Foot drop: Etiology, diagnosis, and treatment

INTRODUCTION — Foot drop (sometimes referred to as "drop foot") refers to an inability to lift the forefoot due to weakness of the dorsiflexors. This condition may be the result of a muscular, skeletal, or nervous system problem. To develop a treatment plan for foot drop, a full evaluation and determination of the cause must be completed for each patient. Just as foot drop can have many causes, foot drop treatment can take many forms.

The etiology, clinical features, diagnosis, and treatment of foot drop will be reviewed here. A general review of peripheral nerve syndromes is provided separately. (See "Overview of lower extremity peripheral nerve syndromes".)

LOWER EXTREMITY ANATOMY — An understanding of the anatomy of the lower extremity is essential for understanding the potential causes of foot drop.

The lower extremity can be thought of as two separate units, the portion above the knee (ie, thigh) and the portion below the knee (ie, leg). Each unit contains a series of compartments that define the relationship between muscles, nerves, and blood vessels.

Muscle compartments

●Thigh – The thigh contains three compartments, the anterior, medial, and posterior compartments, named after their relationship to the femur (figure 1) [1].

●Leg – The leg contains four compartments, named in relation to the tibia and fibula (figure 2) [1].

•Anterior compartment – The anterior compartment contains the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius muscles. These muscles dorsiflex and invert/evert the ankle and extend the toes. The arterial supply is the anterior tibial artery, and the motor nerve is the deep peroneal nerve [1,2].

•Lateral compartment – The lateral compartment contains the peroneus longus and peroneus brevis muscles that evert the foot at the ankle and weakly plantarflex the foot. The peroneal artery and superficial peroneal nerve supply these muscles [1,2].

•Superficial posterior/deep posterior compartments – The posterior compartments contains the muscles that plantarflex and invert the foot at the ankle and flex the toes. The posterior tibial and peroneal arteries supply both compartments. The tibial nerve innervates the superficial and deep posterior compartments [1,2].

-The superficial posterior compartment contains the gastrocnemius, the soleus, and the plantaris (may be absent in 10 to 15 percent of individuals).

-The deep posterior compartment contains the tibialis posterior, flexor hallucis longus, flexor digitorum longus, and popliteus muscles.

Lower extremity innervation

●Lumbar plexus – The lumbar plexus is composed of the anterior rami of spinal nerves L1-L4 (figure 3) as well as contributions from T12. The most superior branches are the iliohypogastric and ilioinguinal nerves, innervating the transversus abdominis and internal oblique muscles and continuing as sensory nerves to the skin of the gluteal region, hypogastrium, and the anterior scrotum or labia. Next is the genitofemoral nerve, innervating the cremaster muscle and continuing to the femoral and genital rami, providing sensation to the skin of the anteromedial thigh and scrotum or mons pubis. The lateral femoral cutaneous nerve provides sensation to the lateral thigh. The obturator nerve provides motor innervation to the muscles of the medial thigh and sensation to the medial thigh. The femoral nerve innervates muscles of the anterior thigh and provides sensation to the anterior thigh. A portion of the femoral nerve continues inferiorly as the saphenous nerve, supplying sensation to the medial aspect of the leg [1,2].

●Sacral plexus – The sacral plexus is composed of the anterior rami of spinal nerves L4-S4 (figure 3) forming the lumbosacral trunk.

The first branch is the superior gluteal nerve, which innervates the gluteus minimus, gluteus medius, and tensor fascia latae. The superior gluteal nerve exits the pelvis above the piriformis muscle, while the inferior gluteal nerve exits below the piriformis muscle, innervating the gluteus maximus [1,2].

The sciatic nerve is a major motor and sensory nerve passing through the gluteal region. The tibial portion of the nerve innervates the muscles in the posterior compartment of the thigh and leg, as well as the sole of the foot. It also provides sensation primarily to the sole of the foot. The nerves innervating the sole of the foot are known as the medial and lateral plantar nerves (figure 4). The common fibular or peroneal division of the sciatic nerve innervates the short head of the biceps femoris, the anterior and lateral compartments of the leg, and the extensor digitorum brevis. This branch also provides sensation to the anterolateral surface of the leg and dorsal aspect of the foot. The nerve innervating the lateral aspect of the leg is known as the sural nerve (figure 5). The first webspace is innervated by the deep peroneal nerve, and the rest of the dorsal foot is innervated by the superficial peroneal nerve (figure 6) [1,2].

