Cerebral Infarction Presenting with Unilateral Isolated Foot Drop

Weakness of the dorsiflexor muscles of the ankle or toe, referred to as foot drop, is a relatively common presentation. In most cases, foot drop is caused by a lower motor neuron disease such as peroneal peripheral neuropathy, L4-5 radiculopathic sciatic neuropathy, or polyneuropathy. Although upper motor neuron lesions can present as foot drop, the incidence is very rare. Here, we report an extremely rare case in which foot drop was the only presenting symptom of cerebral infarction.     

Soleus nerve transfer to deep peroneal nerve for treatment of foot drop

Different mechanisms including knee dislocation, replacement surgery, nerve tumor, lumbar disc herniation, sharp injury, and gunshot wound lead to foot drop. Several surgical techniques have been used for treatment of foot drop, however, they have had sub-optimal outcomes. Soleus branch of tibial nerve is a good donor for nerve transfer for treatment of foot drop. In this is retrospective study, we reviewed medical records of 6 consecutive patients with sustained foot drop following injury to lumbar root or peroneal nerve, who underwent transfer of the soleus branch of tibial nerve to deep peroneal nerve during 2014–2016. The mean age of the patients was 44.8 years and duration of injury to surgery and follow-up was 8.3 and 14.6 months, respectively. At the end of the follow-up, ankle dorsiflexion force was M4 in two patients (with traumatic peroneal nerve injury with M3 toe extension) and was M2 in one patient. There were three patients with lumbar degenerative disease. Of these patients, two showed M0 and one patient experienced M1 ankle dorsiflexion. We recommend that transfer of soleus nerve to deep peroneal nerve is used as an alternative technique for treatment of foot drop.     

Sudden Foot Drop Caused by Foraminal Gas Pseudocyst

A foraminal gas pseudocyst is a rare cause of lumbar radiculopathy. The association with a sudden foot drop has not been previously reported. Here, a 67-year-old woman with sudden foot drop on the left side is reported. Computed tomography and magnetic resonance imaging identified a foraminal gas containing lesion compressing the left L5 root at the L5-S1 foramen. The foraminal gas containing lesion compressing the L5 ganglion was successfully removed by the posterior approach. The histological diagnosis was a gas pseudocyst. This unique case of surgically proven gas pseudocyst indicates that it should be included in the differential diagnosis of patients presenting with sudden foot drop.     

Foot drop: The first sign of an intracranial tumor?

Isolated foot drop due to a brain lesion is rare. A 48-year-old man complained of inability to dorsiflex the right foot. Right dorsiflexion had 0/5 muscle strength and there were no upper neuron findings on his neurological examination. Magnetic resonance imaging of the brain revealed a left parasagittal brain mass. The lesion was removed and muscle activity returned with 3/5 muscle strength 6 weeks after the operation. The parasagittal area is located at the foot of the homunculus. Therefore, in patients with foot drop, lesions of the parasagittal area should be considered.     

Cerebral Infarction Producing Sudden Isolated Foot Drop

Foot drop usually results from lesions affecting the peripheral neural pathway related to dorsiflexor muscles, especially the peroneal nerve. Although a central nervous system lesion is suspected when there is a lack of clinical evidence for a lower motor neuron lesion, such cases are extremely rare. We describe a patient with sudden isolated foot drop caused by a small acute cortical infarction in the high convexity of the precentral gyrus. This report indicates that a cortical infarction may have to be considered as a potential cause of foot drop.     

足下垂的原因分析及其肌电图鉴别诊断价值

目的回顾性分析引起足下垂的各种可能原因,并探讨肌电图对于足下垂的鉴别诊断价值。方法收集2011年9月至2015年6月因足下垂就诊于我科的患者155例,连续入组,符合足下垂肌力评定标准,分析常规神经传导和针肌电图检测的结果。结果电生理显示腓神经单神经病变70例(45.2%)、坐骨神经病变9例、多发性神经病19例、腰骶丛病变9例、腰_5/骶_1神经根病变42例、运动神经元病变(MND)6例。在腓神经单神经病变患者中,腓骨小头处卡压性病变占72.8%(51/70),其他因素占27.2%(P0.05);电生理显示跨腓骨小头传导阻滞占71.4%、速度减慢2.9%、轴索损害25.7%(P0.05)。在多发性神经病、腰骶丛/根病变患者中,足下垂均为伴随表现;1例运动神经元病患者以足下垂为首发症状。结论就诊神经科的足下垂患者,虽然近半数是腓神经单神经病变所致,但鉴别诊断时,需关注下运动神经元其他水平的病变,尤其是全身性疾病的可能,这对于治疗和预后评估很重要;神经电生理检测可以确定病变水平和分布,从而提示病因线索。     

Clinical Characteristics of Peroneal Nerve Palsy by Posture

Objective

Posture induced common peroneal nerve (CPN) palsy is usually produced during the prolonged squatting or habitual leg crossing while seated, especially in Asian culture and is manifested by the onset of foot drop. Because of its similarity to discogenic foot drop, patients may be diagnosed with a lumbar disc disorder, and in some patients, surgeons may perform unnecessary examinations and even spine surgery. The purpose of our study is to establish the clinical characteristics and diagnostic assessment of posture induced CPN palsy.

