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In this paper I discuss how expressive behavior relates to personality and psychopathology, integrating recent findings from my laboratory and the insights of Charles Darwin on this topic. In the first part of the paper I challenge the view, in part espoused by Darwin, that humans are equipped to convey only a limited number of emotions with nonverbal behavior. Our lab has documented displays for several emotions, including embarrassment, love, desire, compassion, gratitude, and awe, to name just a few states that previously were thought not to possess a distinct display. I then present an argument for how individual differences in emotion, although fleeting, shape the social environment. This argument focuses on the functions of nonverbal display: to provide information to others, to evoke responses, and to serve as incentives of preceding or ensuing social behavior. This reasoning sets the stage for the study of the relationships between personality, psychopathology, and expressive behavior, to which I turn in the final part of the paper. Here I show that basic personality traits (e.g., extraversion, agreeableness) and psychological disorders (e.g., externalizing disorder in children, autism) have expressive signatures that shape social interactions and environments in profound ways that might perpetuate and transmit the trait or disorder.
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BACKGROUND: Two core characteristics of pathologic fear are its rapid onset and resistance to cognitive regulation. We hypothesized that activation of the amygdala early in the presentation of fear-relevant visual stimuli would distinguish phobics from nonphobics. METHODS: Chronometry of amygdala activation to phobia-relevant pictures was assessed in 13 spider phobics and 14 nonphobics using functional magnetic resonance imaging (fMRI). RESULTS: Blood oxygen level-dependent (BOLD) responses in the amygdala early in picture processing consistently differentiated between phobic and nonphobic subjects, as well as between phobogenic and nonphobogenic stimuli among phobics. Furthermore, amygdalar BOLD responses associated with timing but not magnitude of activation predicted affective responses to phobogenic stimuli. Computational modeling procedures were used to identify patterns of neural activation in the amygdala that could yield the observed BOLD data. These data suggest that phobic responses were characterized by strong but brief amygdala responses, whereas nonphobic responses were weaker and more sustained. CONCLUSIONS: Results are discussed in the context of the amygdala's role in rapid threat detection and the vigilance-avoidance hypothesis of anxiety. These data highlight the importance of examining the neural substrates of the immediate impact of phobogenic stimuli for understanding pathological fear.
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Previous research indicates that drug motivational systems are instantiated in structures that process information related to incentive, motivational drive, memorial, motor/habit, craving, and cognitive control processing. The present research tests the hypothesis that activity in such systems will be powerfully affected by the combination of drug anticipation and drug withdrawal. Event-related fMRI was used to examine activation in response to a preinfusion warning cue in two experimental sessions that manipulated withdrawal status. Significant cue-induced effects were seen in the caudate, ventral anterior nucleus of the thalamus, the insula, subcallosal gyrus, nucleus accumbens, and anterior cingulate. These results suggest that withdrawal and nicotine anticipation produce (1) different motor preparatory and inhibitory response processing and (2) different craving related processing.
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Attention to internal bodily sensations is a core feature of mindfulness meditation. Previous studies have not detected differences in interoceptive accuracy between meditators and nonmeditators on heartbeat detection and perception tasks. We compared differences in respiratory interoceptive accuracy between meditators and nonmeditators in the ability to detect and discriminate respiratory resistive loads and sustain accurate perception of respiratory tidal volume during nondistracted and distracted conditions. Groups did not differ in overall performance on the detection and discrimination tasks; however, meditators were more accurate in discriminating the resistive load with the lowest ceiling effect. Meditators were also more accurate during the nondistracted tracking task at a lag time of 1 s following the breath. Results provide initial support for the notion that meditators have greater respiratory interoceptive accuracy compared to nonmeditators.
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High vs. low scorers on the Beck Depression Inventory (BDI) were compared on measures of resting EEG activation asymmetry from frontal and parietal brain regions. Depressed subjects showed greater relative right frontal activation compared with nondepressed subjects. Parietal asymmetry did not distinguish between the groups. These data support the hypothesis of right hemisphere hyperactivation in the frontal region of depressed individuals and are consistent with the growing body of literature which suggests that the left and right frontal regions may be differentially specialized for particular positive and negative affects.
