HBOT for Traumatic Brain Injury and Concussion: What the Research Shows

Hyperbaric oxygen therapy (HBOT) for traumatic brain injury (TBI) and persistent post-concussion syndrome is an investigational, off label use: randomized trials using 40 sessions at 1.5 ATA, including Boussi-Gross et al. (2013) and Harch et al. (2020), reported better memory, attention, mood and symptom scores, while several U.S. military sham-controlled trials (Wolf 2012, Cifu 2014, Miller 2015) found no clear difference between HBOT and sham. The FDA has not cleared HBOT for brain injury or concussion, insurance rarely pays for it, and according to a 2022 systematic review by Harch, every chronic mild TBI study it included enrolled fewer than 75 people.

Why Brain Injuries Are So Hard to Treat

When the brain sustains a traumatic injury, whether from a car accident, blast exposure, a fall, or a sports collision, the damage extends far beyond the initial impact site. The mechanical forces stretch and shear axons, disrupt the blood-brain barrier, and trigger a cascade of neuroinflammation that can persist for months or years [1].

This secondary injury cascade creates something called the ischemic penumbra: a zone of brain tissue surrounding the primary damage site where neurons are alive but metabolically impaired. These cells aren’t dead. They’re stuck in a low-energy survival mode because their blood supply is compromised, and they can’t get enough oxygen to function normally [2].

Standard care after the acute phase centers on rest followed by graded activity, physical and vestibular therapy, cognitive rehabilitation, and medications for headache, sleep and mood. These approaches help many people, but none of them directly target brain tissue that remains underperfused and short of oxygen long after the injury.

That gap is where hyperbaric oxygen therapy enters the picture. Most people with a concussion, also called a mild TBI or mTBI, recover within weeks, and the HBOT research focuses on the minority who develop persistent post-concussion syndrome (PPCS), with headaches, brain fog, poor concentration, irritability and sleep problems lasting three months or longer. The post-concussion syndrome overview covers how that diagnosis is made.

How HBOT Addresses Brain Injury

Hyperbaric oxygen therapy, also called hyperbaric oxygen (HBO2) or HBO treatment, means breathing close to 100% oxygen inside a pressurized chamber at more than one atmosphere absolute. Researchers propose five linked mechanisms in the injured brain. Most mechanism data come from laboratory, animal and imaging studies. The hyperbaric oxygen therapy treatment guide explains chambers, pressures and approved uses in more detail.

Oxygen Delivery to Damaged Tissue

Under normal atmospheric pressure, almost all oxygen transport depends on hemoglobin inside red blood cells. In brain regions where capillaries are damaged, swollen, or compressed by edema, red blood cells can’t get through efficiently.

HBOT changes the equation by dramatically increasing dissolved oxygen in blood plasma. At 1.5 to 2.0 ATA breathing 100% oxygen, plasma oxygen levels rise 10-fold or more. This dissolved oxygen is not dependent on hemoglobin or intact capillaries. It diffuses directly through tissue fluid, reaching cells that haven’t had adequate oxygen since the injury [3].

For neurons stuck in the ischemic penumbra, researchers propose that this oxygen influx can support metabolic reactivation rather than continued dormancy.

Angiogenesis: Building New Blood Vessels

Repeated HBOT sessions stimulate the growth of new capillaries into damaged brain tissue. This process, called angiogenesis, is driven by hypoxia-inducible factor (HIF) signaling. According to Hadanny and Efrati (2020), the intermittent nature of HBOT (high oxygen during sessions, normal oxygen between sessions) creates a “relative hypoxia” signal during off-periods that is a potent trigger for new vessel growth, an idea they call the hyperoxic-hypoxic paradox [4].

Over the course of 40 to 60 sessions, these new capillaries are thought to produce a lasting improvement in blood flow to previously ischemic regions. This is one explanation for why many patients in the trials report their largest gains toward the end of a treatment course or in the weeks after it: a new vascular network takes time to mature.

Reduced Neuroinflammation

Chronic neuroinflammation is a hallmark of persistent post-concussion symptoms. Activated microglia, the brain’s resident immune cells, continue releasing inflammatory cytokines long after the initial injury has healed. This ongoing inflammation impairs synaptic function, disrupts neurotransmitter signaling, and contributes to brain fog, mood disturbances, and cognitive decline [5].

