Organized chronic subdural hematoma is a rare form of chronic subdural hematoma. The optimal treatment method is still controversial. Preoperative middle meningeal artery embolization and craniotomy are effective methods for chronic subdural hematoma. However, there are not many reports investigating the effectiveness of these methods in treating organized chronic subdural hematoma. We report the case of a 61-year-old male patient who had a twist-drill craniostomy to treat a left hemisphere subdural hematoma. After surgery, there was a recurrence on the same side in the form of an organized subdural hematoma. The patient received preoperative left middle meningeal artery embolization. After 3 months of follow-up, a small portion of the hematoma remained, causing pressure and slightly shifting the midline to the right by 6.5 mm, and the patient no longer had clinical symptoms.

Background Brain cancer, particularly glioblastoma (GBM), is a global health problem. Despite therapy advances, GBM patients have a poor prognosis. The progression and etiology of GBM may be linked to gene polymorphisms in the VEGFA, TP53, and CTH genes, among others. However, the genetic variations and their interaction in GBM are not fully understood. This study examines the effects of mutations in the VEGFA, TP53, and CTH genes on GBM. Methodology Tissue and blood samples were obtained for hematological, biochemical, and genetic analysis from 18 patients diagnosed with GBM as well as 28 healthy individuals. Standard methods were adopted to perform hematological and biochemical analyses, whereas mutational landscape and expression profiles were obtained from publicly accessible databases. Tissue samples were processed for genomic DNA extraction, and genotype determination was carried out through conventional polymerase chain reaction (PCR) and Sanger sequencing. Results The study involved 18 patients with grade IV GBM before treatment and 28 healthy individuals. The patients consisted of 11 men (61%) and seven females (39%), while healthy individuals included 14 (50%) males and 14 (50%) females. Sixty-seven percent of patients were under 50, 17% between 51 and 60, and 17% over 61, compared to healthy individuals who were 61% under 50, 7% between 51 and 60, and 32% over 60. GBM patients showed higher neutrophil and monocyte counts (median 81% (63.9, 83.5) and 4.2% (3.8-7.3)), respectively, and lower lymphocyte counts (median 13.4% (8.8, 28.40)) compared to controls. The median values of aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) showed no significant differences between the control and GBM groups. GBM patients had significantly higher median CRP levels of 2.55 (1.6, 98) than controls. Analysis of databases revealed a high prevalence of mutations in TP53, with splice region variants, missense variants, and intron variants being the most common. VEGFA and CTH also displayed mutations, primarily missense and intron variants. Gene expression analysis showed significantly higher levels of TP53 and VEGFA in GBM patients compared to controls. CTH expression also exhibited a slight increase in GBM patients. Sanger sequencing identified three mutations in the TP53 gene, including a novel mutation (11915C>A) not previously reported in external databases. Additionally, novel mutations were found in the VEGFA (841G>GA, 919T>TG) and CTH (28398A>AC, 28399A>AT) genes. Conclusions This study highlights the immune dysregulation, inflammation, and genetic variations in GBM. The findings emphasize the potential importance of the TP53, VEGFA, and CTH genes as targets for therapies and diagnostic biomarkers of GBM. Further study is necessary to comprehend these genetic variations\' functional implications and their use in personalized GBM treatment.

BACKGROUND: Lateral neck mass management frequently challenges surgeons. Nerve tissue neoplasms are an uncommon cause of such nodules. Neurogenic tumors form a tiny percentage of the head and neck neoplastic lesions. Considering the number of nerves in this area, it is surprising that such neoplasms are not more frequently seen.
METHODS: A retrospective study was conducted on all patients who presented to the National Cancer Institute of Cairo, Egypt, with head and neck neurogenic neoplasms.
RESULTS: During the last 10 years at the National Cancer Institute of Egypt (2006-2015), 40 cases of neurogenic tumors of the head and neck were treated at the head and neck unit. Patients\' ages ranged from two to 78 years with a mean age of 34.7 years. Childhood neurogenic tumors accounted for nine cases (22.5%) only in this study. Male patients diagnosed with these tumors comprised 16 cases, while female patients comprised 24 cases, with a female-to-male ratio of 1.5:1. Patient presentation depends on the biological behavior of the tumor; for instance, some of them present by slowly growing painless well-circumscribed mobile swelling, and others present by rapidly growing swelling with neurological deficit. Clinical picture and imaging studies such as CT and MRI raise suspicion and may help delineate such tumors, but a definitive diagnosis is obtained by tissue biopsy. Surgery is the mainstay of treatment in most head and neck neurogenic tumors, whereas adjuvant therapy is of limited benefit in some types of neurogenic tumors. The five-year survival rate was 60% for the malignant group, while death was reported in six out of 15 cases (40%).  Conclusion: Most neurogenic head and neck tumors are benign. Accurate preoperative assessment and a high degree of suspicion are the initial steps in the management. Proper treatment involves complete surgical excision; however, debulking procedures have an important role. Malignant neurogenic tumors are aggressive and are treated with combined radical surgical resection and radiation. Chemotherapy is tried for locally advanced unresectable or metastatic disease.

