Treating Veterans with TBI & PTSD

Between 2000 and 2020, more than 430,000 US Service Members have experienced first lifetime Traumatic Brain Injury (TBI), not including service members who incur subsequent TBI’s(1). TBI’s are classified as mild, moderate, severe, or penetrating. They can occur from a sudden blow or jolt to the head from an impact, blast exposure, and even whiplash. Studies suggest that service members and veterans who have sustained a TBI may still have ongoing symptoms of post-concussive syndrome that go untreated. TBI of any severity can cause symptoms across multiple functional domains, including physical, cognitive, and psychological. 

In addition, among veterans with positive TBI screens, 80% indicate comorbid psychiatric diagnosis and up to half meet criteria for Post-Traumatic Stress Disorder (PTSD)(2). From the Vietnam war to Operation Enduring Freedom, Veterans suffering from PTSD has increased from 15% to 20%. PTSD is a complex psychiatric condition that develops in certain individuals after experiencing a major traumatic event(14). Behavioral symptoms of PTSD include re-experiencing the trauma, avoidance behavior, mood alternation, and hyperarousal(15). 

The negative impact that such symptoms and risks can make on one’s quality of life makes it clear that veterans with PTSD and TBI’s require safe, effective treatment options. Unfortunately, less than half of patients receiving traditional psychosocial treatments gain clinically meaningful improvements, and many continue to have residual symptoms(22-23). Thankfully, there is compelling evidence to suggest that Hyperbaric Oxygen Therapy (HBOT) may significantly reduce the negative symptoms experienced by TBI patients and PTSD patients, even years after the incident.

    What is Hyperbaric Oxygen Therapy?

    HBOT involves sitting in a hyperbaric chamber while breathing 100% medical grade oxygen through a mask or hood. The hyperbaric chamber gradually pressurizes to between 1.5 and 2.5 times the normal atmospheric pressure (referred to as 1.5 ATA and 2.5 ATA). This is equivalent to diving between 16 feet (1.5 ATA) and 50 feet (2.5 ATA) below water.

    The majority of HBOT treatments at Extivita are at 2.0 ATA, which is equivalent to 33 feet below surface level. Because oxygen is considered a drug by the FDA, patients must obtain a prescription from a licensed healthcare professional for these therapeutic treatments. The specific pressure is also included in the prescription. Our in-clinic provider can write HBOT prescriptions following your in-person consultation.

     

    Frequently Asked Questions About Hyperbaric Oxygen Therapy

    How do I get started with HBOT (new patients)?

    Before you come into the clinic, you will need to register as a patient in our patient portal. Here you will enter your medical history and primary reason/s for starting HBOT. After this, you will be able to schedule a consultation with Elena Schertz, FNP. You will be all set to begin treatment following your consultation!

    How is HBOT administered? 
    All Extivita patients have their very own hood or mask through which 100% medical grade oxygen is administered. These will be provided after your consultation. 
    What type of HBOT chambers do we use? 
    We have two hard-shell, multi-seat chambers at Extivita. Our biggest chamber can seat up to 12 patients, while our smaller chamber can seat up to 8 patients.  
    What can I do while in the HBOT chamber? 
    Whether it’s reading, watching a movie, or sleeping, there is plenty to do during your HBOT session. We have a TV in our largest chamber that we play movies on during most treatment sessions. In our smaller chamber, we have tablets that you can use to watch TV, browse the internet, or play games on. You are also more than welcome to bring your own book to read during treatment! 
    Will I be by myself during my HBOT session?  

    There will be a trained Extivita supervisor with you in all HBOT sessions. While you may be the only patient in the chamber on some days, most sessions will have other patients in the chamber as well. For additional information on how we are keeping our patients safe during COVID-19, click here.

    How long does an HBOT session last?  
    Most HBOT sessions will last roughly 1 hour and 30 minutes, which includes the time it takes to pressurize the chamber, 1 hour at the prescribed depth, and the time it takes to depressurize the chamber. Certain conditions may require shorter or longer durations at depth.  
    How many HBOT sessions are needed to improve PTSD and TBI Symptoms?

    This depends on the condition that you are receiving treatment for, as well as how your body responds to HBOT. The antioxidant and anti-inflammatory effects of HBOT can typically be felt within the first few sessions. Benefits for acute injuries and soft-tissue damage can typically be seen 5-10 sessions in, while chronic injuries typically require 10-20 sessions. Many conditions require 20-40 HBOT sessions for full healing effects such as stem cell increase.

    For TBI and PTSD patients, an initial HBOT regimen is typically 40 sessions. Symptom improvement is often experienced by patients between 10 and 20 sessions.

