Convolutional neural network-based magnetic resonance image differentiation of filum terminale ependymomas from schwannomas.

PURPOSE: Preoperative diagnosis of filum terminale ependymomas (FTEs) versus schwannomas is difficult but essential for surgical planning and prognostic assessment. With the advancement of deep-learning approaches based on convolutional neural networks (CNNs), the aim of this study was to determine whether CNN-based interpretation of magnetic resonance (MR) images of these two tumours could be achieved. METHODS: Contrast-enhanced MRI data from 50 patients with primary FTE and 50 schwannomas in the lumbosacral spinal canal were retrospectively collected and used as training and internal validation datasets. The diagnostic accuracy of MRI was determined by consistency with postoperative histopathological examination. T1-weighted (T1-WI), T2-weighted (T2-WI) and contrast-enhanced T1-weighted (CE-T1) MR images of the sagittal plane containing the tumour mass were selected for analysis. For each sequence, patient MRI data were randomly allocated to 5 groups that further underwent fivefold cross-validation to evaluate the diagnostic efficacy of the CNN models. An additional 34 pairs of cases were used as an external test dataset to validate the CNN classifiers. RESULTS: After comparing multiple backbone CNN models, we developed a diagnostic system using Inception-v3. In the external test dataset, the per-examination combined sensitivities were 0.78 (0.71-0.84, 95% CI) based on T1-weighted images, 0.79 (0.72-0.84, 95% CI) for T2-weighted images, 0.88 (0.83-0.92, 95% CI) for CE-T1 images, and 0.88 (0.83-0.92, 95% CI) for all weighted images. The combined specificities were 0.72 based on T1-WI (0.66-0.78, 95% CI), 0.84 (0.78-0.89, 95% CI) based on T2-WI, 0.74 (0.67-0.80, 95% CI) for CE-T1, and 0.81 (0.76-0.86, 95% CI) for all weighted images. After all three MRI modalities were merged, the receiver operating characteristic (ROC) curve was calculated, and the area under the curve (AUC) was 0.93, with an accuracy of 0.87. CONCLUSIONS: CNN based MRI analysis has the potential to accurately differentiate ependymomas from schwannomas in the lumbar segment.

Acquired tonsillar herniation related to spontaneous intracranial hypotension: case reports.

Background: Acquired prolapse of the cerebellar tonsils in spontaneous intracranial hypotension (SIH) patients is rare. This study aims to evaluate neuroimaging changes of acquired prolapse of the cerebellar tonsils below the foramen magnum in SIH patients due to spontaneous spinal cerebrospinal fluid leakage, which was treated by targeted epidural blood patches (EBP). Methods: We retrospectively reviewed clinical and neuroimaging characteristics of 5 cases of SIH with acquired prolapse of the cerebellar tonsils that received targeted EBP in our institution from January 2013 to December 2016. Results: Of these SIH patients, all of them suffered from an orthostatic headache. Initial cranial MRI demonstrated descent of the cerebellar tonsils ≥5 mm. Intrathecal gadolinium-enhanced spinal MR myelography and/or spinal MR hydrography were performed to evaluate the level of spinal cerebrospinal fluid leakage. Symptoms were alleviated in all 5 patients after two (n = 4), or three (n = 1) targeted EBP during hospitalization. Follow-up cranial MRI revealed that the descent of cerebellar tonsils was reversed after EBP treatment. Conclusion: Acquired tonsillar herniation can occur in patients with SIH and spinal cerebrospinal fluid leakage. Symptoms of these patients may be resolved and radiologic findings may be reversed after EBP treatment.

Percutaneous Full Endoscopic Management of Spinal Foraminal Schwannomas: Case Series.

