Operant extinction, which features modification of instrumental responses to stimuli following a change in associated reinforcement, is an important form of learning for organisms in dynamic environments. Animal studies have highlighted orbital and medial prefrontal cortex and amygdala as mediators of operant extinction. Yet little is known about the neural mediators of operant extinction learning in humans. Using a novel fMRI paradigm, we report dissociable functional responses in distinct regions of medial orbitofrontal cortex (mOFC) during successful appetitive and aversive based operant extinction. During successful operant extinction, increased activity was observed in frontopolar OFC, while decreased activity was observed in caudal mOFC and rostral anterior cingulate cortex (rACC) relative to both (i) successful control trials where the reinforcement associated with the stimulus does not change; and (ii) successful acquisition trials during initial learning of the stimulus- reinforcement associations. Functional connectivity analysis demonstrated inverse connectivity between frontopolar OFC and both rACC and the amygdala. These data support animal models suggesting the importance of mOFC - amygdala interaction during operant extinction and expand our knowledge of the neural systems in humans. These findings suggest that in humans, frontopolar OFC modulates activity in caudal mOFC, rACC and amygdala during successful operant extinction learning.
frontopolar; amygdala; instrumental; anterior cingulate cortex
The goal of this article is to provide a selective and targeted review of the neuroimaging literature on psychopathic tendencies and antisocial behavior and to explore the extent to which this literature supports recent cognitive neuroscientific models of psychopathy and antisocial behavior. The literature reveals that individuals who present with an increased risk for reactive, but not instrumental, aggression show increased amygdala responses to emotionally evocative stimuli. This is consistent with suggestions that such individuals are primed to respond strongly to an inappropriate extent to threatening or frustrating events. In contrast, individuals with psychopathic tendencies show decreased amygdala and orbitofrontal cortex responses to emotionally provocative stimuli or during emotional learning paradigms. This is consistent with suggestions that such individuals face difficulties with basic forms of emotional learning and decision making.
Amygdala; Orbital frontal cortex; Psychopathy; Instrumental aggression; Reactive aggression
A major controversy in child psychiatry is whether bipolar disorder (BD) presents in children as severe, non-episodic irritability (operationalized here as severe mood dysregulation, SMD), rather than with manic episodes as in adults. Both classic, episodic BD and SMD are severe mood disorders characterized by deficits in processing emotional stimuli. Neuroimaging techniques can be used to test whether the pathophysiology mediating these deficits are similar across the two phenotypes. Amygdala dysfunction during face emotion processing is well-documented in BD, but little is known about amygdala dysfunction in chronically irritable youth. We compared neural activation in SMD (n=19), BD (n=19), and healthy volunteer (HV; n=15) youths during an implicit face-emotion processing task with angry, fearful and neutral expressions. In the right amygdala, both SMD and BD exhibited greater activity across all expressions than HV. However, SMD and BD differed from each other and HV in posterior cingulate cortex, posterior insula, and inferior parietal lobe. In these regions, only SMD showed deactivation in response to fearful expressions, whereas only BD showed deactivation in response to angry expressions. Thus, during implicit face emotion processing, youth with BD and those with SMD exhibit similar amygdala dysfunction but different abnormalities in regions involved in information monitoring and integration.
severe mood dysregulation; bipolar disorder; amygdala; face; emotion
Oxytocin is a neuropeptide that is associated with increases in social affiliative behaviors, particularly toward infants. However, no previous study has investigated healthy adults’ responses to infant faces following oxytocin administration. In addition, given that preliminary evidence suggests that a single nucleotide polymorphism (SNP) of the oxytocin receptor (OXTR) gene, rs53576, may influence behaviors associated with parental sensitivity, we assessed whether such responses vary according to OXTR rs53576 genotype.
The present study assessed the effects of intranasally administered oxytocin and OXTR genotype on human adults’ preferences for infant faces.
A double-blind, between-groups design was used, with 57 genotyped volunteers randomly assigned to receive intranasally administered oxytocin or placebo. Fifty minutes following the administration of oxytocin or placebo, participants viewed infants’ and adults’ faces showing neutral expressions and assessed how appealing they found each face.
Infants’ faces were more strongly preferred following oxytocin inhalation relative to placebo. When participants were separated according to genotype, this effect was only observed for participants homozygous for the rs53576G allele. Parallel effects were not seen for adults’ faces.
