a chronic compartment syndrome can succeed only if the patient is willing to discontinue the inciting activity. The surgical treatment of choice is fasciotomy of the involved compartment.

Neurologic defects

Several neurologic defects can cause foot drop. Equinovarus deformity associated with toe contracture is the most common lower-extremity manifestation of stroke. This can be differentiated from a peripheral neuropathy on examination by eliciting hyperactive deep tendon reflexes and a positive Babinski sign. The patient’s gait pattern can also suggest the etiology. For example, patients with a paretic foot drop bear weight on the heel during initial foot strike, whereas those with a spastic deformity strike with the forefoot.

Another central-nerve insult that can be associated with foot drop is L5 compression. In addition to weakness in the peroneal nerve distribution, weakness of the tibialis posterior is noted. Back pain, sciatica, and limitation of straight leg raising also are seen. Motor conduction velocity may remain normal.

Peroneal neuropathy also may be spontaneous, traumatic, or, less frequently, progressive. It is characterized by weakness in dorsiflexion without back pain, sciatica, or other symptoms. Leprosy neuritis, for example, affects nerves where they are close to the skin and pass through a narrow fibrous or osseous canal. In addition to peroneal nerve palsy, patients with leprosy may have involvement of the posterior tibial nerve at the tarsal tunnel that leads to anesthesia of the sole of the foot.

Foot drop from neuropathy may develop in patients who have undergone bariatric surgery, especially those who experience rapid postoperative weight loss.[10] Deficiencies of micronutrients (eg, vitamin B12) may be a factor in these cases.[11]

Combination of neurologic, muscular, and anatomic dysfunction

Patients with a combination of neurologic, muscular, and anatomic dysfunction typically are diabetic and develop loss of protective sensation and proprioception that leads to unperceived trauma. This is coupled with an autonomic neuropathy that results in loss of sympathetic vasoconstriction and enhanced pedal blood flow, causing demineralization and subsequent bone weakness.

Unperceived trauma, demineralization, and bone weakness culminate in destruction of the tarsal bones. This, in turn, leads to formation of a bony block at the ankle joint and foot drop. Progressive motor neuropathy is also present, in which the muscles weaken in a distal-to-proximal manner, resulting in loss of strength in the anterior compartment. The anterior muscles are overpowered by the Achilles tendon, and this leads to abnormal pronator stress at the midtarsal joint, which further encourages osseous breakdown and foot drop.

Workup of foot drop proceeds according to the suspected cause. In cases where a cause (eg, trauma) is readily identified, no specific diagnostic laboratory studies are required. In cases where unilateral foot drop occurs spontaneously in a previously healthy patient, further investigation into metabolic causes (eg, diabetes, alcohol abuse, and exposure to toxins) is required. The following tests may be helpful:

• Fasting blood sugar
• Hemoglobin A1c
• Erythrocyte sedimentation rate (ESR)
• C-reactive protein (CRP)
• Serum protein electrophoresis/immunoelectro-osmophoresis
• Blood urea nitrogen (BUN)
• Creatinine
• Vitamin B12 level

If foot drop is posttraumatic, plain films of the tibia, fibula, and ankle are appropriate to uncover any bony injury. In the absence of trauma, when anatomic dysfunction (eg, Charcot joint) is suspected, plain films of the foot and ankle provide useful information.

If bleeding is suspected in a patient with a hip or knee prosthesis, ultrasonography can be helpful.

If a tumor or a compressive mass lesion to the peroneal nerve is being investigated, magnetic resonance neurography (MRN) may be considered. MRN has made it possible to produce high-resolution images of peripheral nerves, as well as associated intraneural and extraneural lesions.

MRN can be performed by using a standard 1.5 Tesla magnetic resonance imaging (MRI) system and special phased-array imaging surface coils.[12] Image data are acquired simultaneously from multiple receive-only surface coils. The image data from each coil in the array are combined to form a composite image with an improved signal-to-noise ratio.

Compared with standard MRI, MRN allows faster acquisition of anatomically detailed images, a smaller field of view, higher resolution, and thinner sections. By virtue of these features, MRN images are capable of showing the fascicular organization of normal peripheral nerves, thereby rendering the nerves more clearly distinguishable from other tissue (eg, tumor or blood vessels). In one study, the fascicular structure seen on MRN was found to be functional by using intraoperative electrophysiologic testing; the nonfascicular structures were nonfunctional.

