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Excessive alcohol intake is a major public health problem and can be triggered by stress. Heavy drinking in patients with alcohol use disorder also alters neural, physiological, and emotional stress responses. However, it is unclear whether adaptations in stress-predictive brain networks can be an early marker of risky drinking behavior.Risky social drinkers (regular bingers; n = 53) and light drinker control subjects (n = 51) aged 18 to 53 years completed a functional magnetic resonance imaging-based sustained stress protocol with repeated measures of subjective stress state, during which whole-brain functional connectivity was computed. This was followed by prospective daily ecological momentary assessment for 30 days. We used brain computational predictive modeling with cross-validation to identify unique brain connectivity predictors of stress in risky drinkers and determine the prospective utility of stress-brain networks for subsequent loss of control over drinking.Risky drinkers had anatomically and functionally distinct stress-predictive brain networks (showing stronger predictions from visual and motor networks) compared with light drinkers (default mode and frontoparietal networks). Stress-predictive brain networks defined for risky drinkers selectively predicted future real-world stress levels for risky drinkers and successfully predicted prospective future real-world loss of control over drinking across all participants.These results indicate adaptations in computationally derived stress-related brain circuitry among high-risk drinkers, suggesting potential targets for early preventive intervention and revealing the malleability of the neural processes that govern stress responses.

Stress can powerfully influence episodic memory, often enhancing memory encoding for emotionally salient information. These stress-induced memory enhancements stand at odds with demonstrations that stress and the stress-related hormone cortisol can negatively affect the hippocampus, a brain region important for episodic memory encoding. To resolve this apparent conflict and determine whether and how the hippocampus supports memory encoding under cortisol, we combined behavioral assays of associative memory, high-resolution functional magnetic resonance imaging (fMRI), and pharmacological manipulation of cortisol in a within-participant, double-blinded procedure. Hydrocortisone led to enhanced functional connectivity between hippocampal subregions, which predicted subsequent memory enhancements for emotional information. Cortisol also modified the relationship between hippocampal representations and memory: whereas hippocampal signatures of distinctiveness predicted memory under placebo, relative integration predicted memory under cortisol. Together, these data provide novel evidence that the human hippocampus contains the necessary machinery to support emotional memory enhancements under stress.

Although the feeling of stress is ubiquitous, the neural mechanisms underlying this affective experience remain unclear. Here, we investigate functional hippocampal connectivity throughout the brain during an acute stressor and use machine learning to demonstrate that these networks can specifically predict the subjective feeling of stress. During a stressor, hippocampal connectivity with a network including the hypothalamus (known to regulate physiological stress) predicts feeling more stressed, whereas connectivity with regions such as dorsolateral prefrontal cortex (associated with emotion regulation) predicts less stress. These networks do not predict a subjective state unrelated to stress, and a nonhippocampal network does not predict subjective stress. Hippocampal networks are consistent, specific to the construct of subjective stress, and broadly informative across measures of subjective stress. This approach provides opportunities for relating hypothesis-driven functional connectivity networks to clinically meaningful subjective states. Together, these results identify hippocampal networks that modulate the feeling of stress., Although the feeling of being stressed is ubiquitous and clinically significant, the underlying neural mechanisms are unclear. Using a novel predictive modeling approach, the authors show that functional hippocampal networks specifically and consistently predict the feeling of stress.

BackgroundPosttraumatic stress disorder (PTSD) is triggered by environmental stressors. Empathy may predispose an individual to respond to life events differently if high empathizers are emotionally more sensitive to trauma. For the first time, we test this hypothesis at the genetic level.MethodsWe applied polygenic scoring (PGS) to investigate the shared genetics linking empathy (measured using the Empathy Quotient (EQ), a self-report measure of empathy; N=46,861) and PTSD symptom severity (measured using the 6-item PTSD Checklist 6-item (PCL-6)) in the UK Biobank (N=126,219). Follow-up analyses were performed in the context of (1) experiencing any of 16 potential traumas, (2) the total number of traumas endorsed, and (3) the context of trauma. Autism, depression, generalized anxiety, and PCL-17 PGS were included as covariates to verify the specificity of the effect.ResultsEQPGS associated with PCL-6 (R2=0.012%, P=9.35×10−5). This effect remained significant after accounting for autism, depression, PTSD, and anxiety PGS but was observed only in those who endorsed experiencing at least one traumatic event. EQPGS showed the strongest effect on PCL-6 (β=2.32, s.e.=0.762, P=0.002) among those who endorsed childhood neglect/abuse (felt hated as a child). In the highest EQPGS decile, feeling hated as a child was associated with lower odds of healthy adulthood interpersonal relationships (OR=0.623, 95%CI 0.443-0.885) but this association was not seen in the lowest EQPGS decile.ConclusionsA genetic predisposition to higher empathy, which may index greater emotional sensitivity, predisposes an individual to more severe PTSD symptoms, specifically in the presence of early negative life events.

