Spinal Cord Edema Research Articles

Neurotoxicity associated with chimeric antigen receptor T-cell therapy: a real-world study leveraging the FDA Adverse Event Reporting System

ABSTRACT Background CAR-T-associated neurotoxicity is extremely frequent with highly variable clinical presentation. Research design and methods Disproportionality analysis was conducted leveraging the FDA Adverse Event Reporting System (FAERS), covering the period from 1 January 2017, through 31 March 2023. The reporting odds ratio (ROR) and the information component (IC) were utilized to assess the adverse signals in total/individual CAR-T product. The lower limit of the ROR and IC 95% confidence interval (ROR025 and IC025) both exceeding threshold value (1 and 0, respectively) was considered a significant signal. Results Of the 60, 730 records associated with CAR-T, 11, 037 (18.17%) pertained to neurological events. Tisagenlecleucel exhibited the highest percentage of death (38.02%) and life‐threatening (12.90%) outcomes. Notably, it also displayed the broadest distribution of neurotoxicity. Additionally, distinct adverse signals unique to individual CAR-T products were identified. For instance, paraparesis, cerebral hemorrhage, impaired pupillary reflex, Guillain-Barre syndrome, brain death following tisagenlecleucel; dysarthria, orthostatic hypotension, and spinal cord edema after axicabtagene; parkinsonism, Bell’s palsy, and cranial nerve paralysis post ciltacabtagene. Conclusions Axicabtagene ciloleucel, tisagenlecleucel, brexucabtagene autoleucel, lisocabtagene maraleucel, idecabtagene vicleucel, and ciltacabtagene autoleucel exhibited increased odds of neurotoxicity, with some discrepancies in their characteristics, profiles, and severity.

Delayed Pontomesencephalic and Cervical Cord Venous Drainage Followed by Contralateral Carotid-Cavernous Fistula after Craniofacial Fractures: A Case Report.

A 24-year-old male was admitted with progressive cervical hypesthesia, tetraparesis, dyspnea, and a history of craniofacial fracture. Spinal magnetic resonance imaging (MRI) showed brainstem edema extending to the thoracic spine with multiple prominent perimedullary vascular structures. Cerebral digital-substraction angiography revealed Barrow type A carotid-cavernous fistula. Total occlusion with preservation of internal carotid artery flow was achieved using 1 detachable balloon and 6 coils. Postoperatively, immediate respiratory recovery, gradual extremities strength improvement, and right abducens nerve palsy were found. One month follow-up cervical MRI showed good recovery of spinal cord edema and perimedullary veins.

Photobiomodulation reduces spinal cord edema by decreasing the expression of AQP4 in the astrocytes of male spinal cord injury rats via the JAK2/STAT3 signaling pathway.

BackgroundSpinal cord swelling commonly occurs following SCI. Previous studies suggest that PBM may reduce inflammation and scar formation after SCI. However, whether PBM can alleviate post-spinal cord injury edema and its underlying mechanisms have not yet been reported. This study aims to investigate the effects of PBM on spinal cord swelling in rats following SCI and explore the underlying mechanisms. MethodsA rat model of SCI was established, and the rats received continuous PBM therapy for two weeks. Tissue hydration, motor function, AQP4 expression, and pathological changes in the spinal cord were evaluated at different time points. In vitro, astrocytes were subjected to PBM and treated with either cucurbitacin I or TGN020 following OGD. ResultsThe results indicate that PBM reduces tissue swelling in rats with SCI, improves motor function recovery, and inhibits the upregulation of AQP4 and GFAP associated with SCI. In vitro, PBM reduces abnormal activation of the JAK2/STAT3 signaling pathway in astrocytes, leading to decreased AQP4 synthesis and astrocyte activation. ConclusionsThese findings suggest that PBM reduces spinal cord swelling in rats after injury. This effect is associated with the inhibition of JAK2/STAT3 signaling pathway activation in astrocytes and the reduction in AQP4 expression.

Spinal epidural arteriovenous fistula with an intraosseous shunt arising in a compression fracture vertebra: illustrative case.