Images can be processed further to allow stacking of axial sections and slicing of data in another plane of section. This is helpful in mapping the longitudinal extent of nerve involvement.

In addition to the metabolic disorders listed above, the differential diagnosis of spontaneous foot drop includes spasticity, dystonia, motor neuron disease, L5 radiculopathy, lumbosacral plexopathy, sciatic nerve palsy, compressive peroneal neuropathy, peripheral neuropathy, and some myopathies.

Electromyography (EMG) is useful in differentiating among these diagnoses. This study can confirm the type of neuropathy, establish the site of the lesion, estimate the extent of injury, and provide a prognosis. Sequential studies are useful for monitoring recovery in patients with acute lesions.

Foot drop is highly distressing, and attention to the patient’s psychological needs is very important. Pain should be managed. Optimizing glucose control in diabetic patients and managing vitamin deficiencies with supplements of vitamin B1, B6, or B12 can also be useful.

When foot drop is not amenable to surgical treatment, an ankle-foot orthosis (AFO) is often used. If the foot drop is due to hemiplegia, peroneal nerve stimulation can be considered. Foot drop due to direct trauma to the dorsiflexors generally calls for surgical repair. When nerve insult is the cause of foot drop, treatment is directed at restoring nerve continuity, either by direct repair or by removal of the insult.

If painful paresthesias develop, they can sometimes be effectively managed with sympathetic blocks or laparoscopic synovectomy. Alternative treatments are amitriptyline, nortriptyline, duloxextine, pregabalin, and gabapentin. Local treatment with transdermal capsaicin or diclofenac can also reduce symptoms. Even if there is significant pain, narcotic medications should be kept to a minimum.

Erythropoietin is a naturally occurring hormone that is approved by the US Food and Drug Administration for the treatment of anemia but also has neuroprotective and, possibly, neurotrophic properties. The proposed mechanism of action is antiapoptotic and anti-inflammatory, promoting cell survival. Erythropoietin is given in three doses of 5000 U/kg over 1 week after nerve injury. It has a minimal side-effect profile. An animal study showed that erythropoietin treatment accelerated functional recovery after peripheral nerve injury.[13]

An AFO may be used for foot drop when surgery is not warranted or during surgical or neurologic recovery. The specific purpose of an AFO is to provide toe dorsiflexion during the swing phase, medial or lateral stability at the ankle during stance, and, if necessary, pushoff stimulation during the late stance phase. An AFO is helpful only if the foot can achieve plantigrade position when the patient is standing. Any equinus contracture precludes its successful use.

The most commonly used AFO in foot drop is constructed of polypropylene and inserts into a shoe. If it is trimmed to fit anterior to the malleoli, it provides rigid immobilization. This device is used when ankle instability or spasticity is problematic, as is the case in patients with upper motor neuron diseases or stroke.

If the AFO fits posterior to the malleoli (posterior leaf spring type), plantarflexion at heel strike is allowed, and pushoff returns the foot to neutral for the swing phase. This provides dorsiflexion assistance in instances of flaccid or mild spastic equinovarus deformity. A shoe-clasp orthosis that attaches directly to the heel counter of the shoe also may be used.

A study by Menotti et al suggested that anterior AFOs are associated with lower energy costs of walking and higher levels of perceived comfort than posterior AFOs are and thus may allow people with foot drop to walk longer distances while expending less physical effort.[14]

When foot drop is due to hemiplegia, peroneal nerve stimulation has potential advantages over an AFO, in that it provides active gait correction and can be tailored to individual patients. A short burst of electrical stimulation is applied to the common peroneal nerve between the popliteal fossa and the fibular head. This burst is controlled by a switch in the heel of the affected limb. The stimulator is activated when the foot is lifted and stopped when the foot contacts the ground. This achieves dorsiflexion and eversion during the swing phase of gait.

In a study by Ring et al, the effects of a radiofrequency-controlled neuroprosthesis were compared with those of a standard AFO in 15 patients with foot drop caused by stroke or traumatic brain injury.[15] Compared with the AFO, the neuroprosthesis yielded better balance control during walking and thus managed foot drop more effectively.

The nerve stimulator can be either external or implanted and radiofrequency-activated. In a study of stroke patients with spastic hemiplegia, Chae et al found electrical stimulation to be useful in approximately 2% of the cases.[16] This method may enhance gait speed and quality, and it can contribute to motor relearning.

