Post-Traumatic Seizures Exacerbate Histopathological Damage after Fluid-Percussion Brain Injury

Bao, Yong; Bramlett, Helen M.; Atkins, Coleen M.; Truettner, Jessie; Lotocki, George; Alonso, Ofelia F.; Dietrich, W. Dalton

doi:10.1089/neu.2010.1383

Cited by 51 publications

(28 citation statements)

References 65 publications

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“…[130][131][132] Importantly, PTE is an important secondary injury mechanism that can aggravate damage or impede endogenous recovery mechanisms. [133][134][135][136][137][138][139] In one experimental study, induced periods of PTE were shown to increase the vulnerability of cortical and subcortical structures after experimental TBI. 135 This study first emphasized the potential for a brief episode of PTE to have a significant impact on the vulnerability of the post-traumatic brain.…”

Section: Post-traumatic Epilepsy and Cortical Spreading Depolarizationsmentioning

confidence: 99%

“…[133][134][135][136][137][138][139] In one experimental study, induced periods of PTE were shown to increase the vulnerability of cortical and subcortical structures after experimental TBI. 135 This study first emphasized the potential for a brief episode of PTE to have a significant impact on the vulnerability of the post-traumatic brain. Because recent clinical data have emphasized the high incidence of PTE and episodes of cortical spreading depolarization in TBI patients, these post-traumatic events require more investigation.…”

Section: Post-traumatic Epilepsy and Cortical Spreading Depolarizationsmentioning

confidence: 99%

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Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes

Bramlett

Dietrich

2015

Journal of Neurotrauma

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382

257

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Traumatic brain injury (TBI) is a significant clinical problem with few therapeutic interventions successfully translated to the clinic. Increased importance on the progressive, long-term consequences of TBI have been emphasized, both in the experimental and clinical literature. Thus, there is a need for a better understanding of the chronic consequences of TBI, with the ultimate goal of developing novel therapeutic interventions to treat the devastating consequences of brain injury. In models of mild, moderate, and severe TBI, histopathological and behavioral studies have emphasized the progressive nature of the initial traumatic insult and the involvement of multiple pathophysiological mechanisms, including sustained injury cascades leading to prolonged motor and cognitive deficits. Recently, the increased incidence in age-dependent neurodegenerative diseases in this patient population has also been emphasized. Pathomechanisms felt to be active in the acute and long-term consequences of TBI include excitotoxicity, apoptosis, inflammatory events, seizures, demyelination, white matter pathology, as well as decreased neurogenesis. The current article will review many of these pathophysiological mechanisms that may be important targets for limiting the chronic consequences of TBI.

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Section: Post-traumatic Epilepsy and Cortical Spreading Depolarizationsmentioning

confidence: 99%

Section: Post-traumatic Epilepsy and Cortical Spreading Depolarizationsmentioning

confidence: 99%

Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes

Bramlett

Dietrich

2015

Journal of Neurotrauma

Self Cite

382

257

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“…While true normoxia in room air has an FiO 2 *21%, we elected to maintain ''experimental normoxia'' with a ventilatory mixture of nitrous oxide/oxygen (2:1) to produce an FiO 2 = 33%, which is typically used in rat TBI studies (Bales et al, 2010;Bao et al, 2011;Hall and Lifshitz, 2010). Henceforth in this manuscript ''normoxia'' refers to our ''experimental normoxia,'' with an FiO 2 = 33%.…”