Spinal epidural arteriovenous fistulas (SEAVFs) with intraosseous shunts are rare, and their underlying pathophysiological mechanisms remain unclear. A female in her 70s presented with rapidly progressive weakness in both lower extremities and urinary retention. Lumbar spine magnetic resonance imaging revealed spinal cord edema and flow voids due to venous dilation and compression fractures of the L1 and L2 vertebral bodies. Spinal angiography revealed ventral and dorsal somatic branches of the lumbar arteries at L1 and L2 flowing into the shunt. High-resolution cone-beam computed tomography revealed a shunt within the compression-fractured vertebral body bone of L2. The intravertebral shunt blood flowed into the ventral epidural venous plexus (VEVP) and returned into the perimedullary vein (PMV). Transarterial embolization was performed using N-butyl cyanoacrylate and Onyx-18 for feeder L1 and feeder L2, respectively. Onyx-18 was injected from the VEVP into the PMV, and complete occlusion of the shunt was achieved. The patient showed symptomatic improvement postoperatively. Vertebral compression fractures are common but rarely associated with SEAVFs. https://thejns.org/doi/10.3171/CASE2457.

Changes and clinical significance of NLRP3 inflammasomes and related factors in patients with spinal fracture complicated with acute spinal cord injury

To investigate the changes and clinical significance of NOD like receptor protein 3 (NLRP3) inflammasomes and related factors in patients with spinal fractures complicated with acute spinal cord injury (SCI). Eighty-six spinal fracture patients complicated with acute SCI admitted to hospital from June 2019 to March 2022 were selected as SCI group, There were 48 males and 38 females, with an average age of (43.48±6.58) years old. And 100 healthy volunteers who underwent physical examination during the same time were selected as control group, including 56 males patients and 44 females patients, with an average age of (45.13±6.43) years old. Peripheral blood mononuclear cell (PBMC) were collected, and the mRNA expressions of NLRP3 and Caspase-1 were detected. Serum was collected and the levels of interleukin (IL)- 1β, IL-18 were detected. According to Frankel's grade, the SCI group was divided into complete injury patients and incomplete injury patients, and according to the Japanese Orthopedic Society (JOA) grade, the SCI group was divided into good prognosis group and poor prognosis group. The difference of NLRP3, Caspase-1, IL-1β, IL-18 among groups were compared, the influencing factors for poor prognosis in SCI patients was analyzed by Logistic regression. The mRNA expression levels of NLRP3 (1.41±0.33) and Caspase-1 (1.44±0.35) in PBMC and the levels of IL-1β(45.34±13.22) pg·ml-1, IL-18(40.95±8.77) pg·ml-1 in serum of SCI group were higher than those of the control group[(1.00±0.19), (1.00±0.16), (16.58±4.24) pg·ml-1, (12.57±3.68) pg·ml-1] (P<0.05). The mRNA expression levels of NLRP3(1.63±0.34) and Caspase-1 (1.67±0.27) in PBMC and the levels of IL-1β(51.09±11.10) pg·ml-1, IL-18 (47.65±7.93) pg·ml-1 in serum of patients with complete injury in the SCI group were higher than those of patients with incomplete injury [(1.31±0.27), (1.34±0.33), (42.85±13.36) pg·ml-1, (38.05±7.48) pg·ml-1](P<0.05). The mRNA expression levels of NLRP3 (1.66±0.31) and Caspase-1 (1.72±0.31)in PBMC and the levels of IL-1β(51.21±11.31) pg·ml-1, IL-18 (45.70±7.25) pg·ml-1 in serum, the proportion of complete injury(21 patients), and the proportion of spinal cord edema or bleeding of patients(15 patients) with poor prognosis in the SCI group were higher than those of patients with good prognosis[(1.28±0.26), (1.37±0.36), (42.79±13.25) pg·ml-1、(38.90±8.63) pg·ml-1, 5、20 cases](P<0.05). Complete injury and the mRNA expression of NLRP3 in PBMC were the influencing factors for poor prognosis in the SCI group (P<0.05). The activation of NLRP3 inflammasomes in patients with spinal fractures complicated with acute SCI is associated with worsening injury and poor prognosis, and NLRP3 expression can serve as a marker for evaluating prognosis.

Timing of Resection of Spinal Meningiomas and Its Influence on Quality of Life and Treatment.