In a study of 197 patients who had sustained a stroke approximately 3 months previously, Kluding et al compared use of an AFO with use of a foot-drop stimulator (FDS) for treatment of foot drop.[17] They concluded that whereas both approaches resulted in significant improvement in gait speed and functional outcomes, user satisfaction was higher with the FDS; they also stressed that initial therapy can provide long-term benefit.

Van Swigchem et al studied the potential benefits of peroneal functional electrical stimulation (FES) versus an AFO in regard to the patient’s ability to avoid an obstacle.[18] They concluded that FES was superior and that this finding was particularly relevant to people with low strength in the lower leg muscle.

Chou et al found that application of FES to the upper limbs as well was useful for abnormal arm swing in hemiplegic patients with foot drop.[19]

Bethoux et al carried out a 12-month follow-up analysis of a multicenter unblinded randomized controlled study that compared FES with AFOs over a period of 6 months.[20]  At 12 months, there were no statistically significant differences between the FES group and the AFO group with respect to either primary endpoints (10-Meter Walk Test and device-related serious adverse event rate) or secondary endpoints (6-Minute Walk Test, GaitRite Functional Ambulation Profile, and Modified Emory Functional Ambulation Profile).

Miller et al compared two different FES devices, the Odstock Dropped Foot Stimulator (ODFS) and the Walkaide (WA), in terms of their effect on energy cost and speed of walking.[21]  The ODFS yielded a significant increase in walking speed over what was achieved without FES, and the WA yielded a near-significant increase. Neither walking speed nor energy cost differed significantly between the two FES systems.

In a systematic review and meta-analysis of seven studies (N = 67), Burns et al determined that the main barriers to the use of a transcutaneous foot drop electrical stimulator in patients with neurologic conditions were the aesthetics of the device, usability challenges, the trustworthiness of device in complex environments, and cost.[22]

If foot drop is secondary to lumbar disc herniation (a finding in 1.2-4% of patients with foot drop), discectomy should be considered. In the early phase of this condition, decreased blood flow due to compression is thought to lead to nerve-root ischemia. The nerve root is more susceptible to compression injury than the peripheral nerve is because the vascular network of the nerve root is less developed, with no regional arteriolar blood supply. Foot drop due to nerve-root injury may depend on the magnitude and duration of nerve-root compression.

Early decompression is recommended in cases accompanied by severe motor disturbance, especially in older patients.[7] A Japanese study of 46 patients with degenerative lumbar disease who presented with drop foot noted that palsy duration and preoperative strength were the factors that most affected recovery after surgical intervention.[23]

Foot drop following hip replacement can also be treated with sciatic nerve decompression, particularly if there is any concern about bleeding at the operative site. Shortening of the hip prosthesis may be helpful if the limb was lengthened during surgery.[24]

A review of surgical management of peroneal nerve lesions demonstrated that neural repair is the first priority in selected patients with peroneal nerve palsy.[25] This may be accomplished by means of nerve decompression (either central or peripheral) or nerve grafting or repair. For foot drop from deep peroneal nerve injuries of less than 1 year’s duration, one study reported success in transferring functional fascicles to deep peroneal-innervated muscle groups, with either the superficial peroneal nerve or the tibial nerve used as a donor.[26]

If sufficient recovery is not achieved with those measures, tendon transfer procedures (see below) may be considered. It has been suggested that a tendon transfer may be considered if there is no significant neural recovery at 1 year. If a foot drop is chronic and accompanied by contracture, lengthening of the Achilles tendon may be necessary to achieve adequate dorsiflexion. Several studies have found that tendon transfer increases mobility and self-independency, thereby enhancing patient satisfaction.[27] The choice of surgical technique does not appear to affect outcome. 

In patients in whom foot drop is due to neurologic and anatomic factors (eg, polio or Charcot joint), arthrodesis may be the preferred option. The goal is to achieve a stable, well-aligned foot and ankle. This may be accomplished by means of ankle arthrodesis, Lisfranc arthrodesis, and triple or pantalar arthrodesis, with or without lengthening of the Achilles tendon.

Decisions regarding the appropriate timing of nerve exploration and repair must take into consideration the mechanism of insult.

For sharp laceration with suspected nerve transection, early repair is warranted. Blunt lacerations are repaired 2-4 weeks after injury. Lesions in continuity usually are monitored for several months with clinical examination and electromyography (EMG) for signs of early regeneration. If spontaneous regeneration does not occur, surgical exploration and intraoperative nerve action potential (NAP) recordings are used to determine the need for repair, either with end-to-end sutures or with nerve grafts.

