Hyperbaric Oxygen Therapy & TBI
Hyperbaric Oxygen has been studied in Traumatic Brain Injury
Traumatic brain injury (TBI) is an insult or trauma to the brain caused by external mechanical forces.
The damage caused by TBI can be focal (confined to one area) or diffuse (involving more than one area of the brain). Symptoms of a TBI vary from mild and moderate to severe, depending on the extent of the damage. Patients with TBI are often left with significant cognitive and behavioral disability.
There are no effective standard treatments for TBI patients. Chronic TBI, which is the topic of this review, arises days to weeks after the original insult.
At the time of injury there are different degrees of irreversible damage to the brain tissue termed the primary injury. Next, a chain of events is set off where there is ongoing injury to the brain through edema, hypoxia and ischemia secondary to raised intracranial pressure, microglial activation, excitotoxic neurotransmitters and impaired calcium homeostasis.
Approximately (70–90%) of the TBI are classified as mild TBI (mTBI) or concussion – with a Loss of Consciousness duration of 0–30 minutes, Post Traumatic Amnesia duration of less than a day and Glasgow Coma Scale (GCS) grade of 13–15.
Post concussion syndrome (PCS) is a set of symptoms succeeding mTBI in most patients. The PCS symptoms include headache, dizziness, neuropsychiatric symptoms, and cognitive impairments.
In most patients, PCS may continue for weeks or months, and up to 25% of the patients may experience prolonged PCS (PPCS) in which the symptoms last for over six months
Hyperbaric Mechanisms and TBI
Increased tissue oxygenation
Breathing pure oxygen under Hyperbaric conditions (3.0 ATA) can increase arterial oxygen tensions twenty fold to 2,000 mmHg, and tissue oxygen tensions ten fold to around 500 mmHg and therefore dramatically improve effective cellular oxygenation.
Relevant Hyperbaric Mechanisms include increasing IL-10, reducing microglial activation and decreasing TNF-α and decreasing the expression of MMP-9. HBOT significantly increased the expression of NRF-2. Natural NRF2 activators include curcumin and resveratrol.
Hyperbaric Oxygen increases expression of anti-apoptotic proteins (Bcl-2 and Bcl-xl), preserves mitochondrial integrity and suppresses the activation of the mitochondrial mediated apoptotic pathway.
Hyperbaric Therapy can intensify neuroplastic responses by promoting axonal sprouting and synapse remodeling. HBOT triggers angiogenesis and differentiation of neuronal stem cells as powerful mediators of improved brain function.
At any given time, the brain is utilizing almost all oxygen provided to it for energy production (that is, energy production is at a maximum). The regeneration process after brain injury requires much additional energy. This is where hyperbaric oxygen treatment can help – the increased oxygen level in the blood and body tissues during treatment can supply the additional energy needed for brain repair.
Hyperbaric Oxygen and TBI
In a study by Barrett et al. 1998, 5 patients with chronic TBI, at least 3 years after the initial injury, underwent 120 HBO treatments each at 1.5 ATA for 60 min.
Hyperbaric treated patients had permanent increases in penumbra area cerebral blood flow (area immediately surrounding the area of damage).
Speech fluency, as well as memory and attention improved with Hyperbaric Treatment. The improvement peaked at 80 HBO treatments.
The authors concluded that HBO therapy can improve cognitive function and cerebral blood flow in chronic stable TBI patients (where no improvement would ordinarily be expected 3 years after the injury).
A case report by Harch 2009 in which a 25-year-old male veteran presented with PCS and PTSD three years after loss of consciousness from an explosion in combat. He underwent 39 1.5 ATA HBO treatments and experienced a permanent marked improvement in his post-concussive symptoms, physical exam findings, and brain blood flow and a complete resolution of PTSD symptoms. After treatment he became and has remained employed for eight consecutive months.
In particular, headache was permanently gone after the 1st treatment. After 12 treatments, sleep disruption and fatigue lifted and at the 25th treatment the PTSD symptoms resolved.
In a follow up study by Harch et al. 2012, of the safety and efficacy of Hyperbaric Oxygen in 16 war veterans with chronic blast-induced mild to moderate Blast-Induced TBI/Post-Concussion Syndrome and Post-Traumatic Stress Disorder, each patient received 40 HBO sessions (1.5 ATA for 1 hour) in 30 days
Twelve of 15 subjects (80%) reported improvement in a majority of their symptoms on their prioritized symptom list after HBOT. Eleven of 15 subjects (73%) reported improvement in a majority of symptoms on the primary author's standard symptom questionnaire
An unexpected finding was the confirmation of a reduction in PTSD symptoms in some of the patients as well.
Significant improvements occurred in symptoms, abnormal physical exam findings, cognitive testing, and quality-of-life measurements, with significant improvements in SPECT scans.
Lin 2008 conducted a randomized trial on 44 patients with TBI: 22 patients received HBOT after the condition stabilized, and the other 22 were not treated with HBOT.
The clinical effects were evaluated with the Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS) before and 3 to 6 months after HBOT.
The HBOT protocol was to apply two hour, 2.0 ATA pressures (15 minutes to decompress and recompress allotted). The full treatment course was once a day for 20 days over a 4 week period.
The GCS of the HBOT group was improved from 11.1 to 13.5 and from 10.4 to 11.5 for the control group. It was concluded: "based on this study, HBOT can provide some benefits for the subacute TBI patients with minimal adverse side effects."
