L5 mononeuritis, an uncommon cause of foot drop: illustrative case

Abstract

BACKGROUND

New-onset adult foot drop is commonly encountered in neurosurgical practice and has a broad differential, including radiculopathy, peroneal nerve palsy, demyelinating diseases, and central causes. Etiology is commonly identified with comprehensive history, examination, imaging, and investigations. Despite familiarity with the management of lumbar spondylosis and peroneal nerve compression causes, rare or uncommon presentations of nonsurgical causes are important to consider in order to avoid nonbeneficial surgery.

OBSERVATIONS

The authors report a very uncommon cause of foot drop: new-onset isolated L5 mononeuritis in a 61-year-old nondiabetic male. They provide a review of the etiology and diagnosis of foot drop in neurosurgical practice and detail pitfalls during workup and the strategy for its nonsurgical management.

LESSONS

Uncommon, nonsurgical causes for foot drop, even in the setting of degenerative lumbar spondylosis, should be considered during workup to reduce the likelihood of unnecessary surgical intervention. The authors review strategies for investigation of new-onset adult foot drop and relate these to an uncommon cause, an isolated L5 mononeuritis, and detail its clinical course and response to treatment.

Foot drop is often encountered in clinical practice and is associated with significant morbidity. The etiology is broad,^1,2 with causes ranging from lesions affecting the peripheral nervous system (radiculopathies, common peroneal nerve palsies, trauma, double crush, Charcot-Marie-Tooth),^1–5 pathologies of the central nervous system (stroke, tumor, or cerebral palsy), or both (motor neuron disease). Clinical history, neurological examination, and imaging assist with identifying the site of the lesion.^2,5 Imaging is often confirmatory, with nerve-conduction studies particularly useful for patients with normal lumbar spine magnetic resonance imaging (MRI) findings.^6–8

Despite the available investigative options, diagnosing the cause of foot drop can be challenging, especially in patients with confounding lumbar spondylosis^1,2,5 Common causes of foot drop in neurosurgical practice are peroneal nerve injury,² L5 radiculopathy, sciatic neuropathies, and lumbosacral plexopathies.^2,5 Less common causes, such as mononeuritis multiplex or sciatic neuropathy,^9–12 can be diagnostically challenging, particularly when the cause is underreported in the literature, such as in isolated L5 neuritis.

Understanding less common causes is particularly significant as the literature reports a number of patients with difficult-to-diagnose foot drop with uncommon causes who have undergone nonbeneficial lumbar spine surgery.^8,11,12 Effective management of foot drop involves diagnosis, combined treatment of the underlying cause, symptom management, and rehabilitation.^1,2 In cases of neuropathy or mononeuritis multiplex, steroids and intravenous immunoglobulin have equivocal effect.^8,12 Surgical management often targets compressive structural lesions secondary to lumbar spondylosis, lumbar disc herniations, peripheral nerve tumors, or compression of common peroneal nerve. While surgical interventions may reduce the likelihood of further deterioration in function, meaningful improvement in power usually takes time and recovery is often incomplete.^1–4 Orthoses and physiotherapy remain a mainstay of rehabilitative management.¹ The case reported herein highlights an atypical cause of foot drop and, thus, the importance of comprehensive evaluation to avoid nonbeneficial surgical intervention.

Illustrative Case

A 61-year-old nondiabetic male presented with a 2-month history of right-sided shooting leg pain and numbness confined to the lateral aspect of his leg inferior to the knee involving the dorsum of the right foot. The pain developed across 3 days and had no associated back pain. He described difficulty with initiating micturition that had a temporal relationship with commencing and ceasing a neuropathic analgesic.

He denied any recent viral illnesses and had no other symptoms. There was no significant medical history, but he was a regular smoker. MRI lumbar spine apart from mild degenerative spondylosis was unremarkable and did not show nerve root compression.

On examination, the patient had an antalgic gait, a right foot drop, no wasting, and normal tone, but reduced sensation over the dorsum of the right foot. He had reduced power to 3/5 in dorsiflexion, extensor hallucis longus (EHL), and inversion. Power was preserved in all other myotomes, and provocative tests were unremarkable. Remaining examination was unremarkable.

A repeat lumbosacral MRI confirmed no lumbosacral nerve root compression. Blood tests for vasculitic, autoimmune, metabolic, occult malignancy, or infective causes were negative. A lumbar puncture showed normal cerebrospinal fluid color, cell count, and pressures, negative to culture and viral tests. The patient did not have a coronavirus disease 2019 (COVID-19) test.

