Inborn errors of immunity (IEIs), an expanding group of monogenic disorders with diverse clinical manifestations, are increasingly recognized to include neuroinflammatory disease. Examples of diseases included under this umbrella are Aicardi-Goutières syndrome, deficiency of adenosine deaminase 2, familial haemophagocytic lymphohistiocytosis, neonatal-onset multisystem inflammatory disease, and acute necrotizing encephalopathy, among others. Children with IEIs may develop encephalopathy, seizures, focal neurological deficits, aseptic meningitis, inflammatory lesions on magnetic resonance imaging, or other central or peripheral nervous system manifestations. While systemic features of autoinflammation or autoimmunity are often present and provide important clues that an underlying IEI may be present, neuroinflammation may be the presenting or sole manifestation in some children. Early recognition of neuroinflammatory presentations of IEIs is critical to prompt immunological and genetic investigations, enabling diagnosis and timely initiation of appropriate immunotherapies, and reducing the risk of long-term neurological outcomes. This review highlights paediatric-onset neuroinflammatory phenotypes associated with IEIs and provides practical frameworks for their recognition and investigation in clinical practice.

Leptomeningeal metastases (LM) is a rare but clinically important subtype in central nervous system (CNS) metastasis. Multicentre data was reviewed to detail the epidemiology, clinicopathological associations among patients with positive cerebrospinal fluid cytology (CSF) cytology. Patients with CNS metastasis and clinical data were identified through the Hong Kong Hospital Authority Clinical Data Analysis and Reporting System (CDARS). In total, through 1st January 2000 to 31st December 2024, 38,893 patients with CNS metastasis were retrieved, 1503 had CSF cytology. The most common primary malignancies were lung (54.16%), breast (11.18%) and gastrointestinal (5.66%; colonic: 3.33%, gastric: 1.86%, esophageal: 0.47%). There were 220 (14.64%) patients with positive CSF, they were younger (57.72 years vs. 60.03, p = 0.005), and likely with breast (20.84%, p = 0.016) and lung primaries (16.47%, p = 0.030). The median overall survival (OS) was 113 days. Positive CSF, age > 60 and gastrointestinal primary were correlated with shorter OS (p < 0.05). The inclusion of brain radiotherapy (260 day vs. 82, p < 0.001) and systemic therapy (496 days vs. 61, p < 0.001) for treatment of leptomeningeal metastases was independently associated with longer OS. Positive CSF cytology is a strong independent indicator of poor outcomes. Radiotherapy and systemic therapy improve overall survival for the medium term (6-12 months).

Macrophages in the meninges contribute to immune defense of the central nervous system (CNS), yet their site-specific origin and function remain poorly understood. Using an intravenous model of streptococcal meningoencephalitis in mice, we found bacteria predominantly in the leptomeninges and dura. Nevertheless, monocyte infiltration into the leptomeninges and parenchyma strongly correlated with disease severity. In the dura, infection triggered activation and loss of resident macrophages, followed by rapid engraftment of inflammatory monocytes that transiently replenished the macrophage niche. Under homeostasis, dural monocytes were supplied CCR2 independently from adjacent skull bone marrow. During infection, this local source was insufficient, necessitating recruitment from peripheral bone marrow. Infection further reshaped monocyte ontogeny, increasing monocyte-dendritic cell progenitor-derived monocytes, which expressed higher major histocompatibility complex class II levels and persisted in the brain alongside CD4[+] T cells during resolution. Together, these findings reveal dynamic, compartment-specific remodeling of monocyte recruitment and differentiation across CNS borders during bacterial meningoencephalitis.

Post-neurosurgical bacterial meningitis (PNBM) is one of the major complications that causes high mortality in an era of antimicrobial resistance. Differentiating infective meningitis from aseptic meningitis remains challenging when we rely on culture, as it has lower sensitivity, and conventional cerebrospinal fluid biomarkers cannot differentiate between the two.

Cell culture is a common methodology used in tumor research. However, the manner in which initial tissue conditions, such as storage in the operating theatre, can affect proliferation has not been well‑established. Additionally, there is little information about the behavior of primary cell cultures in meningiomas. Therefore, the present study analyzed the physiology of primary meningioma cultures under different tissue conditions. For the present study, 10 meningioma tissue samples were collected after surgery at Saarland University (Homburg, Germany) between June 2022 and December 2022. Primary cell cultures were separately established on the day of surgery and 1 day later, before the tissues were stored overnight in nutrient solutions. Cultures were split into two flasks, one was used for fluorescence in situ hybridization (FISH), whereas the other was frozen in liquid nitrogen. After 6 months, frozen cultures were thawed and recultivated. The proliferation rates were found to be ≥80% for cell cultures as a minimum. No significant difference was found between cultures established on the surgery day or postoperative day 1 in terms of proliferation rate and growth pattern. FISH revealed loss of the short arm of chromosome 1 (1p) in one meningioma, loss of the long arm of chromosome 22 (22q) in three samples, combined 1p and 22q loss in three samples, and diploid chromosome sets in three samples. In total, 16 out of 17 initially shock‑frozen specimens were successfully recultivated after 6 months of cryopreservation. To conclude, meningioma cultures appeared to proliferate similarly regardless of whether the tissue was processed on the day of surgery or the following day, if viable cells were present. Frozen cultures could be revived after 6 months if cells remained viable. FISH provided evidence that primary meningioma cultures accurately reflected initial chromosomal aberrations of the tumor, even after freezing.