The present results are consistent with the hypothesis that acute oxytocin administration increases sensitivity to reward-relevant features of infants and/or reduces sensitivity to their aversive properties. The results also are consistent with suggestions of more efficient oxytocinergic function in rs53576G homozygotes.
Oxytocin; OXTR; parental; faces; affiliation
Generalized Social Phobia (GSP) and Generalized Anxiety Disorder (GAD) are both associated with emotion dysregulation. In healthy subjects, research implicates dorsal anterior cingulate (dACC) in both explicit emotion regulation and top-down attentional control. While studies have examined these processes in GSP or GAD, no work compares findings across the two disorders. Moreover, no work examines functioning in cases comorbid for both disorders (GSP/GAD). Here we compare the neural correlates of explicit emotion regulation (EER) and top-down attentional control (TAC) in GSP, GAD, and GSP/GAD.
Medication-free adults with GSP (EER n=19; TAC n=18), GAD (EER n=17; TAC n =17), GSP/GAD (EER n=17; TAC=15), or no psychopathology (EER n=18; TAC n=18). During EER, individuals alternatively viewed, up-regulated, and down-regulated responses to emotional pictures. During TAC, they performed an emotional Stroop task.
For both tasks, significant group-by-condition interactions emerged in dACC and parietal cortices. Healthy adults showed significantly increased recruitment during emotion regulation, relative to emotion-picture viewing. GAD, GSP, and GSP/GAD subjects showed no such increases, with all three groups differing from healthy adults but not from each other. Evidence of emotion-related disorder-specificity emerged in medial prefrontal cortex (MPFC) and amygdala. This disorder-specific responding varied as a function of stimulus emotion content but not emotion-regulatory demands.
GSP and GAD both involve reduced capacity for engaging emotion-regulation brain networks, whether explicitly or via top-down attentional control. A reduced ability to recruit regions implicated in top-down attention might represent a general risk factor for anxiety disorders.
imaging; social anxiety; generalized anxiety; emotion regulation; anterior cingulate cortex; top-down attentional control
Bipolar disorder (BD) is highly debilitating in both children and adults. Child and adult BD patients show both behavioral deficits in face emotion processing and abnormal amygdala activation. However, amygdala function in pediatric vs. adult BD patients has never been compared directly.
This study compared amygdala responses to emotional facial expressions in 74 subjects [pediatric (N=18) and adult (N=17) patients with BD, healthy volunteer (HV) children (N=15) and adults (N=22)]. Subjects performed a gender identification task while viewing fearful, angry, and neutral faces.
In response to fearful faces, patients with BD across age-groups showed right amygdala hyperactivity relative to healthy volunteers. However, when responses to all facial expressions were combined, pediatric patients exhibited greater right amygdala activation than either adults with BD or HV children.
Amygdala hyperactivity in response to fearful faces is present in both youths and adults with BD. However, compared to adults with BD or healthy youths, youths with BD show amygdala hyperactivity in response to a broad array of emotional faces. Thus, abnormal amygdala activation during face processing appears to be more pervasive in children than adults with BD.
A major controversy in child psychiatry is whether bipolar disorder (BD) presents in children as severe, non-episodic irritability (operationalized here as severe mood dysregulation, SMD), rather than with manic episodes as in adults. Both classic, episodic BD and SMD are severe mood disorders characterized by deficits in processing emotional stimuli. Neuroimaging techniques can be used to test whether the pathophysiology mediating these deficits are similar across the two phenotypes. Amygdala dysfunction during face emotion processing is well-documented in BD, but little is known about amygdala dysfunction in chronically irritable youth. We compared neural activation in SMD (n = 19), BD (n = 19), and healthy volunteer (HV; n = 15) youths during an implicit face-emotion processing task with angry, fearful and neutral expressions. In the right amygdala, both SMD and BD exhibited greater activity across all expressions than HV. However, SMD and BD differed from each other and HV in posterior cingulate cortex, posterior insula, and inferior parietal lobe. In these regions, only SMD showed deactivation in response to fearful expressions, whereas only BD showed deactivation in response to angry expressions. Thus, during implicit face emotion processing, youth with BD and those with SMD exhibit similar amygdala dysfunction but different abnormalities in regions involved in information monitoring and integration.
•Youths with severe mood dysregulation (SMD), bipolar disorder (BD), controls.•Implicit face-emotion processing fMRI task with angry, fearful, neutral emotions.•In R amygdala, SMD and BD had greater activity across all expressions vs controls.•In whole brain analysis SMD had decreased, BD increased activity vs. other groups.
