Feed

Up to now, Intracerebral hemorrhage (ICH) remains a type of cerebrovascular emergency with high incidence, mortality and disability rates. The secondary brain injury following ICH involves a series of complex pathophysiological mechanisms, including the space-occupying and edema effects of hematoma, abnormal mediation of multiple cell signaling pathways, intense inflammatory storms and immune responses, structural and functional damage to the blood-brain barrier(BBB), progressive increase in intracranial pressure, early hematoma expansion, and neurotoxic effects of blood decomposition product. Over the past few decades, although substantial progress has been made in the construction of risk prediction models, optimization of acute treatment strategies, and improvement of long-term prognosis assessment systems, and dues to the advancement of neuroimaging techniques, improvement in neurocritical care, and innovation in minimally invasive neurosurgery, the overall mortality and disability rates of patients have shown a downward trend. However, it is regrettable that the neurological function recovery of survivors is still generally poor, and the long-term functional improvement rate is very low. Despite extensive and in-depth exploration of the best drug intervention targets and optimal surgical methods for ICH through multiple basic research and clinical trials, these efforts have not yet translated into breakthroughs in clinical treatment outcomes or significant improvements in patient prognosis. This review aims to comprehensively summarize the epidemiological characteristics of spontaneous ICH, the mediation mechanisms of key signaling pathways, the dynamic process of BBB disruption, potential immune-related therapeutic targets, exploration directions of novel drug targets, core mechanisms of secondary brain injury, and key research directions in the future.