The COVID-19 pandemic represents a worldwide stressor. Considering the influence of stress on research participants during this time and beyond may provide new insights and benefit the broader field of human neuroscience., Considering the influence of stress on research participants during the pandemic and beyond may provide new insights and benefit the broader field of human neuroscience.

Acute stress can modulate memory for individual parts of an event (items), but whether it similarly influences memory for associations between items remains unclear. We used a within-subjects design to explore the influence of acute stress on item and associative memory in humans. Participants associated negative words with neutral objects, rated their subjective arousal for each pair, and completed delayed item and paired associative recognition tasks. We found strikingly different patterns of acute stress effects on item and associative memory: for high-arousal pairs, preencoding stress enhanced associative memory, whereas postencoding stress enhanced item memory. Preretrieval stress consistently impaired both forms of memory. We found that the influence of stress-induced cortisol also varied, with a linear relationship between cortisol and item memory but a quadratic relationship between cortisol and associative memory. These findings reveal key differences in how stress, throughout the memory cycle, shapes our memories for items and associations. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Memory for prior drinking experiences may powerfully drive later alcohol use in familiar drinking contexts, yet we know little about what patients with alcohol use disorder (AUD) remember of alcohol-related episodes. Although animal and theoretical models of addiction emphasize the importance of different memory systems for understanding maladaptive use, clinical research parsing what AUD patients remember from alcohol-related episodes is lacking. The current study applied a novel memory task in which moderate drinkers (N = 30) and treatment-seeking individuals with alcohol use disorder (AUD: N = 29) encoded associations between photographs of objects (alcoholic beverages and neutral items) and photographs of neutral scenes. At least 24 h later, two types of memory were assessed: item memory (object recognition) and associative memory (cued recognition of scenes associated with objects). To assess which memories predicted drinking, real-world behavior was assessed in patients with AUD at baseline and for 4 weeks following memory tests. Despite demographic differences, the results showed broadly impaired item memory in AUD compared with moderate drinkers (p

Acute stress has been shown to modulate the engagement of different memory systems, leading to preferential expression of stimulus–response (SR) rather than episodic context memory when both types of memory can be used. However, questions remain regarding the cognitive mechanism that underlies this bias in humans—specifically, how each form of memory is individually influenced by stress in order for SR memory to be dominant. Here we separately measured context and SR memory and investigated how each was influenced by acute stress after learning (Experiment 1) and before retrieval (Experiment 2). We found that postlearning stress, in tandem with increased adrenergic activity during learning, impaired consolidation of context memory and led to preferential expression of SR rather than context memory. Preretrieval stress also impaired context memory, albeit transiently. Neither postlearning nor preretrieval stress changed the expression of SR memory. However, individual differences in cortisol reactivity immediately after learning were associated with variability in initial SR learning. These results reveal novel cognitive mechanisms by which stress can modulate multiple memory systems.

Stress can strongly influence memory, in part by modulating the relative engagement of multiple memory systems. Over the last fifteen years, researchers have demonstrated that stress leads striatal, rather than hippocampal, memory to be dominant in both humans and non-human animals. This shift has been proposed to explain the etiology and maintenance of symptoms of stress-related psychopathology. However, it remains unclear how hippocampal and striatal memory are affected individually in order to facilitate this trade-off. Recent studies provide empirical support for (at least) three different pathways by which stress could modulate these memory systems. Evidence for these diverse effects of stress, and circumstances under which each might occur, are discussed.

