Previous studies have documented the positive effects of mindfulness meditation on executive control. What has been lacking, however, is an understanding of the mechanism underlying this effect. Some theorists have described mindfulness as embodying two facets—present moment awareness and emotional acceptance. Here, we examine how the effect of meditation practice on executive control manifests in the brain, suggesting that emotional acceptance and performance monitoring play important roles. We investigated the effect of meditation practice on executive control and measured the neural correlates of performance monitoring, specifically, the error-related negativity (ERN), a neurophysiological response that occurs within 100 ms of error commission. Meditators and controls completed a Stroop task, during which we recorded ERN amplitudes with electroencephalography. Meditators showed greater executive control (i.e. fewer errors), a higher ERN and more emotional acceptance than controls. Finally, mediation pathway models further revealed that meditation practice relates to greater executive control and that this effect can be accounted for by heightened emotional acceptance, and to a lesser extent, increased brain-based performance monitoring.
A growing body of evidence suggests that empathy for pain is underpinned by neural structures that are also involved in the direct experience of pain. In order to assess the consistency of this finding, an image-based meta-analysis of nine independent functional magnetic resonance imaging (fMRI) investigations and a coordinate-based meta-analysis of 32 studies that had investigated empathy for pain using fMRI were conducted. The results indicate that a core network consisting of bilateral anterior insular cortex and medial/anterior cingulate cortex is associated with empathy for pain. Activation in these areas overlaps with activation during directly experienced pain, and we link their involvement to representing global feeling states and the guidance of adaptive behavior for both self- and other-related experiences. Moreover, the image-based analysis demonstrates that depending on the type of experimental paradigm this core network was co-activated with distinct brain regions: While viewing pictures of body parts in painful situations recruited areas underpinning action understanding (inferior parietal/ventral premotor cortices) to a stronger extent, eliciting empathy by means of abstract visual information about the other's affective state more strongly engaged areas associated with inferring and representing mental states of self and other (precuneus, ventral medial prefrontal cortex, superior temporal cortex, and temporo-parietal junction). In addition, only the picture-based paradigms activated somatosensory areas, indicating that previous discrepancies concerning somatosensory activity during empathy for pain might have resulted from differences in experimental paradigms. We conclude that social neuroscience paradigms provide reliable and accurate insights into complex social phenomena such as empathy and that meta-analyses of previous studies are a valuable tool in this endeavor.
<p>Empathy—the ability to share the feelings of others—is fundamental to our emotional and social lives. Previous human imaging studies focusing on empathy for others' pain have consistently shown activations in regions also involved in the direct pain experience, particularly anterior insula and anterior and midcingulate cortex. These findings suggest that empathy is, in part, based on shared representations for firsthand and vicarious experiences of affective states. Empathic responses are not static but can be modulated by person characteristics, such as degree of alexithymia. It has also been shown that contextual appraisal, including perceived fairness or group membership of others, may modulate empathic neuronal activations. Empathy often involves coactivations in further networks associated with social cognition, depending on the specific situation and information available in the environment. Empathy-related insular and cingulate activity may reflect domain-general computations representing and predicting feeling states in self and others, likely guiding adaptive homeostatic responses and goal-directed behavior in dynamic social contexts.</p>
Anxiety is a debilitating symptom of many psychiatric disorders including generalized anxiety disorder, mood disorders, schizophrenia, and autism. Anxiety involves changes in both central and peripheral biology, yet extant functional imaging studies have focused exclusively on the brain. Here we show, using functional brain and cardiac imaging in sequential brain and cardiac magnetic resonance imaging (MRI) sessions in response to cues that predict either threat (a possible shock) or safety (no possibility of shock), that MR signal change in the amygdala and the prefrontal and insula cortices predicts cardiac contractility to the threat of shock. Participants with greater MR signal change in these regions show increased cardiac contractility to the threat versus safety condition, a measure of the sympathetic nervous system contribution to the myocardium. These findings demonstrate robust neural-cardiac coupling during induced anxiety and indicate that individuals with greater activation in brain regions identified with aversive emotion show larger magnitude cardiac contractility increases to threat.
