Neural, Psychophysiological, and Behavioral Markers of Fear Processing in PTSD: A Review of the Literature

Abstract

As presently defined, post-traumatic stress disorder (PTSD) is an amalgam of symptoms falling into: re-experiencing of the trauma, avoidance of reminders of it, emotional numbing and hyperarousal. PTSD has a well-known proximate cause, commonly occurring after a life-threatening event that induces a response of intense fear, horror, and helplessness. Much of the advancement in understanding of the neurobiology of PTSD has emerged from conceptualizing the disorder as one that involves substantial dysfunction in fear processing. This article reviews recent knowledge of fear processing markers in PTSD. A systematic search was performed of reports within the specific three-year publication time period of January 2010 to December 2012. We identified a total of 31 studies reporting fear processing markers in PTSD. We further categorized them according to the following classification: (1) neural-activation markers (n=10), (2) psychophysiological markers (n=14), and (3) behavioral markers (n=7). Across most studies reviewed here, significant differences between individuals with PTSD and healthy controls were shown. Methodological, theoretical and clinical implications were discussed.

The basolateral amygdala determines the effects of fear memory on sleep in an animal model of PTSD

“…Estimates for victims of rape are up to 80% (Javidi and Yadollahie 2012). Because PTSD is viewed as a disorder of the brain’s fear system (Shvil et al 2013), experimental fear conditioning is one of our most important research models related to PTSD as well as to other anxiety disorders. However, it is important to note that although fear conditioning plays a role in psychopathology, it normally underlies adaptive behavior that extinguishes when the fear-inducing stimulus is withdrawn (Breslau et al 1998).…”

“…PTSD is viewed as a disorder of the brain’s fear system (Shvil et al 2013). As such, experimental fear conditioning is one of our most important research models related to PTSD, as well as of other anxiety disorders (Davis 1990; Davis 1992 ; Foa et al 1992; Grillon et al 1996; Shalev et al 1992).…”

Sex differences in extinction recall in posttraumatic stress disorder: A pilot fMRI study

“…Fear conditioning and extinction paradigms have proven extremely valuable in revealing underlying circuitries of anxiety pathology and for understanding the development and maintenance of PTSD (Pitman et al, 2012; Shvil, Rusch, Sullivan, & Neria, 2013). Recent evidence specifically associates PTSD with impaired capacity to recall extinction memory, demonstrated by increased skin conductance levels to previously extinguished conditioned stimuli (Milad, Pitman, et al, 2009).…”

On the Road to Translation for PTSD Treatment: Theoretical and Practical Considerations of the Use of Human Models of Conditioned Fear for Drug Development

“…In a recent comparative study across subjects reporting primarily PTSD, general anxiety, or depression symptoms, extinction deficits were only observed in subjects with PTSD (Acheson et al 2015b), suggesting that poor extinction is specifically related to trauma-related symptoms as opposed to general symptoms of low mood or ruminative anxiety. PTSD patients also exhibit functional and structural abnormalities in the fear extinction network including the hippocampus, amygdala, and frontal cortex [for review see Acheson et al (2012a), Shvil et al (2013)]. During extinction learning, PTSD is associated with reduced activation of the ventral medial prefrontal cortex and increased activation of the amygdala and dorsal anterior cingulate, suggesting reduced inhibitory modulation by cortical inputs to fear circuits (Shvil et al 2013).…”

“…PTSD patients also exhibit functional and structural abnormalities in the fear extinction network including the hippocampus, amygdala, and frontal cortex [for review see Acheson et al (2012a), Shvil et al (2013)]. During extinction learning, PTSD is associated with reduced activation of the ventral medial prefrontal cortex and increased activation of the amygdala and dorsal anterior cingulate, suggesting reduced inhibitory modulation by cortical inputs to fear circuits (Shvil et al 2013). Twin studies suggest that poor extinction observed in PTSD is associated with symptom state, rather than a vulnerability trait for PTSD (but see Lommen et al 2013;Milad et al 2008), suggesting it could play a role in maintenance of PTSD symptoms once they emerge.…”