Emotional experiences often contain a multitude of details that may be represented in memory as individual elements or integrated into a single representation. How details associated with a negative emotional event are represented in memory can have important implications for extinction strategies designed to reduce emotional responses. For example, is extinguishing one cue associated with an aversive outcome sufficient to reduce learned behavior to other cues present at the time of learning that were not directly extinguished? Here, we used a between-subjects multi-day threat conditioning and extinction task to assess whether participants generalize extinction from one cue to unextinguished cues. On Day 1, one group of participants learned that a compound conditioned stimulus, composed of a tone and colored square, predicted an uncomfortable shock to the wrist (Compound group). A second group learned that the tone and square separately predicted shock (Separate group). On Day 2, participants in both groups were exposed to the tone in the absence of shocks (cue extinction). On Day 3, we tested whether extinction generalized from the extinguished to the unextinguished cue, as well as to a compound composed of both cues. Results showed that configural and elemental learning had unique and opposite effects on extinction generalization. Subjects who initially learned that a compound cue predicted shock successfully generalized extinction learning from the tone to the square, but exhibited threat relapse to the compound cue. In contrast, subjects who initially learned that each cue individually predicted shock did not generalize extinction learning from the tone to the square, but threat responses to the compound were low. These results highlight the importance of whether details of an aversive event are represented as integrated or separated memories, as these representations affect the success or limits of extinction generalization.

Contains fulltext : 173050.pdf (Publisher’s version ) (Open Access) Acute stress has frequently been shown to impair cognitive flexibility. Most studies have examined the effect of stress on cognitive flexibility by measuring how stress changes performance in paradigms that require participants to switch between different task demands. These processes typically implicate pFC function, a region known to be impaired by stress. However, cognitive flexibility is a multifaceted construct. Another dimension of flexibility, updating to incorporate relevant information, involves the dorsal striatum. Function in this region has been shown to be enhanced by stress. Using a within-subject design, we tested whether updating flexibility in a DMS task would be enhanced by an acute stress manipulation (cold pressor task). Participants' cortisol response to stress positively correlated with a relative increase in accuracy on updating flexibility (compared with trials with no working memory interference). In contrast, in line with earlier studies, cortisol responses correlated with worse performance when switching between trials with different task demands. These results demonstrate that stress-related increases in cortisol are associated with both increases and decreases in cognitive flexibility, depending on task demands.

The biological stress response of the body forms one of the foundations of adaptive behavior, including promoting (and impairing) different forms of memory. This response transcends stressful experiences and underlies reactions to challenges and even reinforcers such as addictive substances. Nevertheless, drug-induced stress responses are rarely incorporated into models of addiction. We propose here that drug-induced stress responses (particularly glucocorticoids) play a crucial role in addictive behavior by modulating the formation of memories for substance-use experiences. We review the contributions of amygdala-, striatum-, and hippocampus-based memory systems to addiction, and reveal common effects of addictive drugs and acute stress on these different memories. We suggest that the contributions of drug-induced stress responses to memory may provide insights into the mechanisms driving addictive behavior.

Stress can strongly influence what we learn and remember, including by making memories stronger. Experiments probing stress effects on hippocampus-dependent memory in rodents have revealed modulatory factors and physiological mechanisms by which acute stress can enhance long-term memory. However, extending these findings and mechanisms to understand when stress will enhance declarative memory in humans faces important challenges. This review synthesizes human and rodent studies of stress and memory, examining translational gaps related to measurements of declarative memory and stress responses in humans. Human studies diverge from rodent research by assessing declarative memories that may not depend on the hippocampus and by measuring peripheral rather than central stress responses. This highlights opportunities for future research across species, including assessing stress effects on hippocampal-dependent memory processes in humans and relating peripheral stress responses to stress effects on the function of memory-related brain regions in rodents. Together, these investigations will facilitate the translation of stress effects on memory function from rodents to humans and inform interventions that can harness the positive effects of stress on long-term memory.

BACKGROUND: The role of hippocampus in context-dependent recall of extinction is well recognized. However, little is known about how intervention-induced changes in hippocampal networks relate to improvements in extinction learning. In this study, we hypothesized that mindfulness training creates an optimal exposure condition by heightening attention and awareness of present moment sensory experience, leading to enhanced extinction learning, improved emotion regulation, and reduced anxiety symptoms. METHODS: We tested this hypothesis in a randomized controlled longitudinal study design using a 2-day fear conditioning and extinction protocol. The mindfulness training group included 42 participants (28 female) and the control group included 25 participants (15 female). RESULTS: We show that mindfulness training is associated with differential engagement of the right supramarginal gyrus as well as hippocampal-cortical reorganization. We also report enhanced hippocampal connectivity to primary sensory cortex during retrieval of extinguished stimuli following mindfulness training. CONCLUSION: These findings suggest hippocampal dependent changes in contextual retrieval as one plausible neural mechanism through which mindfulness-based interventions enhance fear extinction and foster stress resilience.

