Finally, the pattern of memory impairments in PTSD demonstrates that PTSD is less associated with problems
with retention, a process mediated by the hippocampus, and much more associated with problems with acquisition and learning, processes more associated with prefrontal system dysfunction.57 There are a number of studies further elucidating the impact of PTSD on the prefrontal cortex (PFC). Stress exposure inhibitor Navitoclax releases glucocorticoids and catecholamines in the Inhibitors,research,lifescience,medical PFC,58, 59 which impair functions mediated by the PFC including working memory, executive function, and the regulation of behavior and emotion.60 Deficits in these areas are also associated with PTSD.5-8, 12, 61-65 Several magnetic resonance imaging (MRI) studies have reported decreased frontal cortex volume in PTSD66-68 and decreased volume in medial prefrontal regions, namely
the anterior cingulate and subcallosal cortex.69-72 A functional imaging study revealed underactivation of the frontal Inhibitors,research,lifescience,medical cortex during a paired-associates learning task in patients with PTSD.73 Particularly in children, findings of Inhibitors,research,lifescience,medical frontal dysfunction are more robust than findings of hippocampal dysfunction.66, 67, 74 Cognitive risk and protective factors in PTSD PTSD is a unique psychiatric disorder in that it is the result of a traumatic Inhibitors,research,lifescience,medical life event. As such, it would be assumed that all neuropsychological and neurobiological abnormalities associated with PTSD are also caused by that event. However, prospective and twin studies offer compelling support, for the model that, pre-existing memory and learning deficits, and related hippocampal dysfunction, increase one’s vulnerability to developing PTSD. Gibertson et al75 studied monozygotic twin pairs who were discordant for combat exposure and found that the identical co-twins of combat veterans with PTSD, who had not, experienced combat exposure or PTSD themselves, showed similar deficits in verbal memory. In addition, both combat, veterans with PTSD and Inhibitors,research,lifescience,medical their co-twins exhibited smaller hippocampi,76
suggesting that a smaller hippocampus and memory impairments in PTSD represent a pre-existing, genetic factor. Further support for this framework Batimastat has come from a recent longitudinal study, where researchers examined the extent, to which poorer neurocognitive functioning prior to a major natural disaster predicted the development, of PTSD symptoms.77 Development of PTSD symptoms was inversely associated with word recall, as well as working memory, www.selleckchem.com/products/Tipifarnib(R115777).html processing speed, and verbal intelligence performance assessed pretrauma. Conclusions It is likely that memory dysfunction is both a pre-existing risk factor for the development of PTSD as well as s a consequence of the disorder.