A Model for the Flash Technique Based on Working Memory and Neuroscience Research

2021 ◽  
pp. EMDR-D-20-00048
Author(s):  
Sik-Lam Wong

This article presents a model for understanding how the Flash Technique (FT) may work in the brain and provides potential avenues for experimental confirmation. In the FT, the client reminds himself of a traumatic memory without dwelling on it but instead focuses on a positive engaging focus and then blinks his eyes as prompted by the therapist. Clients have reported signs of memory reconsolidation, for example, the memory getting blurry and a reduction in emotional response. While the originators of FT did not offer a detailed mechanism for FT, this article proposes that during the blinking, the patient’s periaqueductal gray (PAG) takes over, senses the reminder of the traumatic memory and reflexively triggers the amygdala. As part of a system suggested by Porges (2009) for neuroception, the PAG works reflexively to assess danger without going through the conscious brain. Recent fMRI data show that for posttraumatic stress disorder (PTSD) patients, there is enhanced connectivity from the amygdala to the left hippocampus. As a result, triggering the amygdala may, in turn, activate the left hippocampus, which may then provide a brief access to the traumatic memory. Given the brief access, there is not enough time for the amygdala to go into overactivation. The client remains calm while accessing the traumatic memory, thus setting up the prediction error necessary for memory reconsolidation. This process is repeated many times during blinking in FT to allow memory reconsolidation to proceed, in some cases, to completion. This model is open to experimental confirmation.

2021 ◽  
Vol 15 (3) ◽  
pp. 174-184
Author(s):  
Sik-Lam Wong

Research has shown that the Flash Technique (FT) appears to reduce memory-related disturbance and may reduce symptoms of posttraumatic stress disorder. This paper discusses the connections between FT and eye movement desensitization and reprocessing (EMDR) therapy. In FT, clients remind themselves of a traumatic memory without dwelling on it and focus instead on a positive engaging focus and then blink their eyes when prompted. This paper summarizes numerous models describing how the brain processes traumatic material and presents a model for how FT may work in the brain. It proposes that during the blinking, the patient's periaqueductal gray (PAG) may take over, sensing the reminder of the traumatic memory and reflexively triggering the amygdala. In Porges's neuroception model, the PAG assesses danger without going through the conscious brain. Recent fMRI data show that for patients with posttraumatic stress disorder, there is enhanced connectivity from the amygdala to the left hippocampus. Thus, triggering the amygdala may, in turn, activate the left hippocampus, which may then provide a brief access to the traumatic memory. Given the brief access, there is insufficient time for the amygdala to go into overactivation. The client remains calm while accessing the traumatic memory, thus setting up the prediction error necessary for possible memory reconsolidation. This process is repeated during blinking in FT allowing memory reconsolidation to proceed. This model requires experimental confirmation.


Author(s):  
Jun Inoue ◽  
Kayako Matsuo ◽  
Toshiki Iwabuchi ◽  
Yasuo Takehara ◽  
Hidenori Yamasue

Abstract To characterize the brain responses to traumatic memories in posttraumatic stress disorder (PTSD), we conducted task-employed functional magnetic resonance imaging and, in the process, devised a simple but innovative approach—correlation computation between task conditions. A script-driven imagery task was used to compare the responses to a script of the patients’ own traumatic memories and that of tooth brushing as a daily activity and to evaluate how eye movement desensitization and reprocessing (EMDR), an established therapy for PTSD, resolved the alterations in patients. Nine patients with PTSD (7 females, aged 27–50 years) and nine age- and gender-matched healthy controls participated in this study. Six patients underwent the second scan under the same paradigm after EMDR. We discovered intense negative correlations between daily and traumatic memory conditions in broad areas, including the hippocampus; patients who had an intense suppression of activation during daily recognition showed an intense activation while remembering a traumatic memory, whereas patients who had a hyperarousal in daily recognition showed an intense suppression while remembering a traumatic memory as a form of “shut-down.” Moreover, the magnitude of the discrepancy was reduced in patients who remitted after EMDR, which might predict an improved prognosis of PTSD.


2020 ◽  
Author(s):  
Chantelle S. Lloyd ◽  
Andrew A. Nicholson ◽  
Maria Densmore ◽  
Jean Théberge ◽  
Richard W. J. Neufeld ◽  
...  

2021 ◽  
pp. 216770262199454
Author(s):  
Søren Risløv Staugaard ◽  
Annette Kjær Fuglsang ◽  
Dorthe Berntsen

Studies suggest that general control deficits and elevated affect intensity in posttraumatic stress disorder (PTSD) extend beyond memory for the index trauma. However, few researchers have pursued this possibility experimentally by examining memory for novel events. We used an experimental design to measure the frequency and characteristics of involuntary memories over time. Veterans with and without PTSD saw pictures of neutral and war-related scenes. Half of the participants completed an involuntary-retrieval task immediately after encoding, whereas the other half completed the retrieval task after 1 week. Veterans with PTSD had stronger emotional reactions to their involuntary memories of the scenes regardless of their original valence. The emotional impact and specificity of the memories did not diminish over time in PTSD veterans but did so in the control group. The findings are consistent with an increased emotional response to a range of memories that include—but are not limited to—memories of traumatic events.


2021 ◽  
Vol 79 (4) ◽  
pp. 1723-1734
Author(s):  
Shlomo Sragovich ◽  
Michael Gershovits ◽  
Jacqueline C.K. Lam ◽  
Victor O.K. Li ◽  
Illana Gozes

Background: We recently discovered autism/intellectual disability somatic mutations in postmortem brains, presenting higher frequency in Alzheimer’s disease subjects, compared with the controls. We further revealed high impact cytoskeletal gene mutations, coupled with potential cytoskeleton-targeted repair mechanisms. Objective: The current study was aimed at further discerning if somatic mutations in brain diseases are presented only in the most affected tissue (the brain), or if blood samples phenocopy the brain, toward potential diagnostics. Methods: Variant calling analyses on an RNA-seq database including peripheral blood samples from 85 soldiers (58 controls and 27 with symptoms of post-traumatic stress disorder, PTSD) was performed. Results: High (e.g., protein truncating) as well as moderate impact (e.g., single amino acid change) germline and putative somatic mutations in thousands of genes were found. Further crossing the mutated genes with autism, intellectual disability, cytoskeleton, inflammation, and DNA repair databases, identified the highest number of cytoskeletal-mutated genes (187 high and 442 moderate impact). Most of the mutated genes were shared and only when crossed with the inflammation database, more putative high impact mutated genes specific to the PTSD-symptom cohorts versus the controls (14 versus 13) were revealed, highlighting tumor necrosis factor specifically in the PTSD-symptom cohorts. Conclusion: With microtubules and neuro-immune interactions playing essential roles in brain neuroprotection and Alzheimer-related neurodegeneration, the current mutation discoveries contribute to mechanistic understanding of PTSD and brain protection, as well as provide future diagnostics toward personalized military deployment strategies and drug design.


Author(s):  
Yehezkel Ben-Ari ◽  
Enrico Cherubini ◽  
Massimo Avoli

After over seven decades of neuroscience research, it is now well established that γ-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the brain. In this paper dedicated to Krešimir Krnjević (1927–2021), a pioneer and leader in neuroscience, we briefly highlight the fundamental contributions he made in identifying GABA as an inhibitory neurotransmitter in the brain and our personal interactions with him. Of note, between 1972 and 1978 Dr. Krnjević was a highly reputed Chief Editor of the Canadian Journal of Physiology and Pharmacology.


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