Patients with peroneal nerve palsy after knee arthroplasty or tibial osteotomy should initially be treated by removing all constrictive dressings and repositioning the knee to 20-30° of flexion. If an expanding hematoma is noted, urgent exploration is warranted. If functional recovery does not occur within 2 months, nerve exploration or release is advocated. The time interval between symptom onset and decompression appears to affect the final functional outcome. However, the severity of the preoperative palsy does not seem to affect recovery.

The recommended approach for nerve decompression is through a longitudinal posterolateral incision centered at the fibular head and paralleling the biceps tendon and fibula. The peroneal nerve is identified at the biceps femoris and traced distally. The nerve is released proximally from its fibrous enclosure at the fibular neck. Distally, it is released to the level where it dives into the peroneus longus. The attachment of the peroneus longus at the fibular neck is also released.

A wider exposure should be used for posttraumatic exploration if immediate repair or grafting is anticipated. With the patient prone, a mildly curved incision is made just medial to the short head of the biceps femoris in the lower thigh, extending to the skin posterior to the fibular head and then toward the anterior compartment. Superficial and deep peroneal nerve branches are exposed distal to the fibular head. The peroneal nerve is traced obliquely across the popliteal fossa, and its division can be split away from the tibial fossa if further length is needed.

In general, limited exposure should be avoided, so as to facilitate the performance of intraoperative stimulation and recording studies. Having clear exposure of the lesion, as well as viable nerve proximally and distally, is essential. Surgical exploration with NAP monitoring of lesions in continuity can document sufficient peroneal recovery to allow the surgeon to avoid unnecessary resection and repair. Allograft nerve conduits and allograft cable grafts are an alternative to autografts for nerve reconstruction.

With a tendon transfer, retraining of the transferred tendon and stretching exercises for the Achilles tendon are advocated. Retraining may be avoided with a neurotendinous transposition of the gastrocnemius and the proximal end of the deep peroneal nerve.

This procedure requires very specific patient selection in the subgroup with persistent traumatic peroneal nerve palsy. The common peroneal nerve lesion must be at or distal to the branching from the tibial nerve (to guarantee that intact motor fibers proximal to the lesion are available for transposition). Paralysis must be permanent.

Specifically, there must be no recovery of function for at least 18 months after injury or after the most recent attempt at exploration or repair. Electrodiagnostic changes indicative of permanent damage must be present. Also, there must be good passive range of motion, with at least 90° of dorsiflexion. The muscles innervated by the tibial nerve must be normal. Finally, soft-tissue coverage must be adequate.

A common method of tendon transfer moves the posterior tibial tendon (PTT), with or without complementary lengthening of the Achilles tendon. This procedure is accomplished via an open Z-lengthening of the Achilles tendon to allow a minimum of 15° of passive dorsiflexion.

The route by which the PTT is transferred may be either through the intraosseous membrane or circumtibial. One series that included patients with leprosy concluded that the circumtibial route had an unacceptably high rate of recurrent inversion, leading to ulceration of the lateral border of the foot.[28] Other series have found either method to be acceptable, but a 2009 study argued that the interosseous membrane route is preferred in this patient population.[29]

The circumtibial route is technically easier, but it may be less appealing cosmetically. The intraosseous membrane route can be prone to adhesions if the window in the membrane is too narrow. In addition to discouraging adhesions, a generous window produces a straight line of pull of the posterior tibial muscle-tendon unit from its origin to its new insertion on the dorsum of the foot.

Once a transfer route is selected, the point of fixation of the split PTT may be either tendon-to-tendon or tendon-to-bone. In tendon-to-tendon fixation, the points of attachment are as follows:

• Lateral slip - Peroneus brevis, peroneus tertius, or extensor digitorum longus (EDL) tendons
• Medial slip - Tibialis anterior or extensor hallucis longus (EHL)

In tendon-to-bone fixation, an osseous tunnel in the tarsal or metatarsal bones serves as the point of attachment. One study cited a report of a consequent neuropathic arthropathy of the tarsal joints.

A popular approach to tendon-to-bone attachment is the Bridle procedure, a modification of the Riordan technique described by Rodriguez.[30] This procedure involves insertion of the PTT into the second cuneiform bone, combined with anastomosis of the PTT transfer to the anterior tibial tendon (ATT) and a rerouted peroneus longus tendon in front of the lateral malleolus to balance the foot in dorsiflexion.

