We are interested in investigating white matter connectivity using a novel computational framework that does not use diffusion tensor imaging (DTI) but only uses T1-weighted magnetic resonance imaging. The proposed method relies on correlating Jacobian determinants across different voxels based on the tensor-based morphometry (TBM) framework. In this paper, we show agreement between the TBM-based white matter connectivity and the DTI-based white matter atlas. As an application, altered white matter connectivity in a clinical population is determined.
To test the effects of cortisol on affective experience, the authors orally administered a placebo, 20 mg cortisol, or 40 mg cortisol to 85 men. Participants' affective responses to negative and neutral stimuli were measured. Self-reported affective state was also assessed. Participants in the 40-mg group (showing extreme cortisol elevations within the physiological range) rated neutral stimuli as more highly arousing than did participants in the placebo and 20-mg groups. Furthermore, within the 20-mg group, individuals with higher cortisol elevations made higher arousal ratings of neutral stimuli. However, cortisol was unrelated to self-reported affective state. Thus, findings indicate that acute cortisol elevations cause heightened arousal in response to objectively nonarousing stimuli, in the absence of effects on mood.
Individual differences in emotional reactivity or affective style can be decomposed into more elementary constituents. Several separable of affective style are identified such as the threshold for reactivity, peak amplitude of response, the rise time to peak and the recovery time. latter two characteristics constitute components of affective chronometry The circuitry that underlies two fundamental forms of motivation and and withdrawal-related processes-is described. Data on differences in functional activity in certain components of these are next reviewed, with an emphasis on the nomological network of surrounding individual differences in asymmetric prefrontal The relevance of such differences for understanding the nature affective dysfunction in affective disorders is then considered. The ends by considering what the prefrontal cortex “does” in certain of affective style and highlights some of the important questions for future research.
Functional neuroimaging studies have implicated the fusiform gyri (FG) in structural encoding of faces, while event-related potential (ERP) and magnetoencephalography studies have shown that such encoding occurs approximately 170 ms poststimulus. Behavioral and functional neuroimaging studies suggest that processes involved in face recognition may be strongly modulated by socially relevant information conveyed by faces. To test the hypothesis that affective information indeed modulates early stages of face processing, ERPs were recorded to individually assessed liked, neutral, and disliked faces and checkerboard-reversal stimuli. At the N170 latency, the cortical three-dimensional distribution of current density was computed in stereotactic space using a tomographic source localization technique. Mean activity was extracted from the FG, defined by structure-probability maps, and a meta-cluster delineated by the coordinates of the voxel with the strongest face-sensitive response from five published functional magnetic resonance imaging studies. In the FG, approximately 160 ms poststimulus, liked faces elicited stronger activation than disliked and neutral faces and checkerboard-reversal stimuli. Further, confirming recent results, affect-modulated brain electrical activity started very early in the human brain (approximately 112 ms). These findings suggest that affective features conveyed by faces modulate structural face encoding. Behavioral results from an independent study revealed that the stimuli were not biased toward particular facial expressions and confirmed that liked faces were rated as more attractive. Increased FG activation for liked faces may thus be interpreted as reflecting enhanced attention due to their saliency.
An emotion-modulated acoustic startle paradigm for inducing positive and negative affect was used to address pregoal and postgoal affect. Participants played a computerized lottery task in which they chose digits that could match a subsequently displayed, random set of numbers. In the positive conditions, matches led to monetary rewards. In the negative condition, matches led to an aversive noise blast. In three experiments, we found eyeblink startle magnitude was potentiated just prior to feedback concerning reward outcome, suppressed following the feedback that a monetary reward was won, and potentiated when threatened with an aversive noise. When presented with a 0%, 45%, 90%, or 100% chance of winning, higher probabilities suppressed startle response after feedback whereas the 45% trials did not. These data indicate that postgoal positive affect (winning reward) reliably suppressed the startle response whereas pregoal positive affect did not.
