Continuing Education Activity
Foot drop is a clinical entity that is not frequently seen in primary care settings. There are multiple etiologies of foot drop. Careful neurological examination, in conjunction with metabolic work-up, EMG/NCS, and imaging, usually lead to appropriate diagnosis and management. Adequate knowledge of anatomy and physiology is essential to arrive at the appropriate working diagnosis and management. This activity is intended to review the evaluation, pathophysiology, and management of foot drop, highlighting the role of the interprofessional team in evaluation, management, and potential treatment of patients presenting with a finding of foot drop.
- Identify the common causes of foot drop. A review of anatomy is provided.
- Review the evaluation of foot drop.
- Summarize the pathophysiology of foot drop.
- Outline interprofessional team strategies for care coordination and communication to maximize outcomes.
Foot drop is an inability to lift the forefoot due to the weakness of dorsiflexors of the foot. This, in turn, can lead to an unsafe antalgic gait, potentially resulting in falls.
The etiologies behind this presentation are varied and include muscular, neurologic, spinal, autoimmune, and musculoskeletal disorders. Depending on the etiology, treatment options differ.
A thorough understanding of the underlying pathophysiology is necessary before designing a treatment plan. This article will review the etiology, clinical features, diagnosis, and treatment.
Lumbar Nerve Roots
There are 5 lumbar vertebrae. The lumbar nerve roots emerge from the lateral spinal recess formed by the inferior facet of the rostral vertebrae and the superior facet of the caudal vertebra. The L5 nerve root exits between the L5 and S1 vertebrae.
The lumbar plexus is composed of the anterior rami of spinal nerves L1-L4. Multiple nerves emerge from this plexus. The iliohypogastric and ilioinguinal nerves supply the transverse abdominis and internal oblique muscles. The obturator nerve supplies the adductors of the thigh. The femoral nerve is a large nerve that supplies the quadriceps femoris group and continues as the saphenous nerve, which is the sensory nerve to the medial leg.
The sciatic nerve is the largest branch of the lumbosacral plexus and consists of nerve roots L4 to S4. It travels in the posterior thigh to the popliteal fossa. Here it divides into 2 branches: the tibial and the common fibular (historically peroneal) nerves. The tibial innervates hamstrings, plantar flexors, and invertors of the foot.
Common Fibular Nerve
The common fibular nerve is the lateral terminal branch of the sciatic that runs laterally across the lateral head of the gastrocnemius muscle. It then continues around the fibular head, where it is subcutaneous and so is vulnerable to compression. As it passes between the fibula and fibularis longus muscle, it divides into the deep and superficial fibular nerves. The deep fibular nerve innervates ankle and toe-extensors and supplies sensation to a small area at the first web space between the first and second toes. The superficial fibular nerve supplies the main evertors of the foot, the fibularis longus, and brevis muscles—the superficial fibular sensory branch supplies sensation to the dorsum of the foot and lateral calf.
Entrapment syndromes of the fibular nerve at various locations along its anatomical pathway can lead to compressive neuropathy. Of these, common fibular neuropathy at the fibular head is the most common mononeuropathy affecting the leg. The fibular nerve is quite superficial near the head of the fibula, making it vulnerable to pressure palsies. Anatomic variations of the biceps femoris muscle, between the gastrocnemius and distal biceps, can contribute to forming a tunnel that can predispose to compression of the nerve. Other contributing factors include weight loss, prolonged bedridden status, tight casts, space-occupying lesions, and bone metastasis involving the fibular head.
Sciatic nerve compression between the two heads of the piriformis muscle leading to foot drop has been reported.
Compression palsies in the ICUs due to protracted bed rest have been known to occur. Approximately 10% of patients that stay in the ICU for a period longer than four weeks are expected to develop paresis of the fibular nerve. Critical illness polyneuropathy involving multiple motor and sensory nerves can also present with foot drop. Depending on the extent of involvement, weakness can be bilateral. Patients with diabetes are more vulnerable to these compression neuropathies.
Lumbar radiculopathy is also a common cause of foot drop. L5 radiculopathy is the most common lumbar radiculopathy and typically results from lumbar disc herniation or spondylitis in the spine.
