Etiology of spastic foot drop among 16 patients undergoing electrodiagnostic studies: patient series

Abstract

BACKGROUND

Differentiating foot drop due to upper motor neuron (UMN) lesions from that due to lower motor neuron lesions is crucial to avoid unnecessary surgery or surgery at the wrong location. Electrodiagnostic (EDX) studies are useful in evaluating patients with spastic foot drop (SFD).

OBSERVATIONS

Among 16 patients with SFD, the cause was cervical myelopathy in 5 patients (31%), cerebrovascular accident in 3 (18%), hereditary spastic paraplegia in 2 (12%), multiple sclerosis in 2 (12%), chronic cerebral small vessel disease in 2 (12%), intracranial meningioma in 1 (6%), and diffuse brain injury in 1 (6%). Twelve patients (75%) had weakness of a single leg, whereas 2 others (12%) had bilateral weakness. Eleven patients (69%) had difficulty walking. The deep tendon reflexes of the legs were hyperactive in 15 patients (94%), with an extensor plantar response in 9 patients (56%). Twelve patients (75%) had normal motor and sensory conduction, 11 of whom had no denervation changes of the legs.

LESSONS

This study is intended to raise awareness among surgeons about the clinical features of SFD. EDX studies are valuable in ruling out peripheral causes of foot drop, which encourages diagnostic investigation into a UMN source for the foot drop.

“Foot drop” refers to a disturbance at any central or peripheral location along the motor neural pathway that terminates in the dorsiflexor muscles of the foot.¹ Foot drop is characterized by muscle strength of less than 3/5 when the foot can no longer be actively lifted against gravity and often includes weakness of the tibialis anterior, extensor digitorum longus, and/or extensor hallucis longus and spasticity of the ankle plantar flexors (gastrocnemius and soleus).^1–6 Peripheral (flaccid) foot drop is considerably more common than central (spastic) foot drop and usually involves either an L4 or L5 radiculopathy from a herniated nucleus pulposus/foraminal stenosis or peroneal nerve entrapment at the fibular neck.^2–7 Other peripheral causes of foot drop include trauma to a peripheral nerve, leg compartment syndrome, peripheral polyneuropathies, intraneural tumors, and systemic diseases such as connective tissue disorders, vasculitis, and diabetes mellitus.^4–7

Central foot drop, also known as “spastic foot drop” (SFD), is rare and is caused by disruption of the neural pathway extending from the prefrontal motor cortex, corona radiata, internal capsule, basal ganglia, brainstem, and spinal cord.^2–4 Several conditions have been reported to cause SFD, including brain tumors (meningioma, glioma), metastases, cerebrovascular accidents (CVAs), cervical disc herniations, demyelinating plaques due to multiple sclerosis (MS), traumatic brain injury, cerebral abscess/contusion, spinal cord compression, and neurocysticercosis.^2–10 Cerebral cases may arise in the parasagittal area because of either direct damage or local mass effect because the medial homunculus of the primary motor cortex at the mesial surface and top of the lateral surface of the precentral gyrus are responsible for ankle and toe movements.^3,4 SFD has been reported to occur in 52%–67% of patients with spinal upper motor neuron (UMN) pathology.⁶ A total of 20% of patients develop SFD after a CVA.⁹ Patients with SFD often have motor weakness, have impaired motor control primarily of the distal muscle groups, have gait abnormalities with a tendency to fall, fatigue easily, and experience increased energy expenditure after ambulation.¹¹ SFD may be unilateral or bilateral.

We report 16 patients with SFD, all of whom were referred for electrodiagnostic (EDX) testing to differentiate between lumbar radiculopathy and peroneal nerve palsy. The presenting symptoms, physical examination, and EDX findings are presented. The varying causes of SFD as well as the importance of EDX studies in the diagnostic differentiation between UMN and lower motor neuron (LMN) pathologies are discussed.