Individuals with asthma have twice the risk of developing mood and anxiety disorders as individuals without asthma and these psychological factors are associated with worse outcomes and greater need for medical intervention. Similarly, asthma symptom onset and exacerbation often occur during times of increased psychological stress. Remission from depression, on the other hand, is associated with improvement in asthma symptoms and decreased usage of asthma medication. Yet research aimed at understanding the biological underpinnings of asthma has focused almost exclusively on the periphery. An extensive literature documents the relationship between emotion and asthma, but little work has explored the function of affective neural circuitry in asthma symptom expression. Therefore, the following review integrates neuroimaging research related to factors that may impact symptom expression in asthma, such as individual differences in sensitivity to visceral signals, the influence of expectation and emotion on symptom perception, and changes related to disease chronicity, such as conditioning and plasticity. The synthesis of these literatures suggests that the insular and anterior cingulate cortices, in addition to other brain regions previously implicated in the regulation of emotion, may be both responsive to asthma-related bodily changes and important in influencing the appearance and persistence of symptom expression in asthma.
This article reviews the author's program of research on the neural substrates of emotion and affective style and their behavioral and peripheral biological correlates. Two core dimensions along which affect is organized are approach and withdrawal. Some of the key circuitry underlying approach and withdrawal components of emotion is reviewed with an emphasis on the role played by different sectors of the prefrontal cortex (PFC) and amygdala. Affective style refers to individual differences in valence-specific features of emotional reactivity and regulation. The different parameters of affective style can be objectively measured using specific laboratory probes. Relations between individual differences in prefrontal and amygdala function and specific components of affective style are illustrated. The final section of the article concludes with a brief discussion of plasticity in the central circuitry of emotion and the possibility that this circuitry can be shaped by training experiences that might potentially promote a more resilient, positive affective style. The implications of this body of work for a broader conception of psychophysiology and for training the next generation of psychophysiologists are considered in the conclusion.
This past year has seen significant advances in our understanding of the physiology of emotion. Attention continues to focus on the amygdala and its interconnections with prefrontal cortical regions. New evidence underscores the importance of lateralization for emotion. There are also new findings on the physiological predictors of individual differences in emotional behavior and experience, and on the role of autonomic arousal in emotional memory.
Considerable evidence exists to support an association between psychological states and immune function. However, the mechanisms by which such states are instantiated in the brain and influence the immune system are poorly understood. The present study investigated relations among physiological measures of affective style, psychological well being, and immune function. Negative and positive affect were elicited by using an autobiographical writing task. Electroencephalography and affect-modulated eye-blink startle were used to measure trait and state negative affect. Participants were vaccinated for influenza, and antibody titers after the vaccine were assayed to provide an in vivo measure of immune function. Higher levels of right-prefrontal electroencephalographic activation and greater magnitude of the startle reflex reliably predicted poorer immune response. These data support the hypothesis that individuals characterized by a more negative affective style mount a weaker immune response and therefore may be at greater risk for illness than those with a more positive affective style.
The brain circuitry underlying emotion includes several territories of the prefrontal cortex (PFC), the amygdala, hippocampus, anterior cingulate, and related structures. In general, the PFC represents emotion in the absence of immediately present incentives and thus plays a crucial role in the anticipation of the future affective consequences of action, as well as in the persistence of emotion following the offset of an elicitor. The functions of the other structures in this circuit are also considered. Individual differences in this circuitry are reviewed, with an emphasis on asymmetries within the PFC and activation of the amygdala as 2 key components of affective style. These individual differences are related to both behavioral and biological variables associated with affective style and emotion regulation. Plasticity in this circuitry and its implications for transforming emotion and cultivating positive affect and resilience are considered.
Twenty-six younger (ages 18–36 years) and 19 older (ages 60–88 years) healthy right-handed men and women were tested for interhemispheric transfer by using visual evoked potentials lo laterally presented checkerboards. Interhemispheric transfer time (IHTT) was estimated by subtracting latencies for both P100 and N160 peaks of the waveform contralateral to the stimulus from the waveform ipsilateral to the stimulus for homologous sites. The quality of interhemispheric transfer was estimated by comparing peak-to-peak amplitudes for homologous sites. IHTT did not change across age, but there was a suppression of the waveform over the indirectly stimulated hemisphere in the older participants. The significance of this finding for age-related changes in functions mediated by the corpus callosum is discussed.
