Hyperbaric Oxygen Therapy in Traumatic Brain Injury (TBI)

Personal Experience, Clinical Insight, and a Patient-Centred Pathway to Recovery

As both a clinician who has personally endured persistent post-concussion symptoms—and with my co-founder having faced his own TBI—we know firsthand the gaps that still exist in traumatic brain injury care. Our shared experience is what ultimately led us to establish NUMA.

The research landscape remains undeniably heterogeneous. Differences in injury severity, timing of intervention, and HBOT dosing protocols all shape study outcomes. Most clinical trials, quite rightly, measure cognition, functional neuroimaging, and broad quality-of-life indices. Yet many patients—ourselves once included—live each day wrestling with symptoms that seldom make it into primary endpoints: relentless migraine-like headaches, visual disturbances, piercing sensitivities to light, noise, or smell, nights fragmented by insomnia, and mood or neuroendocrine shifts that derail recovery.

I would welcome trials that evaluate not only cognitive outcomes but also these debilitating neurological symptoms, because in clinical practice they are precisely where we see some of HBOT’s most striking benefits.

At NUMA Hyperbaric Oxygen Clinic, we therefore focus on:

• Early access: intervening as soon as A&E or neurology clears the patient, while secondary injury processes are still modifiable.
• Age-inclusive care: treating adults and children aged 10 years and above, as earlier intervention can meaningfully influence long-term recovery.
• Whole-person outcomes: monitoring not only cognitive scores and brain scans but also headache frequency, sensory tolerances, sleep quality, fatigue, and mood. While forty sessions can feel like a marathon, seeing these “invisible” burdens lift is profoundly rewarding for both patient and team.

I recognise that the evidence base is still evolving, and that larger, multi-centre trials—especially in Persistent Post-Concussive Symptoms (PPCS) —will be invaluable. While we await those data, the physiological rationale and years of clinical experience suggest that HBOT can be a meaningful complement to standard neurorehabilitation. My commitment is to keep this option accessible, explain it transparently, and stand alongside patients and colleagues as we learn and heal together.

Clinical Endorsement

• Strong evidence-based support for the use of HBOT in moderate to severe TBI, acute and chronic phase
• Level A recommendation for improving cognitive and functional outcomes

Proven Track Record

• HBOT has been investigated for over five decades in the treatment of TBI
• Demonstrated significant reductions in disability and improved recovery in both acute and chronic TBI
• Particularly effective when conventional therapies have plateaued

Mechanism of Action:

• Reverses tissue hypoxia → improves cerebral oxygenation and perfusion.
• Stabilises mitochondria → ↑ ATP; ↓ oxidative stress and neuroinflammation.
• Protects the blood–brain barrier → reduces oedema and intracranial pressure.
• Drives neuroplastic repair → neurogenesis, synaptogenesis, remyelination; ↑ BDNF.
• Promotes angiogenesis → restores microcirculation and network connectivity.

Care Strategy

Early Intervention or Subacute Phase:

• 10–20 sessions, initiated soon after injury to modulate inflammation and limit secondary damage
• May improve cerebral oxygenation and reduce ICP (intracranial pressure)

Chronic TBI Recovery:

• 40+ sessions shown to yield:
  • Measurable gains in attention, memory, and executive function
  • Reduced post-concussive symptoms and depression
  • Functional brain imaging improvements (e.g., SPECT, fMRI)

Refractory Cases:

• 60+ sessions often required in cases of prolonged cognitive impairment, where conventional rehabilitation has plateaued
• Individualised protocols recommended based on symptom severity, time since injury, and functional imaging markers

A recent comprehensive literature reviews (1969–2023) evaluated the clinical efficacy of hyperbaric oxygen therapy (HBOT) in traumatic brain injury (TBI) across acute, subacute, and chronic settings. The findings are summarized below (2):

1. Acute and Subacute TBI (Moderate to Severe)

• Evidence Base:
  • 9 Randomized Controlled Trials (RCTs)
  • 1 Meta-analysis
  • 2 Prospective Studies
• Key Findings:
  • Mortality: Significantly reduced in all studies that included it as an endpoint
  • Functional Outcomes: Mixed results among survivors
• Recommendation:
  • Type 2a recommendation, Level A evidence

2. Chronic Mild TBI / Post-Concussion Syndrome

• Evidence Base:
  • 7 Randomized Controlled Trials (RCTs)
  • 6 Prospective Studies
• Key Findings:
  • High-level evidence supports:
    • Improved cognitive function
    • Reduced neurological symptoms
    • Enhanced quality of life
• Recommendation:
  • Type 2a recommendation, Level B-R evidence
  • HBOT should be considered for selected patients with chronic TBI and prolonged post-concussion symptoms, particularly when functional neuroimaging reveals metabolic dysfunction

3. Chronic Severe TBI

• Evidence Base:
  • Limited to small uncontrolled studies and case reports
• Key Findings:
  • Preliminary data suggest possible benefits, but current evidence lacks sufficient quality and consistency -Recommendation:
  • No formal recommendation can be made at this time due to insufficient high-quality evidence

Role of Hyperbaric Oxygen Therapy (HBOT) in Traumatic Brain Injury (TBI)

Why the brain is uniquely vulnerable

• Metabolic demand: The brain receives ~15% of cardiac output, consumes ~20% of the body’s oxygen, and ~25% of the body’s glucose.
• Near-total reliance on aerobic metabolism: It uses almost all delivered oxygen in real time—making even brief hypoxia highly disruptive.

