Endoscopic third ventriculostomy (ETV) is used to treat patients with obstructive hydrocephalus in infants. This study evaluated the postoperative outcomes of ETV among pediatric patients. A retrospective study was undertaken at the Mardan Medical Complex between June 2018 and June 2021. All pediatric patients who underwent the procedure of ETV in both the absence and presence of choroid plexus cauterization (CPC) at our center were included in the study. Using medical history data, a comprehensive survey questionnaire was designed. The findings and effects were evaluated either as a success or failure. A total of 90 cases were reviewed during the study. The rate of in-hospital mortality was 1.1% while the most commonly identified causes of hydrocephalus were myelomeningocele and aqueductal stenosis. A total of 39 (43.33%) patients had a successful surgery. In patients where hydrocephalus was secondary to aqueductal stenosis, the success rate was the highest, while the success rate was quite low for post-infectious hydrocephalus and intraventricular hemorrhage (p < 0.0001). The postoperative complication rate was 55.56% in our study. The rate of in-hospital mortality was 1.1%. We found that the success rate of ETV was dependent upon factors such as the cause of hydrocephalus, type of hydrocephalus, and the age of the patient. Therefore, ETV is not suitable for all patients, and vigilance must be undertaken in selecting patients for the procedure. The rate of postoperative infections in our institution was alarmingly high which is a concerning matter for the institution.

Introduction and importance: Malignant melanotic nerve sheath tumor (MMNST) is a rare and potentially aggressive variant of schwannoma that arises from Schwann cells containing melanin. These tumors most frequently occur in the spinal nerve roots and are often misdiagnosed due to their radiological and histopathological similarities with other pigmented lesions such as malignant melanoma or pigmented meningioma. Accurate diagnosis is crucial, as MMNST carries a higher risk of local recurrence and distant metastasis compared to conventional nerve sheath tumors. Case presentation: We report the case of a 30-year-old male who presented with a 6-month history of progressive left-sided leg pain, lower backache, and paresthesia. Neurological examination revealed decreased perineal sensations and tenderness in the lumbosacral region. MRI of the lumbosacral spine showed an extradural, well-circumscribed, T1 hyperintense lesion with mass effect on the left L5, S1, and S2 nerve roots. The patient underwent surgical resection, and the lesion was found to be encapsulated and pigmented. Histopathology confirmed the diagnosis of MMNST. Immunohistochemistry was positive for S-100 and HMB-45. Postoperative recovery was uneventful, and no recurrence was observed at 6-month follow-up. Clinical discussion: MMNST poses significant diagnostic and therapeutic challenges. While MRI may suggest a pigmented lesion, definitive diagnosis relies on histopathology and immunohistochemical markers. Given its malignant potential, complete surgical resection with long-term follow-up is the mainstay of management. In this case, the tumor’s extradural location and involvement of the sacral nerve roots added to the surgical complexity. Multidisciplinary collaboration was pivotal in planning surgical excision and monitoring for recurrence. Conclusion: MMNST should be considered in the differential diagnosis of pigmented spinal lesions, especially in young adults with progressive neurological symptoms. Early recognition and complete surgical resection remain essential for optimal outcomes. This case highlights the importance of integrating imaging, histopathology, and immunohistochemistry to ensure accurate diagnosis and guide management.

Background Traumatic spinal cord injuries often result in significant disability and impact patients’ functional independence and quality of life. Objective This study aims to evaluate neurological recovery, independence in daily activities, and overall physical performance in trauma patients with spinal injury over a 24-month follow-up, with a focus on outcomes in low-resource settings. Methodology A prospective descriptive observational study was conducted from January 19, 2022, to December 19, 2024. A total of 216 adult patients with acute traumatic spinal injuries were enrolled. Neurological status was assessed using the American Spinal Injury Association (ASIA) Impairment Scale, including motor and sensory subscores, and functional independence was measured with the Spinal Cord Independence Measure (SCIM) at baseline, discharge, and at six, 12, 18, and 24 months post-injury. Data on acute management, complications, specific rehabilitation therapies (physical therapy, occupational therapy, ambulation training), ambulation, and occupational reintegration were collected. Statistical analysis included repeated measures analysis of variance (ANOVA) and Chi-square tests, with significance set at p < 0.05. Results At baseline, 42.59% (n = 92) of patients had severe neurological impairment (ASIA A/B), which decreased to 21.30% (n = 46) at 24 months. The mean SCIM scores improved significantly from 38.60 ± 12.40 at admission to 74.90 ± 15.80 at two years (p < 0.001). Surgical intervention was performed in 68.52% (n = 148) of patients. Independent ambulation was achieved by 38.89% (n = 84), while 41.20% (n = 89) were unemployed due to disability. Common complications included pressure ulcers (11.57%, n = 25) and urinary tract infections (13.89%, n = 30) during hospitalization. Conclusion Significant neurological and functional improvements occur over 24 months, though complications and occupational challenges persist, highlighting the need for cautious interpretation due to heterogeneity in injury levels and rehabilitation protocols, and the importance of optimized rehabilitation in low-resource settings.

