In central nervous system (CNS) surgery, the accurate identification of tumor boundaries, achieving complete resection of the tumor, and safeguarding healthy brain tissue remain paramount challenges. Despite the expertise of neurosurgeons, the infiltrative nature of the tumors into the surrounding brain tissue often hampers intraoperative differentiation between tumorous and non-tumorous tissue, thus hindering total tumor removal. Optical coherence tomography (OCT), with its unique advantages of high-resolution imaging, efficient image acquisition, real-time intraoperative detection, and radiation-free and noninvasive properties, offers accurate diagnostic capabilities and invaluable intraoperative guidance for minimally invasive CNS tumor diagnosis and treatment. Various OCT systems have been employed in neurological tumor research, including polarization-sensitive OCT systems, orthogonal polarization OCT systems, Doppler OCT systems, and OCT angiography systems. In addition, OCT-based diagnostic and therapeutic techniques have been explored for the surgical resection of CNS tumors. This review aims to compile and evaluate the research progress surrounding the principles of OCT systems and their applications in CNS tumors, providing insights into potential future research avenues and clinical applications.

Borderline personality disorder (BPD) is a dysfunctional, stable, and pervasive alteration in personality functioning with the inability to adapt to the environment, mental rigidity, and ego-syntonic. High suicidality in BPD patients underlines the significance of research into its pathology. While extensive research on the psychological and behavioral manifestations of BPD can be found in literature, the neuropsychological aspects of the disorder are still partially unknown, although the roles of certain brain structures in the manifestation of the pathology, such as the amygdala, hippocampus, insula, medial prefrontal and cingulate cortices, nucleus accumbens, and temporo-occipital areas, have already been clarified. This review aims to synthesize current knowledge of the neuroanatomical and functional correlates of BPD, providing insights that may inform future research and therapeutic strategies.

General anesthesia typically involves three key components: amnesia, analgesia, and immobilization. Monitoring the depth of anesthesia (DOA) during surgery is crucial for personalizing anesthesia regimens and ensuring precise drug delivery. Since general anesthetics act primarily on the brain, this organ becomes the target for monitoring DOA. Electroencephalogram (EEG) can record the electrical activity generated by various brain tissues, enabling anesthesiologists to monitor the DOA from real-time changes in a patient's brain activity during surgery. This monitoring helps to optimize anesthesia medication, prevent intraoperative awareness, and reduce the incidence of cardiovascular and other adverse events, contributing to anesthesia safety. Different anesthetic drugs exert different effects on the EEG characteristics, which have been extensively studied in commonly used anesthetic drugs. However, due to the limited understanding of the biological basis of consciousness and the mechanisms of anesthetic drugs acting on the brain, combined with the effects of various factors on existing EEG monitors, DOA cannot be accurately expressed via EEG. The lack of patient reactivity during general anesthesia does not necessarily indicate unconsciousness, highlighting the importance of distinguishing the mechanisms of consciousness and conscious connectivity when monitoring perioperative anesthesia depth. Although EEG is an important means of monitoring DOA, continuous optimization is necessary to extract characteristic information from EEG to monitor DOA, and EEG monitoring technology based on artificial intelligence analysis is an emerging research direction.

Epilepsy is an abnormal neurologic disorder distinguished by the recurrent manifestation of seizures, and the precise underlying mechanisms for its development and progression remain uncertain. In recent years, the hypothesis that inflammatory mediators and corresponding pathways contribute to seizures has been supported by experimental results. The potential involvement of neuroinflammation in the development of epilepsy has garnered growing interest. This review centers attention on the involvement of inflammatory mediators in the emergence and progression of epilepsy within recent years, focusing on both clinical research and animal models, to enhance comprehension of the intricate interplay between brain inflammation and epileptogenesis.

Parkinson's disease (PD) is a neurodegenerative disease characterized by degeneration of dopamine neurons in the substantia nigra pars compacta. The patient exhibits a series of motor symptoms, such as static tremors, which impair their capacity to take care for themselves in daily life. In the late stage, the patient is unable to walk independently and is bedridden for an extended period of time, reducing their quality of life significantly. So far, treatment methods for PD mainly include drug therapy and deep brain stimulation. Pharmacotherapy is aimed at increasing dopamine (DA) levels; however, the treatment effect is more pronounced in the short term, and there is no benefit in improvement in the overall progression of the disease. In recent years, novel therapeutic strategies have been developed, such as cell reprogramming, trying to generate more DA in PD treatment. This review mainly discusses the advantages, methodology, cell origin, transformation efficiency, and practical application shortcomings of cell reprogramming therapy in PD strategy.

Gastrodin, as an effective monomer of gastrodia elata, plays a significant role in anti-inflammatory, antioxidant, antiapoptosis, and other aspects. As the global aging process continues to intensify, diseases of the central nervous system, cardiovascular system, and immune system have brought serious economic and mental burdens to families and have become a major challenge for global public health resources. Many studies have proved that gastrodin may be a potential drug for neurological diseases and ischemic injury but its mechanism of action is still unclear. [Correction added on 19 February 2025, after first online publication: In the preceding sentence, “the treatment of various systemic diseases” has been corrected to “neurological diseases and ischemic injury” in this version.]. In this study, the pharmacological action of gastrodin and the possible mechanism of regulating ferroptosis and pyroptosis were reviewed to provide a new treatment and research direction for clinicians and researchers.

