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On the basis of a review of the extant literature describing emotion-cognition interactions, the authors propose 4 methodological desiderata for studying how task-irrelevant affect modulates cognition and present data from an experiment satisfying them. Consistent with accounts of the hemispheric asymmetries characterizing withdrawal-related negative affect and visuospatial working memory (WM) in prefrontal and parietal cortices, threat-induced anxiety selectively disrupted accuracy of spatial but not verbal WM performance. Furthermore, individual differences in physiological measures of anxiety statistically mediated the degree of disruption. A second experiment revealed that individuals characterized by high levels of behavioral inhibition exhibited more intense anxiety and relatively worse spatial WM performance in the absence of threat, solidifying the authors' inference that anxiety causally mediates disruption. These observations suggest a revision of extant models of how anxiety sculpts cognition and underscore the utility of the desiderata.
Research on the neural substrates of emotion has found evidence for cortical asymmetries for aspects of emotion. A recent article by Nicholls et al. has used a new imaging method to interrogate facial movement in 3D to assess possible asymmetrical action during expressions of happiness and sadness. Greater left-sided movement, particularly during expressions of sadness was observed. These findings have implications for understanding hemispheric differences in emotion and lend support to the notion that aspects of emotion processing might be differentially localized in the two hemispheres.
Compassion is a key motivator of altruistic behavior, but little is known about individuals’ capacity to cultivate compassion through training. We examined whether compassion may be systematically trained by testing whether (i) short-term compassion training increases altruistic behavior, and (ii) individual differences in altruism are associated with training-induced changes in neural responses to suffering. In healthy young adults, we found that compassion training increased altruistic redistribution of funds to a victim encountered outside of the training context. Furthermore, greater altruistic behavior after compassion training was associated with altered activation in regions implicated in social cognition and emotion regulation, including the inferior parietal cortex, dorsolateral prefrontal cortex (DLPFC), and DLPFC connectivity with the nucleus accumbens. These results suggest that compassion can be cultivated with training, where greater altruistic behavior may emerge from increased engagement in neural systems implicated in understanding the suffering of others, executive and emotional control, and reward processing.
Muscle or electromyogenic (EMG) artifact poses a serious risk to inferential validity for any electroencephalography (EEG) investigation in the frequency-domain owing to its high amplitude, broad spectrum, and sensitivity to psychological processes of interest. Even weak EMG is detectable across the scalp in frequencies as low as the alpha band. Given these hazards, there is substantial interest in developing EMG correction tools. Unfortunately, most published techniques are subjected to only modest validation attempts, rendering their utility questionable. We review recent work by our laboratory quantitatively investigating the validity of two popular EMG correction techniques, one using the general linear model (GLM), the other using temporal independent component analysis (ICA). We show that intra-individual GLM-based methods represent a sensitive and specific tool for correcting on-going or induced, but not evoked (phase-locked) or source-localized, spectral changes. Preliminary work with ICA shows that it may not represent a panacea for EMG contamination, although further scrutiny is strongly warranted. We conclude by describing emerging methodological trends in this area that are likely to have substantial benefits for basic and applied EEG research.
Recent years have witnessed a renewed interest in using oscillatory brain electrical activity to understand the neural bases of cognition and emotion. Electrical signals originating from pericranial muscles represent a profound threat to the validity of such research. Recently, McMenamin et al (2010) examined whether independent component analysis (ICA) provides a sensitive and specific means of correcting electromyogenic (EMG) artifacts. This report sparked the accompanying commentary (Olbrich, Jödicke, Sander, Himmerich & Hegerl, in press), and here we revisit the question of how EMG can alter inferences drawn from the EEG and what can be done to minimize its pernicious effects. Accordingly, we briefly summarize salient features of the EMG problem and review recent research investigating the utility of ICA for correcting EMG and other artifacts. We then directly address the key concerns articulated by Olbrich and provide a critique of their efforts at validating ICA. We conclude by identifying key areas for future methodological work and offer some practical recommendations for intelligently addressing EMG artifact.
