Neurotrauma is a significant cause of morbidity and mortality worldwide. For instance, traumatic brain injury (TBI) causes more than 30% of all injury-related deaths in the USA annually. The underlying cause and clinical sequela vary among cases. Patients are liable to both acute and chronic changes in the nervous system after such a type of injury. Cerebrovascular disruption has the most common and serious effect in such cases because cerebrovascular autoregulation, which is one of the main determinants of cerebral perfusion pressure, can be effaced in brain injuries even in the absence of evident vascular injury. Disruption of the blood–brain barrier regulatory function may also ensue whether due to direct injury to its structure or metabolic changes. Furthermore, the autonomic nervous system (ANS) can be affected leading to sympathetic hyperactivity in many patients. On a cellular scale, the neuroinflammatory cascade medicated by the glial cells gets triggered in response to TBI. Nevertheless, cellular and molecular reactions involved in cerebrovascular repair are not fully understood yet. Most studies were done on animals with many drawbacks in interpreting results. Therefore, future studies including human subjects are necessarily needed. This review will be of relevance to clinicians and researchers interested in understanding the underlying mechanisms in neurotrauma cases and the development of proper therapies as well as those with a general interest in the neurotrauma field.

We compared the effectiveness and safety of deep brain stimulation (DBS) and magnetic resonance-guided focused ultrasound (MRgFUS) in patients with essential tremor (ET). A comprehensive search was conducted across four databases (Web of Science, Scopus, PubMed, and Cochrane CENTRAL) till June 2025. Clinical trials and observational studies comparing DBS and MRgFUS in patients with ET were included. Meta-analysis was performed using RevMan version 5.4 and OpenMetaAnalyst, applying a random-effect model. Five cohort studies (463 patients) were included. In the total Clinical Rating Scale for Tremor (CRST) score, there was a significant difference between the two groups favoring DBS (mean difference (MD): 5.12, 95% confidence interval (CI): [1.08, 9.16], P = 0.01), while in part A of the CRST, there was no significant difference ( P = 0.15). No significant difference was found between the two groups in response rate as well ( P = 0.56). Paresthesia (13.3% vs. 2.2%; risk ratio (RR): 4.57, 95% CI: [1.31, 15.94], P = 0.02), gait instability (26.56% vs. 4.06%; RR: 2.85, 95% CI: [1.14, 7.08], P = 0.025), and dysphagia (7.77% vs. 1.37%; RR: 3.40, 95% CI: [1.01, 11.46], P = 0.049) were significantly more frequent in the FUS group compared with DBS. Other serious but rare adverse events (AEs), such as infection and hemorrhage, were more common in the DBS group, but none significantly differed between the two groups. Both DBS and MRgFUS showed similar response rates; however, DBS may provide greater improvement in the total CRST score, potentially due to the comparison of bilateral DBS against predominantly unilateral MRgFUS. Regarding safety, MRgFUS was more associated with sensory and motor AEs, while infrequent but potentially serious complications were only reported with DBS. Future high-quality prospective studies with larger sample sizes and longer follow-up periods are needed.

Objective: To compare the accuracy, efficiency, and safety of robot-assisted versus frame-based stereoelectroencephalography (sEEG) in patients with drug-resistant epilepsy. Methods: In accordance with the PRISMA guidelines, a comprehensive literature search was conducted across four databases (PubMed, Scopus, Web of Science, and Cochrane) up to September 2025. We included comparative studies that evaluated robot-assisted versus frame-based sEEG in patients with drug-resistant epilepsy. A random-effects model was applied to calculate the mean difference (MD) and risk ratio (RR) with corresponding 95% confidence intervals (CI). Results: Eight retrospective comparative cohort studies (758 patients) were included. Regarding accuracy, there was no significant difference between the robot-assisted and frame-based sEEG in depth error (MD: 0.24 mm; 95% CI: -0.79 to 1.27), radial error (MD: 0.07 mm; 95% CI: -0.70 to 0.84), entry point error (EPE; MD: -1.35 mm; 95% CI: -2.74 to 0.04), and target point error (MD: -0.02 mm; 95% CI: -0.57 to 0.53). Robot-assisted sEEG demonstrated a significantly shorter overall operation time (MD: -32.58 min; 95% CI: -47.92 to -17.24) and operation time per electrode (MD: -6.55 min; 95% CI: -8.08 to -5.02). However, pre-implantation time (MD: -1.46 min; 95% CI: -14.02 to 11.11) and electrode number per patient (MD: 0.86; 95% CI: -0.84 to 2.56) were comparable between groups. There was no significant difference between the two groups in overall complication rates, including hemorrhagic events, neurological deficits, infections, and technical complications. Conclusion: Robot-assisted sEEG significantly reduced both overall operation time and operation time per electrode compared with the frame-based group. Both techniques demonstrated comparable accuracy and safety profiles.

Background: Metformin is a routinely prescribed medication for diabetes. Recently, physicians started to prescribe it for a variety of conditions, including polycystic ovarian syndrome (PCOS). It has adverse effects, just like any other medication; lactic acidosis is an uncommon but lethal side effect. The goal of this study was to illustrate the mechanisms of action of metformin in inducing lactic acidosis as well as two undetermined effects, including visceral obesity and the progression of gastroesophageal reflux disease (GERD). Methods: We present a case of a 23-year-old female with GERD who was treated with metformin for PCOS. We observed the emergence of lactic acidosis symptoms, as well as some unexpected symptoms such as visceral fat, and the advancement of GERD from equilibrium to acute, which lasted for up to a year after stopping metformin. Results: We found that metformin advanced GERD from an equilibrium to an acute condition in the presence of stress and a history of GERD. Furthermore, gastrointestinal issues have persisted even after a year of discontinuing metformin. Conclusion: We demonstrated that, despite metformin's powerful effects on the gastrointestinal system, it cannot primarily cause lactic acidosis. Lactic acidosis had developed as a result of metformin interacting with other factors, such as stress and a history of GERD. Our work is the first to capture metformin's connection with GERD; more research is needed to investigate that association and identify the long-term mechanism of metformin, particularly in individuals who have experienced lactic acidosis.