Mild traumatic brain injury results in aberrant free radical generation, which is associated with oxidative stress, secondary injury signaling cascades, mitochondrial dysfunction, and poor functional outcome. Pharmacological targeting of free radicals with antioxidants has been examined as an approach to treatment, but has met with limited success in clinical trials. Conventional antioxidants that are currently available scavenge a single free radical before they are destroyed in the process. Here, we report for the first time that a novel regenerative cerium oxide nanoparticle antioxidant reduces neuronal death and calcium dysregulation after in vitro trauma. Further, using an in vivo model of mild lateral fluid percussion brain injury in the rat, we report that cerium oxide nanoparticles also preserve endogenous antioxidant systems, decrease macromolecular free radical damage, and improve cognitive function. Taken together, our results demonstrate that cerium oxide nanoparticles are a novel nanopharmaceutical with potential for mitigating neuropathological effects of mild traumatic brain injury and modifying the course of recovery.

Background: Surgical outcome prediction has assisted physicians in discussing surgical intervention or expectant management. While increasing pituitary tumor size would seem to be associated with increasing challenge of removal and associated complications, that relationship has not been borne in the literature. Methods: We performed a retrospective review of a consecutive cohort of pituitary surgeries completed at our institution. Data included age at the time of surgery, presenting symptoms and Glasgow Coma scale (GCS), GCS at discharge or 7 days postoperatively, GCS at 6 months, adenoma size, imaging characteristics of the tumor and brain before resection, postoperative complications, the presence of preoperative hydrocephalus, brainstem compression, and patient mortality. Results: Patients with giant adenomas were more likely to present with a cranial nerve palsy (P = 0.019), altered mental status (P = 0.0001), hydrocephalus (P = 0.002), and mass effect on the brainstem (P = 0.020). Patients who experienced a postoperative decline in mental status were more likely to present with altered mental (P = 0.006), had an increased prevalence of mass effect on the brainstem (P = 0.005), and were more likely to have either an ischemic stroke (P = 0.0001) and vasospasms or new intraparenchymal hemorrhage (P = 0.013). Conclusion: The results of this study demonstrate that postoperative mental status declines after pituitary adenoma resection can be directly related to brainstem compression and further surgical irritation of the surrounding vasculature. The intraoperative irritation can be multifactorial and may result as the decompressed brain structures assume their anatomical position.

Introduction:Intracranial hemorrhage (ICH) accounts for significant morbidity and mortality in the United States. Many studies have looked at the benefits of surgical intervention for ICH. Recent results for Minimally Invasive Surgery Plus Recombinant Tissue-type Plasminogen Activator for Intracerebral Hemorrhage-II trials have shown promise for a minimally invasive clot evaluation on improving perihematomal edema. Often rural or busy county medical centers may not have the resources available for immediate operative procedures that are nonemergent. In addition, ICH disproportionally affects the elderly which may not be stable for general anesthetics. This study looks at a minimally invasive bedside approach under conscious sedation for evacuation of ICH.Materials and Methods:Placement of the intraparenchymal hemorrhage drain utilizes bony anatomical landmarks referenced from computed tomography (CT) head to localize the entry point for the trajectory of drain placement. Using the hand twist drill intracranial access is gained the clot accessed with a brain needle. A Frazier suction tip with stylet is inserted along the tract then the stylet is removed. The clot is then aspirated, and suction is then turned off, and Frazier sucker is removed. A trauma style ventricular catheter is then passed down the tract into the center of hematoma and if no active bleeding is noted on postplacement CT and catheter is in an acceptable position then 2 mg recombinant tissue plasminogen activator are administered through the catheter and remaining clot is allowed to drain over days.Results:A total of 12 patients were treated from October 2014 to December 2017. The average treatment was 6.4 days. The glascow coma scale score improved on an average from 8 to 11 posttreatment with a value of P is 0.094. The average clot size was reduced by 77% with a value of P = 0.0000035. All patients experienced an improvement in expected mortality when compared to the predicted ICH score.Discussion:The results for our series of 12 patients show a trend toward improvement in Glasgow Coma Scale after treatment with minimally invasive intraparenchymal clot evacuation and drain placement at the bedside; although, it did not reach statistical significance. There was a reduction in clot size after treatment, which was statistically significant. In addition, the 30-day mortality actually observed in our patients was lower than that estimated using ICH score. Based on our experience, this procedure can be safely performed at the bedside and has resulted in better outcomes for these patients.

A trend was observed in which the closer the fixed dosage approximated the weight-based dosing of phenytoin, the more their CSF phenytoin level increased (and approximated the therapeutic range) with an associated R-squared value of 0.6274. This trend was not found in patients receiving levetiracetam. Conclusions Levetiracetam does not reach levels needed for seizure prophylaxis in human CSF when loaded at standard dosing regimens in the acute setting. Phenytoin does reach levels needed for seizure prophylaxis in human CSF with standardized regimen dosing when dosages approximate weight-based dosing. If needed, in the acute setting phenytoin should have additional doses given prior to six hours after the loading dose to achieve therapeutic CSF levels.