Painless Footdrop in ‎Neurosurgery

Abstract

Context: The inability or difficulty in dorsiflexion of the foot is called foot drop (FD). Neurological cause of FD ranges from central or peripheral etiologies; whilst foot dorsiflexors injuries could be a non-neurological cause, rarely. Painless FD is happening in peripheral peroneal neuropathy and L4-L5 radiculopathy. Painless FD in lumbar disc disease (LDD) is exceptional and even rarer is the bilateral and metachronous presentation of FD.
Methods: To provide up-to-date information on painless FD, we concisely reviewed the painless FD. Using relevant keywords to retrieve researches from PubMed and Medline databases, in form of a narrative review.
Results: The most common involved spinal segment as a cause of FD is L4-L5 level involvement. Differentiating between radiculopathy and peripheral nerve damage or a neurological systemic illness is critical in etiology. The most common condition that is associated with FD is double root compression due to disc herniation. For treatment, surgery should be considered if beneficial effects for restoring nerve function seem achievable and this would most beneficial if the operation is done within the first two days of the paresis. FD needs multimodality treatment. FD has multiple prognostic factors as the location of pathology, duration of FD, the severity of FD, the timing of surgery, and graft length in FD with peripheral origin.
Conclusions: The available evidence in present literature about FD is weak and scarce may be due to its rareness. For closing this gap and planning an effective treatment for FD interdisciplinary outpatient clinics focusing on FD appear to be a practical strategy.

Declarations: 

Research funding: None.

Author contributions: HA, MM, and AK designed the study based on inspiration from their recent patents with FD. Literature review and writing drafts were conducted by all authors. No paid contributors.

Competing interests: None. 

Ethical approval: NA.

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Full Text

Introduction

FD is the inability or difficulty in dorsiflexion of the foot. The etiology of FD is composed of upper or ‎lower motor neuron injury. Peripheral neuropathy is the most common cause of painless FD, followed by ‎central nervous system (CNS) impairment. In most instances of painless FD caused by CNS pathology, FD ‎is coupled with another upper motor neuron clinical feature. An upper motor neuron lesion is a less ‎common cause of FD, and it might manifest as weakness in the ankle dorsiflexors (1,2). Manifestations of ‎FD can increase the suspicion and help in the rapid diagnosis of a central lesion. There are case reports of ‎FD with brain parasagittal region lesion as a central cause of FD (3). ‎

First, we must distinguish between peripheral neuropathy (the most common cause) and radiculopathy ‎related to spinal disease in situations when lower motor neuron damage is the source of FD. If an ‎individual with FD also has sciatica or low back pain, the lumbar spine is the site of the pathogenic region. ‎The L4/5 level is by far the most often implicated spinal segment that causes FD, however, anomalies at ‎the L3/4 and L5/S1 levels can also induce FD. The L5 nerve root accounts for the majority of fibers in the ‎common peroneal nerve, however, fibers from the L4 and S1 roots also intermix in this nerve (4,5). Ankle ‎dorsiflexors (tibialis anterior, extensor hallucis longus, and extensor digitorum longus muscles), foot ‎evertors (proneus longus and brevis muscles), and foot invertors are all innervated by the L5 nerve root ‎through the peroneal nerve. An L5 nerve root injury induces FD, which appears as foot dorsiflexion ‎weakening, foot inversion paresis, and foot eversion paresis. A common peroneal nerve injury promotes ‎FD as well; however, it appears as eversion paresis with intact foot inversion. Electromyography and ‎nerve conduction investigations can be used to determine the site of these lesions (5-8). ‎

The distinction between radiculopathy and peripheral nerve damage or a neurological systemic condition ‎is the most crucial factor to remember when diagnosing the reason for sudden onset FD. History, physical ‎examination, electrodiagnostic investigations, and imaging studies are all relevant in this regard (9,10). ‎The existing data in terms of therapy ideas for FD is minimal, thus it's vital to evaluate the favorable ‎impacts of surgery for restoring nerve function first. The most critical issue in FD treatment is that once ‎the etiology of FD is identified, nerve structure repair is no longer achievable (11). ‎ ‎

Methods

This was a narrative review study. The study scope was focused on painless FD. we reviewed the painless ‎FD. Using relevant keywords to retrieve researches from PubMed and Medline databases, in form of a ‎narrative review.‎

