Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients

Rockswold, Sarah B.; Rockswold, Gaylan L.; Vargo, Janet M.; Erickson, Carla A.; Sutton, Richard L.; Bergman, Thomas; Biros, Michelle H.

doi:10.3171/jns.2001.94.3.0403

Cited by 147 publications

(107 citation statements)

References 52 publications

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“…90 Treatment of TBI patients with normobaric hyperoxia has shown variable results. Significant improvement 91,92 or no improvement 93 in cerebral metabolism, a decrease of lactate levels, 91,94 -96 a reduction of ischemic brain volume 92 and ICP 96 were observed. Hyperoxia treatment has also resulted in either no change 92 and in only some studies a decrease 90,96 of L/P ratio.…”

Section: Clinical Studies With Hyperoxiamentioning

confidence: 94%

Use of Magnesium in Traumatic Brain Injury

Sen¹,

Gulati

2010

Neurotherapeutics

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Summary: Depletion of magnesium is observed in animal brain and in human blood after brain injury. Treatment with magnesium attenuates the pathological and behavioral changes in rats with brain injury; however, the therapeutic effect of magnesium has not been consistently observed in humans with traumatic brain injury (TBI). Secondary brain insults are observed in patients with brain injury, which adversely affect clinical outcome. Systemic administration studies in rats have shown that magnesium enters the brain; however, inducing hypermagnesemia in humans did not concomitantly increase magnesium levels in the CSF. We hypothesize that the neuroprotective effects of magnesium in TBI patients could be observed by increasing its brain bioavailability with mannitol. Here, we review the role of magnesium in brain injury, preclinical studies in brain injury, clinical safety and efficacy studies in TBI patients, brain bioavailability studies in rat, and pharmacokinetic studies in humans with brain injury. Neurodegeneration after brain injury involves multiple biochemical pathways. Treatment with a single agent has often resulted in poor efficacy at a safe dose or toxicity at a therapeutic dose. A successful neuroprotective therapy needs to be aimed at homeostatic control of these pathways with multiple agents. Other pharmacological agents, such as dexanabinol and progesterone, and physiological interventions, with hypothermia and hyperoxia, have been studied for the treatment of brain injury. Treatment with magnesium and hypothermia has shown favorable outcome in rats with cerebral ischemia. We conclude that coadministration of magnesium and mannitol with pharmacological and physiological agents could be an effective neuroprotective regimen for the treatment of TBI.

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Section: Clinical Studies With Hyperoxiamentioning

confidence: 94%

Use of Magnesium in Traumatic Brain Injury

Sen¹,

Gulati

2010

Neurotherapeutics

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“…44,45 The data suggest that HBO 2 enables the brain to use increased FiO 2 in the posttreatment period. Experimental investigations also support the concept of using HBO 2 followed by continued increased O 2 at normobaric pressures as a single treatment.…”

mentioning

confidence: 96%

A prospective, randomized Phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury

Rockswold

Zaun

et al. 2013

JNS

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129

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T he enormous negative social and economic impact of TBI throughout the world cannot be overemphasized. The major issue is premature death and disability both in civilian and military populations. Conservative estimates of the prevalence of long-term disability due to TBI in the United States are well over 3 million people. The economic toll of TBI exceeds $60 billion per year. 18 Our previous investigations of HBO 2 Object. Preclinical and clinical investigations indicate that the positive effect of hyperbaric oxygen (HBO 2 ) for severe traumatic brain injury (TBI) occurs after rather than during treatment. The brain appears better able to use baseline O 2 levels following HBO 2 treatments. In this study, the authors evaluate the combination of HBO 2 and normobaric hyperoxia (NBH) as a single treatment.Methods. Forty-two patients who sustained severe TBI (mean Glasgow Coma Scale [GCS] score 5.7) were prospectively randomized within 24 hours of injury to either: 1) combined HBO 2 /NBH (60 minutes of HBO 2 at 1.5 atmospheres absolute [ATA] followed by NBH, 3 hours of 100% fraction of inspired oxygen [FiO 2 ] at 1.0 ATA) or 2) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Intracranial pressure, surrogate markers for cerebral metabolism, and O 2 toxicity were monitored. Clinical outcome was assessed at 6 months using the sliding dichotomized Glasgow Outcome Scale (GOS) score. Mixedeffects linear modeling was used to statistically test differences between the treatment and control groups. Functional outcome and mortality rates were compared using chi-square tests.Results. There were no significant differences in demographic characteristics between the 2 groups. In comparison with values in the control group, brain tissue partial pressure of O 2 (PO 2 ) levels were significantly increased during and following combined HBO 2 /NBH treatments in both the noninjured and pericontusional brain (p < 0.0001). Microdialysate lactate/pyruvate ratios were significantly decreased in the noninjured brain in the combined HBO 2 /NBH group as compared with controls (p < 0.0078). The combined HBO 2 /NBH group's intracranial pressure values were significantly lower than those of the control group during treatment, and the improvement continued until the next treatment session (p < 0.0006). The combined HBO 2 /NBH group's levels of microdialysate glycerol were significantly lower than those of the control group in both noninjured and pericontusional brain (p < 0.001). The combined HBO 2 /NBH group's level of CSF F2-isoprostane was decreased at 6 hours after treatment as compared with that of controls, but the difference did not quite reach statistical significance (p = 0.0692). There was an absolute 26% reduction in mortality for the combined HBO 2 /NBH group (p = 0.048) and an absolute 36% improvement in favorable outcome using the sliding dichotomized GOS (p = 0.024) as compared with the control group.Conclusions. In this Phase II clinical trial, in comparison with standard care (control t...

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“…The cerebrovascular response to hyperoxia has been investigated in physiological and pathological conditions, and it has been shown that there is a cerebral blood flow (CBF) reduction in response to hyperoxia ranging from 9% to 27% (Johnston et al 2003). In addition, Rockswold et al (2001) investigated the effects of hyperoxia therapy at 1.5 atm on CBF and metabolism. The authors observed that at 1 and 6 h post treatment, there was an increase in CBF in the group with decreased baseline values, whereas there was a decrease in CBF in the patients with increased pretreatment values.…”

Section: Discussionmentioning

confidence: 99%

Effect of normabaric hyperoxia treatment on neuronal damage following fluid percussion injury in the striatum of mice: A morphological approach

et al. 2013

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Traumatic brain injury (TBI) causes significant mortality in most developing countries worldwide. At present, it is imperative to identify a treatment to address the devastating post-TBI consequences. Therefore, the present study has been performed to assess the specific effect of immediate exposure to normabaric hyperoxia (NBO) after fluid percussion injury (FPI) in the striatum of mice. To execute FPI, mice were anesthetised and sorted into (i) a TBI group, (ii) a sham group without injury and (iii) a TBI group treated with immediate exposure to NBO for 3 h. Afterwards, brains were harvested for morphological assessment. The results revealed no changes in morphological and neuronal damage in the sham group as compared to the TBI group. Conversely, the TBI group showed severe morphological changes as well as neuronal damage as compared to the TBI group exposed to NBO for 3 h. Interestingly, our findings also suggested that NBO treatment could diminish the neuronal damage in the striatum of mice after FPI. Neuronal damage was evaluated at different points of injury and the neighbouring areas using morphology, neuronal apoptotic cell death and pan-neuronal markers to determine the complete neuronal structure. In conclusion, immediate exposure to NBO following FPI could be a potential therapeutic approach to reduce neuronal damage in the TBI model.[Muthuraju S, Pati S, Rafiqul M, Abdullah JM and Jaafar H 2013 Effect of normabaric hyperoxia treatment on neuronal damage following fluid percussion injury in the striatum of mice: A morphological approach. J.

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Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients

Cited by 147 publications

References 52 publications

Use of Magnesium in Traumatic Brain Injury

Use of Magnesium in Traumatic Brain Injury

A prospective, randomized Phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury

Effect of normabaric hyperoxia treatment on neuronal damage following fluid percussion injury in the striatum of mice: A morphological approach

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