Myelitis associated with glial fibrillary acidic protein IgG: characterization and comparison with aquaporin-4 IgG and myelin oligodendrocyte glycoprotein IgG myelitis.

Background: Awareness of the characteristics of glial fibrillary acidic protein autoantibody (GFAP-IgG) associated myelitis facilitates early diagnosis and treatment. We explored features in GFAP-IgG myelitis and compared them with those in myelitis associated with aquaporin-4 IgG (AQP4-IgG) and myelin oligodendrocyte glycoprotein IgG (MOG-IgG).

Methods: We retrospectively reviewed data from patients with GFAP-IgG myelitis at the First Affiliated Hospital of Zhengzhou University and Henan Children's Hospital from May 2018 to May 2023.

TRPML1 ameliorates seizures-related neuronal injury by regulating autophagy and lysosomal biogenesis via Ca/TFEB signaling pathway.

Alterations in autophagy have been observed in epilepsy, although their exact etiopathogenesis remains elusive. Transient Receptor Potential Mucolipin Protein 1 (TRPML1) is an ion channel protein that regulates autophagy and lysosome biogenesis. To explore the role of TRPML1 in seizures-induced neuronal injury and the potential mechanisms involved, an hyperexcitable neuronal model induced by Mg-free solution was used for the study.

The cerebral lymphatic drainage system and its implications in epilepsy.

The central nervous system has long been thought to lack a clearance system similar to the peripheral lymphatic system. Therefore, the clearance of metabolic waste in the central nervous system has been a subject of great interest in neuroscience. Recently, the cerebral lymphatic drainage system, including the parenchymal clearance system and the meningeal lymphatic network, has attracted considerable attention.

Mitochondrial-regulated Tregs: potential therapeutic targets for autoimmune diseases of the central nervous system.

Regulatory T cells (Tregs) can eliminate autoreactive lymphocytes, induce self-tolerance, and suppress the inflammatory response. Mitochondria, as the energy factories of cells, are essential for regulating the survival, differentiation, and function of Tregs. Studies have shown that patients with autoimmune diseases of the central nervous system, such as multiple sclerosis, neuromyelitis optica spectrum disorder, and autoimmune encephalitis, have aberrant Tregs and mitochondrial damage.

ATF5 Attenuates Low-magnesium-induced Apoptosis by Inhibiting Endoplasmic Reticulum Stress Via the Regulation of Mitochondrial Reactive Oxygen Species.

Mitochondrial stress and endoplasmic reticulum stress (ERS) are known to be closely linked. ATF5 is a key regulator of mitochondrial stress and is involved in ERS regulation. Previously, we used a seizure model to demonstrate that ATF5 regulates mitochondrial stress.

ATF5-regulated Mitochondrial Unfolded Protein Response Attenuates Neuronal Damage in Epileptic Rat by Reducing Endoplasmic Reticulum Stress Through Mitochondrial ROS.

Endoplasmic reticulum (ER) dysfunction caused by excessive ER stress is a crucial mechanism underlying seizures-induced neuronal injury. Studies have shown that mitochondrial reactive oxygen species (ROS) are closely related to ER stress, and our previous study showed that activating transcription factor 5 (ATF5)-regulated mitochondrial unfolded protein response (mtUPR) modulated mitochondrial ROS generation in a hippocampal neuronal culture model of seizures. However, the effects of ATF5-regulated mtUPR on ER stress and the underlying mechanisms remain uncertain in epilepsy.

Clinical characteristics and prognostic factors for short-term outcomes of autoimmune glial fibrillary acidic protein astrocytopathy: a retrospective analysis of 33 patients.

Background: Autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A) is a recently discovered inflammatory central nervous system (CNS) disease, whose clinical characteristics and prognostic factors for short-term outcomes have not been defined yet. We aimed to assess the symptoms, laboratory tests, imaging findings, treatment, and short-term prognosis of GFAP-A.

Methods: A double-center retrospective cohort study was performed between May 2018 and July 2022.

Activating Transcription Factor 4-mediated Mitochondrial Unfolded Protein Response Alleviates Hippocampal Neuronal Damage in an In Vitro Model of Epileptiform Discharges.