Recent years have seen an explosion of interest in using neural oscillations to characterize the mechanisms supporting cognition and emotion. Oftentimes, oscillatory activity is indexed by mean power density in predefined frequency bands. Some investigators use broad bands originally defined by prominent surface features of the spectrum. Others rely on narrower bands originally defined by spectral factor analysis (SFA). Presently, the robustness and sensitivity of these competing band definitions remains unclear. Here, a Monte Carlo-based SFA strategy was used to decompose the tonic ("resting" or "spontaneous") electroencephalogram (EEG) into five bands: delta (1-5Hz), alpha-low (6-9Hz), alpha-high (10-11Hz), beta (12-19Hz), and gamma (>21Hz). This pattern was consistent across SFA methods, artifact correction/rejection procedures, scalp regions, and samples. Subsequent analyses revealed that SFA failed to deliver enhanced sensitivity; narrow alpha sub-bands proved no more sensitive than the classical broadband to individual differences in temperament or mean differences in task-induced activation. Other analyses suggested that residual ocular and muscular artifact was the dominant source of activity during quiescence in the delta and gamma bands. This was observed following threshold-based artifact rejection or independent component analysis (ICA)-based artifact correction, indicating that such procedures do not necessarily confer adequate protection. Collectively, these findings highlight the limitations of several commonly used EEG procedures and underscore the necessity of routinely performing exploratory data analyses, particularly data visualization, prior to hypothesis testing. They also suggest the potential benefits of using techniques other than SFA for interrogating high-dimensional EEG datasets in the frequency or time-frequency (event-related spectral perturbation, event-related synchronization/desynchronization) domains.
The degree to which perceived controllability alters the way a stressor is experienced varies greatly among individuals. We used functional magnetic resonance imaging to examine the neural activation associated with individual differences in the impact of perceived controllability on self-reported pain perception. Subjects with greater activation in response to uncontrollable (UC) rather than controllable (C) pain in the pregenual anterior cingulate cortex (pACC), periaqueductal gray (PAG), and posterior insula/SII reported higher levels of pain during the UC versus C conditions. Conversely, subjects with greater activation in the ventral lateral prefrontal cortex (VLPFC) in anticipation of pain in the UC versus C conditions reported less pain in response to UC versus C pain. Activation in the VLPFC was significantly correlated with the acceptance and denial subscales of the COPE inventory [Carver, C. S., Scheier, M. F., & Weintraub, J. K. Assessing coping strategies: A theoretically based approach. Journal of Personality and Social Psychology, 56, 267-283, 1989], supporting the interpretation that this anticipatory activation was associated with an attempt to cope with the emotional impact of uncontrollable pain. A regression model containing the two prefrontal clusters (VLPFC and pACC) predicted 64% of the variance in pain rating difference, with activation in the two additional regions (PAG and insula/SII) predicting almost no additional variance. In addition to supporting the conclusion that the impact of perceived controllability on pain perception varies highly between individuals, these findings suggest that these effects are primarily top-down, driven by processes in regions of the prefrontal cortex previously associated with cognitive modulation of pain and emotion regulation.
It has been argued that emotion, pain, and cognitive control are functionally segregated in distinct subdivisions of the cingulate cortex. But recent observations encourage a fundamentally different view. Imaging studies indicate that negative affect, pain, and cognitive control activate an overlapping region of dorsal cingulate, the anterior midcingulate cortex (aMCC). Anatomical studies reveal that aMCC constitutes a hub where information about reinforcers can be linked to motor centers responsible for expressing affect and executing goal-directed behavior. Computational modeling and other kinds of evidence suggest that this intimacy reflects control processes that are common to all three domains. These observations compel a reconsideration of dorsal cingulate’s contribution to negative affect and pain.
Children with an anxious temperament (AT) are at risk for developing psychiatric disorders along the internalizing spectrum, including anxiety and depression. Like these disorders, AT is a multidimensional phenotype and children with extreme anxiety show varying mixtures of physiological, behavioral, and other symptoms. Using a well-validated juvenile monkey model of AT, we addressed the degree to which this phenotypic heterogeneity reflects fundamental differences or similarities in the underlying neurobiology. The rhesus macaque is optimal for studying AT because children and young monkeys express the anxious phenotype in similar ways and have similar neurobiology. Fluorodeoxyglucose (FDG)-positron emission tomography (FDG-PET) in 238 freely behaving monkeys identified brain regions where metabolism predicted variation in three dimensions of the AT phenotype: hypothalamic-pituitary-adrenal (HPA) activity, freezing behavior, and expressive vocalizations. We distinguished brain regions that predicted all three dimensions of the phenotype from those that selectively predicted a single dimension. Elevated activity in the central nucleus of the amygdala and the anterior hippocampus was consistently found across individuals with different presentations of AT. In contrast, elevated activity in the lateral anterior hippocampus was selective to individuals with high levels of HPA activity, and decreased activity in the motor cortex (M1) was selective to those with high levels of freezing behavior. Furthermore, activity in these phenotype-selective regions mediated relations between amygdala metabolism and different expressions of anxiety. These findings provide a framework for understanding the mechanisms that lead to heterogeneity in the clinical presentation of internalizing disorders and set the stage for developing improved interventions.