Results

To move our limbs, first certain impulses are created in the brain, and then they are transported to target ‎muscles through the corticospinal tract. Paresis can be caused by any disorder in this route. Isolated FD ‎can be caused by dorsiflexor weakness in the foot. This is frequently caused by peripheral neuropathy, ‎such as peroneal nerve injury or radiculopathy, and is painless (7-10). ‎

Etiology

 FD can be caused by anterior tibialis weakness. This is frequently linked to extensor hallucis ‎longus and extensor digitorum longus weakness. ‎‎ The main other etiologies of FD are as follows:‎

Lower motor neuron (LMN) Pathology ‎

The most common cause of FD is LMN pathology and the typical common type of this pathology is a ‎disturbance in neural transmission in the deep peroneal nerve (L4/l5). The most prevalent cause of FD is ‎peripheral peroneal neuropathy. The next most common cause of FD is L4/5 radiculopathy (12,13). ‎

Upper motor neuron (UMN) Pathology

The extremely rare cause of FD is UMN pathology. Any pathology affecting neurological pathways can ‎disturb signal transmission to the lumbar nerve roots. Stroke (in 20% of patients) and parasagittal primary ‎brain tumors are among the common central causes of FD (14-16).‎

Other causes

Metabolic diseases, neurodegenerative diseases, neuromuscular diseases, and inflammatory processes ‎such as focal myopathies and multifocal motor neuropathy can also cause foot drop (9).  ‎

Pathophysiology

The axoplasmic flow has a key role in the functional integrity of an axon and its target because this flow ‎transports trophic substances from perikaryon to the axon end. Any pathology disturbes this axoplasmic ‎flow, as laceration or crush injury, damages the functional integrity of the axon. The double-crush ‎phenomenon is a phenomenon that in the presence of a proximal neurogenic insult a distal neurogenic ‎injury occurs so a clinical palsy result. In a patient with preexisting spinal stenosis after doing hip ‎replacement surgery, this phenomenon increases the risk of FD with spinal stenosis as a proximal insult ‎and intraoperative stretch of the sciatic nerve as a distal compromise (17).‎

Diagnosis

History taking

In history taking observing symptoms of the followings are important (9):‎

‎-Common peroneal neuropathy

‎-Sciatic neuropathy ‎

‎-Deep peroneal nerve involvement ‎

‎-Superficial peroneal neuropathy ‎

‎-Lumbosacral plexopathies

Clinical examination

Central foot drop with cerebral lesion can occur without sensory deficits if it is caused by an anterior ‎cerebral artery infarction, while this is rarely the case in patients with middle cerebral artery infarction. ‎Furthermore, the latter is rather associated with a sensorimotor hemiparesis predominantly affecting the ‎arm than with an isolated foot drop (9.18).‎

Because of the limited anatomical space, a spinal cord lesion can be associated with a broad spectrum of ‎combinations of motor, sensory and autonomous deficits. It is rare that an injury to the spinal cord causes ‎only motor deficits, but this may be the case in patients with poliomyelitis, spinal muscle weakness, ‎amyotrophic lateral sclerosis (ALS), and hereditary spastic spinal paralysis. The level of a focal lesion can ‎be concluded from the affected key muscles and dermatomes (12).‎

A radicular lesion of the L5 root is not only associated with foot drop but also with paresis of the gluteus ‎medius muscle and thus can cause a positive Trendelenburg's sign with typical waddling. The key muscle ‎of the L5 root is the tibialis posterior muscle. Therefore, the unilateral absence of the tibialis posterior ‎reflex can also be indicative of a radicular lesion. Here, it is essential to compare the affected side with ‎the healthy side, because this reflex may be absent in healthy individuals too. According to the textbooks, ‎sensory examination in patients with L5 syndrome reveals hypoesthesia of the lateral thigh, the ventral ‎lower leg down to the instep. However, frequently examination findings are not conclusive because of ‎overlapping dermatomes. Since the muscles involved in foot dorsiflexion have a multi-segmental nerve ‎supply, a complete foot drop rather indicates injury to the peroneal nerve and makes an isolated L5 ‎radiculopathy unlikely (12).‎

Furthermore, the clinical examination can help to differentiate between a lesion of the common peroneal ‎nerve and a lesion of one of its branches:‎

‎- Injury to the common peroneal nerve (or to the peroneal fibers of the sciatic nerve): combined ‎impairment of pronation in the ankle and dorsiflexion of the foot with the sensory deficit comprises the ‎ventral lower leg down to the instep, including the area between the great toe and the second toe.‎