Severe mood dysregulation; Bipolar disorder; Amygdala; Face; Emotion
The goal of this paper is to consider anger from a cognitive neuroscience perspective. Five main claims are made: First, reactive aggression is the ultimate behavioral expression of anger and thus we can begin to understand anger by understanding reactive aggression. Second, neural systems implicated in reactive aggression (amygdala, hypothalamus and periaqueductal gray; the basic threat system) are critically implicated in anger. Factors such as exposure to extreme threat that increase the responsiveness of these systems, should be (and are in the context of Post Traumatic Stress Disorder), associated with increased anger. Third, regions of frontal cortex implicated in regulating the basic threat system, when dysfunctional (e.g., in the context of lesions) should be associated with increased anger. Fourth, frustration occurs when an individual continues to do an action in the expectation of a reward but does not actually receive that reward, and is associated with anger. Individuals who show impairment in the ability to alter behavioral responding when actions no longer receive their expected rewards should be (and are in the context of psychopathy) associated with increased anger. Fifth, someone not doing what another person wants them to do (particularly if this thwarts the person’s goal) is frustrating and consequently anger inducing. The response to such a frustrating social event relies on the neural architecture implicated in changing behavioral responses in non-social frustrating situations.
We used functional magnetic resonance imaging (fMRI) to investigate dysfunction in the amygdala and orbitofrontal cortex in adolescents with disruptive behavior disorders and psychopathic traits during a moral judgment task. Fourteen adolescents with psychopathic traits and 14 healthy controls were assessed using fMRI while they categorized illegal and legal behaviors in a moral judgment implicit association task. fMRI data were then analyzed using random-effects analysis of variance and functional connectivity. Youths with psychopathic traits showed reduced amygdala activity when making judgments about legal actions and reduced functional connectivity between the amygdala and orbitofrontal cortex during task performance. These results suggest that psychopathic traits are associated with amygdala and orbitofrontal cortex dysfunction. This dysfunction may relate to previous findings of disrupted moral judgment in this population.
Conduct disorder; psychopathy; moral reasoning; fMRI
Psychopathy is characterized by profound affective deficits, including shallow affect and reduced empathy. Recent research suggests that these deficits may apply particularly to negative emotions, or to certain negative emotions such as fear. Despite increased focus on the cognitive and neural underpinnings of psychopathy, little is known about how psychopathy is associated with emotional deficits across a range of emotions. In addition, the relationship between psychopathy and the subjective experience of emotion has not yet been assessed.
Eighteen 10-17-year-olds with psychopathic traits and 24 comparison children and adolescents reported on their subjective experiences of emotion during five recent emotionally evocative life events, following a paradigm developed by Scherer and colleagues (Scherer & Wallbott, 1994). Group comparisons were then performed to assess variations in subjective experiences across emotions.
As predicted, psychopathy was associated with reductions in the subjective experience of fear relative to other emotions. Children and adolescents with psychopathic traits reported fewer symptoms associated with sympathetic nervous system arousal during fear-evoking experiences.
Rather than being related to uniformly impoverished emotional experience, psychopathic traits appear to be associated with greater deficits in subjective experiences of fear. This pattern of responding supports and extends previous observations that psychopathy engenders deficits in fear learning, physiological responses to threats, and the recognition of fear in others.
Psychopathy; emotion; fear; antisocial behavior; autonomic
Generalized social phobia (GSP) involves the fear of being negatively evaluated. Previous work suggests that self-referentiality, mediated by medial prefrontal cortex (MFPC), plays an important role in the disorder. However, it is not clear whether this anomalous MPFC response to self-related information in patients with GSP concerns an increased representation of their own or others’ opinions. In this paper we examined whether GSP is associated with increased response to own (1st person) or other individuals’ (2nd person) opinions relative to healthy individuals. Unmedicated individuals with GSP (n=15) and age, IQ, and gender-matched comparison individuals (n=15) read 1st (e.g., I’m ugly), and 2nd (e.g., You’re ugly) person viewpoint comments during fMRI. We observed significant group-by-viewpoint interactions within ventral MPFC. Whereas the healthy comparison individuals showed significantly increased (or less decreased) BOLD responses to 1st relative to 2nd person viewpoints, the patients showed significantly increased responses to 2nd relative to 1st person viewpoints. The reduced BOLD responses to 1st person viewpoint comments shown by the patients correlated significantly with severity of social anxiety symptom severity. These results underscore the importance of dysfunctional self-referential processing and MPFC in GSP. We believe that these data reflect a reorganization of self-referential reasoning in the disorder with a self-concept perhaps atypically related to the view of others.