Nerve-conduction studies revealed gross axonal motor and sensory neuropathy in all nerves studied in the right leg, with normal results for the left leg (Table 1). In view of the normal lumbosacral spine MRI and abnormal nerve-conduction study findings, an MRI with contrast of the lumbosacral plexus was conducted, demonstrating right L5 nerve root contrast enhancement. The visualized sciatic nerve was enlarged with hyperintense changes, accompanied by inflammatory changes in the surrounding gluteal musculature (Figs. 1–4).

TABLE 1.

Nerve-conduction studies

Nerve/Sites	Muscle	Latency (msec)	Amp (mV)	Amp (%)	Duration (msec)	Segments	Distance (cm)	Lat Diff (msec)	Velocity (m/sec)
Rt peroneal nerve
Ankle	EDB	6.88	0.2	100	13.54	Ankle - EDB	8
Fibular head	EDB	18.91	0.1	61.3	12.86	Fibular head - ankle	35	12.03	29
Popliteal fossa	EDB	24.32	0.2	69.9	7.76	Popliteal fossa - fibular head	10	5.42	18
Lt peroneal nerve
Ankle	EDB	4.48	2.9	100	9.22	Ankle - EDB	8
Fibular head	EDB	12.50	2.8	96.3	9.37	Fibular head - ankle	35	8.02	44
Popliteal fossa	EDB	14.84	2.4	82.8	9.74	Popliteal fossa - fibular head	10	2.34	43
Rt tibial nerve
Ankle	AH	4.90	1.4	100	3.70	Ankle - AH	8
Popliteal fossa	AH	14.53	1.4	99	4.84	Pop fossa - ankle	45	9.64	47
Lt tibial nerve
Ankle	AH	5.10	8.8	100	4.01	Ankle - AH	8
Popliteal fossa	AH	14.32	4.6	52.5	6.20	Pop fossa - ankle	46	9.22	50

AH = abductor hallucis; Amp = amplitude; EDB = extensor digitorum brevis; Lat Diff = latency differential.

FIG. 1.

Contrast-enhanced axial MRI demonstrating hyperintensity and enlargement of the right L5 nerve root and associated sciatic nerve. The red arrow points to the right L5 nerve root. 1 = gluteus minimus; 2 = ilium; 3 = sacrum; 4 = gluteus maximus; 5 = illiacus.

FIG. 4.

Axial noncontrast T1-weighted MRI demonstrating enlargement of the right L5 nerve root. The red arrow points to the right L5 nerve root. 1 = S1 vertebral body; 2 = gluteus minimus; 3 = psoas muscle; 4 = multifidus muscle; 5 = iliac crest; 6 = iliacus muscle.

FIG. 2.

Contrast-enhanced axial MRI demonstrating enhancement of the right L5 nerve root. The red arrow points to the right L5 nerve root. 1 = L5 vertebral body; 2 = psoas muscle; 3 = central canal; 4 = gluteus minimus.

FIG. 3.

Contrast-enhanced coronal MRI demonstrating enhancement of the right L5 nerve root. The red arrow points to the L5 nerve root moving into lumbosacral trunk. 1 = L5 vertebral body.

The patient was diagnosed with an idiopathic mononeuritis and commenced a course of intravenous steroids and neuropathic analgesia. Several months after commencing treatment, the patient’s lower limb power improved to 4/5 in all affected myotomes. His pain also significantly decreased.

Discussion

Anatomically, foot drop can be caused by disease affecting anterior horn cells, L4 or L5 nerve roots, lumbosacral plexus, the sciatic nerve, or the peroneal nerves.² Common peroneal nerve palsy occurs secondary to compression, trauma, or infiltration,^2–5 and presents with weakness in dorsiflexion of the foot and toes, numbness to the lateral aspect of the leg and dorsum of the foot, and weakness in eversion.² The common peroneal nerve typically originates in the proximal portion of the popliteal fossa.³ It exits the fossa accompanying the tendon of biceps femoris and proceeds to pass around the lateral head of gastrocnemius and around the head of the fibula to the anterolateral portion of the leg.^2,3,5 The lack of epineural tissue and proximity to the head of the fibula make the common peroneal nerve particularly vulnerable to injury.¹³ In contrast, lumbar nerve root compression typically presents with pain and paresthesia in either the L4 or L5 dermatome and weakness in dorsiflexion. Inversion of the foot is commonly weakened as well.^1,2 Central causes of foot drop typically present as part of a larger pattern of paresis, such as a hemiplegia following stroke or weakness from a progressive glioma.¹ Isolated foot drop from a central cause such as a tumor or stroke is rare.^1,2