Laboratory work, including Benson et al. (2003) in human blood-derived immune cells, shows that hyperbaric oxygen lowers production of pro-inflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 [6]. Animal studies suggest it also dampens NF-kB, a transcription factor that drives inflammatory gene expression, and shifts microglia from a pro-inflammatory (M1) toward a reparative (M2) state. These effects are well described in the lab and much less directly measured in human brain injury patients.

Stem Cell Mobilization

A single HBOT session at 2.0 ATA doubles the number of circulating stem cells. After a course of 20 sessions, circulating stem cell counts increase by approximately 800%, according to Thom et al. (2006) [7]. These mobilized stem cells home to damaged tissue and contribute to repair processes. In animal models of brain injury, this includes differentiation into neural progenitor cells and endothelial cells that contribute to new vessel formation.

Neuroplasticity and Axonal Sprouting

HBOT upregulates brain-derived neurotrophic factor (BDNF) and other growth factors that support neuroplasticity. In practical terms, this means the brain may become better at forming new connections to compensate for damaged pathways. SPECT imaging studies before and after HBOT treatment, including Boussi-Gross et al. (2013), report increased metabolic activity in regions that were previously “cold” on the scan [8].

The Clinical Evidence

The clinical evidence for HBOT in brain injury splits into two camps. Civilian trials that compared HBOT with no treatment or delayed treatment mostly report clear gains, while U.S. military trials that compared HBOT with a pressurized sham mostly report that both groups improved by similar amounts. The table below summarizes the main randomized trials in persistent post-concussion symptoms.

The Israeli Civilian TBI Studies

Some of the strongest supportive evidence for HBOT in brain injury comes from the research group led by Dr. Shai Efrati at the Sagol Center for Hyperbaric Medicine and Research at Shamir (Assaf Harofeh) Medical Center in Israel.

In a 2013 randomized prospective trial, Boussi-Gross et al. enrolled patients with mild TBI who were 1 to 5 years post-injury and still experiencing persistent symptoms. The HBOT group received 40 sessions at 1.5 ATA for 60 minutes each. Results showed statistically significant improvements in memory, attention, executive function, and information processing speed. Brain SPECT imaging matched these clinical improvements: previously hypoperfused brain regions showed marked increases in blood flow [8].

The study’s crossover design strengthened the findings. The control group, which initially showed no improvement during the waiting period, demonstrated the same gains once they received HBOT treatment. The design had a limit worth knowing: the control group received no sham chamber sessions, so expectation and the experience of treatment could not be separated from the oxygen itself.

A follow-up study by the same group, Tal et al. (2017), used advanced MRI techniques (diffusion tensor imaging and perfusion MRI) and reported that HBOT improved the microstructural integrity of white matter tracts in post-TBI patients. The authors interpreted this as evidence that the therapy was producing measurable structural change in the brain, not only symptom relief [9].

Military and Veteran TBI Research

The U.S. military has invested heavily in HBOT research for blast-induced TBI, which affects an estimated 400,000 service members from recent conflicts.

Dr. Paul Harch published a phase I study in 2012 examining low-pressure HBOT (1.5 ATA) for military personnel with blast-induced post-concussion syndrome and comorbid PTSD. After 40 sessions, participants showed significant improvements in post-concussive symptoms, PTSD scores, cognitive testing, and quality of life. Brain SPECT imaging demonstrated corresponding improvements in cerebral blood flow [10]. The study had no control group.

Harch et al. (2020) later tested the same dose in a randomized crossover trial of 63 civilian and military adults, 50 of whom completed it. Compared with a no-treatment control period, 40 sessions at 1.5 ATA improved post-concussion symptoms, memory, depression, anxiety, PTSD, sleep and quality of life scores, and the control group showed near-identical gains after crossing over to HBOT [16].

A larger study by Cifu et al. (2014), run at the Naval Air Station in Pensacola, Florida, randomized 61 Marines with mild TBI to 40 chamber sessions at 2.0 ATA. The gas mix was varied so that one group breathed the oxygen equivalent of 1.5 ATA, one the equivalent of 2.0 ATA, and the sham group the equivalent of surface air. The authors found no evidence of efficacy at three months on symptoms, cognition or behavior [11]. Critics point out that every arm, including sham, was compressed to 2.0 ATA, and that pressure itself may act on the brain.