Study Description

We performed a 10-year (January 23, 2012, to February 17, 2022) retrospective analysis of patients referred to our Neurodiagnostic Center for EDX studies to differentiate between a lumbar radiculopathy and peroneal nerve palsy as the cause of foot drop. Over the 10-year time period of this study, a total of 278 patients with foot drop were referred for EDX studies, 16 of whom had SFD. The patients underwent a detailed neurological examination followed by nerve conduction and electromyography (EMG) studies. The EDX studies were performed in our American Association of Neuromuscular & Electrodiagnostic Medicine–accredited facility using the standard protocol of our laboratory.¹² Several metrics were collected including age and gender of the patient, side of the SFD (right/left/bilateral), cause of the SFD, clinical history and neurological examination findings, EDX findings, magnetic resonance imaging (MRI) findings, treatment, and follow-up. The inclusion criteria were the presence of spasticity and hyperreflexia on clinical examination and the absence of signs of lumbar radiculopathy, plexopathy, or peroneal nerve neuropathy on EDX studies.

Clinical Findings and Neurological Examination

Sixteen patients were diagnosed with SFD based on presenting symptoms, neurological examination, and EDX studies (Table 1). The cause of the SFD was cervical myelopathy in 5 patients (31%; Fig. 1A and B), CVAs in 3 (18%), hereditary spastic paraplegia in 2 (12%), MS in 2 (12%), chronic cerebral small vessel disease in 2 (12%), intracranial meningioma in 1 (6%; Fig. 2A and B), and diffuse brain injury in 1 (6%). The mean age was 55.7 years (range, 26–71 years), and the patients were equally divided between males and females. The SFD was bilateral in 9 patients (56%), on the left side in 6 (38%), and on the right side in 1 (6%).

TABLE 1.

Demographics, presenting symptoms, neurological examination, imaging studies, and treatment of patients with SFD referred for EDX studies