Methods

From June 2008 to June 2012, a retrospective study was performed on 26 patients diagnosed with peroneal nerve palsy in neurophysiologic study among patients experiencing foot drop after maintaining a certain posture for a long time.

Results

The inducing postures were squatting (14 patients), sitting cross-legged (6 patients), lying down (4 patients), walking and driving. The mean prolonged neural injury time was 124.2 minutes. The most common clinical presentation was foot drop and the most affected sensory area was dorsum of the foot with tingling sensation (14 patients), numbness (8 patients), and burning sensation (4 patients). The clinical improvement began after a mean 6 weeks, which is not related to neural injury times. Electrophysiology evaluation was performed after 2 weeks later and showed delayed CPN nerve conduction study (NCS) in 24 patients and deep peroneal nerve in 2 patients.

Conclusion

We suggest that an awareness of these clinical characteristics and diagnostic assessment methods may help clinicians make a diagnosis of posture induced CPN palsy and preclude unnecessary studies or inappropriate treatment in foot drop patients.     

Cerebral contusion as a rare cause of foot drop: case report

A 74-year-old woman, taking anticoagulant therapy for chronic heart failure, presented to our emergency room with left dorsiflexion weakness 8 hours from after multitrauma. A detailed neurological examination revealed only 0/5 strength in the left foot dorsiflexion without any upper motor neuron signs. While there was no spinal cord pathology detected, cranial computed tomography demonstrated a lesion in the right parasagittal localization consistent with hemorrhagic contusion. Clinical follow-ups showed an improvement in neurological findings with muscle power of 3/5 in day 5 and 5/5 in day 45 of admission. The parasagittal region has a foot localization in the homonculus and lesions in this area can rarely present with the foot drop sign. Thus, parasagittal region lesions should always be kept in mind in foot drop cases.     

Sudden bilateral foot drop: an unusual presentation of lumbar disc prolapse

Bilateral acute foot drop is reported in a 30-year-old healthy male. He presented with a 7-day history of sudden severe backache, radiating to both the lower limbs and 1-day history of sudden bilateral ankle weakness that progressed to bilateral foot drop within 6 hours. He also developed retention of urine. Investigations revealed a large central disc prolapse at L3-4 with significant canal stenosis at that level. Following surgery the patient had progressive improvement.     

Poststroke subgranular and rostral subventricular zone proliferation in a mouse model of neonatal stroke

Stroke in the neonatal brain is an understudied cause of neurologic morbidity. Recently we have characterized a new immature mouse model of stroke utilizing unilateral carotid ligation alone to produce infarcts and acute seizures in postnatal day 12 (P12) CD‐1 mice. In this study, the amount of poststroke neural progenitor proliferation was examined in the subgranular (SGZ) of the dentate gyrus and the subventricular zone (SVZ) 7, 14, and 21days after ischemia (DAI). A single IP injection (50 mg/kg) of bromodeoxyuridine (BrdU) given 2 hr before perfusion fixation labeled newborn cells. Early cell phenotypes were quantified by colabeling with GFAP, nestin, and DCX. Control mice revealed an age‐dependent decrease in neural proliferation, with an ～50% drop in BrdU‐labeled cell counts at P33 compared with P19 both in the SGZ and in the SVZ. Significant reduction in the amount of neural proliferation in the ipsilateral injured SGZ of ligated mice correlated with both the severity of the stroke‐injury and the acute seizure scores. Similar correlations were not detected contralaterally. Contralateral SGZ neural proliferation was initially lowered at 7 DAI but normalized by 21 DAI. In both injured and control brains, ～90% of newborn SGZ cells colabeled with nestin, ～30% colabeled with GFAP, and a few colabeled with DCX. In contrast, poststroke SVZ cell proliferation was enhanced ipsi‐ more than contralaterally at 7 DAI. In the SVZ, the enhanced neural proliferation normalized to control levels by P33. In conclusion, the neural cell proliferation was differentially altered in the SGZ vs. SVZ after neonatal stroke. © 2009 Wiley‐Liss, Inc.     