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The relation between brain activity and the immune system was evaluated by assessing immune responses in 20 healthy women who manifested extreme differences in the asymmetry of frontal cortex activation. One group showed extreme and stable left frontal activation; the other group showed extreme and stable right frontal activation. As predicted, women with extreme right frontal activation had significantly lower levels of natural killer cell activity (at effector:target cell ratios of 33:1 and 11:1) than did left frontally activated individuals. This difference did not extend to two other immune measures, lymphocyte proliferation and T-cell subsets. However, higher immunoglobulin levels of the M class were observed in the right frontal group. In this study, the immune patterns could not be accounted for by plasma cortisol levels, anxiety- and depression-related symptomatology, or recent health histories. These findings support the hypothesis that there is a specific association between frontal brain asymmetry and certain immune responses.
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Examined whether certain features of infant temperament might be related to individual differences in the asymmetry of resting frontal activation. EEG was recorded from the left and right frontal and parietal scalp regions of 13 normal 10-month-old infants. Infant behavior was then observed during a brief period of maternal separation. Those infants who cried in response to maternal separation showed greater right frontal activation during the preceding baseline period compared with infants who did not cry. Frontal activation asymmetry may be a state-independent marker for individual differences in threshold of reactivity to stressful events and vulnerability to particular emotions.
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<p>It is well known that the eating patterns that restrain chronic dieters (restrained eaters) can be disinhibited by anxiety, which in turn has been associated with relative right frontal brain activity in independent electroencephalographic (EEG) studies. Combining these two lines of evidence, the authors tested the hypothesis that chronic restrained eating is associated with relative right frontal asymmetry. Resting anterior brain asymmetry and self-reported measures of anxiety and depression were collected in 23 restrained and 32 unrestrained eaters. As hypothesized, groups differed in tonic frontal activity, with restrained eaters showing more relative right frontal activity. Furthermore, relative right frontal activity was associated with greater self-reported restraint. Right-sided prefrontal asymmetry may thus represent a diathesis associated with increased vulnerability toward restrained eating.</p>
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Major depression is a heterogeneous condition, and the search for neural correlates specific to clinically defined subtypes has been inconclusive. Theoretical considerations implicate frontostriatal, particularly subgenual prefrontal cortex (PFC), dysfunction in the pathophysiology of melancholia--a subtype of depression characterized by anhedonia--but no empirical evidence has been found yet for such a link. To test the hypothesis that melancholic, but not nonmelancholic depression, is associated with the subgenual PFC impairment, concurrent measurement of brain electrical (electroencephalogram, EEG) and metabolic (positron emission tomography, PET) activity were obtained in 38 unmedicated subjects with DSM-IV major depressive disorder (20 melancholic, 18 nonmelancholic subjects), and 18 comparison subjects. EEG data were analyzed with a tomographic source localization method that computed the cortical three-dimensional distribution of current density for standard frequency bands, allowing voxelwise correlations between the EEG and PET data. Voxel-based morphometry analyses of structural magnetic resonance imaging (MRI) data were performed to assess potential structural abnormalities in melancholia. Melancholia was associated with reduced activity in the subgenual PFC (Brodmann area 25), manifested by increased inhibitory delta activity (1.5-6.0 Hz) and decreased glucose metabolism, which themselves were inversely correlated. Following antidepressant treatment, depressed subjects with the largest reductions in depression severity showed the lowest post-treatment subgenual PFC delta activity. Analyses of structural MRI revealed no group differences in the subgenual PFC, but in melancholic subjects, a negative correlation between gray matter density and age emerged. Based on preclinical evidence, we suggest that subgenual PFC dysfunction in melancholia may be associated with blunted hedonic response and exaggerated stress responsiveness.