BACKGROUND: Schwannoma, a benign peripheral nerve sheath tumor, is perhaps only secondary to degenerative pathology as the most common lesion at neural foramen. The surgical dilemma here is either risking nerve injury because of inadequate exposure or the need for internal fixation because of facet joint sacrifice. OBJECTIVE: To evaluate the feasibility and safety of management of foraminal schwannomas by percutaneous full-endoscopic technique. METHODS: A single-center retrospective review was conducted on patients who underwent full-endoscopic resection of neural foraminal schwannomas. Tumors were grouped into either medial type or lateral type based on relevant location to the neural foramen, and respective surgical approaches were adopted. Data including preoperative neurological status, tumor size, surgery time, the extension of resection, and clinical outcomes were collected. The learning curve was plotted as surgical time/tumor size against case number. RESULTS: A total of 25 patients were treated between May 2015 and March 2022. Gross total resection was achieved in 24 patients, and near-total resection in 1 case, with 1 patient experienced transient voiding difficulty. No tumor recurrence or spinal instability was detected in the short-term follow-up (median follow-up 22 months, range 3 months-6 years). Surgical efficiency improved with the number of cases operated on and remained stable after the initial 10 cases. CONCLUSION: Percutaneous full-endoscopic technique is a safe and minimally invasive technique for the resection of foraminal schwannomas.

Prognostic Factors and Treatments Efficacy in Spontaneous Spinal Epidural Hematoma: A Multicenter Retrospective Study.

BACKGROUND AND OBJECTIVES: Spontaneous spinal epidural hematoma (SSEH) is an uncommon but serious condition with a high morbidity rate. Although SSEH is related to numerous risk factors, its etiology remains unclear. There is a paucity of data on its prognostic factors. We aim to evaluate prognostic factors for SSEH in this study. METHOD: A retrospective study was performed on patients who were admitted for SSEH in 3 academic neurosurgical centers from January 2010 to June 2021. Clinical parameters, including clinical condition on admission, anticoagulants use, imaging modality, the timing and type of surgery performed, and outcomes, were collected. Prognostic factors were analyzed. The Frankel scale was used to assess the clinical condition. RESULTS: A total of 105 patients with SSEH were retrieved from medical records, with a mean age of 51.3 years. Eighty-three patients (79%) complained of acute onset of severe neck or back pain. Eighty-two patients (78%) suffered from moderate to severe neurologic deficits (Frankel scale A-C). Anticoagulation usage was found in 20% of cases. Lower thoracic spine (p = 0.046), use of anticoagulants (p = 0.019), sphincter function disfunction (p = 0.008), severe neurologic deficits at admission (p < 0.001), and rapid deterioration (<1 hour, p = 0.004) were found to be associated with poor outcomes. Surgical decompression was performed in 74 (70%) cases. The univariate and multivariate analysis revealed that preoperative severe neurologic deficits (p = 0.005) and extended paraplegia time (>12 hours, p = 0.004) were independent adverse prognostic factors. The univariate analysis revealed that lower thoracic spine location (p = 0.08) and rapid progression (<6 hours, p = 0.005) were correlated with poor prognosis, but the multivariate analysis failed to identify them as independent prognostic factors. DISCUSSION: Adverse prognostic factors for SSEH might include thoracic segment location, use of anticoagulation, severe neurologic deficits on admission, sphincter dysfunction, and rapid progression. Preoperative neurologic deficit and extended paraplegia time were strongly correlated with the prognosis in the subset of patients who underwent surgical decompression. Timely surgical decompression is recommended for patients with moderate/severe neurologic deficits or progressive neurologic deterioration.

Mast Cells Mediate Inflammatory Injury and Aggravate Neurological Impairment in Experimental Subarachnoid Hemorrhage Through Microglial PAR-2 Pathway.

Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with high mortality and disability. Aberrant neuroinflammation has been identified as a critical factor accounting for the poor prognosis of SAH patients. Mast cells (MCs), the sentinel cells of the immune system, play a critical in the early immune reactions and participate in multiple pathophysiological process. However, the exact role of MCs on the pathophysiological process after SAH has not been fully understood. The current study was conducted to determine the role of MCs and MC stabilization in the context of SAH. Mouse SAH model was established by endovascular perforation process. Mice received saline or cromolyn (MC stabilizer) or compound 48/80 (MCs degranulator). Post-SAH evaluation included neurobehavioral test, western blot, immunofluorescence, and toluidine blue staining. We demonstrated that SAH induced MCs activation/degranulation. Administration of MC stabilizer cromolyn conferred a better neurologic outcome and decreased brain edema when compared with SAH+vehicle group. Furthermore, cromolyn significantly inhibited neuroinflammatory response and alleviated neuronal damage after SAH. However, pharmacological activation of MCs with compound 48/80 dramatically aggravated SAH-induced brain injury and exacerbated neurologic outcomes. Notably, pharmacological inhibition of microglial PAR-2 significantly reversed MCs-induced inflammatory response and neurological impairment. Additionally, the effect of MCs-derived tryptase in mediating neuroinflammation was also abolished by the microglial PAR-2 blockage in vitro. Taken together, MCs yielded inflammatory injury through activating microglia-related neuroinflammation after SAH. These data shed light on the notion that MCs might be a novel and promising therapeutic target for SAH.

Celastrol protects against early brain injury after subarachnoid hemorrhage in rats through alleviating blood-brain barrier disruption and blocking necroptosis.

BACKGROUND: Subarachnoid hemorrhage (SAH) is a life-threatening disease worldwide, and effective pharmaceutical treatment is still lacking. Celastrol is a plant-derived triterpene which showed neuroprotective potential in several types of brain insults. This study aimed to investigate the effects of celastrol on early brain injury (EBI) after SAH. METHODS: A total of sixty-one male Sprague-Dawley rats were used in this study. Rat SAH endovascular perforation model was established to mimic the pathological changes of EBI after SAH. Multiple methods such as 3.0T MRI scanning, immunohistochemistry, western blotting and propidium iodide (PI) labeling were used to explore the therapeutic effects of celastrol on SAH. RESULTS: Celastrol treatment attenuated SAH-caused brain swelling, reduced T2 lesion volume and ventricular volume in MRI scanning, and improved overall neurological score. Albumin leakage and the degradation of tight junction proteins were also ameliorated after celastrol administration. Celastrol protected blood-brain bairrer integrity through inhibiting MMP-9 expression and anti-neuroinflammatory effects. Additionally, necroptosis-related proteins RIP3 and MLKL were down-regulated and PI-positive cells in the basal cortex were less in the celastrol-treated SAH group than that in untreated SAH group. CONCLUSIONS: Celastrol exhibits neuroprotective effects on EBI after SAH and deserves to be further investigated as an add-on pharmaceutical therapy.

Intradural osteomas: Report of two cases.

BACKGROUND: Intradural osteoma is very rarely located in the subdural or subarachnoid space. Unfortunately, intradural osteoma lacks specificity in clinical manifestations and imaging features and there is currently no consensus on its diagnosis method or treatment strategy. Moreover, the pathogenesis of osteoma without skull structure involvement remains unclear. CASE SUMMARY: We describe two cases of intradural osteomas located in the subdural and subarachnoid spaces, respectively. The first case involved a 47-year-old woman who presented with a 3-year history of intermittent headache and dizziness. Intraoperatively, a bony hard mass was found in the left frontal area, attached to the inner surface of the dura mater and compressing the underlying arachnoid membrane and brain. The second case involved a 56-year-old woman who had an intracranial high-density lesion isolated under the right greater wing of the sphenoid. Intraoperatively, an arachnoid-covered bony tumor was found in the sylvian fissure. The pathological diagnosis for both patients was osteoma. CONCLUSION: Surgery and pathological examination are required for diagnosis of intradural osteomas, and craniotomy is a safe and effective treatment.

Intracranial hypertension due to spinal cord tumor misdiagnosed as pseudotumor cerebri syndrome: case report.

BACKGROUND: Isolated onset of intracranial hypertension due to spinal cord tumor is rare, thus, easily leading to misdiagnosis and delay in effective treatment. CASE PRESENTATION: Herein, we describe a 45-year-old female patient who manifested isolated symptoms and signs of intracranial hypertension and whose condition was initially diagnosed as idiopathic intracranial hypertension and transverse sinus stenosis. The patient received a stent implantation; however, no improvements were observed. One year later her symptoms exacerbated, and during rehospitalization a spinal imaging examination revealed a lumbar tumor. Pathologic evaluation confirmed schwannoma, and tumor resection significantly improved her symptoms, except for poor vision. CONCLUSIONS: Space-occupying lesions of the spine should be considered in the differential diagnosis of idiopathic intracranial hypertension, even in the absence of spine-localized signs or symptoms.

