Stress, fear, and memory in healthy individuals

Merz, Christian J.; Elzinga, Bernet M.; Schwabe, Lars

doi:10.1002/9781118356142.ch8

Cited by 8 publications

(11 citation statements)

References 139 publications

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“…The effects of tcVNS blocking inflammatory responses and subjective anger to personalized traumatic script suggests clinical relevance for PTSD. Exposure to traumatic events can produce strongly encoded intrusive memories as well as lasting changes in neurobiology, brain circuits involved in the stress response, and symptoms of PTSD ( Bremner and Pearce, 2016 ; Merz et al., 2016 ). Projections of the vagus through the nucleus tractus solitarius (NTS) extend to the locus coeruleus and hypothalamus, key areas involved in sympathetic hyperarousal in PTSD, as well as brain areas like the amygdala that are involved in the fear response and the medial prefrontal cortex / anterior cingulate, which is involved in both fear extinction and modulation of peripheral neurohormonal responses to stress ( Hardy, 1995 ).…”

Section: Discussionmentioning

confidence: 99%

Transcutaneous vagal nerve stimulation blocks stress-induced activation of Interleukin-6 and interferon-γ in posttraumatic stress disorder: A double-blind, randomized, sham-controlled trial

Bremner

Gurel

Jiao

et al. 2020

Brain, Behavior, & Immunity - Health

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Posttraumatic stress disorder (PTSD) is a highly disabling condition associated with alterations in multiple neurobiological systems, including increases in inflammatory function. Vagus nerve stimulation (VNS) decreases inflammation, however few studies have examined the effects of non-invasive VNS on physiology in human subjects, and no studies in patients with PTSD. The purpose of this study was to assess the effects of transcutaneous cervical VNS (tcVNS) on inflammatory responses to stress. Thirty subjects with a history of exposure to traumatic stress with (N = 10) and without (N = 20) PTSD underwent exposure to stressful tasks immediately followed by active or sham tcVNS and measurement of multiple biomarkers of inflammation (interleukin-(IL)-6, IL-2, IL-1β, Tumor Necrosis Factor alpha (TNFα) and Interferon gamma (IFNγ) over multiple time points. Stressful tasks included exposure to personalized scripts of traumatic events on day 1, and public speech and mental arithmetic (Mental Stress) tasks on days 2 and 3. Traumatic scripts were associated with a pattern of subjective anger measured with Visual Analogue Scales and increased IL-6 and IFNγ in PTSD patients that was blocked by tcVNS (p < .05). Traumatic stress had minimal effects on these biomarkers in non-PTSD subjects and there was no difference between tcVNS or sham. No significant differences were seen between groups in IL-2, IL-1β, or TNFα. These results demonstrate that tcVNS blocks behavioral and inflammatory responses to stress reminders in PTSD.

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Section: Discussionmentioning

confidence: 99%

Transcutaneous vagal nerve stimulation blocks stress-induced activation of Interleukin-6 and interferon-γ in posttraumatic stress disorder: A double-blind, randomized, sham-controlled trial

Bremner

Gurel

Jiao

et al. 2020

Brain, Behavior, & Immunity - Health

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“…In extreme cases, strong and generalized emotional memories will not fade over time and might become overpowering and maladaptive. Strong maladaptive memories underlie posttraumatic stress disorder (PTSD), phobias (Merz et al, 2016), and chronic pain (Elsenbruch and Wolf, 2015).…”

Section: Stress and The Strength Of Emotional Memoriesmentioning

confidence: 99%

Stress modulation of fear and extinction in psychopathology and treatment

et al. 2020

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The glucocorticoid cortisol, a major player in the development of stress-related psychopathology, can also be used for the augmentation of extinction-based psychotherapies (e.g., exposure therapy). Substantial evidence supports its beneficial effects in the treatment of post-traumatic stress disorder and specific phobias. In this review, we first present the role of stress and cortisol in the development of maladaptive emotional memories. Then, we describe the mechanisms that may account for the cortisol-induced augmentation of exposure, namely, the enhancement of extinction memory consolidation and the reduction of the contextual dependency of the extinction memory. Finally, we discuss several considerations and limitations for the use of cortisol in psychotherapy, focusing on the possible adverse effects of cortisol in a reconsolidation-based (as opposed to extinction-based) intervention.

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“…Traumatic stress is known to have lasting effects on neurobiology [ 1 , 2 ] and, in at risk individuals, can result in psychiatric conditions such as posttraumatic stress disorder (PTSD) [ 3 ]. During acute traumatic stress exposure, sympathetic nervous system (SNS) activity increases [ 1 , 4 , 5 ], resulting in a neuroendocrinological cascade with potentially deleterious neural consequences [ 6 – 8 ].…”

Section: Introductionmentioning

confidence: 99%

Non-invasive vagal nerve stimulation decreases brain activity during trauma scripts

et al. 2020

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Background: Traumatic stress can have lasting effects on neurobiology and result in psychiatric conditions such as posttraumatic stress disorder (PTSD). We hypothesize that non-invasive cervical vagal nerve stimulation (nVNS) may alleviate trauma symptoms by reducing stress sympathetic reactivity. This study examined how nVNS alters neural responses to personalized traumatic scripts. Methods: Nineteen participants who had experienced trauma but did not have the diagnosis of PTSD completed this double-blind sham-controlled study. In three sequential time blocks, personalized traumatic scripts were presented to participants immediately followed by either sham stimulation (n = 8; 0–14 V, 0.2 Hz, pulse width = 5s) or active nVNS (n = 11; 0–30 V, 25 Hz, pulse width = 40 ms). Brain activity during traumatic scripts was assessed using High Resolution Positron Emission Tomography (HR-PET) with radiolabeled water to measure brain blood flow. Results: Traumatic scripts resulted in significant activations within the bilateral medial and orbital prefrontal cortex, premotor cortex, anterior cingulate, thalamus, insula, hippocampus, right amygdala, and right putamen. Greater activation was observed during sham stimulation compared to nVNS within the bilateral prefrontal and orbitofrontal cortex, premotor cortex, temporal lobe, parahippocampal gyrus, insula, and left anterior cingulate. During the first exposure to the trauma scripts, greater activations were found in the motor cortices and ventral visual stream whereas prefrontal cortex and anterior cingulate activations were more predominant with later script presentations for those subjects receiving sham stimulation. Conclusion: nVNS decreases neural reactivity to an emotional stressor in limbic and other brain areas involved in stress, with changes over repeated exposures suggesting a shift from scene appraisal to cognitively processing the emotional event.

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Stress, fear, and memory in healthy individuals

Cited by 8 publications

References 139 publications

Transcutaneous vagal nerve stimulation blocks stress-induced activation of Interleukin-6 and interferon-γ in posttraumatic stress disorder: A double-blind, randomized, sham-controlled trial

Transcutaneous vagal nerve stimulation blocks stress-induced activation of Interleukin-6 and interferon-γ in posttraumatic stress disorder: A double-blind, randomized, sham-controlled trial

Stress modulation of fear and extinction in psychopathology and treatment

Non-invasive vagal nerve stimulation decreases brain activity during trauma scripts

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