Objectives: This study aims to explore the expression and functional significance of hub genes in Wilms tumors and their potential as diagnostic biomarkers and therapeutic targets. Methods: Gene expression data from Wilms tumors and normal control samples were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified using the limma package in R, followed by Venn diagram analysis to identify common DEGs. STRING and Cytoscape were employed to construct a protein-protein interaction (PPI) network and identify hub genes. Cell culture of five Wilms tumor cell lines and normal controls was performed to validate gene expression. Functional assays including proliferation, colony formation, and wound healing assays were conducted to assess the impact of SLC12A3 and GSTM3 overexpression. Immune infiltration analysis was carried out using ssGSEA. Results: We identified SLC12A3, CLCNKB, REN, and GSTM3 as hub genes with significant down-regulation across Wilms tumor cell lines and normal controls. Immune infiltration analysis revealed that the expression of these genes was associated with altered levels of immune cell populations, such as activated dendritic cells, CD8+ T cells, macrophages, and NK cells. GSTM3 overexpression enhanced the inflammatory response and reduced DNA damage, indicated by lower γ-H2AX expression. Functional assays showed that induction of SLC12A3 and GSTM3 overexpression significantly inhibited cell proliferation, colony formation, and migration. Conclusion: SLC12A3, CLCNKB, REN, and GSTM3 hub genes play key roles in regulating cellular functions and the immune microenvironment in Wilms tumors. Therefore, these genes could serve as potential biomarker and therapeutic targets in Wilms tumor patients.

Background/introduction The aim of this study was to understand the effectiveness of particular serum and cerebrospinal fluid (CSF) biomarkers for the early diagnosis of cerebral vasospasm (CV) in patients with aneurysmal subarachnoid hemorrhage (aSAH) and to document any correlation with clinical and radiological outcomes. aSAH carries a high risk of CV and delayed cerebral ischemia, which are leading causes of disability and death. Current diagnostic tools like transcranial Doppler and angiography often detect vasospasm only after clinical manifestation, highlighting the need for early predictive biomarkers. This study investigates the potential of serum and CSF biomarkers, specifically IL-6, ET-1, and S100B, to enable early diagnosis of CV and improve correlation with clinical and radiological outcomes. Materials and methods The data were obtained from the Department of Neurosurgery in Mardan Medical Complex Hospital in Mardan, Pakistan, from July 2019 to July 2024. The study included 60 patients aged 18 to 80 years with a diagnosis of aSAH who were admitted within 48 hours of the onset of the disease. Blood and CSF were obtained on days 1, 3, and 7 after ictus. The analyzed biomarkers were interleukin-6 (IL-6), S100 calcium-binding protein B (S100B protein), and endothelin-1 (ET-1). Transcranial Doppler ultrasonography was used to evaluate vasospasm, and computed tomography angiography was used when necessary. SPSS software was used to analyze data, with statistical significance set at p < 0.05. Logistic regression analysis was performed to understand the relationship between biomarker levels and the occurrence of vasospasm. Results Radiology confirmed the diagnosis of vasospasm in 35 (58.3%) of the 60 patients with a mean age of 55.4 ± 12.1 years. On day 3, the levels of IL-6 and endothelin-1 were significantly higher in the vasospasm group than in the non-vasospasm group (p = 0.003 and p = 0.012, respectively), while S100B findings were inconsistent. The risk of vasospasm was 2.5 times higher in patients with increased IL-6 values. Early elevation of biomarkers was associated with poor Glasgow Outcome Scale scores at discharge (p = 0.016). Elevated serum IL-6 (>100 pg/mL) and CSF ET-1 (>10 pg/mL) on day 3 were significant predictors of poor outcome, with odds ratios of 3.2 (95% CI 1.4-7.4; p = 0.005) and 2.8 (95% CI 1.2-6.6; p = 0.015), respectively. Conclusion Serum and CSF biomarkers, particularly IL-6 and endothelin-1, may help identify CV early after aSAH, even without radiological signs. Incorporating these biomarkers into care could enable earlier treatment and improve outcomes, though multicenter studies are needed to establish standardized protocols.

Whether glymphatic dysfunction drives or merely follows brain injury and neurodegeneration remains unresolved. The glymphatic system mediates the transport, exchange, and clearance of solutes between cerebrospinal fluid (CSF) and interstitial fluid (ISF) through paravascular CSF influx, polarized aquaporin-4 (AQP4) at astrocytic endfeet, and meningeal lymphatic drainage. This narrative review synthesizes evidence on glymphatic regulation and its role in traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and neurodegeneration, and appraises imaging, biomarker, and therapeutic approaches. PubMed/MEDLINE and Google Scholar were searched from inception to August 2026, and 128 sources were analyzed. In TBI, mechanical shear and NLR family pyrin domain-containing 3 (NLRP3)-dependent inflammation may alter AQP4 distribution and impair tau and amyloid-beta (Aβ) clearance; however, glymphatic failure has not been established as the causal mediator of later neurodegeneration, which is likely multifactorial. After SAH, blood and fibrin may obstruct perivascular pathways, and hemoglobin, heme, and iron toxicity may further disrupt CSF–ISF exchange; these changes are associated with delayed cerebral ischemia, cortical spreading depolarizations, and post-hemorrhagic hydrocephalus. Impaired clearance of Aβ, phosphorylated tau, and α-synuclein may link glymphatic dysfunction to Alzheimer’s and Parkinson’s diseases, although causality is unproven. Current imaging tools, including diffusion tensor imaging analysis along the perivascular space (DTI-ALPS), and biomarkers do not yet provide a validated measure of glymphatic function. Sleep optimization is a low-risk strategy, and controlled lumbar drainage has the strongest clinical evidence among CSF-dynamics approaches. Translation requires appropriate animal models and prospective TBI/SAH studies combining serial DTI-ALPS with cognitive follow-up.