PTSD is classified as a trauma-related syndrome1 that can develop in individuals who have witnessed or experienced one or more events that involve serious or life-threatening injury or danger. Patients with this disorder persistently re-experience their traumatic events in various ways, including intrusive recollections, nightmares, flashbacks, and physiological reactivity to trauma-related reminders. They often make intense efforts to avoid thinking about the traumatic experience, frequently by utilizing maladaptive coping strategies (including drugs or alcohol), and they may avoid associating with people or going to places that remind them of the trauma. Furthermore, individuals with PTSD can experience symptoms of hyperarousal, such as a heightened startle response, hypervigilance, heightened irritability with others, and difficulties sleeping or concentrating. Alterations in mood can take the form of extreme negative emotions, such as irritability or guilt, feelings of alienation, emotional numbing, and diminished interest in activities they previously enjoyed.
Current models of the neural basis of PTSD have relied prominently on evidence from fMRI aiming to examine alterations in brain function at rest or during the performance of tasks. The most prevalent method in this line of research involves symptom provocation through the presentation of individually tailored or basic trauma-related cues. However, many studies have also examined possible neural variations in the processing of both nonspecific emotional stimuli and neutral stimuli.
This chapter reviews recent research of neural mechanisms implicated in PT SD that have been associated with behavioral, cognitive, and emotional symptomatology ranging from impaired memory to exaggerated response to threat. Specifically examined are studies conducted in the past decade, from 2004 to 2014, considering impairments in fear processing, emotional regulation, memory, and attention, as well as the effects of psychological and pharmacological treatments. Notable outcomes include hyperactivity of the dACC and hypoacti- vation in the vmPFC during fear processing,2 hyperactivity in the amygdala3-11 and insula4,7,8,12,13 in emotional regulation, and widespread alterations in neural networks associated with various memory faculties.6,14,15 Promising findings are emerging that provide neurological support for the efficacy of psychological treatments, including cognitive trauma therapy (CTT),16 as well as possible explanations for poor response to the most commonly prescribed psychological treatment for PTSD, cognitive behavioral therapy (CBT).17 Because PTSD is a chronic condition of long duration, especially when left untreated (Chapter 11), improvements in treatment efficacy will hopefully change the trajectory of illness in a subset of people with PTSD.