Foot Drop

Etiology

Compressive Disorders

Entrapment syndromes involving the fibular nerve at various points along its anatomical course can lead to compressive neuropathy. The most common site is at the fibular head, making common fibular neuropathy the most frequent mononeuropathy of the leg.[1]

The fibular nerve becomes superficial near the fibular head, making it prone to pressure injury. The biceps femoris muscle, located between the gastrocnemius and distal biceps, may have anatomical variations that create a tunnel-like structure capable of compressing the nerve. Additional contributing factors include weight loss, prolonged immobility, tight casts, space-occupying lesions, and bone metastases involving the fibular head.

Sciatic nerve compression between the two heads of the piriformis muscle, resulting in foot drop, has been reported.

Compression palsies due to prolonged bed rest are a known complication in the ICU setting. Approximately 10% of patients who remain in the ICU for more than four weeks develop fibular nerve paresis. Critical illness polyneuropathy, which affects multiple motor and sensory nerves, may also present with foot drop.[2] Depending on the severity, the resulting weakness can be bilateral. Patients with diabetes are particularly susceptible to these compression-related neuropathies.

Lumbar radiculopathy is a common cause of foot drop, with L5 radiculopathy being the most prevalent. This typically results from lumbar disc herniation or spondylitis in the spine.[3]

Extraforaminal compression of the L5 nerve can occur due to disc herniations, as well as compression from bony structures (such as osteophytes or the sacral ala) or ligamentous structures (including the sacroiliac ligament and lumbosacral band).[4] Although uncommon, bone metastasis at the fibular head can also lead to foot drop.

Traumatic Injuries

Orthopedic injuries such as knee dislocations, fractures, blunt trauma, and musculoskeletal injuries can lead to foot drop. Sciatic neuropathy, most often caused by traumatic hip injury or complications from surgery, is the second most common mononeuropathy of the lower extremity and typically presents with foot drop.[5]

Less common causes include lumbosacral plexopathies, which may result from trauma, abdominal or pelvic surgery, or complications related to neoplasms or radiation therapy.

Neurological Disorders

Amyotrophic lateral sclerosis: Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease or Lou Gehrig disease, is a progressive neurodegenerative condition characterized by the degeneration of motor neurons in the anterior horn of the spinal cord. This leads to muscle weakness and difficulties with speech and swallowing. In some cases, the initial presentation may include a painless foot drop.

Cerebrovascular disease: Cerebrovascular accident (CVA) can present with hemiplegia, which may initially manifest as foot drop. Other signs of upper motor neuron involvement include increased muscle tone, hyperreflexia, and circumduction of the lower extremity during walking. Depending on the location of the ischemia, aphasia may also be present.

Mononeuritis multiplex: Mononeuritis multiplex affects one or more sensory and peripheral motor nerves. This condition typically presents with painful, asymmetric symptoms and is associated with conditions such as AIDS, leprosy, hepatitis, granulomatosis with polyangiitis (Wegener granulomatosis), and rheumatoid arthritis. Loss of sensation and movement may result from dysfunction in specific nerves, with the sciatic nerve being one of the most commonly affected. Vasculitis of the small epineurial arteries leads to axonal damage, disrupting nerve conduction and resulting in muscle weakness.

Acute inflammatory demyelinating polyneuropathy: Acute inflammatory demyelinating polyneuropathy (AIDP), also known as Guillain-Barré syndrome, is an autoimmune disorder characterized by progressive motor weakness, sensory loss, and areflexia. Sensory symptoms often precede motor weakness, and autonomic dysfunction is commonly associated with the condition. Myelin sheath damage leads to segmental demyelination, and a hallmark of AIDP is slowed nerve conduction velocities and conduction block. Foot drop may be part of the clinical presentation.

Charcot-Marie-Tooth disease: Charcot-Marie-Tooth (CMT) is a primary congenital demyelinating peripheral neuropathy and one of the most common inherited neuropathies, affecting approximately 1 in 25,000 individuals. This condition affects both motor and sensory nerves, causing foot drop and wasting of the lower leg muscles, resulting in a characteristic "stork leg" appearance.[6]

Somatization and conversion disorders: Somatic symptom disorder and conversion reaction are also possible etiologies of foot drop. In cases with an otherwise unremarkable workup, a psychiatric evaluation should be considered. Both the needle EMG and nerve conduction studies will typically appear normal in patients who exhibit poor or no effort during ankle dorsiflexion or other motor tests.