In clinical practice foot drop generally refers to weakness in tibialis anterior, the main dorsiflexor of the foot.^1,2 This muscle is innervated by the deep peroneal nerve whose fibers derive predominantly from the L4 and L5 nerve roots.^1,2 Extension of the toes usually accompanies foot drop due to the shared innervation of EHL and extensor digitorum longus. These patients typically walk with exaggerated flexion at the hip and knee to compensate for the lack of dorsiflexion at the ankle.^1,2,4,5

Observations

Mononeuritis

Nerve-conduction studies and electromyography can be useful in the diagnosis of mononeuritis.⁶ The neuronal loss associated with an acute neuritis will typically cause a reduction in signal amplitude of the compound muscle action potential in nerve-conduction studies.^6,7,14 Conduction velocity is usually either normal or slightly reduced.¹⁴ Electromyographic findings in patients with neuropathy generally demonstrate motor unit action potentials with large amplitudes and long durations in addition to signs of fibrillation and fasciculations.¹⁴ Table 1 demonstrates that the patient had conduction studies consistent with axonal loss secondary to neuritis. Reduced signal amplitude and reduced conduction velocity were present in the right tibial and common peroneal nerves, both of which receive input from the L5 nerve root.

MRI can also assist with the diagnosis of a mononeuritis.¹⁵ Typical findings include increased nerve caliber, T2 hyperintensity, edema, and loss of perineural fat planes.¹⁶ Neuritis is also reported to demonstrate edema in surrounding musculature.^16,17

Mononeuritis causing foot drop is very uncommon, especially an isolated L5 mononeuritis. A small number of 74 cases of isolated sciatic neuropathy causing weakness have been reported in the literature, with very few reporting associated MRI findings.^8,11,12 This underscores the importance of considering MRI of the lumbosacral plexus for patients when assessing for uncommon causes or challenging-to-diagnose foot drop.

Mononeuritis has a range of underlying etiologies, most commonly diabetes.^18,19 Postviral mononeuropathy can occur following infection with herpes simplex, varicella zoster, Epstein-Barr virus,^17,20,21 hepatitis C, hepatitis E, or human immunodeficiency virus (HIV).²² Nonviral infections, including Lyme disease^23,24 amyloidosis, sarcoidosis, and neuro-Behcet’s disease, are also known to cause neuritis.²² Our patient had no obvious viral prodrome.

Idiopathic mononeuritis typically presents in the form of mononeuritis multiplex.^9–12 Most commonly, these lesions affect the sciatic nerve and isolated idiopathic neuritis of the L5 nerve is underrepresented. Engstrom et al.¹² described 6 patients with idiopathic mononeuropathies of the lower limb; however, none of these patients had the radiological findings described in our case.¹² The patients described in their study presented with generalized weakness rather than an isolated foot drop.¹²

Other recorded idiopathic mononeuropathies have been described as painless, chronic, progressive, and most commonly occurring in young men; interestingly, our patient presented with pain and sensory loss.^8,11 Recent literature also suggests that COVID-19 may be a cause of several emerging mononeuropathies.^10,25

Other causes of neuropathy include repetitive trauma, ischemia, vasculitis, and demyelinating conditions.^2,8,12 Our patient had no history of trauma, and no evidence of demyelinating pathology on lumbar puncture.

Management of this rare condition is challenging, particularly with confounding spondylosis, and is individualized. Surgical exploration of the nerve seems to be unhelpful.¹² Likewise, intravenous immunoglobulin and steroids appear to be nonbeneficial.^8,11 Orthoses prevent falls and help maintain normal gait.¹ Physiotherapy prevents deconditioning.¹ Our patient received a course of intravenous methyl prednisone to uncertain effect. Analgesia proved crucial to the patient’s comfort and allowed continued mobilization, preventing further deconditioning. Neuropathic agents, while not clearly beneficial in this case, may be a consideration when treating severe neurogenic pain.^1,2 Fortunately, with time, the patient reportedly regained a great deal of strength and sensation.

Lessons

Foot drop secondary to idiopathic mononeuropathy is uncommon, and is underrepresented in the literature. We have presented the case of a 61-year-old male with radiological and electroconductive studies consistent with an L5 mononeuritis clinically manifesting as a foot drop. While this clinical entity is uncommon, it is important for the neurosurgeon to consider nonsurgical causes to avoid nonbeneficial surgery.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: All authors. Acquisition of data: Peselzon, Colditz. Analysis and interpretation of data: Colditz. Drafting of the article: all authors. Critically revising the article: all authors. Reviewed submitted version of the manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: Peselzon. Administrative/technical/material support: Maclachlan.