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van Reekum, C. M.

Publications and source records attributed to van Reekum, C. M..

9 recordsLinked to original sources

Cognitive modes involved in emotion regulation identified using Constrained Principal Component Analysis for fMRI (fMRI-CPCA)

Meta-analyses of functional magnetic resonance imaging (fMRI) studies have identified networks of widely distributed brain regions supporting emotion regulation. These overlap with attentional or cognitive control brain networks. The literature is short on data speaking to specific neurocognitive functions of these broad brain networks in reappraisal - a key emotion regulatory strategy involving the reframing of an event according to a goal to increase or decrease experienced emotion. We address this gap by examining both the spatial configuration and temporal profile of event-related blood oxygenation level dependent (BOLD) responses during a task requiring reappraisal. We analysed fMRI datasets obtained from 84 participants (51% female) who were instructed to increase or decrease their emotional response to unpleasant images. We extracted spatial maps and their estimated temporal event-related BOLD signal changes of four components with the highest loadings. Neurocognitive functions were derived by mapping each component onto templates of previously identified task-based cognitive modes. This analysis yielded four cognitive modes: 1) "multiple demand" 2) "response", 3) "re-evaluation", and 4) "default mode". The temporal profiles showed particularly prominent patterns for the increase and decrease conditions in "multiple demand" (mode 1) and "re-evaluation" (mode 3) respectively. These findings highlight a central role for specific neurocognitive processes linked to attentional control ("multiple demand") and switching ("re-evaluation"), as part of the broad brain networks supporting reappraisal. Moreover, the level of neural engagement of these cognitive modes varies depending on the regulatory goal. These findings provide tangible targets for neurocognitive interventions such as neurostimulation when emotion regulation is compromised.

neuroscience↗

The elusive neural signature of emotion regulation capabilities: evidence from a large-scale consortium

Cognitive reappraisal is a fundamental emotion regulation strategy for mental and physical well-being, but how its neural mechanisms relate to individual differences remains poorly understood. In a consortium effort analyzing 40 fMRI datasets (N=2,175), we examined the relationship between neural activation during reappraisal tasks and three core individual difference indices of reappraisal capabilities: (1) trait questionnaires, (2) task-based affective ratings, and (3) amygdala down-regulation. Strikingly, there was no shared overlap across these three common indices. Only a very weak correlation emerged between amygdala down-regulation and task-based affective ratings. Whole-brain analyses revealed no reliable neural associations with trait questionnaires, and associations with task-based affective ratings fell outside canonical emotion regulation networks (e.g., prefrontal circuitry). Moreover, amygdala down-regulation, often interpreted as a stable individual marker, was confounded by person-specific whole-brain responses -- a limitation extending to fMRI research beyond the emotion regulation domain. These findings challenge the assumption that an individuals prefrontal activity is a valid indicator of their reappraisal capabilities and suggest that common trait, behavioral, and neural measures might capture distinct facets of emotion regulation. More broadly, our results highlight concrete methodological challenges for fMRI research on individual differences, with implications extending beyond emotion regulation to the neuroscience of personality, psychopathology, and general well-being.

neuroscience↗

Temporal dynamics of hippocampal activity predict stable patterns of sensitization or habituation to noxious stimulation across sessions.

Acute pain serves to warn an organism of potential damage. When nociceptive stimulation persists, two possible responses emerge: If no risk of harm is anticipated, habituation may occur. If harm is considered possible, pain sensitization is likely. An individuals adaptation to prolonged pain may provide insight into their ability to manage resources, and possibly their likelihood of developing chronic pain. Yet, little is known about the stability of these individual differences or their underlying neural mechanisms. Eighty-five participants undertook a repetitive noxious stimulation task and a resting-state scan in an MRI scanner, in a first session. They then completed the same task outside the scanner on three separate days. Pain adaptation was operationalized as the slope of change in pain ratings within session. Intraclass correlations were calculated between slopes across the four sessions, which demonstrated high stability and association with emotional disposition. Individuals who habituated to repeated stimuli showed increasing activity in the anterior hippocampus and amygdala, while individuals who sensitized showed increasing activity in the sensorimotor cortices. These clusters were then used as seeds in resting state analysis, with habituation associated with higher functional connectivity between hippocampus/amygdala and ventromedial prefrontal cortex(vmPFC), and higher connectivity between sensorimotor regions and the hippocampus, amygdala and insula cortex. Our findings suggest that pain adaptation is a stable phenotypic trait, which may have implications for the prediction of chronic pain. This study implicates neural sensory and appraisal systems in these stable responses, offering insight into the mechanisms underlying trait-like responses to prolonged nociceptive input.

