Survival processing in times of stress

Recent studies have found that processing information according to an evolutionary relevant (i.e., survival) scenario improves its subsequent memorability, potentially as a result of fitness advantages gained in the ancestral past. So far, research has not revealed much about any proximate mechanisms that might underlie this so-called survival processing advantage in memory. Intriguingly, research has shown that the memorability of stressful situations is enhanced via the release of stress hormones acting on brain regions involved in memory. Since survival situations habitually involve some degree of stress, in the present study, we investigated whether stress serves as a proximate mechanism to promote survival processing. Participants rated words for their relevance to either a survival or a neutral (moving) scenario after they had been exposed to a psychosocial stressor or a no-stress control condition. Surprise retention tests immediately following the rating task revealed that survival processing and acute stress independently boosted memory performance. These results therefore suggest that stress does not serve as a proximate mechanism of the survival processing advantage in memory

The Effect of Distress on Susceptibility to False Memories

False memories are of concern in situations involving eyewitness testimony, as inaccurate recollections of events may lead to false convictions. It is especially important to investigate the role of distress in the formation of false memories, due to many eyewitness testimony circumstances involving an event of a negative and traumatic nature. It was the aim of this thesis to investigate several key factors that may contribute to false memories for distressing events, namely Post-Traumatic Stress Disorder (PTSD) symptoms such as avoidance, intrusions, and dissociation, and also the biological marker of cortisol response. In order to investigate these aims, two main techniques were chosen: the Deese-Roediger-McDermott (DRM) word list procedure and the Trauma Film Paradigm (TFP) using narratives to introduce misinformation following the viewing of a film. In Experiment One participants completed the DRM using neutral and trauma-related words along with measu res of dissociation and biases related to threat. Analyses indicated that dissociation was related to false recall for traumatic stimuli; findings related to the biases were less straightforward. In Experiment Two misinformation was introduced following viewing of a neutral or stressful film. Findings indicated dissociation was related to higher distress ratings following the film, but unrelated to acceptance of misinformation. Avoidance scores were related to increased reporting and recognition of misinformation items and reported experiences of intrusions related to greater accuracy. Experiment Three was designed to address discrepant findings between that of the previous two experiments: namely that dissociation was significantly related to falsely remembering trauma words in the DRM task but did not predict false memories for the films. Participants completed both the DRM task and the film task. Results suggested that neither dissociation nor trauma history w as significantly related to DRM false recall. While the dist! ress and state dissociation results of Experiment Two were replicated (specifically that all were higher in response to the trauma film in comparison to the neutral film), the memory results were not. Accuracy on the DRM task predicted accuracy for the film task; however susceptibility to the DRM illusion was unrelated to susceptibility to the misinformation effect. This unexpected finding raised questions regarding whether all false memory tasks are equivalent. Experiment Four builds on the previous experiments by including a biological, objective measure of distress in response to film viewing: cortisol release. Cortisol responders were found to be more susceptible to the misinformation effect than non-responders, depending on sample timing. Dissociation was found to be related to cortisol response, and also confabulations for the film. Chapter Eight ties all four experiments together in the General Discussion. While several limitations were identified, it w as concluded that the findings of how distress experiences following the film affected memory were particularly novel. These findings have important practical implications regarding eyewitness testimony, as well as identifying people at risk of maladaptive distress reactions

A systematic review of the pharmacological modulation of autobiographical memory specificity

BACKGROUND: Over-general autobiographical memory (AM) retrieval is proposed to have a causal role in the maintenance of psychological disorders like depression and PTSD. As such, the identification of drugs that modulate AM specificity may open up new avenues of research on pharmacological modeling and treatment of psychological disorders. AIM: The current review summarizes randomized, placebo-controlled studies of acute pharmacological modulation of AM specificity. METHOD: A systematic search was conducted of studies that examined the acute effects of pharmacological interventions on AM specificity in human volunteers (healthy and clinical participants) measured using the Autobiographical Memory Test. RESULTS: Seventeen studies were identified (986 total participants), of which 16 were judged to have low risk of bias. The presence and direction of effects varied across drugs and diagnostic status of participants (clinical vs. healthy volunteers). The most commonly studied drug-hydrocortisone-produced an overall impairment in AM specificity in healthy volunteers [g = -0.28, CI (-0.53, -0.03), p = 0.03], although improvements were reported in two studies of clinical participants. In general, studies of monoamine modulators reported no effect on specificity. CONCLUSION: Pharmacological enhancement of AM specificity is inconsistent, although monaminergic modulators show little promise in this regard. Drugs that reduce AM specificity in healthy volunteers may be useful experimental-pharmacological tools that mimic an important transdiagnostic impairment in psychological disorders. SYSTEMATIC REVIEW REGISTRATION: PROSPERO, identifier CRD42020199076, https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020199076

LOW RESOLUTION ELECTROMAGNETIC TOMOGRAPHY (LORETA) ANALYSIS OF THE BRAINS ELECTROPHYSIOLOGICAL RESPONSE TO EMOTIONAL VISUAL STIMULI UNDER DIFFERING CONDITIONS

