Brain Injury - Traumatic Brain Injury, Post Traumatic Stress Disorder, Shock Blast Injury, Post Concussion Syndrome ..

  • OXYMED Australia is providing Free Hyperbaric Oxygen Therapy for immediate returning Aussie War Veterans suffering the effects of TBI, Shock Blast, PTSD and Concussion Syndrome
USA Oklahoma Veteran Traumatic Brain Injury Treatment and Recovery Act

  • On the 19 June 2014, Oklahoma became the First State to create a state fund for Hyperbaric Oxygen Therapy to be available for battle casualties suffering the effects of Traumatic Brain Injury and Post Traumatic Stress Disorder.

  • Another 14 USA states have created similar state funded programs enabling returned War Veterans access to HBO. Across other USA states there are numerous 'not for profit' charities collectively under the banner  'Heal Our Heroes'.

  • There is NO provision for Australian returned service men and women to access Hyperbaric Oxygen Therapy for the effects of Traumatic Brain Injury and PTSD.  For the past several years Australian soldiers have been 'directed' to 'privately' attend the USA not for profit HBO centers where they receive 'free HBO treatment'. The USA not for profit clinics have considerable funding support with 'free' treatments typically costing between US $25,000-28,000 for around 80-hours of HBO.

  • Why are these Veterans NOT being directed to OXYMED Melbourne for Hyperbaric Oxygen Therapy?

  • What are the political reasons?

  • Why does the Australian Health Practitioner Regulation Agency (AHPRA) continue to view Hyperbaric Oxygen Therapy and LOKOMAT (Robotic Gait Assisted Walking) as 'novel' and without credit?

  • At OXYMED we have been at the forefront of providing HBO combined with other assertive modalities for neurodegenerative conditions and the effects of catastrophic injuries for the past 20-years. Hyperbaric Oxygen Therapy and Lokomat are considered 'novel and unique' and 'not supported by the greater percentage of medical doctors or organisations in Australia'.

  • We are committed to assisting our Aussie War Vets and in an attempt to get this project going across Australia, OXYMED Australia will continue to provide 'Free HBO or 'immediate' returning War Vets at OXYMED in Melbourne. We are hopeful of other interstate HBO facilities coming on-board to support this initiative. We have 4-monoplace chambers available to assist however we anticipate and currently working toward installing a large multiplace chamber.

  • OXYMED is not a registered charity and receives NO government funding or third party support. This program cannot be sustained without support. Your assistance will ensure that this initiative gains public awareness, partnering together to change the way the Australian Defence treats those that serve this great country.

Common Military Brain Injury

 

MRI shows 'brain scars' in military personnel with blast-related concussion Radiological Society of North America

Dec 2015. MRI shows brain damage in a surprisingly high percentage of active duty military personnel who suffered blast-related mild traumatic brain injury (mTBI), according to a new study appearing online in the journal Radiology.

mTBI, sometimes referred to as a concussion, is very common among U.S. service members returning from conflicts in Iraq and Afghanistan.

  • More than 300,000 service members have been diagnosed with mTBI between 2000 and 2015, according to the Armed Forces Health Surveillance Center.

 

Current assessment of mTBI relies heavily on behavioral observations and on patient recall of events, such as post-traumatic amnesia and loss of consciousness. The need for a more definitive marker spurred Gerard Riedy, M.D., Ph.D., from the National Intrepid Center of Excellence (NICoE) at the Walter Reed National Military Medical Center in Bethesda, Md., to look at advanced brain imaging with MRI as a tool for assessing mTBI.

In what represents the largest study using advanced brain imaging of active military ever performed, Dr. Riedy and colleagues used MRI to study 834 military service members with MTBI related to blast injuries. Slightly more than 84 percent of the patients reported one or more blast-related incidents, and 63 percent reported loss of consciousness at the time of injury.

The MRI scans revealed the presence of white matter T2 hyperintensities, which can be thought of as brain scars, in 52 percent of the mTBI patients.

Hyperbaric Oxygen Therapy for Traumatic Brain Injury:  Bench-to-Bedside Medical Gas Research 2016

Qin Hu1, 2, Anatol Manaenko2, Ting Xu2, Zhenni Guo2, Jiping Tang2, John H. Zhang2, 3, *
1 Discipline of Neuroscience, Department of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai, China 2 Departments of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, USA 3 Department of Neurosurgery, Loma Linda University School of Medicine, Loma Linda, CA, USA *Correspondence to: John H. Zhang, M.D., Ph.D., johnzhang3910@yahoo.com. 

Neuroreport. 2017 Sep 25. doi: 10.1097/WNR.0000000000000901. [Epub ahead of print]

Hyperbaric oxygen promotes neural stem cell proliferation by activating vascular endothelial growth factor/extracellular signal-regulated kinase signaling after traumatic brain injury.

Yang Y1, Wei HZhou XZhang FWang C.

Author information

Abstract

Hyperbaric oxygen (HBO) therapy and neural stem cell (NSC) transplantation can improve traumatic brain injury (TBI) clinically. This study aimed to investigate the mechanism of HBO promoting NSC proliferation and neurological recovery after TBI. Twenty-four Sprague-Dawley rats were divided randomly into three groups: a sham group, a TBI group (constructed using Feeney's free-fall method), and an HBO-treated TBI group. Neurological function was evaluated by Neurological Severity Scores on days 1, 3, and 7, and we found that TBI-induced poor neurological function was improved by HBO. On day 7 after TBI, we observed that TBI promoted NSC proliferation, migration to the lesion area, and the levels of vascular endothelial growth factor (VEGF), VEGFR2, Raf-1, MEK1/2, and phospho-extracellular signal-regulated kinase (ERK) 1/2 protein, which were further boosted by HBO, from immunohistochemistry, immunofluorescence, and Western blot experiments. In vitro, cell injury was applied to NSCs isolated from neonatal Sprague-Dawley rats by the Cell Injury Controller II system. Moreover, data from the BrdU Kit and Western blot showed that in-vitro HBO significantly accelerated NSC proliferation and the levels of proteins related to cell cycle and the VEGF/ERK pathway after cell injury, which was suppressed by the VEGFR2 inhibitor. Taken together, this study indicated that HBO may promote NSC proliferation by activating VEGF/ERK signaling and play a crucial role in neuroprotection after TBI.

Med Gas Res. 2015 May 28;5:7. doi: 10.1186/s13618-015-0028-0. eCollection 2015.

All the right moves: the need for the timely use of hyperbaric oxygen therapy for treating TBI/CTE/PTSD.

Stoller KP1.

Author information

Abstract

BACKGROUND:

The modern age of hyperbaric medicine began in 1937; however, today few know about hyperbaric oxygen's effects on the body and medical conditions outside of diving medicine and wound care centers - a serious ethical issue as there are 20 US military veterans committing suicide every day directly related to Traumatic Brain Injury/Post Traumatic Stress Disorder. The problem is not whether hyperbaric oxygen is effective for treating brain injuries, but why the interference in offering this therapy to those who need it.

DISCUSSION:

Up against black-boxed anti-depressants that are not efficacious, it should be a "no-brainer" to use a safe, off-label drug, but in the case of military veterans, every suicide might be seen as a tremendous cost saving to certain technocrats.