The posterior femoral cutaneous nerve is the next major branch of the lumbosacral trunk, passing inferiorly to the piriformis muscle and providing only sensory innervation to the posterior surface of the thigh, leg, and perineum. These sensory branches are called the perineal branches and inferior cluneal nerves.

The last major branch is the pudendal nerve, providing both motor and sensory innervation. The pudendal nerve innervates the muscles of the perineum and provides sensation to the penis, clitoris, and most of the perineum. Additional branches from the sacral plexus innervate the piriformis, obturator internus, and quadratus femoris muscles [1,2].

ETIOLOGIES

Compressive disorders — Compressive etiologies are the most common cause of peroneal nerve palsies. These occur anywhere along the course of the nerve. Compression of the common peroneal nerve at the level of the fibular head is the most common site of entrapment (figure 6). This is due to the presence of a bony prominence at the fibular head, as well as superficial positioning of the nerve at this level with frequent tethering of the nerve by the peroneus longus tendon in the fibular tunnel [3,4]. However, peripheral compression can also occur at the hip or ankle.

Anatomic variation of the biceps femoris muscle can contribute to the formation of a muscular tunnel between the gastrocnemius muscle and the distal bicep femoris, leading to common peroneal nerve entrapment [5]. The common peroneal nerve may also become trapped in patients with a high division of the sciatic nerve where the peroneal component pierces the piriformis muscle, especially in cases of piriformis scarring or hypertrophy [6]. A less common cause of entrapment may occur from an accessory sesamoid bone called a fabella, which may cause compression at the lateral gastrocnemius attachment, leading to pain in the lateral popliteal fossa [7,8]. In addition, intraneural or extraneural lesions or pathologies may act as a source of compression [9]. Compressive disorders are exacerbated and found more commonly in patients who have a history of significant weight loss, or in those who habitually cross their legs or who perform squatting exercises [10].

In addition to compressive disorders of the periphery, foot drop can occur in patients with lumbar degenerative disease, lumbar disc herniation, and lumbar spinal stenosis with compression of the L4-5 segment. In one review, it was noted that while L5 was the most commonly affected nerve root, L4-S1 involvement, which also contributes nerve fibers to the common peroneal nerve, can also lead to foot drop [11].

Trauma — Traumatic injuries are the second most common cause of peroneal nerve palsy. These often occur in association with orthopedic injuries such as knee dislocations, severe ankle inversions, fractures, blunt trauma, as well as musculoskeletal injuries with nerve traction or direct nerve laceration. Due to its anatomic course, the peroneal nerve is more susceptible to injuries at the level of the knee; however, issues may arise at the hip involving the sciatic nerve or at the ankle [9].

The incidence of peroneal nerve injury in cases of tibial plateau fractures is approximately 1 percent [12]. Acute ligamentous injuries to the knee, especially those involving the anterior cruciate ligament, can also lead to peroneal nerve palsy [13]. Cases have also been noted in the setting of knee dislocation wherein the nerve is placed on significant stretch [14].

Ankle and hip injuries can also lead to nerve dysfunction. In severe ankle sprains, the inversion of a plantar flexed ankle puts significant stretch on the superficial peroneal nerve, leading to injury [15-18]. In the hip, injury to the lateral fibers of the sciatic nerve occurs during acetabular fractures, femur fractures, and posterior hip dislocations, all of which can result in foot drop [19].

Compartment syndrome — Compartment syndromes affecting the leg, either due to trauma or related to ischemia-reperfusion injury, can lead to peroneal nerve ischemia with subsequent foot drop. (See "Clinical features and diagnosis of acute lower extremity ischemia" and "Pathophysiology, classification, and causes of acute extremity compartment syndrome", section on 'Irreversible ischemic endpoints'.)

Iatrogenic — Foot drop secondary to iatrogenic causes is seen most frequently due to surgical procedures or protracted positioning in anesthesia, although other causes such as prolonged bed rest, splinting, and even pneumatic compression devices have been implicated as a cause [20-23]. Surgical procedures that may cause iatrogenic foot drop include those that place a patient in lithotomy position, and others involving orthopedic injuries to the hip, knee, or ankle. (See "Patient positioning for surgery and anesthesia in adults", section on 'Nerve injury'.)