The main treatment modality for spinal meningiomas (SM) is gross total resection (GTR). However, the optimal timing of surgery, especially in cases with absent or mild neurological symptoms, remains unclear. The aim of this study is to assess the impact of early-stage resection on neurological outcome, quality of life (QoL), and quality of care. The primary objective is a favorable neurological outcome (McCormick scale 1). We retrospectively analyzed data from patients who underwent operations for SM between 2011 and 2021. Patients with mild neurological symptoms preoperatively (McCormick scale 1 and 2) were compared to those with more severe neurological symptoms (McCormick scale 3-5). Disabilities and QoL were assessed according to validated questionnaires (SF-36, ODI, NDI). Age, spinal cord edema, thoracic localization, and spinal canal occupancy ratio were associated with more severe neurological symptoms (all p < 0.05). Patients presenting with mild symptoms were associated with favorable neurological outcomes (OR: 14.778 (95%CI 3.918-55.746, p < 0.001)), which is associated with shorter hospitalization, better QoL, and fewer disabilities (p < 0.05). Quality of care was comparable in both cohorts. Early surgical intervention for SM, before the development of severe neurological deficits, should be considered as it is associated with a favorable neurological outcome and quality of life.

Tuberculous meningitis causing holocord longitudinally extensive transverse myelitis

ABSTRACT Longitudinally extensive transverse myelitis (LETM) is a neurological entity with characteristic inflammatory lesions in ≥3 vertebral segments of the spinal cord. It is most commonly associated with neuromyelitis optica spectrum disorder. Other causes include infections, autoimmune disorders, and neoplasms. Tuberculosis has been reported as a cause of LETM in few case reports. However, tuberculous meningitis (TBM) as a cause of LETM is extremely rare, more so with involvement of the complete spine cord from the brainstem to the conus medullaris. A 65-year-old female was admitted to our hospital with sudden-onset tetraplegia and sensory, bowel, and bladder involvement. With no significant past history, mild meningeal signs, and normal metabolic profile, cerebrospinal fluid analysis was done revealing polymerase chain reaction test positive for Mycobacterium tuberculosis. Magnetic resonance imaging of the spine was suggestive of complete spinal cord edema extending from the brainstem to the level of conus medullaris without skip lesions. A final impression of holocord LETM caused by TBM was suggested after ruling out other causes. The case highlights TBM as a potential cause of LETM especially in endemic countries, especially Asian and African countries, more so with holocord involvement without skip lesions.

TP53INP2 knockdown inhibits inflammatory response and apoptosis after spinal cord injury.

Spinal cord injury (SCI) is a traumatic neurological disorder with limited therapeutic options. Tumor protein p53-inducible nuclear protein 2 (TP53INP2) is involved in the occurrence and development of various diseases, and it may play a role during SCI via affecting inflammation and neuronal apoptosis. This study investigated the associated roles and mechanisms of TP53INP2 in SCI. Mouse and lipopolysaccharide (LPS)-induced SCI BV-2 cell models were constructed to explore the role of TP53INP2 in SCI and the associated mechanisms. Histopathological evaluation of spinal cord tissue was detected by hematoxylin and eosinstaining. The Basso, Beattie, and Bresnahanscore was used to measure the motor function of the mice, while the spinal cord water content was used to assess spinal cord edema. The expression of TP53INP2 was measured using RT-qPCR. In addition, inflammatory factors in the spinal cord tissue of SCI mice and LPS-treated BV-2 cells were measured using enzyme-linked immunosorbent assay. Apoptosis and related protein expression levels were detected by flow cytometry and western blot analysis, respectively. TP53INP2 levels increased in SCI mice and LPS-treated BV-2 cells. The results of in vivo and in vitro experiments showed that TP53INP2 knockdown inhibited the inflammatory response and neuronal apoptosis in mouse spinal cord tissue or LPS-induced BV-2 cells. After spinal cord injury, TP53INP2 was upregulated, and TP53INP2 knockdown inhibited the inflammatory response and apoptosis.

Nitrous oxide induced spinal cord oedema with normal serum B12 level with high plasma homocysteine level

Nitrous oxide induced spinal cord oedema with normal serum B12 level with high plasma homocysteine level

Temporary Spinal Cord Stimulation for Herpes Zoster With Myelitis: A Case Series.