Two more Department of Defense trials used a lower pressure sham. In the HOPPS trial, Miller et al. (2015) randomized 72 service members to 40 sessions at 1.5 ATA, sham sessions of room air at 1.2 ATA, or usual care alone, and reported no difference between HBOT and sham [17]. Wolf et al. (2012) compared 30 sessions at 2.4 ATA with sham at 1.3 ATA in 50 service members and found that both groups improved by similar amounts [18]. The HOPPS trial abstract in JAMA Internal Medicine lists the full outcome measures.

Weaver et al. (2018) ran a Phase II trial with 71 service members comparing 40 sessions at 1.5 ATA with sham at 1.2 ATA. At 13 weeks, the HBOT group improved on the Neurobehavioral Symptom Inventory by 3.6 points while the sham group worsened by 3.9 points, and the difference was larger in the 49% of participants who also had PTSD. Those gains regressed by six and twelve months [19].

This “sham problem” has been a recurring issue in HBOT research. Even mild pressurization with ambient air increases dissolved oxygen to some degree, making it difficult to create a truly inert placebo in chamber-based studies. Supporters read the military trials as active treatments compared against each other; skeptics read them as evidence that expectation, attention and time explain much of the improvement.

Sports Concussion

Sports concussion is less studied than military TBI. No large randomized trial has tested HBOT specifically in athletes, and most of what clinicians apply to sports injuries is drawn from the civilian and military post-concussion trials above, which included people injured in falls, collisions and car accidents as well as sport.

Some professional and collegiate sports programs use HBOT as part of concussion recovery, though formal clinical guidelines have not been established and major concussion consensus statements do not recommend it as standard care. Athletes who try it typically use it alongside graded return to play and vestibular rehabilitation.

Children and Teens With Post-Concussion Syndrome

The first double-blind, sham-controlled trial in children was published by Hadanny et al. (2022) in Scientific Reports. It randomized 25 children aged 8 to 15, injured between six months and ten years earlier, to 60 daily HBOT sessions or sham. The HBOT group improved more on general cognitive score, memory, executive function, emotional symptoms and hyperactivity, and those gains tracked with MRI microstructural changes [15]. The trial was small and run at a center that provides HBOT commercially, so it needs independent replication.

Post-Concussion Syndrome: The Chronic Cases

One notable feature of the HBOT brain injury data is that several trials report improvement years after the initial injury. This challenges the conventional neurological assumption that brain recovery plateaus within 12 to 18 months of injury.

The Israeli studies included patients as far out as 5 years post-injury who still demonstrated significant improvement. Dr. Harch has published case reports of patients 15+ years post-TBI showing cognitive and functional gains after HBOT [10]. The Sagol group has reported similar late gains in post-stroke patients, according to Hadanny et al. (2020) [12].

The explanation offered is consistent with the mechanism: if neurons in the ischemic penumbra are alive but metabolically suppressed, they may be reactivated regardless of how long they’ve been in that state. If that holds up in larger trials, the recovery window for HBOT may be longer than for most other TBI interventions.

What Systematic Reviews Conclude

Two reviews frame the evidence. For acute, severe TBI in intensive care, the Cochrane review by Bennett, Trytko and Jonker (2012) pooled 7 trials with 571 people and found that adding HBOT reduced the risk of death (relative risk 0.69) but offered little evidence that survivors had a good functional outcome, with significant lung complications in 13% of HBOT patients versus none in controls [21].

For chronic mild TBI, Harch (2022) reviewed 11 studies, including 6 randomized trials, and concluded that 40 sessions at 1.5 ATA produced significant symptom or cognitive improvement across four randomized trials, with larger gains in patients who also had PTSD. Every study enrolled fewer than 75 people, and the author disclosed co-ownership of a hyperbaric service [20].

The Israeli HBOT Aging Studies: Relevance to Brain Health

While not specifically a TBI intervention, the aging studies from Dr. Efrati’s group provide useful context for understanding how HBOT affects the brain.