Extraforaminal compression of the L5 nerve from disc herniations and bony (osteophytes or sacral ala) or ligamentous (sacroiliac ligament and lumbosacral band) compression is known to occur. Bone metastasis at the fibular head, although uncommon, can cause foot drop.
Traumatic injuries often occur associated with orthopedic injuries as knee dislocations, fractures, blunt trauma, and musculoskeletal injuries. Sciatic neuropathy most commonly results from a traumatic injury of the hip or secondary to surgery. Sciatic neuropathy is the second most common mononeuropathy of the lower extremity and typically presents with foot drop.
A less common cause is lumbosacral plexopathies, resulting from traumatic injury, a complication of abdominal or pelvic surgery, or a complication of neoplasm or radiation therapy.
ALS (Amyotrophic lateral sclerosis), also known as motor neuron disease (MND) or Lou Gehrig disease is a neurodegenerative disease manifested by the death of motor neurons in the anterior horn cells leading to muscle weakness, difficulty speaking and swallowing. Initial presentation can be a painless foot drop.
Cerebrovascular disease (CVA) can present as hemiplegia. Foot drop is a part of this presentation. Other signs of upper motor neuron involvement, as increased muscle tone, hyperreflexia, and circumduction of the lower extremity during ambulation, are also seen. Depending on the location of ischemia, aphasia can be present.
Mononeuritis multiplex is defined as the involvement of one or more sensory and peripheral motor nerves. It is usually painful and asymmetrical. It can be associated with AIDS, leprosy, hepatitis, granulomatis with polyangiitis (Wegener granulomatosis), and rheumatoid arthritis. Loss of sensation and movement may be associated with dysfunction of specific nerves. The sciatic nerve is one of the commonly affected nerves in this condition. Vasculitis of small epineuria arteries leads to damage to the axons disrupting nerve conduction and eventually leading to muscle weakness.
Acute inflammatory demyelinating polyneuropathy (AIDP), also called Guillain-Barré syndrome, is an autoimmune process in which progressive motor weakness, sensory loss, and areflexia are characteristic presentations. Sensory symptoms often precede motor weakness. Autonomic dysfunction is a common accompaniment to this condition. Damage to the myelin sheath leads to segmental demyelination. A hallmark of AIDP is the slowing of nerve conduction velocities and conduction block. Foot drop can be part of the clinical presentation.
Charcot–Marie Tooth (CMT) is a primary congenital demyelinating peripheral neuropathy and is one of the most common inherited neuropathy. It affects both motor and sensory nerves. The incidence is 1 in 25000. One of the main symptoms is foot drop and wasting of the lower leg muscles, giving a typical “stork leg” appearance.
Somatization disorder and conversion reaction are not uncommon etiologies to foot drop. In the event of an otherwise unremarkable workup, psychiatric evaluation should be considered. It should be noted that both the needle EMG and nerve conduction portions of the electrodiagnostic medicine study will appear normal in cases of poor or no effort for ankle dorsiflexion or other motor groups.
The reported incidence of fibular neuropathy is variable. In a study, the prevalence was reported as 19 per 100000 people, more common in males than in females. After total knee replacement, it is reported as 0.79 with a slight male preponderance of 2.8 to 1, respectively. About 90% are unilateral. The right and left sides are equally affected.
ALS -The worldwide incidence of ALS yearly is estimated to be 1.54 per 100000. ALS can affect people at any age, but the peak incidence is 50 to 75 years.
The actual incidence of mononeuritis multiplex in the United States and the rest of the world is not known.
The reported annual incidence for AIDP was 1.0 to 1.2 per 100000 and increased linearly with age, and men are about 1.5 times more affected than women.
To understand the pathophysiology and estimate the future prognosis of peripheral nerve injury, an appreciation of nerve injury classification is necessary. In 1943 Seddon and 1953, Sunderland proposed the following classification: (1) neurapraxia, (2) axonotmesis, and (3) neurotmesis.
In neurapraxia, myelin is damaged, but the axons remain intact. The endoneurium, perineurium, and the epineurium are intact. The conduction of nerve impulses is altered at the site of injury. This is clinically translated as sensory loss and weakness. In EMG, this reflects a prolonged latency and slow nerve conduction velocity across the compressed segment. This type of injury recovers the best.
In axonotmesis, the axon is damaged, but the epineurium and perineurium remain intact. When stimulated, these nerves show sensory and motor deficits below the location of nerve injury. Recovery is possible over a long period but may not always be complete.