The unspoken rationale is that if the military were to embrace hyperbaric oxygen as the efficacious therapy that it is then current active troops that have suffered injuries will come forward and seek treatment and benefits for their Traumatic Brain Injuries now that they know there is a viable therapy and in so doing troop strength will be decimated. So, to attempt to delay the acceptance of hyperbaric oxygen the Department of Defense has funded faux-studies claiming low pressure room air to be a placebo or sham, and then proclaiming there is no statistical difference between treatment arms and sham or placebo treatment arms. With few who understand hyperbaric medicine there is almost no one to call them on this subterfuge and prevarication.

Many peer-reviewed articles have been published in the last decade that demonstrate hyperbaric oxygen is effective in repairing an injured brain even long after that injury took place. One of the most notable showed that blast-induced brain injured war veterans experienced a 15 point IQ increase (p < 0.001).

 

SUMMARY:

Hyperbaric oxygen is an efficacious, benign and humanitarian way to affect brain repair but it has not been adopted because it lacks patent protection and has no large corporate sponsors. It has also met interference because other agendas are present be they the protection of the status quo, myopic budgetary constraints, or perceived liability issues.

1Chief of Hyperbaric Medicine, Hyperbaric Oxygen Clinic of San Francisco, HOCSF/Azzolino CN&IW, 1545 Broadway 1-A, San Francisco, CA 94109 USA.

 

Expert Rev Neurother. 2016 Jul 4:1-13. [Epub ahead of print]

Treatment of persistent post-concussion syndrome due to mild traumatic brain injury: current status and future directions.

Hadanny A1,2, Efrati S1,2,3,4.

Author information

  • 1a The Sagol Center for Hyperbaric Medicine and Research , Assaf Harofeh Medical Center , Zerifin , Israel.

  • 2b Sackler School of Medicine , Tel-Aviv University , Tel-Aviv , Israel.

  • 3c Research and Development Unit , Assaf Harofeh Medical Center , Zerifin , Israel.

  • 4d Sagol School of Neuroscience , Tel-Aviv University , Tel-Aviv , Israel.

Abstract

Persistent post-concussion syndrome caused by mild traumatic brain injury has become a major cause of morbidity and poor quality of life. Unlike the acute care of concussion, there is no consensus for treatment of chronic symptoms. Moreover, most of the pharmacologic and non-pharmacologic treatments have failed to demonstrate significant efficacy on both the clinical symptoms as well as the pathophysiologic cascade responsible for the permanent brain injury. This article reviews the pathophysiology of PCS, the diagnostic tools and criteria, the current available treatments including pharmacotherapy and different cognitive rehabilitation programs, and promising new treatment directions. A most promising new direction is the use of hyperbaric oxygen therapy, which targets the basic pathological processes responsible for post-concussion symptoms; it is discussed here in depth.

Clinical results in brain injury trials using HBO2 therapy: Another perspective

Undersea Hyperb Med. 2015 Jul-Aug;42(4):333-51.

Figueroa XA, Wright JK.

Abstract

The current debate surrounding the use of hyperbaric oxygen (HBO2) for neurological indications, specifically mild to moderate chronic traumatic brain injury (mTBI) and post-concussion syndrome (PCS), is mired in confusion due to the use of non-validated controls and an unfamiliarity by many practitioners of HBO2 therapy with the experimental literature.

In the past 40 years, the use of an air sham (21% oxygen, 1.14-1.5 atmospheres absolute/atm abs) in clinical and animal studies, instead of observational or crossover controls, has led to false acceptance of the null hypothesis (declaring no effect when one is present), due to the biological activity of these "sham" controls. The recent Department of Defense/Veterans Administration (DoD/VA) sponsored trials, previous published reports on the use of HBO2 therapy on stroke and mTBI and preliminary reports from the HOPPS Army trial, have helped to highlight the biological activity of pressurized air, validate the development of a convincing control for future studies and demonstrate the effectiveness of a hyperbaric intervention for mTBI/ PCS.

Approval of HBO2 for neurological indications, especially for mTBI/PCS, should be granted at the federal, state and certifying body levels as a safe and viable treatment for recovery in the post-acute phase.

 

Improved Cognitive Function - Hyperbaric Oxygenation

Clin Neurophysiol. 2015 Jan 24. pii: S1388-2457(15)00030-9. doi: 10.1016/j.clinph.2015.01.010. [Epub ahead of print]

Cognitive enhancement of healthy young adults with hyperbaric oxygen: A preliminary resting-state fMRI study

Yu R1, Wang B2, Li S3, Wang J2, Zhou F1, Chu S1, He X2, Wen X2, Ni X1, Liu L2, Xie Q4, Huang R5.

Author information

  • 1Centre for Hyperbaric Oxygen and Neurorehabilitation, Liuhuaqiao Hospital, Guangzhou, China.

  • 2Centre for Studies of Psychological Application, School of Psychology, South China Normal University, Guangzhou, China.

  • 3Centre for Studies of Psychological Application, School of Psychology, South China Normal University, Guangzhou, China; Department of Medical Imaging, Guangdong No. 2 Provincial People's Hospital, Guangzhou, China.

  • 4Centre for Hyperbaric Oxygen and Neurorehabilitation, Liuhuaqiao Hospital, Guangzhou, China. Electronic address: xqy7180@163.com.

  • 5Centre for Studies of Psychological Application, School of Psychology, South China Normal University, Guangzhou, China. Electronic address: ruiwang.huang@gmail.com.

Abstract

OBJECTIVE:

To date, no study has examined the effect of hyperbaric oxygen (HBO) on the cognitive performance and spontaneous brain activity in healthy adults using resting-state functional magnetic resonance imaging (rsfMRI). Our aim was to reveal the neural mechanism underlying the change in cognitive performance caused by increased oxygen.

METHODS:

In this study, we acquired fMRI data from 20 healthy young adults and used placebo-controlled (PBO) rsfMRI to identify the effect of HBO on the cognitive measures and the regional homogeneity (ReHo) in healthy adults.

RESULTS:

Compared to the PBO group, the HBO group showed the following: (1) the scores of the spatial working memory and memory quotient were significantly increased after HBO administration; (2) the ReHo value was significantly increased in three clusters, the left hippocampus, right inferior frontal, and lingual gyri, and for these three clusters, their functional connectivity with the subcortical brain system was significantly increased after HBO administration; and (3) the changes of ReHo values in these clusters generated by HBO administration were correlated with several aspects of cognitive performance, clarifying the cognitive locus of the effect.

CONCLUSION:

Our results suggested that the increased availability of oxygen can, to some extent, improve memory performance.

SIGNIFICANT:

Our findings may improve our understanding of the role of HBO in clinical and practical applications.

Hyperbaric Oxygen Improves Post Concussion Syndrome Years After Traumatic Brain Injury (TBI)

Citation: Boussi-Gross R, Golan H, Fishlev G, Bechor Y, Volkov O, et al. (2013)

Hyperbaric Oxygen Therapy Can Improve Post Concussion Syndrome Years after Mild Traumatic Brain Injury - Randomized Prospective Trial.

PLoS ONE 8(11): e79995. doi:10.1371/journal.pone.0079995. Published November 15, 2013

 

Traumatic brain injury (TBI) is the leading cause of death and disability in the US. Approximately 70-90% of the TBI cases are classified as mild, and up to 25% of them will not recover and suffer chronic neurocognitive impairments. The main pathology in these cases involves diffuse brain injuries, which are hard to detect by anatomical imaging yet noticeable in metabolic imaging.

The current study tested the effectiveness of Hyperbaric Oxygen Therapy (HBOT) in improving brain function and quality of life in mTBI patients suffering chronic neurocognitive impairments.