Exposure to stress throughout life can cumulatively influence later health, even among young adults. The negative effects of high cumulative stress exposure are well-known, and a shift from episodic to stimulus–response memory has been proposed to underlie forms of psychopathology that are related to high lifetime stress. At the other extreme, effects of very low stress exposure are mixed, with some studies reporting that low stress leads to better outcomes, while others demonstrate that low stress is associated with diminished resilience and negative outcomes. However, the influence of very low lifetime stress exposure on episodic and stimulus–response memory is unknown. Here we use a lifetime stress assessment system (STRAIN) to assess cumulative lifetime stress exposure and measure memory performance in young adults reporting very low and moderate levels of lifetime stress exposure. Relative to moderate levels of stress, very low levels of lifetime stress were associated with reduced use and retention (24 h later) of stimulus–response (SR) associations, and a higher likelihood of using context memory. Further, computational modeling revealed that participants with low levels of stress exhibited worse expression of memory for SR associations than those with moderate stress. These results demonstrate that very low levels of stress exposure can have negative effects on cognition.

To elucidate gaps in the preparedness of clergy and healthcare providers to care for service members (SM) with deployment-related mental health needs. Participants identified clinically relevant symptoms in a standardized video role play of a veteran with deployment-related mental health needs and discussed their preparedness to deal with SM. Clergy members identified suicide and depression most often, while providers identified difficulty sleeping, low energy, nightmares and irritability. Neither clergy nor providers felt prepared to minister to or treat SM with traumatic brain injury. Through a mixed methods approach, we identified gaps in preparedness of clergy and healthcare providers in dealing with the mental health needs of SM.

This study examined differences in disposition decisions among mental health professionals using a standardized Web-based simulation.Using a Web-based simulation that described, across users, the same complex psychiatric patient, credentialed clinicians in a psychiatry department conducted a violence risk assessment and selected a level of follow-up care.Of 410 clinicians who completed the simulation, 60% of psychiatrists were more likely than other types of clinicians to select higher levels of care (inpatient or emergency services) for the standardized virtual patient (odds ratio=2.67, 95% confidence interval=1.67-4.25), even after adjustment for other factors. Virtual actions taken, such as contracting with the patient for safety and discussing hospitalization, elucidated these training differences.Training backgrounds were important determinants of clinicians' actions and the dispositions they recommended for a psychiatric patient at high risk of self-harm and harm to others in the educational setting and may suggest the need for further training to standardize and optimize care.

To provide effective treatments for childhood posttraumatic stress disorder (PTSD) children with PTSD must first be identified. The authors implemented a "screen and treat" program following a widely witnessed school suicide. Three months after the suicide, exposed students received the Child Trauma Symptom Questionnaire at school. Parents received the questionnaire to rate their children's PTSD symptoms. Children with scores >/=5 received follow-up interviews and those diagnosed with PTSD were referred for treatment. Ninety-six percent of exposed students were screened, 14% screened positive, and 6% had PTSD. Child and parent agreement was generally poor. All children with PTSD were successfully referred to treatment. Screen and treat programs using existing clinical instruments are efficient and acceptable for use in school settings following trauma. Language: en

Introduction Autonomic arousal is an important component of understanding learning as it is related to cognitive effort, attention, and emotional arousal. Currently, however, little is known about its relationship to online education. We conducted a study to determine the feasibility of measuring autonomic arousal and engagement in online continuing medical education (CME). Method Using the Computer Simulation Assessment Tool (CSAT) platform, health care providers were randomly assigned to either high- or low-valence versions of a Web-based simulation on risk assessment for a returning veteran. Data were collected on participants' actions within the simulation, self-reported cognitive engagement, knowledge retention, and autonomic arousal measured using galvanic skin response (GSR). Results Participants in the high-valence condition (n = 7) chose a lower percentage of critical actions (M = 79.2, SD = 4.2) than participants in the low valence (n = 8) condition (M = 83.9, SD = 3.6, t(1,14) = 2.44, p = .03). While not statistically significant, high-valence participants reported higher cognitive engagement. Participants in the high-valence condition showed a larger increase in physiologic arousal when comparing mean tonic GSR during the orientation simulation to the study simulation (high-valence mean difference = 4.21 μS, SD = 1.23 vs low-valence mean difference = 1.64 μS, SD = 2.32, t(1,13) = –2.62, p = .01). Discussion In addition to being consistent with previous engagement research, this experiment functioned as a feasibility study for measuring autonomic arousal in online CME. The current study provides a framework for future studies, which may use neurophysiology to identify the critical autonomic and engagement components associated with effective online learning.

