Brain-computer interfaces (BCIs), a remarkable technological advancement in neurology and neurosurgery, mark a significant leap since the inception of electroencephalography in 1924. These interfaces effectively convert central nervous system signals into commands for external devices, offering revolutionary benefits to patients with severe communication and motor impairments due to a myriad of neurological conditions like stroke, spinal cord injuries, and neurodegenerative disorders. BCIs enable these individuals to communicate and interact with their environment, using their brain signals to operate interfaces for communication and environmental control. This technology is especially crucial for those completely locked in, providing a communication lifeline where other methods fall short. The advantages of BCIs are profound, offering autonomy and an improved quality of life for patients with severe disabilities. They allow for direct interaction with various devices and prostheses, bypassing damaged or nonfunctional neural pathways. However, challenges persist, including the complexity of accurately interpreting brain signals, the need for individual calibration, and ensuring reliable, long-term use. Additionally, ethical considerations arise regarding autonomy, consent, and the potential for dependence on technology. Despite these challenges, BCIs represent a transformative development in neurotechnology, promising enhanced patient outcomes and a deeper understanding of brain-machine interfaces.

Background: Hydrocephalus or ventriculomegaly is a condition brought on by an overabundance of cerebrospinal fluid (CSF) in the ventricular system. The major contributor to posttraumatic hydrocephalus (PTH) is traumatic brain injuries (TBIs), especially in individuals with occupations set in industrial settings. A variety of criteria have been employed for the diagnosis of PTH, including the combination of neurological symptoms like nerve deficits and headache, as well as an initial improvement followed by a worsened relapse of altered consciousness and neurological deterioration, which is detected by computed tomography‐brain imaging that reveals gradual ventriculomegaly.Aim: In this article, we discuss and summarize briefly the current understandings and advancements in the management of PTH.Methods: The available literature for this review was searched on various bibliographic databases using an individually verified, prespecified approach. The level of evidence of the included studies was considered as per the Centre for Evidence‐Based Medicine recommendations.Results: The commonly practiced current treatment modality involves shunting CSF but is often associated with complications and recurrence. The lack of a definitive management strategy for PTH warrants the utilization of novel and innovative modalities such as stem cell transplantations and antioxidative stress therapies.Conclusion: One of the worst complications of a TBI is PTH, which has a high morbidity and mortality rate. Even though there hasn't been a successful method in stopping PTH from happening, hemorrhage‐derived blood, and its metabolic by‐products, like iron, hemoglobin, free radicals, thrombin, and red blood cells, may be potential targets for PTH hindrance and management. Also, using stem cell transplantations in animal models and antioxidative stress therapies in future studies can lower PTH occurrence and improve its outcome. Moreover, the integration of clinical trials and theoretical knowledge should be encouraged in future research projects to establish effective and updated management guidelines for PTH.

Chromosomal instability (CIN) is a pivotal factor in gliomas, contributing to their complexity, progression, and therapeutic challenges. CIN, characterized by frequent genomic alterations during mitosis, leads to genetic abnormalities and impacts cellular functions. This instability results from various factors, including replication errors and toxic compounds. While CIN’s role is well documented in cancers like ovarian cancer, its implications for gliomas are increasingly recognized. CIN influences glioma progression by affecting key oncological pathways, such as tumor suppressor genes (e.g., TP53), oncogenes (e.g., EGFR), and DNA repair mechanisms. It drives tumor evolution, promotes inflammatory signaling, and affects immune interactions, potentially leading to poor clinical outcomes and treatment resistance. This review examines CIN’s impact on gliomas through a narrative approach, analyzing data from PubMed/Medline, EMBASE, the Cochrane Library, and Scopus. It highlights CIN’s role across glioma subtypes, from adult glioblastomas and astrocytomas to pediatric oligodendrogliomas and astrocytomas. Key findings include CIN’s effect on tumor heterogeneity and its potential as a biomarker for early detection and monitoring. Emerging therapies targeting CIN, such as those modulating tumor mutation burden and DNA damage response pathways, show promise but face challenges. The review underscores the need for integrated therapeutic strategies and improved bioinformatics tools like CINdex to advance understanding and treatment of gliomas. Future research should focus on combining CIN-targeted therapies with immune modulation and personalized medicine to enhance patient outcomes.