6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase Suppresses Neuronal Apoptosis by Increasing Glycolysis and "cyclin-dependent kinase 1-Mediated Phosphorylation of p27 After Traumatic Spinal Cord Injury in Rats.

Apoptosis is a vital pathological factor that accounts for the poor prognosis of traumatic spinal cord injury (t-SCI). The 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) is a critical regulator for energy metabolism and proven to have antiapoptotic effects. This study aimed to investigate the neuroprotective role of PFKFB3 in t-SCI. A compressive clip was introduced to establish the t-SCI model. Herein, we identified that PFKFB3 was extensively distributed in neurons, and PFKFB3 levels significantly increased and peaked 24 h after t-SCI. Additionally, knockdown of PFKFB3 inhibited glycolysis, accompanied by aggravated neuronal apoptosis and white matter injury, while pharmacological activation of PFKFB3 with meclizine significantly enhanced glycolysis, attenuated t-SCI-induced spinal cord injury, and alleviated neurological impairment. The PFKFB3 agonist, meclizine, activated cyclin-dependent kinase 1 (CDK1) and promoted the phosphorylation of p27, ultimately suppressing neuronal apoptosis. However, the neuroprotective effects of meclizine against t-SCI were abolished by the CDK1 antagonist, RO3306. In summary, our data demonstrated that PFKFB3 contributes robust neuroprotection against t-SCI by enhancing glycolysis and modulating CDK1-related antiapoptotic signals. Moreover, targeting PFKFB3 may be a novel and promising therapeutic strategy for t-SCI.

Flexible endoscope visualization to assist in the removal of a string of 10 schwannomas at the cauda equina: technical case report.

Bead-like schwannomas at the cauda equina are rare but benign intraspinal tumors. They can involve multiple nerve roots and spread within the spinal canal, and open resection would cause significant trauma. The authors have successfully applied a novel minimally invasive technique for the total removal of such schwannomas. A 68-year-old woman presented with a 1-month history of left waist and leg pain. MRI demonstrated multiple intraspinal lesions located from L1 to S1. The diagnosis was bead-like schwannomas at the cauda equina. Two incisions were made at the T12 and L5 levels. A flexible endoscope was introduced into the spinal canal following hemisemilaminectomy under a microscope to identify the relationship between the tumors and the carrying nerves. After dissecting both cranial and caudal ends of the carrying nerve, the string of bead-like tumors was gently pulled out from the caudal end as a whole. The endoscope was reintroduced into the spinal canal to ensure complete tumor removal. The patient recovered quickly, and no tumor residual was found at postoperative MRI. Flexible endoscope-assisted visualization plus microscopic hemisemilaminectomy via 2 incisions is a feasible minimally invasive approach for selected patients with bead-like schwannomas at the cauda equina.

Stimulator of IFN genes mediates neuroinflammatory injury by suppressing AMPK signal in experimental subarachnoid hemorrhage.