Boussi-Gross et al. 2013 conducted the well named " Hyperbaric oxygen therapy can improve post concussion syndrome years after mild traumatic brain injury," a randomized,crossover trial of Hyperbaric Oxygen on 56 mTBI patients 1–5 years after injury with Post Concussive Syndrome. 40 1-hour 1.5 ATA sessions (5 days per week) were used.
56 patients (32 in the treated group and 24 in crossover group) were included in the final analysis. 1–6 years of time elapsed since the injury with 33 months on average and were mostly from car accidents (38/56 patients).
A significant improvement was observed in the treated group after HBOT in all cognitive measures: Information Processing Speed, Attention, Memory, and Executive Functions. Effect sizes were medium to large.
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.
Ultimately, it was concluded: Hyperbaric induced neuroplasticity led to improvement of brain functions and quality of life at a chronic stage with mild TBI.
Mild TBI and HBOT
Weaver 2018 ran a randomized, double-blind, sham-controlled trial that enrolled military personnel with mild TBI and persistent PCS using 40, 60 minute 1.5 ATA HBO treatments over 12 weeks.
The HBO group had improved 13-week scores (improved post-concussive and PTSD symptoms) including sleep quality, some anger and memory outcomes (improved cognitive processing speed) as well as functional balance improvements and reduced vestibular complaints at 13 weeks compared to a worsening in the sham group. Oddly, improvements appeared to regressed at 6 months, perhaps indicating the need for maintenance treatments.
Shytle 2019 published a paper outlining cases of three veterans with chronic TBI/PTSD symptoms where 20-35, 60 minute HBO treatments at 1.5-1.75 ATA were used.
In the first case, significant improvements in judgment, memory, social interactions, anxiety, and stress were noted as well as frequent headaches and episodes of nausea also resolved. In the second case, reduced anxiety, better sleep and motivation as well as gradual and progressive improvements in his memory and mood. In the final case, improvements were seen in impulsivity, anxiety, fatigue, sleep and depression.
Harch 2020 looked at persistent post concussion syndrome (PPCS) after mild TBI (mTBI) from blunt or blast in a randomized controlled crossover study. Sixty-three civilian and military subjects with mTBI/PPCS were randomized to either 40 HBOTs at for 60 minutes, once daily, 5 days per week for 8 weeks to a control group. The control group was then crossed over to HBOT.
Treatment was done on average 4.6 years after their last TBI and 50 subjects were in the final analysis.
Anderson ND TBI Protocol
Paul Anderson is a Naturopathic Doctor has lectured about the experience of his clinic in Seattle using Hyperbaric Oxygen Therapy and Nutritional IV Therapy.
Anderson Standard HBOT + IV Head Trauma Protocol:
IV three-part formula:
At home oral supplements:
•Vitamin-C: 1 gram 2-3X a day
• Cover-3 gel
Anderson Case Study
Combination HBOT & IV Nutrient Therapy
“SM” with mTBI - Recent MVA
Schedule for HBOT + IV:
Outcome - SUBJECTIVE: Felt about 80% recovered from the accident with improved endurance and stamina after 16 treatments.
Naturopathic Medicine and TBI
Omega 3 Fatty Acids have been found in Animal models to improves cognitive function, reduce neuronal edema, stabilizes cellular energy homeostasis, increase dendrite growth and deficient levels of Omega 3's impair recovery.
In a clinical trial by Oliver 2016, (Neurofilamentlight (NFL)) or whole season • DHA supplementation reduced NFL (Neurofilamentlight - surrogate marker of TBI). Our Naturopathic doctors usually suggest dietary augmentation (fresh fatty fish) for phospholipid bound DHA as well as oral supplementation as part of an adjunctive Naturopathic protocol.
Curcumin has been studied primarily in TBI in animal models - Animal studies where post supplementation reduces lipid peroxidation, protein oxidation, edema and behavioral impairment. Furthermore, Curcumin reduces microglia activation.
In terms of nutritional augmentation our approach is heavily centered on B-Vitamins, Magnesium, Zinc and Glutathione.
B-Vitamins (B1, B2, B3, B5, B12) and magnesium are intimately involved in neuronal energy production and as mentioned above the regeneration process after brain injury requires much additional energy. Large proportion of TBI patients are deficient in Magnesium and Zinc and both help modulate NMDA receptor activity - all of which are easy to give in an IV Therapy context which our Naturopaths include as part of our TBI IV treatments.
Vitamin E, as fat soluble antioxidant, animal studies show reduced brain damage and improved function with Vitamin E supplementation. Our Naturopaths usually round off Vitamin E supplementation which tends to protect membranes with Vitamin C which tends to protect the cell cytosol.
Several studies have reported that brain Glutathione levels are reduced following TBI. Strategies aimed at enhancing brain Glutathione may be a viable approach to mitigate secondary injury processes induced by TBI.
Glutathione and its precursor including N-acetylcysteine have neuroprotective effects in animal models of TBI through amelioration of neuronal injury.
For these reasons, our Naturopathic doctors use high doses of IV Glutatione in our Edmonton PCS/TBI patients. We've seen excellent, rapid and durable clinical responses giving IV Glutathione with supportive Glutathione nutrients such as Vitamin C and Selenium with the IV therapy treatment.
Regular IV Therapy treatments (1x weekly) have proven sufficient for numerous PCS/TBI patients with a goal of cessation of treatment within 12 treatments.
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