Neurotmesis is the most severe type of nerve injury. Myelin, axons, and supportive connective tissue are damaged. Wallerian degeneration occurs distal to the site of injury. This is clinically reflected as sensory and motor deficits. Spontaneous recovery is not possible. Surgical intervention, which may include nerve grafting or tendon transfer, is sometimes necessary.
Depending on the level of compression, inflammation, or trauma, neurapraxia, axonotmesis, or complete neurotmesis can occur.
Neurapraxia results in temporary damage to the myelin sheath but leaves the nerve intact. Recovery is usually complete.
Axonotmesis involves the interruption of the axon and myelin. But the connective tissue is preserved. Wallerian degeneration occurs. Electromyography (EMG) performed 2 to 4 weeks later shows denervation potentials called fibrillations and positive sharp waves in the involved muscles distal to the injury site.
Axonotmesis is usually the result of a more severe crush or contusion but can also occur when the nerve is stretched (without damage to the epineurium). Through regeneration, the nerves attempt regrowth distally as fast as 2 to 3 mm per day or as slowly as 1.5 mm per day. Regeneration occurs over weeks to years.
Neurotmesis is an injury in which the nerve is completely divided, such as in penetrating trauma. There is no intact myelin, and axons are completely disrupted. Endoneurium tubes and connective tissue components are damaged, disrupted, and/or transected, and the perineurium may be preserved. Recovery has no potential to occur without surgical re-anastomosis.
A wide variety of chemicals and other toxins can have an adverse effect on skeletal muscle, central, and peripheral nervous system directly. The specifics of these agents and their effects are likely not always symmetric, and beyond the intended scope of this article, however, toxic effects and a thorough history of chemical exposure should be considered and obtained in the workup of any patient with weakness.
History and Physical
A careful history and physical exam can help identify the likely cause of foot drop.
Standard musculoskeletal testing asking the patient to toe stand, heel stand, and do a deep knee bend should be observed. MRC scale rating 0-5 for the major muscle groups to the lower extremities, including ankle plantarflexion, ankle dorsiflexion, ankle inversion, ankle eversion, knee extension, knee flexion, and hip flexion, should be performed and graded. A neurosensory exam for pinprick should be performed in the distribution, looking for both peripheral nerves and lumbar dermatomes. Muscle mass with the side-to-side comparison observing the major muscle group bulk areas can be done well doing manual motor testing. Side-to-side circumference measurements can be made and documented to note progression or recovery of mass further down the road. The ASIA (American Spinal Cord Injury Association) point and motor groups are a standardization convenient for communication between professionals; however, it does not include evaluation of specific peripheral sensory nerves.
A formal electrodiagnostic medicine consult, including EMG and nerve conduction studies, is considered to be an extension of the physical examination and may need to be obtained from the subspecialist who is not commonly the first clinician to be involved in the care of the patient.
Any damage affecting the neuraxis from the roots to the peripheral nerve can weaken the muscles supplied by that nerve.
A lesion of the L5 root, lumbar plexus, sciatic nerve, common peroneal, or the deep peroneal nerve can potentially lead to foot drop due to the weakness of the anterior compartment musculature. The presenting symptom is the inability to ambulate as before. More specifically, weakness of the muscles in the foot that assist in dorsiflexion. There may or may not be a pain. The person will be unable to dorsiflex during the heel strike. The foot remains flat on the ground. Sometimes can also cause toe drag and inability to clear the foot. This can potentially lead to falls.
Radiculopathy affecting the fifth lumbar nerve root typically results in neuropathic pain starting in the lumbar region and radiating down the posterior thigh, anterolateral leg to the foot down to the big toe. Sensory symptoms include the medial aspect of the foot, including the first webspace. Motor symptoms include weakness of dorsiflexors and evertors of the foot.
Lumbosacral plexopathies can present with similar sensory and motor deficits that are similar to sciatic neuropathy. Weakness may also affect hip girdle muscles, including hip abduction (gluteus medius) and hip extension (gluteus maximus).