In a 2020 randomized controlled trial, Hadanny et al. randomized 63 healthy adults over 64 to 60 HBOT sessions at 2.0 ATA or to a control group, using a protocol with intermittent oxygen exposure (periods of 100% oxygen alternating with periods of breathing normal air within the chamber). This protocol was designed to maximize the hypoxia-hyperoxia signaling that drives regenerative pathways. The HBOT group improved in global cognitive function, with the largest gains in attention and information processing speed, and perfusion MRI showed increased cerebral blood flow in several frontal and parietal regions [13].

A separate prospective study by Hachmo et al. (2020) gave 60 sessions to 35 healthy adults aged 64 and older, without a control group. It reported that telomeres lengthened by over 20% in several immune cell populations while senescent T helper cells fell by about 37% and senescent cytotoxic T cells by about 11% [14].

These findings suggest that HBOT may improve some measures of brain function even in the absence of overt injury, and that the same mechanisms (improved perfusion, reduced inflammation, enhanced neuroplasticity) studied in brain injury patients may also affect cognitive aging. Several authors of these studies disclosed commercial ties to a company that operates hyperbaric clinics, and none of the aging results have yet been replicated by an independent group.

Is HBOT FDA Approved for Traumatic Brain Injury or Concussion?

No. The U.S. Food and Drug Administration (FDA) has cleared hyperbaric chambers for a defined list of conditions, such as decompression sickness, carbon monoxide poisoning, gas embolism, certain non-healing wounds and radiation injury, and traumatic brain injury and concussion are not on that list. The Undersea and Hyperbaric Medical Society (UHMS) does not include TBI in its approved indications either.

This means HBOT for brain injury is an off label use. A licensed physician can still prescribe it, and many hyperbaric clinics offer it, but it is usually cash pay and the patient carries the cost of an unsettled evidence base. The list of FDA cleared HBOT indications shows exactly which uses insurers recognize.

Protocols for Brain Injury

The most studied protocols for TBI share several common elements:

• Pressure: 1.5 to 2.0 ATA. Most civilian TBI studies use 1.5 ATA, while some military studies have used 2.0 ATA and one used 2.4 ATA. There is no consensus on which pressure is optimal, and some clinicians argue that lower pressures (1.3 to 1.5 ATA) may be better for certain patients, particularly in the early post-injury period.
• Duration: 60 minutes at treatment pressure per session, plus 5 to 10 minutes each for compression and decompression.
• Frequency: 5 sessions per week is standard in the research. Some clinics offer twice-daily sessions to shorten the treatment course, an approach the trials have not tested.
• Total sessions: 40 sessions is the most common research protocol. Many clinicians extend to 60 sessions for more severe injuries or longstanding symptoms. Periodic reassessment (every 20 sessions) helps determine whether continuing treatment is producing additional benefit.

Some practitioners use a protocol that incorporates “air breaks,” brief periods during the session where the patient breathes normal air instead of pure oxygen. This intermittent approach mimics the Israeli aging study protocol and may enhance the regenerative signaling response.

Efrati Protocol and Harch Protocol

Two named approaches dominate brain injury HBOT. The Efrati protocol, used at the Sagol Center, typically runs 60 sessions at 2.0 ATA with scheduled air breaks. The Harch protocol, from Louisiana State University, centers on 40 sessions at 1.5 ATA, the dose used in the Harch 2020 trial and the 2022 dosage review [16][20]. The comparison of the Efrati and Harch HBOT protocols covers the differences session by session.

Side Effects and Risks of HBOT for Brain Injury

HBOT is generally well tolerated at the 1.5 to 2.0 ATA pressures used in brain injury trials, but it carries real risks. The most common side effect is middle ear barotrauma, a feeling of pressure, pain or fullness in the ears caused by trouble equalizing during compression. Sinus pain, temporary changes in near vision and fatigue after sessions are also reported.

Less common but more serious risks include oxygen toxicity seizures, lung barotrauma and claustrophobia or anxiety inside the chamber. Seizure risk deserves extra attention after TBI because post-traumatic epilepsy is more common in this group. An untreated pneumothorax (collapsed lung) rules out HBOT, and certain chemotherapy drugs, recent ear or chest surgery and uncontrolled seizures require a physician’s review first. The full breakdown of hyperbaric chamber side effects lists warning signs to report during a course.