This article reviews the modern literature on two key aspects of the central circuitry of emotion - the prefrontal cortex (PFC) and the amygdala. There are several different functional divisions of the PFC including the dorsolateral, ventromedial and orbitofrontal sectors. Each of these regions plays some role in affective processing that shares the feature of representing affect in the absence of immediate rewards and punishments as well as in different aspects of emotional regulation. The amygdala appears to be crucial for the learning of new stimulus-threat contingencies and also appears to be important in the expression of cue-specific fear. Individual differences in both tonic activation and phasic reactivity in this circuit play an important role in governing affective style. Emphasis is placed upon affective chronometry, or the time course of emotional responding, as a key attribute of emotion that varies across individuals and is regulated by this circuitry.
Asthma, like many inflammatory disorders, is affected by psychological stress, suggesting that reciprocal modulation may occur between peripheral factors regulating inflammation and central neural circuitry underlying emotion and stress reactivity. Despite suggestions that emotional factors may modulate processes of inflammation in asthma and, conversely, that peripheral inflammatory signals influence the brain, the neural circuitry involved remains elusive. Here we show, using functional magnetic resonance imaging, that activity in the anterior cingulate cortex and insula to asthma-relevant emotional, compared with valence-neutral stimuli, is associated with markers of inflammation and airway obstruction in asthmatic subjects exposed to antigen. This activation accounts for > or =40% of the variance in the peripheral markers and suggests a neural basis for emotion-induced modulation of airway disease in asthma. The anterior cingulate cortex and insula have been implicated in the affective evaluation of sensory stimulation, regulation of homeostatic responses, and visceral perception. In individuals with asthma and other stress-related conditions, these brain regions may be hyperresponsive to disease-specific emotional and afferent physiological signals, which may contribute to the dysregulation of peripheral processes, such as inflammation.
Meditation refers to a family of complex emotional and attentional regulatory practices, which can be classified into two main styles – focused attention (FA) and open monitoring (OM) – involving different attentional, cognitive monitoring and awareness processes. In a functional magnetic resonance study we originally characterized and contrasted FA and OM meditation forms within the same experiment, by an integrated FA–OM design. Theravada Buddhist monks, expert in both FA and OM meditation forms, and lay novices with 10 days of meditation practice, participated in the experiment. Our evidence suggests that expert meditators control cognitive engagement in conscious processing of sensory-related, thought and emotion contents, by massive self-regulation of fronto-parietal and insular areas in the left hemisphere, in a meditation state-dependent fashion. We also found that anterior cingulate and dorsolateral prefrontal cortices play antagonist roles in the executive control of the attention setting in meditation tasks. Our findings resolve the controversy between the hypothesis that meditative states are associated to transient hypofrontality or deactivation of executive brain areas, and evidence about the activation of executive brain areas in meditation. Finally, our study suggests that a functional reorganization of brain activity patterns for focused attention and cognitive monitoring takes place with mental practice, and that meditation-related neuroplasticity is crucially associated to a functional reorganization of activity patterns in prefrontal cortex and in the insula.
OBJECTIVE: The purpose of this study was to use functional magnetic resonance imaging (fMRI) to probe the neural circuitry associated with reactivity to negative and positive affective stimuli in patients with major depressive disorder before treatment and after 2 and 8 weeks of treatment with venlafaxine. Relations between baseline neural activation and response to treatment were also evaluated. METHOD: Patients with major depressive disorder (N=12) and healthy comparison subjects (N=5) were scanned on three occasions, during which trials of alternating blocks of affective and neutral pictorial visual stimuli were presented. Symptoms were evaluated at each testing occasion, and both groups completed self-report measures of mood. Statistical parametric mapping was used to examine the fMRI data with a focus on the group-by-time interactions. RESULTS: Patients showed a significant reduction in depressive symptoms with treatment. Group-by-time interactions in response to the negative versus neutral stimuli were found in the left insular cortex and the left anterior cingulate. At baseline, both groups showed bilateral activation in the visual cortices, lateral prefrontal cortex, and amygdala in response to the negative versus neutral stimuli, with patients showing greater activation in the visual cortex and less activation in the left lateral prefrontal cortex. Patients with greater relative anterior cingulate activation at baseline in response to the negative versus neutral stimuli showed the most robust treatment response. CONCLUSIONS: The findings underscore the importance of the neural circuitry activated by negative affect in depression and indicate that components of this circuitry can be changed within 2 weeks of treatment with antidepressant medication.