Neurologic disorders — Primary and secondary neurologic disorders are other causes of foot drop.

Charcot-Marie-Tooth, a primary peripheral nerve disorder occurring in 1 in 2500 people, is the most commonly inherited peripheral nerve disorder. It affects both sensory and motor nerves. Presentation usually occurs during childhood or early adulthood, although it may present later in life. One of the initial symptoms is foot drop; however, other symptoms and progression of the disease vary [24]. Other less frequent neurologic disorders, such as amyotrophic lateral sclerosis or multiple sclerosis, may present with foot drop as a presenting symptom or as part of a constellation of initial symptoms. (See "Charcot-Marie-Tooth disease: Genetics, clinical features, and diagnosis" and "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease", section on 'Clinical symptoms and signs' and "Clinical presentation, course, and prognosis of multiple sclerosis in adults".)

Patients with long-standing diabetes who suffer from peripheral neuropathy are also at a risk for distal motor neuropathy. In these patients, deterioration of the function of the peroneal nerve can lead to dysfunction of the foot and ankle muscles that it supplies, leading to foot drop. (See "Epidemiology and classification of diabetic neuropathy", section on 'Peripheral mononeuropathy'.)

CLINICAL FEATURES — Foot drop, which refers to an inability to lift the forefoot due to weakness of the dorsiflexion muscles in the foot, may be partial or complete, developing acutely or over a period of days to weeks. The presence of foot drop is associated with a number of etiologies. (See 'Etiologies' above.)

A detailed clinical evaluation is necessary to ensure an accurate diagnosis and proper treatment planning. Clinical evaluation begins with a complete review of the medical history and patient-reported symptoms.

Patients may complain of dragging their toes, problems walking or climbing stairs, or frequent falls [4,25]. Depending on the underlying cause of foot drop, other symptoms may also be present.

When foot drop occurs due to peripheral nerve entrapment, the symptoms will differ depending on the affected nerve and site of entrapment. Foot drop caused by entrapment of the peroneal nerve may also result in decreased sensation, tingling, numbness, or burning from the lower lateral leg to the top of the foot [25]. Numbness may be present along the lateral leg, dorsal foot, and/or first toe webspace. Pain may be present but is not a common complaint in patients with foot drop due to peroneal nerve entrapment [4]. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Fibular (peroneal) nerve'.)

Patients with L5 radiculopathy or compression of the sciatic nerve may present with deficits similar to those with peroneal neuropathy, including foot drop, as well as lateral lower limb pain, and dorsal foot pain. However, the presence of concurrent low back pain or posterolateral thigh pain suggests the presence of lumbar radiculopathy [9]. Patients with foot drop caused by sciatic neuropathy may also complain of weakness in knee flexion and hamstring weakness [26]. Lumbosacral plexopathy may result in foot drop as well as weakness of knee flexion, internal hip rotation, and hip abduction [9]. (See "Overview of lower extremity peripheral nerve syndromes", section on 'Lumbosacral plexopathy'.)

Patients who experience foot drop resulting from muscle or nerve disorders often present with a number of additional symptoms specific to their condition. (See 'Neurologic disorders' above.)

Physical examination — The physical examination includes a full sensorimotor and vascular evaluation of the lower extremity, evaluating for signs of trauma, previous surgery, vascular insufficiency, ulcers, and edema [4,9]. Familiarity with the sensory and motor innervation of the nerves in the leg is essential to accurately interpret physical examination findings. (See 'Lower extremity anatomy' above.)

Patients should be instructed to remove any braces and walk toward and away from the examiner, allowing the clinician to observe any obvious deficits while walking. A strength and sensory examination should be completed, comparing the affected extremity to the unaffected side. Muscle strength testing should include testing specific muscle functions as described in the table (table 1) [27].

Weakness of the ankle dorsiflexors, toe extensors, and ankle evertors are all present in the diagnosis of "foot drop." A sensory examination of the leg and foot may reveal areas of decreased or abnormal sensation. Testing for Tinel's sign should be conducted during the physical examination to locate areas of nerve irritation or entrapment. Specifically, Tinel's sign should also be tested over the peroneal nerve at the fibular head (figure 6).

