Traumatic Brain Injury & Concussion
The effects of Hyperbaric Oxygen Therapy in the treatment of traumatic brain injury are well documented and are becoming more well known. There is a faction that doesn't want it to become well known and are fond of publishing papers that claim pressurized air is a placebo or a sham treatment copared to 100% oxygen, but even pressurized air increases the partial pressure of oxygen and apparently does so enough to signal DNA to heal even tho the absolute oxygen level is not 100%. Nevertheless, these papers will state that there is no performance significance between the so-called "sham" treatment group and the 100% oxygen group and so this faction will say HBOT is no better than sham, and they think the public and 3rd party payers will believe this, and they usually do, but for how long? Eventually the truth comes out, eventually wrongs are righted, but it will take the man on the street creating the atmosphere for that to happen.
Research & Studies
Hyperbaric Oxygen Therapy Can Improve Post Concussion Syndrome
Years after Mild Traumatic Brain Injury –
Randomized Prospective Trial
Published: November 15, 2013
Rahav Boussi-Gross, Haim Golan, Gregori Fishlev, Yair Bechor, Olga Volkov, Jacob Bergan, Mony Friedman, Dan Hoofien, Nathan Shlamkovitch, Eshel Ben-Jacob, Shai Efrati
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 post-concussion 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 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.
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.
Cerebral Blood Flow Changes & Cognitive Improvement in Chronic Stable Traumatic Brain Injuries Treated with Hyperbaric Oxygen Therapy
Neurol, April, 1998 (Suppl):A178-A179. Kevin F. Barrett, Brent E. Masel, Galveston, TX, Paul G. Harch, New Orleans, LA Fred Ingram, Kevan P. Corson, Jon T. Mader, Galveston, TX.
Objective: To determine if hyperbaric oxygen therapy in patients with chronic stable traumatic brain injuries can produce: 1) neurological and cognitive improvements; 2) changes in cerebral blood flow to ischemic penumbral areas as determined by ECD-Tc99m SPECT brain scanning.
Background: Numerous studies have shown that cognitive improvement after severe traumatic brain injury (TBI) is most dramatic in the first six months after injury, and is fairly static after 18 months. Anecdotal reports exist that attest to the efficacy of hyperbaric oxygen therapy (HBOT) to improve post traumatic neurologic deficits by increasing blood flow in the ischemic penumbra despite protocol differences. Cerebral blood flow, speech, neurological and neuropsychometric testing have not been studied serially in patients undergoing HBOT for chronic stable TBI.
Design/Methods: Five patients with TBI, at least three years post injury, underwent 120 HBOT’s at 1.5 atmospheres absolute of oxygen for 60 minutes. They received a set of 80 HBOT’s, a five month rest, and a second set of 40 HOBT’s. Patients were studied sequentially to determine HOB’s effects on: cerebral blood flow, speech fluency, neurologic, neuropsychometric and progressive exercise testing. Six TBI controls were not treated with HBOT, but underwent serial SPECT scanning to study time related alterations in cerebral blood flow. Five non-TBI controls underwent SPECT scanning, one HBOT, and a repeat scan to study HBOT influence on cerebral blood flow in normal subjects. SPECT brain scans were performed serially on the HBO treated group. Scans were spatial and intensity normalized and subjected to statistical parametric mapping.
Results: Serial SPECT imaging showed: TBI controls had no significant consistent change in CBF over time; non-TBI controls had essentially no influence from one HBOT upon CBF; the treated TBI patients had permanent increases in CBF to penumbral areas and a reqression to a mean CBF range. In the HOB treated group, no changes were seen in progressive exercise and neurologic testing. Speech fluency improved in all cases, as did group mean scores of memory, attention, and executive function. Improvement peaked at 80 HBOT, suggesting a possible maximum length of treatment between 80 and 120 HBOT.
Conclusions: Our pilot study findings suggest that HBOT at 1.5 ATA is a promising therapy for permanently improving penumbral brain blood flow and cognitive function in chronic stable TBI where no improvement would have been expected.
Neuroprotective Effect of Hyperbaric oxygen therapy in brain injury is mediated by preservation of mitochondrial membrane properties
Palzur E, Zaaroor M, Vlodavsky E, Milman F, Soustiel JF
Brain Res. 2008 Jul 24;1221:126-33. Epub 2008 May 11.
Recent experimental data have shown that hyperbaric oxygen therapy (HBOT) was associated increased Bcl-2 expression at the injury site that correlated with reduced apoptosis. We hypothesized that HBOT mediated enhancement of Bcl-2 expression and increased intracellular oxygen bio-availability may both contribute to preserve mitochondrial integrity and reduce the activation of the mitochondrial pathway of apoptosis. For this purpose, a cortical lesion was created in the parietal cortex of Sprague-Dawley rats by dynamic cortical deformation (DCD) and outcome measures in non-treated animals were compared with that of HBOT treated rats. Morphological analysis showed a profound reduction in neuronal counts in the perilesional area and a marked rarefaction of the density of the axonal-dendritic network. In treated animals, however, there was a significant attenuation of the impact of DCD over perilesional neurons, characterized by significantly higher cell counts and denser axonal network. In mitochondria isolated from injured brain tissue, there was a profound loss of mitochondrial transmembrane potential (Deltapsi(M)) that proved to be substantially reversed by HBOT. This finding correlated with a significant reduction of caspases 3 and 9 activation in HBOT treated animals but not of caspase 8, indicating a selective effect over the intrinsic pathway of apoptosis. Altogether, our results indicate that the neuroprotective effect of HBOT may represent the consequence of preserved mitochondrial integrity and subsequent inhibition of the mPTP and reduction of the mitochondrial pathway of apoptosis.