Traumatic Brain Injury (TBI)
The treatment of TBI is critical; it is estimated that between 3.2 and 5.3 million Americans live with permanent disabilities as a direct result of a TBI(1). Traumatic brain injuries (TBI) refer to injuries to the brain caused by an external physical force(2). Such injuries result in brain dysfunction, which can lead to cognitive impairments such as decreased attention, memory loss, and reduced cognitive flexibility as well as motor issues(3). However, there is compelling evidence to suggest that HBOT may significantly reduce the negative symptoms experienced by TBI patients, even years after the incident.
Extivita Therapies for TBI:
Extivita Therapies Traumatic Brain Injury Recovery:
Hyperbaric Oxygen Therapy
Neurofeedback
Supplements
Nutritional IV Therapy
Pulsed Electromagnetic Field Therapy
Hyperbaric Oxygen Therapy for Traumatic Brain Injury:
Research suggests that increased tissue oxygenation, improved cellular metabolism and mitochondrial function, and improved inflammatory response, to name a few, are responsible for improving the following cognitive impairments(5):
- Improved Memory (most improvement)
- Reduced Attention Problems (high improvement)
- Improved Executive Function
- Increased Information Processing Speed
- Improved Motor Skills
Effects of HBOT on Traumatic Brain Injury:
Decreased Inflammation
Increased Stem Cell Activity
New Blood Vessel Formation
Hyperbaric oxygen therapy stimulates the formation of new blood vessels, healing injured tissues that were unable to get nutrients and oxygen.
Neurofeedback for Traumatic Brain Injury:
Neurofeedback has been shown to improve many of the cognitive issues that patients with traumatic brain injuries (TBIs) experience post-injury(6, 7). After a TBI, the brain must form new neural pathways to account for any brain tissue damaged by the TBI. These new connections play a vital role in restoring healthy brain function, and neurofeedback has been shown to help establish and help strengthen such connections(6). Most studies that use neurofeedback to help TBIs train to increase theta and alpha brainwaves in the occipital lobe (towards the back of the head). This has been shown to improve reduce stress (which has a negative physiological and emotional effect in TBIs), increase relaxation, and improve cognitive measures such as memory and processing speed. (6, 7, 8, 9).
IV Therapy for Traumatic Brain Injury:
The combination of the Myer’s cocktail and glutathione IV’s can improve cognitive and motor function following traumatic brain injury. A principal issue post-TBI is the degree neuroinflammation, which is directly correlated to the severity of the short-term and long-term consequences of TBI. In TBI patients, the mitochondria in brain cells become damaged, activating immune cells (glia, microglia, and astrocytes). These immune cells release inflammatory cytokines which recruit even more inflammatory cells to the area. This results in brain cell swelling, death, decreased energy production, all of which lead to impaired cognitive and motor function(10).
The Myers cocktail IV contains Vitamin C and other antioxidants which have been shown to decrease oxidative stress and inflammatory responses. By doing do, the Myer’s cocktail can help minimize further cells damage and improve brain health and function after a TBI(11, 12). Glutathione, the master antioxidant, has been used to reduce oxidative stress and enhance cellular detoxification and can be part of a multi-modal therapy in correcting the metabolic crisis in TBI.
Pulsed Electromagnetic Field Therapy for Traumatic Brain Injury:
Micro vessels play a significant role in overall course of vascular diseases. Dysfunction to this system has been linked to a multitude of illnesses. The PEMF device has been shown to optimize the microcirculatory system, increasing perfusion to tissues and organs. When used in conjunction with HBOT, oxygen rich blood can be delivered to these areas, where healing can begin (13).
News & Research for for Traumatic Brain Injury:
Executive summary: The Brain Injury and Mechanism of Action of Hyperbaric Oxygen for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury (mTBI) (BIMA) Study.
The Brain Injury and Mechanism of Action of Hyperbaric Oxygen for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury (mTBI) (BIMA) study, sponsored by the Department of Defense and held under an investigational new drug application by the Office of the Army Surgeon General, is one of the largest and most complex clinical trials of hyperbaric oxygen (HBO₂) for post-concussive symptoms (PCS) in U.S. military service members.
Hyperbaric oxygen for mild traumatic brain injury: Design and baseline summary.
The Brain Injury and Mechanisms of Action of Hyperbaric Oxygen for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury (mTBI) (BIMA) study, sponsored by the Department of Defense, is a randomized double-blind, sham-controlled clinical trial that has a longer duration of follow-up and more comprehensive assessment battery compared to recent HBO₂ studies. BIMA randomized 71 participants from September 2012 to May 2014. Primary results are expected in 2017. Randomized military personnel received hyperbaric oxygen (HBO₂) at 1.5 atmospheres absolute (ATA) or sham chamber sessions at 1.2 ATA, air, for 60 minutes daily for 40 sessions. Outcomes include neuropsychological, neuroimaging, neurological, vestibular, autonomic function, electroencephalography, and visual systems evaluated at baseline, immediately following intervention at 13 weeks and six months with self-report symptom and quality of life questionnaires at 12 months, 24 months and 36 months. Characteristics include: median age 33 years (range 21-53); 99% male; 82% Caucasian; 49% diagnosed post-traumatic stress disorder; 28% with most recent injury three months to one year prior to enrollment; 32% blast injuries; and 73% multiple injuries. This manuscript describes the study design, outcome assessment battery, and baseline characteristics. Independent of a therapeutic role of HBO₂, results of BIMA will aid understanding of mTBI.