BACKGROUND: Anxious temperament (AT) is identifiable early in life and predicts the later development of anxiety disorders and depression. Neuropeptide Y (NPY) is a putative endogenous anxiolytic neurotransmitter that adaptively regulates responses to stress and might confer resilience to stress-related psychopathology. With a well-validated nonhuman primate model of AT, we examined expression of the NPY system in the central nucleus (Ce) of the amygdala, a critical neural substrate for extreme anxiety. METHODS: In 24 young rhesus monkeys, we measured Ce messenger RNA (mRNA) levels of all members of the NPY system that are detectable in the Ce with quantitative real time polymerase chain reaction. We then examined the relationship between these mRNA levels and both AT expression and brain metabolism. RESULTS: Lower mRNA levels of neuropeptide Y receptor 1 (NPY1R) and NPY5R but not NPY or NPY2R in the Ce predicted elevated AT; mRNA levels for NPY1R and NPY5R in the motor cortex were not related to AT. In situ hybridization analysis provided for the first time a detailed description of NPY1R and NPY5R mRNA distribution in the rhesus amygdala and associated regions. Lastly, mRNA levels for these two receptors in the Ce predicted metabolic activity in several regions that have the capacity to regulate the Ce. CONCLUSIONS: Decreased NPY signaling in the Ce might contribute to the altered metabolic activity that is a component of the neural substrate underlying AT. This suggests that enhancement of NPY signaling might reduce the risk to develop psychopathology.
Anhedonia, the loss of pleasure or interest in previously rewarding stimuli, is a core feature of major depression. While theorists have argued that anhedonia reflects a reduced capacity to experience pleasure, evidence is mixed as to whether anhedonia is caused by a reduction in hedonic capacity. An alternative explanation is that anhedonia is due to the inability to sustain positive affect across time. Using positive images, we used an emotion regulation task to test whether individuals with depression are unable to sustain activation in neural circuits underlying positive affect and reward. While up-regulating positive affect, depressed individuals failed to sustain nucleus accumbens activity over time compared with controls. This decreased capacity was related to individual differences in self-reported positive affect. Connectivity analyses further implicated the fronto-striatal network in anhedonia. These findings support the hypothesis that anhedonia in depressed patients reflects the inability to sustain engagement of structures involved in positive affect and reward.
Individuals show marked variation in their responses to threat. Such individual differences in “behavioral inhibition” (BI) play a profound role in mental and physical wellbeing. BI is thought to reflect variation in the sensitivity of a distributed neural system responsible for generating anxiety and organizing defensive responses in response to threat and punishment. Although progress has been made in identifying the key constituents of this behavioral inhibition system (BIS) in humans, the involvement of dorsolateral prefrontal cortex (dlPFC) remains unclear. Here, we acquired self-reported BIS-sensitivity and high-density EEG from a large sample (n=51). Using the enhanced spatial resolution afforded by source modeling techniques, we show that individuals with greater tonic activity in right posterior dlPFC rate themselves as more behaviorally inhibited. This observation provides novel support for recent conceptualizations of BI and clues to the mechanisms that might underlie variation in threat-induced negative affect.
Stress can fundamentally alter neural responses to incoming information. Recent research suggests that stress and anxiety shift the balance of attention away from a task-directed mode, governed by prefrontal cortex (PFC), to a sensory-vigilance mode, governed by the amygdala and other threat-sensitive regions. A key untested prediction of this framework is that stress exerts dissociable effects on different stages of information processing. This study exploited the temporal resolution afforded by event-related potentials to disentangle the impact of stress on vigilance, indexed by early perceptual activity, from its impact on task-directed cognition, indexed by later post-perceptual activity in humans. Results indicated that threat-of-shock amplified stress, measured using retrospective ratings and concurrent facial electromyography (EMG). Stress also double-dissociated early sensory-specific from the later task-directed processing of emotionally-neutral stimuli: stress amplified N1 (184-236 ms) and attenuated P3 (316-488 ms) activity. This demonstrates that stress can have strikingly different consequences at different processing stages. Consistent with recent suggestions, stress amplified earlier extrastriate activity in a manner consistent with vigilance for threat (N1), but disrupted later activity associated with the evaluation of task-relevant information (P3). These results provide a novel basis for understanding how stress can modulate information processing in everyday life and stress-sensitive disorders.
