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Blind rage? Heightened anger is associated with altered amygdala responses to masked and unmasked fearful faces
Abstract
We investigated anger-related variability in the BOLD fMRI response to crude/masked and detailed/unmasked fearful faces. Anger expression positively covaried with amygdala activation to crude fear, while trait anger negatively covaried with amygdala responses to detailed fear. This differential processing may trigger aggression without the subsequent inhibition associated with distress cues.
... Meanwhile, a recent study suggests the right and left amygdala are involved in processing different types of fearful faces (Carlson, Greenberg, & Mujica-Parodi, 2010). Specifically, individuals who score higher in anger expression have increased neural activity in the left amygdala to crude representations of fearful faces, which may reflect a mechanism triggering aggressive behaviors. ...
... In contrast, trait anger negatively covaried with the right amygdala response to detailed fear expressions. In other words, the left amygdala is more related to antisocial or aggressive behaviors (Blair, 2003), while the right amygdala is more related to trait anger and fear processing (Carlson et al., 2010). Because of its functional dissociation between the left and right amygdala, the hemispheric asymmetry of the amygdala in the relation between unsatisfied needs and trait anger, if any, may help elucidate its role in aggression (i.e., approach-related behaviors) or fear (i.e., withdrawal behaviors). ...
... We found that the right amygdala GMV was negatively correlated with trait anger. Because previous studies also show that the right amygdala is involved in processing perceived threats (Blair, 2012;Carlson et al., 2010), and low relatedness satisfaction is associated with threatened ego (Baumeister et al., 1996), it is not surprising that the right amygdala was also found to be related to unsatisfied relatedness, which further mediated its relation to anger. ...
Anger is a common negative emotion in social life. Behavioral research suggests that unsatisfied relatedness, autonomy, and competence are related to anger. However, it remains unclear whether these unsatisfied needs all contribute to anger or just a particular unsatisfied need is the main source of anger. In addition, little is known about the neural substrate between unsatisfied needs and anger. To address these two questions, we used voxel-based morphometry (VBM) to explore the neural substrate underlying the relation between unsatisfied needs and trait anger. Behaviorally, we found that although all three unsatisfied needs were correlated with trait anger, unsatisfied relatedness was the only factor that was uniquely related to trait anger. Neurally, the gray matter volume of the right amygdala was correlated with trait anger, which fits nicely with the role of the amygdala as a core region for processing anger. Importantly, the right amygdala mediated the total effect of unsatisfied relatedness on trait anger, even after controlling for general personality dispositions. Our results contribute to the theoretical conceptualization of anger by elucidating the unique role of unsatisfied relatedness in anger and the neural substrate underlying such relation.
... Moreover, trait anger apparently is highly predictive for social aggression, which is marked by reduced sensitivity to the victim's fearful expression (see (Marsh & Blair, 2008) for a review). In strong agreement, trait anger is related to reduced amygdala reactivity when perceiving fearful faces (Carlson, Greenberg, & Mujica-Parodi, 2010). Additionally, trait anger has repeatedly been linked to reward-sensitivity and approach motivation (Carver, 2004;Harmon-Jones, 2004). ...
... It must however be noted that, based on the present data, we cannot entirely exclude that trait anger also reduces gaze-imitation towards threat. Indeed, trait anger is associated with reduced amygdala activity when perceiving fearful faces (Carlson et al., 2010), and reduced sensitivity for fearful facial expressions, which is argued to underlie social aggression (Marsh & Blair, 2008). The present data are however in favor of increased reward-sensitivity in relation to trait anger, and we therefore assume that the trait anger shift from threat to reward in gaze- imitation is driven by angry individuals imitating happy gaze more strongly, thereby reducing the general imitation bias for fearful gaze-shifts. ...
... Although the correlational analysis shows us that the reduced threat-bias in relation to trait anger is most likely the result of increased gaze-imitation towards reward, we cannot exclude that gaze-imitation towards threat might also be reduced. Both interpretations are supported in the literature ( Carlson et al., 2010;Carver, 2004;Harmon-Jones, 2004;Marsh & Blair, 2008), and future research on gaze-imitation should therefore address this issue. ...