After TBI: the secondary injury you can still modify

• Hypoxia drives the cascade: Reduced oxygen shifts neurons to anaerobic metabolism → acidosis, diminished metabolic reserve, ionic pump failure, membrane degradation, and ultimately irreversible neuronal death in some cells.
• Network dysfunction even without cell death: Hypoxia suppresses neuronal metabolism and activity, causing synaptic loss and impaired connectivity that underlie persistent symptoms.

How HBOT helps

A) Early phase (acute/subacute): stabilise and protect HBOT delivers high dissolved oxygen to ischaemic tissue, aiming to interrupt the secondary injury cascade:

• Restore aerobic metabolism: Increases oxygen availability, reduces lactate accumulation, and supports ATP production.
• Improve tissue oxygenation & perfusion: Enhances brain tissue oxygen and can improve cerebral blood flow.
• Protect structure: Helps preserve the blood–brain barrier, stabilise mitochondrial membranes, and reduce oedema and intracranial pressure.
• Attenuate the inflammatory response: Dampens microgliosis and astrogliosis, lowering neuroinflammation.
• Cellular rescue mechanisms: Supports mitochondrial health and may facilitate astrocyte-to-neuron mitochondrial transfer, aiding injured neurons’ recovery.

B) Chronic phase (subacute–delayed): repair and rewire With the acute crisis past, HBOT promotes long-term neurorepair:

• Neuroplasticity: Stimulates cell proliferation, endogenous neurogenesis, axonal regeneration, remyelination, and strengthened network connectivity.
• Mitochondrial restoration: Improves mitochondrial function in neurons and glia; reduces apoptosis and oxidative stress.
• Neurotrophic support: Increases neurotrophic factors—particularly BDNF, which supports neuronal survival, synaptic plasticity, hippocampal LTP, and cognitive recovery.
• Astrocyte support: Modulates neuroinflammation and facilitates synaptic repair and homeostasis.

C) Vascular remodelling for sustained recovery

• Angiogenesis: HBOT induces new capillary growth that underpins axonal regeneration, neurogenesis, and synaptogenesis.
• Correct hypoperfusion: Resolves local and diffuse cerebral hypoperfusion—a key brake on recovery—improving delivery of oxygen and nutrients required for long-term tissue regeneration.

Clinical Features 

Most patients with mild traumatic brain injury (mTBI) recover fully within four weeks. However, a proportion of patients continue to experience physical, cognitive, or emotional symptoms beyond this timeframe. When symptoms persist for more than four weeks, the condition is referred to as Persistent Post-Concussive Symptoms (PPCS).

PPCS encompasses a constellation of symptoms that may span several functional domains. These include:

• Physical: Headache (most prevalent), dizziness, balance impairment, nausea, fatigue, light and noise sensitivity, and visual disturbances.
• Cognitive: Reduced attention span, memory difficulties, slowed processing speed, and subjective cognitive inefficiency (“brain fog”).
• Emotional and Behavioural: Irritability, anxiety, low mood, emotional lability, and reduced stress tolerance.
• Sleep-related: Insomnia, hypersomnia, fragmented sleep, and difficulty initiating or maintaining sleep.

These symptoms can significantly impact quality of life and daily functioning. Early recognition and a structured, multidisciplinary management approach are essential to support recovery and mitigate long-term complications.

Management Approach

Recovery after traumatic brain injury (TBI) is best supported through a comprehensive, integrative strategy that addresses the full spectrum of symptoms and promotes long-term function.

• Multidisciplinary care: Involving neurology, neuropsychology, physiotherapy, ENT, and vestibular rehabilitation.
• Cognitive rehabilitation: Focused programmes to improve memory, attention, and executive function.
• Hyperbaric Oxygen Therapy (HBOT): A well-established treatment since the 1950s, increasingly supported by research for its ability to enhance brain oxygenation, reduce neuroinflammation, and promote recovery. When introduced early, HBOT can help limit secondary injury; when used later, it can support neuroplastic repair, especially when integrated within a broader neurorehabilitation programme to amplify gains in cognition, function, and symptom relief.
• Education and reassurance: Helping patients understand their condition and fostering confidence, as most improve over time with consistent, targeted care.