Case No.	Age (yrs)/Gender	Side	Cause	Presenting Symptoms at EDX	Neurological Examination at EDX	MRI	Treatment/FU
1	26/F	Lt	CVA	Lt hemiparesis, uses cane	SFD, contracture of Achilles tendon	NA	HO botulinum toxin injections, bracing, PT
2	58/M	Bilat	Cervical myelopathy	Lt leg weak, limping	Bilat patellar/lt DTR hyperactive; extensor plantar response bilat; lt patellar/ankle clonus; bilat decreased pinprick sensation feet, bilat spastic gait	Cervical: severe spinal stenosis/abnl cord signal C5–6	HO lumbar laminectomy L4–5; no treatment after EDX studies
3	65/M	Lt	Intracranial meningioma	Numbness/weakness in lt leg	0/5 strength in dorsiflexors/evertors lt ankle/extensors of toes, weakness plantar flexors lt ankle/toe flexors, rt w/ extensor plantar response, decreased pinprick sensation dorsal/lateral lt leg	Brain: 4.7 × 3.4–cm meningioma rt parietal parafalcine	HO lumbar laminectomy L4–5 3 yrs before EDX studies, meningioma resection 2 yrs before EDX studies; no treatment after EDX studies
4	50/F	Lt	CVA	Lt hemiparesis, difficulty walking, seizures	Spasticity/hyperreflexia in lt leg, shortening of Achilles tendon	NA	Lioresal, PT, botulinum toxin injections
5	50/M	Bilat	Cervical myelopathy	Bilat numbness in hands/legs, lt leg weak, gait/balance abnl, LBP/leg pain, jerky movements/pruritus/pricking sensation in legs	4/5 strength lt dorsiflexors/plantar flexors/hip flexion/extension, bilat DTR hyperactive, decreased pinprick sensation bilat distal legs/feet, vibration sense decreased malleoli	Cervical myelogram: diffuse cervical spinal stenosis; solid fusion C5–6, incomplete fusion C6–7; significant foraminal stenosis C5–6, C6–7 bilat; myelomalacia C5–6; lumbar myelogram: bilat facet hypertrophic changes L4–5, L5–S1	HO ACDF C5–6, C6–7 18 mos before EDX; cyclobenzaprine, diazepam
6	61/F	Bilat	CVA	LBP/leg pain, difficulty walking, uses wheelchair	Rt ankle dorsiflexors/plantar flexors weak, hyperactive bilat patellar DTR, rt plantar reflex extensor, decreased pinprick sensation rt foot	Brain: remote infarctions of posterior rt MCA territory, rt occipital lobe, lt caudate nucleus; lumbar: multilevel spinal stenosis/spondylolisthesis	Neurosurgery recommended lumbar laminotomies/fusion L3–5
7	35/M	Bilat	Hereditary spastic paraplegia w/ some features of Charcot-Marie-Tooth disease	Bilat weakness in legs, trip/fall, numbness in bilat feet	Bilat club feet, weakness bilat dorsiflexors ankles w/ contracture of Achilles tendons, spasticity of legs bilat; hyperreflexia/positive Babinski bilat, loss of vibration sense ankles bilat, pinprick sensation decreased bilat feet, hyperreflexia arms	Cervical/thoracic: minor disc bulges	HO tethered cord release, transforaminal lumbar interbody fusion; Lioresal, pregabalin, PT, botulinum toxin injections
8	63/M	Bilat	Cervical myelopathy	Bilat weakness in legs, difficulty walking	Bilat weakness dorsiflexors ankles, bilat hyperactive DTR, rt plantar response extensor, decreased pinprick sensation/light touch bilat feet	Cervical: moderate to severe spinal stenosis C6–7, C7–T1	Decompression/fusion C5–T2 1 mo after EDX
9	40/F	Bilat	Hereditary spastic paraplegia w/ positive family history	LBP/leg pain bilat, trip while walking, uses walker	Lt pes cavus, bilat weakness extensors toes/EHL/peronei, spastic muscles, bilat hyperreflexia, lt extensor plantar response, decreased pinprick sensation bilat forefeet, hyperactive DTR bilat arms	Brain: Nl; cervical: mild multilevel canal stenosis & cord flattening due to disc protrusion; thoracic: disc protrusion & mild cord flattening T9–10	No treatment after EDX studies
10	67/F	Lt	Chronic cerebral small vessel disease	LBP/leg pain bilat, weakness lt leg	Lt weakness dorsiflexors/evertors/ plantar flexors ankle, contracture lt Achilles tendon, lt Achilles DTR hyperactive, lt extensor plantar response	Brain: chronic small vessel disease; lumbar: Nl	HO TIAs; no treatment after EDX studies
11	69/F	Bilat	Spastic paraplegia from MS	Weakness rt leg, LBP/leg pain/numbness bilat	Lt DTR hyperactive, decreased pinprick sensation bilat feet	Brain: findings consistent w/ MS; cervical/thoracic/lumbar: multilevel spinal & foraminal stenosis	HO MS, posterior & interbody fusion L4–5 5 yrs before EDX studies; PT
12	65/M	Bilat	Traumatic cervical myelopathy	Lt leg weak, spasms in bilat legs	Spasticity bilat legs w/ extensor spasms, bilat hyperactive patellar DTR, lt weak dorsiflexors	Cervical: severe stenosis w/ cord compression C3–5; lumbar: severe stenosis L3–5	HO paraplegia after MVA age 25; celecoxib; neurosurgery recommended cervical laminoplasty C3–7 w/ rt foraminotomies C5–7: patient declined; lumbar decompression L3–S1 on lt 7 yrs after EDX studies
13	65/F	Lt	Diffuse brain injury	Lt foot weak, numbness, tingling	Bilat hyperreflexia patellar DTR, lt extensor plantar response, decreased pinprick sensation lt foot, inability to dorsiflex lt ankle/toes	Ankle: osteoarthritis	HO head injury 2 yrs before EDX, in coma × 7 days
14	71/M	Rt	Chronic cerebral small vessel disease	Rt leg weak, difficulty w/ walking, ataxia, micturition precipitancy, difficulty getting up from seated position	Bilat spasticity in legs; bilat hyperreflexia patellar DTR, lt extensor plantar response, rt weak dorsiflexors/extensor hallucis longus/plantar flexion, lt weak dorsiflexors, loss of position sense toes bilat, vibration sense absent in ankles bilat, absent pinprick/light touch sensation rt lower leg/lt ankle	Brain MRI: chronic small vessel disease; cervical/thoracic/lumbar MRI: multilevel degenerative changes	HO fall, 1 episode TIA, rt peroneal nerve decompression, several surgeries for lumbosacral radiculopathy
15	39/M	Bilat	Spastic paraplegia from MS	LBP/rt hip pain, weakness rt leg, pain bilat feet, difficulty walking	Weakness rt dorsiflexors/evertors ankle; difficulty w/ plantar flexion inversion rt foot; hyperreflexia rt patellar DTR, rt arm; bilat extensor plantar response; decreased pinprick sensation rt arm, leg; abnl gait w/ circumduction rt leg	Brain: hyperintense lesion pons; cervical: 2 areas signal abnl cord; thoracic: Nl; lumbar: disc bulges L4–S1	Diagnosed w/ MS; gabapentin, Lioresal, carisoprodol, wears AFO
16	67/F	Lt	Cervical myelopathy	Paresthesia/ weakness/pain in lt leg, difficulty walking, uses cane, bladder control problems	Spasticity lt leg, weak lt dorsiflexion, lt patellar DTR hyperreflexia w/ clonus, lt Achilles DTR hyperreflexia	Cervical myelogram: multilevel diffuse congenital & acquired spinal stenosis; thoracic myelogram: disc protrusion T6–7 w/ cord flattening; lumbar myelogram: foraminal stenosis w/ flattening of L5 roots, pelvic screw over cortex of lt S1 foramen	HO MVA 4 yrs before EDX w/ pelvic fractures; lumbar interbody fusion L3–5 after MVA; ketamine injections, pregabalin, duloxetine, spinal cord stimulator

