Predicting Posttraumatic Stress Disorder: From Circuits to Communities

Neurocircuitry of Personality Traits and Intent in Decision-Making

“…Additional evidence supporting the idea of fear-based impulsiveness and lack of consideration for future consequences linked to neuroticism can be found in the observation of acquired brain injury patients, where damage to the OFC is linked to behavior guided by immediate outcomes [6,[30][31][32]. As seen above, the mPFC can also contribute to the aspect of neglecting to reason about future consequences [18,19,24], although not necessarily implying that aggressivity would be a definite trait.…”

Neurobiological Features of Posttraumatic Stress Disorder (PTSD) and Their Role in Understanding Adaptive Behavior and Stress Resilience

“…In a recent narrative review on neuroanatomical components involved in emotional regulation in PTSD, Fitzgerald and colleagues (2018) described an overall under-engagement of prefrontal areas during emotional processing in individuals with PTSD [ 15 ]. It is known that low levels of norepinephrine in the brain binding to norepinephrine alpha1 receptors can increase the activation of prefrontal neurons, while higher concentrations have an adverse effect of lowering the activation of those neurons; in other words, low levels of stress can be helpful for information processing, while high levels can be detrimental for those processes, leading to hypoactivation in the PFC [ 22 ]. This level of hypoactivation can also be observed in other disorders of the anxiety spectrum [ 23 ].…”

“…With the purpose of understanding the role of the AM in behavior, a variety of studies have been performed since its discovery, from lesion-based to pharmacological manipulation, with the results reinforcing the AM’s role in social behavior and emotionally driven learning processes [ 48 ]. Hyperactivation of the AM ( Figure 1 ) has been associated with excessive fear learning in PTSD individuals during stimulation, fear conditioning, extinction learning, and recall [ 12 , 13 , 14 , 15 , 22 ]. These aptitudes of the AM and the difficulties that individuals with PTSD experience with such emotional and behavioral processes are most likely the result of the lack of reciprocal inhibition, as discussed above, in the circuitry between the AM, the mPFC, and the saCC [ 7 ].…”

“…Decreased HPC and PHG GMV, and decreased volume in all temporal gyri ( Figure 1 ), have been abundantly reported in studies [ 7 , 11 , 12 , 27 , 31 , 32 , 33 ]. One of the sources of these changes is probably the interrupted neurogenesis observed in hippocampal neurons under chronic stress conditions, modifying behavior and leading to more generalized responses to threats, instead of analysis of specific events and possible hazards [ 22 ], which has been observed in exaggerated responses to triggers in individuals with PTSD, as well as in abnormal behavior in other stress-related mental health disorders.…”