Background Subarachnoid block (SAB) is a widely practiced regional anesthetic for lower limb surgeries. The patient position for subarachnoid block induction, either sitting or lateral decubitus, may affect hemodynamic stability and block quality. Objective To compare the incidence of hypotension and the onset times of block in these two positions. Method In this prospective single-center observational comparative study, 108 patients, who were scheduled to undergo elective lower limb surgery, were equally assigned to subarachnoid block in sitting position (SP) and Lateral decubitus position (LP) groups. An intrathecal dose of hyperbaric Bupivacaine 0.5% (15 mg) was given. Hemodynamic variables, onset of sensory and motor block, maximum level of sensory and motor block and any complications including hypotension and bradycardia were recorded and compared. Categorical variables were analyzed using the Chi-square test, and continuous variables were compared using the unpaired Student's t-test. Result The incidence of hypotension was greater in sitting position group (20.41%) than in LP group (16.67%), but the difference was not statistically significant. Out of these, bradycardia was more frequent in sitting position (9.2%) as compared to lateral decubitus position (7.4%). The onset times of sensory and motor blocks in the lateral decubitus position group were significantly shorter (p < 0.05). Conclusion Lateral decubitus position results in superior early hemodynamic stability and shorter time to sensory and motor block onset as compared to sitting in subarachnoid block for elective lower limb surgeries.

Spina bifida (SB) is a neurodevelopmental disorder characterised by the incomplete closure of the embryonic neural tube, resulting in a neural tube defect (NTD) that affects the development of the spine and spinal cord. Both genetic and non-genetic factors contribute to the occurrence of SB, including deficiencies in folic acid and vitamin B12, maternal obesity, smoking, epilepsy, alcohol consumption, drug use, and a history of previous pregnancies affected by SB. Complications associated with SB include meningitis, hydrocephalus, neonatal paralysis, and urinary or faecal incontinence. Considerable advancements have been made in raising awareness, improving diagnostic capabilities, and establishing specialised clinics and multidisciplinary teams (MDTs) dedicated to SB management. However, several gaps persist in its management. These include inadequate awareness and education among healthcare professionals, limited access to healthcare services, a scarcity of surgical workforce and MDTs, social stigma and discrimination, and research and data accessibility gaps. The implications of these management gaps in SB care encompass diminished quality of life, increased morbidity and mortality rates, and economic consequences related to surgical management. To improve SB management outcomes in Africa, strategic interventions should focus on enhancing healthcare infrastructure and resources, strengthening education and awareness programs for SB prevention and support, addressing cultural concerns, improving neonatal surgical care, and enhancing research and guidelines. By addressing these gaps through targeted, equity-focused interventions in healthcare infrastructure, education, cultural adaptation, neonatal surgical care, research, and policy, substantial improvements can be made in SB care and outcomes in Africa, reducing the disproportionate burden of disability in low-resource settings.

Tuberculous meningitis (TBM), the most severe form of Mycobacterium tuberculosis infection, is characterized by high mortality and neurological sequelae, largely attributed to blood-brain barrier (BBB) disruption. While recent studies identified GSDMD-mediated endothelial pyroptosis as a key mechanism of inflammatory BBB damage, the full molecular landscape in TBM remains unclear.

Against the backdrop of widespread implementation of intrapartum prophylaxis for group B streptococcus (GBS), E. coli has emerged as a major pathogen of early-onset neonatal sepsis (EOS) and neonatal meningitis. Vaginal colonization of pregnant women with highly virulent E. coli is not uncommon and has been associated with adverse obstetric outcomes, including preterm birth, chorioamnionitis, and neonatal infection. Available evidence suggests that the maternal colonization rate is approximately 20-30%, and vertical transmission during delivery occurs frequently. Colonizing strains often harbor virulence determinants associated with extraintestinal pathogenic E. coli (ExPEC), with virulence profiles resembling those of uropathogenic E. coli and neonatal meningitis-associated strains. Although most exposed neonates may remain asymptomatically colonized, once invasive infection occurs, the disease can rapidly progress to sepsis or meningitis, resulting in substantial mortality and long-term neurodevelopmental sequelae. In recent years, the spread of multidrug-resistant strains, particularly extended-spectrum β-lactamase (ESBL)-producing isolates, has further complicated perinatal prevention and empirical treatment. This review summarizes current advances in perinatal E. coli infection, with a focus on maternal colonization and vertical transmission, pathogenic mechanisms, clinical manifestations, antimicrobial resistance trends, and emerging preventive strategies.

Listeria monocytogenes is an important food-borne pathogen that is responsible for contamination of a variety of food products. It causes listeriosis which is one of the most severe and serious foodborne diseases, whose main severe clinical forms include septicaemia, meningitis, and mateoneonatal infections. Also because of its ability to adhere to industrials' surfaces, it is difficult for them to come up against this danger. Although there are researches in L. monocytogenes proteome, most of them are based on the study of a single strain, yet little is known about the proteome of more of the microbe's strains. By studying the proteome of the microorganism with state-of-the-art mass spectrometry technology in terms of proteomics, we will be able to have an overall picture of the pathogenicity of the bacterium, as this is largely based on its ability to adapt to certain environments and to project its toxicity in them. To address that we provide a dataset of 2227 different proteins from 4 strains of L. monocytogenes, grouped by their molecular function and their biological process. The identified proteins confirm the complex molecular mechanisms of the bacterium.