OBJECTIVE: Happiness, sadness, and disgust are three emotions that differ in their valence (positive or negative) and associated action tendencies (approach or withdrawal). This study was designed to investigate the neuroanatomical correlates of these discrete emotions. METHOD: Twelve healthy female subjects were studied. Positron emission tomography and [15O]H2O were used to measure regional brain activity. There were 12 conditions per subject: happiness, sadness, and disgust and three control conditions, each induced by film and recall. Emotion and control tasks were alternated throughout. Condition order was pseudo-randomized and counterbalanced across subjects. Analyses focused on brain activity patterns for each emotion when combining film and recall data. RESULTS: Happiness, sadness, and disgust were each associated with increases in activity in the thalamus and medial prefrontal cortex (Brodmann's area 9). These three emotions were also associated with activation of anterior and posterior temporal structures, primarily when induced by film. Recalled sadness was associated with increased activation in the anterior insula. Happiness was distinguished from sadness by greater activity in the vicinity of ventral mesial frontal cortex. CONCLUSIONS: While this study should be considered preliminary, it identifies regions of the brain that participate in happiness, sadness, and disgust, regions that distinguish between positive and negative emotions, and regions that depend on both the elicitor and valence of emotion or their interaction.
Recent theoretical and empirical work in cognitive science and neuroscience is brought into contact with the concept of the flow experience. After a brief exposition of brain function, the explicit-implicit distinction is applied to the effortless information processing that is so characteristic of the flow state. The explicit system is associated with the higher cognitive functions of the frontal lobe and medial temporal lobe structures and has evolved to increase cognitive flexibility. In contrast, the implicit system is associated with the skill-based knowledge supported primarily by the basal ganglia and has the advantage of being more efficient. From the analysis of this flexibility/efficiency trade-off emerges a thesis that identifies the flow state as a period during which a highly practiced skill that is represented in the implicit system's knowledge base is implemented without interference from the explicit system. It is proposed that a necessary prerequisite to the experience of flow is a state of transient hypofrontality that enables the temporary suppression of the analytical and meta-conscious capacities of the explicit system. Examining sensory-motor integration skills that seem to typify flow such as athletic performance, writing, and free-jazz improvisation, the new framework clarifies how this concept relates to creativity and opens new avenues of research.
In children, behavioral inhibition (BI) in response to potential threat predicts the development of anxiety and affective disorders, and primate lesion studies suggest involvement of the orbitofrontal cortex (OFC) in mediating BI. Lesion studies are essential for establishing causality in brain-behavior relationships, but should be interpreted cautiously because the impact of a discrete lesion on a complex neural circuit extends beyond the lesion location. Complementary functional imaging methods assessing how lesions influence other parts of the circuit can aid in precisely understanding how lesions affect behavior. Using this combination of approaches in monkeys, we found that OFC lesions concomitantly alter BI and metabolism in the bed nucleus of stria terminalis (BNST) region and that individual differences in BNST activity predict BI. Thus it appears that an important function of the OFC in response to threat is to modulate the BNST, which may more directly influence the expression of BI.
Positive affect elicited in a mother toward her newborn infant may be one of the most powerful and evolutionarily preserved forms of positive affect in the emotional landscape of human behavior. This study examined the neurobiology of this form of positive emotion and in so doing, sought to overcome the difficulty of eliciting robust positive affect in response to visual stimuli in the physiological laboratory. Six primiparous human mothers with no indications of postpartum depression brought their infants into the laboratory for a photo shoot. Approximately 6 weeks later, they viewed photographs of their infant, another infant, and adult faces during acquisition of functional magnetic resonance images (fMRI). Mothers exhibited bilateral activation of the orbitofrontal cortex (OFC) while viewing pictures of their own versus unfamiliar infants. While in the scanner, mothers rated their mood more positively for pictures of their own infants than for unfamiliar infants, adults, or at baseline. The orbitofrontal activation correlated positively with pleasant mood ratings. In contrast, areas of visual cortex that also discriminated between own and unfamiliar infants were unrelated to mood ratings. These data implicate the orbitofrontal cortex in a mother's affective responses to her infant, a form of positive emotion that has received scant attention in prior human neurobiological studies. Furthermore, individual variations in orbitofrontal activation to infant stimuli may reflect an important dimension of maternal attachment.