BACKGROUND: Neuroinflammation is closely associated with the poor prognosis in subarachnoid hemorrhage (SAH) patients. This study was aimed to determine the role of stimulator of IFN genes (STING), an essential regulator to innate immunity, in the context of SAH. METHODS: A total of 344 male C57BL/6 J mice were subjected to endovascular perforation to develop a model of SAH. Selective STING antagonist C-176 and STING agonist CMA were administered at 30 min or 1 h post-modeling separately. To investigate the underlying mechanism, the AMPK inhibitor compound C was administered intracerebroventricularly at 30 min before surgery. Post-SAH assessments included SAH grade, neurological test, brain water content, western blotting, RT-PCR, and immunofluorescence. Oxygenated hemoglobin was introduced into BV2 cells to establish a SAH model in vitro. RESULTS: STING was mainly distributed in microglia, and microglial STING expression was significantly increased after SAH. Administration of C-176 substantially attenuated SAH-induced brain edema and neuronal injury. More importantly, C-176 significantly alleviated both short-term and persistent neurological dysfunction after SAH. Meanwhile, STING agonist CMA remarkably exacerbated neuronal injury and deteriorated neurological impairments. Mechanically, STING activation aggravated neuroinflammation via promoting microglial activation and polarizing into M1 phenotype, evidenced by microglial morphological changes, as well as the increased level of microglial M1 markers including IL-1ß, iNOS, IL-6, TNF-α, MCP-1, and NLRP3 inflammasome, while C-176 conferred a robust anti-inflammatory effect. However, all the mentioned beneficial effects of C-176 including alleviated neuroinflammation, attenuated neuronal injury and the improved neurological function were reversed by AMPK inhibitor compound C. Meanwhile, the critical role of AMPK signal in C-176 mediated anti-inflammatory effect was also confirmed in vitro. CONCLUSION: Microglial STING yielded neuroinflammation after SAH, while pharmacologic inhibition of STING could attenuate SAH-induced inflammatory injury at least partly by activating AMPK signal. These data supported the notion that STING might be a potential therapeutic target for SAH.

Lack of association between insulin resistance as estimated by homeostasis model assessment and stroke risk: A systematic review and meta-analysis.

Epidemiologic studies have reported conflicting results on the association between insulin resistance and risk of stroke. This meta-analysis sought to evaluate the association between homeostasis model assessment-insulin resistance (HOMA-IR) and risk of stroke. Eligible studies were identified by searching PubMed and Emabse databases up to December 2018. Prospective observational studies investigating the association between HOMA-IR and incident stroke were included. Seven studies involving 36,343 participants were identified. The pooled risk ratio (RR) of stroke was 1.29 (95% confidence intervals [CI] 0.89-1.87) for the highest versus the lowest HOMA-IR category. Similarly, individuals with insulin resistance did not significantly increase the risk of ischemic stroke (RR 1.65; 95%CI 0.76-3.56). Likewise, insulin resistance was also not associated with higher risk of stroke in the general population (RR 1.38; 95%CI 0.88-2.18) and non-diabetic population subgroup (RR 1.76; 95%CI 0.71-4.35). This meta-analysis suggests lack of association between HOMA-IR and risk of stroke. However, interpretation of these findings should be with caution due to the small number of studies analyzed and significant heterogeneity across studies.

The Neuroprotective Effects of Necrostatin-1 on Subarachnoid Hemorrhage in Rats Are Possibly Mediated by Preventing Blood-Brain Barrier Disruption and RIP3-Mediated Necroptosis.

Despite the substantial efforts to elucidate the role of early brain injury in subarachnoid hemorrhage (SAH), an effective pharmaceutical therapy for patients with SAH continues to be unavailable. This study aims to reveal the role of necroptosis after SAH, and explore whether the disruption of the blood-brain barrier (BBB) and RIP3-mediated necroptosis following SAH in a rat SAH model are altered by necrostatin-1 via its selective inhibition of receptor-interacting protein kinase 1 (RIP1). Sixty-five rats were used in the experiments. The SAH model was established using endovascular perforation. Necrostatin-1 was intracerebroventricularly injected 1 h before SAH induction. The neuroprotective effects of necrostatin-1 were evaluated with multiple methods such as magnetic resonance imaging (MRI) scanning, immunohistochemistry, propidium iodide (PI) labeling, and western blotting. Pretreatment with necrostatin-1 attenuated brain swelling and reduced the lesion volume on T2 sequence and ventricular volume on MRI 72 h after SAH induction. Albumin leakage and the degradation of tight junction proteins were also ameliorated by necrostatin-1 administration. In addition, necrostatin-1 decreased the number of PI-positive cells in the basal cortex, reduced the levels of the RIP3 and MLKL proteins, and inhibited the production of the pro-inflammatory cytokines IL-1ß, IL-6, and TNF-α. Based on the findings from the present study, the selective RIP1 inhibitor necrostatin-1 functioned as a neuroprotective agent after SAH by attenuating brain swelling and BBB disruption. Moreover, the necrostatin-1 pretreatment prevented SAH-induced necroptosis by suppressing the activity of the RIP3/MLKL signaling pathway. These results will provide insights into new drugs and pharmacological targets to manage SAH, which are worth further study.