    Are there any side-effects to HBOT? 

    HBOT is generally considered one of the safest therapies in use today. Any serious side effects can be prevented by pre-HBOT screening that all patients receive during their consultation. One side effect that is some people experience is mild ear pain while the chamber pressurizes. However, this can be reduced through proper sinus clearing and it typically goes away as you receive more treatments.

    News & Research for Veterans with PTSD & TBI:

    References:
    1. Report to Congress, Study and Report on Traumatic Brain Injury Mitigation Efforts Final Report, July 2021. US Department of Defense. https://www.cdc.gov/traumaticbraininjury/pdf/Report_to_Congress_on_Traumatic_Brain_Injury_2013-a.pdf
    2. Mac Donald CL, Johnson AM, Wierzechowski L, et al. Outcome Trends after US Military Concussive Traumatic Brain Injury. J Neurotrauma. 2017;34(14):2206-2219. doi:10.1089/neu.2016.443
    3. O’Neil ME, Carlson K, Storzbach D, Brenner L, Freeman M, Quiñones A, Motu’apuaka M, Ensley M, Kansagara D. Complications of Mild Traumatic Brain Injury in Veterans and Military Personnel: A Systematic Review [Internet]. Washington (DC): Department of Veterans Affairs (US); 2013 Jan. PMID: 24600749.
    4. 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.
    5. 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
    6. 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
    7. 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
    8. 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.
    9. 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.
    10. 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.
    11. 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.
    12. 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
    13. 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
    14. 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
    15. https://www.imin-org.eu/images/science/Haug-Report-Bemer_2016_Englisch.pdf
    16. NIMH » Post-Traumatic Stress Disorder (PTSD). https://www.nimh.nih.gov/health/statistics/post-traumatic-stress-disorder-ptsd#part_155467. Accessed 2 June 2021.
    17. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th edn. American Psychiatric Publishing, Arlington, VA, 2013.
    18. Michopoulos, Vasiliki, et al. “Posttraumatic Stress Disorder: A Metabolic Disorder in Disguise?” Experimental Neurology, vol. 284, no. Pt B, Oct. 2016, pp. 220–29. PubMed, doi:10.1016/j.expneurol.2016.05.038.
    19. Mellon, Synthia H., et al. “Metabolism, Metabolomics, and Inflammation in Posttraumatic Stress Disorder.” Biological Psychiatry, vol. 83, no. 10, May 2018, pp. 866–75. PubMed, doi:10.1016/j.biopsych.2018.02.007.
    20. Edmondson, Donald, et al. “Posttraumatic Stress Disorder and Risk for Coronary Heart Disease: A Meta-Analytic Review.” American Heart Journal, vol. 166, no. 5, Nov. 2013, pp. 806–14. PubMed, doi:10.1016/j.ahj.2013.07.031.
    21. O’Donovan, Aoife, et al. “Elevated Risk for Autoimmune Disorders in Iraq and Afghanistan Veterans with Posttraumatic Stress Disorder.” Biological Psychiatry, vol. 77, no. 4, Feb. 2015, pp. 365–74. PubMed, doi:10.1016/j.biopsych.2014.06.015.
    22. Song, Huan, et al. “Association of Stress-Related Disorders With Subsequent Autoimmune Disease.” JAMA, vol. 319, no. 23, June 2018, pp. 2388–400. PubMed, doi:10.1001/jama.2018.7028.
    23. Miller, Mark W et al. “Oxidative Stress, Inflammation, and Neuroprogression in Chronic PTSD.” Harvard review of psychiatry vol. 26,2 (2018): 57-69. doi:10.1097/HRP.0000000000000167
    24. Bradley, Rebekah, et al. “A Multidimensional Meta-Analysis of Psychotherapy for PTSD.” The American Journal of Psychiatry, vol. 162, no. 2, Feb. 2005, pp. 214–27. PubMed, doi:10.1176/appi.ajp.162.2.214.
    25. Jonas, Daniel E., et al. Psychological and Pharmacological Treatments for Adults With Posttraumatic Stress Disorder (PTSD). Agency for Healthcare Research and Quality (US), 2013. PubMed, http://www.ncbi.nlm.nih.gov/books/NBK137702/.