abnl = abnormal; ACDF = anterior cervical discectomy with fusion; AFO = ankle foot orthosis; EHL = extensor hallucis longus; FU = follow-up; HO = history of; LBP = low back pain; MCA = middle cerebral artery; MVA = motor vehicle accident; NA = not applicable; Nl = normal; PT = physical therapy; TIA = transient ischemic attack.

FIG. 1.

Sagittal (A) and axial (B) MRI scans displaying severe cervical spinal stenosis at C5–6 (arrows) with myelomalacia presenting with bilateral foot drop.

FIG. 2.

Coronal (A) and axial (B) MRI scans of a right parasagittal meningioma (arrowheads) that presented with a left foot drop.

Upon presentation for EDX testing, all patients had evidence of SFD. Twelve patients (75%) had weakness of a single leg, whereas 2 others (12%) had hemiparesis. Eleven patients (69%) had difficulty walking. A total of 6 patients (38%) had numbness of the legs/feet and 2 (12%) had bladder control problems. On examination, the deep tendon reflexes (DTRs) of the legs were hyperactive in 15 patients (94%) on the side of the SFD, with an extensor plantar response in 9 patients (56%).

EDX Studies

The EDX findings for patients with SFD are presented in Table 2. Twelve patients (75%) had normal motor and sensory conduction as confirmed by the nerve conduction studies, 11 of whom had no denervation changes of the legs by needle EMG. One of the patients with normal motor and sensory conduction had fibrillations/positive waves in the gastrocnemius due to prior botulinum toxin injections for reducing spasticity. Three patients (19%) had evidence of a sensory motor peripheral neuropathy in addition to the SFD. Another patient had rupture of the tibialis anterior tendon.

TABLE 2.