Methods and Findings: The trial population included 56 mTBI patients 1–5 years after injury with prolonged postconcussion syndrome (PCS). The HBOT effect was evaluated by means of prospective, randomized, crossover controlled trial: the patients were randomly assigned to treated or crossover groups.

Patients in the treated group were evaluated at baseline and following 40 HBOT (60-minute) sessions; patients in the crossover group were evaluated three times: at baseline, following a 2-month control period of no treatment, and following subsequent 2-months of 40 HBOT sessions.

The HBOT protocol included 40 treatment sessions (5 days/week), 60 minutes each, with 100% oxygen at 1.5 ATA. ‘‘Mindstreams’’ was used for cognitive evaluations, quality of life (QOL) was evaluated by the EQ-5D, and changes in brain activity were assessed by SPECT imaging.

Significant improvements were demonstrated in cognitive function and QOL in both groups following HBOT but no significant improvement was observed following the control period. SPECT imaging revealed elevated brain activity in good agreement with the cognitive improvements.

Conclusions: HBOT can induce neuroplasticity leading to repair of chronically impaired brain functions and improved quality of life in mTBI patients with prolonged PCS at late chronic stage.

Page 11 - Linking elevated oxygen, metabolism and brain activity to neuroplasticity

 

The changes in SPECT images after treatment indicate that HBOT led to reactivation of neuronal activity in stunned areas that seemed normal under CT and MRI imaging.

While SPECT imaging has a limited spatial resolution (compared, for example, to fMRI, the changes in activity were sufficiently robust to be clearly detected by the SPECT images. Recently, Kan et al. [57] discussed the need for potent interventions, such as elevated tissue oxygen, capable of repairing microenvironment alterations after mTBI (e.g impairments in vascular changes, in cerebral blood flow and in perfusion), leading to reduced oxygen availability followed by reduced metabolism, which in turn leads to reduced neuronal activity, loss of synapses and tampered neuronal connectivity.

The observed reactivation of neuronal activity in the stunned areas found here, along with similar results in post-stroke patients [3], imply that increasing the plasma oxygen concentration with hyperbaric oxygenation is a potent means of delivering to the brain sufficient oxygen for tissue repair. HBOT might initiate a cellular and vascular repair mechanism and improve cerebral vascular flow [34,58,59,60]. More specifically, HBOT induces regeneration of axonal white matter [61,62,63,64, has positive effect upon the myelinization and maturation of injured neural fibers [65], and can stimulate axonal growth and increase the ability of neurons to function and communicate with each other [66].

In addition, HBOT was found to have a role in initiation and/or facilitation of angiogenesis and cell proliferation processes needed for axonal regeneration [67]. At the cellular level, HBOT can improve cellular metabolism, reduce apoptosis, alleviate oxidative stress and increase levels of neurotrophins and nitric oxide through enhancement of mitochondrial function (in both neurons and glial cells). Moreover, the effects of HBOT on neurons can be mediated indirectly by glial cells, including astrocytes [23].

HBOT may promote the neurogenesis of endogenous neural stem cells [24]. With regard to secondary injury mechanisms in mTBI, HBOT can initiate vascular repair mechanism and improve cerebral vascular flow [58,59,68,69], promote blood brain barrier integrity and reduce inflammatory reactions [28] as well as brain edema [20,21,22,26,34,70].

A drawback to the above-mentioned findings is that the different effects have been tested at different experimental setups and while utilizing different protocols of HBOT.

However, it is well noticed that there is at least one common denominator to all repair/regeneration mechanisms: Figure 6. Assessments of the mean relative changes and standard errors in quality of life measurements. The changes are shown for the crossover group following control period (green bars) and following HBOT (blue bars), and for the treated group following HBOT (red bars). Note that, according to the questionnaire structure, in the EQ-5D measurement improvement is reflected as score decrease, hence the negative values of change they are all energy/oxygen dependent.

  • It might be possible that HBOT enables the metabolic change simply by supplying the missing energy/oxygen needed for those regeneration processes.

Med Sci Monit. 2016 Jan 26;22:284-8.

Hyperbaric Oxygen Alleviates Secondary Brain Injury After Trauma Through Inhibition of TLR4/NF-κB Signaling Pathway

Meng XE1, Zhang Y1, Li N1, Fan DF1, Yang C1, Li H1, Guo DZ1, Pan SY1.

Author information

  • 1Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).

Abstract

BACKGROUND The aim of this study was to investigate the efficacy of hyperbaric oxygen in secondary brain injury after trauma and its mechanism in a rat model.

MATERIAL AND METHODS A rat model of TBI was constructed using the modified Feeney's free-fall method, and 60 SD rats were randomly divided into three groups - the sham group, the untreated traumatic brain injury (TBI) group, and the hyperbaric oxygen-treated TBI group. The neurological function of the rats was evaluated 12 and 24 hours after TBI modeling; the expression levels of TLR4, IκB, p65, and cleaved caspase-3 in the peri-trauma cortex were determined by Western blot; levels of TNF-α, IL-6, and IL-1β were determined by ELISA; and apoptosis of the neurons was evaluated by TUNEL assay 24 hours after TBI modeling.

RESULTS Hyperbaric oxygen therapy significantly inhibited the activation of the TLR4/NF-κB signaling pathway, reduced the expression of cleaved caspase-3, TNF-α, IL-6 and IL-1β (P<0.05), reduced apoptosis of the neurons and improved the neurological function of the rats (P<0.05).

CONCLUSIONS Hyperbaric oxygen therapy protects the neurons after traumatic injury, possibly through inhibition of the TLR4/NF-κB signaling pathway.

Cell Physiol Biochem. 2016;38(6):2323-36. doi: 10.1159/000445586. Epub 2016 May 23.

Hyperbaric Oxygen Intervention Modulates Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats: Possible Involvement of TLR4/NF-x03BA; B-Mediated Signaling Pathway.

Liu H, Yang M, Pan L, Liu P, Ma L.

Abstract

BACKGROUND/AIMS:

Previous studies have proved that the activation of TLR4/NF-x03BA; B signaling pathway is involved in inflammatory processes in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Hyperbaric oxygen (HBO) intervention has successfully been used to treat several animal models of tissue injury via its anti-inflammation property. This study was undertaken to investigate the influence of HBO administration on the TLR4/NF-x03BA; B signaling pathway in rats at the early stage of SAH.

METHODS:

Male Sprague-Dawley rats (n = 150) were randomly divided into 5 groups: the sham, the sham + 2.8 atmospheres absolute (ATA) HBO group, the SAH group, the SAH + 2.0ATA HBO group, the SAH + 2.8ATA HBO group. Each group (n = 30) was randomly subdivided into three subgroups that were examined at the following time points: 24 h, 48 h and 72 h post-injury. HBO (100% O2, 2.0ATA or 2.8ATA for 90mins) was initiated 12 h after injury. Neurological deficit, brain edema and blood-brain barrier (BBB) permeability were assessed to evaluate the development of EBI. The expressions of TLR4, NF-x03BA; B and pro-inflammatory cytokines in the cortical were determined by real time polymerase chain reaction (RT-PCR), western blot, immunohistochemistry, or enzyme-linked immunosorbent assay (ELISA).

RESULTS:

Our study showed that treatment with HBO significantly decreased the expressions of TLR4, NF-x03BA; B and the downstream inflammatory agents, such as TNF-α, IL-6, IL-1β and ICAM-1, and also improved brain edema, blood-brain barrier permeability and neurologic function.

