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The neural basis of flashback formation: the impact of viewing trauma

BACKGROUND: Psychological traumatic events, such as war or road traffic accidents, are widespread. A small but significant proportion of survivors develop post-traumatic stress disorder (PTSD). Distressing, sensory-based involuntary memories of trauma (henceforth ‘flashbacks’) are the hallmark sympt...

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Detalles Bibliográficos
Autores principales: Bourne, C., Mackay, C. E., Holmes, E. A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cambridge University Press 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3806039/
https://www.ncbi.nlm.nih.gov/pubmed/23171530
http://dx.doi.org/10.1017/S0033291712002358
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author Bourne, C.
Mackay, C. E.
Holmes, E. A.
author_facet Bourne, C.
Mackay, C. E.
Holmes, E. A.
author_sort Bourne, C.
collection PubMed
description BACKGROUND: Psychological traumatic events, such as war or road traffic accidents, are widespread. A small but significant proportion of survivors develop post-traumatic stress disorder (PTSD). Distressing, sensory-based involuntary memories of trauma (henceforth ‘flashbacks’) are the hallmark symptom of PTSD. Understanding the development of flashbacks may aid their prevention. This work is the first to combine the trauma film paradigm (as an experimental analogue for flashback development) with neuroimaging to investigate the neural basis of flashback aetiology. We investigated the hypothesis that involuntary recall of trauma (flashback) is determined during the original event encoding. METHOD: A total of 22 healthy volunteers viewed a traumatic film whilst undergoing functional magnetic resonance imaging (fMRI). They kept a 1-week diary to record flashbacks to specific film scenes. Using a novel prospective fMRI design, we compared brain activation for those film scenes that subsequently induced flashbacks with both non-traumatic control scenes and scenes with traumatic content that did not elicit flashbacks (‘potentials’). RESULTS: Encoding of scenes that later caused flashbacks was associated with widespread increases in activation, including in the amygdala, striatum, rostral anterior cingulate cortex, thalamus and ventral occipital cortex. The left inferior frontal gyrus and bilateral middle temporal gyrus also exhibited increased activation but only relative to ‘potentials’. Thus, these latter regions appeared to distinguish between traumatic content that subsequently flashed back and comparable content that did not. CONCLUSIONS: Results provide the first prospective evidence that the brain behaves differently whilst experiencing emotional events that will subsequently become involuntary memories – flashbacks. Understanding the neural basis of analogue flashback memory formation may aid the development of treatment interventions for this PTSD feature.
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spelling pubmed-38060392013-10-23 The neural basis of flashback formation: the impact of viewing trauma Bourne, C. Mackay, C. E. Holmes, E. A. Psychol Med Original Articles BACKGROUND: Psychological traumatic events, such as war or road traffic accidents, are widespread. A small but significant proportion of survivors develop post-traumatic stress disorder (PTSD). Distressing, sensory-based involuntary memories of trauma (henceforth ‘flashbacks’) are the hallmark symptom of PTSD. Understanding the development of flashbacks may aid their prevention. This work is the first to combine the trauma film paradigm (as an experimental analogue for flashback development) with neuroimaging to investigate the neural basis of flashback aetiology. We investigated the hypothesis that involuntary recall of trauma (flashback) is determined during the original event encoding. METHOD: A total of 22 healthy volunteers viewed a traumatic film whilst undergoing functional magnetic resonance imaging (fMRI). They kept a 1-week diary to record flashbacks to specific film scenes. Using a novel prospective fMRI design, we compared brain activation for those film scenes that subsequently induced flashbacks with both non-traumatic control scenes and scenes with traumatic content that did not elicit flashbacks (‘potentials’). RESULTS: Encoding of scenes that later caused flashbacks was associated with widespread increases in activation, including in the amygdala, striatum, rostral anterior cingulate cortex, thalamus and ventral occipital cortex. The left inferior frontal gyrus and bilateral middle temporal gyrus also exhibited increased activation but only relative to ‘potentials’. Thus, these latter regions appeared to distinguish between traumatic content that subsequently flashed back and comparable content that did not. CONCLUSIONS: Results provide the first prospective evidence that the brain behaves differently whilst experiencing emotional events that will subsequently become involuntary memories – flashbacks. Understanding the neural basis of analogue flashback memory formation may aid the development of treatment interventions for this PTSD feature. Cambridge University Press 2013-07 2012-10-18 /pmc/articles/PMC3806039/ /pubmed/23171530 http://dx.doi.org/10.1017/S0033291712002358 Text en © Cambridge University Press 2012 The online version of this article is published within an Open Access environment subject to the conditions of the Creative Commons Attribution licence <http://creativecommons.org/licenses/by/3.0/
spellingShingle Original Articles
Bourne, C.
Mackay, C. E.
Holmes, E. A.
The neural basis of flashback formation: the impact of viewing trauma
title The neural basis of flashback formation: the impact of viewing trauma
title_full The neural basis of flashback formation: the impact of viewing trauma
title_fullStr The neural basis of flashback formation: the impact of viewing trauma
title_full_unstemmed The neural basis of flashback formation: the impact of viewing trauma
title_short The neural basis of flashback formation: the impact of viewing trauma
title_sort neural basis of flashback formation: the impact of viewing trauma
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3806039/
https://www.ncbi.nlm.nih.gov/pubmed/23171530
http://dx.doi.org/10.1017/S0033291712002358
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