Current methods of diagnosing and monitoring stress include: observing changes in the severity of existing symptoms, the development of new symptoms, hormone level tests, and stress self-assessment surveys. Self-assessment surveys are subject to bias and false reporting. This project focuses on analyzing electroencephalogram (EEG) using Low Resolution Electromagnetic Tomography (LORETA) to identify differences within current source location of emotionally elicited event related potentials (ERPs), in order to aid physicians in stress diagnostics and management. For this study twenty-one participants took the Penn State Worry Questionnaire which classifies the participants into high-stress and low-stress groups. The individuals had their EEG recorded while viewing pleasant, neutral, and unpleasant stimuli. CURRY, the current reconstruction program, was used to filter, epoch, and average the data to obtain event related potentials (ERPs) for each participant. Using group-averaged ERPs as the data input, LORETA was used to calculate the current distribution within the brain. One and two-tailed t-tests were performed to examine for current source distribution differences between high-stress/low-stress conditions and pleasant, unpleasant and neutral stimuli. The results of the experiment indicate that there is a difference in current source location between high-stress and low-stress individuals. The current source distribution differences are within regions of the frontal lobe and the parietal lobe associated with emotional processing

Psychopharmacology of memory and emotion in humans

Tesis inédita de la Universidad Complutense de Madrid, Facultad de Psicología, Departamento de Psicología Básica I (Procesos Cognitivos), leída el 16-06-2017El principal propósito de esta tesis ha sido ahondar en el conocimiento del mecanismo neural subyacente a la influencia de la emoción y el sistema motor en la memoria. El primero de los estudios presentados incide sobre la posibilidad de disminuir la memoria episódica, mientras que el segundo estudio presentado incide sobre la viabilidad de aumentarla. En el primer capítulo, se resumen las principales teorías sobre los procesos de memoria, desde las teorías clásicas a las más actuales. El segundo capítulo repasa los principales sistemas de neurotransmisores del sistema nervioso central y su relación con la emoción y la memoria, presentando los principales estudios en humanos o en animales. En el tercer y cuarto capítulos, se presentan dos estudios novedosos, que son una réplica y ampliación de dos estudios previos. Las teorías clásicas han considerado la memoria como una facultad monolítica e inmutable de la mente. Sin embargo, las nuevas actualizaciones provenientes de las investigaciones realizadas en las últimas décadas, abren una puerta a la modificación de memorias previamente consolidadas. La teoría de la reconsolidación establece la posibilidad de reactivar de nuevo una memoria mediante la presentación de una “clave” relacionada con la misma. Una vez la memoria es reactivada es susceptible de ser modificada dentro de una ventana de tiempo, mediante la administración de diferentes tipos de manipulaciones, tanto de carácter conductual como farmacológico; necesitando ser consolidada de nuevo después de la reactivación. La reconsolidación de la memoria ha sido observada en diferentes especies animales y en humanos, así como con diferentes tareas y tipos de memoria...The main objective of this thesis has been to deepen the knowledge of the neural mechanism underlying the influence of emotion as well as the motor system in memory. The first of the studies presented focuses on the possibility of decreasing episodic memory, while the second study refers to the feasibility of increasing it. In the first chapter, the main theories about the processes of memory are summarized, from the classic theories to the more actual ones. The second chapter reviews the main neurotransmitter systems of the central nervous system and its relation to emotion and memory, presenting the main studies in humans or animals. In the third and fourth chapters, two novel studies are presented, which are a replication and extension of two previous studies. Classical theories have considered memory as a monolithic and immutable faculty of mind. However, new updates from the research carried out in the last decades, opens a door to the modification of previously consolidated memories. The theory of reconsolidation postulates that upon reactivation, memories can become labile and susceptible to manipulation, requiring a new restabilization process in order to maintain them. The reconsolidation of memory has been observed in different animal species and in humans, as well as with different tasks and types of memory. The first study presented (Chapter 3) is based on the hypothesis of the implication of the GABAergic system in the deterioration of the reconsolidation of an episodic emotional memory. For the accomplishment of this experiment it was counted on the participation of patients who were going to undergo an endoscopy procedure and therefore, to receive a scheduled sedation. The results show the impairment of the emotional memory by the administration of propofol, an anesthetic agent, immediately after the reactivation. A significant proportion of the population is affected by psychiatric disorders that have at their core a traumatic or maladaptive emotional memory. The possibility of modifying this type of memory opens a range to new treatments and adjuvant therapies to those already existing...Depto. de Psicología Experimental, Procesos Cognitivos y LogopediaFac. de PsicologíaTRUEunpu