Compartment Syndrome

Compartment syndrome may result from ischemia-reperfusion injury or trauma to the leg. These events can lead to peroneal nerve ischemia, which may present clinically as foot drop.[7]

Iatrogenic Factors

Several iatrogenic factors can contribute to the development of foot drop, including:

• Surgical procedures, particularly when patients are placed in the lithotomy position
• Prolonged bed rest
• Protracted positioning in anesthesia
• Improper splinting
• Use of pneumatic compression devices [8]

Epidemiology

The reported incidence of fibular neuropathy is variable. A study reported a prevalence of 19 cases per 100,000 individuals, with a higher incidence in males than females. Following total knee replacement, the prevalence is reported at 0.79, with a slight male predominance of 2.8:1.[9] A total of 90% of presentations are unilateral, occurring equally on the right or left side with equal frequency.

The global annual incidence of ALS is estimated at 1.54 per 100,000 individuals.[10] Although ALS can affect people of any age, its peak onset occurs between 50 and 75 years. The true incidence of mononeuritis multiplex remains unknown both in the United States and worldwide. The reported annual incidence of AIDP ranges from 1.0 to 1.2 cases per 100,000 individuals, with a linear increase in incidence with age. Men are approximately 1.5 times more likely to be affected by this condition than women.[11]

Pathophysiology

Understanding the pathophysiology and estimating the prognosis of peripheral nerve injuries requires a standardized classification system. Seddon (1943) and Sunderland (1953) proposed the following categories of nerve injury—neurapraxia, axonotmesis, and neurotmesis.

In neurapraxia, the myelin sheath is damaged while the axons remain intact. The endoneurium, perineurium, and epineurium are also preserved. Nerve impulse conduction is disrupted at the site of injury, leading to clinical signs such as sensory loss and muscle weakness. Electromyography (EMG) typically shows prolonged latency and reduced nerve conduction velocity across the affected segment. Neurapraxia carries the best prognosis among nerve injuries.

In axonotmesis, the axon is damaged, but the epineurium and perineurium remain intact. Nerve stimulation leads to sensory and motor deficits below the site of injury. Recovery is possible over an extended period, although full recovery may not always be achieved.

Neurotmesis is the most severe type of nerve injury, involving damage to the myelin, axons, and supporting connective tissues. Wallerian degeneration occurs distal to the site of injury. Clinically, this presents as both sensory and motor deficits. Spontaneous recovery is not possible, and surgical intervention, such as nerve grafting or tendon transfer, may be required.[12] Please see StatPearls' companion resource, "Anatomy, Bony Pelvis and Lower Limb: Extensor Hallucis Longus Muscle," for more information.

Histopathology

The type of nerve injury—neurapraxia, axonotmesis, or neurotmesis—depends on the severity of compression, inflammation, or trauma.

• Neurapraxia involves temporary damage to the myelin sheath while preserving the integrity of the nerve itself, and recovery is typically complete.

• Axonotmesis involves the disruption of both the axon and its myelin sheath, while the connective tissue surrounding the nerve remains intact. Despite this, Wallerian degeneration occurs distal to the injury site. EMG performed 2 to 4 weeks later typically reveals denervation potentials, such as fibrillations and positive sharp waves, in the muscles affected by the injury. Axonotmesis usually results from a more severe crush or contusion, but can also occur when the nerve is stretched, as long as the epineurium remains undamaged. Nerves may attempt to regenerate distally, typically at a rate of 1.5 to 3 mm per day. This regeneration process can take anywhere from weeks to years.

• Neurotmesis is a severe nerve injury in which the nerve is completely severed, as seen in penetrating trauma. There is no intact myelin, and the axons are entirely disrupted. The endoneurium, along with other connective tissue components, is damaged or transected, although the perineurium may remain intact. Recovery is unlikely without surgical reanastomosis.

Toxicokinetics

Chemicals and other toxins can have adverse effects on skeletal muscle and the nervous system. The effects of these agents are not always symmetrical and are beyond the intended scope of this article. However, toxic effects, along with a thorough history of chemical exposure, should be considered and obtained when evaluating any patient presenting with weakness.

History and Physical

A detailed history and physical examination are essential for identifying the underlying cause of foot drop.

Musculoskeletal testing involves observing the patient performing functional movements such as toe standing, heel standing, and deep knee bending. Strength testing should be conducted using the Medical Research Council (MRC) scale (0 to 5) for major lower extremity muscle groups, including ankle plantarflexion, dorsiflexion, inversion, eversion, as well as knee extension, knee flexion, and hip flexion. Additionally, a neurosensory examination should be performed using pinprick testing to assess sensory function in the distribution of peripheral nerves and lumbar dermatomes. 