Studies on aging and emotion suggest an increase in reported positive affect, a processing bias of positive over negative information, as well as increasingly adaptive regulation in response to negative events with advancing age. These findings imply that older individuals evaluate information differently, resulting in lowered reactivity to, and/or faster recovery from, negative information, while maintaining more positive responding to positive information. We examined this hypothesis in an ongoing study on Midlife in the US (MIDUS II) where emotional reactivity and recovery were assessed in a large number of respondents (N = 159) from a wide age range (36-84 years). We recorded eye-blink startle magnitudes and corrugator activity during and after the presentation of positive, neutral and negative pictures. The most robust age effect was found in response to neutral stimuli, where increasing age is associated with a decreased corrugator and eyeblink startle response to neutral stimuli. These data suggest that an age-related positivity effect does not essentially alter the response to emotion-laden information, but is reflected in a more positive interpretation of affectively ambiguous information. Furthermore, older women showed reduced corrugator recovery from negative pictures relative to the younger women and men, suggesting that an age-related prioritization of well-being is not necessarily reflected in adaptive regulation of negative affect.
OBJECTIVE: The underlying changes in biological processes that are associated with reported changes in mental and physical health in response to meditation have not been systematically explored. We performed a randomized, controlled study on the effects on brain and immune function of a well-known and widely used 8-week clinical training program in mindfulness meditation applied in a work environment with healthy employees. METHODS: We measured brain electrical activity before and immediately after, and then 4 months after an 8-week training program in mindfulness meditation. Twenty-five subjects were tested in the meditation group. A wait-list control group (N = 16) was tested at the same points in time as the meditators. At the end of the 8-week period, subjects in both groups were vaccinated with influenza vaccine. RESULTS: We report for the first time significant increases in left-sided anterior activation, a pattern previously associated with positive affect, in the meditators compared with the nonmeditators. We also found significant increases in antibody titers to influenza vaccine among subjects in the meditation compared with those in the wait-list control group. Finally, the magnitude of increase in left-sided activation predicted the magnitude of antibody titer rise to the vaccine. CONCLUSIONS: These findings demonstrate that a short program in mindfulness meditation produces demonstrable effects on brain and immune function. These findings suggest that meditation may change brain and immune function in positive ways and underscore the need for additional research.
Experientially opening oneself to pain rather than avoiding it is said to reduce the mind's tendency toward avoidance or anxiety which can further exacerbate the experience of pain. This is a central feature of mindfulness-based therapies. Little is known about the neural mechanisms of mindfulness on pain. During a meditation practice similar to mindfulness, functional magnetic resonance imaging was used in expert meditators (>10,000 h of practice) to dissociate neural activation patterns associated with pain, its anticipation, and habituation. Compared to novices, expert meditators reported equal pain intensity, but less unpleasantness. This difference was associated with enhanced activity in the dorsal anterior insula (aI), and the anterior mid-cingulate (aMCC) the so-called 'salience network', for experts during pain. This enhanced activity during pain was associated with reduced baseline activity before pain in these regions and the amygdala for experts only. The reduced baseline activation in left aI correlated with lifetime meditation experience. This pattern of low baseline activity coupled with high response in aIns and aMCC was associated with enhanced neural habituation in amygdala and pain-related regions before painful stimulation and in the pain-related regions during painful stimulation. These findings suggest that cultivating experiential openness down-regulates anticipatory representation of aversive events, and increases the recruitment of attentional resources during pain, which is associated with faster neural habituation.
The primary taste cortex consists of the insula and operculum. Previous work has indicated that neurons in the primary taste cortex respond solely to sensory input from taste receptors and lingual somatosensory receptors. Using functional magnetic resonance imaging, we show here that expectancy modulates these neural responses in humans. When subjects were led to believe that a highly aversive bitter taste would be less distasteful than it actually was, they reported it to be less aversive than when they had accurate information about the taste and, moreover, the primary taste cortex was less strongly activated. In addition, the activation of the right insula and operculum tracked online ratings of the aversiveness for each taste. Such expectancy-driven modulation of primary sensory cortex may affect perceptions of external events.
