Lower Limb Weakness Research Articles

Analysis of clinical features and genetic variants in three children with late-onset Multiple acyl-Coenzyme A dehydrogenase deficiency

To explore the clinical characteristics and genetic variants in three children with late-onset Multiple acyl-Coenzyme A dehydrogenase deficiency (MADD type Ⅲ). Clinical data of three children diagnosed with late-onset MADD at the Children's Hospital Affiliated to Zhengzhou University between March 2020 and March 2022 were retrospectively analyzed. All children were subjected to whole exome sequencing (WES), and candidate variants were verified by Sanger sequencing. All children had received improved metabolic therapy and followed up for 1 ~ 3 years. The children had included 2 males and 1 female, and aged from 2 months to 11 years and 7 months. Child 1 had intermittent vomiting, child 2 had weakness in lower limbs, while child 3 had no symptom except abnormal neonatal screening. Tandem mass spectrometry of the three children showed elevation of multiple acylcarnitines with short, medium and long chains. Children 1 and 2 showed increased glutaric acid and multiple dicarboxylic acids by urine Gas chromatography-mass spectrometry (GC-MS) analysis. All children were found to harbor compound heterozygous variants of the ETFDH gene, including a paternal c.1211T>C (p.M404T) and a maternal c.488-22T>G variant in child 1, a paternal c.1717C>T (p.Q573X) and a maternal c.250G>A (p.A84T) variant in child 2, and a paternal c.1285+1G>A and maternal c.629A>G (p.S210N) variant in child 3. As for the treatment, high-dose vitamin B2, levocarnitine and coenzyme Q10 were given to improve the metabolism, in addition with a low fat, hypoproteinic and high carbohydrate diet. All children showed a stable condition with normal growth and development during the follow-up. The compound heterozygous variants of the ETFDH gene probably underlay the muscle weakness, remittent vomiting, elevated short, medium, and long chain acylcarnitine, as well as elevated glutaric acid and various dicarboxylic acids in the three children with type Ⅲ MADD.

A randomized cross-over study protocol to evaluate long-term gait training with a pediatric robotic exoskeleton outside the clinical setting in children with movement disorders.

Individuals with neuromuscular disorders display a combination of motor control deficits and lower limb weakness contributing to knee extension deficiency characterized by exaggerated stance phase knee flexion. There is a lack of evidence for long-term improvement of knee extension deficiency with currently available clinical treatment programs. Our previous work testing a wearable robotic exoskeleton with precisely timed assistive torque applied at the knee showed immediate increases in knee extension during walking for children with cerebral palsy, which continued to improve over an acute practice period. When we applied interleaved assistance and resistance to knee extension, we observed improvements in knee extension and increased muscle activation indicating the potential for muscle strengthening when used over time. There is a need for additional, high-quality trials to assess the impact of dosage, intensity and volume of training necessary to see persistent improvement in lower limb function for these patient populations. This randomized crossover study (ClinicalTrials.gov: NCT05726591) was designed to determine whether 12 weeks of overground gait training with a robotic exoskeleton outside of the clinical setting, following an initial in clinic accommodation period, has a beneficial effect on walking ability, muscle activity and overall motor function. Participants will be randomized to either complete the exoskeleton intervention or continue their standard therapy for 12 weeks first, followed by a crossover to the other study component. The primary outcome measure is change in peak knee extension angle during walking; secondary outcome measures include gait speed, strength, and validated clinical scales of motor function and mobility. Assessments will be completed before and after the intervention and at 6 weeks post-intervention, and safety and compliance will be monitored throughout. We hypothesize that the 12-week exoskeleton intervention outside the clinical setting will show greater improvements in study outcome measures than the standard therapy.

Spinal muscular atrophy caused by compound heterozygous SMN1 mutations: two cases and literature review.

Spinal muscular atrophy (SMA) is a rare neuromuscular disease, which is characterized by the degeneration of motor neurons, leading to symmetrical muscle weakness and atrophy.Description of two novel SMN1 mutations (patient1: c.683T > A, p.Leu228Ter; patient2: c.347 T > C, p.Ile116 Thr).We reported two patients with SMN1 mutations with the clinical features, and provided a literature review of the previously reported 22 cases.Two SMA patients showed progressive proximal lower limb weakness and milder clinical symptom. In a total of 22 cases, the most commonly observed SMN1 gene alteration was missense mutation (55%), followed by splicing defect (27%), nonsense (9%) and frameshift (9%).We discuss the possible decisive role of these intragenic mutations in the phenotypic results, which enriched the SMN 1 fine mutation database.