DIAGNOSIS — A diagnosis of foot drop is generally clinically apparent from the history and physical examination. Extremity imaging is useful for ruling out fracture or other anatomic abnormalities, to help identify a likely etiology. Most patients will undergo electromyography (EMG), unless there has been an obvious traumatic nerve transection.

Imaging — Extremity imaging (eg, plain radiography or computed tomography [CT]) is useful to evaluate for fractures, masses, arthritis, or tumor if the medical history suggests one of these etiologies. Magnetic resonance (MR) imaging of the lumbar spine, knee, or ankle may be considered to evaluate for potential soft tissue lesions that may be compressing a nerve. Later-generation MR technology may even allow characterization of the nerve (eg, increased nerve dimension, deformation of the nerve, or loss of nerve integrity) [9,26].

Electrodiagnostic studies — EMG and nerve conduction studies (NCS) can also be helpful in localizing the lesion. Motor nerve conduction studies of the peroneal nerve and tibial nerve and sensory nerve conduction studies of the sural and superficial peroneal nerves are recommended. (See "Overview of electromyography" and "Overview of nerve conduction studies".)

EMG typically examines at least two muscles innervated by the deep peroneal nerve (eg, tibialis anterior, extensor hallucis longus) and at least one muscle innervated by the superficial peroneal nerve (eg, peroneus longus, peroneus brevis).

EMG studies may also be performed on the tibialis posterior, another muscle innervated by the tibial nerve (eg, medial head of gastrocnemius) and the short head of the biceps femoris to identify more proximal lesions. If these findings are abnormal, further testing should be conducted on the more proximal muscles innervated by the sciatic nerve, gluteal muscles, and lumbosacral muscles to identify the level of lesion [4,9].

By indicating the site and severity of nerve injury, electrodiagnostic test results can help to determine the best course of treatment. Depending on the exact origin and nature of the problem, different surgical treatment options may offered. This is especially true in compressive disorders as different areas will be targeted for decompression based on EMG findings.

TREATMENT

Approach to the patient — A number of surgical and nonsurgical treatment options are available for the management of foot drop. The approach to the patient depends upon the etiology of foot drop and the localization of the lesions. Treatment plans are individualized based upon the evaluation and diagnostic findings.

●For nerve transection (traumatic, iatrogenic), surgical nerve reconstruction should ideally occur within 72 hours of the injury. Stimulation of the distal nerve end helps with identification. However, after 72 hours, the distal synapse experiences irreversible degradation of neurotransmitters, making this impossible. Nerve reconstruction may be performed using primary nerve repair techniques, an autologous nerve graft, or nerve conduits, depending on the severity of nerve injury. (See 'Nerve repair' below.)

●For other etiologies, treatment is often initially conservative due to the fact that partial or complete resolution of symptoms may occur spontaneously over time. Patients who do not respond adequately to conservative care or who experience deterioration may be candidates for surgical intervention, which usually occurs three to six months after the onset of symptoms. (See 'Conservative care' below.)

●For patients with a confirmed nerve compression, nerve decompression and neurolysis should be performed. Nerve transfers, tendon transfers, and combined procedures play an important role in cases of significant nerve dysfunction such as in patients unresponsive to decompression, or those with irreversible damage. Patients with an equinus contracture should undergo treatment for this at the same time as their foot drop surgery. (See 'Nerve or tendon transfer' below.)

●For patients who are not a candidate for, or who do not improve with the above-mentioned procedures, ankle fusion may relieve pain and improve function. (See 'Ankle fusion' below.)

Conservative care — The goal of conservative management is to stabilize the gait and prevent "foot slap," as well as to prevent contracture of the denervated muscles [3]. Conservative care includes physical therapy and/or splinting, and pharmacologic therapy to manage neuropathic pain, as needed. Patients are followed for signs of possible improvement with interval electromyography (EMG).

Surgical intervention may be indicated if there are no signs of improvement or further deterioration is observed. Surgical treatment should be offered within three to six months after the onset of symptoms.