The Bridle procedure makes use of five incisions (see the first image below). The PTT insertion is secured through incision 1 on the medial foot. Incision 2 is used to retrieve the end of the PTT proximal to the tarsal canal into the posterior compartment of the leg (see the second image below).

Incision 3, on the anterior leg proximal to the ankle, provides wide exposure of the interosseous membrane. The PTT is pulled through the interosseous membrane and a longitudinally split ATT, then into the anterior compartment between the tibia and the ATT. The PTT is anastomosed to the ATT with the foot in full dorsiflexion (see the image below).

Incision 4, posterior to the lateral malleolus, accesses the peroneus longus and brevis tendons proximal to the lateral retinaculum. The peroneus longus is transected about 5 cm proximal to the tip of the lateral malleolus. The distal transected end of the peroneus longus is retrieved into the foot distal to the superior and inferior peroneal retinaculum, then transposed via a direct subcutaneous tunnel that is anterior to the lateral malleolus. The proximal end of the transected peroneus longus is anastomosed to the peroneus brevis tendon.

Incision 5 accesses the distal stump of the PTT as it is brought to the dorsum of the foot via a subcutaneous tunnel. Here, the tendon is secured to the second cuneiform bone while full dorsiflexion of the foot is maintained. Ideally, if the tendon has sufficient length, it should be anastomosed to itself through a tunnel in the second cuneiform bone. If this is not feasible, the tendon may be secured to the bone with sutures or tunneled through and secured with a button.

In a study comparing 19 patients with foot drop who underwent the Bridle procedure with 10 matched control subjects, Johnson et al found that although the procedure did not restore foot and ankle strength and balance to normal, it was successful in that patients with a functional posterior tibial muscle had significantly better outcomes and were able to discontinue using an AFO.[31] All of the Bridle-procedure patients had good-to-excellent outcomes and stated that they would undergo the operation again.

Werner et al, in a study of 10 patients with peroneal nerve injury resulting from multiligament instability, evaluated nonoperative treatment (n=5) against PTT transfer (n=5); there was also a control group (n=4) who did not have peroneal nerve injury.[32] Compared with the nonoperative group, the PTT-transfer group showed increased dorsiflexion at initial contact and at mid-late swing phase. Compared with the control group, the PTT-transfer group had similar gait patterns but tended to be more everted. Overall, gait analysis demonstrated significantly improved sagittal-plane ankle kinematics with PTT transfer, with some degree of subtle instability as the tradeoff.

A series of hemiplegic patients demonstrated favorable results when anterior transfer of the long-toe flexors (flexor hallucis longus [FHL] or flexor digitorum longus [FDL]) was combined with Achilles-tendon lengthening. The flexor was transferred intraosseously to the fourth metatarsal. If the foot drop was accompanied by a marked varus deformity, lengthening of the PTT was also performed. Short-toe flexors were released if the patient had severe hammertoes.

Another method of reconstruction involving the coaptation of the EHL to the tibialis anterior was investigated in eight patients who had had polio. At final review, only two of the patients maintained efficient dorsiflexion. These poor results were thought to be due to stretching of the coaptation.

During neurotendinous transposition, the lateral head of the gastrocnemius is transposed to the tendons of the anterior muscle group simultaneously with transposition of the proximal end of the deep peroneal nerve. The nerve is sutured to the motor nerve of the lateral head of the gastrocnemius, restoring active voluntary foot dorsiflexion and automatic walking. By avoiding use of an antagonist muscle to the paralytic group of muscles, this transfer avoids retraining to achieve dorsiflexion, providing physiologic muscle balance and fully automatic walking.

Mohavedi Yeganeh et al described the use of a triple tendon transfer (involving the PTT, the FHL tendon, and the FDL tendon) to correct toe drop associated with common peroneal nerve palsy, which is not addressed by anterior PTT transfer alone.[33]  Excellent postoperative results for foot drop correction were achieved in nine cases (60%), good results in five (33%), and moderate results in one (7%). Excellent postoperative extension of the toes was achieved in seven cases (47%), good extension in five (33%), and moderate extension in three (20%).