Natrium Benzoate Alleviates Neuronal Apoptosis via the DJ-1-Related Anti-oxidative Stress Pathway Involving Akt Phosphorylation in a Rat Model of Traumatic Spinal Cord Injury.

This study aimed to explore the neuroprotective effects and mechanisms of natrium benzoate (NaB) and DJ-1 in attenuating reactive oxygen species (ROS)-induced neuronal apoptosis in traumatic spinal cord injury (t-SCI) in rats. T-SCI was induced by clip compression. The protein expression and neuronal apoptosis was evaluated by Western blotting, double immunofluorescence staining and transmission electron microscope (TEM). ROS level, spinal cord water content (SCWC) and Evans blue (EB) extravasation was also examined. Locomotor function was evaluated by Basso, Beattie, and Bresnahan (BBB) and inclined plane test (IPT) scores. We found that DJ-1 is expressed in spinal cord neurons and increased after t-SCI. At 24 h post-injury, the levels of DJ-1, p-Akt, SOD2, ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3 increased, while the Bcl-2/Bax ratio decreased. NaB upregulated DJ-1, p-Akt, and SOD2, decreased ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3, and increased the Bcl-2/Bax ratio, which were reversed by DJ-1 siRNA. The proportion of CC-3- and TUNEL-positive neurons also increased after t-SCI and was reduced by NaB. These effects were reversed by MK2206. Moreover, the level of oxDJ-1 increased after t-SCI, which was decreased by DJ-1 siRNA, NaB or the combination of them. NaB also reduced mitochondrial vacuolization, SCWC and EB extravasation, and improved locomotor function assessed by the BBB and IPT scores. In conclusion, NaB increased DJ-1, and thus reduced ROS and ROS-induced neuronal apoptosis by promoting Akt phosphorylation in t-SCI rats. NaB shows potential as a therapeutic agent for t-SCI, with DJ-1 as its main target.

Utilizing real-time contrast medium to detect the fistula of giant spinal arachnoid cyst and treat with minimal invasive surgery.

BACKGROUND: Spinal arachnoid cysts are rare and have varied clinical manifestations depending on the affected spinal region and nerve roots. A complete cyst excision with fistula closure is the first choice of treatment. However, it might be difficult to localize the specific position of the fistula because previous images have no enhancements or the fistula is too tiny to be detected. CASE PRESENTATION: This case is a giant lumbar extradural arachnoid cyst. We administered a lumbar injection with contrast medium into subarachnoid space under digital subtraction angiography (DSA) and disclosed the fistula. Confirming the location of fistula enabled us to perform minimally invasive surgery to ligate the fistula. Surgical intervention for a spinal arachnoid cyst might encounter the problem of the formation of a postoperative cerebrospinal fluid (CSF) fistula. We propose the option of detecting the fistula preoperatively for minimal invasive surgery. Recurrence depends on the long-term follow-up, and more cases are needed to further evaluate our technique. CONCLUSIONS: The real-time contrast medium technique for spinal arachnoid cysts contributes to the complete ligation with minimally invasive surgery.

MANF attenuates neuronal apoptosis and promotes behavioral recovery via Akt/MDM-2/p53 pathway after traumatic spinal cord injury in rats.

