Hyperbaric Oxygen for Treatment of Closed Head Injury

Neubauer, Richard A.; Gottlieb, Sheldon F.; Pevsner, N.

doi:10.1097/00007611-199409000-00015

Cited by 48 publications

(26 citation statements)

References 4 publications

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“…However, in each instance, the effects of hyperoxia on the mCNS are attributed to the oxidative effects of ROS (60-63, 70, 107, 205). For example, the mCNS response to hyperoxia can range from a moderate, but reversible change in neural activity (22, 51,142,150,152), possibly with therapeutic benefits for improved neurological function (33,38,158,203), to violent and reversible seizures at higher levels of Pti O 2 (5,60,63), to irreversible motor deficits (and even death) at the highest dosages of hyperoxia (9,12). The use of graded levels of hyperoxia at room pressure (normobaric hyperoxia) and increased ambient pressure (hyperbaric hyperoxia, or HBO 2 ), therefore, is a useful model for studying the wide-ranging effects of oxidative stress on neurological function, which complements more traditional in vitro models of oxidative stress used at normobaric pressure (e.g., Refs.…”

Section: Hyperoxia As a Model Of Oxidative Stressmentioning

confidence: 99%

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Dean¹,

Mulkey²,

Garcia³

et al. 2003

Journal of Applied Physiology

175

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III. Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures. J Appl Physiol 95: 883-909, 2003; 10.1152/japplphysiol.00920.2002.-As ambient pressure increases, hydrostatic compression of the central nervous system, combined with increasing levels of inspired PO 2, PCO2, and N2 partial pressure, has deleterious effects on neuronal function, resulting in O 2 toxicity, CO2 toxicity, N2 narcosis, and high-pressure nervous syndrome. The cellular mechanisms responsible for each disorder have been difficult to study by using classic in vitro electrophysiological methods, due to the physical barrier imposed by the sealed pressure chamber and mechanical disturbances during tissue compression. Improved chamber designs and methods have made such experiments feasible in mammalian neurons, especially at ambient pressures Ͻ5 atmospheres absolute (ATA). Here we summarize these methods, the physiologically relevant test pressures, potential research applications, and results of previous research, focusing on the significance of electrophysiological studies at Ͻ5 ATA. Intracellular recordings and tissue PO 2 measurements in slices of rat brain demonstrate how to differentiate the neuronal effects of increased gas pressures from pressure per se. Examples also highlight the use of hyperoxia (Յ3 ATA O 2) as a model for studying the cellular mechanisms of oxidative stress in the mammalian central nervous system. anesthesia; carbon dioxide toxicity; free radicals; high-pressure nervous syndrome; membrane potential; nitrogen narcosis; oxidative stress; oxygen toxicity; polarographic oxygen electrode MOST HUMANS ARE PHYSIOLOGICALLY adapted to live and work near sea level, where ambient pressure is ϳ1 atmosphere absolute (ATA).1 Nonetheless, we exploit a continuum of barometric pressure (PB) ranging from the near vacuum of outer space, which we survive during Space Shuttle extravehicular activity by wearing a 4.3 lb./in.2 absolute (psia) pressure suit (30,300 ft. pressure equivalent, 0.29 ATA) (120, 220), down to the summit of Mt. Everest at 29,029 ft., where PB is 0.31 ATA (221), to ocean depths as great as 2,300 ft. of sea water (fsw), where PB increases to ϳ70 ATA (18). These situations are the pressure extremes of our inhabitable environment, which only relatively few highly trained individuals have ever occupied.Military personnel, medical personnel, and other humans, however, frequently encounter levels of hyperbaric pressure (i.e., Ͼ1 ATA) of lesser degrees in their normal work environments. Examples of moderate hyperbaric environments (e.g., Ͻ5 ATA) include the following: patients and medical attendants undergoing hyperbaric O 2 therapy (HBOT) (38,203); diving with an underwater breathing apparatus for recreational, professional (oil and salvage companies), and combat purposes (89); simulated dry and wet dives for hyperbaric research and dive training (217); and working in the compressed atmosphere of a subterranean environment (117). Abnormal work environments resulting from catastrophic accident...