Among younger adults, the ability to willfully regulate negative affect, enabling effective responses to stressful experiences, engages regions of prefrontal cortex (PFC) and the amygdala. Because regions of PFC and the amygdala are known to influence the hypothalamic-pituitary-adrenal axis, here we test whether PFC and amygdala responses during emotion regulation predict the diurnal pattern of salivary cortisol secretion. We also test whether PFC and amygdala regions are engaged during emotion regulation in older (62- to 64-year-old) rather than younger individuals. We measured brain activity using functional magnetic resonance imaging as participants regulated (increased or decreased) their affective responses or attended to negative picture stimuli. We also collected saliva samples for 1 week at home for cortisol assay. Consistent with previous work in younger samples, increasing negative affect resulted in ventral lateral, dorsolateral, and dorsomedial regions of PFC and amygdala activation. In contrast to previous work, decreasing negative affect did not produce the predicted robust pattern of higher PFC and lower amygdala activation. Individuals demonstrating the predicted effect (decrease < attend in the amygdala), however, exhibited higher signal in ventromedial prefrontal cortex (VMPFC) for the same contrast. Furthermore, participants displaying higher VMPFC and lower amygdala signal when decreasing compared with the attention control condition evidenced steeper, more normative declines in cortisol over the course of the day. Individual differences yielded the predicted link between brain function while reducing negative affect in the laboratory and diurnal regulation of endocrine activity in the home environment.
Despite growing evidence on the neural bases of emotion regulation, little is known about the mechanisms underlying individual differences in cognitive regulation of negative emotion, and few studies have used objective measures to quantify regulatory success. Using a trait-like psychophysiological measure of emotion regulation, corrugator electromyography, we obtained an objective index of the ability to cognitively reappraise negative emotion in 56 healthy men (Session 1), who returned 1.3 years later to perform the same regulation task using fMRI (Session 2). Results indicated that the corrugator measure of regulatory skill predicted amygdala-prefrontal functional connectivity. Individuals with greater ability to down-regulate negative emotion as indexed by corrugator at Session 1 showed not only greater amygdala attenuation but also greater inverse connectivity between the amygdala and several sectors of the prefrontal cortex while down-regulating negative emotion at Session 2. Our results demonstrate that individual differences in emotion regulation are stable over time and underscore the important role of amygdala-prefrontal coupling for successful regulation of negative emotion.
Anxious temperament (AT) in human and non-human primates is a trait-like phenotype evident early in life that is characterized by increased behavioural and physiological reactivity to mildly threatening stimuli. Studies in children demonstrate that AT is an important risk factor for the later development of anxiety disorders, depression and comorbid substance abuse. Despite its importance as an early predictor of psychopathology, little is known about the factors that predispose vulnerable children to develop AT and the brain systems that underlie its expression. To characterize the neural circuitry associated with AT and the extent to which the function of this circuit is heritable, we studied a large sample of rhesus monkeys phenotyped for AT. Using 238 young monkeys from a multigenerational single-family pedigree, we simultaneously assessed brain metabolic activity and AT while monkeys were exposed to the relevant ethological condition that elicits the phenotype. High-resolution (18)F-labelled deoxyglucose positron-emission tomography (FDG-PET) was selected as the imaging modality because it provides semi-quantitative indices of absolute glucose metabolic rate, allows for simultaneous measurement of behaviour and brain activity, and has a time course suited for assessing temperament-associated sustained brain responses. Here we demonstrate that the central nucleus region of the amygdala and the anterior hippocampus are key components of the neural circuit predictive of AT. We also show significant heritability of the AT phenotype by using quantitative genetic analysis. Additionally, using voxelwise analyses, we reveal significant heritability of metabolic activity in AT-associated hippocampal regions. However, activity in the amygdala region predictive of AT is not significantly heritable. Furthermore, the heritabilities of the hippocampal and amygdala regions significantly differ from each other. Even though these structures are closely linked, the results suggest differential influences of genes and environment on how these brain regions mediate AT and the ongoing risk of developing anxiety and depression.
