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Query: UMLS:C0848237 (acute stress)
4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rationale underpinning the diagnosis of acute stress disorder is that cognitive mechanisms result in avoidant processing of aversive experiences. This study investigated acutely traumatized participants with either acute stress disorder (ASD; n = 15) or no ASD (n = 14) and nontraumatized comparison participants (n = 16). Participants were administered intermixed presentations on a computer screen of positive, neutral, and trauma-related words that were followed by instructions to either remember or forget each word. On a subsequent recall test, ASD participants displayed poorer recall of to-be-forgotten trauma-related words than did non-ASD participants. Severity of psychopathology was negatively correlated with to-be-remembered positive words. These findings are consistent with the proposal that people who develop ASD display an aptitude for superior forgetting of aversive material.
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PMID:Directed forgetting in acute stress disorder. 1186 70

Acute stress disorder is characterized by dissociative responses that are theorized to result in deficient encoding and retrieval of trauma-related material. This study examined retrieval inhibition using the list method of the directed forgetting paradigm in traumatized individuals with acute stress disorder (ASD; n = 14), no ASD (n = 14), and a nontraumatized control group (n = 15). Participants were presented with a list of intermixed positive, neutral, and trauma-related words. Instructions to forget that list and instead remember a second list were then given, and a new list presented. ASD participants exhibited poorer recall of to-be-forgotten trauma words than the non-ASD and control groups. The ASD group also demonstrated deficient recognition of to-be-remembered and to-be-forgotten positive words. Severity of acute posttraumatic stress response was associated with retrieval impairments. The cumulative findings suggest that ASD is associated with impoverished memory for trauma-related and positive material.
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PMID:An investigation of retrieval inhibition in acute stress disorder. 1628 Dec 17

This study investigated the relationship between ongoing posttraumatic adjustment and encoding style. Eleven acute stress disorder (ASD) participants and 14 non-traumatized controls completed the item method of directed forgetting and were retested 1 year later. Trauma-related, positive and neutral words were followed by a "remember" or "forget" instruction. At Time 1, ASD participants demonstrated directed forgetting for trauma and neutral words; controls showed directed forgetting for all word types. At Time 2, directed forgetting was replicated in controls for each word type, but only for neutral words in the ASD group. Directed forgetting effects were absent for positive words in the ASD group. The findings raise the possibility that individuals who develop ASD possess an encoding style for positive material that reflects a trait-like manner of information processing.
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PMID:Avoidant encoding in acute stress disorder: a prospective study. 1793 16

When acute stress is experienced shortly after an event is encoded into memory, this can slow the forgetting of the study event, which is thought to reflect the effect of cortisol on consolidation. In addition, when events are encoded under conditions of high reward they tend to be remembered better than those encoded under non-rewarding conditions, and these effects are thought to reflect the operation of the dopaminergic reward system. Although both modulatory systems are believed to impact the medial temporal lobe regions critical for episodic memory, the manner, and even the extent, to which these two systems interact is currently unknown. To address this question in the current study, participants encoded words under reward or non-reward conditions, then one half of the participants were stressed using the social evaluation cold pressor task and the other half completed a non-stress control task. After a two-hour delay, all participants received a free recall and recognition memory test. There were no significant effects of stress or reward on overall memory performance. However, for the non-reward items, increases in stress-related cortisol in stressed participants were related to increases in recall and increases in recollection-based recognition responses. In contrast, for the reward items, increases in stress-related cortisol were not related to increases in memory performance. The results indicate that the stress and the reward systems interact in the way they impact episodic memory. The results are consistent with tag and capture models in the sense that cortisol reactivity can only affect non-reward items because plasticity-related products are already provided by reward anticipation.
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PMID:Reward anticipation modulates the effect of stress-related increases in cortisol on episodic memory. 2917 14

Unwanted imaginations of future fears can, to some extent, be avoided. This is achieved by control mechanisms similar to those engaged to suppress and forget unwanted memories. Suppression-induced forgetting relies on the executive control network, whose functioning is impaired after exposure to acute stress. This study investigates whether acute stress affects the ability to intentionally control future fears and, furthermore, whether individual differences in executive control predict a susceptibility to these effects. The study ran over two consecutive days. On day 1, the working memory capacity of one hundred participants was assessed. Thereafter, participants provided descriptions and details of fearful episodes that they imagined might happen in their future. On day 2, participants were exposed to either the stress or no-stress version of the Maastricht Acute Stress Test, after which participants performed the Imagine/No-Imagine task. Here, participants repeatedly imagined some future fears and suppressed imaginings of others. Results demonstrated that, in unstressed participants, suppression successfully induced forgetting of the episodes' details compared to a baseline condition. However, anxiety toward these events did not differ. Acute stress was found to selectively impair suppression-induced forgetting and, further, this effect was moderated by working memory capacity. Specifically, lower working memory predicted a susceptibility to these detrimental effects. These findings provide novel insights into conditions under which our capacity to actively control future fears is reduced, which may have considerable implications for understanding stress-related psychopathologies and symptomatologies characterized by unwanted apprehensive thoughts.
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PMID:The impairing effect of acute stress on suppression-induced forgetting of future fears and its moderation by working memory capacity. 3277 89

Accumulating evidence suggests that forgetting is not necessarily a passive process but that we can, to some extent, actively control what we remember and what we forget. Although this intentional control of memory has potentially far-reaching implications, the factors that influence our capacity to intentionally control our memory are largely unknown. Here, we tested whether acute stress may disrupt the intentional control of memory and, if so, through which neural mechanism. We exposed healthy men and women to a stress (n = 27) or control (n = 26) procedure before they aimed repeatedly to retrieve some previously learned cue-target pairs and to actively suppress others. While control participants showed reduced memory for suppressed compared with baseline pairs in a subsequent memory test, this suppression-induced forgetting was completely abolished after stress. Using magnetoencephalography (MEG), we show that the reduced ability to suppress memories after stress is associated with altered theta activity in the inferior temporal cortex when the control process (retrieval or suppression) is triggered and in the lateral parietal cortex when control is exerted, with the latter being directly correlated with the stress hormone cortisol. Moreover, the suppression-induced forgetting was linked to altered connectivity between the hippocampus and right dorsolateral prefrontal cortex (PFC), which in turn was negatively correlated to stress-induced cortisol increases. These findings provide novel insights into conditions under which our capacity to actively control our memory breaks down and may have considerable implications for stress-related psychopathologies, such as posttraumatic stress disorder (PTSD), that are characterized by unwanted memories of distressing events.SIGNIFICANCE STATEMENT It is typically assumed that forgetting is a passive process that can hardly be controlled. There is, however, evidence that we may actively control, to some extent, what we remember and what we forget. This intentional memory control has considerable implications for mental disorders in which patients suffer from unwanted (e.g., traumatic) memories. Here, we demonstrate that the capacity to intentionally control our memory breaks down after stress. Using magnetoencephalography (MEG), we show that this stress-induced memory control deficit is linked to altered activity in the lateral parietal cortex and the connectivity between the hippocampus and right prefrontal cortex (PFC). These findings provide novel insights into conditions under which memory control fails and are highly relevant in the context of stress-related psychopathologies.
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PMID:Stress Impairs Intentional Memory Control through Altered Theta Oscillations in Lateral Parietal Cortex. 3286 59