Journal of neurotrauma
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Journal of neurotrauma · Aug 2012
Severe brief pressure-controlled hemorrhagic shock after traumatic brain injury exacerbates functional deficits and long-term neuropathological damage in mice.
Hypotension after traumatic brain injury (TBI) worsens outcome. We published the first report of TBI plus hemorrhagic shock (HS) in mice using a volume-controlled approach and noted increased neuronal death. To rigorously control blood pressure during HS, a pressure-controlled HS model is required. ⋯ CA3 cell loss was seen after CCI+HS (p<0.05 at 24 h and 7 days). CA1 cell loss at 21 days was seen only in CCI+HS animals (p<0.05). Brief, severe, pressure-controlled HS after CCI produces robust functional deficits and exacerbates neuropathology versus CCI or HS alone.
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Journal of neurotrauma · Aug 2012
Intensity- and interval-specific repetitive traumatic brain injury can evoke both axonal and microvascular damage.
In the experimental setting several investigators have recently reported exacerbations of the burden of axonal damage and other neuropathological changes following repetitive traumatic brain injuries (TBI) that were sustained at intervals from hours to days following the initial insult. These same studies also revealed that prolonging the interval between the first and second insult led to a reduction in the burden of neuropathological changes and/or their complete elimination. Although demonstrating the capability of repetitive TBI to evoke increased axonal and other neuropathological changes, these studies did not address the potential for concomitant microvascular dysfunction or damage, although vascular dysfunction has been implicated in the second-impact syndrome. ⋯ With the extension of the interval between injuries to 10 h, neither axonal nor vascular changes were found. Collectively, these studies reaffirm the existence of significant axonal damage following repetitive TBI administered within a relatively short time frame. Additionally, they also demonstrate that these axonal changes parallel changes in the cerebral microcirculation, which also may have adverse consequences for the injured brain.
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Journal of neurotrauma · Aug 2012
Galveston Brain Injury Conference 2010: clinical and experimental aspects of blast injury.
Blast injury is the most prevalent source of mortality and morbidity among combatants in Operations Iraqi and Enduring Freedom. Blast-induced neurotrauma (BINT) is a common cause of mortality, and even mild BINT may be associated with chronic cognitive and emotional deficits. In addition to military personnel, the increasing use of explosives by terrorists has resulted in growing numbers of blast injuries in civilian populations. ⋯ The attention focused on BINT has led to increased financial support for research on blast effects, contributing to the development of better experimental models of blast injury and a clearer understanding of the mechanisms of BINT. This more thorough understanding of blast injury mechanisms will result in novel and more effective therapeutic and rehabilitative strategies designed to reduce injury and facilitate recovery, thereby improving long-term outcomes in patients suffering from the devastating and often lasting effects of BINT. The following is a summary of the 2010 Galveston Brain Injury Conference, that included presentations related to the diagnosis and treatment of acute BINT, the evaluation of the long-term neuropsychological effects of BINT, summaries of current experimental models of BINT, and a debate about the relative importance of primary blast effects on the acute and long-term consequences of blast exposure.
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Journal of neurotrauma · Aug 2012
ReviewBrain tissue oxygen monitoring and hyperoxic treatment in patients with traumatic brain injury.
Cerebral ischemia is a well-recognized contributor to high morbidity and mortality after traumatic brain injury (TBI). Standard of care treatment aims to maintain a sufficient oxygen supply to the brain by avoiding increased intracranial pressure (ICP) and ensuring a sufficient cerebral perfusion pressure (CPP). Devices allowing direct assessment of brain tissue oxygenation have showed promising results in clinical studies, and their use was implemented in the Brain Trauma Foundation Guidelines for the treatment of TBI patients in 2007. ⋯ With the increased availability of advanced neuromonitoring devices such as brain tissue oxygen monitors, it was shown that some patients might benefit from this therapeutic approach. In this article, we review the pathophysiological rationale and technical modalities of brain tissue oxygen monitors, as well as its use in studies of brain tissue oxygen-directed therapy. Furthermore, we analyze hyperoxia as a treatment option in TBI patients, summarize the results of clinical trials, and give insights into the recent findings of hyperoxic effects on cerebral metabolism after TBI.
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Journal of neurotrauma · Aug 2012
An FMRI study of auditory orienting and inhibition of return in pediatric mild traumatic brain injury.
Studies in adult mild traumatic brain injury (mTBI) have shown that two key measures of attention, spatial reorienting and inhibition of return (IOR), are impaired during the first few weeks of injury. However, it is currently unknown whether similar deficits exist following pediatric mTBI. The current study used functional magnetic resonance imaging (fMRI) to investigate the effects of semi-acute mTBI (<3 weeks post-injury) on auditory orienting in 14 pediatric mTBI patients (age 13.50±1.83 years; education: 6.86±1.88 years), and 14 healthy controls (age 13.29±2.09 years; education: 7.21±2.08 years), matched for age and years of education. ⋯ In contrast, functional imaging results indicated that patients with mTBI demonstrated significantly decreased activation within the bilateral posterior cingulate gyrus, thalamus, basal ganglia, midbrain nuclei, and cerebellum. The spatial topography of hypoactivation was very similar to our previous study in adults, suggesting that subcortical structures may be particularly affected by the initial biomechanical forces in mTBI. Current results also suggest that fMRI may be a more sensitive tool for identifying semi-acute effects of mTBI than the procedures currently used in clinical practice, such as neuropsychological testing and structural scans. fMRI findings could potentially serve as a biomarker for measuring the subtle injury caused by mTBI, and documenting the course of recovery.