Bilateral lower limb weakness due to transverse myelitis as a first presentation of ankylosing spondylitis

Abstract: The occurrence of transverse myelitis (TM) in ankylosing spondylitis (AS) patients is a rarely reported event with only a few reports of similar cases in existing literature. When faced with a patient with TM, attention should be focused on determining the cause. AS should be kept in mind as a possible etiology. We report the case of a 58-year-old female patient who presented at Al-Ahli Hospital in Palestine, with a 3-day history of lower limb weakness, preceded by a 1-month history of lower back pain with radiation to lower limbs. Based on clinical findings and a comprehensive diagnostic work-up, the patient was diagnosed with TM along with AS. Steroid therapy was started, with pulse therapy having minimal effect. Due to the poor response to steroid therapy, plasmapheresis was done with a good response. After careful consideration, our patient was discharged on low-dose oral glucocorticoids for her TM, and methotrexate for her AS, with close follow-up by a neurologist and a rheumatologist.

The Effectiveness of Strengthening Exercise on Improving Physical Function in Chronic Dialysis with Comorbidity: A Case Study

BACKGROUND: Individuals living with End stage renal disease (ESRD) on long term hemodialysis (HD) generally has a sedentary life style. This leads to reduction of physical function and poor quality of life. Exercise intervention improves muscular strength, physical fitness and Quality of life (QOL) in maintained hemodialysis Individuals. CASE SCENARIO: A 67-year-old female presented with chronic hemodialysis period was carried on wheelchair with the help of relative as she was referred to physiotherapy department with chief complain of weakness in both lower limb and difficulty in walking for 1 year. In this case along with chronic dialysis related dysfunction, patient had atherosclerosis had an acute coronary event and she was on AKT since last one year as she was having pott’s spine. METHODOLOGY: In our evaluation, she had full range of motion of lower limb with muscle weakness by manual muscle testing (MMT=3-4/5), Reduced balance and physical performance by short physical performance battery (SPPB=4/12), and partially dependent for functional activity by functional independent measure (FIM= 81/126). In Physiotherapy intervention: Exercise program started with active exercise, cycling, balance and gait training. Progressively in active exercise increased weight with weight cuff, increase cycling time and task specific balance activities with independent walking each week. RESULT: After four week of intervention improvement in muscle strength (MMT=4-5/5), balance (SPPB=7/12), minimal assistance in functional activities (FIM=109/126). CONCLUSION: Individualized strengthening exercise program improve physical function and muscle strength in chronic dialysis patient. Keywords: Hemodialysis, physical function, muscle strength.

Management of Guillain–Barre Syndrome through Basti (Medicated Enema) and Composite Ayurveda Treatment: A Case Report

Abstract BACKGROUND: Guillain–Barre syndrome (GBS) is a condition characterized by polyradiculoneuropathy associated with an immune-mediated response. Conventional therapies such as intravenous immunoglobulins and plasma exchange have been used to manage this condition, but they often result in unpleasant clinical and electrophysiological outcomes. The present case report describes traditional Ayurveda treatments, specifically Basti (medicated enema) and composite Ayurveda treatment, used to manage GBS. This report aims to provide insights into the effectiveness of traditional Ayurvedic treatments in managing GBS. MATERIALS AND METHODS: In this case, the patient presented with complaints of tingling and numbness in the bilateral upper and lower limbs for 2 months, weakness in bilateral upper and lower limbs for 1 month, inability to stand and walk, pain in the lumbar region, intermittent constipation, and dysphagia since 1 month. The patient was diagnosed with Guillain–Barre syndrome based on clinical findings, electromyography, and nerve conduction velocity test (EMG-NCV). He received treatment from a private hospital, but his symptoms were aggravated, so he was referred to Government Ayurveda Hospital Nagpur for further clinical management. Plasma transfusion was done at PVT Hospital 15 days before. He was treated based on the treatment principles of Vatavyadhi Chikitsa, Vata Dosha Upkram, and Santarpan Chikitsa. The primary goals of the therapy were to nourish the bodily tissues (Santarpan) and pacify the Pitta Dosha (Pittaghna). RESULTS: The patient’s electromyography and nerve conduction velocity test (EMG-NCV) results showed acute demyelinating sensorimotor polyneuropathy involving both the upper limbs and lower limbs. Compared to before treatment, EMG-NCV studies showed definite improvement in compound motor action potential (CMAP) amplitudes more prominently in upper limbs after 4 months of therapy. The muscle power grade increased from 0 to 5, indicating a significant improvement. The bedridden patient can walk alone after the completion of treatment. CONCLUSION: This case study reveals that Ayurvedic treatment has the potential for significant recovery in GBS instances.

