Intracranial-Pressure-Monitoring-Assisted Management Associated with Favorable Outcomes in Moderate Traumatic Brain Injury Patients with a GCS of 9–11

Objective: With a mortality rate of 10–30%, a moderate traumatic brain injury (mTBI) is one of the most variable traumas. The indications for intracranial pressure (ICP) monitoring in patients with mTBI and the effects of ICP on patients’ outcomes are uncertain. The purpose of this study was to examine the indications of ICP monitoring (ICPm) and its effects on the long-term functional outcomes of mTBI patients. Methods: Patients with Glasgow Coma Scale (GCS) scores of 9–11 at Tangdu hospital, between January 2015 and December 2021, were enrolled and treated in this retrospective cohort study. We assessed practice variations in ICP interventions using the therapy intensity level (TIL). Six-month mortality and a Glasgow Outcome Scale Extended (GOS-E) score were the main outcomes. The secondary outcome was neurological deterioration (ND) events. The indication and the estimated impact of ICPm on the functional outcome were investigated by using binary regression analyses. Results: Of the 350 patients, 145 underwent ICP monitoring-assisted management, and the other 205 patients received a standard control based on imaging or clinical examinations. A GCS ≤ 10 (OR 1.751 (95% CI 1.216–3.023), p = 0.003), midline shift (mm) ≥ 2.5 (OR 3.916 (95% CI 2.076–7.386) p < 0.001), and SDH (OR 1.772 (95% CI 1.065–2.949) p = 0.028) were predictors of ICP. Patients who had ICPm (14/145 (9.7%)) had a decreased 6-month mortality rate compared to those who were not monitored (40/205 (19.5%), p = 0.011). ICPm was linked to both improved neurological outcomes at 6 months (OR 0.815 (95% CI 0.712–0.933), p = 0.003) and a lower ND rate (2 = 11.375, p = 0.010). A higher mean ICP (17.32 ± 3.52, t = −6.047, p < 0.001) and a more significant number of ICP > 15 mmHg (27 (9–45.5), Z = −5.406, p < 0.001) or ICP > 20 mmHg (5 (0–23), Z = −4.635, p < 0.001) 72 h after injury were associated with unfavorable outcomes. The best unfavorable GOS-E cutoff value of different ICP characteristics showed that the mean ICP was >15.8 mmHg (AUC 0.698; 95% CI, 0.606–0.789, p < 0.001), the number of ICP > 15 mmHg was >25.5 (AUC 0.681; 95% CI, 0.587–0.774, p < 0.001), and the number of ICP > 20 mmHg was >6 (AUC 0.660; 95% CI, 0.561–0.759, p < 0.001). The total TIL score during the first 72 h post-injury in the non-ICP group (9 (8, 11)) was lower than that of the ICP group (13 (9, 17), Z = −8.388, p < 0.001), and was associated with unfavorable outcomes. Conclusion: ICPm-assisted management was associated with better clinical outcomes six months after discharge and lower incidences of ND for seven days post-injury. A mean ICP > 15.8 mmHg, the number of ICP > 15 mmHg > 25.5, or the number of ICP > 20 mmHg > 6 implicate an unfavorable long-term prognosis after 72 h of an mTBI

Ependymomas with extraneural metastasis to lung in children: A case report and literature review

Ependymomas, which account for 10% of pediatric central nervous system (CNS) tumors, arise from the ependymal cells that line the cerebral ventricles and the central canal of the spinal cord. Extraneural metastasis to lung is rare for ependymomas primary tumors. Repeated surgeries that disrupt the blood-brain barrier may contribute to haematogenous spread, but the mechanism remains unclear. We present a case of ependymoma with extraneural metastasis to lung in a child and discuss reported cases of extracranial metastatic ependymoma with this presentation

Risk factors for hemorrhage in patients with long-term aspirin therapy undergoing emergency external ventricular drainage/intracranial pressure probe placement

Background: Studies have been inconclusive on the risk for hemorrhage in patients with a history of aspirin use who underwent emergency external ventricular drainage (EVD)/intracranial pressure (ICP) probe placement. The aim of this study was to explore hemorrhage-related risk factors in order to reduce the risk for hemorrhage in these patients. Methods: Between July 2014 and July 2020, patients were retrospectively divided into EVD/ICP-related hemorrhage and non-hemorrhage groups. The collected data included age, gender, major diagnosis, medical history, imaging examinations, conventional coagulation test data, thromboelastography with platelet mapping (TEG-PM), surgical procedures and discharge conditions. Results: In total 94 patients, 21 in the hemorrhage group (15 males, 6 females) and 73 in the non-hemorrhage group (52 males, 21 females) were included. The majority of hemorrhages were recorded in EVD patients (19/21; 90.5%). Platelet AA pathway inhibition rate of ≥75% (sensitivity: 79.45% specificity: 52.38%) (P = 0.014) and SBP ≥125 mmHg (P = 0.006) were significantly related to hemorrhage. When the platelet AA pathway inhibition rate was ≥75% and the during-procedure SBP was ≥125 mmHg, the hemorrhage rate was significantly higher (83.3%) than with SBP  0.05). Multivariate logistic regression analysis revealed that a platelet AA pathway inhibition rate ≥75% (OR = 5.183, 95% CI: 1.683–15.960) and during-procedure SBP ≥125 mmHg (OR = 4.609, 95% CI: 1.466–14.484) were independent risk factors for EVD/ICP-related hemorrhage. Conclusion: Patients with long-term aspirin therapy, a platelet AA pathway inhibition rate ≥75% and during-procedure SBP ≥125 mmHg had a significantly higher risk of hemorrhage, which could be reduced by adjusting the SBP to <125 mmHg

Astrocyte‐Derived Extracellular Vesicular miR‐143‐3p Dampens Autophagic Degradation of Endothelial Adhesion Molecules and Promotes Neutrophil Transendothelial Migration after Acute Brain Injury

Abstract Pivotal roles of extracellular vesicles (EVs) in the pathogenesis of central nervous system (CNS) disorders including acute brain injury are increasingly acknowledged. Through the analysis of EVs packaged miRNAs in plasma samples from patients with intracerebral hemorrhage (ICH), it is discovered that the level of EVs packaged miR‐143‐3p (EVs‐miR‐143‐3p) correlates closely with perihematomal edema and neurological outcomes. Further study reveals that, upon ICH, EVs‐miR‐143‐3p is robustly secreted by astrocytes and can shuttle into brain microvascular endothelial cells (BMECs). Heightened levels of miR‐143‐3p in BMECs induce the up‐regulated expression of cell adhesion molecules (CAMs) that bind to circulating neutrophils and facilitate their transendothelial cell migration (TEM) into brain. Mechanism‐wise, miR‐143‐3p directly targets ATP6V1A, resulting in impaired lysosomal hydrolysis ability and reduced autophagic degradation of CAMs. Importantly, a VCAM‐1–targeting EVs system to selectively deliver miR‐143‐3p inhibitor to pathological BMECs is created, which shows satisfactory therapeutic effects in both ICH and traumatic brain injury (TBI) mouse models. In conclusion, the study highlights the causal role of EVs‐miR‐143‐3p in BMECs’ dysfunction in acute brain injury and demonstrates a proof of concept that engineered EVs can be devised as a potentially applicable nucleotide drug delivery system for the treatment of CNS disorders