How HBOT Compares With Other TBI and Concussion Treatments

HBOT is one of several options for persistent post-concussion symptoms, and most specialists use it, when they use it at all, alongside standard rehabilitation rather than instead of it. The table compares HBOT with the treatments it is most often combined with.

The neurofeedback therapy guide and the TMS treatment guide explain how those options are delivered.

How Much Does HBOT for Brain Injury Cost, and Does Insurance Cover It?

HBOT for traumatic brain injury is almost always self-pay in the United States, because Medicare and most private insurers cover HBOT only for a defined list of approved indications that does not include brain injury. Clinics typically charge $150 to $300 per session for brain injury protocols, and a 40 to 60 session course multiplies that figure into the thousands of dollars.

Some patients use health savings accounts or package pricing, and veterans can ask their VA or TRICARE team about research and community care programs. The guide to HBOT cost breaks down pricing by chamber type and setting.

Limitations and Honest Assessment

HBOT for brain injury is promising, but the evidence has real limitations that deserve honest acknowledgment:

• Most published studies are small, typically 30 to 70 participants. Large multi-center randomized controlled trials are still lacking.
• The sham control problem means that some “negative” studies may have inadvertently used active treatments as placebos, while some “positive” studies had no sham at all.
• Insurance coverage for HBOT in TBI is almost nonexistent in the United States, making treatment expensive for patients (typically $150 to $300 per session).
• Not every patient responds. Response rates in published studies range from 60 to 80%, meaning a meaningful fraction of patients do not see significant improvement.
• There are no reliable biomarkers to predict which patients will respond before starting treatment.
• The optimal pressure, number of sessions, and timing relative to injury remain subjects of active debate.
• Several of the most positive trials come from investigators who run or co-own hyperbaric services, which they disclose, and independent replication is limited.

Despite these gaps, multiple research groups in Israel and the United States have reported benefits backed by brain imaging that tracks with symptom change. The fair summary is that HBOT for chronic post-concussion symptoms is supported by several small trials, contradicted by others, and not yet settled.

What Patients Should Know Before Starting

If you’re considering HBOT for a brain injury or persistent concussion symptoms, keep the following in mind:

• Get baseline neuropsychological testing and, if possible, brain imaging (SPECT or perfusion MRI) before starting. This provides objective measures to track progress.
• Plan for the full protocol if you start. Stopping at 10 to 15 sessions and concluding that HBOT “didn’t work” does not match how the trials were run, because the proposed mechanisms, particularly angiogenesis, require sustained treatment.
• Work with a provider experienced in neurological HBOT applications, not just wound care. The clinical reasoning and protocol adjustments differ significantly.
• Be patient. Some patients notice cognitive improvements within the first 10 to 20 sessions. Others don’t experience their primary gains until weeks after completing the full course.
• Combine HBOT with other evidence-based brain recovery strategies: quality sleep, anti-inflammatory nutrition, targeted supplementation, and cognitive rehabilitation exercises.
• Ask the clinic in writing what pressure, oxygen concentration, session count and total price it proposes, and how it will measure whether you are improving.

Who Provides HBOT for Brain Injury and How to Find a Clinic

HBOT for brain injury is usually supervised by a physician with board certification in Undersea and Hyperbaric Medicine, a subspecialty certified through the American Board of Emergency Medicine and the American Board of Preventive Medicine. Chambers are run by certified hyperbaric technologists (CHT), and brain injury programs often work alongside neurologists, physiatrists (physical medicine and rehabilitation physicians), neuropsychologists and vestibular therapists. UHMS runs a facility accreditation program that patients can ask about.

The directory of hyperbaric oxygen therapy clinics in the US lists providers by state and city. Listing order is not paid ranking. Featured slots are labeled and capped, and a Verified label means the clinic completed credential checks, not that it paid for placement. Regenerated.com is free for patients, and inclusion in the directory is not an endorsement. The guide to Featured, Verified and organic listings explains each label.

Ask any clinic on the list which brain injury protocol it follows and whether a physician is on site during sessions. The traumatic brain injury condition page covers diagnosis and the wider range of treatments to discuss with your care team.

Frequently asked questions

Does hyperbaric oxygen therapy help with concussion?