Physical therapy — Physical therapy focuses on stretching and strengthening both the muscles affected by the palsy, as well as the opposing musculature. The initial focus of therapy is to stretch the contralateral muscle groups with the addition of electrical stimulation of the weakened dorsiflexors and evertors. Once autonomous muscle contractions are present, there is a transition to strengthening the muscles.

Splinting — Splints and braces are used in conjunction with physical therapy to optimize treatment outcomes. Different types of footwear and splints are used, depending on the location of the nerve injury and the extent of physical manifestation of peroneal nerve dysfunction.

In cases of isolated superficial peroneal nerve palsy with weakness of the evertors, only a lateral wedge shoe inset is necessary to prevent supination. However, if there is an inability to dorsiflex the ankle, an ankle foot orthosis (AFO) will be needed [9]. Bracing may be incorporated into a patient's treatment plan to prevent contractures from developing.

Pain management — Pain management may include topical analgesics, as well as selective serotonin reuptake inhibitors, antiepileptics, opioids, or µ-receptor agonists [9]. These modalities may provide symptom relief but do not address the underlying cause of pain. (See "Evaluation of chronic non-cancer pain in adults" and "Approach to the management of chronic non-cancer pain in adults".)

Surgical management

Nerve repair — A lacerated nerve may undergo direct primary repair if there is a minimal gap between the ends of the nerve [28]. If primary repair is not possible due to a significant gap, using an autologous nerve graft (most commonly using the sural nerve) is recognized as the standard of care [4]. If the nerve gap is less than 3 cm, a nerve conduit, which is an alternative to autologous nerve grafting, can be used with similar results [29].

Neurolysis — Cases of foot drop caused by compressive disorders should undergo decompression surgery based on the cause and location of the nerve palsy. Nerve decompression and neurolysis should be offered to relieve compression at the fibular head, fibular tunnel, or any other anatomic areas that are a source of pressure. Favorable outcomes have been reported following surgical intervention, with return to function observed in 97 percent of cases [30].

Compressive masses that are extraneural are resected to reduce pressure on the nerve [31]. Intraneural lesions are dissected out using microsurgical techniques with intraoperative nerve monitoring to prevent any harm to adjacent healthy nerve structures [32,33]. Any lesion suspicious of malignancy should be confirmed with biopsy or frozen section.

Nerve or tendon transfer — Nerve transfers and tendon transfers play an important role in improving dorsiflexion in cases of foot drop where there is significant nerve dysfunction, such as when nerve decompression or direct nerve reconstruction with primary repair or grafting has failed or would result in poor outcomes. Nerve transfer can restore ankle dorsiflexion with minimal morbidity. Patients with limited improvement after nerve transfer still have the opportunity to undergo tendon transfer. Some surgeons may also choose to perform a combined nerve transfer/tendon transfer procedure [34].

With nerve transfer, a functional but less important nerve is transferred to a distal but more important denervated nerve [35]. For the treatment for foot drop, functional fascicles of either the superficial peroneal or tibial nerve (eg, donor nerve fascicles innervating the soleus muscle, flexor digitorum longus, flexor hallucis longus) are used as the donor to reinnervate the deep peroneal nerve (figure 7) [34,36,37]. In a small study, 14 patients underwent these nerve transfers with 11 of the patients experiencing return of ankle dorsiflexion function with greater than three motor grades of recovery [38].

Tendon transfers may also be used to restore function in refractory cases. This procedure involves transferring one of the flexor or invertor muscles to the dorsum of the foot for dorsiflexion function [3]. The most common procedure involves transferring the posterior tibial tendon (figure 8). The tendon is passed through the interosseous membrane and is then anchored to the dorsal foot or to the anterior tibialis tendon. The first of these is favored as the tendon-to-tendon repair may decrease dorsiflexion strength resulting in an unbalanced foot [39,40]. A double tendon transfer can restore balance and may eliminate the need for supporting orthoses. The second transfer strengthens ankle dorsiflexion and reanimates toe extension.

A double tendon transfer can be performed by transferring the posterior tibialis tendon to the anterior tibialis tendon and the flexor digitorum longus to the extensor digitorum longus and extensor hallucis longus tendons. A small case series reported "good" to "excellent" results in greater than 80 percent of patients who underwent a double tendon transfer (as described above) [41].

