Brain activation related to fear-associated learning during early post-trauma period

Pain and traumatic stress symptoms occur immediately after injury caused by a traumatic event, severities of acute symptoms are associated with risk of development of post-traumatic stress disorder (PTSD) and chronic pain following injury. Deficits in fear-associated learning may contribute to the d...

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Bibliographic Details
Main Author: Walkosz, Maciej Jan
Other Authors: Wang, Xin
Language:en_US
Published: 2018
Subjects:
Online Access:https://hdl.handle.net/2144/31289
Description
Summary:Pain and traumatic stress symptoms occur immediately after injury caused by a traumatic event, severities of acute symptoms are associated with risk of development of post-traumatic stress disorder (PTSD) and chronic pain following injury. Deficits in fear-associated learning may contribute to the development of these disorders. A fear associated learning task (FALT) has revealed altered brain activations in patients with PTSD and chronic pain; however, FALT brain activations have not been studied in the early post-trauma period. This study examined FALT brain activation within weeks after traumatic injury to investigate this issue. Within 2 weeks after a traumatic injury, 51 trauma survivors underwent a FALT, comprised of acquisition, extinction, and extinction recall phases during functional magnetic resonance imaging (fMRI). Symptoms were assessed with the PTSD Check List (PCL), Acute Stress Disorder Questionnaire (ASDQ), Pain Anxiety Symptom Scale (PASS20), Pain Catastrophizing Scale (PCS), and the National Pain Score (NPS). Contrast between conditioned stimuli that were (CS+) or were not (CS-) paired with an aversive stimulus revealed activations in the medial-prefrontal (mPFC)/dorsal anterior cingulate (dACC), right insula, and right dorsolateral prefrontal cortices (dlPFC) during acquisition; bilateral sensorimotor, right dlPFC and superior lateral-occipital/superior parietal cortices during extinction; left insular and right lateral occipital cortices during recall. Negative correlations were significant between mPFC/dACC activation during acquisition and both PASS20 and PCS scores. The results suggest emotion regulatory regions are associated with pain stress symptoms within weeks following trauma. These deficits may contribute to development of symptoms of both PTSD and chronic pain. Further studies will examine the relationships between FALT activations and other symptoms.