Although the co-occurrence of negative affect and pain is well recognized, the mechanism underlying their association is unclear. To examine whether a common self-regulatory ability impacts the experience of both emotion and pain, we integrated neuroimaging, behavioral, and physiological measures obtained from three assessments separated by substantial temporal intervals. Our results demonstrated that individual differences in emotion regulation ability, as indexed by an objective measure of emotional state, corrugator electromyography, predicted self-reported success while regulating pain. In both emotion and pain paradigms, the amygdala reflected regulatory success. Notably, we found that greater emotion regulation success was associated with greater change of amygdalar activity following pain regulation. Furthermore, individual differences in degree of amygdalar change following emotion regulation were a strong predictor of pain regulation success, as well as of the degree of amygdalar engagement following pain regulation. These findings suggest that common individual differences in emotion and pain regulatory success are reflected in a neural structure known to contribute to appraisal processes.
The amygdalae are important, if not critical, brain regions for many affective, attentional and memorial processes, and dysfunction of the amygdalae has been a consistent finding in the study of clinical depression. Theoretical models of the functional neuroanatomy of both normal and psychopathological affective processes which posit cortical hemispheric specialization of functions have been supported by both lesion and functional neuroimaging studies in humans. Results from human neuroimaging studies in support of amygdalar hemispheric specialization are inconsistent. However, recent results from human lesion studies are consistent with hemispheric specialization. An important, yet largely ignored, feature of the amygdalae in the primate brain--derived from both neuroanatomical and electrophysiological data--is that there are virtually no direct interhemispheric connections via the anterior commissure (AC). This feature stands in stark contrast to that of the rodent brain wherein virtually all amygdalar nuclei have direct interhemispheric connections. We propose this feature of the primate brain, in particular the human brain, is a result of influences from frontocortical hemispheric specialization which have developed over the course of primate brain evolution. Results consistent with this notion were obtained by examining the nature of human amygdalar interhemispheric connectivity using both functional magnetic resonance imaging (FMRI) and positron emission tomography (PET). We found modest evidence of amygdalar interhemispheric functional connectivity in the non-depressed brain, whereas there was strong evidence of functional connectivity in the depressed brain. We interpret and discuss the nature of this connectivity in the depressed brain in the context of dysfunctional frontocortical-amygdalar interactions which accompany clinical depression.
BACKGROUND: Autism is a syndrome of unknown cause, marked by abnormal development of social behavior. Attempts to link pathological features of the amygdala, which plays a key role in emotional processing, to autism have shown little consensus. OBJECTIVE: To evaluate amygdala volume in individuals with autism spectrum disorders and its relationship to laboratory measures of social behavior to examine whether variations in amygdala structure relate to symptom severity. DESIGN: We conducted 2 cross-sectional studies of amygdala volume, measured blind to diagnosis on high-resolution, anatomical magnetic resonance images. Participants were 54 males aged 8 to 25 years, including 23 with autism and 5 with Asperger syndrome or pervasive developmental disorder not otherwise specified, recruited and evaluated at an academic center for developmental disabilities and 26 age- and sex-matched community volunteers. The Autism Diagnostic Interview-Revised was used to confirm diagnoses and to validate relationships with laboratory measures of social function. MAIN OUTCOME MEASURES: Amygdala volume, judgment of facial expressions, and eye tracking. RESULTS: In study 1, individuals with autism who had small amygdalae were slowest to distinguish emotional from neutral expressions (P=.02) and showed least fixation of eye regions (P=.04). These same individuals were most socially impaired in early childhood, as reported on the Autism Diagnostic Interview-Revised (P<.04). Study 2 showed smaller amygdalae in individuals with autism than in control subjects (P=.03) and group differences in the relation between amygdala volume and age. Study 2 also replicated findings of more gaze avoidance and childhood impairment in participants with autism with the smallest amygdalae. Across the combined sample, severity of social deficits interacted with age to predict different patterns of amygdala development in autism (P=.047). CONCLUSIONS: These findings best support a model of amygdala hyperactivity that could explain most volumetric findings in autism. Further psychophysiological and histopathological studies are indicated to confirm these findings.
