HBOT studied for post-stroke neurological recovery, including chronic cases years after the event. 2013 Boussi-Gross RCT showed improvement at 6–36 months post-stroke.
Quality: Low Weak recommendation
Efrati 2013 crossover trial supports late-window benefit; replication in independent centres limited. Off-label worldwide.
HBOT for post-stroke recovery has been studied in both acute and chronic phases. The 2013 Boussi-Gross RCT demonstrated significant improvements in patients 6 months to 3 years post-stroke using 40 sessions at 2.0 ATA. Mechanisms are hypothesised to include angiogenesis, mitochondrial recovery, and neuroplasticity induction in surviving but dormant penumbra tissue.
The post-stroke brain contains a mix of permanently infarcted tissue and surviving-but-dormant tissue in the ischaemic penumbra. HBOT appears to selectively benefit this penumbra tissue. Elevated plasma oxygen reaches cells with marginal blood supply; HIF-1α stabilisation drives angiogenesis and improves microcirculation in previously hypoperfused regions; neuroplasticity signalling (BDNF, growth factors) is upregulated. SPECT and perfusion MRI consistently show increased perfusion in brain areas corresponding to clinical gains. Importantly, infarcted tissue cannot be rescued — HBOT does not regenerate dead neurons.
| Typical protocol | 40 sessions at 2.0 ATA, 90 minutes each, 5 days/week |
|---|---|
| Evidence level | Phase 2 RCTs — Moderate evidence |
| FDA / regulatory status | Not FDA-approved for stroke |
The Boussi-Gross protocol delivers 40 sessions at 2.0 ATA over 8 weeks. Sessions include scheduled air breaks, pre- and post-treatment neurocognitive and functional assessment (NIH Stroke Scale, cognitive batteries, imaging), and interim evaluation. Patients continue standard rehabilitation during the HBOT course.