CONCLUSIONS:

These findings indicate that HBO treatment may result in abatement of the development of EBI after SAH, possibly through suppression of TLR4/NF-x03BA; B signaling pathway.

 

J Phys Ther Sci. 2015 Oct;27(10):3271-4. doi: 10.1589/jpts.27.3271. Epub 2015 Oct 30.

Protection mechanism of early hyperbaric oxygen therapy in rats with permanent cerebral ischemia.

Yu M1, Xue Y2, Liang W1, Zhang Y1, Zhang Z1.

Author information

Abstract

[Purpose] The purpose of this study was to investigate whether early hyperbaric oxygen is useful in rats with permanent cerebral ischemia, and whether its mechanism relates to the inhibition of the tumor necrosis factor-alpha-protein kinase C-alpha pathway. [Subjects] Healthy, male Sprague-Dawley rats (N = 108) were the subjects. [Methods] After middle cerebral artery occlusion models were successfully made, rats were randomly divided into sham-operated, cerebral ischemia, and hyperbaric oxygen groups. At 4 and 12 hours after modeling, the volume of cerebral infarction was determined by triphenyltetrazolium chloride staining, and brain water content was measured using the dry and wet method. The expression of tumor necrosis factor-alpha and protein kinase C-alpha in the ischemic penumbra tissue was measured using Western blot analysis.

[Results] The data showed that at 4 and 12 hours after modeling, cerebral infarct volume and brain water content decreased in the hyperbaric oxygen group, and expression of tumor necrosis factor-alpha and phospho-protein kinase C-alpha in the ischemic penumbra tissue also decreased.

  • Our study demonstrates that early hyperbaric oxygen therapy has protective effects on brain tissue after cerebral ischemia, possibly via inhibition of tumor necrosis factor-alpha and phospho-protein kinase C-alpha.

Undersea Hyperb Med. 2015 Jul-Aug;42(4):333-51

Clinical results in brain injury trials using HBO2 therapy: Another perspective

Figueroa XA, Wright JK.

Abstract

The current debate surrounding the use of hyperbaric oxygen (HBO2) for neurological indications, specifically mild to moderate chronic traumatic brain injury (mTBI) and post-concussion syndrome (PCS), is mired in confusion due to the use of non-validated controls and an unfamiliarity by many practitioners of HBO2 therapy with the experimental literature.

In the past 40 years, the use of an air sham (21% oxygen, 1.14-1.5 atmospheres absolute/atm abs) in clinical and animal studies, instead of observational or crossover controls, has led to false acceptance of the null hypothesis (declaring no effect when one is present), due to the biological activity of these "sham" controls.

The recent Department of Defense/Veterans Administration (DoD/VA) sponsored trials, previous published reports on the use of HBO2 therapy on stroke and mTBI and preliminary reports from the HOPPS Army trial, have helped to highlight the biological activity of pressurized air, validate the development of a convincing control for future studies and demonstrate the effectiveness of a hyperbaric intervention for mTBI/ PCS.

  • Approval of HBO2 for neurological indications, especially for mTBI/PCS, should be granted at the federal, state and certifying body levels as a safe and viable treatment for recovery in the post-acute phase.

 

J Formos Med Assoc. 2014 Sep;113(9):620-8. doi: 10.1016/j.jfma.2014.03.012. Epub 2014 Apr 29.

Repetitive hyperbaric oxygen therapy provides better effects on brain inflammation and oxidative damage in rats with focal cerebral ischemia

Chen LF1, Tian YF2, Lin CH3, Huang LY4, Niu KC4, Lin MT5.

Author information

  • 1Nursing Department, Cheng Kung University Hospital and Department of Nursing, Chang Jung University, Tainan, Taiwan.

  • 2Department of Surgery, Chi Mei Medical Center, Tainan, Taiwan; Department of Health and Nutrition, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan. Electronic address: cmh7590@mail.chimei.org.tw.

  • 3Department of Nursing, Shu-Zen Junior College of Medicine and Management, Kaohsiung, Taiwan; Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan.

  • 4Department of Hyperbaric Oxygen, Chi Mei Medical Center, Tainan, Taiwan.

  • 5Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan. Electronic address: 891201@mail.chimei.org.tw.

Abstract

BACKGROUND/PURPOSE:

Repetitive hyperbaric oxygen (HBO2) therapy may cause excessive generation of reactive oxygen species. This study assessed whether repetitive or 2-4-day trials of HBO2 therapy (2 treatments daily for 2-4 consecutive days) provides better effects in reducing brain inflammation and oxidative stress caused by middle cerebral artery occlusion (MCAO) in rats than did a 1-day trial of HBO2 therapy (2 treatments for 1 day).

METHODS:

Rats were randomly divided into four groups: sham; MCAO without HBO2 treatment; MCAO treated with 1-day trial of HBO2; and MCAO treated with 2-4-day trials of HBO2. One treatment of HBO2 (100% O2 at 253 kPa) lasted for 1 hour in a hyperbaric chamber.

RESULTS:

Therapy with the 2-4-day trials of HBO2 significantly and dose-dependently attenuated the MCAO-induced cerebral infarction and neurological deficits more than the 1-day trial of HBO2 therapy.

  • The beneficial effects of repetitive HBO2 therapy were associated with: (1) reduced inflammatory status in ischemic brain tissues (evidenced by decreased levels of tumor necrosis factor-α, interleukin-1β, and myeloperoxidase activity); (2) decreased oxidative damage in ischemic brain tissues (evidenced by decreased levels of reactive oxygen and nitrogen species, lipid peroxidation, and enzymatic pro-oxidants, but increased levels of enzymatic antioxidant defenses); and (3) increased production of an anti-inflammatory cytokine, interleukin-10.

 

CONCLUSION:

The results provide the apparently contradictory finding that heightened oxygen tension reduced oxidative stress (and inflammation), which was reflected by increased antioxidant and decreased oxidant contents under focal cerebral ischemia.

Neuroscience. 2013 Nov 27. pii: S0306-4522(13)00983-4. doi: 10.1016/j.neuroscience.2013.11.036. [Epub ahead of print]

Interleukin-10 mediates the neuroprotection of hyperbaric oxygen therapy against traumatic brain injury in mice

Chen X1, Duan XS1, Xu LJ1, Zhao JJ2, She ZF1, Chen WW1, Zheng ZJ1, Jiang GD3.

Author information

  • 1Department of Hyperbaric Oxygen, The 113th Hospital of PLA, Ningbo, Zhejiang, China.

  • 2Department of Neurology, The 305th Hospital of PLA, Beijing, China.

  • 3Department of Hyperbaric Oxygen, The 113th Hospital of PLA, Ningbo, Zhejiang, China. Electronic address: jianggd2013@hotmail.com.

Abstract

The aim of present study was to elucidate the role of Interleukin-10 (IL-10) in the neuroprotection of hyperbaric oxygen (HBO) against traumatic brain injury (TBI) in mice. The TBI in mice was induced by controlled cortical impact (CCI). HBO was given for 1h at 2.0 ATA in 100% O2.

  • HBO enhanced the serumal and cerebral IL-10 protein levels in both sham-operated and TBI mice. HBO therapy after TBI reduced lesion volume, attenuated cerebral edema, improved neurological status including motor and cognitive function, inhibited apoptosis evidenced by decreased ratio of cleaved caspase-3 (C3) to pro-C3 and Bax expression and increased bcl-2 expression, and attenuated inflammation marked by reduced expression of IL-1β, IL-6, macrophage inflammatory protein-2 (MIP-2), and monocyte chemoattractant protein-1 (MCP-1) and activity of matrix metalloproteinase-9 (MMP9).

