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Abstract
Cerebral edema (CE) and resultant intracranial hypertension are associated with unfavorable
prognosis in traumatic brain injury (TBI). CE is a leading cause of in-hospital mortality,
occurring in >60% of patients with mass lesions, and ∼15% of those with normal initial
computed tomography scans. After treatment of mass lesions in severe TBI, an important
focus of acute neurocritical care is evaluating and managing the secondary injury
process of CE and resultant intracranial hypertension. This review focuses on a contemporary
understanding of various pathophysiologic pathways contributing to CE, with a subsequent
description of potential targeted therapies. There is a discussion of identified cellular/cytotoxic
contributors to CE, as well as mechanisms that influence blood-brain-barrier (BBB)
disruption/vasogenic edema, with the caveat that this distinction may be somewhat
artificial since molecular processes contributing to these pathways are interrelated.
While an exhaustive discussion of all pathways with putative contributions to CE is
beyond the scope of this review, the roles of some key contributors are highlighted,
and references are provided for further details. Potential future molecular targets
for treating CE are presented based on pathophysiologic mechanisms. We thus aim to
provide a translational synopsis of present and future strategies targeting CE after
TBI in the context of a paradigm shift towards precision medicine. This article is
part of the Special Issue entitled "Novel Treatments for Traumatic Brain Injury".