A Comprehensive Approach to Foot Drop: A Clinical Review for the Internist

Dr Neeraj Manikath , claude.ai

Abstract

Foot drop, characterized by weakness of ankle dorsiflexion, represents a common yet diagnostically challenging presentation in internal medicine. This review provides a systematic, evidence-based approach to evaluating and managing foot drop, with particular emphasis on clinical pearls that enhance diagnostic accuracy and therapeutic outcomes.

Introduction

Foot drop—the inability to dorsiflex the foot at the ankle—affects approximately 20 per 100,000 individuals annually and frequently presents to internists as an incidental finding or chief complaint. While often attributed reflexively to common peroneal nerve injury, the differential diagnosis spans the entire neuraxis from cerebral cortex to muscle fiber. A methodical approach prevents diagnostic oversimplification and ensures appropriate, timely intervention.

Anatomical Framework: Understanding the Pathway

Ankle dorsiflexion requires integrity along the entire motor pathway. The primary muscles involved include the tibialis anterior (L4-L5), extensor hallucis longus (L5-S1), and extensor digitorum longus (L5-S1), all innervated by the deep peroneal nerve. The common peroneal nerve, branching from the sciatic nerve at the fibular head, is superficial and vulnerable to compression—hence its notorious involvement in foot drop presentations.

Clinical Pearl #1: Always examine ankle inversion strength (tibialis posterior, L5, tibial nerve). Preserved inversion with weak dorsiflexion localizes pathology to the peroneal nerve rather than the L5 root. This simple bedside test dramatically narrows the differential diagnosis.

The Systematic Approach: A Stepwise Algorithm

Step 1: Characterize the Presentation

Temporal Profile: Acute onset suggests vascular events (stroke, spinal cord infarction), trauma, or acute compression. Subacute progression over weeks suggests inflammatory or infectious etiologies. Chronic, insidious onset points toward degenerative, neoplastic, or hereditary conditions.

Unilateral versus Bilateral: Unilateral foot drop typically indicates peripheral nerve or nerve root pathology. Bilateral presentation should prompt consideration of central lesions (parasagittal lesions affecting leg motor areas), polyradiculopathy, polyneuropathy, or motor neuron disease.

Clinical Pearl #2: The "overnight foot drop" following prolonged leg crossing, anesthesia, or lithotomy position is classic common peroneal neuropathy at the fibular head. However, don't miss the "weekend foot drop" in intoxicated patients who compress the nerve during prolonged unconsciousness—this requires scrutiny for rhabdomyolysis and compartment syndrome.

Step 2: Localize the Lesion Through Examination

A structured neurological examination efficiently localizes pathology:

Upper Motor Neuron Signs:

• Hyperreflexia, spasticity, Babinski sign
• Weakness in pyramidal distribution (extensors > flexors in upper limb; flexors > extensors in lower limb)
• Localizes to brain or spinal cord

Lower Motor Neuron Signs:

• Hyporeflexia, atrophy, fasciculations
• Localizes to anterior horn cell, nerve root, plexus, or peripheral nerve

Examination Sequence for Foot Drop:

1. Gait assessment: Steppage gait (high stepping to clear the dropped foot) indicates peripheral pathology. Circumduction suggests central lesion with spasticity.

2. Strength testing:

   • Ankle dorsiflexion (L4-L5, deep peroneal)
   • Toe extension (L5, deep peroneal)
   • Ankle eversion (L5-S1, superficial peroneal)
   • Ankle inversion (L5, tibial nerve)—the localizing test
   • Knee flexion (S1, sciatic)
   • Hip abduction (L5, superior gluteal)

3. Sensory examination: Peroneal neuropathy produces sensory loss over the dorsum of the foot and first web space. L5 radiculopathy causes lateral calf and dorsal foot numbness extending to the great toe. Sciatic neuropathy involves both peroneal and tibial distributions.

4. Reflexes: Ankle reflex (S1) should be preserved in isolated peroneal neuropathy but diminished in sciatic neuropathy or S1 radiculopathy. Knee reflex (L4) assessment helps differentiate L4 from L5 pathology.

Clinical Pearl #3 (The Oyster): In patients with apparent foot drop and normal strength on formal testing, consider the "pseudofoot drop" of severe plantar flexor spasticity from upper motor neuron lesions. The foot appears dropped due to overpowering plantarflexion, not true dorsiflexor weakness. Palpate the contracted gastrocnemius and observe the plantarflexed posture at rest.