EDX studies of patients with SFD

Case No.	Nerve Conduction Studies	Needle EMG	Impression
1	Nl motor conduction lt common peroneal/lt tibial	No denervation changes in TA/PL: recruited 3–4 motor units; positive waves/fibrillations in gastrocnemius–recruited 2–3 motor units	Spastic weakness from UMN involvement; fibrillations/positive waves in gastrocnemius due to botulinum toxin injections
2	Decreased motor conduction velocity/prolonged distal motor latency lt common peroneal nerve; no sensory potentials of bilat medial plantar nerves; Nl H-reflex bilat tibial nerves	Increased polyphasic units lt TA, gastrocnemius	Spastic weakness; motor sensory peripheral polyneuropathy; needle EMG findings due to previously treated L5 radiculopathy
3	Nl motor conduction lt common peroneal; Nl sensory conduction in superficial peroneal nerve	No denervation changes lt TA–could not recruit motor units; 1–2 polyphasic motor units lt PL	Spastic weakness from UMN involvement due to rt parietal meningioma
4	Nl motor conduction lt peroneal/ tibial; Nl sensation lt sural/superficial/peroneal/plantar	No denervation changes lt TA/PL/gastrocnemius; recruited 2–3 motor units lt TA/gastrocnemius but none in PL	Spastic hemiparesis; no neuropathy of lt peroneal/tibial
5	Nl motor conduction studies bilat peroneal; nl sensory conduction bilat superficial peroneal; tibial nerve evoked H-reflex w/ Nl latency bilat	No denervation or reinnervation changes in legs/lumbar paraspinal muscles	Spastic weakness from cervical myelopathy; no lumbosacral radiculopathy bilat L4–S1; no peripheral neuropathy
6	Nl motor conduction rt peroneal nerve w/ Nl amplitude of CMAPs over EDB; Nl sensory conduction rt superficial peroneal nerve; Nl H-reflex rt tibial nerve	No denervation changes rt TA/PL–recruited few motor units; no reinnervation changes	Spastic weakness from UMN involvement from CVA; no rt peroneal nerve neuropathy
7	CMAPs w/ Nl amplitude w/ prolonged latency/decreased motor conduction velocity bilat peroneal nerves/rt tibial nerve; no sensory potentials of plantar, superficial peroneal, sural nerves	Decreased motor units/increased polyphasic in bilat TA/gastrocnemius	Spastic weakness from hereditary spastic paralysis; motor sensory peripheral neuropathy
8	Nl motor conduction bilat peroneal/tibial nerves; Nl sensory conduction bilat plantar, sural, & superficial peroneal nerves	No denervation/reinnervation changes	Spastic weakness from UMN involvement due to cervical myelopathy; no LMN disorder or peripheral polyneuropathy
9	Nl motor conduction bilat peroneal/tibial nerves; Nl sensory conduction peroneal, sural, plantar nerves	No denervation changes	Spastic weakness from hereditary spastic paralysis; no lumbosacral radiculopathy L4, L5, or S1 and no peripheral polyneuropathy
10	Nl motor conduction bilat common peroneal nerve/lt tibial nerve; Nl sensory conduction bilat plantar/superficial peroneal nerves; bilat tibial nerve H-reflex w/ Nl latency	No denervation/reinnervation changes bilat L3, L4, L5, S1	Spastic weakness from UMN due to chronic cerebral small vessel disease
11	Nl motor conduction bilat common peroneal nerves; decreased amplitude CMAPs over EDB; Nl sensory conduction bilat superficial peroneal nerves	No denervation changes bilat L4, L5, S1; recruited motor units rt TA/PL	Spastic weakness from UMN due to MS
12	Nl motor conduction bilat peroneal/tibial nerves; H-reflex bilat tibial nerves w/ Nl latency; Nl sensory conduction bilat sural nerves	Decreased recruitment lt TA w/ no fibrillations/positive waves	Spastic weakness from corticospinal tract involvement due to posttraumatic cervical myelopathy; no lumbosacral radiculopathy L4–5
13	CMAP w/ low amplitude/prolonged latency over EDB w/ stimulation of lt common peroneal nerve; Nl motor conduction lt tibial nerve; Nl sensory conduction lt plantar nerves; no sensory potential lt superficial peroneal nerve	Decreased motor units/increased polyphasic units bilat legs	Spastic weakness from UMN due to diffuse brain injury; rupture of lt TA tendon; anterior tarsal tunnel syndrome; US: lt TA tendon rupture
14	No CMAPs over EDB on stimulation of rt common peroneal nerve; decreased motor conduction lt common peroneal nerve/rt tibial nerve; no sensory potentials bilat plantar/superficial peroneal nerves	Fibrillations/positive waves w/ 1–2 small motor units rt TA; fasciculations/decreased motor units/increased polyphasics lt TA; decreased motor units/increased polyphasics bilat gastrocnemius; increased polyphasics VM/VL	Spastic weakness from UMN due to chronic cerebral small vessel disease; rt peroneal nerve axonopathy; sensory peripheral polyneuropathy of legs
15	Nl motor conduction rt peroneal/tibial nerves; Nl sensory conduction rt superficial peroneal nerves; no H-reflex rt tibial nerve	Positive sharp waves rt TA/gastrocnemius; decreased motor unit recruitment w/ increased size of motor units	Spastic paraplegia from UMN due to MS
16	Nl motor conduction bilat peroneal/tibial nerves; Nl sensory conduction bilat superficial peroneal nerves	No denervation changes lt L4–S1	Spastic weakness due to cervical myelopathy