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BACKGROUND: Functional magnetic resonance imaging (fMRI) holds promise as a noninvasive means of identifying neural responses that can be used to predict treatment response before beginning a drug trial. Imaging paradigms employing facial expressions as presented stimuli have been shown to activate the amygdala and anterior cingulate cortex (ACC). Here, we sought to determine whether pretreatment amygdala and rostral ACC (rACC) reactivity to facial expressions could predict treatment outcomes in patients with generalized anxiety disorder (GAD). METHODS: Fifteen subjects (12 female subjects) with GAD participated in an open-label venlafaxine treatment trial. Functional magnetic resonance imaging responses to facial expressions of emotion collected before subjects began treatment were compared with changes in anxiety following 8 weeks of venlafaxine administration. In addition, the magnitude of fMRI responses of subjects with GAD were compared with that of 15 control subjects (12 female subjects) who did not have GAD and did not receive venlafaxine treatment. RESULTS: The magnitude of treatment response was predicted by greater pretreatment reactivity to fearful faces in rACC and lesser reactivity in the amygdala. These individual differences in pretreatment rACC and amygdala reactivity within the GAD group were observed despite the fact that 1) the overall magnitude of pretreatment rACC and amygdala reactivity did not differ between subjects with GAD and control subjects and 2) there was no main effect of treatment on rACC-amygdala reactivity in the GAD group. CONCLUSIONS: These findings show that this pattern of rACC-amygdala responsivity could prove useful as a predictor of venlafaxine treatment response in patients with GAD.
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<p>BACKGROUND: Functional magnetic resonance imaging (fMRI) techniques were used to identify the neural circuitry underlying emotional processing in control and depressed subjects. Depressed subjects were studied before and after treatment with venlafaxine. This new technique provides a method to noninvasively image regional brain function with unprecedented spatial and temporal resolution. METHOD: Echo-planar imaging was used to acquire whole brain images while subjects viewed positively and negatively valenced visual stimuli. Two control subjects and two depressed subjects who met DSM-IV criteria for major depression were scanned at baseline and 2 weeks later. Depressed subjects were treated with venlafaxine after the baseline scan. RESULTS: Preliminary results from this ongoing study revealed three interesting trends in the data. Both depressed patients demonstrated considerable symptomatic improvement at the time of the second scan. Across control and depressed subjects, the negative compared with the positive pictures elicited greater global activation. In both groups, activation induced by the negative pictures decreased from the baseline scan to the 2-week scan. This decrease in activation was also present in the control subjects when they were exposed to the positive pictures. In contrast, when the depressed subjects were presented with the positive pictures they showed no activation at baseline, whereas after 2 weeks of treatment an area of activation emerged in right secondary visual cortex. CONCLUSION: While preliminary, these results demonstrate the power of using fMRI to study emotional processes in normal and depressed subjects and to examine mechanisms of action of antidepressant drugs.</p>
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It is the central hypothesis of this paper that the mental states commonly referred to as altered states of consciousness are principally due to transient prefrontal cortex deregulation. Supportive evidence from psychological and neuroscientific studies of dreaming, endurance running, meditation, daydreaming, hypnosis, and various drug-induced states is presented and integrated. It is proposed that transient hypofrontality is the unifying feature of all altered states and that the phenomenological uniqueness of each state is the result of the differential viability of various frontal circuits. Using an evolutionary approach, consciousness is conceptualized as hierarchically ordered cognitive function. Higher-order structures perform increasingly integrative functions and thus contribute more sophisticated content. Although this implies a holistic approach to consciousness, such a functional hierarchy localizes the most sophisticated layers of consciousness in the zenithal higher-order structure: the prefrontal cortex. The hallmark of altered states of consciousness is the subtle modification of behavioral and cognitive functions that are typically ascribed to the prefrontal cortex. The theoretical framework presented yields a number of testable hypotheses.

