Traumatic brain injury (TBI) often results in long-lasting patterns of neurological deficits including motor, sensory, and cognitive abnormalities. Cranial gunshot survivors are among the most disabled TBI patients and face a lifetime of disability with no approved strategies to protect or repair the brain after injury. Recent studies using a model of penetrating TBI (pTBI) have reported that human neural stem cells (hNSCs) transplantation can lead to dose and location-dependent neuroprotection. Evidence for regional patterns of microglial activation has also been reported after pTBI with evidence for microglial cell death by pyroptosis. Because of the importance of injury-induced microglial activation in the pathogenesis of TBI, we tested the hypothesis that dose-dependent hNSC mediated neuroprotection after pTBI was associated with reduced microglial activation in pericontusional cortical areas. To test this hypothesis, quantitative microglial/macrophage Iba1 immunohistochemistry and Sholl analysis was conducted to investigate the arborization patterns using four experimental groups including, (i) Sham operated (no injury) + low dose (0.16 million cells/rat), (ii) pTBI + vehicle (no cells), (iii) pTBI + low dose hNSCs (0.16 million/rat), and (iv) pTBI + high dose hNSCs (1.6 million cells/rat). At 3 months post-transplantation (transplants at one week after pTBI), the total number of intersections was significantly reduced in vehicle treated pTBI animals versus sham operated controls indicating increased microglia/macrophage activation. In contrast, hNSC transplantation led to a dose-dependent increase in the number of intersections compared to pTBI vehicle indicating less microglia/macrophage activation. The peak of Sholl intersections at 1 μm from the center of the microglia/macrophages ranged from ~6,500–14,000 intersections for sham operated, ~250–500 intersections for pTBI vehicle, ~550–1,000 intersections for pTBI low dose, and ~2,500–7,500 intersections for pTBI high dose. Plotting data along the rostrocaudal axis also showed that pericontusional cortical areas protected by hNSC transplantation had increased intersections compared to nontreated pTBI animals. These studies using a non-biased Sholl analysis demonstrated a dose-dependent reduction in inflammatory cell activation that may be associated with a neuroprotective effect driven by the cellular transplant in perilesional regions after pTBI.

Pediatric hydrocephalus results from the overproduction, obstruction, or inability to resorb cerebrospinal fluid (CSF), which may lead to ventricular enlargement. Hydrocephalus may be secondary to other pathologies, including intraventricular hemorrhage (IVH). Surgical intervention may include a ventricular access device or a ventriculosubgaleal shunt in premature infants who are too small for permanent CSF diversion. Hydrocephalus, an inflammatory pathology, involves activation of the inflammasome. Elevation in pro-inflammatory proteins is often associated with worsening clinical outcomes in pediatric pathologies. Whether inflammasome proteins are reliable biomarkers for pediatric hydrocephalus has not been established. We analyzed CSF samples via an ELLA assay from pediatric hydrocephalic patients with IVH of prematurity vs. controls and compared changes in inflammasome protein concentrations post-reservoir surgery at different time points. The area under the curve was calculated using receiver operator characteristic curves. The levels of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), caspase-1, and interleukin-18 were significantly elevated in pediatric hydrocephalic patients with IVH vs. controls. Thus, these proteins are reliable biomarkers of the inflammatory response in pediatric hydrocephalus following ROC analysis, with an AUC of 1.0 and high sensitivity and specificity at the corresponding cut-off points. Ongoing work seeks to validate these findings in a larger cohort of pediatric hydrocephalic patients with varying etiologies.

Background: Endoscopic spine surgery (ESS) is an established minimally invasive approach for degenerative spinal conditions. Advances in instrumentation and visualization have expanded its application to spinal tumor resection. This review synthesizes reported clinical outcomes and technical considerations of ESS for primary spinal tumors. Methods: PubMed was queried from 2000 to 2025 for studies reporting endoscopic resection of primary spinal tumors. Studies involving metastatic disease or non-resective interventions were excluded. Data were descriptively analyzed given heterogeneity and limited sample size. Results: Eleven patients across seven studies were included (mean age = 50.3 years). Pathologies comprised schwannoma (n = 5), meningioma (n = 3), osteoid osteoma (n = 2), and Ewing sarcoma (n = 1). Seven tumors were intradural extramedullary (63.6%) and four were extradural (36.4%); no intramedullary lesions were included. Of the seven intradural cases, one was performed via uniportal full-endoscopic technique, one via biportal endoscopy, and five via tubular retractor-assisted endoscopy. Across all eleven patients, gross total resection was achieved in 90.9% of cases. Gross total resection was achieved in 100% of cases in which it was the operative intent (10/10); the remaining case was a planned biopsy of recurrent Ewing sarcoma. One transient postoperative lower extremity weakness was reported; no cerebrospinal fluid leaks, reoperations, or perioperative deaths occurred. No recurrences were observed across a mean follow-up of 21.9 months (range 4–48 months), though this duration may be insufficient to assess long-term recurrence for slow-growing tumors such as meningioma and schwannoma. Conclusions: ESS of primary spinal tumors appears feasible and safe in carefully selected cases, particularly for small, well-circumscribed lesions in favorable anatomical locations. Intradural resection introduced distinct technical challenges, including irrigation management and dural closure, which influence platform selection. These findings are limited by small sample size, short follow-up, and likely publication bias. ESS should be considered an emerging minimally invasive option rather than a replacement for established microsurgical approaches. Prospective comparative studies are needed to better define its role in spinal oncology.