Foot drop: where, why and what to do?

Foot drop is a common and distressing problem that can lead to falls and injury. Although the most frequent cause is a (common) peroneal neuropathy at the neck of the fibula, other causes include anterior horn cell disease, lumbar plexopathies, L5 radiculopathy and partial sciatic neuropathy. And even when the nerve lesion is clearly at the fibular neck there are a variety of causes that may not be immediately obvious; habitual leg crossing may well be the most frequent cause and most patients improve when they stop this habit. A meticulous neurological evaluation goes a long way to ascertain the site of the lesion. Nerve conduction and electromyographic studies are useful adjuncts in localising the site of injury, establishing the degree of damage and predicting the degree of recovery. Imaging is important in establishing the cause of foot drop be it at the level of the spine, along the course of the sciatic nerve or in the popliteal fossa; ultrasonography, CT and MR imaging are all useful. For patients with a severe foot drop of any cause, an ankle foot orthosis is a helpful device that enables them to walk better and more safely.     

Intrapartum maternal lumbosacral plexopathy

There are many conflicting theories regarding the mechanism and prognosis of acute foot drop during labor. We report seven women who had arrested labor and foot drop. Six had short stature and one had a large newborn. All had weakness of ankle dorsiflexion, eversion, and inversion, and sensory loss in the L-5 dermatome. Superficial peroneal sensory nerve action potentials (SNAPs) were small or absent in six patients, and the sural SNAP was attenuated in one. Peroneal compound muscle action potential (CMAP) amplitude (recording from extensor digitorum brevis) was low in five, whereas the tibial CMAP was normal in all patients. Peroneal CMAP amplitude (recording from the tibialis anterior) was normal in three and small in three. Needle electromyography revealed decreased recruitment and fibrillation potentials in L-5-innervated muscles, mostly below the knee. We conclude that intrapartum foot drop occurs mostly in short women and is caused by lumbosacral trunk compression by the fetal head at the pelvic brim. The primary pathology is predominantly demyelination and recovery is complete in up to 5 months.     

Calpainopathy presenting as foot drop in a 41 year old

Mutations in the gene encoding muscle-specific calpain 3 protease cause limb girdle muscular dystrophy type 2A. Calpainopathy is characterised by progressive symmetrical atrophy of pelvic, scapular and trunk muscles with an elevated creatine kinase. Most patients develop symptoms in childhood and lose the ability to walk by the age of 40 years. We describe a man who presented with foot drop at the age of 41 years, together with neurophysiological, histopathological and genetic data. This is the first report of calpainopathy presenting as foot drop, and widens the phenotype associated with this disease.     

弥漫性轴突损伤形态学改变的实验研究

目的　观察弥漫性轴突损伤的常见部位, 病理改变过程, 以及其发生原因和机制。探讨其与临床的相关性。方法　用 Ｍａｒｍａｒｏｕ 的落体打击装置致伤动物, 大鼠脑组织标本在光镜和电镜下观察。结果　轴突回缩球密度在桥脑基底部和小脑上脚最高。伤后轴突内的微丝、微管结构紊乱, 轴突肿胀。伤后３ 天, 多数肿胀的轴突断裂, 形成轴突回缩球。１ 小时组轴突内钙颗粒数量是对照组的１７ 倍, 提示钙的内流。结论　本实验中弥漫性轴突损伤的最常见部位是桥脑基底部和小脑上脚。轴突损伤的过程为： 轴突内结构的紊乱, 轴突肿胀及断裂。轴突损伤的主要发生原因和机制可能是细胞外钙的内流。在伤后１２ 小时以内, 损伤轴突尚未断裂, 可能仍存在可逆性, 这可能是临床上有效治疗的最佳时机。     

Feasibility of Using Peroneal Nerve Recordings for Deriving Stimulation Timing in a Foot Drop Correction System

The objective of this research was to demonstrate the potential of using peroneal nerve activity to derive timing control for stimulation in foot drop correction and to attempt recording and stimulation through the same electrode. Two subjects were implanted with cuff electrodes on the peroneal nerve. An input domain was derived from the recorded electroneurogram (ENG) and fed to a detection algorithm based on an Adaptive Logic Network (ALN) for predicting stimulation timing. A switching circuit was furthermore built for switching between stimulator and recorder for combined use of the cuff electrode. The detection was successful, but the accuracy depended on the signal to noise ratio of the recorded ENG. The switching circuit successfully allowed for simultaneous recording and stimulation through the same cuff electrode. We conclude that the peroneal nerve can potentially be used to record sensory information for derivation of a stimulator control signal in a foot drop application, while at the same time being stimulated to activate foot dorsiflexors.     

