Functional Neuroanatomy of Emotion and Its Regulation in PTSD

Abstract

Posttraumatic stress disorder (PTSD) is a devastating disorder, linked to profound mental, physical, occupational, and functional impairment. In addition, it is a highly complex disorder, characterized by symptom heterogeneity across multiple domains. Nevertheless, emotion dysregulation arising from the exaggerated response to threat or from the inability to regulate negative emotional states plays a defining role in the pathophysiology of PTSD. In order to improve our understanding of how emotion dysregulation manifests in this illness, functional neuroimaging research over the past 20 years provides great insight into underlying neuroanatomy of each component of emotion dysregulation in the context of PTSD. While prior reviews exist on the topic of neuroimaging findings in PTSD, the present review synthesizes that work through the lens of emotion and its regulation. Studies that employed tasks of emotional responding and symptom provocation, implicit regulation (e.g., emotional Stroop and interference), explicit regulation (e.g., cognitive reappraisal), and fear conditioning/extinction were reviewed. Findings demonstrate that emotion dysregulation in PTSD arises from complications within a large neurocircuitry involving the amygdala, insula, hippocampus, anterior cingulate cortex, and prefrontal cortex. Although an exaggerated response in the amygdala and insula to negative emotional triggers is pervasive, PTSD is also marked by deficient appraisal, resolution, and management of negative emotional states subserved by the anterior cingulate cortex and prefrontal cortex during regulation. These findings further support the importance of studying emotion-regulation deficits in tandem with exaggerated symptom provocation in order to better understand the constellation of symptoms present in those with PTSD.

Concurrent Mild Traumatic Brain Injury and Posttraumatic Stress Disorder Is Associated With Elevated Tau Concentrations in Peripheral Blood Plasma

“…Higher concentrations of tau following an mTBI in service members and veterans with PTSD may also relate to the observed reductions in overall neuronal volume (Averill et al, 2017), specifically in the volume and function of the hypothalamus, prefrontal cortex, and amygdala (Fitzgerald, DiGangi, & Phan, 2018). Therefore, it may be that the increased tau concentrations observed following TBIs increases vulnerability of neurons and may relate to a higher risk for PTSD and other chronic symptoms.…”

Noradrenergic α1-Adrenoceptor Actions in the Primate Dorsolateral Prefrontal Cortex

“…Although the initial focus of prazosin research was on reducing nightmares, data also show reduced daytime PTSD symptoms, especially in those taking higher doses or longeracting treatments (Taylor et al, 2006;Ruff et al, 2012;Koola et al, 2014;Smith and Koola, 2016). Because PTSD symptomology is related to PFC dysfunction (Aupperle et al, 2012;Kühn and Gallinat, 2013;Fitzgerald et al, 2018), including weaker dlPFC regulation of emotional response (Aupperle et al, 2012), the cur- Figure 9. Schematic illustration of ␣1-AR actions in the primate dlPFC.…”

“…Treatment of PFC disorders often involves medications that have ␣1-AR-blocking actions. For example, PTSD symptoms involve impaired PFC regulation of emotion (Fitzgerald et al, 2018) and the ␣1-AR antagonist prazosin is in widespread use for the treatment of PTSD in veterans, active duty soldiers, and civilians (for review, see Arnsten et al, 2015). ␣1-AR blockade is also a common characteristic of atypical antipsychotic drug actions (Baldessarini et al, 1992;Bymaster et al, 1996) used to treat mental disorders that involve dysfunction of the dorsolateral PFC (dlPFC; Glantz and Lewis, 2000).…”

A comparison of physical comorbidities in patients with posttraumatic stress disorder developed after a terrorist attack or other traumatic event

“…Various neuroanatomical structures are involved in the pathogenesis of posttraumatic stress disorder (PTSD), but only a subgroup of individuals who experience trauma develop the disorder. Genetic studies show that memory disorders associated with trauma are genetically inheritable through protein transmission (Chitrala, Nagarkatti, & Nagarkatti, ; Fitzgerald, DiGangi, & Phan, ). Familiarity and early traumatic experiences are considered to be vulnerability factors (Chitrala et al, ; Fitzgerald et al, ; Szeszko, Lehrner, & Yehuda, ).…”

“…that memory disorders associated with trauma are genetically inheritable through protein transmission (Chitrala, Nagarkatti, & Nagarkatti, 2016;Fitzgerald, DiGangi, & Phan, 2018). Familiarity and early traumatic experiences are considered to be vulnerability factors (Chitrala et al, 2016;Fitzgerald et al, 2018;Szeszko, Lehrner, & Yehuda, 2018). Other variables, including race, and ethnocultural and social background, influence the onset and symptom patterns of the disorder (Roberts, Gilman, Breslau, Breslau, & Koenen, 2011).…”