Tracking the silent epidemic and educating the public: CDC's traumatic brain injury-associated activities under the TBI Act of 1996 and the Children's Health Act of 2000

National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Atlanta, GA, USA.
Journal of Head Trauma Rehabilitation (Impact Factor: 2.92). 05/2005; 20(3):196-204. DOI: 10.1097/00001199-200505000-00003
Source: PubMed

ABSTRACT The Traumatic Brain Injury Act of 1996 and the Children's Health Act of 2000 authorized the Centers for Disease Control and Prevention to conduct several activities associated with traumatic brain injury. This article describes how the Centers for Disease Control and Prevention responded to the legislation in 2 key areas: traumatic brain injury surveillance, and education and awareness.

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    • "In spite of numerous studies of TBI, patient outcomes remain poor (Langlois et al. 2005). Amongst the different forms of TBI, penetrating traumatic brain injuries (PTBI) are associated with the worst outcomes and highest death rates and especially affect young people (Binder et al. 2005). "
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    ABSTRACT: Traumatic brain injury (TBI) is still the leading cause of disability in young adults worldwide. The major mechanisms - diffuse axonal injury, cerebral contusion, ischemic neurological damage, and intracranial hematomas have all been shown to be associated with mitochondrial dysfunction in some form. Mitochondrial dysfunction in TBI patients is an active area of research, and attempts to manipulate neuronal/astrocytic metabolism to improve outcomes have been met with limited translational success. Previously, several preclinical and clinical studies on TBI induced mitochondrial dysfunction have focused on opening of the mitochondrial permeability transition pore (PTP), consequent neurodegeneration and attempts to mitigate this degeneration with cyclosporine A (CsA) or analogous drugs, and have been unsuccessful. Recent insights into normal mitochondrial dynamics and into diseases such as inherited mitochondrial neuropathies, sepsis and organ failure could provide novel opportunities to develop mitochondria-based neuroprotective treatments that could improve severe TBI outcomes. This review summarizes those aspects of mitochondrial dysfunction underlying TBI pathology with special attention to models of penetrating traumatic brain injury, an epidemic in modern American society.
    Journal of Bioenergetics 10/2014; 47(1-2). DOI:10.1007/s10863-014-9589-1 · 3.21 Impact Factor
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    • "Traumatic brain injury is recognized as a critical public health problem worldwide, and it has been estimated that in the USA, a TBI occurs every 21 s [1] [2]. As the problems experienced by those suffering from TBI may not be visible (e.g., impairments in memory or cognition ), the disease is often referred to as a " silent epidemic " [3]. Depending on the location and type of brain injury, TBI can lead to a variety of comorbidities (Fig. 1). "
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    ABSTRACT: Traumatic brain injury (TBI) can cause a myriad of sequelae depending on its type, severity, and location of injured structures. These can include mood disorders, posttraumatic stress disorder and other anxiety disorders, personality disorders, aggressive disorders, cognitive changes, chronic pain, sleep problems, motor or sensory impairments, endocrine dysfunction, gastrointestinal disturbances, increased risk of infections, pulmonary disturbances, parkinsonism, posttraumatic epilepsy, or their combinations. The progression of individual pathologies leading to a given phenotype is variable, and some progress for months. Consequently, the different post-TBI phenotypes appear within different time windows. In parallel with morbidogenesis, spontaneous recovery occurs both in experimental models and in human TBI. A great challenge remains; how can we dissect the specific mechanisms that lead to the different endophenotypes, such as posttraumatic epileptogenesis, in order to identify treatment approaches that would not compromise recovery? This article is part of a Special Issue entitled “NEWroscience 2013”.
    Epilepsy & Behavior 09/2014; 38. DOI:10.1016/j.yebeh.2014.01.013 · 2.26 Impact Factor
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    • "I t is estimated that 1.5 million individuals suffer traumatic brain injury (TBI) each year in the United States (Langlois et al., 2005), which is associated with costly health problems and high mortality and morbidity in previously healthy populations. TBI involves primary and secondary injury cascades resulting in delayed neuron dysfunction, synapse loss, and cell death (Sullivan et al., 1998; Biegon et al., 2004; Scheff et al., 2005). "
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    ABSTRACT: Cortical contusion injury can result in the partial loss of ipsilateral CA3 neurons within 48 h, leading to a proportional reduction in the number of afferent fibers to CA1 stratum radiatum. While the loss of afferent input to CA1 exhibits a remarkable, albeit incomplete, recovery over the next few weeks, little is known about the functional status of presynaptic afferents during the depletion and recovery phases following injury. Here, we prepared hippocampal slices from adult Sprague Dawley rats at 2, 7, and 14 days after lateral cortical contusion injury and measured fiber volley (FV) amplitudes extracellularly in CA1 stratum radiatum. Field excitatory post-synaptic potentials (EPSPs) were also measured and plotted as a function of FV amplitude to assess relative synaptic strength of residual and/or regenerated synaptic contacts. At 2 days post-injury, FV amplitude and synaptic strength were markedly reduced in the ipsilateral, relative to the contralateral, hippocampus. FV amplitude in ipsilateral CA1 showed a complete recovery by 7 days, indicative of a post-injury sprouting response. Synaptic strength in ipsilateral CA1 also showed a dramatic recovery over this time; however, EPSP-to-FV curves remained slightly suppressed at both the 7 and 14 day time points. Despite these deficits, ipsilateral slices retained the capacity to express long-term potentiation, indicating that at least some mechanisms for synaptic plasticity remain intact, or are compensated for. These results are in agreement with anatomical evidence showing a profound deafferentation, followed by a remarkable re-enervation, of ipsilateral CA1 in the first few weeks after traumatic brain injury. Although plasticity mechanisms appear to remain intact, synaptic strength deficits in CA1 could limit information throughput in the hippocampus, leading to persistent memory dysfunction.
    Journal of neurotrauma 08/2009; 26(12):2269-78. DOI:10.1089/neu.2009.1029 · 3.71 Impact Factor
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