ITPR1 variant-induced autosomal dominant hereditary spastic paraplegia in a Chinese family.

Hereditary spastic paraplegia (HSP) is a rare neurodegenerative disease prominently characterized by slowly progressive lower limb weakness and spasticity. The significant genotypic and phenotypic heterogeneity of this disease makes its accurate diagnosis challenging. In this study, we identified the NM_001168272: c.2714A > G (chr3.hg19: g.4716912A > G, N905S) variant in the ITPR1 gene in a three-generation Chinese family with multiple individuals affected by HSP, which we believed to be associated with HSP pathogenesis. To confirm, we performed whole exome sequencing, copy number variant assays, dynamic mutation analysis of the entire family, and protein structure prediction. The variant identified in this study was in the coupling domain, and this is the first corroborated report assigning ITPR1 variants to HSP. These findings expand the clinical and genetic spectrum of HSP and provide important data for its genetic analysis and diagnosis.

A Multidisciplinary Extended Approach to Physiotherapy Rehabilitation in Guillain-Barre Syndrome as Sequelae of COVID-19: A Single Case Study

Introduction: Coronaviruses can cause widespread systemic infections, the most common of which are respiratory complications, which are close to the symptoms of serious acute respiratory syndrome coronavirus (SARS-CoV). Case Description: We report a case of a 16-year-old boy who developed weakness in bilateral lower limbs, difficulty in coughing, and generalized weakness for 2 days. He was diagnosed with post-COVID Guillain-Barre syndrome (GBS). Cerebrospinal fluid (CSF) analysis manifested a CSF protein of 117 mg/dL, a white blood cell count of 6-7/mm3 , and a glucose of too low to comment. Magnetic resonance investigation of the brain revealed mucosal thickening in the bilateral maxillary, ethmoid, and left frontal sinuses. Nerve conduction studies concluded evidence of sensory-motor polyneuropathy. Physiotherapy intervention included patient education, breathing retraining, airway clearance techniques, positioning, a combination of chest proprioceptive neuromuscular facilitation (PNF) techniques, a walking program with supplemented oxygen, and psychological support. Results: Outcome measures have shown enhancement in functional independence and performance of activities of daily living. Conclusion: The evidence from this study suggests that pulmonary rehabilitation plays a pivotal role in managing a patient who is diagnosed with post-COVID GBS, which includes patient education, breathing retraining, airway clearing techniques, a combination of chest PNF techniques, positioning, a walking program with augmented oxygen, and psychological support.

Nerve Cuff Reconstruction for Sacral Duct Tarlov Cyst

ObjectiveTo investigate factors influencing the long-term prognosis of patients with sacral Tarlov syndrome after nerve root cuff reconstruction. MethodsA total of 42 patients with sacral Tarlov cysts who underwent nerve root cuff reconstruction at the First Medical Center of the Chinese PLA General Hospital between December 2015 and December 2021 were retrospectively reviewed. All cases were confirmed using magnetic resonance imaging and pathology. All patients were followed up for 24 months after surgery. Improvement in self-evaluation of health was defined as a good prognosis, while a decline in self-evaluation of health was defined as a poor prognosis. The demographic characteristics and clinical data were compared between patients with good and poor prognoses. Multivariate logistic regression analysis was performed, taking poor prognosis as the dependent variable and parameters with P<0.1 in the univariate analysis as independent variables to identify the risk factors. ResultsSignificant differences were observed in disease duration, lower limb weakness, defecation dysfunction, and defecation dysfunction between patients with good and poor prognoses. Multivariate logistic regression analysis showed that disease duration (Odds ratio [OR]: 0.961, 95% CI: 0927–0.995) and defecation dysfunction (OR: 0.005, 95% CI: 0.0–0.368) were independent risk factors for poor prognosis after nerve cuff reconstruction in patients with sacral Tarlov cysts (all P < 0.05). ConclusionsPatients with sacral Tarlov cysts undergoing nerve root cuff reconstruction, particularly those with longer preoperative disease duration and dysuria, are at increased risk of poor long-term prognosis.

