Journal of neurotrauma
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Journal of neurotrauma · May 2012
Continuous monitoring of the Monro-Kellie doctrine: is it possible?
The Monro-Kellie doctrine describes the principle of homeostatic intracerebral volume regulation, which stipulates that the total volume of the parenchyma, cerebrospinal fluid, and blood remains constant. Hypothetically, a slow shift (e.g., brain edema development) in the irregular vasomotion-driven exchanges of these compartmental volumes may lead to increased intracranial hypertension. To evaluate this paradigm in a clinical setting and measure the processes involved in the regulation of systemic intracranial volume, we quantified cerebral blood flow velocity (CBFv) in the middle cerebral artery, arterial blood pressure (ABP), and intracranial pressure (ICP), in 238 brain-injured subjects. ⋯ The mortality rate is 5% when ICC is less than 0, and 43% when above 0.7. ICC above 0.7 was associated with terminally elevated ICP (chi-square p=0.026). We propose that the Monro-Kellie doctrine can be monitored in real time to illustrate the state of intracranial volume regulation.
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Journal of neurotrauma · May 2012
Comparative StudyDifferential effects of voluntary and forced exercise on stress responses after traumatic brain injury.
Voluntary exercise increases levels of brain-derived neurotrophic factor (BDNF) after traumatic brain injury (TBI) when it occurs during a delayed time window. In contrast, acute post-TBI exercise does not increase BDNF. It is well known that increases in glucocorticoids suppress levels of BDNF. ⋯ Forced exercise did not increase levels of BDNF in any group. It did, however, decrease hippocampal glucocorticoid receptors in the control group. The results suggest that exercise regimens with strong stress responses may not be beneficial during the early post-injury period.
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Journal of neurotrauma · May 2012
Trends in the incidence of physician-diagnosed mild traumatic brain injury among active duty U.S. military personnel between 1997 and 2007.
Mild traumatic brain injury (mTBI) has been described as the most common form of traumatic brain injury within military populations; however, few epidemiologic studies have examined incidence rates for mTBI in this population. The objective of this study was to examine trends in the incidence of mTBI among active-duty U. S. service members between 1997 and 2007. ⋯ Overall, for 2006-2007 versus 1997-2005, the rate ratio was 1.61 (95% CI 1.58,1.65). The greatest increase in the rate of mTBI was observed among those serving in Iraq, who experienced a 38.4% (95% CI 35.4%,41.1%) annual increase in new cases. The observed increase in the incidence of mTBI in this population has significant policy implications in terms of allocating appropriate health care resources.
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Journal of neurotrauma · May 2012
Comparative StudyStatins improve outcome in murine models of intracranial hemorrhage and traumatic brain injury: a translational approach.
Traumatic brain injury (TBI) and intracerebral hemorrhage (ICH) are leading causes of neurological mortality and disability in the U. S. However, therapeutic options are limited and clinical management remains largely supportive. ⋯ Administration of rosuvastatin following TBI was also associated with downregulation of inflammatory gene expression in the brain. Following ICH, treatment with simvastatin 1 mg/kg was associated with the greatest improvement in functional outcomes, an effect that was independent of hemorrhage volume. Clinically relevant models of acute brain injury may be used to define variables such as optimal statin and dosing paradigms to facilitate the rational design of pilot clinical trials.
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Journal of neurotrauma · May 2012
Preventing flow-metabolism uncoupling acutely reduces axonal injury after traumatic brain injury.
We have previously presented evidence that the development of secondary traumatic axonal injury is related to the degree of local cerebral blood flow (LCBF) and flow-metabolism uncoupling. We have now tested the hypothesis that augmenting LCBF in the acute stages after brain injury prevents further axonal injury. Data were acquired from rats with or without acetazolamide (ACZ) that was administered immediately following controlled cortical impact injury to increase cortical LCBF. ⋯ Furthermore, early LCBF augmentation prevented the injury-associated increase in the number of stained axons from 3-24 h. Additional robust stereological analysis of impaired axonal transport and neurofilament compaction in the corpus callosum and cingulum underlying the injury core confirmed the amelioration of β-APP axon density, and showed a trend, but no significant effect, on RMO14-positive axons. These data underline the importance of maintaining flow-metabolism coupling immediately after injury in order to prevent further axonal injury, in at least one population of injured axons.