Introduction: Spinal cord injury (SCI) is associated with microenvironment imbalance, thereby resulting in poor regeneration and recovery of the spinal cord. Gene therapy can be used to balance the inflammatory response, however target genes cannot exist in localized injured areas. Methods: A genetically engineered electrospun scaffold (GEES) to achieve long-term immunoregulation and nerve repair was constructed. By combining the microfluidic and electrospinning techniques, interleukin-10 plasmid (pIL10) was loaded into lipid nanoparticles (LNPs) (pIL10-LNP), which was encapsulated to the nerve growth factor (NGF). Immunofluorescence staining, qRT-PCR, ELISA, flow cytometry, and other tests were employed to comprehensively assess the role of GEES in modulating macrophage polarization and facilitating neural repair. Results: The results showed that the scaffold released >70% of the pIL10-LNP within 10 d and continued slow release within 30 d. In vitro cell experiments have demonstrated that GEES effectively stimulates macrophages to secrete anti-inflammatory cytokines and facilitates the differentiation of neural stem cells into neuronal cells. In rat T9 SCI model, the GEES significantly inhibited the inflammatory response in the acute and chronic phases of SCI by transfecting local tissues with slow-release pIL10-LNP to promote the release of the anti-inflammatory factor IL10, thereby creating a favorable microenvironment. With the addition of NGF, the repair and regeneration of nerve tissues was effectively promoted, and the post-SCI motor function of rats improved. Discussion: GEES can regulate post-SCI immune responses through continuous and effective gene delivery, providing a new strategy for the construction of electrospun scaffolds for nerve repair in gene therapy.

Glioblastoma (GBM) causes nearly universal mortality as a result of the failure of conventional therapies including surgical resection, targeted radiation therapy, and chemotherapy. An increasingly important treatment option is combining immunotherapy with other therapies in both preclinical and clinical studies. The central nervous system (CNS) has been historically considered an immune privileged area, but increasing evidence, including the recent rediscovery of meningeal lymphatic vessels (MLVs), has overturned this notion. MLVs are populated by multiple immune cells and connect the CNS to the periphery by draining cerebrospinal fluid with soluble CNS antigens and immune cells into cervical lymph nodes. In the past few years, more and more studies have indicated that MLVs are involved in the regulation of inflammation and the immune response in the pathogenesis of various CNS diseases including GBM. Here, we explore the critical interlinkages between MLVs and GBM therapies including chemotherapy, radiotherapy and immunotherapy, and propose the meningeal lymphatic vasculature as a general target for GBM therapy.

Chorea-acanthocytosis (ChAc) is a rare autosomal recessive inherited syndrome with heterogeneous symptoms, which makes it a challenge for early diagnosis. The mutation of VPS13A is considered intimately related to the pathogenesis of ChAc. To date, diverse mutation patterns of VPS13A, consisting of missense, nonsense, and frameshift mutations, have been reported. In this study, we first report a clinical case that was misdiagnosed as epilepsy due to recurrent seizures accompanied by tongue bite for 9 months, which was not rectified until seizures were controlled and involuntary orolingual movements with awareness became prominent and were confirmed to be orolingual dyskinesia. The patient was eventually diagnosed as ChAc based on whole-exome sequencing revealing novel homozygous c.2061dup (frameshift mutation) and c.6796A > T dual mutations in VPS13A. The patient from a family with consanguineous marriage manifested epileptic seizures at onset, including both generalized tonic-clonic seizures and absence but normal long-term electroencephalography, and gradually developed orofacial dyskinesia, including involuntary tongue protrusion, tongue biting and ulcers, involuntary open jaws, occasionally frequent eye blinks, and head swings. The first test of the peripheral blood smear was negative, and repeated checks confirmed an elevated percentage of acanthocytes by 15-21.3%. Structural brain MRI indicated a mildly swollen left hippocampus and parahippocampal gyrus and a progressively decreased volume of the bilateral hippocampus 1 year later, along with atrophy of the head of the caudate nucleus but no progression in 1 year. We deeply analyzed the reasons for long-term misdiagnosis in an effort to achieve a more comprehensive understanding of ChAc, thus facilitating early diagnosis and treatment in future clinical practice.

