Articles: traumatic-brain-injuries.
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Blast-induced neurotrauma (BINT) has increased in incidence over the past decades and can result in cognitive issues that have debilitating consequences. The exact primary and secondary mechanisms of injury have not been elucidated and appearance of cellular injury can vary based on many factors, such as blast overpressure magnitude and duration. Many methodologies to study blast neurotrauma have been employed, ranging from open-field explosives to experimental shock tubes for producing free-field blast waves. ⋯ While cellular injury mechanisms have been identified following blast exposure, the various experimental models present both concurrent and conflicting results. Furthermore, the temporal response and progression of pathology after blast exposure have yet to be detailed and remain unclear due to limited resemblance of methodologies. This chapter summarizes the current state of blast neuropathology and emphasizes the need for a standardized preclinical model of blast neurotrauma.
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The pathophysiological mechanisms underlying mild traumatic brain injury (mTBI) are not well understood, but likely involve neuroinflammation. Here the controlled cortical impact model of mTBI in rats was used to test this hypothesis. Mild TBI caused a rapid (within 6 h post-mTBI) upregulation of synthesis of TNF-α and IL-1β in the cerebral cortex and hippocampus, followed by an increase in production of neutrophil (CXCL1-3) and monocyte (CCL2) chemoattractants. ⋯ The monocyte influx was not observed until 24 h post-mTBI, and these inflammatory cells predominantly entered the ipsilateral SAS and CVI, with a limited invasion of brain parenchyma. These observations indicate that the endothelium of pial microvessels responds to injury differently than that of intraparenchymal microvessels, which may be associated with the lack of astrocytic ensheathment of cerebrovascular endothelium in pial microvessels. These findings also suggest that neuroinflammation represents the potential therapeutic target in mTBI.
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Weight drop models in rodents have been used for several decades to advance our understanding of the pathophysiology of traumatic brain injury. Weight drop models have been used to replicate focal cerebral contusion as well as diffuse brain injury characterized by axonal damage. More recently, closed head injury models with free head rotation have been developed to model sports concussions, which feature functional disturbances in the absence of overt brain damage assessed by conventional imaging techniques. ⋯ In the second part, we describe the development of our own weight drop closed head injury model that features impact plus rapid downward head rotation, no structural brain injury, and long-term cognitive deficits in the case of multiple injuries. This rodent model was developed to reproduce key aspects of sports concussion so that a mechanistic understanding of how long-term cognitive deficits might develop will eventually follow. Such knowledge is hoped to impact athletes and war fighters and others who suffer concussive head injuries by leading to targeted therapies aimed at preventing cognitive and other neurological sequelae in these high-risk groups.
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Morphologic features of computed tomography (CT) scans of the brain can be used to estimate intracranial pressure (ICP) via an image-processing algorithm. Clinically, such estimations can be used to prognosticate outcomes and avoid placement of invasive intracranial monitors in certain patients with severe traumatic brain injury. Features on a CT scan that may correlate with measurements of low ICP are sought. ⋯ This method permits a noninvasive means of identifying patients who are low risk for having elevated ICP; by following Brain Trauma Foundation guidelines strictly such a patient may be subjected to an unnecessary, invasive procedure. This work is a promising pilot study that will need to be analyzed for a larger population.
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Acta Neurochir. Suppl. · Jan 2016
Early Changes in Brain Oxygen Tension May Predict Outcome Following Severe Traumatic Brain Injury.
We report on the change in brain oxygen tension (PbtO2) over the first 24 h of monitoring in a series of 25 patients with severe traumatic brain injury (TBI) and relate this to outcome. The trend in PbtO2 for the whole group was to increase with time (mean PbtO2 17.4 [1.75] vs 24.7 [1.60] mmHg, first- vs last-hour data, respectively; p = 0.002). However, a significant increase in PbtO2 occurred in only 17 patients (68 %), all surviving to intensive care unit discharge (p = 0.006). ⋯ The cumulative length of time that PbtO2 was <20 mmHg was not significantly different among these three groups. In conclusion, although for the cohort as a whole PbtO2 increased over the first 24 h, the individual trends of PbtO2 were related to outcome. There was a significant association between improving PbtO2 and survival, despite these patients having cumulative durations of hypoxia similar to those of non-survivors.