Spinal Adhesive Arachnoiditis Following Surgical Treatment for an Intramedullary Tuberculoma of the Conus Medullaris: A Case Report from Western Mexico

Objectives: Describe a rare case of intramedullary tuberculoma (IMT) complicated by chronic adhesive arachnoiditis (CAA). Presentation of Case: A 19-year-old woman presented with complaints of weight loss, progressive weakness of both lower limbs, and urinary retention. Neurological examination corroborated the motor dysfunction of the lower limbs, associated with sensory disturbances. Magnetic resonance imaging (MRI) detected a ring-enhancing intramedullary mass that expanded the conus medullaris. A provisional diagnosis of neoplastic origin lesion was made and the patient received complete resection of the mass. Histopathology was consistent with tuberculoma. 8 months after beginning postoperative antituberculous therapy, neurological symptoms worsened and follow-up MRI showed a distorted spinal cord with arachnoid cysts and septations, findings that corresponded to CAA. Despite a new surgical intervention, the patient remained with lasting disability. Discussion: IMT is an uncommon presentation of spine tuberculosis. The clinical manifestations mimic those of any space-occupying lesion (SOL), and are dependent on the location in the spine, thus a differential diagnosis with neoplastic, inflammatory, and other granulomatous lesions is required. Being IMT an encapsulated lesion, it is unexpected that the inflammatory response extends to pia-arachnoid layers conducting to complications, such as CAA. The association between IMT and CAA must be recognized, since it undermines the outcomes of therapeutical interventions. Conclusion: The diagnosis of IMT complicated by CAA is challenging due to its low frequency. Therefore, this report emphasizes the importance of recognizing the clinical and radiological features of this association to allow an early diagnosis, and facilitate the selection of therapeutic interventions.

Two homozygous adjacent novel missense mutations in DYSF gene caused dysferlinopathy due to splicing abnormalities.

Background: Dysferlinopathy is an autosomal recessive disorder caused by mutations in the DYSF gene. This study reported two homozygous adjacent missense mutations in the DYSF gene, presenting clinically with bilateral lower limb weakness and calf swelling. Two homozygous adjacent missense mutations in the DYSF gene may be associated with the development of dysferlinopathy, but the exact mechanism needs further investigation. Methods: A retrospective analysis of clinical data from a dysferlinopathy-affected family was conducted. Peripheral blood samples were collected from members of this family for whole-exome sequencing (WES) and copy number variation analysis. Sanger sequencing was employed to confirm potential pathogenic variants. The Human Splicing Finder, SpliceAI, and varSEAK database were used to predict the effect of mutations on splicing function. The pathogenic mechanism of aberrant splicing in dysferlinopathy due to two homozygous adjacent missense mutations in the DYSF gene was determined by an in vivo splicing assay and an in vitro minigene assay. Results: The proband was a 42-year-old woman who presented with weakness of the lower limbs for 2 years and edema of the lower leg. Two homozygous DYSF variants, c.5628C>A p. D1876E and c.5633A>T p. Y1878F, were identified in the proband. Bioinformatics databases suggested that the mutation c.5628C>A of DYSF had no significant impact on splicing signals. Human Splicing Finder Version 2.4.1 suggested that the c.5633A>T of DYSF mutation caused alteration of auxiliary sequences and significant alteration of the ESE/ESS motif ratio. VarSEAK and SpliceAI suggested that the c.5633A>T of DYSF mutation had no splicing effect. Both an in vivo splicing assay and an in vitro minigene assay showed two adjacent mutations: c.5628C>A p. D1876E and c.5633A>T p. Y1878F in the DYSF gene leading to an Exon50 jump that resulted in a 32-aa amino acid deletion within the protein. Point mutation c.5628C>A p. D1876E in the DYSF gene affected splicing in vitro, while point mutation c.5633A>T p. Y1878F in the DYSF gene did not affect splicing function. Conclusion: This study confirmed for the first time that two homozygous mutations of DYSF were associated with the occurrence of dysferlinopathy. The c.5628C>A p. D1876E mutation in DYSF affected the splicing function and may be one of the contributing factors to the pathogenicity.

Intradural extramedullary epidermoid cyst: Case report

Spinal epidermoid cysts are benign tumors. They are most commonly extramedullary intradural tumors. Intramedullary localization is the exception. In this review, we report the case of a 45-year-old patient with a dorsal intradural extramedullary epidermoid cyst, revealed by dorsal spinal pain and right lower limb weakness, we discuss the clinical aspects, radiological features, and neurosurgical treatment.

