Title of article: Foot Drop
Author: Yahya Firas Mohammad Al-shgerat.
Editors: Almutazballlah Qablan, Sadeen Eid
Reviewer: Dr. Adam M. Abdallah
Keywords: Peroneal neuropathy, foot drop, drop foot, sciatic nerve, Leg crossing, Radiculopathy, common peroneal nerve palsy, common fibular nerve palsy
One of the common problems that lead to falls and injuries is foot drop. Foot drop, or common fibular nerve (CFN) palsy, describes a significant weakness of ankle and toe dorsiflexors including tibialis anterior, extensor hallucis longus (EHL), and extensor digitorum longus (EDL) which are innervated by the peroneal nerve. These muscles control the swinging of the foot during walking and control plantarflexion on heel strikes. Foot drop can occur due to conditions including muscular, neurologic, spinal, autoimmune, and musculoskeletal disorders. Depending on the etiology, treatment options differ.1
Lumbar Nerve Roots
There are 5 lumbar vertebrae. The lumbar nerve roots arise from the lateral spinal recess. The L5 nerve root emerges between the L5 and S1 vertebrae.
The spinal nerves L1–L4’s anterior rami combine to create the lumbar plexus. Multiple nerves exit this plexus. The iliohypogastric and ilioinguinal nerves innervate the transversus abdominis and internal oblique muscles. The obturator nerve provides neural supply to the adductor muscles of the thigh. The femoral nerve is a major 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 includes nerve roots L4-S4. It courses in the posterior thigh to the popliteal fossa. Here it splits into 2 branches: the tibial and the common fibular (historically peroneal) nerves. The tibial nerve supplies the hamstrings, plantar flexors, and investors of the foot.
Common Fibular Nerve
The deep fibular nerve innervates the anterior compartment of the leg. It is an offshoot of the common fibular nerve, of the sciatic nerve. The sciatic nerve splits at the apex of the popliteal fossa into the tibial and common fibular nerves. The tibial nerve further courses down the leg, posterior to the tibia, supplying the deep muscles of the posterior leg. It terminates by separating into the medial and lateral plantar nerves of the foot. The common fibular nerve twists around the neck of the fibula and then divides and terminates into the superficial and deep fibular nerves. The superficial peroneal innervates the lateral compartment of the leg and the sensation to the dorsum of the foot. The deep fibular will supply the motor innervation to the anterior compartment of the leg and sensation to the first dorsal toe webspace.2
Entrapment syndromes of the fibular nerve at any spot along its anatomical pathway can lead to compressive neuropathy. Common fibular neuropathy at the fibular head is the most common mononeuropathy that alters the leg.3 The fibular nerve is quite superficial near the head of the fibula, making it prone to pressure palsies. Anatomic variations of the biceps femoris muscle, between the gastrocnemius and distal biceps, can contribute to forming a tunnel that can increase the chances of nerve compression. Other contributing factors include weight loss, prolonged bedridden position, tight casts, space-occupying lesions, and bone metastasis involving the fibular head. According to reports, the piriformis muscle’s two heads can compress the sciatic nerve, causing foot drop.
Compression palsies in the ICUs due to prolonged bed rest can occur. 10% of patients who stay in the ICU for longer than four weeks may develop paresis of the fibular nerve. Critical illness polyneuropathy in motor and sensory nerves can present with foot drop.4 Weakness can be bilateral. Diabetic patients are more vulnerable to such compression neuropathies.
Lumbar radiculopathy is a common cause of foot drop; L5 radiculopathy is the most common lumbar radiculopathy and often results from lumbar disc herniation or spondylitis in the spine.5
There were cases of disc herniations, bony (osteophytes or sacral ala) or ligamentous (lumbosacral band and sacroiliac ligament) compression of the L5 nerve which occurs extraforaminately.6Bone metastasis at the fibular head, can rarely cause foot drop.
Traumatic injuries occur associated with orthopedic injuries such as knee dislocations, fractures, blunt trauma, and musculoskeletal injuries. Sciatic neuropathy 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 presents with foot drop.7
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.
Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease (MND) or Lou Gehrig disease, is a neurodegenerative condition that causes muscular weakness, difficulties speaking and swallowing, and motor neuron loss in the anterior horn cells. The first presentation can be a painless foot drop.
Cerebrovascular disease (CVA) can manifest as hemiplegia. Foot drop is a domain of this presentation. Additional signs of upper motor neuron involvement include heightened muscular tone, hyperreflexia, and circumduction of the lower extremities when walking. Depending on the site of ischemia, aphasia can be present.
Mononeuritis multiplex involves one or more sensory and peripheral motor nerves. It is painful and asymmetrical. It can be along with AIDS, leprosy, hepatitis, granulomatosis with polyangiitis (Wegener granulomatosis), and rheumatoid arthritis. Specific nerve dysfunction can cause loss of sensation and movement. A common issue is a sciatic nerve. Vasculitis of small epineuria arteries leads to damage to the axons disrupting nerve conduction and causing muscle weakness.
Acute inflammatory demyelinating polyneuropathy (AIDP), also called Guillain-Barré syndrome, is an autoimmune process that presents progressive motor weakness, sensory loss, and areflexia. Sensory symptoms oftentimes precede motor weakness. Autonomic dysfunction usually comes with this condition. Disruption in the myelin sheath leads to segmental demyelination. Slowing of nerve conduction velocities and conduction block is a hallmark of AIDP. Foot drop can be in the clinical presentation.
One of the most common hereditary neuropathies, Charcot-Marie Tooth (CMT) is a primary congenital demyelinating peripheral neuropathy. It affects motor and sensory nerves. The reported incidence is 1 in 25000. One of the major symptoms is foot drop and atrophy of the lower leg muscles, presenting a typical “stork leg” appearance.8
Somatization disorder and conversion reaction can cause foot drop. Consider a psychiatric evaluation if the workup is unremarkable. Needle electromyography (EMG) and nerve conduction studies (NCS) will appear normal in cases of poor or no effort for ankle dorsiflexion or other motor groups.
The incidence of fibular neuropathy is variable. According to research, the prevalence was 19 per 100000 persons, with more men than women affected. After total knee replacement, the incidence is reported as 0.79 with a slight male overbalance of 2.8: 1, respectively.9 Roughly 90% are unilateral. The effect was equal on both sides.
ALS -The worldwide incidence of ALS yearly is assessed to be 1.54 per 100000.10 ALS can affect people at any age, but the highest incidence is at 50 to 75 years. The actual incidence of mono neuritis multiplex in the United States and the rest of the world is unknown. The reported incidence of AIDP was 1.0 to 1.2 per 100000 every year and increased linearly with age, men are more affected than women by 1.5 times.11
To understand the pathophysiology and predict the future prognosis of peripheral nerve injury, it is necessary to understand the nerve injury classification. In 1943 Seddon and 1953, Sunderland proposed the classification: (1) neurapraxia, (2) axonotmesis, and (3) neurotmesis.
In neuropraxia, myelin is damaged, but the axons are intact. The endoneurium, perineurium, and epineurium remain uninjured. The conduction of nerve impulses is changed at the site of injury. This is clinically interpreted as sensory loss and weakness. In EMG, this reflects latency and slow nerve conduction velocity across the compressed segment. This type of injury heals the best.
In axonotmesis, the axon is damaged, but the epineurium and perineurium remain undamaged. These nerves show sensory and motor deficits below the location of nerve injury when stimulated. Recovery is possible over the long term but unguaranteed.
Neurotmesis is the worst type of nerve injury. Myelin, axons, and supportive connective tissue are altered. Wallerian degeneration happens distal to the site of injury. This is clinically manifested as sensory and motor deficits. Unplanned recovery is not possible. Surgical intervention, including nerve grafting or tendon transfer, is sometimes necessary.12,13
Depending on the level of compression, inflammation, or trauma, neurapraxia, axonotmesis, or complete neurotmesis can happen.
Neurapraxia results in transient damage to the myelin sheath but spares the nerve. Recovery is often complete. Axonotmesis includes the interruption of the axon and myelin. While the connective tissue is preserved. Wallerian degeneration occurs. EMG performed 2 to 4 weeks later shows denervation potentials called fibrillations and positive sharp waves in the included muscles distal to the injury.