Simulation is used increasingly in psychiatry and mental health as a tool for clinician education, patient care, and research. Requiring realistic and evocative interpersonal interactions, as well as presentations of complex psychological symptom profiles for clinician training or emotionally salient stimuli for patient treatment, psychiatry pushes the boundaries of simulation design. Varying modalities, from simple audio tracks to immersive and interactive virtual environments, have been used to accomplish these goals. This chapter reviews current and future uses of simulation in psychiatry, focusing on the nuances of educational and therapeutic objectives as well as challenges inherent in using different simulation modalities.

Introduction: The controversy surrounding commercial support for continuing medical education (CME) programs has led to policy changes, but data show no significant difference in perceived bias between commercial and noncommercial CME. Indeed, what attendees perceive as commercial influence is not fully understood. We sought to clarify what sources contribute to attendees' perceptions of commercial influence in non-industry-supported CME programs, and how attendees perceive that this influence manifests itself on both speaker and program levels. Methods: Evaluation forms were received from 1 544 attendees at 14 live noncommercially supported CME programs in 2006, 2007, and 2010. Attendees rated perceived commercial influence for each lecture and the entire program. Using open-ended and “check all that apply'' questions, participants specified perceived sources and manifestations of commercial influence. Results: Attendees rating individual lectures but not the entire program as commercially influenced accounted for 59.9% of those who identified bias. The most frequently endorsed source of commercial influence was individual speakers' funding, and the most listed manifestations were speakers' mentions of pharmaceuticals and expressions of personal opinions. Rating the entire program commercially influenced correlated with whether attendees considered the funding of referenced research a source of influence. Discussion: CME attendees consider a broad spectrum of factors when reporting commercial influence. Evaluation forms should include bias questions per lecture as well as items to clarify perceived sources and manifestations of commercial influence.

Background Obtaining informed consent in the clinical setting is an important yet challenging aspect of providing safe and collaborative care to patients. While the medical profession has defined best practices for obtaining informed consent, it is unclear whether these standards meet the expressed needs of patients, their families as well as healthcare providers. The authors sought to address this gap by comparing the responses of these three groups with a standardised informed consent paradigm. Methods Piloting a web-based ‘reverse’ simulation paradigm, participants viewed a video showing a standardised doctor engaging in an informed consent discussion. The scenario depicted a simulated patient with psychotic symptoms who is prescribed an atypical antipsychotic medication. 107 participants accessed the simulation online and completed a web-based debriefing survey. Results Survey responses from patients, family members and healthcare providers indicated disparities in information retention, perception of the doctor9s performance and priorities for required elements of the consent process. Conclusions To enhance existing informed consent best practices, steps should be taken to improve patient retention of critical information. Adverse events should be described in the short-term and long-term along with preventative measures, and alternative psychosocial and pharmacological treatment options should be reviewed. Information about treatment should include when the medication takes therapeutic effect and how to safely maintain the treatment. The reverse simulation design is a model that can discern gaps in clinical practice, which can be used to improve patient care.

Article-at-a-Glance Background Ongoing professional practice evaluation (OPPE) activities consist of a quantitative, competency-based evaluation of clinical performance. Hospitals must design assessments that measure clinical competencies, are scalable, and minimize impact on the clinician's daily routines. A psychiatry department at a large academic medical center designed and implemented an interactive Web-based psychiatric simulation focusing on violence risk assessment as a tool for a departmentwide OPPE. Methods Of 412 invited clinicians in a large psychiatry department, 410 completed an online simulation in April–May 2012. Participants received scheduled e-mail reminders with instructions describing how to access the simulation. Using the Computer Simulation Assessment Tool, participants viewed an introductory video and were then asked to conduct a risk assessment, acting as a clinician in the encounter by selecting actions from a series of drop-down menus. Each action was paired with a corresponding video segment of a clinical encounter with a standardized patient. Participants were scored on the basis of their actions within the simulation (Measure 1) and by their responses to the open-ended questions in which they were asked to integrate the information from the simulation in a summative manner (Measure 2). Results Of the 410 clinicians, 381 (92.9%) passed Measure 1, 359 (87.6%) passed Measure 2, and 5 (1.2%) failed both measures. Seventy-five (18.3%) participants were referred for focused professional practice evaluation (FPPE) after failing either Measure 1, Measure 2, or both. Conclusions Overall, Web-based simulation and e-mail engagement tools were a scalable and efficient way to assess a large number of clinicians in OPPE and to identify those who required FPPE.