The mitochondrial unfolded protein response (mtUPR) has been shown to restore protein homeostasis and cell function under stress, and recent studies have confirmed that the activating transcription factor 4 (ATF4) regulates mtUPR. However, the role of ATF4-mediated mtUPR in a hippocampal neuronal culture model of seizures remains unclear. Our results showed that the expression of mtUPR-related proteins (HSP60 and CLpP) increased in primary hippocampal neurons with seizures induced by a magnesium-free solution, suggesting mtUPR activation.

A nested case-control study investigating short-term prognosis, clinical and imaging features in acute ischemic stroke patients with systemic lupus erythematosus.

Objectives: To investigate acute ischemic stroke (AIS) patients with systemic lupus erythematosus (SLE) clinical and imaging features, and to explore the impact of SLE on the short-term prognosis of AIS patients.

Methods: A nested case-control study was conducted in The First Affiliated Hospital of Zhengzhou University between October 1, 2019, and May 31, 2021. The case group consisted of 28 AIS patients diagnosed with SLE, and 112 AIS patients without SLE were selected by incidence density sampling as a control group.

Single internal carotid cavernous sinus aneurysm presented as bilateral painful ophthalmoplegia: a case report.

Background: Intracranial aneurysms are the most common vascular cause of painful ophthalmoplegia. Symptoms include retro-orbital pain, diplopia, ophthalmoplegia, trigeminal neuropathy, or a combination of these. Most single aneurysms cause ipsilateral, painful ophthalmoplegia.

ATF5 Attenuates Apoptosis in Hippocampal Neurons with Seizures Evoked by Mg-Free Medium via Regulating Mitochondrial Unfolded Protein Response.

The mitochondrial unfolded protein response (mtUPR)-a stress response pathway for maintaining protein homeostasis-is critical in seizures-induced neuronal injury. The activating transcription factor 5 (ATF5) regulates mtUPR; however, whether ATF5-regulated mtUPR has a role in neuronal injury in epilepsy remains uncertain. Here, we investigated the effects of ATF5-regulated mtUPR on neuronal injury in hippocampal neurons with seizures evoked by Mg-free medium.

Autoimmune encephalitis with coexistent LGI1 and GABAR1 antibodies: case report.

Background: Autoimmune encephalitis (AE) with multiple auto-antibodies is of great clinical significance because its complex clinical manifestations and atypical imaging increase the difficulty of diagnosis, differential diagnosis and treatment, which may aggravate the disease, increase the recurrence rate and mortality. The coexistence of anti-Leucinie-rich Glioma Inactivated 1 (LGI1) and anti-γ-aminobutyric acid-beta-receptor 1 (GABAR1) has not been published before.

Case Presentation: We herein present the case of a 60-year-old man with slow response, behavioral changes, psychosis and sleep disorders.

FAM134B-Mediated ER-Phagy in Mg-Free Solution-Induced Mitochondrial Calcium Homeostasis and Cell Death in Epileptic Hippocampal Neurons.

Mitochondrial-associated endoplasmic reticulum (ER) membranes (MAMs) regulate calcium (Ca) homeostasis via Ca transport-related proteins such as inositol-1,4,5-triphosphate receptor (IP3R). FAM134B-mediated ER-phagy plays an important role in ER homeostasis. However, it remains unknown whether FAM134B-mediated ER-phagy affects mitochondrial Ca homeostasis and cell death through MAMs.

Antagomirs targeting miR-142-5p attenuate pilocarpine-induced status epilepticus in mice.

MicroRNAs (miRNAs) are reported to involve in pathogenesis of temporal lobe epilepsy (TLE). miR-142-5p is found increased in TLE, but its role remains unknown. In the study, we established a mouse model of status epilepticus (SE) with pilocarpine and a cell model of TLE.

CGRP Plasma Levels Decrease in Classical Trigeminal Neuralgia Patients Treated with Botulinum Toxin Type A: A Pilot Study.

Objective: The aim of this study was to investigate the changes of calcitonin gene-related peptide (CGRP) plasma levels in patients with classical trigeminal neuralgia (TN) and if plasma CGRP concentrations could be used to predict the response to botulinum toxin type A (BTX-A).

