Abstract
Traumatic brain injury (TBI) is a major public health issue in the USA, with over 1.7 million cases per year. At least 5.3 million Americans currently live with ongoing disability due to TBI (Walker and Tesco 2013). The long-term consequences of TBI can be complex and progressive: 10–15% of individuals diagnosed with mild TBI continue to suffer from persistent symptoms, while as many as 50% of patients with moderate TBI experience long-term dysfunction (Bales et al. 2009; Walker and Tesco 2013). In addition to the post-injury development of cognitive deficits in attention, memory, and executive function (Bales et al. 2009), a chronic inflammatory state can persist in the brain for months, and even years, following TBI (Opii et al. 2007; Piao et al. 2013). Despite the prevalence of these chronic dysfunctions following TBI, elucidating the mechanisms that underlie these symptoms has proven challenging. It is understood that the post-injury processes of TBI involve a primary and a secondary phase of injury. Primary injury occurs during the initial insult, resulting from the displacement of the physical structures within the brain. Secondary injury occurs over time and involves an interdependent series of cellular dysfunctions that persist long after injury (Giza and Hovda 2001; Nilsson et al. 1996; Park et al. 2008; Walker and Tesco 2013; Werner and Engelhard 2007). Currently, it is not well understood how the acute mechanical injury of TBI, and subsequent secondary injury processes, can result in serious long-term dysfunctions that can persist for years.
Published Version
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