Neuropsychological assessments in a hyperbaric trial of post-concussive symptoms.
Results of studies addressing the effect of mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) on symptoms and neuropsychological assessments are mixed regarding cognitive deficits in these populations. Neuropsychological assessments were compared between U.S. military service members with mTBI only (n=36) vs. those with mTBI÷ PTSD (n=35) from a randomized interventional study of mTBI participants with persistent post-concussive symptoms (PCS). The mTBI group endorsed worse symptoms than published norms on PCS, PTSD and pain scales (⟩50% abnormal on Neurobehavioral Symptom Inventory (NSI), PTSD Checklist-Civilian, McGill Pain Questionnaire-Short Form) and some quality of life domains. Worse symptom reporting was found in the mTBI÷ PTSD group compared to mTBI (e.g., mean NSI total score in mTBI 27.5 (SD=12.7), mTBI÷ PTSD 39.9 (SD=13.6), p⟨0.001). The mTBI÷PTSD group performed worse than mTBI on the Weschler Adult Intelligence Scale digit span (mean difference -1.5, 95% CI[-2.9,-0.1], p=0.04) and symbol search (mean difference -1.5, 95% CI[-2.7,-0.2], p=0.03) and Grooved Pegboard (dominant hand mean difference -7.0, 95% CI[-11.5,-2.4], p=0.003; non-dominant mean difference -9.8, 95% CI[-14.9,-4.7], p⟨0.001). Differences were detected in ANAM simple reaction time (p=0.04) and mathematical processing (p=0.03) but not verbal fluency or visuospatial memory assessments. Results indicate increased symptom severity and some cognitive deficits in mTBI÷ PTSD compared to mTBI alone.
References
- Tbi_report_to_congress_epi_and_rehab-a.Pdf.” Accessed June 2, 2019. https://www.cdc.gov/traumaticbraininjury/pdf/tbi_report_to_congress_epi_and_rehab-a.pdf.
- Silver, J.M., T.W. McAllister, and D.B. Arciniegas. Textbook of Traumatic Brain Injury. American Psychiatric Publishing, 2018. https://books.google.com/books?id=ViKMDwAAQBAJ.
- Hadanny A, Abbott S, Suzin G, et al. Effect of hyperbaric oxygen therapy on chronic neurocognitive deficits of post-traumatic brain injury patients: retrospective analysis. BMJ Open 2018;8:e023387. doi: 10.1136/bmjopen-2018-023387 https://bmjopen.bmj.com/content/bmjopen/8/9/e023387.full.pdf
- 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 https://www.ncbi.nlm.nih.gov/pubmed/24260334
- Efrati S, Ben-Jacob E. Reflections on the neurotherapeutic effects of hyperbaric oxygen. Expert Rev Neurother 2014;14:233–6. https://www.tandfonline.com/doi/full/10.1586/14737175.2014.884928
- Munivenkatappa, Ashok, et al. “EEG Neurofeedback Therapy: Can It Attenuate Brain Changes in TBI?” NeuroRehabilitation, vol. 35, no. 3, IOS Press, Jan. 2014, pp. 481–84. content.iospress.com, doi:10.3233/NRE-141140.
- Bennett, Cathlyn N., et al. “Clinical and Biochemical Outcomes Following EEG Neurofeedback Training in Traumatic Brain Injury in the Context of Spontaneous Recovery:” Clinical EEG and Neuroscience, SAGE PublicationsSage CA: Los Angeles, CA, Dec. 2017. Sage CA: Los Angeles, CA, journals.sagepub.com, doi:10.1177/1550059417744899.
- Reddy, Rajakumari Pampa, et al. “Silent Epidemic: The Effects of Neurofeedback on Quality-of-Life.” Indian Journal of Psychological Medicine, vol. 36, no. 1, 2014, pp. 40–44. PubMed Central, doi:10.4103/0253-7176.127246.
- Reddy, Rajakumari P., et al. “Neurofeedback Training to Enhance Learning and Memory in Patient with Traumatic Brain Injury: A Single Case Study.” The Indian Journal of Neurotrauma, vol. 6, no. 1, June 2009, pp. 87–90. ScienceDirect, doi:10.1016/S0973-0508(09)80037-3.
- Cheng, G., Kong, R.‐h., Zhang, L.‐m. and Zhang, J.‐n. (2012), Mitochondria in traumatic brain injury and mitochondrial‐targeted multipotential therapeutic strategies. British Journal of Pharmacology, 167: 699-719. doi:10.1111/j.1476-5381.2012.02025.x
- KC, Sagan et al. “Vitamin C enters mitochondria via facilitative glucose transporter 1 (Glut1) and confers mitochondrial protection against oxidative injury.” FASEB journal : official publication of the Federation of American Societies for Experimental Biology vol. 19,12 (2005): 1657-67. doi:10.1096/fj.05-4107com
- Zhang, Xiao-Ying et al. “Vitamin C alleviates LPS-induced cognitive impairment in mice by suppressing neuroinflammation and oxidative stress.” International immunopharmacology vol. 65 (2018): 438-447. doi:10.1016/j.intimp.2018.10.020
- https://www.imin-org.eu/images/science/Haug-Report-Bemer_2016_Englisch.pdf