 

In addition, HBO after TBI improved the blood-brain barrier, and upregulated the expression of tight junction proteins including zonula occludens-1 (ZO-1) and claudin-5.

  • IL-10 deficiency aggravated TBI-induced damage in the brain and abrogated the beneficial effects of HBO on neuroinflammation, apoptosis, and edema after TBI. IL-10 deficiency itself had no significant effect on brain water content and neurological status. In conclusion, IL-10 played an important role in the neuroprotection of HBO therapy against TBI in mice.

J Surg Res. 2013 Oct;184(2):1076-84. doi: 10.1016/j.jss.2013.04.070. Epub 2013 May 21.

Microglial activation induced by traumatic brain injury is suppressed by postinjury treatment with hyperbaric oxygen therapy

Lim SW, Wang CC, Wang YH, Chio CC, Niu KC, Kuo JR.

Author information

  • Department of Neurosurgery, Chi-Mei Medical Center, Tainan, Taiwan. Electronic address: kuojinnrung@gmail.com.

Abstract

BACKGROUND:

The mechanisms underlying the protective effects of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) are unclear. TBI initiates a neuroinflammatory cascade characterized by activation of microglia and increased production of proinflammatory cytokines. In this study, we attempted to ascertain whether the occurrence of neuroinflammation exhibited during TBI can be reduced by HBO.

METHODS:

TBI was produced by the fluid percussion technique in rats. HBO (100% O2 at 2.0 absolute atmospheres) was then used at 1 h (HBO I) or 8 h (HBO II) after TBI. Neurobehavior was evaluated by the inclined plane test on the 72 h after TBI and then the rats were killed. The infarction area was evaluated by Triphenyltetrazolium chloride. Immunofluorescence staining was used to evaluate neuronal apoptosis (TUNEL + NeuN), microglial cell aggregation count (OX42 + DAPI), and tumor necrosis factor-alpha (TNF-α) expression in microglia cell (OX42 + TNF-α).

RESULTS:

The maximum grasp angle in the inclined plane test and cerebral infarction of the rats after TBI were significantly attenuated by HBO therapy regardless of whether the rats were treated with HBO 1 or 8 h after TBI compared with the controls. TBI-induced microglial activation, TNF-α expression, and neuronal apoptosis were also significantly reduced by HBO therapy.

CONCLUSIONS:

Our results demonstrate that treatment of TBI during the acute phase of injury can attenuate microgliosis and proinflammatory cytokine TNF-α expression resulting in a neuroprotective effect. Even treating TBI with HBO after 8 h had a therapeutic effect.

 

Undersea Hyperb Med. 2013 Mar-Apr;40(2):165-93

A prospective trial of hyperbaric oxygen for chronic sequelae after brain injury (HYBOBI)

Churchill S, Weaver LK, Deru K, Russo AA, Handrahan D, Orrison WW Jr, Foley JF, Elwell HA.

Source

LDS Hospital, Salt Lake City, Utah; Intermountain Medical Center, Murray, Utah, USA.

OBJECTIVE:

Some practitioners advocate hyperbaric oxygen (HBO2) for sequelae following brain injury. This study assessed recruitment, tolerance and safety in preparation for a randomized clinical trial. Design: Prospective, open-label feasibility study.

SETTING:

Hyperbaric medicine department of a tertiary academic hospital. Participants: Participatory adult outpatients with problems from stroke (n=22), anoxia (13) or trauma (28) that occurred at least 12 months before enrollment, without contraindications to HBO2. Sixty-three participants enrolled in the study (21 females,42 males). Age was 45 +/- 16 years (18-76) and time from injury was 6.9 +/- 7.1 years (1.0-29.3). Fifty-three completed the study intervention, and 55 completed the assessment battery.

METHODS:

Participants underwent 60 daily HBO2 sessions (1.5 atm abs, 100% oxygen, 60 minutes). Assessments were conducted at baseline, after the HBO2 course, and six months later. Main outcome measurements: The prime outcome was feasibility. To estimate the immediate and long-term effects of HBO2, we assessed neuropsychological measures, questionnaires, neurologic exam and physical functioning measures. Some participants also had pre- and post-HBO2 speech evaluation (n=27) and neuroimaging (n=17).

RESULTS:

The study met our a prior definition for feasibility for recruitment, but 44% required additional time to complete the 60 sessions (up to 105 days). HBO2-related adverse events were rare and not serious. Although many participants reported improvement in symptoms (51% memory, 51% attention/concentration, 48% balance/coordination, 45% endurance, 20% sleep) post-HBO2, and 93% reported that they would participate in the study again, no standardized testing showed clinically important improvement. In the small subset of those undergoing neuroimaging, apparent improvement was observed in auditory functional MRI (8/13), MR spectroscopy (9/17) and brain perfusionby CT angiography (5/9).

CONCLUSIONS:

Conducting an HBO2 clinical trial in this population was feasible. Although many participants reported improvement, the lack of concurrent controls limits the strength of inferences from this trial, especially considering lack of change in standardized testing. The clinical relevance of neuroimaging changes is unknown. The findings of this study may indicate a need for caution when considering the broad application of HBO2 more than one year after brain injury due to stroke, severe TBI and anoxia, until there is more compelling evidence from carefully designed sham-controlled, blinded clinical trials.

 

Neuropsychiatr Dis Treat. 2010 Dec 6;6:785-9. doi: 10.2147/NDT.S16071.

Hyperbaric oxygen ameliorates worsening signs and symptoms of post-traumatic stress disorder

Eovaldi B, Zanetti C.

Source

Department of Medicine, Chicago College of Osteopathic Medicine, Chicago, IL, USA. eovaldi@gmail.com

Abstract

Hyperbaric oxygen therapy at 2.4 atmospheric pressure absolutes for 90 minutes per day ameliorated the signs and symptoms of agitation, confusion, and emotional distress in a 27-year-old male seven days following a traumatic accident.

Hyperbaric oxygen was used to treat the patient's crush injury and underlying nondisplaced pelvic fractures which were sustained in a bicycle versus automobile traffic accident. Its effect on the patient's neuropsychiatric symptoms was surprising and obvious immediately following the initial hyperbaric oxygen treatment.

  • Complete cognitive and psychiatric recovery was achieved by the seventh and final hyperbaric oxygen treatment. We propose that hyperbaric oxygen was effective in improving the patient's neuropsychiatric symptoms by reducing cerebral oxidative stress, inflammation, vasogenic edema, and hippocampal neuronal apoptosis.

Further investigation into the use of hyperbaric oxygen as a novel therapy for the secondary prevention of post-traumatic stress disorder that often accompanies post-concussive syndrome may be warranted. We acknowledge that hyperbaric oxygen therapy has been shown to have a strong placebo effect on neurologic and psychiatric diseases.

J Neurotrauma 2013 Jun 3. [Epub ahead of print]

The Therapeutic Role of Interleukin-10 after Spinal Cord Injury

Source

University of Wisconsin , Neurological Surgery, 600 Highland Avenue, Madison, Wisconsin, United States, 53792, 608-265-8800 ; cthompson5@wisc.edu.