Sciatic neuropathy classically presents with sensory loss of the whole foot and weakness of ankle plantar flexors (gastrocnemius, soleus) and ankle inversion. It can result in a 'flail foot.' Hamstring muscles may also be involved resulting in knee flexion weakness. It is not uncommon for an incomplete sciatic neuropathy to present as a common peroneal neuropathy. Often, the peroneal fascicles in the sciatic nerve are more susceptible to injury than the tibial fascicles.
In common fibular neuropathy, the patient presents with sensory and motor deficits. History may include leg crossing, prolonged kneeling, immobility, or trauma. Sensory loss or paresthesias affect the lateral leg below the knee and the anterolateral foot. Muscle weakness affects both ankle dorsiflexion (tibialis anterior), toe extension (e.g., extensor hallucis longus), and ankle evertors (peroneus longus and brevis).
If only the deep fibular portion is affected, only minimal sensory deficits (limited to the web space between the first two digits) and isolated weakness of toe and ankle extensors are seen. Ankle eversion and inversion are normal.
Isolated superficial fibular neuropathy is rare and presents as the sensory deficit of the foot except for the first webspace. Only ankle eversion/inversion may be affected.
60% of the normal gait cycle consists of the stance phase and 40% of the swing phase. When one foot is in the swing phase, the other is in the stance phase. The gait cycle starts with a heel strike and ends with a heel strike on the same side. During the stance phase, the foot remains flat on the ground. The foot is in dorsiflexion in the heel strike, preparing for gradual lowering before the stance phase. In the absence of dorsiflexors, the foot remains in plantar flexion during the stance phase. This prevents the ability to clear the ground and prepare for the next phase of the gait cycle. The patient either drags their toes or lifts the foot high to clear the ground.
After a careful physical exam, diagnostic testing should include plain radiographs of the pelvis and tibia, and fibula to rule out fracture or dislocation. MRI may be indicated .in suspected plexopathies due to masses or tumors. MRI of the lumbar spine, knee, and or ankle may be indicated for potential soft tissue masses in cases of compressive neuropathies. MSK ultrasound is also utilized for evidence of swelling at or proximal to the site of compression.
In the case of collagen vascular diseases, rheumatoid factors, ANA, and other relevant labs should be checked. CBC differential and chemistry panel to rule out other etiologies should be considered.
In many cases, an electrodiagnostic study is an important test to confirm the clinical diagnosis or provide an alternate localization and diagnosis. This study can also define the injury severity and provide information regarding prognosis. This study contains two parts .1) NCS (nerve conduction studies) and needle electromyography. (EMG).
Nerve conduction studies provide information regarding the viability of myelin. Nerve compression is reflected as a delay in conduction latency. The presence of delayed latency, slow velocity, coupled with conduction block at the involved segment, indicates nerve compression.
Needle electromyography: Monopolar needles are introduced into muscles supplied by the nerve under study. Motor unit potential thus obtained are studied for amplitude, firing rates, and recruitment patterns. Denervation of a muscle is evidenced by the presence of potentials called positive sharp waves and fibrillation potentials, which indicate axonal involvement. Nerve conduction studies and EMG together help the electromyographer to identify the location, severity of the lesion and estimate the prognosis for recovery. The absence of denervation potentials coupled with the presence of sufficient, viable motor units on needle EMG points to a good prognosis.
Evidence of denervation potentials coupled with a lack of viable motor units denotes a poor prognosis for recovery.
Autoimmune and critical illness neuropathy and myopathy often exist across the spectrum, and often a thorough, extensive workup simply results in a "clinical syndrome" rather than a perfect clear-cut diagnosis.
Treatment / Management
Approach to the Patient
The approach to a patient depends upon the etiology of foot drop and the nature of the compressive lesion. Based on the evaluation and diagnostic findings, many options exist.
In trauma cases, for nerve transection, nerve reconstruction should take place within 72 hours of injury. Primary nerve repair techniques, autologous nerve grafts are usually performed.
For complete nerve compression, necrolysis and nerve decompression should be performed. Return to function has been reported in about 97%. A surgical release may be necessary for patients with equinus deformity.
In cases of significant nerve dysfunction, nerve or tendon transfers may be required. A detailed discussion of surgical options is beyond the scope of this article.
For the other etiologies, treatment is initially conservative because there may be a chance of partial or complete resolution of symptoms spontaneously overtime.