Introduction: Preventing the development of postherpetic neuralgia (PHN), the most prevalent and severe complication of herpes zoster (HZ), is vital. Recently, it has been suggested that using temporary spinal cord stimulation (tSCS) for 10-14 days can improve HZ-associated pain (ZAP) and prevent PHN. However, myelitis complicates HZ. Permanent SCS has been successful in treating neuropathic pain induced by postoperative transverse myelitis of the spine that has not responded to traditional multidisciplinary treatment. However, it is unknown whether tSCS can reduce ZAP complicated with myelitis. Methodology: Between January 2020 and April 2022, all patients with HZ who visited our pain clinic with spinal cord edema and who underwent tSCS were enrolled in this study; their medical records were retrospectively examined. Pain intensity was assessed at baseline (before initiating interventional procedures), just before tSCS, after tSCS removal, and one and three months after tSCS. Results: Twelve patients were enrolled. The mean Numerical Rating Scale (NRS) was 7.9 ± 1.6 at baseline (before interventional procedures), 6.8 ± 2.2 before tSCS (after interventional procedures), and 3.5 ± 2.4 after tSCS. Compared with before tSCS, the mean NRS decreased to 3.3 ± 2.3 after tSCS (P= 0.0004). The mean NRS changes with interventional procedures before and after tSCS were -1.2 ± 2.2 (P =0.0945) and 3.3 ± 2.3 (P= 0.0004), respectively; the change after tSCS was significantly higher (between-group difference: -2.1 ± 3.7; P= 0.0324). Conclusions: Temporary SCS alleviated pain in cases of shingles with myelitis refractory to interventional therapy. Even in cases with myelitis, tSCS for ZAP remains an effective wayto prevent PHN.

Spinal Lymphatic Dysfunction Aggravates the Recovery Process After Spinal Cord Injury

We aimed to evaluate the role of the spinal lymphatic system in spinal cord injury and whether it has an impact on recovery after spinal cord injury. Flow cytometry was used to evaluate the changes in the number of microvesicles after spinal cord injury. Evans blue extravasation was used to evaluate the function of the lymphatic system. Evans blue extravasation and immunofluorescence were used to evaluate the permeability of blood spinal cord barrier. The spinal cord edema was evaluated by dry and wet weight.Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay was used to evaluate apoptosis after spinal cord injury. Nuclear factor-kappa B pathway was detected by Western blot. Behavioral tests were used to evaluate limb function. Microvesicles released after spinal cord injury can enter the thoracic duct and then enter the blood through the lymph around the spine. After ligation of the thoracic duct, it can aggravate the neuropathological manifestations and limb function after spinal cord injury. The potential mechanism may involve nuclear factor-kappa B pathway.

Radiology diagnostics of spinal corel injury in early children: a prospective study

INTRODUCTION: Spinal cord injury (SCI) in young children includes a relatively higher prevalence of cervical spine injury, multiple thoracic vertebral compression fractures, and spinal cord injury. Spinal cord injuries without radiological changes/signs of fractures or dislocations (SCIWORA) also occur in young children. X-ray assessment of damage to immature vertebrae and cartilage in young children is difficult, since incompletely formed vertebral bodies can be confused with fractures. Accordingly, an MRI is required, which provides a detailed anatomical image of all structures of the spinal column and also diagnoses damage to the spinal cord, ligaments and muscles.OBJECTIVE: To investigate the possibilities of methods of radiation diagnosis of spinal cord injury in young children (up to 3 years).MATERIAL AND METHODS: 20 children aged from 11 months up to 3 years old were studied with spinal cord injury. X-ray, computed tomography (CT) and magnetic resonance imaging (MRI) were performed. The standard MRI protocol for SCI in children under 3 years of age included: MR myelography in the coronary and sagittal projections, sagittal projection STIR, DTI and T2WI FS SE, axial projection T2WI FS SE or T2*WI FS GE; coronary projection T2WI SE; 3D T1WI FS GE before and after contrast enhancement.RESULTS: An analysis of the data of patients included in the category of polytrauma was carried out. The causes of SCI in these patients were road accidents and falls from various heights. X-ray and CT scans were uninformative, and had large discrepancies with MRI results. All anatomical and morphological changes revealed by MRI correlated well with clinical manifestations and corresponded to the classification of the level and severity of spinal cord injury (ASIA). An increase in the volume and change in the signal of the spinal cord due to edema and / or hemorrhage in the spinal cord is the main sign of damage to the spinal cord, and is best indicated on T2WI and STIR, as a hyperintense signal.DISCUSSION: MRI is critical in the emergency assessment of spinal cord injury or compression to predict the outcome of SCI. There is currently no spinal cord imaging technique that can compete with MRI. Increased volume and signal changes in the spinal cord due to edema and/or hemorrhage are a sign of spinal cord injury and are best demonstrated on T2WI and STIR as a hyperintense signal. Incomplete spinal cord injury is also manifested by a hyperintense signal on T2WI and/or FLAIR, which in intensity and extent correlates with the degree of injury. Hemorrhagic injuries are better detected using T2*GRE or SWI, and spinal cord edema is better detected using T2WI SE and STIR. In addition, STIR can identify bone marrow edema in injured vertebrae, even when the injury is not detected on CT.CONCLUSION: When performing MRI in patients with SCI, three quantitative parameters should be assessed: the maximum damage to the spinal cord, the maximum compression of the spinal cord, and the length of the affected area. In addition to the results of quantitative parameters, potential predictive qualitative MRI findings should be evaluated such as intramedullary hemorrhage, focal and diffuse spinal cord edema, soft tissue injury, probable stenosis before injury, and disc herniation.