Complications are plausible events during surgical operations. Surgical complications profoundly impact surgeons, often called “second victims” of adverse events. These complications trigger a range of emotional and psychological responses, including guilt, anxiety, heightened empathy, and the looming threat of burnout. Moreover, the toll extends to physical health, with chronic stress and sleep disturbances taking their toll. Surgeons’ social lives are not immune to the fallout, and their career satisfaction may wane, pushing some towards defensive medicine practices. While mentorship, counselling, and peer support are crucial support mechanisms, they encounter barriers such as time constraints and the fear of negative perceptions. This paper suggests practical recommendations, including comprehensive wellness programmes, a streamlined badge card system for easy access to resources, and mindfulness training to mitigate stress and burnout. Recognising and proactively addressing these multifaceted impacts is imperative for cultivating a resilient medical community capable of providing optimal patient care.

Cerebrovascular diseases (CVDs) include conditions such as stroke, cerebral amyloid angiopathy (CAA) and cerebral small vessel disease (CSVD), which contribute significantly to global morbidity and healthcare burden. The pathophysiology of CVD is complex, involving inflammatory, cellular and vascular mechanisms. Recently, research has focused on triggering receptor expressed on myeloid cells 2 (TREM2), an immune receptor predominantly found on microglia. TREM2 interacts with multiple signalling pathways, particularly toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB), inhibiting patients' inflammatory response. This receptor plays an essential role in both immune regulation and neuroprotection. TREM2 deficiency or dysfunction is associated with impaired microglial responses, exacerbated neurodegeneration and neuroinflammation. Up until recently, TREM2 related studies have focused on neurodegenerative diseases (NDs), however a shift in focus towards CVDs is beginning to take place. Advancements in CVD research have focused on developing therapeutic strategies targeting TREM2 to enhance recovery and reduce long-term deficits. These include the exploration of TREM2 agonists and combination therapies with other anti-inflammatory agents, which may synergistically reduce neuroinflammation and promote neuroprotection. The modulation of TREM2 activity holds potential for innovative treatment approaches aimed at improving patient outcomes following cerebrovascular insults. This review compiles current research on TREM2, emphasising its molecular mechanisms, therapeutic potential, and advancements in CNS disease research.

Whole-exome sequencing (WES), a ground-breaking technology, has emerged as a linchpin in neurology and neurosurgery, offering a comprehensive elucidation of the genetic landscape of various neurological disorders. This transformative methodology concentrates on the exonic portions of DNA, which constitute approximately 1% of the human genome, thus facilitating an expedited and efficient sequencing process. WES has been instrumental in advancing our understanding of neurodegenerative diseases, neuro-oncology, cerebrovascular disorders, and epilepsy by revealing rare variants and novel mutations and providing intricate insights into their genetic complexities. This has been achieved while maintaining a substantial diagnostic yield, thereby offering novel perspectives on the pathophysiology and personalized management of these conditions. The utilization of WES boasts several advantages over alternative genetic sequencing methodologies, including cost-effectiveness, reduced incidental findings, simplified analysis and interpretation process, and reduced computational demands. However, despite its benefits, there are challenges, such as the interpretation of variants of unknown significance, cost considerations, and limited accessibility in resource-constrained settings. Additionally, ethical, legal, and social concerns are raised, particularly in the context of incidental findings and patient consent. As we look to the future, the integration of WES with other omics-based approaches could help revolutionize the field of personalized medicine through its implications in predictive models and the development of targeted therapeutic strategies, marking a significant stride toward more effective and clinically oriented solutions. Graphical Abstract