‎-An isolated injury to the deep branch of the peroneal nerve: FD without impairment of pronation with the ‎sensory loss is limited to the area between the great toe and the second toe (9).‎

Electrophysiological measurement

Electrophysiological measurement can differentiate between a lesion of the long tracts, radiculopathy and ‎a peripheral nerve injury. In nerve conduction studies (neurography), a circumscribed myelin lesion, e.g. ‎as the result of chronic pressure, causes a conduction block. The response to stimulation proximal to the ‎lesion is less intense compared to the response distal of the lesion. In the presence of axonal damage, ‎compound muscle action potentials (CMAP) have a low amplitude, regardless of the stimulation site. Ten ‎to 14 days after a nerve injury, electromyography (EMG) shows abnormal spontaneous activity. If the ‎damage is limited to myelin, no abnormal spontaneous activity is observed. In addition, the EMG detects ‎reinnervation potentials which are of positive prognostic value even before clinical improvements are ‎seen (19-21).‎

In addition, sensory neurography can differentiate between preganglionic and postganglionic nerve ‎damage over time: In contrast to postganglionic lesions, preganglionic lesions do not result in the ‎development of Wallerian degeneration in a proximal-to-distal manner. Thus, in patients with a ‎postganglionic lesion, sensory neurography will show an abnormal finding in the clinical course which ‎can be used to locate the lesion and to distinguish, for example, between a radicular lesion and a plexus ‎lesion or peripheral nerve damage. By contrast, in acute cases, sensory neurography will be unremarkable ‎even if the patient reports sensory deficits. Furthermore, neurography can detect any additional, ‎potentially asymptomatic nerve lesions, for example as part of a polyneuropathy. In the case of normal ‎neurography findings, it can be useful to obtain sensory and motor evoked potentials to the peroneal ‎nerve and the L5 dermatome (19-21). ‎

Imaging

Imaging exams are helpful in determining the origins of FD, particularly in determining the spinal cord ‎and brain causes of FD. Neuroimaging can also identify the specific location and shape of a lesion in ‎peripheral nerve abnormalities. Magnetic resonance imaging (MRI), MR neurography, and nerve ‎ultrasonography are imaging procedures that can help diagnose the cause of FD. There is a substantial ‎association between electrophysiologically observable axonal damage and nerve alterations on ‎ultrasonography, according to retrospective research. The electrophysiological nerve conduction block, ‎on the other hand, did not show such a link (22,23).‎

Treatment

From a treatment viewpoint, the present literature is weak in FD treatment and more conclusive detailed ‎studies are needed. In the treatment concept first of all must determine whether a surgical intervention has ‎positive effects for restoring nerve function. For clarification of this, FD etiology should completely ‎clarify. However, at the time of diagnosis of etiology of FD restoration of the nerve structures is often no ‎longer possible (9). As the only goal of surgery for degenerative lumbar disease with FD is improvement ‎in the strength of the tibialis anterior, caution must be exercised when considering surgery for these ‎patients with longstanding palsy (24). A retrospective clinical series to investigate the prognostic factors ‎for the postoperative improvement of FD caused by degenerative lumbar disease concluded that age, ‎preoperative tibialis anterior muscle strength, and duration of FD were statistically significant prognostic ‎factors of recovery from FD. Surgery within 2 months after the onset of FD may improve postoperative ‎outcomes (24). ‎

Nerve function preservation and regeneration operation

The range of surgical treatment in FD is wide and extends from tumor resection in the brain or spine to ‎discectomy for a disc herniation to peripheral nerve surgery. Whether these interventions are effective or ‎not depends on the patient-perceived limitations, the location of the lesion, and the duration and severity ‎of the paresis. However, how much time interval is the precise time frame for effective positive results in ‎surgical treatment? For answering this there are scarce clinical data and most of these data are ‎experimental (9,25).‎

Peripheral and central nervous system repairing process

As a rule, in the peripheral nervous system if the nerve cell nucleus remains intact following injury axonal ‎sprouting can occur up to 6 months after injury. However, due to the various changes in the distal stump, ‎regeneration markedly declines already after 3 months and consequently, the outcomes of surgery are less ‎favorable. In the central nervous system for the prevention of uncontrolled growth processes neural ‎regeneration is inhibited by the extracellular environment. Thus, any damage is generally definite other ‎than space-occupying lesions which displace or compress it, instead of destroying it by infiltrative ‎growth. In irreversible damage, damaged tissue is quickly replaced by a glial scar (25).‎