A variety of recent research indicates that when subjects are induced to experience certain negative emotions, there is greater suppression of alpha power in the right than left frontal region, while during the experience of positive emotion, alpha power asymmetry in this region shows the opposite pattern. We have conceptualized this assymetry as reflecting specialization for approach and withdrawal processes in the left and right frontal regions, respectively. In this experiment, reward and punishment contingencies were directly manipulated to produce approach and withdrawal response motional states. In addition, subjects responded to imperative stimuli using either an approach response (finger press) or a withdrawal response (finger lift). EEG was recorded from multiple scalp locations. During the foreperiod prior to the response to the imperative stimuli, the EEG was extracted, Fourier-transformed and power computed in the theta, alpha and beta frequency bands. In addition, the contingent negative variation (CNV) was derived from the identical epoch. Reward trials were associated with greater left frontal alpha power suppression than punishment trials, while during the latter trials, there was greater right-sided frontal alpha power suppression than during reward trials. There was also some evidence to indicate that withdrawal responses were associated with greater right-sided alpha power suppression in the temporo-parietal region compared with approach responses. Power in the theta and beta bands did not systematically vary with condition. The CNV was larger during trials on which subjects responded quickly compared with slow trials, but did not differentiate between reward and punishment contingencies. The findings support the hypothesis that approach-related processes can be differentiated from withdrawal-related processes on the basis of asymmetrical shifts in alpha power in the frontal region. They also indicate that the CNV and spectral power estimates from the identical epochs reflect different neural processes.
This article presents an overview of the author's recent electrophysiological studies of anterior cerebral asymmetries related to emotion and affective style. A theoretical account is provided of the role of the two hemispheres in emotional processing. This account assigns a major role in approach- and withdrawal-related behavior to the left and right frontal and anterior temporal regions of two hemispheres, respectively. Individual differences in approach- and withdrawal-related emotional reactivity and temperament are associated with stable differences in baseline measures of activation asymmetry in these anterior regions. Phasic state changes in emotion result in shifts in anterior activation asymmetry which are superimposed upon these stable baseline differences. Future directions for research in this area are discussed.
OBJECTIVE: The anterior cingulate cortex has been implicated in depression. Results are best interpreted by considering anatomic and cytoarchitectonic subdivisions. Evidence suggests depression is characterized by hypoactivity in the dorsal anterior cingulate, whereas hyperactivity in the rostral anterior cingulate is associated with good response to treatment. The authors tested the hypothesis that activity in the rostral anterior cingulate during the depressed state has prognostic value for the degree of eventual response to treatment. Whereas prior studies used hemodynamic imaging, this investigation used EEG. METHOD: The authors recorded 28-channel EEG data for 18 unmedicated patients with major depression and 18 matched comparison subjects. Clinical outcome was assessed after nortriptyline treatment. Of the 18 depressed patients, 16 were considered responders 4-6 months after initial assessment. A median split was used to classify response, and the pretreatment EEG data of patients showing better (N=9) and worse (N=9) responses were analyzed with low-resolution electromagnetic tomography, a new method to compute three-dimensional cortical current density for given EEG frequency bands according to a Talairach brain atlas. RESULTS: The patients with better responses showed hyperactivity (higher theta activity) in the rostral anterior cingulate (Brodmann's area 24/32). Follow-up analyses demonstrated the specificity of this finding, which was not confounded by age or pretreatment depression severity. CONCLUSIONS: These results, based on electrophysiological imaging, not only support hemodynamic findings implicating activation of the anterior cingulate as a predictor of response in depression, but they also suggest that differential activity in the rostral anterior cingulate is associated with gradations of response.
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