Despite growing interest in emotion regulation, the degree to which psychophysiological measures of emotion regulation are stable over time remains unknown. We examined four-week test-retest reliability of corrugator electromyographic and eyeblink startle measures of negative emotion and its regulation. Both measures demonstrated similar sensitivity to the emotion manipulation, but only individual differences in corrugator modulation and regulation showed adequate reliability. Startle demonstrated diminished sensitivity to the regulation instructions across assessments and poor reliability. This suggests that corrugator represents a trait-like measure of voluntary emotion regulation, whereas startle should be used with caution for assessing individual differences. The data also suggest that corrugator and startle might index partially dissociable constructs and underscore the need to collect multiple measures of emotion.
Planned and reflexive behaviors often occur in the presence of emotional stimuli and within the context of an individual's acute emotional state. Therefore, determining the manner in which emotion and attention interact is an important step toward understanding how we function in the real world. Participants in the current investigation viewed centrally displayed, task-irrelevant, face distractors (angry, neutral, happy) while performing a lateralized go/no-go continuous performance task. Lateralized go targets and no-go lures that did not spatially overlap with the faces were employed to differentially probe processing in the left (LH) and right (RH) cerebral hemispheres. There was a significant interaction between expression and hemisphere, with an overall pattern such that angry distractors were associated with relatively more RH inhibitory errors than neutral or happy distractors and happy distractors with relatively more LH inhibitory errors than angry or neutral distractors. Simple effects analyses confirmed that angry faces differentially interfered with RH relative to LH inhibition and with inhibition in the RH relative to happy faces. A significant three-way interaction further revealed that state anxiety moderated relations between emotional expression and hemisphere. Under conditions of low cognitive load, more intense anxiety was associated with relatively greater RH than LH impairment in the presence of both happy and threatening distractors. By contrast, under high load, only angry distractors produced greater RH than LH interference as a function of anxiety.
Muscle electrical activity, or "electromyogenic" (EMG) artifact, poses a serious threat to the validity of electroencephalography (EEG) investigations in the frequency domain. EMG is sensitive to a variety of psychological processes and can mask genuine effects or masquerade as legitimate neurogenic effects across the scalp in frequencies at least as low as the alpha band (8-13 Hz). Although several techniques for correcting myogenic activity have been described, most are subjected to only limited validation attempts. Attempts to gauge the impact of EMG correction on intracerebral source models (source "localization" analyses) are rarer still. Accordingly, we assessed the sensitivity and specificity of one prominent correction tool, independent component analysis (ICA), on the scalp and in the source-space using high-resolution EEG. Data were collected from 17 participants while neurogenic and myogenic activity was independently varied. Several protocols for classifying and discarding components classified as myogenic and non-myogenic artifact (e.g., ocular) were systematically assessed, leading to the exclusion of one-third to as much as three-quarters of the variance in the EEG. Some, but not all, of these protocols showed adequate performance on the scalp. Indeed, performance was superior to previously validated regression-based techniques. Nevertheless, ICA-based EMG correction exhibited low validity in the intracerebral source-space, likely owing to incomplete separation of neurogenic from myogenic sources. Taken with prior work, this indicates that EMG artifact can substantially distort estimates of intracerebral spectral activity. Neither regression- nor ICA-based EMG correction techniques provide complete safeguards against such distortions. In light of these results, several practical suggestions and recommendations are made for intelligently using ICA to minimize EMG and other common artifacts.
EEG and EEG source-estimation are susceptible to electromyographic artifacts (EMG) generated by the cranial muscles. EMG can mask genuine effects or masquerade as a legitimate effect-even in low frequencies, such as alpha (8-13 Hz). Although regression-based correction has been used previously, only cursory attempts at validation exist, and the utility for source-localized data is unknown. To address this, EEG was recorded from 17 participants while neurogenic and myogenic activity were factorially varied. We assessed the sensitivity and specificity of four regression-based techniques: between-subjects, between-subjects using difference-scores, within-subjects condition-wise, and within-subject epoch-wise on the scalp and in data modeled using the LORETA algorithm. Although within-subject epoch-wise showed superior performance on the scalp, no technique succeeded in the source-space. Aside from validating the novel epoch-wise methods on the scalp, we highlight methods requiring further development.