Step 3: Differential Diagnosis by Anatomical Localization

Central Causes (5-10% of cases):

• Stroke affecting leg motor cortex or internal capsule
• Parasagittal lesions (meningioma, metastases)
• Multiple sclerosis
• Cervical spondylotic myelopathy

Spinal Cord Lesions:

• Conus medullaris lesions
• Spinal cord infarction (anterior spinal artery)

Anterior Horn Cell:

• Amyotrophic lateral sclerosis (look for upper motor neuron signs elsewhere)
• Poliomyelitis (historical consideration)

Nerve Root (L5 radiculopathy—20-30% of cases):

• Lumbar disc herniation (L4-L5 most common)
• Spinal stenosis
• Neoplastic infiltration
• Diabetic radiculoplexopathy

Lumbosacral Plexus:

• Diabetic amyotrophy
• Retroperitoneal hemorrhage
• Pelvic masses or radiation

Sciatic Nerve:

• Gluteal compartment masses
• Hip arthroplasty complications
• Prolonged lithotomy positioning
• Deep intramuscular injections

Common Peroneal Nerve (30-40% of cases):

• Compression at fibular head (habitual leg crossing, casts, weight loss)
• Knee trauma or surgery
• Ganglion cysts
• Vasculitis (especially in diabetes or connective tissue disease)

Deep Peroneal Nerve:

• Anterior compartment syndrome
• Tight-fitting boots or ski boots ("ski boot paralysis")

Muscle/Neuromuscular Junction:

• Myopathies (inclusion body myositis affecting tibialis anterior)
• Myasthenia gravis (rare presentation, look for fatigability)

Clinical Pearl #4: The presence of pain significantly narrows the differential. Painless foot drop suggests common peroneal compression or motor neuron disease. Painful presentations point toward radiculopathy, vasculitic neuropathy, or compartment syndrome (acute pain).

Step 4: Targeted Investigations

Initial Laboratory Testing:

• Complete blood count, ESR, CRP (inflammatory/vasculitic)
• Glucose, HbA1c (diabetic neuropathy/radiculopathy)
• Vitamin B12, folate (nutritional neuropathy)
• Thyroid function (myopathy)
• Creatine kinase (myopathy, rhabdomyolysis)

Electrodiagnostic Studies:

Nerve conduction studies (NCS) and electromyography (EMG) performed 3-4 weeks post-symptom onset provide definitive localization:

• Peroneal neuropathy: Prolonged distal motor latency, reduced conduction velocity across fibular head, reduced compound muscle action potential (CMAP) amplitude
• L5 radiculopathy: Normal peroneal NCS with denervation in L5-innervated paraspinal and limb muscles sparing peroneus longus
• Plexopathy: Abnormal studies in multiple nerve territories beyond single nerve or root distribution

Clinical Pearl #5 (The Hack): Order EMG/NCS at least 3 weeks after symptom onset. Earlier testing may be falsely negative as Wallerian degeneration requires 10-21 days to manifest fibrillation potentials. If urgent localization is needed, MRI provides faster answers.

Imaging:

• MRI lumbosacral spine: For suspected radiculopathy (disc herniation, stenosis, tumor)
• MRI pelvis: For sciatic nerve or lumbosacral plexus lesions
• Ultrasound: Increasingly useful for visualizing nerve entrapment, masses, or fascicular disruption at the fibular head
• Brain/cervical spine MRI: For upper motor neuron signs

Step 5: Specific Clinical Scenarios and Their Unique Features

Scenario 1: The Hospitalized Patient

Iatrogenic foot drop occurs in 0.3-1% of surgical patients. Risk factors include prolonged surgery (>3 hours), lithotomy position, poorly padded stirrups, and hypotension. Prevention requires meticulous positioning and padding of the fibular head.

Scenario 2: The Diabetic Patient

Diabetics develop foot drop through multiple mechanisms: L5 radiculopathy (diabetic radiculoplexopathy), peroneal mononeuropathy, and distal polyneuropathy with preferential peroneal involvement. The key discriminator is the examination pattern and EMG/NCS localization.

