| Summary: | Summary: Over the last two decades, neurological researchers have uncovered many pathophysiological mechanisms associated with subarachnoid haemorrhage (SAH), with early brain injury and delayed cerebral ischaemia both contributing to morbidity and mortality. The current dilemma in SAH management inspired us to rethink the nature of the insult in SAH: sudden bleeding into the subarachnoid space and hypoxia due to disturbed cerebral circulation and increased intracranial pressure, generating exogenous stimuli and subsequent pathophysiological processes. Exogenous stimuli are defined as factors which the brain tissue is not normally exposed to when in the healthy state. Intersections of these initial pathogenic factors lead to secondary brain injury with related metabolic changes after SAH. Herein, we summarized the current understanding of efforts to monitor and analyse SAH-related metabolic changes to identify those precise pathophysiological processes and potential therapeutic strategies; in particular, we highlight the restoration of normal cerebrospinal fluid circulation and the normalization of brain-blood interface physiology to alleviate early brain injury and delayed neurological deterioration after SAH.
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