<p>In this commentary I discuss the integration of mindful procedures in cognitive therapy of generalized anxiety disorder (CAD) and attempt to answer questions concerning the effects of mindfulness on information processing and on mechanisms purported to maintain CAD in the meta-cognitive model of this disorder. Different techniques that promote mindfulness can be identified, including mindfulness meditation and attention training. These techniques are intended to disrupt repetitive styles of dysfunctional thinking. I argue that the effect of mindfulness strategies on information processing in emotional disorder can be conceptualized in meta-cognitive terms as (a) activating a meta-cognitive mode of processing; (b) disconnecting the influence of maladaptive beliefs on processing; (c) strengthening flexible responding to threat; and (d) strengthening meta-cognitive plans for controlling cognition. Although mindfulness meditation may have general treatment applications, the meta-cognitive model of CAD suggests caution in using this treatment in CAD. It is unclear which dimension of worry should be targeted, and mindfulness meditation does not contain information that can lead to unambiguous disconfirmation of erroneous beliefs about worry.</p>

BACKGROUND: The broad autism phenotype includes subclinical autistic characteristics found to have a higher prevalence in unaffected family members of individuals with autism. These characteristics primarily affect the social aspects of language, communication, and human interaction. The current research focuses on possible neurobehavioral characteristics associated with the broad autism phenotype. METHODS: We used a face-processing task associated with atypical patterns of gaze fixation and brain function in autism while collecting brain functional magnetic resonance imaging (fMRI) and eye tracking in unaffected siblings of individuals with autism. RESULTS: We found robust differences in gaze fixation and brain function in response to images of human faces in unaffected siblings compared with typically developing control individuals. The siblings' gaze fixations and brain activation patterns during the face processing task were similar to that of the autism group and showed decreased gaze fixation along with diminished fusiform activation compared with the control group. Furthermore, amygdala volume in the siblings was similar to the autism group and was significantly reduced compared with the control group. CONCLUSIONS: Together, these findings provide compelling evidence for differences in social/emotional processing and underlying neural circuitry in siblings of individuals with autism, supporting the notion of unique endophenotypes associated with the broad autism phenotype.
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Although there are many imaging studies on traditional ROI-based amygdala volumetry, there are very few studies on modeling amygdala shape variations. This paper presents a unified computational and statistical framework for modeling amygdala shape variations in a clinical population. The weighted spherical harmonic representation is used to parameterize, smooth out, and normalize amygdala surfaces. The representation is subsequently used as an input for multivariate linear models accounting for nuisance covariates such as age and brain size difference using the SurfStat package that completely avoids the complexity of specifying design matrices. The methodology has been applied for quantifying abnormal local amygdala shape variations in 22 high functioning autistic subjects.
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BACKGROUND: Although it has been hypothesized that glucocorticoid hypersecretion in depressed patients leads to neuronal atrophy in the hippocampus, magnetic resonance imaging (MRI) -based morphometry studies of the hippocampus to date have produced mixed results. METHODS: In our MRI study, hippocampal volumes were measured in 25 depressed patients (13 with melancholia and 12 without melancholia) and 15 control subjects. RESULTS: No significant differences in hippocampus volumes were found between any of the subject groups, although within subjects right hippocampal volumes were found to be significantly larger than left hippocampal volumes. Additionally, right and total (left + right) hippocampal volumes in control and depressed subjects were found to be positively correlated with trait anxiety as measured by the state/trait anxiety inventory. CONCLUSIONS: Because our subject group is younger than those in studies reporting hippocampal atrophy, we conclude that longitudinal studies will be necessary for investigation of the lifelong course of hippocampal volumetry.