This includes physical therapy and or splinting and pharmacological therapy to manage pain. The goals of conservative management are to stabilize the gait, prevention of falls and contractures. Physical therapy focuses on stretching and strengthening muscles. Electrical stimulation techniques of the weekend dorsi flexors have shown promise. A home exercise program should be an integral part of therapy- specifically to maintain the strength and range of motion of muscle groups that are working in the prevention of flexion contracture.
Splinting is utilized to minimize contractures. For complete nerve palsies with insufficient recovery, an ankle-foot orthosis (AFO) to prevent further plantarflexion should be ordered. Sufficient education and training should be included to assist in the proper usage and maintenance of the brace.
For patients with numbness, instructions for skincare to prevent abrasions and ulcerations are a significant part of management and are often coordinated with the orthotist fabricating the AFO.
For pain management, topical analgesics, serotonin reuptake inhibitors, membrane stabilizers, and opioids can be used. But are not likely to result in clinical recovery.
Follow up electrodiagnostic studies to reassess the situation, looking for reinnervation should also be part of the treatment planning.
- Upper motor neuron involvement - CVA can cause weakness of the whole extremity. Due to spasticity, the limb is artificially long. To ambulate, the person rotates the leg in a semicircular fashion, also referred to as circumduction. Dysphagia, aphasia, or upper limb weakness are also evident.
- Cerebellar gait - The cerebellum is responsible for the smoothness and balance of gait. Cerebellar gait deficits are seen as ataxia and failure to walk in tandem.
- Ataxic gait - Presentation is bilateral. Due to the involvement of long tracks of the spinal cord, position and vibration senses are lost. This leads to high steppage and side to side sway, as can be seen in alcohol use disorder.
- Severe L5 lumbar radiculopathy
- Parkinsonian gait - Involvement of substantia nigra causes failure of the smooth transition of the gait cycle leading to initiation problems coupled with short and fast steps called festinate gait.
- Lumbar plexus involvement such as autoimmune, compressive-tumor,
- Diabetic amyotrophy
- Conversion reaction, somatization disorder, and malingering should be considered if the workup is unremarkable, and there is potential for substantial secondary gain, depression, anxiety, or other suspected psychological issues.
The potential exists for the space-occupying lesion to affect the lumbosacral plexus and result in leg weakness. Underlying malignancy in cases of otherwise unexplained weakness and potential other constitutional signs and symptoms should be considered. However, a predilection for genital femoral neuropathy and weakness of knee extension is more common in these cases.
A history of radiation treatment can result in radiation-induced plexopathy. Typically the electrodiagnostic study shows specific "myokymic discharges." In cases where patients have required radiation treatment to the region, consideration should be given to potential recurrence.
Early range of motion and potential strengthening should be planned. The electrodiagnostic study may assist in helping plan as to whether or not the patient will be needed for long-term bracing and or whether or not the weakness is likely to get worse or spread to other motor groups. Early placement into the ankle dorsiflexor brace improves gait mechanics, decreases falls and helps to minimize other secondary musculoskeletal complaints from the altered gait cycle.
Toxicity and Side Effect Management
If a toxic or other metabolic etiology is discovered, it is best treated early and avoidance or withdrawal of the offending agent.
Medical oncologic issues may arise in cases of underlying malignancy, or space-occupying lesions. Previous chemotherapeutic agents can also result in peripheral neuropathy, which is typically symmetric and distal. However, this or any etiology for underlying peripheral neuropathy may make peripheral nerves more prone to compression.
Preparation for long-term care, bracing, and adaptive equipment should be considered. Rehabilitation medicine services and other therapy should be directed toward the underlying etiology in addition to the foot drop itself. Staging will depend upon the underlying diagnosis such as multiple sclerosis or Lou Gehrig disease being treated differently in terms of staging compared to lumbar spinal pathology.
Prognosis depends both upon the degree of injury and the underlying diagnosis.
Neurapraxia has the best prognosis, and patients usually recover in about three months.
In the case of axonal loss, recovery follows over 6 to 12 months. Neurotmesis has a guarded prognosis and may require surgical treatment with either a nerve transfer or tendon transfer. The appropriate time to refer to a peripheral nerve surgeon is approximately 6 to 9 months after injury. Denervated muscle does not recover significant function after 18 months.
In cases of other etiologies such as Lou Gehrig's disease or space-occupying lesions, the prognosis will differ and depend upon the diagnosis itself rather than the peripheral nerve involvement.
