Authors
Kozin A. I.
Scientific department of Russian armed forces1
ORCID iD: 0009-0004-1845-3865
1Federal State Budgetary Military Educational Institution of Higher Education «S. M. Kirov Military Medical Academy», Saint Petersburg, Russia
Corresponding author
Kozin Alexander Igorevich; e-mail: virko-viktor@mail.ru
Funding
The study had no sponsorship.
Conflict of interest
The authors declare no conflict of interest.
Received
03.04.2026
Accepted for publication
11.05.2026
Abstract
Severe traumatic brain injury (TBI) remains one of the leading causes of death and disability worldwide. The key pathogenetic mechanism is secondary brain injury driven by excitotoxicity, neuroinflammation, oxidative stress, and neuronal apoptosis. Sedative therapy in neurocritical care has traditionally been used to control intracranial pressure and synchronize with the ventilator, but current evidence indicates its potential as an active neuroprotective intervention. Objective. To analyze current understanding of the molecular mechanisms of neuroprotection achieved with sedative and anesthetic agents in patients with severe TBI, evaluate the clinical efficacy of various sedation strategies, and identify promising directions for the development of this method. A review of Russian and international literature from 2012 to 2026 was conducted using PubMed, Scopus, eLibrary, and Cochrane Library databases. Systematic reviews, meta-analyses, clinical guidelines were included, randomized controlled trials, experimental studies on neuroprotective effects of sedative drugs. Results. Sedative agents exert neuroprotective effects by modulating key components of secondary injury: inhibition of NMDA receptors (xenon, ketamine), activation of PI3K/Akt/mTOR and Nrf2 signaling pathways (sevoflurane, xenon), and suppression of NLRP3 inflammasome and neuroinflammation (dexmedetomidine, sevoflurane). Clinical studies have demonstrated that propofol and sevoflurane effectively reduce intracranial pressure, while dexmedetomidine and xenon improve cerebral oxygenation and neurological outcomes. Promising directions include inhaled sedation (sevoflurane, xenon, argon), the use of new drugs (ciprofol, remimazolam), and combined strategies. Conclusions. Sedative therapy in TBI extends beyond symptomatic control, becoming an active neuroprotective intervention. An optimal strategy requires a personalized approach that considers the pharmacological properties of the drugs, the specific features of the injury course and individual patient factors.
Key words
traumatic brain injury, neuroprotection, sedation, intracranial pressure, neuroinflammation, intravenous anesthetics, inhalation anesthetics
DOI
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