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Cultivation of mindfulness, the nonjudgmental awareness of experiences in the present moment, produces beneficial effects on well-being and ameliorates psychiatric and stress-related symptoms. Mindfulness meditation has therefore increasingly been incorporated into psychotherapeutic interventions. Although the number of publications in the field has sharply increased over the last two decades, there is a paucity of theoretical reviews that integrate the existing literature into a comprehensive theoretical framework. In this article, we explore several components through which mindfulness meditation exerts its effects: (a) attention regulation, (b) body awareness, (c) emotion regulation (including reappraisal and exposure, extinction, and reconsolidation), and (d) change in perspective on the self. Recent empirical research, including practitioners’ self-reports and experimental data, provides evidence supporting these mechanisms. Functional and structural neuroimaging studies have begun to explore the neuroscientific processes underlying these components. Evidence suggests that mindfulness practice is associated with neuroplastic changes in the anterior cingulate cortex, insula, temporo-parietal junction, fronto-limbic network, and default mode network structures. The authors suggest that the mechanisms described here work synergistically, establishing a process of enhanced self-regulation. Differentiating between these components seems useful to guide future basic research and to specifically target areas of development in the treatment of psychological disorders.
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Neurosurgical treatment of psychiatric disorders has been influenced by evolving neurobiological models of symptom generation. The advent of functional neuroimaging and advances in the neurosciences have revolutionized understanding of the functional neuroanatomy of psychiatric disorders. This article reviews neuroimaging studies of depression from the last 3 decades and describes an emerging neurocircuitry model of mood disorders, focusing on critical circuits of cognition and emotion, particularly those networks involved in the regulation of evaluative, expressive and experiential aspects of emotion. The relevance of this model for neurotherapeutics is discussed, as well as the role of functional neuroimaging of psychiatric disorders.
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Two hundred and nine pupils were randomly allocated to either a cognitive behaviourally based stress management intervention (SMI) group, or a non-intervention control group. Mood and motivation measures were administered pre and post intervention. Standardized examinations were taken 8–10 weeks later. As hypothesized, results indicated that an increase in the functionality of pupils’ cognitions served as the mechanism by which mental health improved in the SMI group. In contrast, the control group demonstrated no such improvements. Also, as predicted, an increase in motivation accounted for the SMI group's significantly better performance on the standardized, academic assessments that comprise the United Kingdom's General Certificate of Secondary Education. Indeed, the magnitude of this enhanced performance was, on average, one-letter grade. Discussion focuses on the theoretical and practical implications of these findings.

Baseline resting electroencephalogram activity was recorded with 3 different reference montages from 15 clinically depressed and 13 control subjects. Power in all frequency bands was extracted by fast Fourier transformation. There was a significant Group X Hemisphere interaction in the mid-frontal region, for the alpha band power only. Depressed subjects had less left-sided activation (i.e., more alpha activity) than did normal control subjects. This pattern of diminished left-sided frontal activation is interpreted as indicating a deficit in approach mechanisms in depressed subjects.
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Autism is a neurodevelopmental disorder affecting behavioral and social cognition, but there is little understanding about the link between the functional deficit and its underlying neuroanatomy. We applied a 2D version of voxel-based morphometry (VBM) in differentiating the white matter concentration of the corpus callosum for the group of 16 high functioning autistic and 12 normal subjects. Using the white matter density as an index for neural connectivity, autism is shown to exhibit less white matter concentration in the region of the genu, rostrum, and splenium removing the effect of age based on the general linear model (GLM) framework. Further, it is shown that the less white matter concentration in the corpus callosum in autism is due to hypoplasia rather than atrophy.
