CNS function and dysfunction during exposure to hyperbaric oxygen in operational and clinical settings.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and pathophysiology without systematic search methodology or new empirical human data.
PubMed 30902504 · doi:10.1016/j.redox.2019.101159
What was done
The authors reviewed literature on central nervous system oxygen toxicity (CNS-OT) occurring during hyperbaric oxygen breathing in clinical therapy and undersea/submarine operations. The review discusses underlying pathophysiology, involved brain regions, neural and redox signaling mechanisms in seizure genesis, factors accelerating onset, and investigational mitigation strategies targeting redox stress.
What was found
No quantitative data, sample sizes, or numerical results are reported in the abstract. The authors describe that CNS-OT is preceded by a safe latent period that varies widely between and within individuals, limiting predictable exposure limits. Symptoms progress from non-convulsive cranial nerve, autonomic, and cardiorespiratory signs of brainstem origin to generalized tonic-clonic seizures via cortical spread.
Why it matters
Clarifying the redox and neural pathways driving oxygen toxicity helps identify potential neuroprotective strategies that could extend safe hyperbaric oxygen exposure in medical and diving contexts.
Limits
As a narrative review, it presents no original data, statistical analyses, or systematic review methodology. Specific exposure thresholds, effect sizes of mitigation strategies, and quantitative variability are not reported in the abstract.
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.