neuroscience↗

Resting EEG Periodic and Aperiodic Components Predict Cognitive Decline Over 10 Years

Measures of intrinsic brain function at rest show promise as predictors of cognitive decline in humans, including EEG metrics such as individual alpha peak frequency (IAPF) and the aperiodic exponent, reflecting the strongest frequency of alpha oscillations and the relative balance of excitatory:inhibitory neural activity, respectively. Both IAPF and the aperiodic exponent decrease with age and have been associated with worse executive function and working memory. However, few studies have jointly examined their associations with cognitive function, and none have examined their association with longitudinal cognitive decline rather than cross-sectional impairment. In a preregistered secondary analysis of data from the longitudinal Midlife in the United States (MIDUS) study, we tested whether IAPF and aperiodic exponent measured at rest predict cognitive function (N = 235; age at EEG recording M = 55.10, SD = 10.71) over 10 years. The IAPF and the aperiodic exponent interacted to predict decline in overall cognitive ability, even after controlling for age, sex, education, and lag between data collection timepoints. Post-hoc tests showed that "mismatched" IAPF and aperiodic exponents (e.g., higher exponent with lower IAPF) predicted greater cognitive decline compared to "matching" IAPF and aperiodic exponents (e.g., higher exponent with higher IAPF; lower IAPF with lower aperiodic exponent). These effects were largely driven by measures of executive function. Our findings provide the first evidence that IAPF and the aperiodic exponent are joint predictors of cognitive decline from midlife into old age and thus may offer a useful clinical tool for predicting cognitive risk in aging. Significance StatementMeasures of intrinsic brain function at rest assessed noninvasively from the scalp using electroencephalography (EEG) show promise as predictors of cognitive decline in humans. Using data from 235 participants from the Midlife in the United States (MIDUS) longitudinal study, we found two resting EEG markers (individual peak alpha frequency and aperiodic exponent) interacted to predict cognitive decline over a span of 10 years. Follow-up analyses revealed that "mismatched" markers (i.e., high in one and low in the other) predicted greater cognitive decline compared to "matching" markers. Because of the low cost and ease of collecting EEG data at rest, the current research provides evidence for possible scalable clinical applications for identifying individuals at risk for accelerated cognitive decline.

neuroscience↗

Heart Rate Variability Covaries with Amygdala Functional Connectivity During Voluntary Emotion Regulation

The Neurovisceral Integration Model posits that shared neural networks support the effective regulation of emotions and heart rate, with heart rate variability (HRV) serving as an objective, peripheral index of prefrontal inhibitory control. Prior neuroimaging studies have predominantly examined both HRV and associated neural functional connectivity at rest, as opposed to contexts that require active emotion regulation. The present study sought to extend upon previous resting-state functional connectivity findings, examining HRV and corresponding amygdala functional connectivity during a cognitive reappraisal task. Seventy adults (52 old and 18 young adults, 18-84 years, 51% male) received instructions to cognitively reappraise negative and neutral affective images during functional MRI scanning. HRV measures were derived from a finger pulse signal throughout the scan. During the task, young adults exhibited a significant inverse association between HRV and amygdala-medial prefrontal cortex (mPFC) functional connectivity, in which higher HRV was correlated with weaker amygdala-mPFC coupling, whereas old adults displayed a slight positive, albeit non-significant correlation. Furthermore, voxelwise whole-brain functional connectivity analyses showed that higher HRV was linked to weaker right amygdala-posterior cingulate cortex connectivity across old and young adults, and in old adults, higher HRV positively correlated with stronger right amygdala - right ventrolateral prefrontal cortex connectivity. Collectively, these findings highlight the importance of assessing HRV and neural functional connectivity during active regulatory contexts to further identify neural concomitants of HRV and adaptive emotion regulation.

neuroscience↗

How Cognitive and Affective Empathy Relate to Emotion Regulation: Divergent Patterns from Trait and Task-Based Measures