Section: Ventilation and Controlled Hypoxiamentioning

confidence: 99%

Post-Traumatic Hypoxia Exacerbates Neuronal Cell Death in the Hippocampus

Feng

Zhao

Gurkoff

et al. 2012

Journal of Neurotrauma

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Hypoxia frequently occurs in patients with traumatic brain injury (TBI) and is associated with increased morbidity and mortality. This study examined the effects of immediate or delayed post-traumatic hypoxia (fraction of inspired oxygen [FiO 2 ] 11%) on acute neuronal degeneration and long-term neuronal survival in hippocampal fields after moderate fluid percussion injury in rats. In Experiment 1, hypoxia was induced for 15 or 30 min alone or immediately following TBI. In Experiments 2 and 3, 30 min of hypoxia was induced immediately after TBI or delayed until 60 min after TBI. In Experiment 1, acute neurodegeneration was evaluated in the hippocampal fields 24 h after insults using Fluoro-Jade staining and stereological quantification. During hypoxia alone, or in combination with TBI, mean arterial blood pressure was significantly reduced by approximately 30%, followed by a rapid return to normal values upon return to pre-injury FiO 2 . Hypoxia alone failed to cause hippocampal neuronal degeneration when measured at 24 h after insult. TBI alone resulted in neuronal degeneration in each ipsilateral hippocampal field, predominantly in CA2-CA3 and the dentate gyrus. Compared to TBI alone, TBI plus immediate hypoxia for either 15 or 30 min significantly increased neuronal loss in most ipsilateral hippocampal fields and in the contralateral hilus and dentate gyrus. In Experiment 2, TBI plus hypoxia delayed 30 min significantly increased degeneration only in ipsilateral CA2-CA3. In Experiment 3, 30 min of immediate hypoxia significantly reduced the numbers of surviving neurons in the CA3 at 14 days after TBI. The greatly increased vulnerability in all hippocampal fields by immediate 30 min post-traumatic hypoxia provides a relevant model of TBI complicated with hypoxia/hypotension. These data underscore the significance of the secondary insult, the necessity to better characterize the range of injuries experienced by the TBI patient, and the importance of strictly avoiding hypoxia in the early management of TBI patients.

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“…Posttraumatic epilepsy (PTE) is commonly observed in patients with moderate to severe TBI and promotes secondary injury processes and long-term cognitive deficits (Bao, et al, 2011, Vespa, et al, 2010). In models of epilepsy, evidence for acute increases in neurogenesis, similar to that seen after TBI have been reported (Parent, et al, 1997, Scott, et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Posttraumatic hypothermia increases doublecortin expressing neurons in the dentate gyrus after traumatic brain injury in the rat

Bregy

Nixon

Lotocki

et al. 2012

Experimental Neurology

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Previous studies have demonstrated that moderate hypothermia reduces histopathological damage and improves behavioral outcome after experimental traumatic brain injury (TBI). Further investigations have clarified the mechanisms underlying the beneficial effects of hypothermia by showing that cooling reduces multiple cell injury cascades. The purpose of this study was to determine whether hypothermia could also enhance endogenous reparative processes following TBI such as neurogenesis and the replacement of lost neurons. Male Sprague-Dawley rats underwent moderate fluid-percussion brain injury and then were randomized into normothermia (37°C) or hypothermia (33°C) treatment. Animals received injections of 5-bromo-2′-deoxyuridine (BrdU) to detect mitotic cells after brain injury. After 3 or 7 days, animals were perfusion-fixed and processed for immunocytochemistry and confocal analysis. Sections were stained for markers selective for cell proliferation (BrdU), neuroblasts and immature neurons (doublecortin), and mature neurons (NeuN) and then analyzed using non-biased stereology to quantify neurogenesis in the dentate gyrus (DG). At 7 days after TBI, both normothermic and hypothermic TBI animals demonstrated a significant increase in the number of BrdU-immunoreactive cells in the DG as compared to sham-operated controls. At 7 days post-injury, hypothermia animals had a greater number of BrdU (ipsilateral cortex) and doublecortin (ipsilateral and contralateral cortex) immunoreactive cells in the DG as compared to normothermia animals. Because adult neurogenesis following injury may be associated with enhanced functional recovery, these data demonstrate that therapeutic hypothermia sustains the increase in neurogenesis induced by TBI and this may one of the mechanisms by which hypothermia promotes reparative strategies in the injured nervous system.

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Post-Traumatic Seizures Exacerbate Histopathological Damage after Fluid-Percussion Brain Injury

Cited by 51 publications

References 65 publications

Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes

Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes

Post-Traumatic Hypoxia Exacerbates Neuronal Cell Death in the Hippocampus

Posttraumatic hypothermia increases doublecortin expressing neurons in the dentate gyrus after traumatic brain injury in the rat

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