Central Nervous System Oxygen Toxicity and Hyperbaric Oxygen Seizures.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing physiological and molecular mechanisms without systematic methodology or primary human trial data.
PubMed 27099087 · doi:10.3357/AMHP.4463.2016
What was done
The author conducted a narrative literature review across multiple fields to examine the physiological changes and molecular mechanisms underlying central nervous system (CNS) oxygen toxicity and seizures resulting from elevated partial pressures of oxygen during hyperbaric oxygen therapy.
What was found
The abstract reports no quantitative data or statistical findings. Mechanistically, it describes that elevated partial pressure of oxygen (Po2) saturates endogenous protective antioxidant enzymes, shifting biochemical reactions toward reactive-species-mediated neural network overstimulation. Vulnerability varies across CNS regions, and sustained elevated Po2 can precipitate tonic-clonic seizures and death.
Why it matters
As hyperbaric oxygen therapy use increases, clarifying the mechanisms of CNS oxygen toxicity highlights the biological limits and seizure risks associated with high partial pressures of oxygen.
Limits
This is a non-systematic narrative review with no defined search criteria, human trial data, or reported study count. The abstract provides no quantitative thresholds, incidence rates, or primary empirical measurements.
Cited by
- supports Hyperbaric oxygen therapy guidelines cap exposure at three atmospheres because of the risk of tonic-clonic central nervous system oxygen toxicity seizures above that level.