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Section: Hyperoxia As a Model Of Oxidative Stressmentioning

confidence: 99%

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Dean¹,

Mulkey²,

Garcia³

et al. 2003

Journal of Applied Physiology

175

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“…Ischemic as well as post traumatic penumbra are characterized as potentially viable tissue exposed to secondary deleterious events wherein energy failure is prominent. In this regard, increasing attention has been recently drawn to the beneficial effect of hyperbaric oxygen therapy (HBOT) for the reduction of delayed neuronal death (Neubauer et al, 1994). However, conflicting results regarding the benefits of hyperbaric oxygen have also been reported (Nighoghossian and Trouillas, 1997).…”

Section: Introductionmentioning

confidence: 99%

Hyperbaric Oxygen Therapy for Reduction of Secondary Brain Damage in Head Injury: An Animal Model of Brain Contusion

Palzur¹,

Vlodavsky²,

Mulla³

et al. 2004

Journal of Neurotrauma

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Cerebral contusions are one the most frequent traumatic lesions and the most common indication for secondary surgical decompression. The purpose of this study was to investigate the physiology of perilesional secondary brain damage and evaluate the value of hyperbaric oxygen therapy (HBOT) in the treatment of these lesions. Five groups of five Sprague-Dawley rats each were submitted to dynamic cortical deformation (DCD) induced by negative pressure applied to the cortex. Cerebral lesions produced by DCD at the vacuum site proved to be reproducible. The study protocol entailed the following: (1) DCD alone, (2) DCD and HBOT, (3) DCD and post-operative hypoxia and HBOT, (4) DCD, post-operative hypoxia and HBOT, and (5) DCD and normobaric hyperoxia. Animals were sacrificed after 4 days. Histological sections showed localized gross tissue loss in the cortex at injury site, along with hemorrhage. In all cases, the severity of secondary brain damage was assessed by counting the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 3-positive cells in successive perilesional layers, each 0.5 mm thick. Perilesional TUNEL positive cells suggested the involvement of apoptosis in group 1 (12.24% of positive cells in layer 1). These findings were significantly enhanced by post-operative hypoxia (31.75%, p < 0.001). HBOT significantly reduced the severity and extent of secondary brain damage expressed by the number of TUNEL positive cells in each layer and the volume of the lesion (4.7% and 9% of TUNEL positive cells in layer 1 in groups 2 and 4 respectively, p < 0.0001 and p < 0.003). Normobaric hyperoxia also proved to be beneficial although in a lesser extent. This study demonstrates that the vacuum model of brain injury is a reproducible model of cerebral contusion. The current findings also suggest that HBOT may limit the growth of cerebral contusions and justify further experimental studies.

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“…A review of the literature on the effectiveness of HBOT in brain injury confirms this. These studies are limited to anecdotal conclusions based on the clinical experience of the author, along with some single-subject or small group studies (Hawkins et al, 2000;Mahi, 1998;Neubauer & Walker, 2000;Neubauer et al, 1994;Walker, 1996).…”

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confidence: 99%

Improvement in Cerebral Metabolism in Chronic Brain Injury After Hyperbaric Oxygen Therapy

Golden

Neubauer

Golden

et al. 2002

International Journal of Neuroscience

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While no research study has yet demonstrated convincing evidence for the efficacy of Hyperbaric Oxygen Therapy (HBOT) in patients with chronic neurological disorders (CND), anecdotal studies have been supportive of its use in improving healing of the damaged brain. The current study hypothesized that (1) individuals with CND show increases in cerebral blood flow and metabolism as measured by Single Positron Emission Computed Tomography (SPECT) in the cerebral hemispheres, but not on measures of cerebellar and pons blood flow; and (2) younger patients show more improvement than older patients. The study used archival data to compare 25 older and 25 younger subjects who were given SPECT scans pretherapy, midtherapy, and posttherapy. ANOVAs using the SPECT scans as a within subjects variable and age as a between subjects variable confirmed the hypothesis that the cerebral measures all changed but that the cerebellar and pons measures did not. Post-hoc t-tests confirmed that there was improvement in blood flow from the beginning to the end of the study. An age effect was found on only two of the five measures; however, there were no interactions. Analysis by post-hoc t-tests showed that the younger group had higher blood flows, but not more improvement than the older group. The results provided the first statistical research data to show the effectiveness of HBOT in improving blood flow in CND. These results indicate that HBOT can be an effective part of the treatment for such clients. The implications of these findings and future research directions were discussed.

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Hyperbaric Oxygen for Treatment of Closed Head Injury

Cited by 48 publications

References 4 publications

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Hyperbaric Oxygen Therapy for Reduction of Secondary Brain Damage in Head Injury: An Animal Model of Brain Contusion

Improvement in Cerebral Metabolism in Chronic Brain Injury After Hyperbaric Oxygen Therapy

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