Muscle mass assessment can be performed by comparing side-to-side differences in the bulk of major muscle groups through manual motor testing. Circumference measurements of affected muscle groups can be documented to monitor changes over time and track progression or recovery. The ASIA (American Spinal Cord Injury Association) motor and sensory scoring system provides a standardized framework for interprofessional communication; however, it does not specifically evaluate individual peripheral sensory nerves.

A formal electrodiagnostic medicine consultation, including EMG and nerve conduction studies, is considered an extension of the physical examination and may need to be obtained from a subspecialist, who is not commonly the first clinician involved in the patient's care.

Any damage to the neuraxis, from the nerve roots to the peripheral nerve, can weaken the muscles innervated by that nerve.

A lesion involving the L5 nerve root, lumbar plexus, sciatic nerve, common peroneal nerve, or deep peroneal nerve can lead to foot drop due to weakness of the anterior compartment muscles. The primary symptom is reduced ambulation compared to the patient’s previous activity level. A more specific indicator is weakness in the dorsiflexor muscles of the foot, which may or may not be associated with pain. During gait, the patient is unable to dorsiflex the foot during heel strike, causing it to remain flat on the ground. Toe drag and difficulty clearing the foot may also be observed, increasing the risk of falls.

Radiculopathy involving the L5 nerve root typically presents with neuropathic pain originating in the lumbar region and radiating down the posterior thigh, anterolateral leg, and into the foot, including the big toe. Sensory symptoms often involve the medial aspect of the foot, particularly the first web space. Motor symptoms typically include weakness in the dorsiflexors and evertors of the foot.

Lumbosacral plexopathies can present with sensory and motor deficits resembling those seen in sciatic neuropathy. However, weakness may also involve the hip girdle muscles, affecting hip abduction through the gluteus medius and hip extension through the gluteus maximus.

Sciatic neuropathy typically presents with sensory loss involving the entire foot, along with weakness in the ankle plantar flexors (gastrocnemius and soleus) and ankle inversion. This can lead to a condition known as "flail foot." The hamstring muscles may also be affected, resulting in impaired knee flexion. Incomplete sciatic neuropathy often mimics common peroneal neuropathy, as the peroneal fascicles within the sciatic nerve are generally more vulnerable to injury than the tibial fascicles.

Patients with common fibular neuropathy typically present with both sensory and motor deficits. The history may reveal contributing factors such as habitual leg crossing, prolonged kneeling, immobility, or trauma. Sensory loss or paresthesias are often noted in the lateral leg below the knee and the anterolateral aspect of the foot. Motor involvement includes weakness in ankle dorsiflexion (tibialis anterior), toe extension (extensor hallucis longus), and ankle eversion (peroneus longus, brevis, and tertius).

If only the deep fibular portion is affected, minimal sensory deficits are typically observed, limited to the web space between the first and second toes. Isolated weakness of the toe and ankle extensors is present, while ankle eversion and inversion remain normal. Isolated superficial fibular neuropathy is rare and primarily presents with sensory deficits on the foot, excluding the first web space. In this case, only ankle eversion and inversion may be affected.

About 60% of the normal gait cycle consists of the stance phase, with the remaining 40% allocated to the swing phase. While one foot is in the swing phase, the other remains in the stance phase. The gait cycle begins with a heel strike and concludes with a heel strike on the same side. During the stance phase, the foot remains flat on the ground. At heel strike, the foot is in dorsiflexion, preparing for a gradual lowering throughout the stance phase. In the absence of functioning dorsiflexors, the foot stays in plantar flexion during the stance phase, preventing it from clearing the ground and preparing for the next phase of the gait cycle. As a result, patients may drag their toes or lift their foot higher to clear the ground. Specific muscles, as outlined in Table 1, should be examined for weakness that could contribute to foot drop.[5]

Table 1. Assessment of Muscle Strength

Evaluation

After a thorough physical examination, diagnostic testing should include plain radiographs of the pelvis, tibia, and fibula to rule out fractures or dislocations.[5] Magnetic resonance imaging (MRI) may be indicated for suspected plexopathies due to masses or tumors. Additionally, MRI of the lumbar spine, knee, and ankle may be useful for detecting potential soft tissue masses in cases of compressive neuropathies. Advanced MRI techniques can also assess nerve characteristics, such as nerve deformation, increased nerve size, or loss of nerve integrity. Musculoskeletal ultrasound can also be used to evaluate swelling at or proximal to the site of compression.

Laboratory testing for rheumatoid factors and antinuclear antibodies can help assess the presence of collagen vascular diseases. Additionally, a complete blood count (CBC) with differential and a chemistry panel should be considered to rule out other potential etiologies.