<Emphasis Type="Italic">MYH7</Emphasis> mutation associated with two phenotypes of myopathy

The mutations of MYH7 (slow skeletal/β-cardiac myosin heavy chain) are commonly found in familial hypertrophic/dilated cardiomyopathy, and also can cause Laing early-onset distal myopathy (LDM), myosin storage myopathy (MSM), and congenital myopathy with fiber-type disproportion (CFTD). Here we report two cases whose diagnosis was hereditary myopathy according to clinical feature and muscle pathology analysis. High-throughput genomic sequencing (next generation sequencing) was performed to validate the diagnosis. Two MYH7 mutations, p.R1845W and p.E1687del, were identified. p.R1845W was found in a male patient showing weakness of both terminal lower legs without foot drop. Muscle pathology stainings characteristically showed the hyaline body in the intracytoplasmic location. The novel mutation p.E1687del was found in a family with seven patients. The proband showed foot drop, scoliosis, and winged scapula, while his mother only showed mild foot drop and winged scapula. Muscle pathology analysis showed congenital centronucleus myopathy. Both cases only showed muscular disorder and had no cardiomyopathy. This study, for the first time, reports the MYH7 mutations associated with centronucleus myopathy.     

A case of foot drop as an expression of brain metastases?

Foot drop can be defined as a significant weakness in ankle and toe dorsiflexion. Injury to the dorsiflexors or to any point along the neural pathways that supply these muscles can result in a foot drop. Injury to the peroneal nerve is usually the major precipitant. Other causes vary from trauma to surgical nerve injury, as well as leg compartment syndromes or dorsiflexor injuries, peripheral nerve injuries, stroke, neuropathies, drug toxicities, spinal stenosis, L5 sciaticas, systemic diseases such as connective tissue diseases, vasculidities, or diabetes. This report focuses on a patient presenting with a foot drop as an unusual manifestation of brain metastasis. His minimal symptomatology seemed to point towards a local process. Therefore, early recognition and prompt treatment are essential. The central nervous system must be the target of investigations when the workup fails to disclose the proper etiology. Potential diagnostic delays may occur. Certain cases may require a more aggressive approach.     

Real Time Foot Drop Correction using Machine Learning and Natural Sensors

The objective of this study was to investigate and test a real time system implemented for Functional Electrical Stimulation (FES) assisted foot drop correction, deriving control timing from signals recorded from a peripheral sensory nerve. A hemiplegic participant was attached with a cuff electrode on the sural nerve connected to a telemetry controlled implanted neural amplifier, and a stimulation cuff electrode on the peroneal nerve connected to an implanted stimulator. An input domain was derived from the recorded electroneurogram (ENG) and fed to a detection algorithm based on an Adaptive Logic Network (ALN) for controlling the timing of the peroneal stimulation. The detection system was tested in real time over a period of 392 days, covering a variety of walking tasks. The detection system's ability to detect heel strike and foot lift without errors and to detect the difference between walking and standing proved to be stable for the duration of the study. We conclude that using ALNs and natural sensors provide a stable and accurate control signal for FES foot drop correction.     

Two differential cavities in syringomyelia of pediatric Chiari I malformation presenting with unilateral foot drop

IntroductionPatients with Chiari I malformation (CM1) may have chronic symptoms of syringomyelia, including numbness and weakness of the upper limbs, typically during young adulthood. Acute or subacute presentation of unilateral foot drop has been rarely reported as a first symptom of CM1-associated syringomyelia exclusively in childhood or adolescence. Why these patients do not show any symptoms of the upper limbs although holocord syringomyelia is always observed on magnetic resonance imaging (MRI) is unclear.Case presentationA four-year-old girl presented rapidly with isolated left foot drop. Conventional MRI revealed holocord syringomyelia associated with CM1. Three-dimensional constructive interference in steady state (3D-CISS) imaging further demonstrated that the syringomyelia was comprised of two differential cavities that communicated with each other via a small pore: a centrally positioned upper cavity and a left-deviated lower one. Surgical decompression of the foramen magnum resolved the symptom with radiological improvement of the two cavities.ConclusionIn contrast to a centrally enlarged syrinx that is often asymptomatic, a paracentrally extended syrinx usually produces segmental signs related to its levels. Thus, the left foot drop in this case would have been due to the ipsilaterally deviated lower cavity that was distinguished from the central upper cavity by 3D-CISS imaging. Further reports using this imaging technique are needed to verify the hypothetic pathology.