Traumatic brain injury (TBI) is a leading cause of death and disability among U.S. adolescents. The authors sought to determine causes and trends for TBI-related hospitalizations in the U.S. adolescent population (10-19 years). The authors identified common causes and trends of adolescent TBI, overall and within two-year age categories, using hospitalization data from 2005 to 2009 in the Nationwide Inpatient Sample. The leading cause of adolescent TBI overall was motor vehicle occupant accidents (35%), which are also the leading cause in 14-15, 16-17, and 18-19 year age groups. Falls were the cause of most TBI in the 10-11 year (23%) and 12-13 year (20%) groups. For both unintentional and intentional mechanisms of injury, there was evidence of increasing hospitalizations with increasing age. From 2005 to 2009, the overall annual incidence of adolescent TBI hospitalizations decreased 21% from an estimated 75.5 to 59.3 per 100,000 (p<0.001). These rates declined for mild, moderate, and severe TBI, and decreased for two-year age groups, except 18-19 year olds. For TBI attributable to motor vehicle occupants, rates declined 27% from 27.6 to 20.2 per 100,000 (p<0.001). Motor vehicle occupant injuries account for 42% of in-hospital mortality in adolescent TBI; however, firearms are the most lethal mechanism with 46% proportional mortality among victims of firearm-related TBI. Rates of adolescent TBI-related hospitalizations have decreased overall. Motor vehicle accidents and firearms were identified as leading causes of injury and mortality for adolescent TBI and represent potential targets for intervention. Keywords: [Epidemiology], [Traumatic Brain Injury], [Pediatric Brain Injury], [Head Trauma].
"and 850.0e854.19, as recommended by the CDC])  . Within this group, we identified those whose records included data for sex, in-hospital mortality status, external mechanism of injury, severity of head injury, comorbidities, and insurance type, as well as hospital characteristics such as region, location, and teaching status for study inclusion. "
"Moreover, individuals with a history of TBI are more likely to receive welfare or disability payments and to develop neurologic disorders that are disabling in their own right (Ma et al., 2014)— for example, Alzheimer's disease (Fleminger et al., 2003). The incidence of TBI is particularly high in younger age groups, with motor vehicle accidents being the leading cause (Asemota et al., 2013). The direct costs of TBI have been estimated at $13.1 billion per year (in 2013) in the United States (Ma et al., 2014); additionally, $64.7 billion per year are lost through missed work and lost productivity, and total medical costs range from $63.4 to $79.1 billion per year (Ma et al., 2014). "
[Show abstract][Hide abstract] ABSTRACT: Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Despite improvements in acute intensive care, there are currently no specific therapies to ameliorate the effects of TBI. Successful therapeutic strategies for TBI should target multiple pathophysiologic mechanisms that occur at different stages of brain injury. The kallikrein-kinin system is a promising therapeutic target for TBI as it mediates key pathologic events of traumatic brain damage, such as edema formation, inflammation, and thrombosis. Selective and specific kinin receptor antagonists and inhibitors of plasma kallikrein and coagulation factor XII have been developed, and have already shown therapeutic efficacy in animal models of stroke and TBI. However, conflicting preclinical evaluation, as well as limited and inconclusive data from clinical trials in TBI, suggests that caution should be taken before transferring observations made in animals to humans. This review summarizes current evidence on the pathologic significance of the kallikrein-kinin system during TBI in animal models and, where available, the experimental findings are compared with human data.
"The majority of TBI cases can be attributed to motor vehicle accidents, motorcycle accidents, bicycle accidents, and pedestrian injuries . Survivors are often are left with debilitating neurological deficits after injury [121, 122], so in addition to the enormous personal burden to victims and their families, the financial impact for the community in terms of hospitalization, treatment, rehabilitation, and specialized care runs into the billions of dollars annually. "
[Show abstract][Hide abstract] ABSTRACT: Classical inflammation is a well-characterized secondary response to many acute disorders of the central nervous system. However, in recent years, the role of neurogenic inflammation in the pathogenesis of neurological diseases has gained increasing attention, with a particular focus on its effects on modulation of the blood-brain barrier BBB. The neuropeptide substance P has been shown to increase blood-brain barrier permeability following acute injury to the brain and is associated with marked cerebral edema. Its release has also been shown to modulate classical inflammation. Accordingly, blocking substance P NK1 receptors may provide a novel alternative treatment to ameliorate the deleterious effects of neurogenic inflammation in the central nervous system. The purpose of this paper is to provide an overview of the role of substance P and neurogenic inflammation in acute injury to the central nervous system following traumatic brain injury, spinal cord injury, stroke, and meningitis.
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