Methods: Forty-seven patients with classical TN were recruited and treated with BTX-A. A patient was considered a responder when the visual analog scale (VAS) score and number of episodes were reduced by at least 50% compared with baseline data.

FAM134B Attenuates Seizure-Induced Apoptosis and Endoplasmic Reticulum Stress in Hippocampal Neurons by Promoting Autophagy.

Autophagy plays a critical role in epileptic neuronal injury, and recent studies have demonstrated that FAM134B plays an important role in regulating autophagy. However, the effect of FAM134B on epileptic neuronal injury remains unclear. In this study, we investigated the role of FAM134B in neuronal apoptosis and endoplasmic reticulum (ER) stress using the hippocampal neuronal culture model of acquired epilepsy (AE) in vitro.

A new compound heterozygous mutation in adult-onset Krabbe disease.

Krabbe disease (KD) or globoid cell leukodystrophy is an autosomal recessive lysosomal disorder caused by a lack of the lysosomal enzyme galactocerebrosidase (GALC) because of mutations in . Patients with KD exhibit a wide spectrum of clinical symptoms; therefore, their diagnosis can be challenging. We report the clinical features and gene mutations in a 48-year-oldpatient with adult-onset KD.

Role of the mitochondrial calcium uniporter in Mg-free-induced epileptic hippocampal neuronal apoptosis.

Mitochondrial Ca overload is closely associated with seizure-induced neuronal damage. The mitochondrial calcium uniporter (MCU) plays a crucial role in regulating mitochondrial Ca homeostasis. However, the role of the MCU in seizure-induced neuronal damage remains elusive.

Relationship between elevated plasma trimethylamine N-oxide levels and increased stroke injury.

Objective: To investigate whether elevated plasma trimethylamine N-oxide (TMAO) levels are associated with initial stroke severity and infarct volume.

Methods: This cross-sectional study included 377 patients with acute ischemic stroke and 50 healthy controls. Plasma TMAO levels were assessed at admission.

Factors affecting the therapeutic effect of botulinum toxin A on trigeminal neuralgia: A follow-up retrospective study of 152 patients.

Botulinum toxin A (BTX-A) is a promising therapeutic modality against trigeminal neuralgia (TN) with certain controversies pertaining to its application. To provide further information on factors influencing the treatment outcomes of BTX-A, a retrospective study with 152 patients with TN treated with BTX-A was performed. The starting time and duration of the therapeutic effect, as well as side effects, of BTX-A in the treatment of TN were analyzed by sex, age, course of disease, number of branches and injected dose.

Low-Dose Tirofiban Treatment Improves Neurological Deterioration Outcome After Intravenous Thrombolysis.

Background and Purpose- Early use of antiplatelet drugs within 24 hours after intravenous thrombolysis (IVT) has always been a confusing clinical problem. The purpose of this study was to assess the safety and efficacy of early low-dose tirofiban treatment in patients with early neurological deterioration (END) within the first 24 hours after IVT. Methods- This was a retrospective analysis of prospectively collected data of 1764 consecutive patients with acute ischemic stroke treated with IVT between January 2017 and September 2018.

Angioplasty and/or stenting after thrombectomy in patients with underlying intracranial atherosclerotic stenosis.

Purpose: To investigate the imaging and clinical outcomes of emergent angioplasty and/or stenting or neither in patients of emergent large-vessel occlusion (ELVO) with underlying severe intracranial atherosclerotic stenosis (ICAS).

Methods: In this multicenter prospective cohort study, we included patients of ELVO with underlying ICAS. Patients received emergent angioplasty and/or stenting or neither after mechanical thrombectomy at the interventionists' discretion.

Both left upper lobectomy and left pneumonectomy are risk factors for postoperative stroke.

Retrospective studies have found that left upper lobectomy (LUL) may be a new risk factor for stroke, and the potential mechanism is pulmonary vein thrombosis, which more likely develops in the left superior pulmonary vein (LSPV) stump. The LSPV remaining after left pneumonectomy is similar to that remaining after LUL. However, the association between left pneumonectomy, LUL, and postoperative stroke remains unclear.