The aggregation of β-amyloid (Aβ) peptides has been associated with the onset of Alzheimer's disease (AD) by causing neurotoxicity due to oxidative stress and apoptosis. Cordycepin is a natural derivative of the nucleoside adenosine that displays potent antioxidant, antitumor, anti-inflammatory, and neuroprotective properties. However, the mechanism of the neuroprotective effect of cordycepin toward Aβ-induced neurotoxicity, as well as underlying mechanisms, is still unclear. In this study, we found that cordycepin conferred neuroprotection to catecholaminergic PC12 neuronal cell cultures exposed to Aβ_1–42-insult by reducing the production of reactive oxygen species, restoring the mitochondrial membrane potential, and inhibiting apoptosis. Cordycepin stimulated the phosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP-responsive element-binding protein (CREB) in a time- and concentration-dependent manner. Inhibition of the ERK pathway reduced the neuroprotective effect of cordycepin. Similar results were obtained with hippocampal HT22 neuronal cell cultures. Cumulatively, these findings suggest that cordycepin-induced neuroprotection toward Aβ_1–42 neurotoxic insult may involve activation of the ERK/CREB pathway. This study expands our knowledge of the neuroprotective function of cordycepin and suggests that it holds promise as a natural lead compound for drug development in AD.

This study aimed to investigate the causal relationship between systemic lupus erythematosus (SLE) and juvenile myoclonic epilepsy (JME). Univariable and reverse Mendelian randomization (MR) analyses were performed to investigate the potential causal associations between SLE, systemic autoimmune disorders (SADs), and JME. Two-step mediation MR analysis was further performed to explore indirect factors that may influence the relationship between SLE and JME. Summary data on SADs were extracted from the Integrative Epidemiology Unit Open genome-wide association study database, and summary statistics for JME were acquired from the International League Against Epilepsy Consortium. The inverse-variance weighted (IVW) method was used for primary analysis, supplemented by MR-Egger and weighted median. In the univariable MR analysis, IVW results indicated a causal relationship between SLE and an increased risk of JME (odds ratio = 1.0030, 95% confidence interval, 1.0004–1.0057; p = 0.023). The subsequent mediation MR analysis showed that inflammatory cytokines may not be the mediating factors between SLE and JME, while the inverse MR analysis found no significant relationship. Our study indicated that genetic susceptibility to SLE was causally linked to JME. However, subsequent mediation analysis failed to identify the potential mediators that could influence this relationship. Moreover, evidence suggested that other SADs were not causally associated with JME. This study may provide guidance for screening risk factors for seizures and exploring potential treatments in SLE and JME, and even all SADs and JME.

A middle-aged man experienced intermittent acupuncture-like pain in the skin of the right scrotum and medial thigh 1 month after undergoing laparoscopic high ligation of the right hernial sac for a right indirect inguinal hernia in November 2020, and the pain persisted for 6 months. Under ultrasound guidance, ilioinguinal and genitofemoral nerve block and local adhesion water separation were performed with a mixture of 0.25% lidocaine (6 mL) plus prednisolone acetate (10 mg), and the same drugs and methods were repeated five times once a week. After five treatments, the visual analogue scale (VAS) score was reduced from 7 before treatment to 1. During the follow-up period, at 3 months after the end of treatment, the VAS score remained at 0, and this score was sustained at 0 even at the 6-month follow-up. These outcomes indicate that ultrasound-guided nerve block combined with water separation technology can effectively alleviate neuralgia caused by surgical adhesion, which holds important clinical significance in managing such conditions.

A 57-year-old man who suffered from a headache for 1 year, accompanied by blurred vision for 7 months and numbness in his left face for 1 week was admitted to the Affiliated Hospital of Zunyi Medical University on May 7, 2022. One year ago, the patient had no obvious precipitating factor of paroxysmal stabbing pain in the whole skull with dizziness, which could be relieved by oneself after lasting for 1–2 min each time, with about 20 episodes per day. The cranial magnetic resonance imaging revealed changes in bilateral frontal lobe ischemic foci, bilateral frontal, ethmoid, sphenoid and maxillary sinusitis, and retinal macular degeneration. After hormone shock treatment, the condition improved. He suffered from headaches again with blurred vision in the right eye 7 months ago and was initially diagnosed with multiple sclerosis. He then was discharged after improvement due to hormone shock therapy. Oral hormone therapy was continued outside the hospital, but he stopped it due to drug side effects (details remained unclear). After cutting off, he developed a headache and visited our hospital once more, the relevant tests were performed and the patient was diagnosed with idiopathic hypertrophic pachymeningitis (IHP). The symptoms were slightly abated after hormone therapy. We hope that through this case report, we can deepen the clinicians' understanding of IHP, and improve the diagnosis rate of the disease through relevant examinations in future clinical work, so that patients can receive timely treatment and the mental pressure and economic burden caused by the disease on patients are reduced.