Identification of clinical, radiological, and laboratory variables as well as new biomarkers independently associated with cognitive outcome remains an important challenge for further work involving severe TBI patients. With an incidence rate of 150–300 per 100,000 per year of hospitalized selleckchem and fatal traumatic brain injuries (TBIs) in Europe – and higher in other parts of the world – head trauma
is likely to be the most probable aetiology of cognitive disorders due to a general medical condition (Bales, Wagner, Kline, & Dixon, 2009; Markowitsch & Staniloiu, 2012). TBI patients frequently suffer from long-term sequelae, which have personal, family, and social impact (Diaz et al., 2012; Marsh & Kersel, 2006). These sequelae are highly heterogeneous, comprising cognitive deficits, psychiatric disorders, motor and sensory impairments, epilepsy, and others (Diaz et al., 2012; Ietswaart, Milders, Crawford, Currie, & Scott, 2008; Schwarzbold et al., 2010). Cognitive deficits, however, stand out due to its elevated prevalence and impact in daily life (Larson, Perlstein, Demery, & Stigge-Kaufman, 2006).
Studies on moderate and severe TBI have found a significant impairment of cognition in up to 50% of patients (Kersel, Marsh, Havill, & Sleigh, 2001; Vakil, 2005). Studies on mild TBI have revealed SP600125 order more variable results, with cognitive changes affecting less than 1%–20% of patients (Arciniegas, Anderson, Topkoff, & McAllister, 2005; Carroll et al., 2004). TBI can affect several domains of cognition, in particular attention, working, and long-term memory, processing speed, and executive functions (Mathias & Wheaton, 2007). Although patients tend to experience some improvement with time, cognitive Vasopressin Receptor deficits frequently have a chronic evolution particularly after severe TBI, being present many years after trauma (Hoofien, Gilboa, Vakil, & Donovick, 2001; Ruttan, Martin, Liu, Colella, & Green, 2008). Moreover, cognitive deficits have been associated with poor psychosocial function, as well as behavioural and emotional problems (Chamelian & Feinstein, 2006; Mazaux et al.,
1997). Despite its importance, the mechanisms and determinants of cognitive impairment following TBI are poorly understood. From a neuroanatomical point of view, it is reasonable to consider that damage in a specific brain region may impair its function with regard to cognition. For example, damage to the dorsolateral prefrontal is likely to affect executive function and orbitofrontal damage seems to affect decision making (Bechara, Damasio, & Damasio, 2000). Temporal lesions may affect declarative memory (Markowitsch & Staniloiu, 2012). However, such neuroanatomical explanations are of limited value in the case of TBI, as TBI typically involves damage of a diffuse nature or in areas remote to the impact (Sidaros et al., 2008).