Axonotmesis is usually the result of a more severe crush or contusion but can occur when the nerve is extended (without damage to the epineurium). Through regeneration, the nerves regrow distally as fast as 2 to 3 mm per day or as slowly as 1.5 mm per day. Regeneration happens over weeks to years.
Neurotmesis is an injury in which the nerve is completely cut, such as in penetrating trauma. There is no intact myelin, and the axons are completely damaged. Endoneurium tubes and connective tissue components are damaged, disrupted, and/or transected, and the perineurium may be protected. Recovery has no chance to occur without surgical re-anastomosis.
A wide variety of chemicals and other toxins can affect skeletal muscles, central, and peripheral nervous systems directly. The properties of these agents and their effects are not always symmetric and are beyond the intended scope of this article, however, toxic effects and a thorough history of chemical exposure should be thought of in the workup of any patient with weakness.
History and Physical
A careful history and physical exam can help recognize the cause of foot drop.
You should watch the patient do the toe stand, heel stand, and deep knee bend exercises prescribed by standard musculoskeletal testing. Medical research council (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 attained. Finding peripheral nerves and lumbar dermatomes should be the aim of a neurosensory pinprick examination in the distribution. Manual motor testing may effectively measure muscle mass using a side-by-side comparison, identifying the primary muscle group bulk locations. Side-to-side circumference measurements can be obtained and documented to note the 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 healthcare professionals, but it does not include evaluation of specific peripheral sensory nerves.
A formal electrodiagnostic medicine consult, including EMG and NCS, 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 incapacitate the muscles supplied by that nerve.
A lesion of the L5 root, lumbar plexus, sciatic nerve, common peroneal, or deep peroneal nerve can lead to foot drop due to the weakness of the anterior compartment musculature. The presenting symptom is the inability to walk as before. Weakness of the muscles in the foot that aid in dorsiflexion in particular. Pain may or may not be present. The person will not be able to dorsiflex during the heel strike. The foot will remain flat on the ground. Sometimes can also cause toe drag and incapability to clear the foot. This can lead to falls.
Radiculopathy affecting the fifth lumbar nerve root 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 and the first webspace. Motor symptoms involve weakness of dorsiflexion and eversion of the foot.
Lumbosacral plexopathies can present with similar sensory and motor problems that are similar to sciatic neuropathy. Weakness may also involve hip girdle muscles, including hip abduction (gluteus medius) and hip extension (gluteus maximus).
Sciatic neuropathy presents with sensory loss of the whole foot and weakness of ankle plantar flexors (gastrocnemius, soleus) and ankle inversion. A “flail foot” may result from it. Knee flexion may alter as a result of the involvement of the hamstring muscles as well. Incomplete sciatic neuropathy can present as a common peroneal neuropathy. Often, the peroneal fascicles in the sciatic nerve are more prone to injury than the tibial fascicles.
In common fibular neuropathy, the patient complains of sensory and motor deficits. History may include leg crossing, continuous kneeling, immobility, or trauma. Sensory loss or paresthesia impacts the lateral leg below the knee and the anterolateral foot. Muscle weakness affects ankle dorsiflexion (tibialis anterior), toe extension (e.g., extensor hallucis longus), and ankle evertor muscles (peroneus longus and brevis).
If only the deep fibular portion is affected, 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 will be normal.
Isolated superficial fibular neuropathy is infrequent and presents as the sensory deficit of the foot except for the first webspace. Ankle eversion/inversion may be affected merely.
60% of the normal gait cycle comprises the stance phase and 40% of the swing phase. When one foot is in the swing phase, the other foot is in the stance phase. The cycle starts with a heel strike and ends with a heel strike on the same side. Throughout the stance phase, the foot remains flat. The foot is in dorsiflexion in the heel strike, preparing for gradual lowering prior to the stance phase. In the malfunction of dorsiflexion, the foot remains in plantar flexion during the stance phase. This arrests the ability to clear the ground and prepare for the next phase of the gait cycle. The patients either pull their toes or lifts their foot high to clear the ground.
