World Neurosurg. 2026 Jun 30:125167. doi: 10.1016/j.wneu.2026.125167. Online ahead of print.
ABSTRACT
The role of cerebral autoregulation in the management of traumatic brain injury (TBI) is of increasing interest. Though oxygen is potently vasoactive, its role in autoregulation is under-appreciated despite the importance of brain oxygen monitoring and pervasive availability of supplemental oxygen in clinical environments. This narrative review intends to provide historical scientific context for oxygen-driven cerebral autoregulation-hereby termed oxygenic autoregulation-and its therapeutic potential, particularly during intracranial pressure (ICP) crises. A review of original research from 1900-2025 identified sparse but consistent evidence, concentrated in the late 20th century, that hyperoxia and hypoxia have significant effects on cerebral vasomotion and ICP. Clinical studies of hyperoxia were conducted primarily using hyperbaric oxygen therapy (HBOT), which consistently reduced ICP, but often with a rebound to baseline levels or above both during and after treatment. Hypoxic high altitude cerebral edema was frequently associated with increased non-invasive estimates of ICP. The Brain Trauma Foundation's pre-hospital guidelines recommend the provision of supplemental oxygen to those suspected of having a brain injury. However much remains to be learned about the mechanism underlying this benefit, as well as the harms of hyperoxic therapy (such as oxidative stress or rebound ICP elevation), especially over the longer term. New research is needed to understand if supplemental oxygen reliably induces autoregulatory vasoconstriction which in turn reduces intracranial hypertension. At the present time, given the lack of recent research on this "oxygenic" mechanism of autoregulation, there is insufficient evidence for the therapeutic use of normobaric hyperoxic therapy for the treatment of intracranial hypertension.
PMID:42379473 | DOI:10.1016/j.wneu.2026.125167