Social Phobia; fMRI; self-referentiality; medial prefrontal cortex; amygdala
Mentalization is the process by which an observer views a target as possessing higher cognitive faculties such as goals, intentions and desires. Mentalization can be assessed using action identification paradigms, in which observers choose mentalistic (goals-focused) or mechanistic (action-focused) descriptions of targets’ actions. Neural structures that play key roles in inferring goals and intentions from others’ observed or imagined actions include temporo-parietal junction, ventral premotor cortex and extrastriate body area. We hypothesized that these regions play a role in action identification as well. Data collected using functional magnetic resonance imaging (fMRI) confirmed our predictions that activity in ventral premotor cortex and middle temporal gyrus near the extrastriate body area varies both as a function of the valence of the target and the extent to which actions are identified as goal-directed. In addition, the inferior parietal lobule is preferentially engaged when participants identify the actions of mentalized targets. Functional connectivity analyses suggest support from other regions, including the medial prefrontal cortex and amygdala, during mentalization. We found correlations between action identification and Autism Quotient scores, suggesting that understanding the neural correlates of action identification may enhance our understanding of the underpinnings of essential social cognitive processes.
fMRI; action identification; mentalize; ventral premotor cortex; extrastriate body area; amygdale
The psychological and neurobiological processes underlying moral judgment have been the focus of extensive recent research. Here we show that serotonin transporter (5-HTTLPR) genotype predicts responses to moral dilemmas featuring foreseen harm to an innocent.
Participants in this study judged the acceptability of actions that would unintentionally or intentionally harm an innocent victim in order to save others' lives. An analysis of variance revealed a genotype × scenario interaction, F(2, 63) = 4.52, p = .02. Results showed that, relative to long allele homozygotes (LL), carriers of the short (S) allele showed particular reluctance to endorse utilitarian actions resulting in foreseen harm to an innocent individual. LL genotype participants rated perpetrating unintentional harm as more acceptable (M = 4.98, SEM = 0.20) than did SL genotype participants (M = 4.65, SEM = 0.20) or SS genotype participants (M = 4.29, SEM = 0.30). No group differences in moral judgments were observed in response to scenarios featuring intentional harm.
The results indicate that inherited variants in a genetic polymorphism that influences serotonin neurotransmission influence utilitarian moral judgments as well. This finding is interpreted in light of evidence that the S allele is associated with elevated emotional responsiveness.
Generalized social phobia (GSP) is defined by a persistent fear of social disapproval. However, the neural underpinnings of this increased fear and its mediating factors are unclear. Using event-related fMRI, we examined whether the intent of an event, which mediates the neural response to social disapproval in healthy individuals, differentially affects response in GSP. Specifically, would patients with GSP show particularly increased response to embarrassing, unintentional transgressions?
Sixteen patients with GSP and sixteen age, IQ, and gender matched healthy individuals read stories during fMRI scans that either involved neutral social events, unintentional social transgressions (e.g., choking on food at party, and coughing it up), or intentional social transgressions (e.g., disliking food at party, and spitting it out).
Significant group-by-transgression interactions were observed within ventral regions of medial prefrontal cortex (MPFC). Healthy individuals tended to show increased BOLD responses to intentional, relative to unintentional transgressions. The patients with GSP, however, showed significantly increased responses to the unintentional transgressions. In addition, they rated the unintentional transgressions as significantly more embarrassing than the comparison individuals. We also observed significant group main effects within the amygdala and bilateral insula, reflecting elevated GSP responses within these regions to all event types.
These results further implicate the MPFC in the pathophysiology of GSP, specifically through its involvement in distorted self-referential processing. In addition, the current results further underscore the extended role of the amygdala and insula in the processing of social stimuli more generally in GSP.
Generalized social phobia (GSP) is characterized by fear/avoidance of social situations. Previous studies have examined the neural responses in GSP to one class of social stimuli, facial expressions. However, studies have not examined the neural response in GSP to another equally important class of social stimuli, the communication of praise or criticism.
To examine the neural response to receipt of praise or criticism in GSP; specifically, to determine whether patients with GSP show an increased response to the receipt of both praise and criticism and whether self-relevance modulates this relationship.
Government clinical research institute.
Unmedicated individuals with GSP (n=17) and age-, IQ-, and sex-matched healthy comparison individuals (n=17).