After a thorough physical exam, diagnostic testing should include plain radiographs of the pelvis and tibia, and fibula to rule out fracture or dislocation. MRI can be indicated in suspected plexopathies due to space-occupying masses. MRI of the lumbar spine, knee, and or ankle may be indicated for possible soft tissue masses in cases of compressive neuropathies. MSK ultrasound is also obtained for evidence of swelling at or proximal to the site of compression.
In the case of collagen vascular diseases; rheumatoid factors, ANA, and relevant labs should be checked. You might consider performing a CBC differential and a chemistry panel to exclude other etiologies.
In many cases, an electrodiagnostic study is an important test to confirm the clinical diagnosis or provide an alternative localization and diagnosis. This study can also assess the injury severity and provide information regarding prognosis. This study contains two domains: NCS (nerve conduction studies) and needle electromyography (EMG).
Nerve conduction studies provide information about the viability of myelin. Nerve compression is interpreted as a delay in conduction latency. The presence of delayed latency, and slow velocity, along with the conduction block at the involved segment, indicates nerve compression.
Needle electromyography: Muscles supplied by the nerve under study get injections from monopolar needles. Motor unit potential thus obtained is noticed for amplitude, firing rates, and recruitment patterns. Positive sharp waves and fibrillation potentials, which indicate axonal involvement, are potentials that indicate the presence of muscle innervation. Nerve conduction studies and EMG together help the observer to identify the site, and severity of the lesion and estimate the prognosis for recovery. The absence of denervation potentials along with the presence of sufficient, viable motor units on needle EMG points to a good prognosis.14
Evidence of denervation potentials coupled with an absence of viable motor units denotes a poor prognosis for recovery.
Autoimmune and critical illness neuropathy and myopathy usually exist across the spectrum, and often a thorough, extensive workup simply results in a “clinical syndrome” rather than a perfect crystal-clear diagnosis.
Approach to the Patient
The approach to a patient counts on the etiology of foot drop and the nature of the compressive lesion. Based on the evaluation and diagnostic findings, multiple options exist.
In trauma cases, for nerve transection, nerve reconstruction must take place within 72 hours of injury. Primary nerve repair techniques and autologous nerve grafts are usually performed.
For complete nerve compression, necrolysis and nerve decompression surgery should be performed. Return to function has accounted for about 97%.15 A surgical release may be a must for patients with equinus deformity.
When there is severe nerve dysfunction, tendon or nerve transfers may be necessary.5 A detailed discussion of surgical modalities is beyond the scope of this article.
For the other etiologies, treatment is conservative as a first step because there may be a chance of partial or complete resolution of symptoms spontaneously over time.
This includes physical therapy and or splinting and pharmacological therapy to control pain. The goals of conservative management are to stabilize the gait and prevent falls and contractures. Muscle strengthening and stretching are the main focuses of physical therapy. Electrical stimulation techniques for weakened dorsiflexion have shown some hope. A home exercise program should be an integral part of therapy- specifically to maintain muscle groups’ strength and range of motion that prevent flexion contracture.
Using splinting reduces contractures. For complete nerve palsies with insufficient recovery, an ankle-foot orthosis (AFO) is indicated to prevent further plantarflexion. Sufficient education and training should be included to aid in the proper usage and maintenance of the brace. For patients with numbness, instructions for skincare to prevent abrasions and ulcerations are an important part of management and are often coordinated with the orthotist fabricating the AFO.
The management of pain may involve the use of opioids, membrane stabilizers, serotonin reuptake inhibitors, and topical analgesics. But are not likely to result in clinical recovery.
Follow-up electrodiagnostic studies to reappraise the situation, and look for reinnervation should also be part of the treatment planning.
Upper motor neuron involvement
- ٍStroke can induce weakness of the whole extremity. Due to spasticity, the limb appears artificially long. To ambulate, the person rotates the leg in a semicircular fashion, also known as circumduction. Dysphagia, aphasia, or upper limb weakness are also apparent.
- Cerebellar gait, The cerebellum is responsible for the delicate and balanced gait. Cerebellar gait deficits exhibit ataxia and failure to walk in tandem.
