Injuries of the central (CNS) and peripheral nervous system (PNS) are a serious problem of the modern healthcare system. The situation is complicated by the lack of clinically effective neuroprotective drugs that can protect damaged neurons and glial cells from death. In addition, people who have undergone neurotrauma often develop mental disorders and neurodegenerative diseases that worsen the quality of life up to severe disability and death. Hydrogen sulfide (H₂S) is a gaseous signaling molecule that performs various cellular functions in normal and pathological conditions. However, the role of H₂S in neurotrauma and mental disorders remains unexplored and sometimes controversial. In this large-scale review study, we examined the various biological effects of H₂S associated with survival and cell death in trauma to the brain, spinal cord, and PNS, and the signaling mechanisms underlying the pathogenesis of mental illnesses, such as cognitive impairment, encephalopathy, depression and anxiety disorders, epilepsy and chronic pain. We also studied the role of H₂S in the pathogenesis of neurodegenerative diseases: Alzheimer’s disease (AD) and Parkinson’s disease (PD). In addition, we reviewed the current state of the art study of H₂S donors as neuroprotectors and the possibility of their therapeutic uses in medicine. Our study showed that H₂S has great neuroprotective potential. H₂S reduces oxidative stress, lipid peroxidation, and neuroinflammation; inhibits processes associated with apoptosis, autophagy, ferroptosis and pyroptosis; prevents the destruction of the blood-brain barrier; increases the expression of neurotrophic factors; and models the activity of Ca²⁺ channels in neurotrauma. In addition, H₂S activates neuroprotective signaling pathways in psychiatric and neurodegenerative diseases. However, high levels of H₂S can cause cytotoxic effects. Thus, the development of H₂S-associated neuroprotectors seems to be especially relevant. However, so far, all H₂S modulators are at the stage of preclinical trials. Nevertheless, many of them show a high neuroprotective effect in various animal models of neurotrauma and related disorders. Despite the fact that our review is very extensive and detailed, it is well structured right down to the conclusions, which will allow researchers to quickly find the proper information they are interested in.

Background: Connexins (Cx) are a family of transmembrane proteins that form gap junctions and connexin hemichannels (HCs), enabling direct intercellular communication within the nervous system. Connexin 43 (Cx43), the principal astrocytic connexin, exhibits a context-dependent dual role: under physiological conditions it maintains tissue homeostasis and metabolic support, whereas under pathological conditions excessive activation of Cx43 hemichannels promotes neuroinflammation, excitotoxicity, blood–brain barrier disruption, and secondary neural tissue damage. Other connexin isoforms also contribute to the pathogenesis of neurological and psychiatric disorders through alterations in neuronal synchronization, glial signaling, and myelin integrity. Objective: To systematize current evidence on the role of key connexin isoforms in acute nervous system injuries—including stroke, traumatic brain injury, spinal cord injury, and peripheral nerve injury—as well as chronic disorders such as neurodegenerative diseases, epilepsy, and psychiatric disorders, with particular emphasis on the functional duality of connexin channels and the therapeutic potential of their selective modulation. Methods: A systematic literature search was conducted in the PubMed, Scopus, and Web of Science databases in accordance with the PRISMA framework and the PRISMA Extension for Scoping Reviews guidelines. The review included data from experimental models, postmortem brain studies, genetic association analyses, and pharmacological intervention studies. The retrieved studies were screened, assessed for eligibility, and integrated using a qualitative narrative synthesis approach. Results: In acute neural injuries, hyperactivation of Cx43 hemichannels amplifies inflammatory signaling, edema formation, and neuronal death, whereas selective HCs inhibitors reduce lesion volume and improve functional outcomes in experimental models. Connexin 36 (Cx36) contributes to cortical spreading depolarization and seizure propagation, while Connexin 32 (Cx32) and Connexin 47 (Cx47) are critically involved in oligodendrocyte function and white-matter demyelination. In PNI, Cx43 upregulation contributes to neuropathic pain, whereas mutations in Cx32 cause hereditary demyelinating neuropathies. In neurodegenerative diseases—including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis—Cx43 hemichannel activity promotes neuroinflammation and pathological protein accumulation, while reduced Cx32/Cx47 expression disrupts metabolic support of axons. In psychiatric disorders such as major depressive disorder, bipolar disorder, and schizophrenia, decreased astrocytic connexin expression (Cx43 and Cx30) has been associated with impaired glial–neuronal communication and cognitive–emotional dysfunction. In epilepsy, increased Cx43/Cx30 expression contributes to neuronal hypersynchronization and blood–brain barrier dysfunction, whereas selective hemichannel blockade suppresses seizure activity. Conclusions: Cx—particularly Cx43—occupies a central position in the molecular mechanisms of secondary neural injury and network dysfunction. The dual functional properties of gap junctions and hemichannels determine their context-dependent effects across neurological and psychiatric diseases. Selective inhibition of pathological HCs activity shows significant neuroprotective and anticonvulsant potential and represents a promising direction for the development of targeted therapeutic strategies. Further studies are required to determine optimal therapeutic time windows, tissue-specific effects, and the long-term safety of Cx modulation.

Objective. To summarize data on indications for microsurgical resection of brain metastases, effect of resection technique on local control and leptomeningeal dissemination, as well as the role of stereotactic radiosurgery in improving local control. Material and methods. A descriptive review of data on surgical treatment of brain metastases was performed. We reviewed the PubMed/MEDLINE, the Cochrane Library (CENTRAL), PubMed Central, and eLIBRARY/RSCI databases between 2000 and January 2025 using the keywords “brain metastases”, “en bloc resection”, “piecemeal resection”, “local control”, “leptomeningeal disease”, “preoperative SRS” and “postoperative SRS”. Clinical studies, systematic reviews, meta-analyses, guidelines, and consensus documents were included. Studies on primary central nervous system tumors, samples ≤10 patients, and publications without extractable clinical outcomes were excluded. Results. The first part of the review considers indications for microsurgical resection in relation to clinical goals, survival and functional status. Surgery is reasonable for symptomatic large lesions, mass effect, diagnostic uncertainty, local recurrence, or complications after radiotherapy. Surgical technique should account for growth pattern of brain metastases: en bloc resection and, in selected cases, extended resection of peritumoral zone may improve local control. Retrospective data consistently associate piecemeal resection with higher risk of leptomeningeal dissemination, particularly for posterior fossa lesions and metastases adjacent to cerebrospinal fluid pathways. Conclusion. Surgical treatment is presented as a component of a personalized multimodal strategy. Decision-making on surgery should rely on survival prognosis and likelihood of clinically meaningful benefit. When technically feasible, en bloc resection may be considered as a preferable approach, especially when the risk of leptomeningeal dissemination is clinically relevant.

Late-onset Vitamin K deficiency bleeding is a rare disease that develops as a manifestation of Vitamin K deficiency in children from 8 days to 6 months of age with an incidence of 4.4 to 72 cases per 100,000 newborns in countries where prophylaxis with Vitamin K1 preparations is not carried out and of 0 to 3 cases per 100,000 in countries where prophylaxis is carried out. In Russia the prophylaxis is carried out using menadione sodium bisulfite, a Vitamin K3 preparation, the effectiveness of which is questionable. One of the specific manifestations of the late-onset Vitamin K deficiency bleeding is intracranial hemorrhage (ICH), which occurs in more than half of all cases of the disease. This disease has not been described in patients with hemophilia A until now. Authors represent a clinical case report of the development of the late-onset Vitamin K deficiency bleeding by a massive ICH in a patient with hemophilia A.