The oxygen isn't a top-up. It's a signal.

Give the body a burst of very high oxygen, then let it return to normal, and the cells respond as though they had just survived a shortage — mounting the same adaptive repair response, but with none of the damage a real shortage causes.

This is the counter-intuitive engine of the whole therapy. The signal that normally says "we were starved of oxygen, start repairing" can be triggered by the withdrawal of a surplus. So HBOT recruits the body's own recovery machinery — the machinery evolved to handle hypoxia — while actually flooding the tissue with oxygen.

The significance of this model is that all six pathways operate on the shared downstream pathophysiology of neural injury — mitochondrial failure, the oxidative cascade, neuroinflammation, oedema, disrupted connectivity — rather than on the specific initiating event.

That is why a treatment studied in traumatic brain injury also has a coherent rationale in post-concussion syndrome, PTSD, ischaemic stroke and cognitive decline. A hurt, swollen, oxygen-short brain looks much the same downstream whatever hurt it — and HBOT acts there, on the injury itself.