An electrodiagnostic study can confirm the clinical diagnosis or offer an alternate localization and diagnosis. This also helps define the severity of the injury and provides valuable information regarding prognosis. This study consists of 2 parts—nerve conduction studies and needle EMG—as outlined below.

Nerve Conduction Studies

Nerve conduction studies assess the viability of myelin. Nerve compression is indicated by a delay in conduction latency. Findings such as delayed latency, slow velocity, and conduction block at the affected segment suggest nerve compression.

Needle Electromyography

During EMG procedures, monopolar needles are inserted into muscles innervated by the nerve under investigation. The motor unit potential is analyzed for amplitude, firing rates, and recruitment patterns. Denervation of a muscle is indicated by the presence of positive sharp waves and fibrillation potentials, which signal axonal damage. Typically, EMG examines at least one muscle innervated by the superficial peroneal nerve and at least 2 muscles innervated by the deep peroneal nerve.[13] Additionally, EMG may be conducted on muscles innervated by the tibial nerve.

Nerve conduction studies and EMG assist in identifying the location and severity of the lesion, as well as estimating the prognosis for recovery. The absence of denervation potentials, along with the presence of sufficient and viable motor units on needle EMG, suggests a favorable prognosis.[14]

Evidence of denervation potentials combined with a lack of viable motor units indicates a poor prognosis for recovery. Autoimmune and critical illness neuropathy or myopathy are often identified during the evaluation of foot drop. A comprehensive workup typically leads to a "clinical syndrome" rather than a definitive diagnosis.

Treatment / Management

Approaching the Patient

The approach to treating a patient with foot drop depends on the underlying etiology and the characteristics of the compressive lesion. Treatment options are determined based on the evaluation and diagnostic findings.

Surgical Options

In cases of traumatic nerve transection, nerve reconstruction should be performed within 72 hours of the injury. Common surgical approaches include primary nerve repair and the use of autologous nerve grafts.

For cases involving complete nerve compression, neurolysis and nerve decompression are recommended. Functional recovery has been reported in approximately 97% of cases.[15] Depending on the severity of the nerve injury, reconstruction may involve the use of an autologous nerve graft, primary nerve repair techniques, or nerve conduits. Additionally, a surgical release may be required for patients with equinus deformity.

For patients with significant nerve dysfunction, nerve or tendon transfers may be necessary to restore function.[3] A detailed discussion of these surgical options is beyond the scope of this article. Treatment is usually conservative initially for other etiologies, as there is a possibility that symptoms may partially or completely resolve over time.

Conservative Management

The management includes physical therapy, splinting, and pharmacologic treatment to manage pain. The primary goals of conservative management include stabilizing gait and preventing falls and contractures. Physical therapy focuses on exercises that stretch and strengthen muscles to improve mobility and overall function. Electrical stimulation techniques of the weekend dorsiflexors have shown promising results. A structured home exercise program should be an essential component of therapy to maintain muscle strength, preserve range of motion, and prevent flexion contractures.

Splinting helps minimize contractures. An ankle-foot orthosis should be used to prevent excessive plantarflexion and aid in managing complete nerve palsies with inadequate recovery. Proper education and training on the correct use and maintenance of the brace are essential. For patients with numbness, instructions on skincare to prevent abrasions and ulcerations are a crucial part of management. These guidelines are typically coordinated with the orthotist responsible for fabricating the ankle-foot orthosis.

For pain management, topical analgesics, serotonin reuptake inhibitors, membrane stabilizers, and opioids may be used. However, these agents alone are unlikely to lead to clinical recovery. Follow-up electrodiagnostic studies should be conducted to reassess the condition and evaluate reinnervation, which should be incorporated into the treatment plan.

Surgical Management

Nerve repair: Direct primary repair may be performed if the gap between the nerve ends is small.[16] A nerve conduit is performed if the gap is less than 3 cm.[17] For larger gaps, an autologous nerve graft, typically involving the sural nerve, is the preferred option.[13](B3)

Neurolysis: Neurolysis and nerve decompression may be performed to relieve compression at the fibular tunnel, fibular head, or other anatomical areas where pressure is causing nerve impairment.[18](B3)

Nerve or tendon transfer: Nerve transfer can restore ankle dorsiflexion with minimal morbidity. If the nerve transfer procedure is unsuccessful, a tendon transfer, typically involving the posterior tibial tendon, may be considered.[19](B2)

Ankle fusion: This procedure is reserved for cases that are refractory to other treatments and have not responded to conservative management. The ankle is fused in a 90° position relative to the tibia, either through a pantalar fusion (involving the talocalcaneal, talonavicular, and tibiotalar joints) or a tibiotalar fusion.

Differential Diagnosis

The various differential diagnoses associated with foot drop are discussed below.