TA= tibialis anterior; PL = peroneus longus; US = ultrasound; CMAP = compound muscle action potential; EDB = extensor digitorum brevis; TA = tibialis anterior; PL = peroneus longus; VM = vastas medialis; VL = vastus lateralis; Nl = normal.

Follow-Up

After the EDX studies, most patients received appropriate treatment for SFD, including botulinum toxin injections, physical therapy, bracing or ankle foot orthoses, spinal cord stimulator, and medications (Lioresal, cyclobenzaprine, diazepam, carisoprodol). Of the 5 patients with cervical myelopathy, only 1 patient underwent a cervical decompression and fusion 1 month after the EDX studies.

Discussion

A thorough history and neurological examination are imperative in the evaluation of patients with foot drop. Physical examination findings are useful in differentiating between foot drop due to UMN or LMN pathology. In a peripheral cause of foot drop, muscle hypotonia and decreased DTRs are often observed.² Increased muscle tone, hyperreflexia, ankle clonus, and Babinski sign (extensor plantar response) on the side of the foot drop are typical with SFD.^2,3,6,7 EDX studies are valuable in distinguishing between a central and a peripheral foot drop.^1,6 Nerve conduction studies may show conduction block or demyelination in the peroneal nerve. Additionally, denervation changes in muscles innervated by the peroneal nerve in foot drop caused by lesions of ventral horn cells, nerve roots, and peroneal division of the sciatic nerve and the peroneal nerve may be observed. EMG testing may reveal only decreased recruitment patterns of the tibialis anterior and extensor digitorum brevis muscles in SFD.⁷ Imaging such as MRI, magnetic resonance angiography, and myelography are also useful in the diagnostic assessment of foot drop, because they may be able to confirm a pathological condition in the brain or cervical/thoracic spinal cord that may be causing the SFD.

Treatment of SFD is aimed at correctly identifying the cause of the SFD and whether surgical intervention may be beneficial to the patient. In cases of cervical myelopathy, a cervical discectomy or decompression may ameliorate the signs and symptoms associated with SFD.⁶ Similarly, resection of a causative lesion such as a meningioma may also improve the SFD. Botulinum toxin intramuscular injections are reversible, painless, and selective and may reduce ankle spasticity by impairing the release of acetylcholine at the neuromuscular junctions.^1,9,11,13,14 Patients with post-CVA hemispasticity and SFD who received botulinum toxin injections every 3 months for 1 year were more likely to attain continued benefits with a reduction of muscle tone and increased active range of motion.¹⁴ Additionally, functional electrical stimulation and botulinum toxin injections can work synergistically to improve SFD by enhancing the antispasticity effect.⁹ Other appropriate therapies include passive muscle stretching, physical therapy, splinting, ankle-foot orthotic devices, intrathecal Lioresal, and medications (Lioresal, tizanidine, dantrolene, and benzodiazepines).^1,9