Following nerve and tendon transfers, patients are placed in an ankle foot orthosis (AFO) with heel touch. Patients begin early motion protocol a few days postoperatively.

Ankle fusion — Ankle fusion, also known as arthrodesis, is reserved for patients who are not candidates for any of the above-mentioned treatments, or who have failed treatment. With this procedure, the ankle is fused in the 90 degree position relative to the tibia either through a tibiotalar fusion or a pantalar fusion. This procedure is considered the last resort in foot drop treatment as all motion is removed from the ankle joint.

While arthrodesis may provide patients with pain relief and improved function, there is also a risk of complications, including malunion, hardware-related issues, and arthritic changes in the adjacent bones [3].

OUTCOMES — Left untreated, foot drop leads to reduced mobility and overall functioning, which in association with chronic pain can severely impact a patient's quality of life.

When foot drop is confirmed to be due to compression of the common peroneal nerve, decompression surgery is very effective for improving motor strength, decreasing pain, and improving sensory impairment, with low associated morbidity [42]. Although direct nerve repair is not always a feasible surgical treatment option for common peroneal nerve injuries, it can provide properly selected patients with significant functional improvements postoperatively. Direct repair of common peroneal nerve injuries achieves grade 3 or better functional outcomes in 84 percent of patients (grade 3: peronei muscles and anterior tibial muscles contract against gravity and some resistance; grade 4: peronei muscles and anterior tibial muscles contract against moderate resistance; grade 5: peronei muscles and anterior tibial muscles contract against great resistance) [30].

A study that evaluated the long-term results of patients who underwent tendon transfers for foot drop correction found near-normal load distribution on gait analysis with almost all patients being able to walk without visible limping or the need for orthotic devices [43]. Patient satisfaction was high, and most patients reported a significant increase in quality of life, with greatest improvements noted in symptom-related quality of life, recreational activity, walking, private life, and fitness for work.

Nerve transfers also provide appropriately selected patients with significant improvements in range of motion and restored walking ability. In a review of patients who underwent nerve transfers of either the superficial peroneal nerve or the tibial nerve fascicles, significant clinical improvements in ankle dorsiflexion, eversion, and toe extension were identified in 80 percent of their patients [36]. The remaining 20 percent of patients experienced good improvement in ankle eversion, but poor or no ankle dorsiflexion.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Neuropathy".)

SUMMARY AND RECOMMENDATIONS

●Foot drop – Foot drop refers to an inability to lift the front part of the foot due to weakness of the dorsiflexion muscles in the foot. This may be the result of a muscular, skeletal, or nervous system problem. An understanding of the anatomy and innervation of the leg is essential for understanding the potential causes of foot drop. (See 'Introduction' above and 'Lower extremity anatomy' above and 'Etiologies' above.)

●Clinical features and diagnosis – Patients complain of dragging their toes, problems walking or climbing stairs, or frequent falls, and depending on the underlying cause of foot drop, other symptoms may also be present. To identify the underlying etiology, the evaluation should include a review of medical history and physical examination, as well as lower extremity imaging and electrodiagnostic studies, when appropriate. (See 'Clinical features' above and 'Diagnosis' above.)

●Treatment

•Conservative care – The initial treatment approach for many cases of foot drop is conservative and includes physical therapy, splinting, and pain management. (See 'Conservative care' above.)

•Timing of surgery – Timing varies for surgical treatment depending on the etiology of foot drop. (See 'Approach to the patient' above.)

-For nerve transection (traumatic, iatrogenic), surgical nerve reconstruction should ideally occur within 72 hours of the injury.

-For other etiologies, surgical intervention may be indicated if there are no signs of improvement, or if further deterioration is observed. When indicated, surgical intervention should be offered within three to six months after the onset of symptoms.

•Nerve reconstruction – Nerve reconstruction may be performed using primary nerve repair techniques, an autologous nerve graft, or nerve conduits, depending upon the severity of nerve injury. Nerve decompression and neurolysis should be performed for patients with a confirmed nerve compression. Nerve transfers, tendon transfers, and combined procedures play an important role in cases of significant nerve dysfunction. Patients who are not a candidate for or who do not improve from the above-mentioned procedures may experience pain relief and improved function following ankle fusion. (See 'Surgical management' above.)