Abstract

Spinal cord injury (SCI) is a devastating condition affecting 270,000 people in the United States. A potential treatment for decreasing the secondary inflammation, excitotoxic damage, and neuronal apoptosis associated with SCI is the anti-inflammatory cytokine interleukin-10.

  • The best characterized effects of IL-10 are anti-inflammatory-it down-regulates pro-inflammatory species IL-1β, IL-2, IL-6, tumor necrosis factor-α, interferon-γ, matrix metalloproteinase-9, nitric oxide synthase, myeloperoxidase, and reactive oxygen species. Pro-apoptotic factors cytochrome c, caspase 3, and Bax are down-regulated by IL-10, whereas anti-apoptotic factors Bcl-2 and Bcl-xl are up-regulated by IL-10.

  • IL-10 also provides trophic support to neurons through the IL-10 receptor. Increased tissue sparing, functional recovery, and neuroprotection are seen with an immediate post-SCI systemic administration of IL-10.

  • Treatment of SCI with IL-10 has been used successfully in combination with Schwann cell and olfactory glial cell grafts as well as methylprednisolone.

  • Minocycline, tetramethylpyrazine, and hyperbaric oxygen treatment all increase IL-10 levels in a SCI models and result in increased tissue sparing and functional recovery. A chronic systemic administration of IL-10 does not appear to be beneficial to SCI recovery and causes increased susceptibility to septicemia, pneumonia, and peripheral neuropathy. However, a localized up-regulation of IL-10 has been shown to be beneficial and can be achieved by herpes simplex virus gene therapy, injection of poliovirus replicons, or surgical placement of a slow-release compound. IL-10 shows promise as a treatment for SCI, although research on local IL-10 delivery timeline and dosage needs to be expanded upon.

 

 

J Pain. 2013 May 14. pii: S1526-5900(13)00839-0. doi: 10.1016/j.jpain.2013.02.003. [Epub ahead of print]

Repetitive Hyperbaric Oxygen Treatment Attenuates Complete Freund's Adjuvant-Induced Pain and Reduces Glia-Mediated Neuroinflammation in the Spinal Cord.

Source

Institute of Nautical Medicine, Jiangsu Key laboratory of Neuroregeneration, Nantong University, Nantong, China.

Abstract

Hyperbaric oxygen (HBO) therapy is reported to attenuate pain in both clinical pain conditions and animal pain models, but the underlying mechanism remains to be investigated. Here, we show that 7 daily 60-minute HBO (100% oxygen, 2 atmosphere absolute) treatments effectively and persistently inhibited heat hyperalgesia, mechanical allodynia, and paw edema induced by peripheral injection of complete Freund's adjuvant (CFA). Five daily 60-minute HBO treatments also produced a prolonged reversal effect of the ongoing inflammatory pain.

Furthermore, such an HBO treatment reduced CFA-induced activation of glial cells, phosphorylation of mitogen-activated protein kinases, and production of a variety of proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-1 beta [IL-1β], and interleukin-6 [IL-6]) and chemokines (monocyte chemoattractant protein-1 [MCP-1], keratinocyte-derived chemokine [KC], and IFN-gamma-inducible protein 10 [IP-10]) in the spinal cord. HBO treatment also decreased lipopolysaccharide-induced mRNA expression of these cytokines and chemokines in primary cultures of astrocytes and microglia.

In addition, the mRNA expressions of IL-1β, IL-6, MCP-1, KC, and IP-10 in the inflamed paw skin were decreased by HBO. Taken together, these data suggest that HBO treatment is an effective therapy for inflammatory pain in animals. The inhibition of the neuroinflammation that is mediated by glial cells and inflammatory mediators may, at least in part, contribute to the antinociceptive effect of HBO therapy.

PERSPECTIVE: Our results suggest that repetitive HBO treatment attenuates CFA-induced pain and reduces glial activation and inflammatory mediators' production. These findings provide the evidence of the antinociception effect of HBO on inflammatory pain and characterize some of the underlying mechanisms.

 

J Neurosurg 2013 Jun;118(6):1317-28. doi: 10.3171/2013.2.JNS121468. Epub 2013 Mar 19.

A prospective, randomized Phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury.

Rockswold SB, Rockswold GL, Zaun DA, Liu J.

Source

Department of Physical Medicine and Rehabilitation.

Abstract

Object Preclinical and clinical investigations indicate that the positive effect of hyperbaric oxygen (HBO2) for severe traumatic brain injury (TBI) occurs after rather than during treatment. The brain appears better able to use baseline O2 levels following HBO2 treatments. In this study, the authors evaluate the combination of HBO2 and normobaric hyperoxia (NBH) as a single treatment. Methods Forty-two patients who sustained severe TBI (mean Glasgow Coma Scale [GCS] score 5.7) were prospectively randomized within 24 hours of injury to either: 1) combined HBO2/NBH (60 minutes of HBO2 at 1.5 atmospheres absolute [ATA] followed by NBH, 3 hours of 100% fraction of inspired oxygen [FiO2] at 1.0 ATA) or 2) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Intracranial pressure, surrogate markers for cerebral metabolism, and O2 toxicity were monitored. Clinical outcome was assessed at 6 months using the sliding dichotomized Glasgow Outcome Scale (GOS) score. Mixed-effects linear modeling was used to statistically test differences between the treatment and control groups. Functional outcome and mortality rates were compared using chi-square tests. Results There were no significant differences in demographic characteristics between the 2 groups. In comparison with values in the control group, brain tissue partial pressure of O2 (PO2) levels were significantly increased during and following combined HBO2/NBH treatments in both the noninjured and pericontusional brain (p < 0.0001). Microdialysate lactate/pyruvate ratios were significantly decreased in the noninjured brain in the combined HBO2/NBH group as compared with controls (p < 0.0078). The combined HBO2/NBH group's intracranial pressure values were significantly lower than those of the control group during treatment, and the improvement continued until the next treatment session (p < 0.0006). The combined HBO2/NBH group's levels of microdialysate glycerol were significantly lower than those of the control group in both noninjured and pericontusional brain (p < 0.001). The combined HBO2/NBH group's level of CSF F2-isoprostane was decreased at 6 hours after treatment as compared with that of controls, but the difference did not quite reach statistical significance (p = 0.0692). There was an absolute 26% reduction in mortality for the combined HBO2/NBH group (p = 0.048) and an absolute 36% improvement in favorable outcome using the sliding dichotomized GOS (p = 0.024) as compared with the control group.

Conclusions In this Phase II clinical trial, in comparison with standard care (control treatment) combined HBO2/NBH treatments significantly improved markers of oxidative metabolism in relatively uninjured brain as well as pericontusional tissue, reduced intracranial hypertension, and demonstrated improvement in markers of cerebral toxicity. There was significant reduction in mortality and improved favorable outcome as measured by GOS. The combination of HBO2 and NBH therapy appears to have potential therapeutic efficacy as compared with the 2 treatments in isolation. Clinical trial registration no.: NCT00170352 ( ClinicalTrials.gov ).

 

Med Gas Res 2011 Sep 6;1(1):21. doi: 10.1186/2045-9912-1-21.

Hyperbaric oxygen therapy for traumatic brain injury.

Department of Biophysics & Bioengineering, Loma Linda University, Griggs Hall, Room 227, 11065 Campus St,, Loma Linda, California, 92354, USA. aobenaus@llu.edu.

