Foot Drop Treatment & Management

Foot drop is very distressing, and attention to the patient's psychological needs is very important. If painful paresthesias develop, they can sometimes be effectively managed with sympathetic blocks or laparoscopic synovectomy. Alternative treatments are amitriptyline, nortriptyline, 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. Optimizing glucose control in diabetic patients and managing vitamin deficiencies with supplements of B-1, B-6, or B-12 can also be useful.

Erythropoietin is a naturally occurring hormone that is approved by the Food and Drug Administration for the treatment of anemia but also has neuroprotective and possibly neurotrophic properties. The proposed mechanism of action is anti-apoptotic and anti-inflammatory, promoting cell survival. Erythropoietin is given in 3 doses of 5000 U/kg over a week following nerve injury. It has a minimal side-effect profile. An animal study showed that erythropoietin treatment accelerated functional recovery after peripheral nerve injury.^[9]

Treatment of foot drop is directed to its etiology. If foot drop is not amenable to surgery, an ankle-foot orthosis (AFO) often is used. An AFO also is used during surgical or neurologic recovery. The specific purpose of an AFO is to provide toe dorsiflexion during the swing phase, medial and/or lateral stability at the ankle during stance, and, if necessary, push-off stimulation during the late stance phase. An AFO is helpful only if the foot can achieve plantigrade position when standing. Any equinus contracture prohibits 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 is used when ankle instability or spasticity is problematic, such as in patients with upper motor neuron diseases or stroke. If the AFO fits posterior to the malleoli (posterior leaf spring type), plantar flexion at heel strike is allowed, and push-off 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.

In patients in whom foot drop is due to hemiplegia, peroneal nerve stimulation can be considered. This type of stimulation was first applied in 1961. Nerve stimulation has advantages to the AFO, as it provides active gait correction and can be tailored to individual patients. In this system, a short burst of electrical stimulation is applied to the common peroneal nerve between the popliteal fossa and fibular head. A switch in the heel of the affected limb controls this burst. The stimulator is activated when the foot is lifted, and it is then 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 ankle-foot orthosis (AFO) in 15 patients with foot drop caused by stroke or traumatic brain injury. The authors found that compared with AFO, the studied neuroprosthesis enhanced balance control during walking and, thus, more effectively managed foot drop.^[10]

The nerve stimulator can be either external or implanted and radiofrequency activated. The use of electrical stimulation in stroke patients with spastic hemiplegia was reported to be useful in approximately 2% of the cases. This method may enhance the gait speed and quality, and it can contribute to motor relearning.^[11]

Foot drop due to direct trauma to the dorsiflexors generally requires 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 foot drop is secondary to lumbar disc herniation (a finding in 1.2-4% of patients with this condition), consider discectomy. 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 is the peripheral nerve 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.^[12] 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.^[13]

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.^[14]

A review of surgical management of peroneal nerve lesions demonstrated that neural repair is the first priority in selected patients with peroneal nerve palsy.^[15] This may be accomplished with nerve decompression (either central or peripheral) or nerve grafting or repair. For foot drop from deep peroneal nerve injuries of less than 1-year duration, one study has reported success with transfer of functional fascicles to deep peroneal-innervated muscle groups, using either the superficial peroneal or tibial nerve as a donor.^[16] Failing sufficient recovery with those measures, tendon transfer procedures 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, Achilles tendon lengthening may be necessary to achieve adequate dorsiflexion.

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

Nerve exploration, decompression, or repair

Decisions regarding appropriate timing of nerve exploration and repair take into consideration the mechanism of insult. Sharp laceration where nerve transection is suspected warrants early repair. Blunt lacerations are repaired 2-4 weeks after injury. Lesions in continuity usually are monitored for several months by clinical examination and 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 by end-to-end sutures or nerve grafts.

Treat patients who are status post knee arthroplasty or tibial osteotomy with peroneal nerve palsy initially by removing all constrictive dressings and repositioning the knee to 20 or 30 º of flexion. If an expanding hematoma is noted, urgent exploration is warranted. If functional recovery does not occur within 2 months, nerve exploration and/or release has been advocated. The time interval between symptom onset and decompression appears to affect final functional outcome. However, severity of the preoperative palsy does not seem to affect recovery.

Tendon transfer

If a patient is to undergo tendon transfer surgery, 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 of patients with persistent traumatic peroneal nerve palsy. The lesion of the common peroneal nerve must be at, or distal to, its branching from the tibial nerve. This guarantees 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 following 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 º of dorsiflexion. The muscles innervated by the tibial nerve must be normal. Finally, soft tissue coverage must be adequate.