There is mounting evidence that prefrontal cortex (PFC) is activated during mnemonic operations such as working memory maintenance and also during response-related operations. In the current study, we examine the neural organization of mnemonic and response operations with respect to each other within PFC. Stimulus-evoked and sustained functional MRI activity was recorded during performance of a mental calculation task. The presence or absence of mnemonic and response demands was manipulated in a 2 x 2 factorial design with conditions requiring: (1) memory encoding and maintenance (M+); (2) response selection and execution (R+); (3) encoding, maintenance, and response execution (M+R+); (4) neither mnemonic nor response-related processes (M-R-). The first step of the analyses identified PFC voxels exhibiting differential activity during (M+) vs. (R+) trials. Within these voxels, we then examined activity during multiple phases of (M+R+) trials. Greater stimulus-evoked and sustained activity was observed within the anterior extent of dorsolateral prefrontal cortex (BA 46) during R+ vs. M+ trials. In contrast, greater activity was observed in the posterior extent of dorsolateral PFC during M+ vs. R+ trials. Importantly, both regions were activated during (M+R+) trials. Activity levels during all of these conditions exceeded levels observed during (M-R-) control trials. These results suggest that integrative functions of PFC that allow past information to guide future actions may emerge from communication between discrete subregions supporting mnemonic and response operations.
Pain can be modulated by several cognitive techniques, typically involving increased cognitive control and decreased sensory processing. Recently, it has been demonstrated that pain can also be attenuated by mindfulness. Here, we investigate the underlying brain mechanisms by which the state of mindfulness reduces pain. Mindfulness practitioners and controls received unpleasant electric stimuli in the functional magnetic resonance imaging scanner during a mindfulness and a control condition. Mindfulness practitioners, but not controls, were able to reduce pain unpleasantness by 22% and anticipatory anxiety by 29% during a mindful state. In the brain, this reduction was associated with decreased activation in the lateral prefrontal cortex and increased activation in the right posterior insula during stimulation and increased rostral anterior cingulate cortex activation during the anticipation of pain. These findings reveal a unique mechanism of pain modulation, comprising increased sensory processing and decreased cognitive control, and are in sharp contrast to established pain modulation mechanisms.
Increasing research indicates that concepts are represented as distributed circuits of property information across the brain's modality-specific areas. The current study examines the distributed representation of an important but under-explored category, foods. Participants viewed pictures of appetizing foods (along with pictures of locations for comparison) during event-related fMRI. Compared to location pictures, food pictures activated the right insula/operculum and the left orbitofrontal cortex, both gustatory processing areas. Food pictures also activated regions of visual cortex that represent object shape. Together these areas contribute to a distributed neural circuit that represents food knowledge. Not only does this circuit become active during the tasting of actual foods, it also becomes active while viewing food pictures. Via the process of pattern completion, food pictures activate gustatory regions of the circuit to produce conceptual inferences about taste. Consistent with theories that ground knowledge in the modalities, these inferences arise as reenactments of modality-specific processing.
The experience of pain arises from both physiological and psychological factors, including one's beliefs and expectations. Thus, placebo treatments that have no intrinsic pharmacological effects may produce analgesia by altering expectations. However, controversy exists regarding whether placebos alter sensory pain transmission, pain affect, or simply produce compliance with the suggestions of investigators. In two functional magnetic resonance imaging (fMRI) experiments, we found that placebo analgesia was related to decreased brain activity in pain-sensitive brain regions, including the thalamus, insula, and anterior cingulate cortex, and was associated with increased activity during anticipation of pain in the prefrontal cortex, providing evidence that placebos alter the experience of pain.
<p>Measures of left-right asymmetry in resting brain activity were derived from spectral estimates of electroencephalogram (EEG) alpha-band power density in 13 homologous scalp electrode pairs from 81 right-handed individuals (43 F) on two occasions separated by 6 weeks. At a third, later session, these individuals completed a cognitive task, comparing word-pairs that systematically differed in affective tone. For an extended series of paired-comparisons, the subject chose the one word-pair that 'went together best'. Objectively, associative strength was comparable for both word-pairs. Individuals with relatively greater left-sided anterior frontal resting activity were more likely to select the more pleasant word-pair. Relations between word-pair selection and asymmetry in resting brain activity at central and posterior sites were not significant.</p>
Individuals with fragile X syndrome (FXS) commonly display characteristics of social anxiety, including gaze aversion, increased time to initiate social interaction, and difficulty forming meaningful peer relationships. While neural correlates of face processing, an important component of social interaction, are altered in FXS, studies have not examined whether social anxiety in this population is related to higher cognitive processes, such as memory. This study aimed to determine whether the neural circuitry involved in face encoding was disrupted in individuals with FXS, and whether brain activity during face encoding was related to levels of social anxiety. A group of 11 individuals with FXS (5 M) and 11 age- and gender-matched control participants underwent fMRI scanning while performing a face encoding task with online eye-tracking. Results indicate that compared to the control group, individuals with FXS exhibited decreased activation of prefrontal regions associated with complex social cognition, including the medial and superior frontal cortex, during successful face encoding. Further, the FXS and control groups showed significantly different relationships between measures of social anxiety (including gaze-fixation) and brain activity during face encoding. These data indicate that social anxiety in FXS may be related to the inability to successfully recruit higher level social cognition regions during the initial phases of memory formation.
