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See References

  1. Tibbles, Patrick M., Edelsberg, John S. Hyperbaric-oxygen therapy. (1996). Hyperbaric-oxygen therapy. N Engl J Med 1996; 334:1642-1648. Doi: 10.1056/NEJM199606203342506
  2. McDonagh M, Helfand M, Carson S, Russman BS. Hyperbaric oxygen therapy for traumatic brain injury: a systematic review of the evidence. Arch Phys Med Rehabil. 2004;85:1198–1204. doi: 10.1016/j.apmr.2003.12.026.[PubMed]
  3. Hyder F, Patel AB, Gjedde A, Rothman DL, Behar KL, Shulman RG. Neuronal-glial glucose oxidation and glutamatergic-GABAergic function. J Cereb Blood Flow Metab. 2006;26:865–877. doi: 10.1038/sj.jcbfm.9600263. [PubMed] [Cross Ref]
  4. Neubauer RA, Walker M. Hyperbaric oxygen therapy. Garden City Park, NY: Avery Publishing Group; 2000.
  5. Efrati, S., and Ben-Jacob, E. (2014). Reflections on the neurotherapeutic effects of hyperbaric oxygen. Expert Rev. Neurother. 14, 233–236.
  6. Efrati, S., Fishlev, G., Bechor, Y., Volkov, O., Bergan, J., Kliakhandler,K., et al. (2013). Hyperbaric oxygen induces late neuroplasticity in post stroke patients–randomized, prospective trial. PLoS ONE 8:e53716
  7. Zamboni WA, et al. Morphological analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen. Plast Reconstr Surg 1993;91:1110-1123.
  8. Thom SR. Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. Toxicol Appl Pharmacol 1993;123:248-256.
  9. Mink RB, Dutka AJ. Hyperbaric oxygen after global cerebral ischemia in rabbits reduces brain vascular permeability and blood flow. December, 1995. Stroke;26(12):2307-2312.
  10. Yamada T, et al. The protective effect of hyperbaric oxygenation on the small intestine in ischemia-reperfusion injury. Journal of Ped Surg, June, 1995;30(6):786-90.
  11. Siddiqui A, et al. Ischemic tissue oxygen capacitance after hyperbaric oxygen therapy: a new physiologic concept. Plast Reconstr Surg, 1995;99:148-155.
  12. Wu L, Mustoe TA. Effect of ischemia on growth factor enhancement of incisional wound healing. Surgery, 1995;117:570.
  13. Buras JA, et al. Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. Am J Physiol Cell Physiol. 2000;278:292-302.
  14. Zhao LL, et al. Effect of hyperbaric oxygen and growth factors on rabbit ear ischemic ulcers. Arch Surg, 1994;129:1043.
  15. Reenstra WR, et al. Hyperbaric oxygen increases human dermal fibroblast proliferation, growth factor receptor number and in vitro wound closure. Undersea & Hyperb Med, 1998a;25:53.
  16. Reenstra WR, et al. Hyperbaric oxygen increases human dermal fibroblast expression of EGF-receptors (EGFR). Undersea & Hyperb Med, 1998b;25:54.
  17. Brown GL, Thomson PD, Mader JT, Hilton JG, Browne ME, Wells CH. Effects of hyperbaric oxygen upon S. aureus, Ps. aeruginosa and C. albicans. Aviat Space Environ Med 1979;50:717–720.
  18. Brismar K, Lind F, Kratz G. Dose-dependent hyperbaric oxygen stimulation of human fibroblast proliferation. Wound Repair Regen 1997;5:147–150.
  19. Reng JJ, Hussan MZ, Constant J, Hunt TK. Angiogenesis in wound healing. J Surg Pathol 1998;3:1–7.
  20. Hu, Q., Liang, X., Chen, D., Chen, Y., Doycheva, D., Tang, J., et al. (2014). Delayed hyperbaric oxygen therapy promotes neurogenesis through reactive oxygen species/hypoxia-inducible factor-1alpha/beta-catenin pathway in middle cerebral artery occlusion rats. Stroke 45, 1807–1814.
  21. Harch PG, Gottieb SF, Van Meter Kw, Staab P. HMPAO SPECT brain imagine and low pressure HBOT in the diagnosis and treatment of chronic traumatic, ischemic, hypoxic and anoxic encephalopathies. Undersea Hyperb Med 1995;21 (Supple):30.
  22. Achiron, A., Chapman, J., Magalashvili, D., Dolev, M., Lavie, M., Bercovich E., et al. (2013). Modeling of cognitive impairment by disease durationin multiple sclerosis: a cross-sectional study. PLoS ONE 8:e71058.
  23. Alaudek G, Hofler H, Pinter H et al.[Hyperbaric oxygen therapy in experimental necrotizing pancreatitis (author’s transl.)]. Dtsch. Z. Verdau. Stoffwechselkr 1982; 42: 7-13.
Hyperbaric Oxygen Therapy (HBOT)

Hyperbaric Oxygen Therapy (HBOT)

  • What is it?

    Hyperbaric Oxygen therapy (HBOT) is a non-invasive procedure during which clients immerse themselves in specially designed chamber pressurized greater than the earth’s (1). Administration is relatively simple with the sensation experienced similar to that flying and/or landing an airplane, or swimming to the bottom of a swimming pool. While in the chamber, subjects may comfortably watch television, listen to music or sleep.

  • Why is it important?

    Although HBOT was originally developed as a treatment for the “bends” in divers, with extensive research on the mechanisms by which increased oxygen saturation and availability is utilized, it has now become very popular as a part of the treatment plans for conditions such as, accelerated wound healing (17-19), Traumatic Brain Injury/Concussion (3,5,8), stroke (6), headache (6,8), Cerebral Palsy (CP) (21), Multiple Sclerosis (MS) (22), Pancreatitis (23), and more.

  • How does it work?

    Oxygen is the key element that cells, especially in the central nervous system (CNS), thrive on due to the high demand associated with neuronal signal transduction, synaptic transmission, and action potential nerve excitability (2). The use of high-pressure oxygen allows for additional oxygen to dissolve into the blood plasma, where it is only usually present in small amounts, increasing the amount of available oxygen to cells.

  • How does it help?

    This increases blood flow and promotes blood vessel development within the body, but most importantly, the brain. It has been argued that this increase in cerebral blood flow increases the function of neurons by stimulating axonal growth, thus increasing the communicative capacity of each neuron and neuronal network (3) while promoting neurogenesis and endogenous stem cell growth (4-6). HBOT has also been proven to be a powerful inhibitor of reperfusion injury (7-9), occurring when blood flow is re-established to deprived tissue, commonly seen in global ischemia, anoxia, and even coma (10-12).

    Also, undergoing HBOT, blood flow has been seen to be reduced to damaged areas, decreasing inflammation/edema without compromising oxygenation, signaling DNA to effect trophic (growth) tissue changes (14-16), enhancing neutrophil killing ability, and promoting collagen synthesis (17-19). It makes sense, that with such foundational consequences, HBOT therapy can induce neuroplasticity and increase immune function even years after an initial insult (20).

  • References

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