Neurosurgical Review最新文献

Tardigrades are microscopic organisms known for their remarkable resilience to extreme environmental conditions, including radiation and desiccation. Two key proteins, Dsup (Damage suppressor protein) and CAHS D (Cytoplasmic Abundant Heat Soluble protein D), play crucial roles in this resilience. Dsup protects DNA from radiation-induced damage, while CAHS D stabilizes cellular structures during desiccation by interacting with, but not retaining, water. These unique mechanisms have significant potential applications in neurosurgery and neuroscience. Dsup could inspire the development of protective agents for neural tissues during radiation-based treatments, minimizing collateral damage and improving patient outcomes. Meanwhile, CAHS D's stabilization properties could lead to new neuroprotective strategies, safeguarding brain cells under stress. Together, these tardigrade proteins offer innovative solutions for enhancing neural protection, opening new avenues for treating neurological conditions and improving the safety and efficacy of neurosurgical procedures.

The study by Canisius et al. (2022) explores the expression of decitabine-targeted oncogenes (TRIM58, FAM84B, ELOVL2, DIO3) in meningiomas, aiming to evaluate decitabine's therapeutic potential for high-grade tumors. Using immunohistochemical staining and RT-PCR in over 100 patient samples, the authors found significant correlations between oncogene expression and tumor grade, with elevated ELOVL2 levels being linked to tumor recurrence. This work highlights the role of decitabine in modulating oncogene expression and suggests its potential in treating refractory meningiomas. Despite the robust methodology, limitations such as the small sample size and the lack of comprehensive molecular data were noted. Future research should incorporate larger sample sizes and advanced genomic techniques like RNA sequencing to better understand oncogenic mechanisms. The study emphasizes the need for further in situ analyses of decitabine's efficacy, setting the foundation for future neuro-oncological treatments.

Chordomas of the skull base are rare, slow growing, locally invasive cancers with limited long-term survival analysis reported in the literature. We seek to provide comparative survival analysis of patients on a long-term (20-year) basis using population-level data. The Surveillance, Epidemiology, and End Results (SEER) program was queried for cases of chordoma relegated to the base of the skull, diagnosed between 2000 and 2020. Demographic, disease, and treatment information were analyzed using Cox proportional hazards and log-rank comparisons. 630 patients with chordoma of the skull base were identified. Age ≤ 49 years at diagnosis was associated with increased five-, 10-, and 20-year overall survival (hazard ratio (HR) = 0.39, 0.33, and 0.30, respectively; p < 0.001 for all). Treatment with surgery and adjuvant radiotherapy was associated with increased five-, 10-, and 20-year survival (HR = 0.71, 0.79, and 0.79, respectively; p < 0.001 for all). On univariate analysis, widowed patients had decreased survival (20-year overall survival = 34.8% [15.3%-34.8%] compared to married patients (74.4% [68.1%-80.8%]. Surgery remains the primary treatment associated with increased survival among patients with chordoma of the skull base, with adjuvant radiotherapy serving a complimentary role. Demographic factors such as marital status are also associated with changes in survival.

The article by Liu et al. (2024) investigates the progression of ossification of the posterior longitudinal ligament (OPLL) in 29 patients post-cervical laminoplasty. The study meticulously tracks transverse and longitudinal OPLL progression, providing crucial insights into surgical planning and patient outcomes. While the research design is commendable, reliance on X-ray imaging limits precision compared to CT or MRI scans. The sample size, though adequate for initial findings, may not fully capture OPLL variability, and the follow-up period could be extended to better assess long-term outcomes. Future studies should incorporate advanced imaging techniques, larger cohorts, and patient-reported outcomes to enhance the understanding of OPLL progression, thereby refining surgical strategies and improving personalized care for OPLL patients.

A variety of treatment modalities currently exist for epilepsy, a debilitating disorder. With the emergence of drug-resistant epilepsy, however, new options are being explored. Deep brain stimulation is a neuromodulation technique that can prove to be a ground-breaking treatment option for pediatric epilepsy. It employs a neurosurgical method in which electrodes are implanted within the brain that send impulses to control abnormal brain activity. Significant gaps exist in literature, thereby emphasizing the importance of further research in this promising approach.

The article "Decoding pediatric spinal tumors: a single-center retrospective case series on etiology, presentation, therapeutic strategies, and outcomes" by Lenga et al. (2024) provides essential insights into pediatric spinal tumors, a rare and challenging area of medical research. The authors present a thorough analysis of clinical presentations, treatment strategies, and patient outcomes, offering valuable data to refine therapeutic approaches and improve outcomes. However, the study's retrospective design, confined to a single center, introduces potential biases and limits the generalizability of findings. The lack of long-term follow-up data and a control group further restricts the study's scope. Future research should prioritize multi-center collaborations, incorporate control groups, and extend follow-up durations to better understand long-term outcomes. The establishment of standardized treatment protocols is also recommended to enhance consistency in managing pediatric spinal tumors across diverse clinical settings.

Wu et al. (2021) investigated the neuroprotective effects of hypoxia preconditioning (HPC) in a rat model of traumatic brain injury (TBI). The study demonstrated that HPC enhances brain resilience to TBI by upregulating glucose transporters GLUT1 and GLUT3 through the HIF-1α signaling pathway. Comprehensive molecular and histological analyses confirmed increased expression of these transporters, correlating with reduced neuronal apoptosis and cerebral edema. The robust methodology, including rigorous statistical validation and time-course assessments, underscores HPC's potential therapeutic role in mitigating neuronal loss and improving glucose transport post-injury. However, the study could be strengthened by incorporating additional preconditioning controls, comparative analyses with other neuroprotective strategies, and exploring downstream metabolic effects in greater detail. Furthermore, expanding the research to include diverse animal models and examining sex-dependent responses would enhance the generalizability and translational relevance of the findings. Future studies should also integrate metabolic flux analysis and advanced imaging techniques to further elucidate HPC's mechanisms of action.