Hyperbaric oxygen therapy helped persistent concussion symptoms in several small civilian trials, including Boussi-Gross et al. (2013) and Harch et al. (2020), which used 40 sessions at 1.5 ATA and reported better memory, attention, mood and sleep. Sham-controlled military trials such as Miller et al. (2015) found sham sessions worked about as well. HBOT is studied mainly for symptoms lasting three months or more, not for fresh concussions, and it remains off label.

How many HBOT sessions are needed for a brain injury?

Most brain injury trials used 40 sessions of 60 minutes at 1.5 ATA, given five days a week over about eight weeks. The Sagol Center protocol and the 2022 pediatric trial used 60 sessions. Clinicians often reassess every 20 sessions to judge whether more treatment is adding benefit. No trial has shown that a short course of 10 to 20 sessions produces lasting change, and the right number for any one patient is not established.

Is HBOT for traumatic brain injury covered by insurance?

HBOT for traumatic brain injury is rarely covered by insurance in the United States, because TBI and concussion are not FDA cleared or UHMS approved indications for hyperbaric oxygen. Most patients pay out of pocket, with clinics typically charging $150 to $300 per session. Some use health savings accounts or package pricing, and veterans can ask the VA or TRICARE about research and community care programs, which change over time.

Can HBOT help years after a brain injury?

Several trials report improvement years after injury. Boussi-Gross et al. (2013) treated adults 1 to 5 years after mild TBI, Hadanny et al. (2022) treated children injured up to 10 years earlier, and Dr. Paul Harch has described gains in patients more than 15 years out. The proposed reason is that underperfused but living brain tissue can still respond to oxygen. These are small studies, so a late benefit is possible but not assured.

Is hyperbaric oxygen therapy safe for people with brain injuries?

Hyperbaric oxygen therapy is generally well tolerated at the 1.5 to 2.0 ATA used in brain injury trials, but it carries risks. Ear barotrauma is the most common problem, followed by sinus pain, temporary vision changes and fatigue. Oxygen toxicity seizures are rare but matter more after TBI, when seizure risk is already raised. A physician should screen for collapsed lung, recent surgery, seizure history and certain chemotherapy drugs before the first session.

What is the difference between mild HBOT and clinical HBOT for brain injury?

Clinical HBOT uses hard-shell chambers pressurized to 1.5 ATA or more with close to 100% oxygen, which is the dose tested in the brain injury trials. Mild HBOT uses soft chambers that usually reach about 1.3 ATA, often with concentrated rather than pure oxygen. Because no randomized brain injury trial has tested soft home chambers at that oxygen level, results from clinical HBOT studies should not be assumed to apply to mild HBOT.