We examined whether resting anterior electroencephalographic (EEG) asymmetry in the alpha frequency band has psychometric properties that would be expected of a measure assessing individual differences. In each of two experimental sessions, separated by three weeks, resting EEG in midfrontal and anterior temporal sites was recorded from 85 female adults during eight 60-s baselines. Resting alpha asymmetry demonstrated acceptable test-retest stability and excellent internal consistency reliability. Analyses including other frequency bands indicated that degree of stability varied somewhat as a function of band and region. In addition, asymmetry was less stable than absolute power. Discussion focuses on the implications of the present findings for the measurement and conceptualization of resting anterior asymmetry.
BACKGROUND: Anhedonia, a reduced ability to experience pleasure, is a chief symptom of major depressive disorder and is related to reduced frontostriatal connectivity when attempting to upregulate positive emotion. The present study examined another facet of positive emotion regulation associated with anhedonia-namely, the downregulation of positive affect-and its relation to prefrontal cortex (PFC) activity. METHODS: Neuroimaging data were collected from 27 individuals meeting criteria for major depressive disorder as they attempted to suppress positive emotion during a positive emotion regulation task. Their PFC activation pattern was compared with the PFC activation pattern exhibited by 19 healthy control subjects during the same task. Anhedonia scores were collected at three time points: at baseline (time 1), 8 weeks after time 1 (i.e., time 2), and 6 months after time 1 (i.e., time 3). Prefrontal cortex activity at time 1 was used to predict change in anhedonia over time. Analyses were conducted utilizing hierarchical linear modeling software. RESULTS: Depressed individuals who could not inhibit positive emotion-evinced by reduced right ventrolateral prefrontal cortex activity during attempts to dampen their experience of positive emotion in response to positive visual stimuli-exhibited a steeper anhedonia reduction slope between baseline and 8 weeks of treatment with antidepressant medication (p < .05). Control subjects showed a similar trend between baseline and time 3. CONCLUSIONS: To reduce anhedonia, it may be necessary to teach individuals how to counteract the functioning of an overactive pleasure-dampening prefrontal inhibitory system.
Working memory (WM) comprises operations whose coordinated action contributes to our ability to maintain focus on goal-relevant information in the presence of distraction. The present study investigated the nature of distraction upon the neural correlates of WM maintenance operations by presenting task-irrelevant distracters during the interval between the memoranda and probes of a delayed-response WM task. The study used a region of interest (ROIs) approach to investigate the role of anterior (e.g., lateral and medial prefrontal cortex--PFC) and posterior (e.g., parietal and fusiform cortices) brain regions that have been previously associated with WM operations. Behavioral results showed that distracters that were confusable with the memorandum impaired WM performance, compared to either the presence of non-confusable distracters or to the absence of distracters. These different levels of distraction led to differences in the regional patterns of delay interval activity measured with event-related functional magnetic resonance imaging (fMRI). In the anterior ROIs, dorsolateral PFC activation was associated with WM encoding and maintenance, and in maintaining a preparatory state, and ventrolateral PFC activation was associated with the inhibition of distraction. In the posterior ROIs, activation of the posterior parietal and fusiform cortices was associated with WM and perceptual processing, respectively. These findings provide novel evidence concerning the neural systems mediating the cognitive and behavioral responses during distraction, and places frontal cortex at the top of the hierarchy of the neural systems responsible for cognitive control.
Baseline resting electroencephalogram (EEG) activity was recorded from 6 normothymic depressives and 8 controls using three different reference montages. Power in all frequency bands was extracted by Fourier transformation. Significant Group X Region X Hemisphere interactions were found consistently for alpha band power only. Previously depressed subjects had less left-sided anterior and less right-sided posterior activation (i.e., more alpha activity) than did never depressed subjects. Previously depressed subjects had no history of pharmacological treatment and did not differ from controls in emotional state at the time of testing. The pattern of anterior and posterior asymmetry in the previously depressed subjects is similar to that found in acutely depressed subjects and suggests that this may be a state-independent marker for depression.