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      Hyperbaric oxygen therapy for traumatic brain injury

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          Abstract

          Traumatic brain injury (TBI) is a major public health issue. The complexity of TBI has precluded the use of effective therapies. Hyperbaric oxygen therapy (HBOT) has been shown to be neuroprotective in multiple neurological disorders, but its efficacy in the management of TBI remains controversial. This review focuses on HBOT applications within the context of experimental and clinical TBI. We also discuss its potential neuroprotective mechanisms. Early or delayed multiple sessions of low atmospheric pressure HBOT can reduce intracranial pressure, improve mortality, as well as promote neurobehavioral recovery. The complimentary, synergistic actions of HBOT include improved tissue oxygenation and cellular metabolism, anti-apoptotic, and anti-inflammatory mechanisms. Thus HBOT may serve as a promising neuroprotective strategy that when combined with other therapeutic targets for TBI patients which could improve long-term outcomes.

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          The Neurometabolic Cascade of Concussion.

          Christopher C Giza, David A. Hovda (2001)
          OBJECTIVE: To review the underlying pathophysiologic processes of concussive brain injury and relate these neurometabolic changes to clinical sports-related issues such as injury to the developing brain, overuse injury, and repeated concussion. DATA SOURCES: Over 100 articles from both basic science and clinical medical literature selected for relevance to concussive brain injury, postinjury pathophysiology, and recovery of function. DATA SYNTHESIS: The primary elements of the pathophysiologic cascade following concussive brain injury include abrupt neuronal depolarization, release of excitatory neurotransmitters, ionic shifts, changes in glucose metabolism, altered cerebral blood flow, and impaired axonal function. These alterations can be correlated with periods of postconcussion vulnerability and with neurobehavioral abnormalities. While the time course of these changes is well understood in experimental animal models, it is only beginning to be characterized following human concussion. CONCLUSIONS/RECOMMENDATIONS: Following concussion, cerebral pathophysiology can be adversely affected for days in animals and weeks in humans. Significant changes in cerebral glucose metabolism can exist even in head-injured patients with normal Glasgow Coma Scores, underscoring the need for in-depth clinical assessment in an effort to uncover neurocognitive correlates of altered cerebral physiology. Improved guidelines for clinical management of concussion may be formulated as the functional significance and duration of these postinjury neurometabolic derangements are better delineated.
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            Bcl-2/Bax: a rheostat that regulates an anti-oxidant pathway and cell death.

            Z Oltvai, John R. Shutter, S Korsmeyer … (1993)
            The maintenance of homeostasis in normal tissues reflects a balance between cell proliferation and cell death. The importance of both positive and negative regulators of cell growth has been well documented in neoplasia. Bcl-2 argues for the existence of a new category of oncogenes, regulators of cell death. The bcl-2 gene was identified at the chromosomal breakpoint of t(14; 18) bearing B cell lymphomas. Bcl-2 has proved to be unique among protooncogenes in blocking programmed cell death rather than promoting proliferation. In adults, bcl-2 is topographically restricted to progenitor cells and longlived cells but is much more widespread in the developing embryo. Transgenic mice that overexpress bcl-2 in the B cell lineage demonstrate extended cell survival, and progress to high grade lymphomas. Bcl-2 has been localized to mitochondria, endoplasmic reticulum and nuclear membranes, also the sites of reactive oxygen species generation. Bcl-2 does not appear to influence the generation of oxygen free radicals but does prevent oxidative damage to cellular constituents including lipid membranes. Bcl-2 deficient mice complete embryonic development and display relatively normal haematopoietic differentiation but undergo fulminant lymphoid apoptosis of thymus and spleen. Moreover, they demonstrate two potentially oxidation related pathologies: polycystic kidney disease and hair hypopigmentation. A family of bcl-2 related genes is emerging that includes Bax, a conserved homolog that heterodimerizes in vivo with bcl-2. A pre-set ratio of Bcl-2/Bax appears to determine the survival or death of cells following an apoptotic stimulus.
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              Hyperbaric oxygen: its uses, mechanisms of action and outcomes.

              Jennifer A Gill, Jeffrey A. Bell (2004)
              Article 0 comments Cited 68 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Med Gas Res
                Title: Medical Gas Research
                Publisher: BioMed Central
                ISSN (Electronic): 2045-9912
                Publication date Collection: 2011
                Publication date (Electronic): 6 September 2011
                Volume: 1
                Page: 21
                Affiliations
                [1 ]Department of Biophysics & Bioengineering, Loma Linda University, Griggs Hall, Room 227, 11065 Campus St., Loma Linda, California, 92354, USA
                [2 ]Department of Pediatrics, Loma Linda University, CSP A1010, 11175 Campus St., Loma Linda, California, 92354, USA
                [3 ]Department of Radiology, Loma Linda University Medical Center, CSP A1010, 11175 Campus St., Loma Linda, California, 92354, USA
                [4 ]Department of Radiation Medicine, Loma Linda University, CSP A1010, 11175 Campus St., Loma Linda, California, 92354, USA
                [5 ]Department of Neuroscience, University of California, Riverside, 1140 Batchelor Hall, University of California, Riverside, California, 92521, USA
                Article
                Publisher ID: 2045-9912-1-21
                DOI: 10.1186/2045-9912-1-21
                PMC ID: 3231802
                PubMed ID: 22146562
                SO-VID: 98816801-e112-4af4-9df8-7b106dfa18e6
                Copyright © Copyright ©2011 Huang and Obenaus; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 May 2011
                Date accepted : 6 September 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: intracranial pressure,metabolism,apoptosis,inflammation,tissue oxygenation,cerebral blood flow
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: intracranial pressure, metabolism, apoptosis, inflammation, tissue oxygenation, cerebral blood flow

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