Nerve exploration, decompression, or repair

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 also is 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. The incision extends to the skin posterior to the head of the fibula and then toward the anterior compartment of the leg. Superficial and deep peroneal nerve branches are exposed distal to the head of the fibula. 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 to perform intraoperative stimulation and recording studies. Having clear exposure of the lesion, as well as viable nerve proximally and distally, is essential. Surgical exploration with nerve action potential (NAP) monitoring of lesions in continuity can document enough peroneal recovery to avoid unnecessary resection and repair.

Tendon transfer

A common method of tendon transfer moves the posterior tibial tendon, with or without complementary Achilles tendon lengthening. This procedure is accomplished via an open Z-lengthening of the Achilles to allow for a minimum of 15° of passive dorsiflexion. Route of transfer of the posterior tibial tendon may be through the intraosseous membrane or circumtibial. Ober described the circumtibial method in 1933. 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.^[17] Other series have demonstrated either method to be acceptable, but a recent study also argued that the interosseus route is preferred in this patient population.^[18]

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 posterior tibial tendon may be tendon-to-tendon or tendon-to-bone. In tendon-to-tendon fixation, the points of attachment are (1) the peroneus brevis or tertius or extensor digitorum longus tendons for the lateral slip and (2) the tibialis anterior or extensor hallucis longus for the medial slip. 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 procedure involving the tendon-to-bone attachment is the Bridle procedure, a modification of the Riordan technique described by Rodriguez (see images below).^[19] This procedure involves insertion of the posterior tibial tendon into the second cuneiform bone, combined with anastomosis of the posterior tibial tendon transfer to the anterior tibial tendon and a rerouted peroneus longus tendon in front of the lateral malleolus to balance the foot in dorsiflexion.

Five incisions are used in this technique, as seen in the first image above. The posterior tibial tendon insertion is secured through incision 1 on the medial foot. Incision 2 is used to retrieve the end of the tendon of the posterior tibial proximal to the tarsal canal into the posterior compartment of the leg, as seen in the first two images above. Incision 3, on the anterior leg proximal to the ankle, provides wide exposure of the interosseous membrane. The posterior tibial tendon is pulled through the interosseous membrane and a longitudinally split anterior tibial tendon into the anterior compartment between the tibia and anterior tibial tendon. The posterior tibial tendon is anastomosed to the anterior tibial tendon with the foot in full dorsiflexion, as seen in the last image above.

Incision 4, posterior to the lateral malleolus, accesses the peroneus longus and brevis tendons proximal to the lateral retinaculum (see first image below). The peroneus longus is transected about 2 inches 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. This is then transposed via a direct subcutaneous tunnel, which is anterior to the lateral malleolus. The proximal end of the transected peroneus longus is anastomosed to the peroneus brevis tendon (see second image below).

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

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

Another method of reconstruction involving the coaptation of the extensor hallucis longus to the tibialis anterior was investigated in 8 patients who had had polio. At final review, only 2 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 with simultaneous 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. This restores active voluntary dorsiflexion of the foot and automatic walking. This transfer avoids use of an antagonist muscle to the paralytic group of muscles, avoiding retraining to achieve dorsiflexion. This provides physiologic muscle balance and fully automatic walking.

Nerve exploration, decompression, or repair

Following a nerve exploration or graft procedure, weight bearing as tolerated is allowed with a 2-3 day period of immobilization of the knee in a Robert-Jones dressing. An AFO may be used while awaiting neural recovery.

Tendon transfer

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

As with any surgical procedure, wound infection may occur. Nerve graft failure also can occur. In tendon transfer procedures, recurrent deformity is reported. In arthrodeses or fusion procedures, there may be pseudoarthrosis, delayed union, or nonunion.

As treatment of foot drop varies according to the cause, so too do prognosis and outcomes. In a peripheral compressive neuropathy, recovery can be expected in up to 3 months, as long as further compression is avoided. A partial peroneal nerve palsy following total knee replacement has a uniformly good prognosis.^[20] A variable amount of recovery is seen with a complete postoperative palsy. Follow-up EMG and nerve conduction studies may be useful to assess recovery. A partial palsy recovers faster due to local sprouting. Complete axon loss reinnervates by proximal-to-distal axonal growth only, usually proceeding at 1 mm per day. Therefore, 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 of longer than 6 months duration, a negative straight leg raising test, and old age were considered poor prognostic factors for recovery of dorsiflexion.^[12]

When there is direct injury to the peroneal nerve, a more favorable outcome is noted with sharp versus blunt trauma. A traction or stretch injury to the nerve has an intermediate outcome. When nerve grafting is used, functional recovery depends upon the severity of injury and, therefore, the length of graft used. Good functional recovery in grafts longer than 12 cm is rarely seen.