Acute effects of alcohol on trauma memories

Memory disturbances following a trauma are a characteristic feature of posttraumatic stress disorder. Despite alcohol’s frequent involvement in real-life traumatic events, our understanding of its contribution to trauma-related symptoms is unclear. The research in this thesis aimed to determine the way in which alcohol intoxication during a traumatic experience might influence memory for the event. Experiment 1 showed that alcohol impaired recognition associated with recollection with greater reductions as dose increased (0, 0.4, 0.6, 0.8g/kg); in contrast, recognition associated with familiarity was preserved. Experiments 2 and 3 utilised an analogue trauma film to examine how low (0.4g\kg) and high (0.8g/kg) doses of alcohol affected intrusive imagery and explicit memory for the footage. Alcohol during encoding resulted in a dose-dependent inverted U-shaped curve on intrusive imagery, with increased intrusions only following a low dose. Explicit memory for the footage was reduced in a dose-dependent linear manner. In addition, experiment 3 concurrently assessed same- and shifted-view object location recognition to determine the mechanisms that might underpin alcohol’s effects on trauma memory. Results showed that a low dose of alcohol selectively impaired shifted-view recognition, thought to rely on an allocentric representation. However, same-view recognition was preserved, suggesting a spared egocentric representational system. In contrast, the high dose disrupted both same- and shifted-view recognition, suggesting a global disruption in both memory systems. Experiment 4 examined the effects of alcohol (0.4/kg) on contextual fear acquisition and extinction and both same- and shifted-view recognition. Fear acquisition was unaffected by alcohol, whilst extinction learning was impaired with persistent conditioned responses throughout extinction. Alcohol-induced reductions in extinction learning were highly correlated with decreases in shifted-view recognition, supporting the role of contextual encoding in extinction. The findings of these studies suggest that alcohol dose-dependently influences trauma memories and this could result in a distinct set of trauma-related symptoms

Uncertainty and stress: Why it causes diseases and how it is mastered by the brain

The term 'stress' - coined in 1936 - has many definitions, but until now has lacked a theoretical foundation. Here we present an information-theoretic approach - based on the 'free energy principle' - defining the essence of stress; namely, uncertainty. We address three questions: What is uncertainty? What does it do to us? What are our resources to master it? Mathematically speaking, uncertainty is entropy or 'expected surprise'. The 'free energy principle' rests upon the fact that self-organizing biological agents resist a tendency to disorder and must therefore minimize the entropy of their sensory states. Applied to our everyday life, this means that we feel uncertain, when we anticipate that outcomes will turn out to be something other than expected - and that we are unable to avoid surprise. As all cognitive systems strive to reduce their uncertainty about future outcomes, they face a critical constraint: Reducing uncertainty requires cerebral energy. The characteristic of the vertebrate brain to prioritize its own high energy is captured by the notion of the 'selfish brain'. Accordingly, in times of uncertainty, the selfish brain demands extra energy from the body. If, despite all this, the brain cannot reduce uncertainty, a persistent cerebral energy crisis may develop, burdening the individual by 'allostatic load' that contributes to systemic and brain malfunction (impaired memory, atherogenesis, diabetes and subsequent cardio- and cerebrovascular events). Based on the basic tenet that stress originates from uncertainty, we discuss the strategies our brain uses to avoid surprise and thereby resolve uncertainty

Associations between sleep architecture, cortisol concentrations, cognitive performance, and quality of life in patients with Addison's disease

Recent literature in the neurosciences suggests that there are mechanistic relations between sleep disruption and cognitive (particularly memory) deficits, and that varying concentrations of the hormone cortisol may play a particularly important role in mediating those relations. Because patients with Addison’s disease (AD) experience consistent and predictable periods of sub- and supra-physiological cortisol concentrations (due to lifelong glucocorticoid replacement therapy), and because they frequently report disrupted sleep and poor memory, those presenting with that endocrinological disorder form an ideal population to use in studies testing hypotheses about the ways in which (a) disrupted sleep is related to impaired consolidation of previously learned material (and, hence, poor performance on tests assessing memory for that material), and (b) cortisol concentrations may mediate this relationship between sleep and memory. This dissertation presents four studies that, together, tested those hypotheses. Study 1 (n = 60 per group) found that patients with AD self-reported significantly more disturbed sleep and poorer cognition and quality of life compared to matched healthy controls. Importantly, our analyses suggested that disrupted sleep, and not AD per se, accounted most strongly for the reported cognitive impairment. Study 2 (n = 35 per group) found that patients had significantly poorer objectively-measured declarative memory performance compared to matched healthy controls, but that other domains of cognition were relatively unimpaired. Study 3 (n = 10 per group) suggested that matched healthy controls retained significantly more declarative information than patients. Importantly, while controls retained significantly more declarative information when a period of sleep, rather than waking, separated learning from recall, patients derived no such benefit. Study 4 (n = 7 per group) suggested that, relative to matched healthy controls, patients had different patterns of night-time cortisol secretion, accompanied by significantly reduced slow-wave sleep. Together, these four studies suggest that, despite being on replacement medication, patients with AD still experience disrupted sleep and memory deficits. These disruptions and deficits may be related to the failure of replacement regimens to restore a normal circadian rhythm of cortisol secretion. This pattern of results provides support for existing theoretical frameworks which posit that (in AD and other neuroendocrine, neurological, or psychiatric disorders) disrupted sleep is an important biological mechanism that underlies, at least partially, the memory impairments that patients frequently report experiencing. With specific regard to patients with AD, the findings presented here suggest that future initiatives aimed at improving patients’ cognitive performance (and, indeed, their overall quality of life) should prioritise optimizing sleep. More generally, this dissertation advances our understanding of sleep as a critical biological process essential for cognitive well-being