Main Outcome Measure
Blood oxygenation level–dependent signal, as measured via functional magnetic resonance imaging. During functional magnetic resonance imaging scans, individuals read positive (eg, You are beautiful), negative (eg, You are ugly), and neutral (eg, You are human) comments that could be either about the self or about somebody else (eg, He is beautiful).
Hypothesized significant group×valence×referent interactions were observed within regions of the medial prefrontal cortex and bilateral amygdala. In these regions, the patients with GSP showed significantly increased blood oxygenation level–dependent responses, relative to comparison individuals, to negative comments (criticism) referring to themselves. However, in contrast, there were no significant group differences with respect to negative comments referring to others or neutral or positive comments referring to self or others.
These results implicate the medial prefrontal cortex, involved in the representation of the self, together with the amygdala, in the pathophysiology of GSP. Further, findings demonstrate a meaningful effect of psychological context on neural-circuitry hyperactivity in GSP.
Generalized Social Phobia (GSP) involves the fear/avoidance of social situations while Generalized Anxiety Disorder (GAD) involves an intrusive worry about everyday life circumstances. It remains unclear whether these, highly comorbid, conditions represent distinct disorders or alternative presentations of a single underlying pathology. In this study, we examined stimulus-reinforcement based decision-making in GSP and GAD.
Twenty unmedicated patients with GSP, sixteen unmedicated patients with GAD and nineteen age, IQ, and gender matched healthy comparison individuals completed the Differential Reward/ Punishment Learning Task (DRPLT). In this task, the subject chooses between two objects associated with different levels of reward or punishment. Thus, response choice indexes not only reward/ punishment sensitivity but also sensitivity to reward/ punishment level according to between-object reinforcement distance.
We found that patients with GAD committed a significantly greater number of errors compared to both the patients with GSP and the healthy comparison individuals. In contrast, the patients with GSP and the healthy comparison individuals did not differ in performance on this task.
These results link GAD with an anomalous non-affective based decision-making. Further, they are indicative that GSP and GAD are associated with distinct pathophysiologies.
Psychopathy is a developmental disorder marked by emotional hypo-responsiveness and an increased risk for antisocial behavior. Influential attention based accounts of psychopathy have long been made; however, these accounts have made relatively little reference to general models of attention in healthy individuals. The current paper has three aims: (1) To briefly describe current cognitive neuroscience data on differing attentional systems; (2) To examine the functional integrity of these attentional systems in individuals with psychopathy; (3) To consider the implications of these data for attention and emotion dysfunction accounts of psychopathy.
Generalized Social Phobia (GSP) is characterized by a marked fear of most social situations. It is associated with an anomalous neural response to emotional stimuli, and individuals with the disorder frequently show interpretation bias in social situations. From this it might be suggested that GSP involves difficulty in accurately perceiving, using, understanding and managing emotions. Here we applied the Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT) to medication-free GSP (n=28) and no pathology (n=21) individuals. Patients with GSP performed within the normal range on the measure however severity of social anxiety significantly correlated with emotional intelligence (EI). Specifically, there was a negative correlation between social anxiety severity and Experiential (basic-level emotional processing) EI. In contrast, there was no significant correlation between social anxiety severity and Strategic (higher-level conscious emotional processing) EI. These results suggest that EI may index emotional processing systems that mitigate the impact of systems causally implicated in GSP.
generalized social phobia; emotional responding; emotional intelligence; MSCEIT
Status hierarchies constitute a fundamental organizing principle of human society. However, little is known about the neural systems that process nonverbal cues that indicate status. Preliminary neuropsychological work has suggested a role for the ventrolateral and ventromedial prefrontal cortex (VLPFC/VMPFC) and the superior temporal cortex (STC). We used functional magnetic resonance imaging to delineate the nature of these roles. Analyses revealed signal changes in the right VLPFC in connection with two primary functions attributed to status cues. Status cues moderate behavior and the right VLPFC showed increased signal for high-status relative to neutral and low-status cues. The VLPFC also showed increased signal for high-status cues displayed by individuals of the opposite gender to the perceiver; this may be relevant to the role status cues play in moderating mate choice behavior. Connectivity results indicated significant positive connectivity between the VLPFC and both the VMPFC and the STC. We suggest that the VLPFC retrieves information from these regions when processing hierarchy cues to facilitate socially adaptive behavior.