    26. Passos, Ives Cavalcante et al. “Inflammatory markers in post-traumatic stress disorder: a systematic review, meta-analysis, and meta-regression.” The lancet. Psychiatry vol. 2,11 (2015): 1002-12. doi:10.1016/S2215-0366(15)00309-0
    27. Miller, Mark W et al. “Oxidative Stress, Inflammation, and Neuroprogression in Chronic PTSD.” Harvard review of psychiatry vol. 26,2 (2018): 57-69. doi:10.1097/HRP.0000000000000167
    28. Neigh, Gretchen N, and Fariya F Ali. “Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment.” Current opinion in pharmacology vol. 29 (2016): 104-10. doi:10.1016/j.coph.2016.07.011
    29. Godman, Cassandra A et al. “Hyperbaric oxygen treatment induces antioxidant gene expression.” Annals of the New York Academy of Sciences vol. 1197 (2010): 178-83. doi:10.1111/j.1749-6632.2009.05393.x
    30. Szeszko, Philip R., and Rachel Yehuda. “Magnetic Resonance Imaging Predictors of Psychotherapy Treatment Response in Post-Traumatic Stress Disorder: A Role for the Salience Network.” Psychiatry Research, vol. 277, July 2019, pp. 52–57. ScienceDirect, doi:10.1016/j.psychres.2019.02.005.
    31. Akiki, Teddy J., et al. “Default Mode Network Abnormalities in Posttraumatic Stress Disorder: A Novel Network-Restricted Topology Approach.” NeuroImage, vol. 176, Aug. 2018, pp. 489–98. ScienceDirect, doi:10.1016/j.neuroimage.2018.05.005.
    32. Ros, Tomas, et al. “Mind over Chatter: Plastic up-Regulation of the FMRI Salience Network Directly after EEG Neurofeedback.” NeuroImage, vol. 65, Jan. 2013, pp. 324–35. ScienceDirect, doi:10.1016/j.neuroimage.2012.09.046.
    33. Kluetsch, R. C., et al. “Plastic Modulation of PTSD Resting-State Networks and Subjective Wellbeing by EEG Neurofeedback.” Acta Psychiatrica Scandinavica, vol. 130, no. 2, 2014, pp. 123–36. Wiley Online Library, doi:https://doi.org/10.1111/acps.12229.
    34. Kolk, Bessel A. van der, et al. “A Randomized Controlled Study of Neurofeedback for Chronic PTSD.” PLOS ONE, vol. 11, no. 12, Public Library of Science, Dec. 2016, p. e0166752. PLoS Journals, doi:10.1371/journal.pone.0166752.
    35. Nicholson, Andrew A., et al. “Intrinsic Connectivity Network Dynamics in PTSD during Amygdala Downregulation Using Real-Time FMRI Neurofeedback: A Preliminary Analysis.” Human Brain Mapping, vol. 39, no. 11, 2018, pp. 4258–75. Wiley Online Library, doi:10.1002/hbm.24244.
    36. Rogel, Ainat, et al. “The Impact of Neurofeedback Training on Children with Developmental Trauma: A Randomized Controlled Study.” Psychological Trauma: Theory, Research, Practice, and Policy, vol. 12, no. 8, Educational Publishing Foundation, 2020, pp. 918–29. APA PsycNET, doi:10.1037/tra0000648.
    37. Gapen, Mark, et al. “A Pilot Study of Neurofeedback for Chronic PTSD.” Applied Psychophysiology and Biofeedback, vol. 41, no. 3, Sept. 2016, pp. 251–61. Springer Link, doi:10.1007/s10484-015-9326-5.
    38. Miller, Mark W et al. “Oxidative Stress, Inflammation, and Neuroprogression in Chronic PTSD.” Harvard review of psychiatry vol. 26,2 (2018): 57-69. doi:10.1097/HRP.0000000000000167
    39. S. Brody, R. Preut, K. Schommer, T.H. Schürmeyer A randomized controlled trial of high dose ascorbic acid for reduction of blood pressure, cortisol, and subjective responses to psychological stress Psychopharmacology (Berl), 159 (2002), pp. 319-324, 10.1007/s00213-001-0929-6
    40. Peters, E M et al. “Vitamin C supplementation attenuates the increases in circulating cortisol, adrenaline and anti-inflammatory polypeptides following ultramarathon running.” International journal of sports medicine vol. 22,7 (2001): 537-43. doi:10.1055/s-2001-17610
    41. Michels L, Schulte-Vels T, Schick M, O’Gorman RL, Zeffiro T, Hasler G, et al. Prefrontal GABA and glutathione imbalance in posttraumatic stress disorder: preliminary findings. Psychiatry Res. 2014;224(3):288–95.
    42. Ross, Christina L., et al. “The Use of Pulsed Electromagnetic Field to Modulate Inflammation and Improve Tissue Regeneration: A Review.” Bioelectricity, vol. 1, no. 4, Mary Ann Liebert, Inc., publishers, Dec. 2019, pp. 247–59. liebertpub.com (Atypon), doi:10.1089/bioe.2019.0026.