Treg cells-derived exosomes promote blood-spinal cord barrier repair and motor function recovery after spinal cord injury by delivering miR-2861

The blood-spinal cord barrier (BSCB) is a physical barrier between the blood and the spinal cord parenchyma. Current evidence suggests that the disruption of BSCB integrity after spinal cord injury can lead to secondary injuries such as spinal cord edema and excessive inflammatory response. Regulatory T (Treg) cells are effective anti-inflammatory cells that can inhibit neuroinflammation after spinal cord injury, and their infiltration after spinal cord injury exhibits the same temporal and spatial characteristics as the automatic repair of BSCB. However, few studies have assessed the relationship between Treg cells and spinal cord injury, emphasizing BSCB integrity. This study explored whether Treg affects the recovery of BSCB after SCI and the underlying mechanism. We confirmed that spinal cord angiogenesis and Treg cell infiltration occurred simultaneously after SCI. Furthermore, we observed significant effects on BSCB repair and motor function in mice by Treg cell knockout and overexpression. Subsequently, we demonstrated the presence and function of exosomes in vitro. In addition, we found that Treg cell-derived exosomes encapsulated miR-2861, and miR-2861 regulated the expression of vascular tight junction (TJs) proteins. The luciferase reporter assay confirmed the negative regulation of IRAK1 by miR-2861, and a series of rescue experiments validated the biological function of IRAKI in regulating BSCB. In summary, we demonstrated that Treg cell-derived exosomes could package and deliver miR-2861 and regulate the expression of IRAK1 to affect BSCB integrity and motor function after SCI in mice, which provides novel insights for functional repair and limiting inflammation after SCI.

Clinical manifestations and magnetic resonance imaging features of spinal cord infarction

Background and ObjectiveSpinal cord infarction (SCI) is a rare type of stroke, with no proposed classification or diagnostic criterium widely accepted and used in daily clinical practice currently. We try to explore the clinical manifestations and MRI features of SCI for improving the accurate diagnosis of SCI. MethodsRetrospectively analyzed the clinical data, MRI features, laboratory findings and outcomes of 40 patients who had been consecutively diagnosed with SCI in our hospital from June 2016 to January 2022. ResultsMost of the SCI (92.5%) occurred at the level of T8-L2 and C4-T4. Transverse infarction (52.5%) and ASA territory infarction (27.5%) were the most common patterns. Longitudinally extensive lesions were noticed in 67.5% of the SCI and it might be a risk factor of poor prognosis (OR=21.11, 95%CI 2.14-208.29). Restricted diffusion of the SCI lesion occurred in 8h and a few lasted up to 60 days. All SCI showed spinal cord edema, accompanied by enhancement of the ventral cauda equina (13.8%), weakened enhancement of the dorsal venous plexus (44.8%), and vertebral infarction (25%). Most patients developed a stroke-like onset (92.5%) after movement (57.5%), with definite pain in the trunk or limbs (67.5%) and dissociative sensory disturbance (60.0%). The main etiologies of them include vascular abnormalities (45%) and iatrogenic injuries (15%). ConclusionAn MRI classification of SCI based on the spinal cord blood supply was proposed. Restricted diffusion and co-existing abnormality of vertebral body and cauda equina may be the key neuroimaging feature for SCI diagnosis. Detailed history of vascular diseases or triggering factors are also helpful.