UNASSIGNED: Traumatic brain injury (TBI) is one of the leading causes of all injury-related deaths and disabilities in the world, especially in low to middle-income countries (LMICs) which also suffer from lower levels of funding for all levels of the health care system for patients suffering from TBI. These patients do not generally get comprehensive diagnostic workup, monitoring, or treatment, and return to work too quickly, often with undiagnosed post-traumatic deficits which in turn can lead to subsequent incidents of physical harm.
UNASSIGNED: Here, we share methods and results from our research project to establish innovative, simple, and scientifically based practices that dramatically leverage technology and validated testing strategies to identify post-TBI deficits quickly and accurately, to circumvent economic realities on the ground in LMICs. We utilized paper tests such as the Montreal cognitive assessment (MoCA), line-bisection, and Bell\'s test. Furthermore, we combined modifications of neuroscience computer tasks to aid in assessing peripheral vision, memory, and analytical accuracies. Data from seventy-one subjects (51 patients and 20 controls, 15 females and 56 males) from 4 hospitals in Ethiopia are presented. The traumatic brain injury group consists of 17 mild, 28 moderate, and 8 severe patients (based on the initial Glasgow Comma Score). Controls are age and education-matched subjects (no known history of TBI, brain lesions, or spatial neglect symptoms).
UNASSIGNED: We found these neurophysiological methods can: 1) be implemented in LMICs and 2) test impairments caused by TBI, which generally affect brain processing speed, memory, and both executive and cognitive controls.
UNASSIGNED: The main findings indicate that these examinations can identify several deficits, especially the MoCA test. These tests show great promise to assist in the evaluation of TBI patients and support the establishment of dedicated rehabilitation centers. Our next steps will be expansion of the cohort size and application of the tests to other settings.

UNASSIGNED: Motor neurons (MNs) within the nucleus ambiguus innervate the skeletal muscles of the larynx, pharynx, and oesophagus. These muscles are activated during vocalisation and swallowing and must be coordinated with several respiratory and other behaviours. Despite many studies evaluating the projections and orientation of MNs within the nucleus ambiguus, there is no quantitative information regarding the dendritic arbours of MNs residing in the compact, and semicompact/loose formations of the nucleus ambiguus..
UNASSIGNED: In female and male Fischer 344 rats, we evaluated MN number using Nissl staining, and MN and non-MN dendritic morphology using Golgi-Cox impregnation Brightfield imaging of transverse Nissl sections (15 μm) were taken to stereologically assess the number of nucleus ambiguus MNs within the compact and semicompact/loose formations. Pseudo-confocal imaging of Golgi-impregnated neurons within the nucleus ambiguus (sectioned transversely at 180 μm) was traced in 3D to determine dendritic arbourisation.
UNASSIGNED: We found a greater abundance of MNs within the compact than the semicompact/loose formations. Dendritic lengths, complexity, and convex hull surface areas were greatest in MNs of the semicompact/loose formation, with compact formation MNs being smaller. MNs from both regions were larger than non-MNs reconstructed within the nucleus ambiguus.
UNASSIGNED: Adding HBLS to the diet could be a potentially effective strategy to improve horses\' health.

Objectives: We recently introduced a frameless, navigated, robot-driven laser tool for depth electrode implantation as an alternative to frame-based procedures. This method has only been used in cadaver and non-recovery studies. This is the first study to test the robot-driven laser tool in an in vivo recovery animal study. Methods: A preoperative computed tomography (CT) scan was conducted to plan trajectories in sheep specimens. Burr hole craniotomies were performed using a frameless, navigated, robot-driven laser tool. Depth electrodes were implanted after cut-through detection was confirmed. The electrodes were cut at the skin level postoperatively. Postoperative imaging was performed to verify accuracy. Histopathological analysis was performed on the bone, dura, and cortex samples. Results: Fourteen depth electrodes were implanted in two sheep specimens. Anesthetic protocols did not show any intraoperative irregularities. One sheep was euthanized on the same day of the procedure while the other sheep remained alive for 1 week without neurological deficits. Postoperative MRI and CT showed no intracerebral bleeding, infarction, or unintended damage. The average bone thickness was 6.2 mm (range 4.1-8.0 mm). The angulation of the planned trajectories varied from 65.5° to 87.4°. The deviation of the entry point performed by the frameless laser beam ranged from 0.27 mm to 2.24 mm. The histopathological analysis did not reveal any damage associated with the laser beam. Conclusion: The novel robot-driven laser craniotomy tool showed promising results in this first in vivo recovery study. These findings indicate that laser craniotomies can be performed safely and that cut-through detection is reliable.

Positron emission tomography/computed tomography (PET/CT) has dramatically altered the landscape of noninvasive glioma evaluation, offering complementary insights to those gained through magnetic resonance imaging (MRI). PET/CT scans enable a multifaceted analysis of glioma biology, supporting clinical applications from grading and differential diagnosis to mapping the full extent of tumors and planning subsequent treatments and evaluations. With a broad array of specialized radiotracers, researchers and clinicians can now probe various biological characteristics of gliomas, such as glucose utilization, cellular proliferation, oxygen deficiency, amino acid trafficking, and reactive astrogliosis. This review aims to provide a recent update on the application of versatile PET/CT radiotracers in glioma research and clinical practice.