Differentiating between UMN and LMN pathology may prove challenging when patients present with signs and symptoms of peripheral neuropathy and SFD.^4,7,8 Narenthiran et al.⁴ reported the case of a patient with a 5-year history of progressive right-sided foot drop who had previously undergone biopsy of an abnormality relating to the right C7–T1 facet, which was benign. Physical examination revealed UMN signs in the ipsilateral foot. Brain MRI demonstrated a 3.0-cm left parasagittal lesion consistent with a meningioma. Because of her extensive medical history, the patient declined resection of the meningioma. These authors discussed the diagnostic uncertainty of the cause of foot drop when patients have simultaneous lumbar and thoracocervical spine disease.⁴ They stressed that the diagnosis of the central cause of foot drop may be delayed and that patients may undergo needless surgeries. Kim et al.⁸ reported a case of a patient with complaints of weakness of the left foot with a normal physical examination. Lumbar MRI showed a ruptured disc with compression of the left L4–5 nerve root. EDX studies revealed decreased amplitude and prolonged latency of compound muscle action potentials in the left peroneal and tibial muscles. The patient was diagnosed with lumbar radiculopathy at L4–5 and underwent a lumbar decompression and fusion with no improvement of the left foot weakness. On postoperative day 8, the left Achilles DTR was increased, and there was left ankle clonus. Brain MRI demonstrated an infarction in the right parietal cortex with anterior cerebral artery and posterior cerebral artery stenosis on the left. The patient was treated with daily antiplatelet and adjuvant physiotherapy for SFD. The motor deficit gradually improved within 1 month postoperatively. These authors encouraged awareness of patients who have both a peripheral lesion in the lumbar spine and a central lesion in the primary motor cortex, as the UMN lesion was masked by the LMN lesion.⁸

These previous cases are similar to our case 3 with the concurrent lumbar spinal pathology and a UMN lesion. All of these cases underwent unnecessary spinal surgical procedures (lumbar in 2 cases and cervical facet biopsy in 1 case) before the definitive cause of the SFD was diagnosed, that is, a meningioma in 2 cases and cerebral infarction in the other. Central causes of foot drop should be considered and eliminated in suspicious clinical situations before lumbar surgeries are performed in patients with SFD.

Unilateral SFD may be caused by lesions affecting the corticospinal tract anywhere between the paracentral area of the brain to the lower thoracic spinal cord. Patients with isolated unilateral foot drop may have either UMN or LMN pathology.⁴ Abnormalities in the central nervous system such as a cerebral infarction or other lesion in the parasagittal area should be considered when a patient presents with isolated foot drop that mimics a peripheral lesion.⁷ Another clinical situation is when patients with amyotrophic lateral sclerosis present with unilateral foot drop and examination shows SFD along with LMN features such as fasciculations and muscle atrophy; EDX studies often show diagnostic features in these cases.

Observations

The strength of the present study is the large number of patients who were diagnosed with SFD from different causes and referred for EDX studies, most often with a clinically suspected diagnosis of lumbar radiculopathy or peroneal nerve palsy. While certain causes of SFD have been previously reported, including CVA, meningioma, MS, and cervical myelopathy, our study is the first, to our knowledge, to report SFD arising from hereditary spastic paraplegia, diffuse brain injury, and chronic cerebral small vessel disease. EDX studies play an important role in differentiating between UMN and LMN pathology when a patient is referred for lumbar radiculopathy. However, EDX testing is unable to localize SFD except in situations where a combination of UMN and LMN involvement occurs, as in amyotrophic lateral sclerosis or myeloradiculopathy. Although SFD can be easily diagnosed by clinical examination, it is often missed unless it occurs in the context of hemiplegia or quadri-/paraplegia. The spastic nature of foot drop is frequently not recognized by the referring physician. The value of our study is to raise awareness among physicians and surgeons about the clinical features and causes of SFD. The limitation of this study is its retrospective nature.

Lessons

Our study demonstrates the importance of adequate neurological examination and the integration of EDX studies to the clinical findings in the diagnosis of SFD. EDX testing is able to rule out peripheral causes of foot drop, which encourages diagnostic investigation into a UMN source of the foot drop. Surgeons should be alert to the characteristic features of SFD and perform brain and complete spinal imaging studies to confirm a central cause for the SFD. Prompt surgical intervention may be appropriate in certain cases of brain tumors and spinal cord compression to improve or resolve the SFD. Functional electrical stimulation may significantly improve gait and reduce falls in SFD.

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: CB Shields, LBE Shields, Iyer. Acquisition of data: CB Shields, LBE Shields, Iyer. Analysis and interpretation of data: CB Shields, LBE Shields, Iyer. Drafting the article: LBE Shields. Critically revising the article: all authors. Reviewed submitted version of manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: CB Shields. Administrative/technical/material support: CB Shields, LBE Shields. Study supervision: CB Shields, LBE Shields.