Cho et al reported on 17 patients who underwent PTT transfer for foot drop secondary to peroneal nerve palsy (follow-up, ≥3 years).[34] Mean American Orthopaedic Foot & Ankle Society (AOFAS) score, Foot and Ankle Outcome Score (FAOS), and Foot and Ankle Ability Measure (FAAM) improved significantly at final follow-up: from 65.1 to 86.2, from 55.6 to 87.8, and from 45.7 to 84.4, respectively. However, all functional evaluation scores were significantly lower than in the control group. Mean peak torque was 7.1 Nm for ankle dorsiflexors, 39.2 Nm for plantarflexors, 9.8 Nm for invertors, and 7.3 Nm for evertors at final follow-up. These values were significantly lower than corresponding values in the control group.

No significant differences in radiographic measurements were found, and no patients presented with a postoperative flatfoot deformity.[34] One patient (5.9%) needed an AFO for occupational activity. Cho et al concluded that although restoration of dorsiflexion strength postoperatively was about 33% of the normal ankle, function in daily activities and gait ability were satisfactorily improved. In addition, PTT transfer demonstrated no definitive radiographic or clinical progression to postoperative flatfoot deformity at intermediate-term follow-up.

After a nerve exploration or graft procedure, weight-bearing as tolerated is allowed with a 2- to 3-day period of immobilization of the knee in a Robert-Jones dressing (a bulky compressive bandage composed of multiple layers of soft material). An AFO may be used while neural recovery is being awaited.

After a tendon transfer procedure, the patient is placed in a cast and restricted to nonweightbearing ambulation for 6 weeks. Subsequently, the patient receives physical therapy for gait training.

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Class Summary

The analgesic properties of certain agents in this class may improve symptoms if painful paresthesias develop.

Amitriptyline

Amitriptyline is an analgesic for certain chronic and neuropathic pain. It blocks the reuptake of norepinephrine and serotonin, which increases their concentration in the central nervous system (CNS). Amitriptyline decreases pain by inhibiting spinal neurons involved in pain perception. This agent is highly anticholinergic. It is often discontinued because of somnolence and dry mouth. Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval after reaching the target level is advised. Up to 1 month may be needed to obtain clinical effects.

Nortriptyline (Pamelor)

Nortriptyline increases the concentration of serotonin and norepinephrine in the central nervous system by inhibiting their reuptake by the presynaptic neuronal membrane. It has demonstrated effectiveness in the treatment of chronic pain.

Desipramine (Norpramin)

This is the original tricyclic antidepressant used for depression. These agents have been suggested to act by inhibiting reuptake of noradrenaline at synapses in central descending pain modulating pathways located in the brainstem and spinal cord.

Class Summary

Pharmacologic agents with reuptake inhibition of serotonin and norepinephrine such as duloxetine (Cymbalta) may be helpful in a variety of mood and anxiety disorders. Duloxetine is also cleared for use for chronic musculoskeletal pain, anxiety, and depression. It can be used for neuropathy and has also been used for fibromyalgia.

Duloxetine (Cymbalta, Irenka)

Duloxetine is a potent inhibitor of neuronal serotonin and norepinephrine uptake, and antidepressant action is thought to be due to serotonergic and noradrenergic potentiation in the central nervous system.

Class Summary

Some agents in this category have shown benefit by improving symptoms if painful paresthesias develop.

Pregabalin (Lyrica)

Pregabalin is a structural derivative of gamma-aminobutyric acid (GABA). Its mechanism of action is unknown. The drug binds with high affinity to the alpha2-delta site (a calcium channel subunit). In vitro, it reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. Pregabalin has been approved by the US Food and Drug Administration (FDA) for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.

Gabapentin (Neurontin)

Gabapentin, a membrane stabilizer, is a structural analogue of the inhibitory neurotransmitter GABA, although, paradoxically, it is thought not to exert an effect on GABA receptors. It appears to exert its action via the alpha2delta1 and alpha2delta2 auxiliary subunits of voltage-gaited calcium channels. Gabapentin is used to manage pain and provide sedation in neuropathic pain.

Class Summary

Agents in this class may be used for the treatment of anemia but also has neuroprotective and possibly neurotrophic properties.

Epoetin alfa (Epogen, Procrit)

This is a recombinant erythropoietin that has been shown to accelerate functional recovery after peripheral nerve injury. The proposed mechanism of action is antiapoptotic and anti-inflammatory, promoting cell survival. Erythropoietin is given in 3 doses of 5000 U/kg over 1 week after nerve injury.