Abstract

Traumatic brain injury (TBI) is a major public health issue. The complexity of TBI has precluded the use of effective therapies. Hyperbaric oxygen therapy (HBOT) has been shown to be neuroprotective in multiple neurological disorders, but its efficacy in the management of TBI remains controversial. This review focuses on HBOT applications within the context of experimental and clinical TBI. We also discuss its potential neuroprotective mechanisms.

  • Early or delayed multiple sessions of low atmospheric pressure HBOT can reduce intracranial pressure, improve mortality, as well as promote neurobehavioral recovery. The complimentary, synergistic actions of HBOT include improved tissue oxygenation and cellular metabolism, anti-apoptotic, and anti-inflammatory mechanisms.

  • Thus HBOT may serve as a promising neuroprotective strategy that when combined with other therapeutic targets for TBI patients which could improve long-term outcomes.

 

Brain Inj. 2012;26(10):1273-84. Epub 2012 May 9.

Hyperbaric oxygenation improves locomotor ability by enhancing neuroplastic responses after cortical ablation in rats.

Institute of Medical Physiology 'Richard Burian', School of Medicine, University of Belgrade, Serbia.

Abstract

To investigate whether hyperbaric oxygenation (HBO) can improve the recovery of motor functions in rats after suction ablation of the right sensorimotor cortex.

The experimental paradigm implies the following groups: Control animals (C), Control + HBO (CHBO), Sham controls (S), Sham control + HBO (SHBO), Lesion group (L), right sensorimotor cortex was removed by suction, Lesion + HBO (LHBO). Hyperbaric protocol: pressure applied 2.5 atmospheres absolute, for 60 minutes, once a day for 10 days. A beam walking test and grip strength meter were used to evaluate the recovery of motor functions. Expression profiles of growth-associated protein 43 (GAP43) and synaptophysin (SYP) were detected using immunohistochemistry.

The LHBO group achieved statistically superior scores in the beam walking test compared to the L group. Additionally, the recovery of muscle strength of the affected hindpaw was significantly enhanced after HBO treatment. Hyperbaric oxygenation induced over-expression of GAP43 and SYP in the neurons surrounding the lesion site.

Data presented suggest that hyperbaric oxygen therapy can intensify neuroplastic responses by promoting axonal sprouting and synapse remodelling, which contributes to the recovery of locomotor performances in rats. This provides the perspective for implementation of HBO in clinical strategies for treating traumatic brain injuries.

 

J Trauma Acute Care Surg. 2012 Mar;72(3):650-9.

Attenuating inflammation but stimulating both angiogenesis and neurogenesis using hyperbaric oxygen in rats with traumatic brain injury.

Department of Biotechnology, Southern Taiwan University, Tainan, Taiwan.

Erratum in J Trauma Acute Care Surg. 2012 Jul;73(1):295-6.

Abstract

Inflammation, angiogenesis, neurogenesis, and gliosis are involved in traumatic brain injury (TBI). Several studies provide evidence supporting the neuroprotective effect of hyperbaric oxygen (HBO2) therapy in TBI. The aim of this study was to ascertain whether inflammation, angiogenesis, neurogenesis, and gliosis during TBI are affected by HBO2 therapy.

Rats were randomly divided into three groups: TBI + NBA (normobaric air: 21% O2 at 1 absolute atmospheres), TBI + HBO2, and Sham operation + NBA. TBI + HBO2 rats received 100% O2 at 2.0 absolute atmospheres for 1 hr/d for three consecutive days. Behavioral tests and biochemical and histologic evaluations were done 4 days after TBI onset.

TBI + NBA rats displayed: (1) motor and cognitive dysfunction; (2) cerebral infarction and apoptosis; (3) activated inflammation (evidenced by increased brain myeloperoxidase activity and higher serum levels of tumor necrosis factor-α); (4) neuronal loss (evidenced by fewer NeuN-positive cells); and (5) gliosis (evidenced by more glial fibrillary protein-positive cells).

  • In TBI + HBO2 rats, HBO2 therapy significantly reduced TBI-induced motor and cognitive dysfunction, cerebral infarction and apoptosis, activated inflammation, neuronal loss, and gliosis. In addition, HBO2 therapy stimulated angiogenesis (evidenced by more bromodeoxyuridine-positive endothelial and vascular endothelial growth factor-positive cells), neurogenesis (evidenced by more bromodeoxyuridine-NeuN double-positive and glial cells-derived neurotrophic factor-positive cells), and overproduction of interleukin-10 (an anti-inflammatory cytokine).

  • Collectively, these results suggest that HBO2 therapy may improve outcomes of TBI in rats by inhibiting activated inflammation and gliosis while stimulating both angiogenesis and neurogenesis in the early stage.

Neuroprotective Effects of Hyperbaric Oxygen Treatment in Traumatic Brain Injury of Rat.

Wang G, Jiang Z. Institute of Nautical Medicine, Department of Neuropharmacology, Department of Neuropharmacology, Institute of Nautical Medicine, Nantong University, 19 Qixiu Road, Chongchuan District, Nantong, Jiangsu 226001, China, Nantong, China, 226001, 86-513-85051799, 86-513-85051796; wgh@ntu.edu.cn. J Neurotrauma. 2010 Jun 23. [Epub ahead of print]

Abstract: This study was designed to evaluate the potential benefits of hyperbaric Oxygen (HBO) in the treatment of traumatic brain injury (TBI). The right cerebral cortex of rats was injured by the impact of a 20 g object dropped from a standard predetermined height. Rats received HBO treatment at 3 ATA for 60 min after TBI. Neurological behavior score, brain water content, morphological changes in the hippocampus, and cell apoptosis in brain tissue surrounding the primary injury were examined to reflect the brain damage severity. Three and six hours after TBI, HBO-treated rats displayed a significant reduction of brain damage. However, 12 h after TBI, the efficacy of HBO treatment was considerably attenuated. Furthermore, 24 h, 48 h and 72 h after TBI, the HBO treatment did not show notable effects. In contrast, multiple HBO treatments (3 or 5 times totally), even started from 48 h after TBI, remarkably reduced the neurology deficit score and the loss of neuronal number in the hippocampus. Although multiple treatments started from 48 h significantly improved the neurological behaviors and reduced the brain injury, the overall benefic effects were substantially weaker than the ones observed after single treatment from 6 h.

These results suggest that: 1) HBO treatment could alleviate brain damage after TBI. 2) Single treatment of HBO has a time limitation of 12 h post-TBI. 3) Multiple HBO treatments have the possibility to extend the post-TBI delivery time-window. Therefore, our results clearly suggest the validity of HBO therapy for the treatment of TBI.

 

Undersea Hyperb Med 2012 Nov-Dec;39(6):1075-82.

Hyperbaric side effects in a traumatic brain injury randomized clinical trial.

Wolf EG, Prye J, Michaelson R, Brower G, Profenna L, Boneta O.

Source

USAF School of Aerospace Medicine, Hyperbaric Medicine Department, Lackland AFB, Texas, USA. earl.wolf.ctr@us.af.mil

Abstract

OBJECTIVE:

To catalog the side effects of 2.4 atmospheres absolute (atm abs) hyperbaric oxygen (HBO2) vs. sham on post-concussion symptoms in military service members with combat-related, mild traumatic brain injury (TBI).

METHODS:

Fifty subjects diagnosed with TBI were randomized to either a sham (1.3 atm abs breathing air) or treatment (2.4 atm abs breathing 100% oxygen) hyperbaric profile. Forty-eight subjects completed 30 exposures. Medical events during hyperbaric exposures were separately annotated by medical staff and chamber operators. After the blind was broken, events were segregated into the exposure groups.