Sources

1. Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurol. 2008;7(8):728-741. doi:10.1016/S1474-4422(08)70164-9. PMID: 18635021 ↩
2. Astrup J, Siesjö BK, Symon L. Thresholds in cerebral ischemia: the ischemic penumbra. Stroke. 1981;12(6):723-725. doi:10.1161/01.STR.12.6.723. PMID: 6272455 ↩
3. Gill AL, Bell CN. Hyperbaric oxygen: its uses, mechanisms of action and outcomes. QJM. 2004;97(7):385-395. doi:10.1093/qjmed/hch074. PMID: 15208426 ↩
4. Hadanny A, Efrati S. The hyperoxic-hypoxic paradox. Biomolecules. 2020;10(6):958. doi:10.3390/biom10060958. PMID: 32604837 ↩
5. Loane DJ, Kumar A. Microglia in the TBI brain: the good, the bad, and the dysregulated. Exp Neurol. 2016;275 Pt 3(0 3):316-327. doi:10.1016/j.expneurol.2015.08.018. PMID: 26342753 ↩
6. Benson RM, Minter LM, Osborne BA, Granowitz EV. Hyperbaric oxygen inhibits stimulus-induced proinflammatory cytokine synthesis by human blood-derived monocyte-macrophages. Clin Exp Immunol. 2003;134(1):57-62. doi:10.1046/j.1365-2249.2003.02248.x. PMID: 12974755 ↩
7. Thom SR, Bhopale VM, Velazquez OC, Goldstein LJ, Thom LH, Buerk DG. Stem cell mobilization by hyperbaric oxygen. Am J Physiol Heart Circ Physiol. 2006;290(4):H1378-H1386. doi:10.1152/ajpheart.00888.2005. PMID: 16299259 ↩
8. Boussi-Gross R, Golan H, Fishlev G, et al. Hyperbaric oxygen therapy can improve post concussion syndrome years after mild traumatic brain injury: randomized prospective trial. PLoS One. 2013;8(11):e79995. doi:10.1371/journal.pone.0079995. PMID: 24260334 ↩
9. Tal S, Hadanny A, Sasson E, Suzin G, Efrati S. Hyperbaric oxygen therapy can induce angiogenesis and regeneration of nerve fibers in traumatic brain injury patients. Front Hum Neurosci. 2017;11:508. doi:10.3389/fnhum.2017.00508. PMID: 29097988 ↩
10. Harch PG, Andrews SR, Fogarty EF, et al. A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder. J Neurotrauma. 2012;29(1):168-185. doi:10.1089/neu.2011.1895. PMID: 22026588 ↩
11. Cifu DX, Walker WC, West SL, et al. Hyperbaric oxygen for blast-related postconcussion syndrome: three-month outcomes. Ann Neurol. 2014;75(2):277-286. doi:10.1002/ana.24067. PMID: 24255008 ↩
12. Hadanny A, Abbott S, Engelman G, et al. Hyperbaric oxygen therapy improves neurocognitive functions of post-stroke patients: a retrospective analysis. Restor Neurol Neurosci. 2020;38(1):93-107. doi:10.3233/RNN-190959. PMID: 31985478 ↩
13. Hadanny A, Daniel-Kotovsky M, Suzin G, et al. Cognitive enhancement of healthy older adults using hyperbaric oxygen: a randomized controlled trial. Aging (Albany NY). 2020;12(13):13740-13761. doi:10.18632/aging.103571. PMID: 32589613 ↩
14. Hachmo Y, Hadanny A, Abu Hamed R, et al. Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial. Aging (Albany NY). 2020;12(22):22445-22456. doi:10.18632/aging.202188. PMID: 33206062 ↩
15. Hadanny A, Catalogna M, Yaniv S, et al. Hyperbaric oxygen therapy in children with post-concussion syndrome improves cognitive and behavioral function: a randomized controlled trial. Sci Rep. 2022;12(1):15233. doi:10.1038/s41598-022-19395-y. PMID: 36151105 ↩
16. Harch PG, Andrews SR, Rowe CJ, et al. Hyperbaric oxygen therapy for mild traumatic brain injury persistent postconcussion syndrome: a randomized controlled trial. Med Gas Res. 2020;10(1):8-20. doi:10.4103/2045-9912.279978. PMID: 32189664 ↩
17. Miller RS, Weaver LK, Bahraini N, et al. Effects of hyperbaric oxygen on symptoms and quality of life among service members with persistent postconcussion symptoms: a randomized clinical trial. JAMA Intern Med. 2015;175(1):43-52. doi:10.1001/jamainternmed.2014.5479. PMID: 25401463 ↩
18. Wolf G, Cifu D, Baugh L, Carne W, Profenna L. The effect of hyperbaric oxygen on symptoms after mild traumatic brain injury. J Neurotrauma. 2012;29(17):2606-2612. doi:10.1089/neu.2012.2549. PMID: 23031217 ↩
19. Weaver LK, Wilson SH, Lindblad AS, et al. Hyperbaric oxygen for post-concussive symptoms in United States military service members: a randomized clinical trial. Undersea Hyperb Med. 2018;45(2):129-156. PMID: 29734566 ↩
20. Harch PG. Systematic review and dosage analysis: hyperbaric oxygen therapy efficacy in mild traumatic brain injury persistent postconcussion syndrome. Front Neurol. 2022;13:815056. doi:10.3389/fneur.2022.815056. PMID: 35370898 ↩
21. Bennett MH, Trytko B, Jonker B. Hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury. Cochrane Database Syst Rev. 2012;12:CD004609. doi:10.1002/14651858.CD004609.pub3. PMID: 23235612 ↩

Related Reading

• Hyperbaric Oxygen Therapy: Benefits, Evidence, and What to Expect
• Brain Fog: Causes, Testing, and Evidence-Based Ways to Clear It
• Supplements for Brain Fog: What Actually Works (and What Doesn’t)