Therapeutic choices for Common peroneal nerve (CPN) injuries are: ‎

conservative measures, neurolysis, direct nerve repair, nerve grafting, nerve transfers, and tendon ‎transfers (26-28). In open trauma with laceration, immediate surgical exploration must be done. For blunt ‎trauma, conservative therapy and observation must be done for 3-6 months from injury onset and if there ‎is no functional improvement or in cases with persistent neuropathic pain surgical exploration is ‎indicated. Surgical options for treatment of CPN injuries are as follows (29-31): ‎

‎-Neurolysis: It includes a release of myofascial and scarring/ fibrosis compressions and adhesions around ‎the nerve. Neurolysis may improve nerve function if there is improvement in multimodal intraoperative ‎monitoring. As injury at the knee region is one of the most common injury sites in compressive and ‎traction injuries, decompression at this site and down to nerve divisions should be performed (31-32). ‎

‎-Direct nerve repair: It is indicated in laceration injuries. However, for contusive and stretching injuries, it ‎is rarely indicated, since nerve lesion may involve several centimeters of length. Direct nerve repair is ‎possible if the gap is small and nerve stumps can be re-approximated without tension, an end-to-end ‎suture can be performed. In the associated musculoskeletal injuries, the need for a workable ‎immobilization should be evaluated because nerve anastomosis must be maintained in place and without ‎movement for lengthy periods (11,24). ‎

‎-Nerve grafting: It is indicated in two conditions.First after resectioning a nonconductive in-continuity ‎neuroma and second when nerve stumps cannot be reapproximated without tension. The sural nerve, if ‎not injured, is often an optimal donor nerve source for autologous nerve reconstruction. The best ‎outcomes are observed with grafts less or equal to 6 cm of length (33). ‎

‎-Nerve transfers recently have become an object of study in CPN injuries reconstruction by using tibial ‎nerve branches. Outcomes in the most recently reported series remain inferior as compared to other ‎reconstructive techniques (34). ‎

‎-Tendon transfers by transferring posterior tibial tendon to different tendinous targets (anterior tibial ‎tendon (ATT) alone or ATT plus toes extensors and peroneus tendons) or anchoring the tendon to tarsal or ‎metatarsal bones. Many years ago, this technique was used as a salvage procedure when nerve ‎reconstruction failed. However, in recent works, its use is advocated for early reconstruction in ‎combination with nerve surgery (35,36).‎

In lumbar radiculopathy as a cause of FD based on the Glocker F, et al in the current DGN( Deutsche ‎Gesellschaft für Neurologie )guideline there is relative(for muscle strengths >3/5) and absolute(for ‎muscle strengths=3/5) indication for surgery. The severity of the paresis has a clear correlation with the ‎recovery of paresis but the duration of the paresis does not have any clear correlation with the recovery of ‎paresis. If the patient undergoes an operation within 48 hours of the onset of paresis there are better ‎recovery results (37).‎

Botulinum toxin

Botulinum toxin is a therapeutic option in patients with spastic FD. Calf muscles injection of type A ‎botulinum toxin has the following results: effective, dose-dependent decrease in ankle spasticity, a ‎reduction in usage of aids, and improvement of pain that is associated with spastic FD. In cases with ‎severe spasticity, we can consider a combined treatment with botulinum toxin and physiotherapeutic ‎redressement procedures. In this approach, the plaster casts are applied and dorsal extension is weekly ‎increased to overwhelm shortening of the Achilles tendon by continuous stretching(38-40).‎

Orthoses

In patients with irreversible foot drop, ankle-foot orthoses as called peroneus splints are planned to ‎improve patients,s daily mobility. Two types of orthoses are available as dynamic and stiff versions. ‎Disadvantages are the weight of orthoses, the appearance of orthoses, as well as pressure points due to ‎insufficient adaption to the foot and shoe shape. Orthoses usage doesn't cause a normal gait pattern. ‎Patients should be encouraged to at times abstain from the use of the orthosis in a barrier-free ‎environment(41).‎

Conclusions

FD is an exceptionally important disorder. The present literature has weak retrospective data about FD. ‎Because of this detailed conclusive studies for the etiologies of FD are needed. Interdisciplinary ‎outpatient clinics concentrating on foot drop appear to be a useful technique in the treatment of FD for ‎bridging information gaps and providing logistic therapy. ‎ For clarification of multiple aspects of FD from ‎etiology to treatment(conservative versus surgical) more conclusive detailed studies are obligatory.‎