Evidence suggests that empathy and emotion regulation may be related, but few studies have directly investigated this relationship. Here we report two experiments which examined: 1) how different components of empathy (cognitive & affective) relate to the habitual use of cognitive reappraisal to regulate emotions (N=220), and 2) how these components of empathy relate to implicit reappraisal in a context-framing task (N=92). In study 1, a positive correlation between cognitive empathy and reappraisal use was observed. Affective empathy showed no relationship with reappraisal use. In study 2, participants completed an implicit reappraisal task in which previously viewed negative images were paired with either a neutralising (intended to reduce negative emotionality) or descriptive (which simply described the image) framing sentence. Participants then reported how unpleasant/pleasant each image made them feel. In contrast to study 1, a positive correlation between affective empathy and the implicit reappraisal task metric (rating of neutralising-descriptive framing conditions) was observed. There was no relationship between cognitive empathy and implicit reappraisal. These findings suggest that both components of empathy are related to reappraisal, but in different ways: Cognitive empathy is related to more deliberate use of reappraisal, while affective empathy is associated with more implicit reappraisal processes.

animal behavior and cognition↗

The devil is in the detail: The role of threat level and intolerance of uncertainty in extinction

Recent evidence suggests that individual differences in intolerance of uncertainty (IU) are associated with disrupted threat extinction. However, it is unknown what maintains the learned threat association in high IU individuals: is it the experienced uncertainty during extinction or the combination of experienced uncertainty with potential threat during extinction? Here we addressed this question by running two independent experiments with uncertain auditory stimuli that varied in threat level (Experiment 1, aversive human scream (n = 30); Experiment 2, benign tone (n = 47) and mildly aversive tone (n = 49)). During the experiments, we recorded skin conductance responses and subjective ratings to the learned cues during acquisition and extinction. In experiment 1, high IU was associated with heightened skin conductance responding to the learned threat vs. safe cue during extinction. In experiment 2, high IU was associated only with larger skin conductance responding to the learned cues with threatening properties during extinction i.e. mildly aversive tone. These findings suggest that uncertainty in combination with threat, even when mild, disrupts extinction in high IU individuals. Such findings help us understand the link between IU and threat extinction, and its relevance to anxiety disorder pathology.

neuroscience↗

Out with the old and in with the new: The role of intolerance of uncertainty in reversal of threat and safety

The ability to learn and reverse threat associations is crucial for survival. The extent to which old threat associations are inhibited and new threat associations are formed may depend on sensitivity to future threat uncertainty. To assess the extent to which Intolerance of Uncertainty (IU) predicts threat learning and reversal, we recorded expectancy ratings and skin conductance in 44 healthy participants during an associative learning paradigm, where threat and safety contingencies were reversed. During acquisition and reversal, we observed larger SCR magnitude and expectancy ratings for threat vs. safety cues. However, during reversal higher IU was associated with larger SCR magnitude to new threat vs. new safety cues, compared to lower IU. These results were specific to IU-related variance, over shared variance with trait anxiety (STAIX-2). Overall, these findings suggest that individuals high in IU are able to reverse threat and safety associations in the presence of direct threat. Such findings help us understand the recently revealed link between IU and threat extinction, where direct threat is absent. Moreover, these findings highlight the potential relevance of IU in clinical intervention and treatment for anxiety disorders.

neuroscience↗

Multimodal evidence for delayed fear extinction in adolescence and young adulthood.

Previous research in rodents and humans points to an evolutionarily conserved profile of blunted fear extinction during adolescence, underpinned by brain structures such as the amygdala and medial prefrontal cortex (mPFC). In this study, we examine age-related effects on the function and structural connectivity of this system in fear extinction in adolescence and young adulthood. Younger age was associated with greater amygdala activity and delayed mPFC engagement to learned threat cues as compared to safety cues. Furthermore, greater structural integrity of the uncinate fasciculus, a white matter tract that connects the amygdala and mPFC, mediated the relationship between age and acceleration of mPFC engagement during extinction. These findings suggest that age-related changes in the structure and function of amygdala-mPFC circuitry may underlie the protracted maturation of fear regulatory processes, rendering younger individuals more vulnerable to anxiety disorders, which emerge during development.

neuroscience↗