Clinical Pearl #6: Diabetic amyotrophy (also called lumbosacral radiculoplexus neuropathy) presents with asymmetric lower limb weakness, severe pain, and weight loss. Though often affecting proximal muscles, it can cause foot drop through L5 involvement. Most patients improve spontaneously over 6-18 months with glycemic control and immunomodulation.

Scenario 3: The Weight Loss Patient

Rapid weight loss—whether from bariatric surgery, malignancy, or intentional dieting—predisposes to compression neuropathy through loss of protective subcutaneous fat padding at the fibular head. This "slimmer's paralysis" is increasingly common and typically recovers with weight stabilization and nerve protection.

Management: From Diagnosis to Recovery

Conservative Management

For Compressive Peroneal Neuropathy:

• Avoid precipitating behaviors (leg crossing, kneeling)
• Knee padding during sleep
• Physical therapy focusing on range-of-motion exercises
• Ankle-foot orthosis (AFO) to prevent contracture and improve gait

Clinical Pearl #7: Fit AFOs early. Prolonged foot drop leads to Achilles tendon contracture, making eventual recovery functionally inadequate even if nerve function returns. Prevention of contracture is as important as treating the nerve.

Surgical Intervention

Surgical exploration and decompression is considered for:

• Progressive weakness despite conservative management (3-6 months)
• Complete nerve transection identified on imaging
• Mass lesions compressing the nerve
• Failed conservative therapy in young, active patients

Recovery rates following decompression vary: 50-80% experience meaningful improvement when performed within 6 months of symptom onset; outcomes deteriorate significantly beyond this window.

Disease-Specific Therapies

• L5 radiculopathy: NSAIDs, neuropathic pain agents, epidural steroid injections, surgical decompression for refractory cases
• Vasculitic neuropathy: Immunosuppression (corticosteroids, cyclophosphamide)
• Central lesions: Treat underlying pathology; intensive rehabilitation
• Motor neuron disease: Supportive care, multidisciplinary management

Prognosis and Recovery Predictors

Prognosis depends critically on etiology and severity:

Favorable Prognostic Factors:

• Incomplete weakness (ability to move toes)
• Preserved sensory function
• Short duration (<6 months)
• Younger age
• Compressive rather than traumatic etiology
• Neuropraxia (conduction block without axonal loss)

Poor Prognostic Indicators:

• Complete paralysis
• Extensive axonal loss on EMG
• Delayed presentation (>12 months)
• Neurotmesis (complete transection)

Clinical Pearl #8: Serial EMG at 3-6 months demonstrating reinnervation potentials (motor unit action potentials of increased amplitude and duration) predicts functional recovery even before clinical strength improvement becomes apparent.

Red Flags Requiring Urgent Evaluation

• Bilateral foot drop (consider cauda equina, motor neuron disease)
• Associated bowel/bladder dysfunction (cauda equina syndrome)
• Progressive weakness despite conservative management
• Severe pain suggesting compartment syndrome or aggressive pathology
• Upper motor neuron signs (central lesion)
• Constitutional symptoms (fever, weight loss, night pain suggesting malignancy or infection)

Conclusion

Foot drop exemplifies the diagnostic reasoning central to excellent internal medicine practice. The clinician who systematically localizes pathology through careful history and examination, judiciously applies investigations, and thoughtfully manages each patient will achieve superior outcomes. Remember: foot drop is a sign, not a diagnosis. The internist's mandate is uncovering the underlying cause and implementing appropriate, timely therapy.

Key Practice Points

1. Always test ankle inversion to distinguish peroneal neuropathy from L5 radiculopathy
2. Delay EMG/NCS for 3-4 weeks post-symptom onset for optimal sensitivity
3. Fit AFOs early to prevent contractures
4. Consider diabetic amyotrophy in diabetics with painful, asymmetric weakness
5. Investigate bilaterality and upper motor neuron signs urgently
6. Surgical decompression outcomes optimize when performed within 6 months
7. Weight loss and hospitalization are common, preventable causes

Note: While this review references general clinical principles established in neurology and internal medicine literature over decades, specific citation formatting for journal submission would require formal references to primary sources including: Stewart JD. Foot drop: where, why and what to do? Pract Neurol. 2008;8(3):158-169; Katirji B. Peroneal neuropathy. Neurol Clin. 1999;17(3):567-591; and comprehensive neurology texts such as those by Aids to the Examination of the Peripheral Nervous System and monographs on electrodiagnostic medicine.