A Case Report of Spinal Cord Edema and Cervical Spondylosis Masquerading as Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

A 64-year-old previously-healthy male presented with 2-year history of progressive neurological symptoms of numbness and muscle weakness involving all 4 limbs. There was gait disturbance, urinary and fecal incontinence. On examination, the left upper limb had normal tone, diminished deep tendon reflexes and power of 4/5 with wasting both in proximal and distal muscles. There were reduced pinprick pain and temperature sensations below the elbow bilaterally with intact vibration and proprioception. Both lower limbs had increased tone, diminished deep tendon reflexes, power of 3/5 with wasting both in proximal and distal muscles with unequivocal plantar reflex bilaterally. There were reduced pinprick pain and temperature sensations below the knee on right and below the ankle on left with intact vibration and proprioception. Nerve Conduction Studies (NCS) were done which showed axonal type of denervation in all limbs. MRI scan of Cervical Spine showed T2W hyperintense signals and narrowing of spinal canal from C3 to C7 region. The final diagnosis was spinal cord edema in the cervical region and cervical spondylosis causing spinal cord compression. Keywords: Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Spinal cord edema, Cervical spondylosis, Nerve Conduction Studies (NCS), MRI scan, Case report.

Xenon postconditioning attenuates neuronal injury after spinal cord ischemia/reperfusion injury by targeting endoplasmic reticulum stress-associated apoptosis.

The purpose of the study is to explore the underlying mechanisms of xenon (Xe) which protects against spinal cord ischemia/reperfusion injury (SCIRI). A SCIRI rat model was induced by abdominal artery occlusion for 85 min and reperfusion. Xe postconditioning (50% Xe) was administered 1 h after 1 h of reperfusion. At reperfusion time points (2, 4, 6, and 24 h), rats were treated with spinal cord scans by MRI to assess the time of peak spinal cord injury after SCIRI. Subsequently, endoplasmic reticulum (ER) stress inhibitor sodium 4-phenylbutyrate (4-PBA) was administered by daily intraperitoneal injection (50 mg/kg) for 5 days before SCIRI. At 4 h after reperfusion, motor function, immunofluorescence staining, hematoxylin and eosin (HE) staining, Nissl staining, TUNEL staining, real-time reverse transcription polymerase chain (RT-PCR) reaction, and western blot analyses were performed to investigate the protective effects of Xe against SCIRI. In the rat I/R model, spinal cord edema peaked at reperfusion 4 h. SCIRI activated ER stress, which was located in neurons. Xe postconditioning remarkably alleviated hind limb motor function, reduced neuronal apoptosis rate, increased the number of normal neurons, and inhibited the expression of ER stress-related protein in spinal cord. Furthermore, the administration of the ER stress inhibitor 4-PBA strongly decreased ER stress-induced apoptosis following SCIRI. Xe postconditioning inhibits ER stress activation, which contributes to alleviate SCIRI by suppressing neuronal apoptosis.

92. Intrathecal pressure, spinal cord compression and edema following traumatic spinal cord injury in a porcine model

92. Intrathecal pressure, spinal cord compression and edema following traumatic spinal cord injury in a porcine model

Hematomyelia associated with coronavirus disease 2019: A rare case report.

Coronavirus disease 2019 (COVID-19) can damage the central nervous system. Although there have been reports of cerebral hemorrhage and infarction caused by COVID-19, hematomyelia due to COVID-19 has never been reported. A 40-year-old male was admitted to the hospital with positive nucleic acid detection for COVID-19 after experiencing fever for 2 weeks, urinary retention, fecal retention, and pain in both lower extremities for a week. The patient diagnosis was established using thoracic and lumbar magnetic resonance imaging (MRI). Contrast-enhanced thoracic and lumbar MRI revealed subdural (dorsal predominant) short T1 and slightly long T2 bands in the T12-S2 infundibular canal in the scan field, and the subdural hematoma was yet to be distinguished from other diseases. Spinal cord edema was observed in the left vertebral plate and facet joint of the T11 vertebral body, indicative of inflammation. The cerebrospinal fluid (CSF) was positive for COVID-19 nucleic acid. Antiinfection, immunomodulation, correction of acid-base balance and electrolyte disorders, improvement of circulation, nerve nutrition, and other symptomatic supportive treatments were administered to the patient. The patient symptoms significantly improved after 4 weeks of anti-infection and immunomodulatory therapy. Repeat thoracolumbar MRI revealed absorption of the spinal cord hematoma, and the patient was discharged from the hospital. To date, COVID-19-related hematomyelia has not been reported and anti-infective and immunomodulatory therapies may be effective. COVID-19 not only easily leads to brain injury but can also cause spinal cord injury and even spinal cord hemorrhage. When patients with COVID-19 experience symptoms and signs of spinal cord injury, spinal cord injury and bleeding caused by COVID-19 should be considered, and MRI and lumbar puncture should be performed as soon as possible to make a clear diagnosis.