The aim of this study was to investigate the potential effect and mechanism of action of MANF in attenuating neuronal apoptosis following t-SCI. A clip compressive model was used to induce a crush injury of the spinal cord in a total of 230 rats. The Basso, Beattie, and Bresnahan (BBB) score, spinal cord water content, and blood spinal cord barrier (BSCB) permeability were evaluated. The expression levels of MANF and its downstream proteins were examined by western blotting. Immunofluorescence staining of MANF, NeuN, GFAP, Iba-1, cleaved caspase-3, and TUNEL staining were also performed. Cells were counted in six randomly selected fields in the gray matter regions of the sections from two spinal cord sites (2 mm rostral and caudal to the epicenter of the injury) per sample. A cell-based mechanical injury model was also conducted using SH-SY5Y cells. Cell apoptosis and viability were assessed by flow cytometry, an MTT assay, and trypan blue staining. Subcellular structures were observed by transmission electron microscopy. MANF was mainly expressed in neurons. The expression levels of MANF, and its downstream target, p-Akt, were gradually increased and after t-SCI. Treatment with MANF increased Bcl-2 and decreased Bax and CC-3 levels; these effects were reversed on treatment with MK2206. The BBB score, spinal cord water content, and BSCB destruction were also ameliorated by MANF treatment. MANF decreases neuronal apoptosis and improves neurological function through Akt/MDM-2/p53 pathway after t-SCI. Therefore, MANF might be a potential treatment for patients with t-SCI.© 2018 BioFactors, 2018.

Percutaneous Endoscopic Removal of Cervical Foraminal Schwannoma via Interlaminar Approach: A Case Report.

BACKGROUND AND IMPORTANCE: Cervical foraminal schwannomas commonly originate from spinal nerves that pass through the intervertebral foramen of the cervical vertebrae. Because of the proximity of this type of tumor to the vertebral artery and spinal nerves, surgical management remains a major challenge. Conventional open spine surgery usually requires the removal of the articular process and is supplemented by a simultaneous posterolateral spine fusion surgery. To decrease the associated risks of surgical complications by further reducing invasiveness, percutaneous spinal endoscopy may be used for resection of foraminal spinal neoplasm. CLINICAL PRESENTATION: A 52-yr-old female who presented with neck pains with duration of 1 yr was admitted to our hospital. Physical examination revealed moderate rigidity in the neck and grade 5 muscle strength in both upper and lower limbs. Preoperative magnetic resonance imaging (MRI) scans demonstrated a left-sided lesion at the C3-C4 intervertebral foraminal area. Under C-arm fluoroscopy navigation and neuromonitoring, the endoscope was properly positioned on the same side of the tumor, and a small part of the left C3 inferior and C4 superior lamina were first removed by an endoscopic drill to enlarge the interlaminar space. Next, through an endoscopic working canal, the left intervertebral ligamentum flavum was removed to fully expose the tumor. The tumor mass was finally resected in a piecemeal approach. Postoperative MRI confirmed complete tumor resection. CONCLUSION: This is the first case report of a total removal of a cervical foraminal schwannoma with a percutaneous spinal endoscopic procedure.

Melatonin-mediated mitophagy protects against early brain injury after subarachnoid hemorrhage through inhibition of NLRP3 inflammasome activation.

The NLRP3 inflammasome is activated in the early period following subarachnoid hemorrhage(SAH), resulting in inflammatory responses. Recent studies have shown that activation of NLRP3 inflammasome is suppressed by autophagy, but the potential mechanism is unclear. In this study, we examined whether mitophagy was involved in the beneficial effect of melatonin and its relationship with NLRP3 inflammasome activation after SAH. In total, 130 adult-male SD rats were randomly divided into four groups: sham group, SAH + vehicle group, SAH + melatonin group, and SAH + 3-methyladenine (3-MA) + melatonin group. Brain samples were used for brain water content analysis, ROS assay, Western blot, immunohistochemistry and transmission electron microscopy. The results showed that melatonin treatment markedly increased the expression of both autophagy markers(LC3-II/LC3-I and Atg 5), and mitophagy markers(Parkin and PINK-1) following SAH induction. Additionally, melatonin treatment attenuated pathological changes in mitochondria and reduced ROS generation, which are closely related to NLRP3 inflammasome activation. Consequently, melatonin-mediated upregulation of proteins associated with mitophagy inhibited NLRP3 inflammasome activation and significantly reduced pro-inflammatory cytokine levels after SAH. Conversely, 3-MA, an autophagy inhibitor, reversed these beneficial effects of melatonin on mitophagy and the NLRP3 inflammasome. These results suggest that mitophagy-associated NLRP3 inflammasome inhibition by melatonin is neuroprotective against early brain injury post-SAH in rats.