RESULTS:

These side effects were observed as rate (sham/treatment): ear block (ear barotrauma) 5.51% (1.09%/5.91%), sinus squeeze 0.14% (0.0%/0.27%), and confinement anxiety 0.27% (0.27%/0.27%). Other conditions that occurred included: headache 0.61% (0.68%/0.54%); nausea 0.2% (0.14%/0.27%); numbness 0.07% (0%/0.13%); heartburn 0.07% (0.14%/0%); musculoskeletal chest pain 0.07% (0%/0.13%); latex allergy 0.07% (0.14%/0%); and hypertension 0.07% (0.14%/0%).

CONCLUSION:

This study demonstrated no major adverse events, such as pulmonary barotraumas, pulmonary edema or seizure. Given the infrequent, mild side effect profile, the authors feel the study demonstrated that hyperbaric oxygen therapy (HBO2T) was safe at a relatively high treatment pressure in TBI subjects, and these data can be used to evaluate the risk/ benefit calculation when deciding to utilize HBO2T for treatment of various diseases in the TBI population.

 

J Surg Res. 2013 May 21. pii: S0022-4804(13)00442-3. doi: 10.1016/j.jss.2013.04.070. [Epub ahead of print]

Microglial activation induced by traumatic brain injury is suppressed by postinjury treatment with hyperbaric oxygen therapy.

Lim SW, Wang CC, Wang YH, Chio CC, Niu KC, Kuo JR.

Source

Department of Neurosurgery, Chi-Mei Medical Center, Tainan, Taiwan. Electronic address: kuojinnrung@gmail.com.

Abstract

BACKGROUND:

The mechanisms underlying the protective effects of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) are unclear. TBI initiates a neuroinflammatory cascade characterized by activation of microglia and increased production of proinflammatory cytokines. In this study, we attempted to ascertain whether the occurrence of neuroinflammation exhibited during TBI can be reduced by HBO.

METHODS:

TBI was produced by the fluid percussion technique in rats. HBO (100% O2 at 2.0 absolute atmospheres) was then used at 1 h (HBO I) or 8 h (HBO II) after TBI. Neurobehavior was evaluated by the inclined plane test on the 72 h after TBI and then the rats were killed. The infarction area was evaluated by Triphenyltetrazolium chloride. Immunofluorescence staining was used to evaluate neuronal apoptosis (TUNEL + NeuN), microglial cell aggregation count (OX42 + DAPI), and tumor necrosis factor-alpha (TNF-α) expression in microglia cell (OX42 + TNF-α).

RESULTS:

The maximum grasp angle in the inclined plane test and cerebral infarction of the rats after TBI were significantly attenuated by HBO therapy regardless of whether the rats were treated with HBO 1 or 8 h after TBI compared with the controls. TBI-induced microglial activation, TNF-α expression, and neuronal apoptosis were also significantly reduced by HBO therapy.

CONCLUSIONS:

Our results demonstrate that HBO treatment of TBI during the acute phase of injury can attenuate microgliosis and proinflammatory cytokine TNF-α expression resulting in a neuroprotective effect. Even treating TBI with HBO after 8 h had a therapeutic effect.

 

J Neurotrauma. 2012 Jan 1;29(1):168-85. doi: 10.1089/neu.2011.1895. Epub 2011 Nov 22.

A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder.

Harch PG,

Department of Medicine, Section of Emergency and Hyperbaric Medicine, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, USA. paulharchmd@gmail.com

Abstract

This is a preliminary report on the safety and efficacy of 1.5 ATA hyperbaric oxygen therapy (HBOT) in military subjects with chronic blast-induced mild to moderate traumatic brain injury (TBI)/post-concussion syndrome (PCS) and post-traumatic stress disorder (PTSD). Sixteen military subjects received 40 1.5 ATA/60 min HBOT sessions in 30 days. Symptoms, physical and neurological exams, SPECT brain imaging, and neuropsychological and psychological testing were completed before and within 1 week after treatment. Subjects experienced reversible middle ear barotrauma (5), transient deterioration in symptoms (4), and reversible bronchospasm (1); one subject withdrew. Post-treatment testing demonstrated significant improvement in: symptoms, neurological exam, full-scale IQ (+14.8 points; p<0.001), WMS IV Delayed Memory (p=0.026), WMS-IV Working Memory (p=0.003), Stroop Test (p<0.001), TOVA Impulsivity (p=0.041), TOVA Variability (p=0.045), Grooved Pegboard (p=0.028), PCS symptoms (Rivermead PCSQ: p=0.0002), PTSD symptoms (PCL-M: p<0.001), depression (PHQ-9: p<0.001), anxiety (GAD-7: p=0.007), quality of life (MPQoL: p=0.003), and self-report of percent of normal (p<0.001), SPECT coefficient of variation in all white matter and some gray matter ROIs after the first HBOT, and in half of white matter ROIs after 40 HBOT sessions, and SPECT statistical parametric mapping analysis (diffuse improvements in regional cerebral blood flow after 1 and 40 HBOT sessions). Forty 1.5 ATA HBOT sessions in 1 month was safe in a military cohort with chronic blast-induced PCS and PTSD. Significant improvements occurred in symptoms, abnormal physical exam findings, cognitive testing, and quality-of-life measurements, with concomitant significant improvements in SPECT.

 

Low pressure hyperbaric oxygen therapy and SPECT brain imaging in the treatment of blast-induced chronic traumatic brain injury (post-concussion syndrome) and post traumatic stress disorder

Paul G Harch*1, Edward F Fogarty2, Paul K Staab1 and Keith Van Meter1. Section of Emergency Medicine, Department of Medicine, Louisiana State University Health Sciences Center, 2021 Perdido St, Room W535, New Orleans, Louisiana, 70112, USA and 2Department of Radiology, University of North Dakota School of Medicine and Health Sciences,

Abstract

A 25-year-old male military veteran presented with diagnoses of post concussion syndrome and post traumatic stress disorder three years after loss of consciousness from an explosion in combat. The patient underwent single photon emission computed tomography brain blood flow imaging before and after a block of thirty-nine 1.5 atmospheres absolute hyperbaric oxygen treatments. The patient experienced a permanent marked improvement in his post-concussive symptoms, physical exam findings, and brain blood flow. In addition, he experienced a complete resolution of posttraumatic stress disorder symptoms. After treatment he became and has remained employed for eight consecutive months. This case suggests a novel treatment for the combined diagnoses of blast-induced post-concussion syndrome and post-traumatic stress disorder.

 

Low Pressure Hyperbaric Oxygen Therapy For Traumatic Brain Injury

Abstract

Traumatic brain injury (TBI) is a major public health issue. The complexity of TBI has precluded the use of effective therapies. Hyperbaric oxygen therapy (HBOT) has been shown to be neuroprotective in multiple neurological disorders, but its efficacy in the management of TBI remains controversial. This review focuses on HBOT applications within the context of experimental and clinical TBI. We also discuss its potential neuroprotective mechanisms.

  • Early or delayed multiple sessions of low atmospheric pressure HBOT can reduce intracranial pressure, improve mortality, as well as promote neurobehavioral recovery. The complimentary, synergistic actions of HBOT include improved tissue oxygenation and cellular metabolism, anti-apoptotic, and anti-inflammatory mechanisms. Thus HBOT may serve as a promising neuroprotective strategy that when combined with other therapeutic targets for TBI patients which could improve long-term outcomes.

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