Complications can be a result of nerve damage itself or a consequence of gait aids and braces.
Nerve damage leading to foot drop impairs the ability to clear the ground resulting in a fall. Gait aids as walkers and canes can also be an impediment, especially on uneven surfaces. Anesthetic skin can be a source of ulceration. Abrasions can be a result of poor fitting braces. Bracing may need to be variable depending upon bulk change. In cases such as renal failure and congestive heart failure, different braces for different phases of edema and swelling may need to be provided.
Postoperative and Rehabilitation Care
As outlined above, physical therapy, occupational therapy can play a major role in whether the patient had conservative or surgical management.
If the diagnosis is in question, consultation with either a neurologist or physiatrist is necessary. Referral to an electrodiagnostic laboratory is essential to confirm the localization of injury and determine severity, which impacts the outcome. Referral to physical therapy for gait evaluation and fall prevention, and brace management is indicated. Consultation with an Orthotist is necessary whether the patient requires a temporary brace while awaiting regeneration of the nerve or a permanent brace in case of poor recovery. Psychiatric referral, hematology, oncology, neurosurgery, and orthopedic surgery may all have potential roles in the patient's comprehensive care presenting with foot drop.
Deterrence and Patient Education
The involvement of the patient in every step of the decision-making process is vital for a successful outcome. Education to the patient and family members should be provided regarding pathology, etiology, diagnosis, and severity of the disease process. Handouts and specific instructions should include home exercise programs, skincare, and brace maintenance.
The clinician needs to be able to reach out to the orthotist in between medical visits for maintaining functional braces since all braces eventually wear out and need replacement and maintenance. Follow-up instructions should be provided so that any future adjustments in therapy, bracing, or further diagnostic testing can be monitored.
Pearls and Other Issues
- Foot drop is an inability to lift the forefoot due to the weakness of the dorsiflexors.
- This may be a result of muscular-skeletal or nervous system pathology.
- A thorough evaluation should include medical history, physical examination and necessary imaging, and or electrodiagnostic studies.
- Depending upon the etiology, either surgical or non-surgical options are exercised.
- Prognosis depends upon the extent of nerve damage and the viability of the remaining muscles.
- A comprehensive approach, including referrals to appropriate services, will result in a better outcome.
- Careful analysis of the presenting history and physical examination is essential to arrive at the proper diagnosis.
- Management is contingent upon diagnosis and severity.
Enhancing Healthcare Team Outcomes
Foot drop is not a commonly seen condition. Patients may present to ERs, primary care settings, and other medical clinics. The primary provider may or may not be comfortable handling such a case but can recognize the clinical syndrome and direct care in the proper direction. Prompt diagnosis and identification are necessary since time is essential, especially if a patient requires surgery.[Level 2] the nurse practitioner or a primary care specialist needs to coordinate a multispecialty consultation team as soon as possible. A neurologist, PM&R physician, physical therapists, pharmacy, nursing, and orthotists are the main team players in care coordination. [Level 5].
A thorough anatomical and neurologic background is the mainstay in management and evaluation. Prompt diagnosis, by utilization of appropriate imaging modalities, to rule out bone lesions and other more serious space-occupying entities is crucial. A neurologist and a PM&R specialist play a major role in providing diagnosis and prognosis. PM&R physicians also coordinate a prosthetic/orthotic team to provide the initial brace and take charge of the aftercare. They also supervise Physical and occupational therapy to ensure the patient is making progress, lack of which should prompt consideration for other options. PT and OTs provide muscle reeducation, balance, coordination, and fall prevention strategies. A nurse can be essential in providing education for skincare. For pain management, a consultation with a pharmacist may be necessary. Regular follow-up services should include skincare, maintenance of the brace and other ambulation devices, and review of exercise protocols. Initial EMG studies and follow-up (in 3-4 months following the initial presentation) will further strengthen the outcomes.
The following is an example of the care coordination plan.
- A thorough history and physical examination
- Assessment of risk factors
- Consultation with neurology and PMR
- Order diagnostic imaging, EMG
- Provision of pain management
- Provision of the brace as needed with orthotist
- Referrals to PT and OT
- potential surgical consultation and or intervention
- Review of skincare, fall prevention
- Follow up appointments as needed