Sedation in Acute Ischemic Stroke: Pathophysiological Basis and Evidence for Commonly Used Agents.

Sedation is frequently required in the acute management of ischemic stroke (AIS), yet its potential to influence secondary brain injury and systemic complications remains insufficiently integrated into clinical practice. This narrative review examines experimental and clinical evidence on the biological effects of commonly used sedatives in neurocritical care, propofol, dexmedetomidine, and ketamine, and explores their potential role as active therapeutic agents in AIS. Experimental studies consistently show that propofol reduces oxidative injury and apoptotic signalling, dexmedetomidine attenuates neuroinflammation and sympathetic overactivation, and ketamine limits excitotoxicity through N-methyl-D-aspartate receptor blockade. Together, these mechanisms provide a plausible basis for mitigating infarct progression and protecting vulnerable neural networks during the acute phase. Clinical data remain limited, predominantly observational, and heterogeneous, but suggest that sedative choice may influence neurological recovery, hemodynamic stability, and extra-cerebral organ function. These potential benefits must be weighed against known risks, including hemodynamic effects of propofol, blood pressure reductions with dexmedetomidine, and historical concerns regarding ketamine and intracranial dynamics. At present, the absence of standardized sedation strategies for AIS and the variability in study design preclude firm conclusions. Recognizing sedation as an intervention with possible neuroprotective and systemic effects, rather than solely a means of comfort or procedural facilitation, may open new avenues for targeted multiorgan protection in early stroke care. Rigorous clinical trials are needed to define how propofol, dexmedetomidine, or ketamine can be optimally integrated into AIS management.