AP2A2 mutation and defective endocytosis in a Malian family with hereditary spastic paraplegia

Hereditary spastic paraplegia (HSP) comprises a large group of neurogenetic disorders characterized by progressive lower extremity spasticity. Neurological evaluation and genetic testing were completed in a Malian family with early-onset HSP. Three children with unaffected consanguineous parents presented with symptoms consistent with childhood-onset complicated HSP. Neurological evaluation found lower limb weakness, spasticity, dysarthria, seizures, and intellectual disability. Brain MRI showed corpus callosum thinning with cortical and spinal cord atrophy, and an EEG detected slow background in the index patient. Whole exome sequencing identified a homozygous missense variant in the adaptor protein (AP) complex 2 alpha-2 subunit (AP2A2) gene. Western blot analysis showed reduced levels of AP2A2 in patient-iPSC derived neuronal cells. Endocytosis of transferrin receptor (TfR) was decreased in patient-derived neurons. In addition, we observed increased axon initial segment length in patient-derived neurons. Xenopus tropicalis tadpoles with ap2a2 knockout showed cerebral edema and progressive seizures. Immunoprecipitation of the mutant human AP-2-appendage alpha-C construct showed defective binding to accessory proteins. We report AP2A2 as a novel genetic entity associated with HSP and provide functional data in patient-derived neuron cells and a frog model. These findings expand our understanding of the mechanism of HSP and improve the genetic diagnosis of this condition.

No quadriceps muscle weakness following anterior quadratus lumborum block compared with placebo: a randomized, non-inferiority, blinded, volunteer trial

Background and aimsAnterior quadratus lumborum block is a truncal block, applied in close proximity to the lumbar plexus, potentially causing lower limb weakness. This trial aimed to evaluate whether a...

Integrating incentive spirometry and progressive muscle training in managing respiratory compromise in Guillain–Barré syndrome

BackgroundGuillain–Barré syndrome (GBS) is one of the most common causes of acute neuromuscular paralysis in developed and developing countries. It is a complex autoimmune disorder characterized by progressive skeletal muscle weakness, potentially involving respiratory muscles. The purpose of this case report was to explore the importance of combined use of incentive spirometry and progressive muscle training as essential therapies in a 20-year-old male diagnosed with GBS.Case presentationThis is a case report of a 20-year-old Nigerian male university student who was brought to the trauma center on a wheelchair with weakness of both upper and lower limbs which was said to be progressive, and a diagnosis of GBS was made by the attending physician. On examination, he was discovered to have quadriparesis with mild respiratory muscle involvement. He deteriorated with cardiopulmonary compromise and was transferred into intensive care unit. He was managed with supplementary oxygen therapy until there was significant improvement and he was weaned off oxygen therapy and then needed further evaluation and management. The patient was placed on immunoglobulin in conjunction with incentive spirometry, progressive strengthening exercise and exercise training which proved to be effective as he regained all the lost function within a few weeks of symptoms.ResultsThis intervention delves into the synergistic potential of fortifying respiratory muscles and improving respiratory function alongside overall muscle strength which resulted in the patient regaining all the lost function within a few weeks.ConclusionsThe combined use of incentive spirometry and progressive muscle training in addition to immunoglobulin was effective in modulating GBS related impairments. We recommend the use of a multifaceted strategy in the management of patients with GBS and other similar health conditions.

A Young Man With Hereditary Motor And Sensory Neuropathy: A Rare Genetic Association

Hereditary motor and sensory neuropathies with early onset are uncommon conditions that include Dejerine-Sottas neuropathy, which begins in infancy, and congenital hypomyelinating neuropathy, which manifests in the early postnatal period. However, these two historically defined disease entities are only small parts of the clinical spectrum. It is well recognized that very early onset hereditary neuropathies are frequently caused by de novo dominant mutations in PMP22, MPZ, and EGR2. In addition, mutations in several other dominant and recessive genes for Charcot-Marie-Tooth disease may lead to similar phenotypes. A 20-year-old boy had complaints of weakness of both lower limbs for 1 year, followed by wasting and foot drop, which subsequently involved the upper limbs. Nerve conduction velocity and electromyography of both lower limbs revealed demyelinating sensory motor polyneuropathy. Histological examination of the sural nerve revealed a nerve trunk with perineural soft tissue, with the nerve bundles being irregular and separated by fibrous tissue bands. The later reveals small perivascular infiltration of chronic inflammatory cells, and no granuloma or AFB is seen. The genetic test of whole exome screening for heriditatory neuropathy showed pathogenic (PM2, PVS, PP5) with a gene impact of (NF2: c.363+1G&gt;T), which is a rare entity in our case study to consider the diagnosis despite negative family history. We highlight this rare disease in young man with a high index of clinical suspicion for its diagnosis. Bangladesh J Medicine 2024; 35: 101-105

Identification of a Novel Intronic Mutation in VMA21 Associated with a Classical Form of X-Linked Myopathy with Autophagy.