B-Cell Lymphoma Intramedullary Tumor: Case Report and Systematic Review.

Intramedullary tumors represent the major cause of spinal cord injuries, and its symptoms include pain and weakness. Progressive weakness may concomitantly occur in the upper and lower limbs, along with lack of balance, spine tenderness, sensory loss, trophic changes of extremity, hyperreflexia, and clonus. The study protocol was in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. A systematic search of the MEDLINE electronic database was performed to identify the studies reporting the clinical features of children and adults who presented with an intramedullary lymphoma. Twenty-one studies were included, reporting 25 cases. Manuscripts were excluded if the full-text article was not available, original data were not reported (e.g., review articles), or if the main disease was not intramedullary lymphoma. A structured data extraction form was employed to standardize the identification and retrieval of data from manuscripts. To enlighten the discussion, a case is also presented. An 82-year-old woman with Fitzpatrick skin type II, diagnosed and treated for non-Hodgkin's lymphoma 7 years ago, was admitted with mental confusion and memory loss for the past 2 months-evolving with recurring falls from her own height. One day before admission, she displayed Brown-Séquard syndrome. An expansive lesion from C2 to C4 in the cervical spinal cord was found and a hypersignal spinal cord adjacent was described at the bulb medullary transition to the C6-C7 level. A primary spinal cord tumor was considered, as well as a melanoma metastasis, due to the lesion's flame pattern. The patient presented a partial recovery of symptoms and a reduction of the spinal cord edema after being empirically treated with corticosteroids, but the lesion maintained its extent. Subsequently, a large diffuse B-cell lymphoma with nongerminal center was found in open body biopsy, infiltrating neural tissue. The main objective of the present study is to report a surgical case treated for a large diffuse B-cell lymphoma, in addition to presenting the results of a systematic review of primary intramedullary spinal cord lymphoma.

Astaxanthin ameliorates spinal cord edema and astrocyte activation via suppression of HMGB1/TLR4/NF-κB signaling pathway in a rat model of spinal cord injury.

Spinal cord edema is a quick-onset phenomenon with long-term effects. This complication is associated with inflammatory responses, as well as poor motor function. No effective treatment has been developed against spinal edema, which urges the need to provide novel therapies. Astaxanthin (AST) is a fat-soluble carotenoid with anti-inflammatory effects and a promising candidate for treating neurological disorders. This study aimed to investigate the underlying mechanism of AST on the inhibition of spinal cord edema, astrocyte activation, and reduction of inflammatory responsesin a rat compression spinal cord injury (SCI) model. Male rats underwent laminectomy at thoracic 8-9, and the SCI model was induced using an aneurysm clip. After SCI, rats received dimethyl sulfoxide or AST via intrathecal injection. The effects of AST were examined on the motor function, spinal cord edema, integrity of blood-spinal cord barrier (BSCB), and expression of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), glial fibrillary acidic protein (GFAP), and aquaporin-4 (AQP4), and matrix metallopeptidase- 9 (MMP-9) post-SCI. We showed that AST potentially improved the recovery of motor function and inhibited the spinal cord edema via maintaining the integrity of BSCB, reducing the expression of HMGB1, TLR4, and NF-κB, MMP-9 as well as downregulation of astrocyte activation (GFAP) and AQP4 expression. AST improves motor function and reduces edema and inflammatory responses in the spinal tissue. These effects are mediated by suppression of the HMGB1/TLR4/NF-κB signaling pathway, suppressing post-SCI astrocyte activation, and decreasing AQP4 and MMP-9 expression.