• Upper motor neuron involvement: A CVA can cause weakness in the entire extremity. Due to spasticity, the affected limb may appear artificially long. During ambulation, the individual may exhibit a semicircular leg movement known as "circumduction." Additional symptoms, such as dysphagia, aphasia, or upper limb weakness, may also be present.

• Cerebellar gait: The cerebellum is crucial for coordinating smooth and balanced musculoskeletal movements, including gait. Deficits in cerebellar function often result in ataxia and difficulty walking in a coordinated manner, such as an inability to walk in tandem.

• Ataxic gait: This condition typically presents bilaterally. Involvement of the long tracts of the spinal cord results in the loss of proprioception and vibratory sensation. As a consequence, patients exhibit a high-steppage gait with side-to-side swaying, resembling the gait seen in individuals with alcohol use disorder.

• Severe L5 lumbar radiculopathy.

• Parkinsonian gait: Pathophysiological changes involving the substantia nigra lead to a failure of smooth transitions during the gait cycle. This results in difficulty initiating movement, accompanied by short, rapid steps known as "festinate gait."

• Lumbar plexus dysfunction: As previously noted, various conditions, including compressive tumors or autoimmune disorders, that affect the lumbar plexus may present with foot drop.

• Diabetic amyotrophy.

• Psychological causes: Foot drop may result from psychological conditions such as conversion disorder, somatization, depression, or anxiety. Malingering should be considered if the diagnostic workup is unremarkable and there is a potential for significant secondary gain.

Surgical Oncology

A space-occupying lesion can affect the lumbosacral plexus, resulting in leg weakness. Thus, underlying malignancy should be considered in patients with unexplained weakness accompanied by other constitutional signs and symptoms. However, these patients are more commonly associated with genitofemoral neuropathy and weakness during knee extension.

Radiation Oncology

A history of radiation treatment should raise suspicion for radiation-induced plexopathy. Electrodiagnostic studies often reveal characteristic "myokymic discharges." In patients who have received radiation therapy to the affected region, clinicians should also consider the possibility of tumor recurrence.

Treatment Planning

A light exercise regimen that emphasizes early range of motion and strengthening should be initiated. Electrodiagnostic studies can help determine whether long-term bracing is necessary for the patient and predict the potential for worsening or spread of weakness to other motor groups. Early placement of an ankle dorsiflexor brace enhances gait mechanics, reduces the likelihood of falls, and helps minimize other secondary musculoskeletal issues caused by the altered gait cycle.

Toxicity and Adverse Effect Management

If a toxic etiology is identified, the offending agent should be discontinued. Medications contributing to toxicity that cannot be stopped abruptly should be tapered gradually under medical supervision.

Medical Oncology

Medical oncologic concerns can arise in patients with underlying malignancy or space-occupying lesions. Prior exposure to chemotherapeutic agents may also lead to peripheral neuropathy, which is typically symmetric and distal. Regardless of the cause, preexisting peripheral neuropathy can increase the risk of peripheral nerve compression.

Staging

Clinicians and patients should collaboratively discuss the potential need for long-term care, bracing, and adaptive equipment, if indicated. Rehabilitation services and other therapies should be directed toward the underlying etiology and the foot drop. Staging depends on the underlying diagnosis; for example, conditions such as multiple sclerosis or ALS require a different staging approach compared to traumatic lumbar spinal fractures.

Prognosis

The prognosis depends on both the severity of the injury and the underlying diagnosis. As noted earlier, neurapraxia generally has the most favorable outcome, with most patients achieving full recovery within approximately 3 months.

For patients with axonal loss, recovery may take up to 12 months. Neurotmesis carries a guarded prognosis and often requires surgical intervention, such as nerve repair or tendon transfer. Patients should be referred to a peripheral nerve surgeon if insufficient progress has been made 6 to 9 months after the injury. A denervated muscle is unlikely to recover significant function after 18 months.[15]

In other etiologies, such as ALS or space-occupying lesions, the prognosis will differ and depend on the underlying diagnosis and the patient's response to treatment, rather than solely on peripheral nerve involvement.

Complications

Complications can arise from nerve damage itself or improper use or overuse of gait aids and braces.

Nerve damage resulting in foot drop impairs the ability to clear the ground, increasing the risk of falls. Gait aids, such as walkers and canes, can be detrimental, especially on uneven surfaces. Anesthetic skin may become a site for chronic soft tissue injuries, such as ulcers. Poorly fitting braces can cause abrasions, and the bracing may need to be adjusted depending on changes in bulk. For conditions such as renal failure and congestive heart failure, different braces may be required to accommodate varying phases of edema and swelling.