Introduction VMA21 -related myopathy is one of the rare forms of slowly progressive myopathy observed in males. Till now, there have been only a handful of reports, mainly from Europe and America, and two reports from India. Method Here, we describe a case of genetically confirmed VMA21 -associated myopathy with clinical, histopathological, and imaging features with a list of known VMA21 mutations. Results A 29-year-old man had the onset of symptoms at 18 years of age with features of proximal lower limb weakness. Muscle magnetic resonance imaging showed the preferential involvement of vasti and adductor magnus. A biopsy of the left quadriceps femoris showed features of autophagic vacuolar myopathy with vacuoles containing granular eosinophilic materials. In targeted next-generation sequencing, hemizygous mutation in the 3' splice site of intron 2 of the VMA21 gene (c.164-7 T > A) was identified and confirmed the diagnosis of X-linked myopathy with excessive autophagy. Conclusion This report expands the phenotypic and genotypic profile of VMA21 -related myopathy, with a yet unreported mutation in India.

Whole spinal transverse myelitis in neuromyelitis optica spectrum disorder

Background: Spinal cord is one of the prominent targets of autoimmune mechanisms in Neuromyelitis Optica Spectrum Disorder (NMOSD). Rarely, NMOSD causes damage to the entire length of the spinal cord, from cervical segments to conus medullaris, which has not been characterized in the existing literature.Material and method: We reviewed medical records, demographic information, and magnetic resonance imaging (MRI) sequences of 174 NMOSD patients from January 2011 to January 2023 who were admitted to Isfahan Multiple Sclerosis center to find patients with whole spinal transverse myelitis (TM).Results: Whole spinal TM was present in five patients (2.9 %). Three patients were seropositive for Aquaporin-4 (AQP4) antibody; Myelin Oligodendrocyte Glycoprotein antibody (MOG IgG) tested negative for all of them. Lower limb weakness was the most frequent clinical complaint. Two patients presented with optic neuritis; One patient reported having episodes of nausea and vomiting. These patients, overall, yielded a higher expanded disability status scale (EDSS) score than the other NMOSD patients.Conclusion: Whole spinal TM is a rare finding in NMOSD, which is strongly associated with a higher severity and a worse outcome of the disease. The role of anti-AQP4 antibodies in the extent of myelitis in NMOSD has yet to be investigated.

Spinal dural arteriovenous fistula: a case-based review

Spinal dural arteriovenous fistula is an abnormal connection between radicular arteries and spinal venous plexus. This condition is relatively rare with annual incidence of five-ten cases per million. We present a case of a 62-year-old male with complaints of tingling in feet since six months and weakness in legs since 1 hour. Lower limb weakness progressed over a day to complete paralysis and bladder incontinence. Magnetic resonance imaging (MRI) spine showed a dural hypointensity over D6-D11 with abnormal vessels around spinal cord. Patient underwent spinal angiography which showed an intramedullary arteriovenous malformation causing compression. Arterial embolization was done within 24 hours from symptom onset and he ambulated within a week. AV malformations are a rare cause of compressive myelopathy presenting with acute paraplegia. Advances in endovascular techniques have made it possible to treat them early and prevent irreversible damage.

A rare case of spontaneous spinal epidural hematoma with spontaneous resolution

Spontaneous spinal epidural hematoma (SSEH) is an uncommon cause of acute spinal cord compression. It is a neurological emergency that requires urgent imaging and appropriate treatment to prevent permanent neurological sequelae. Here, we present the case of a 30-year-old male with no known comorbidities who presented to the emergency department with a history of sudden onset of upper backache and chest discomfort followed by bilateral lower limb weakness. On examination, the blood pressure was 220/120 mmHg, and neurological examination showed decreased tone and power of 2/5 in bilateral lower limbs. In view of the initial chest discomfort, a cardiac evaluation was done, which was normal, followed by magnetic resonance imaging of the whole spine, which showed a lesion in the anterior epidural space suggestive of hematoma, causing spinal cord compression. A final diagnosis was C6-T2 dorsal SSEH secondary to a hypertensive emergency.