Frontiers in neurology
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Frontiers in neurology · Jan 2012
Intracerebral hemorrhage: toward physiological imaging of hemorrhage risk in acute and chronic bleeding.
Despite improvements in management and prevention of intracerebral hemorrhage (ICH), there has been little improvement in mortality over the last 30 years. Hematoma expansion, primarily during the first few hours is highly predictive of neurological deterioration, poor functional outcome, and mortality. For each 10% increase in ICH size, there is a 5% increase in mortality and an additional 16% chance of poorer functional outcome. ⋯ However, clinical efficacy has yet to be proven. There is compelling evidence that cerebral amyloid angiopathy (CAA) may precede the radiographic evidence of vascular disease and as such contribute to microbleeding. The interplay between microbleeding, CAA, CTA Spot Sign and genetic composition (ApoE genotype) may be crucial in developing a risk model for ICH.
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Blast-induced traumatic brain injury (TBI) has been a major cause of morbidity and mortality in the conflicts in Iraq and Afghanistan. How the primary blast wave affects the brain is not well understood. In particular, it is unclear whether blast injures the brain through mechanisms similar to those found in non-blast closed impact injuries (nbTBI). ⋯ Unlike the findings in nbTBI animal models, levels of the β-secretase, β-site APP cleaving enzyme 1, and the γ-secretase component presenilin-1 were unchanged following blast exposure. These studies have implications for understanding the nature of blast injury to the brain. They also suggest that strategies aimed at lowering Aβ production may not be effective for treating acute blast injury to the brain.
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Recent studies have shown an increase in the frequency of traumatic brain injuries related to blast exposure. However, the mechanisms that cause blast neurotrauma are unknown. Blast neurotrauma research using computational models has been one method to elucidate that response of the brain in blast, and to identify possible mechanical correlates of injury. ⋯ Intracranial pressures ranged from 80 to 390 kPa as a result of the blast and were notably lower than the shock tube reflected pressures of 300-2830 kPa, indicating pressure attenuation by the skull up to a factor of 8.4. Peak head accelerations were measured from 385 to 3845 G's and were well correlated with peak incident overpressure (R(2) = 0.90). One SD corridors for the surface pressure, intracranial pressure (ICP), and head acceleration are presented to provide experimental data for computer model validation.
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Frontiers in neurology · Jan 2012
Deep brain stimulation and cognitive decline in Parkinson's disease: a clinical review.
Parkinson's disease is a common and often debilitating disorder, with a growing prevalence accompanying global population aging. Current drug therapy is not satisfactory enough for many patients, especially after a few years of symptom progression. This is mainly due to the motor complications that frequently emerge as disease progresses. ⋯ On the other hand it has been observed that certain aspects of cognitive performance may decline after DBS, namely when the therapeutic target is the widely used subthalamic nucleus. These are important pieces of information for patients, their families, and health care professionals. This manuscript reviews these aspects and their clinical implications.
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Frontiers in neurology · Jan 2012
A Multiscale Approach to Blast Neurotrauma Modeling: Part II: Methodology for Inducing Blast Injury to in vitro Models.
Due to the prominent role of improvised explosive devices (IEDs) in wounding patterns of U. S. war-fighters in Iraq and Afghanistan, blast injury has risen to a new level of importance and is recognized to be a major cause of injuries to the brain. However, an injury risk-function for microscopic, macroscopic, behavioral, and neurological deficits has yet to be defined. ⋯ We have also injured a simplified in vitro model of the blood-brain barrier, which exhibits disrupted integrity immediately following exposure to 581 ± 10.0 kPa peak overpressure with a 1.067 ± 0.006-ms duration and 222 ± 6.9 kPa-ms impulse in-air. To better prevent and treat bTBI, both the initiating biomechanics and the ensuing pathobiology must be understood in greater detail. A well-characterized, in vitro model of bTBI, in conjunction with animal models, will be a powerful tool for developing strategies to mitigate the risks of bTBI.