- Ataxic gait, Presents bilaterally. Due to the involvement of long tracks of the spinal cord, position, and vibration impulses are lost. This leads to excessive steppage and swaying from side to side, a symptom of alcohol use disorder.
extreme L5 lumbar radiculopathy.
Involvement of substantia nigra causes failure of the smooth transition of the gait cycle leading to initiation problems along with short and fast steps called festinate gait.
Lumbar plexus pathologies
- The potential exists for the space-occupying lesion to affect the lumbosacral plexus and end in leg weakness. In situations with otherwise inexplicable weakness, it is important to investigate underlying cancer as well as any other constitutional complaints. However, a propensity for genital femoral neuropathy and weakness of knee extension is more common in these cases.
- A history of radiation treatment can cause radiation-induced plexopathy. Typically, the electrodiagnostic study manifests specific “myokymic discharges.” Patients who need radiation therapy to the region should take the possibility of recurrence into consideration. It is essential to plan the patient’s early range of motion and potential strengthening. If the patient requires long-term bracing, the electrodiagnostic examination may be useful in determining whether or not this is the best course of action. It may also assist determine whether the weakness is likely to worsen or spread to other motor groups. Early placement into the ankle dorsiflexor brace improves gait mechanics, decreases falls, and aids in minimizing other secondary musculoskeletal complaints from the altered gait cycle.
Medical oncologic issues may emerge in cases of underlying malignancy, or space-occupying lesions. Previous chemotherapeutic agents can also result in peripheral neuropathy, which is often symmetric and distal. However, this or any etiology for underlying peripheral neuropathy may cause peripheral nerves to be more prone to compression.
Conversion reaction, somatization disorder, and malingering should be investigated if the workup is unremarkable, and there is potential for substantial secondary gain, depression, anxiety, or other suspected psychological issues.
It is essential to consider bracing, adapted equipment, and long-term management preparation. In addition to treating the foot drop itself, rehabilitation medicine treatments and other forms of therapy should target the underlying etiology. Staging will depend upon the underlying pathology such as multiple sclerosis or Lou Gehrig’s disease being treated differently in terms of staging compared to lumbar spinal pathology.
The prognosis depends both upon the degree of insult and the underlying diagnosis.
Neurapraxia has the best prognosis, and patients often recover in about three months. In the case of axonal loss, recovery shows over 6 to 12 months. Neurotmesis has a guarded prognosis and may require surgery with either a nerve transfer or tendon transfer. The best time to refer to a peripheral nerve surgeon is approximately 6 to 9 months after injury. Denervated muscle does not recover significantly after 18 months.15
In cases of other etiologies such as Lou Gehrig’s disease or space-occupying lesions, the prognosis will be different and depend upon the diagnosis itself rather than the peripheral nerve involvement.
Complications can be a result of nerve damage itself or a result of gait aids and braces. Nerve damage leading to foot drop impairs the ability to clear the foot resulting in a fall. Gait aids such as walkers and canes can also be helpful, especially on uneven surfaces. Anesthetic skin can be a source of ulceration and infection. Abrasions can be a consequence of poorly fitting braces. Bracing may need to be variable depending upon muscle bulk change. In cases such as renal failure and congestive heart failure, different brace sizes for different phases of edema and swelling may need to be provided.
Postoperative and Rehabilitation Care
As outlined above, physical therapy and occupational therapy can play an important role in whether the patient had conservative or surgical management.
The involvement of the patient in every step of the decision-making process is essential for a successful outcome. It is important to educate the patient and their family on the pathology, etiology, diagnosis, and severity of the disease process. Handouts and specific instructions should involve home exercise programs, skincare, and brace maintenance.
Foot drop is an inability to lift the forefoot because of weakness in the dorsiflexors. This can be a result of muscular-skeletal or nervous system pathology. A full evaluation should include medical history, physical examination and necessary imaging, and or electrodiagnostic studies. There are surgical and non-surgical procedures available, depending on the etiology. The prognosis depends upon the range of nerve damage and the viability of the remaining muscles. A comprehensive approach, including referrals to appropriate services, will give a better outcome. Careful analysis of the presenting history and physical examination is vital to arrive at the proper diagnosis. Management is subjunctive upon diagnosis and severity.
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