The Modulatory Role of Hypothermia in Poststroke Brain Inflammation: Mechanisms and Clinical Implications

Acute ischemic stroke remains a major contributor to mortality and disability worldwide. The use of hypothermia has emerged as a promising neuroprotective strategy, with proven effectiveness in cardiac arrest and neonatal hypoxic-ischemic injury.

This review explores the therapeutic potential of hypothermia in ischemic stroke by examining its impact on poststroke inflammatory responses. We synthesized evidence from basic and clinical studies to illustrate the inhibitory effects of hypothermia on poststroke brain inflammation. The underlying mechanisms include modulation of microglial activation and polarization; downregulation of key inflammatory pathways such as MAPKs, NF-KB, and JAK/STAT; protection of the blood-brain barrier integrity; and reduction of immune cell infiltration into the brain. We also discuss the current limitations of hypothermia treatment in clinical practice and highlight future research directions for optimizing protocols and evaluating its clinical efficacy in stroke patients.

Therapeutic hypothermia (TH) has evolved significantly with advancements in medical technologies, especially with the introduction of automated cooling devices, both intravascular and surface based. However, a refined, highly individualized, and effective hypothermia protocol may stand robust against the devastating consequences of ischemic stroke, and we think it should become the future development goal.