The current paper examines the functional contributions of the amygdala and ventromedial prefrontal cortex (vmPFC) and the evidence that the functioning of these systems is compromised in individuals with psychopathy. The amygdala is critical for the formation of stimulus–reinforcement associations, both punishment and reward based, and the processing of emotional expressions. vmPFC is critical for the representation of reinforcement expectancies and, owing to this, decision making. Neuropsychological and neuroimaging data from individuals with psychopathy are examined. It is concluded that these critical functions of the amygdala and vmPFC, and their interaction, are compromised in individuals with the disorder. It is argued that these impairments lead to the development of psychopathy.
amygdala; venromedial perfrontal cortex; psychopathy
Amygdala and ventrolateral prefrontal cortex (vlPFC) dysfunction manifests in adolescents with anxiety disorders when they view negatively valenced stimuli in threatening contexts. Such fear-circuitry dysfunction may also manifest when anticipated social evaluation leads socially anxious adolescents to misperceive peers as threatening.
To determine whether photographs of negatively evaluated smiling peers viewed during anticipated social evaluation engage the amygdala and vlPFC differentially in adolescents with and without social anxiety.
Government clinical research institute.
Fourteen adolescents with anxiety disorders associated with marked concerns of social evaluation and 14 adolescents without a psychiatric diagnosis matched on sex, age, intelligence quotient, and socioeconomic status.
Main Outcome Measures
Blood oxygenation level–dependent signal measured with event-related functional magnetic resonance imaging. Before and during neuroimaging scans, participants anticipating social evaluation completed peer- and self-appraisals. Event-related analyses were tailored to participants’ ratings of specific peers.
Participants classified 40 pictures of same-age peers as ones with whom they did or did not want to engage in a social interaction. Anxious adolescents showed greater amygdala activation than healthy adolescents when anticipating evaluation from peers previously rated as undesired for an interaction. Psychophysiological interaction connectivity analyses also revealed a significant positive association between amygdala and vlPFC activation in anxious vs healthy adolescents in response to these stimuli.
Anticipating social evaluation from negatively perceived peers modulates amygdala and vlPFC engagement differentially in anxious and healthy adolescents. Amygdala and vlPFC dysfunction manifests in adolescent anxiety disorders in specific contexts of anticipated peer evaluation.
Social dominance and physical size are closely linked. Nonverbal dominance displays in many non-human species are known to increase the displayer's apparent size. Humans also employ a variety of nonverbal cues that increase apparent status, but it is not yet known whether these cues function via a similar mechanism: by increasing the displayer's apparent size.
We generated stimuli in which actors displayed high status, neutral, or low status cues that were drawn from the findings of a recent meta-analysis. We then conducted four studies that indicated that nonverbal cues that increase apparent status do so by increasing the perceived size of the displayer. Experiment 1 demonstrated that nonverbal status cues affect perceivers' judgments of physical size. The results of Experiment 2 showed that altering simple perceptual cues can affect judgments of both size and perceived status. Experiment 3 used objective measurements to demonstrate that status cues change targets' apparent size in the two-dimensional plane visible to a perceiver, and Experiment 4 showed that changes in perceived size mediate changes in perceived status, and that the cue most associated with this phenomenon is postural openness.
We conclude that nonverbal cues associated with social dominance also affect the perceived size of the displayer. This suggests that certain nonverbal dominance cues in humans may function as they do in other species: by creating the appearance of changes in physical size.
Children with narrow phenotype bipolar disorder (NP-BD; i.e., history of at least one hypomanic or manic episode with euphoric mood) are deficient when labeling face emotions. It is unknown if this deficit is specific to particular emotions, or if it extends to children with severe mood dysregulation (SMD; i.e., chronic irritability and hyperarousal without episodes of mania). Thirty-nine NP-BD, 31 SMD, and 36 control subjects completed the emotional expression multimorph task, which presents gradations of facial emotions from 100% neutrality to 100% emotional expression (happiness, surprise, fear, sadness, anger, and disgust). Groups were compared in terms of intensity of emotion required before identification occurred and accuracy. Both NP-BD and SMD youth required significantly more morphs than controls to label correctly disgusted, surprised, fearful, and happy faces. Impaired face labeling correlated with deficient social reciprocity skills in NP-BD youth and dysfunctional family relationships in SMD youth. Compared to controls, patients with NP-BD or SMD require significantly more intense facial emotion before they are able to label the emotion correctly. These deficits are associated with psychosocial impairments. Understanding the neural circuitry associated with face-labeling deficits has the potential to clarify the pathophysiology of these disorders.