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<p>A long-standing problem in stress research has been that individuals' reports of their tendencies to become anxious are often inconsistent with relevant behavioral and physiological indices. This study investigated the distinction between (a) truly low-anxious Ss, who report low trait anxiety on the Taylor Manifest Anxiety Scale and low defensiveness on the Marlowe-Crowne Social Desirability Scale, and (b) repressors, who report low anxiety but high defensiveness. These groups were compared with a moderately high-anxious one. Heart rate, spontaneous skin resistance responses, and forehead muscle tension were recorded from 40 male college students during a phrase association task. Significant differences in the 3 physiological measures as well as in 3 behavioral ones (reaction time, content avoidance, and verbal interference) all indicated that the repressors were more stressed than the low-anxious Ss despite their claims of lower trait anxiety. The high-anxious group exhibited a 3rd pattern suggesting an intermediate level of anxious responding. These data document the need to distinguish between repressors and truly low-anxious persons in research concerned with relations between self-reported anxiety and behavioral and physiological responses to stress. (42 ref)</p>
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INTRODUCTION: Major depressive disorder (MDD) is characterized by cognitive biases in attention, memory and language use. Language use biases often parallel depression symptoms, and contain over-representations of both negative emotive and death words as well as low levels of positive emotive words. This study further explores cognitive biases in depression by comparing the effect of current depression status to cumulative depression history on an elaborated verbal recall of emotional photographs. METHODS: Following a negative mood induction, fifty-two individuals (42 women) with partially-remitted depression viewed - then recalled and verbally described - slides from the International Affective Picture System (IAPS). Descriptions were transcribed and frequency of depression-related word use (positive emotion, negative emotion, sex, ingestion and death) was analyzed using the Linguistic Inquiry and Word Count program (LIWC). RESULTS: Contrary to expectations and previous findings, current depression status did not affect word use in any categories of interest. However, individuals with more than 5 years of previous depression used fewer words related to positive emotion (t(50) = 2.10, p = .04, (d = 0.57)), and sex (t(48) = 2.50, p = .013 (d = 0.81)), and there was also a trend for these individuals to use fewer ingestion words (t(50) = 1.95, p = .057 (d = 0.58)), suggesting a deficit in appetitive processing. CONCLUSIONS: Our findings suggest that depression duration affects appetitive information processing and that appetitive word use may be a behavioral marker for duration related brain changes which may be used to inform treatment.
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Self-conscious emotions such as embarrassment and shame are associated with 2 aspects of theory of mind (ToM): (a) the ability to understand that behavior has social consequences in the eyes of others and (b) an understanding of social norms violations. The present study aimed to link ToM with the recognition of self-conscious emotion. Children with and without autism identified facial expressions conscious of self-conscious and non-self-conscious emotions from photographs. ToM was also measured. Children with autism performed more poorly than comparison children at identifying self-conscious emotions, though they did not differ in the recognition of non-self-conscious emotions. When ToM ability was statistically controlled, group differences in the recognition of self-conscious emotion disappeared. Discussion focused on the links between ToM and self-conscious emotion.
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Patients in the placebo arms of randomized controlled trials (RCT) often experience positive changes from baseline. While multiple theories concerning such “placebo effects” exist, peculiarly, none has been informed by actual interviews of patients undergoing placebo treatment. Here, we report on a qualitative study (n = 27) embedded within a RCT (n = 262) in patients with irritable bowel syndrome. Besides identical placebo acupuncture treatment in the RCT, the qualitative study patients also received an additional set of interviews at the beginning, midpoint, and end of the trial. Interviews of the 12 qualitative subjects who underwent and completed placebo treatment were transcribed. We found that patients (1) were persistently concerned with whether they were receiving placebo or genuine treatment; (2) almost never endorsed “expectation” of improvement but spoke of “hope” instead and frequently reported despair; (3) almost all reported improvement ranging from dramatic psychosocial changes to unambiguous, progressive symptom improvement to tentative impressions of benefit; and (4) often worried whether their improvement was due to normal fluctuations or placebo effects. The placebo treatment was a problematic perturbation that provided an opportunity to reconstruct the experiences of the fluctuations of their illness and how it disrupted their everyday life. Immersion in this RCT was a co-mingling of enactment, embodiment and interpretation involving ritual performance and evocative symbols, shifts in bodily sensations, symptoms, mood, daily life behaviors, and social interactions, all accompanied by self-scrutiny and re-appraisal. The placebo effect involved a spectrum of factors and any single theory of placebo—e.g. expectancy, hope, conditioning, anxiety reduction, report bias, symbolic work, narrative and embodiment—provides an inadequate model to explain its salubrious benefits.
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