The terms approach and avoidance are used to describe appetitive motivation and fear of punishment. In a social context fear is indeed linked to avoidance, but approach motivation is also expressed with anger and aggression as means to achieve goals at the expense, or through social correction, of others. Therefore, in the social competition of most mammalian species approach-avoidance is strongly linked to dominance-submissiveness, whereby the motivation to dominate others reflects appetitive motivation as well as socially aggressive tendencies. The steroid testosterone is a social hormone that is heavily involved in approach-avoidance and dominance-submissiveness, and is in many species associated with reduced fear and increased reactive social aggression. Recent evidence indicates, however, that testosterone can also promote fairness in humans. In this thesis we first describe a neural framework rooted in animal research and based on a study in five human subjects with selective brain damage in the basolateral amygdala, in which we show that this structure is heavily involved in the inhibition of fear-vigilance. Next, we use several newly developed interactive eye-tracking paradigms to show that anger is indeed related to reward sensitivity, and anxiety to threat avoidance. Furthermore, when confronted with angry facial expressions, submissiveness predicts rapid gaze aversion from eye-contact, and dominance motives as well as testosterone administration lead to reflexive preservation of eye-contact. In sum, dominance-submissiveness seems to involve reflexive mechanisms, and testosterone induces reactive dominance behavior. In the next part of this thesis we show that testosterone also influences cognitive behavior and decision-making in the absence of a direct status-threat. Earlier research already showed that testosterone can reduce cognitive empathy, and here we show that testosterone adaptively reduces trust, but can also increase social cooperative behavior. Translating evidence from rodent and primate research, we argue therefore that reactive-reflexive dominance, and deliberate social cooperation are both approach behaviors by which testosterone promotes survival and reproduction through an increase of social status. First, testosterone inhibits basal fear responsivity at the level of the basolateral amygdala and hypothalamus providing for a general fearlessness that facilitates approach oriented behavior. Second, when social status is directly challenged testosterone promotes reactive aggression and reflexive dominance by upregulating vasopressin gene-expression in the central-medial amygdala. Third, testosterone reduces cortical control over the amygdala, resulting in the general social vigilance that underlies conscious decision making that is beneficial to social status. In sum, testosterone boosts unconscious-reflexive dominance, but can also increase cooperative behaviors depending on the social context. However, both on the level of this reflexive behavior and in conscious decision making, testosterone promotes approach oriented behavior that helps to defend and increase social status.
... Moreover, trait anger apparently is highly predictive for social aggression, which is marked by reduced sensitivity to the victim's fearful expression (see (Marsh & Blair, 2008) for a review). In strong agreement, trait anger is related to reduced amygdala reactivity when perceiving fearful faces (Carlson, Greenberg, & Mujica-Parodi, 2010). Additionally, trait anger has repeatedly been linked to reward-sensitivity and approach motivation (Carver, 2004;Harmon-Jones, 2004). ...
... It must however be noted that, based on the present data, we cannot entirely exclude that trait anger also reduces gaze-imitation towards threat. Indeed, trait anger is associated with reduced amygdala activity when perceiving fearful faces (Carlson et al., 2010), and reduced sensitivity for fearful facial expressions, which is argued to underlie social aggression (Marsh & Blair, 2008). The present data are however in favor of increased reward-sensitivity in relation to trait anger, and we therefore assume that the trait anger shift from threat to reward in gaze- imitation is driven by angry individuals imitating happy gaze more strongly, thereby reducing the general imitation bias for fearful gaze-shifts. ...
... Although the correlational analysis shows us that the reduced threat-bias in relation to trait anger is most likely the result of increased gaze-imitation towards reward, we cannot exclude that gaze-imitation towards threat might also be reduced. Both interpretations are supported in the literature ( Carlson et al., 2010;Carver, 2004;Harmon-Jones, 2004;Marsh & Blair, 2008), and future research on gaze-imitation should therefore address this issue. ...
The terms approach and avoidance are used to describe appetitive motivation and fear of punishment. In a social context fear is indeed linked to avoidance, but approach motivation is also expressed with anger and aggression as means to achieve goals at the expense, or through social correction, of others. Therefore, in the social competition of most mammalian species approach-avoidance is strongly linked to dominance-submissiveness, whereby the motivation to dominate others reflects appetitive motivation as well as socially aggressive tendencies. The steroid testosterone is a social hormone that is heavily involved in approach-avoidance and dominance-submissiveness, and is in many species associated with reduced fear and increased reactive social aggression. Recent evidence indicates, however, that testosterone can also promote fairness in humans.
In this thesis we first describe a neural framework rooted in animal research and based on a study in five human subjects with selective brain damage in the basolateral amygdala, in which we show that this structure is heavily involved in the inhibition of fear-vigilance. Next, we use several newly developed interactive eye-tracking paradigms to show that anger is indeed related to reward sensitivity, and anxiety to threat avoidance. Furthermore, when confronted with angry facial expressions, submissiveness predicts rapid gaze aversion from eye-contact, and dominance motives as well as testosterone administration lead to reflexive preservation of eye-contact. In sum, dominance-submissiveness seems to involve reflexive mechanisms, and testosterone induces reactive dominance behavior.
In the next part of this thesis we show that testosterone also influences cognitive behavior and decision-making in the absence of a direct status-threat. Earlier research already showed that testosterone can reduce cognitive empathy, and here we show that testosterone adaptively reduces trust, but can also increase social cooperative behavior. Translating evidence from rodent and primate research, we argue therefore that reactive-reflexive dominance, and deliberate social cooperation are both approach behaviors by which testosterone promotes survival and reproduction through an increase of social status. First, testosterone inhibits basal fear responsivity at the level of the basolateral amygdala and hypothalamus providing for a general fearlessness that facilitates approach oriented behavior. Second, when social status is directly challenged testosterone promotes reactive aggression and reflexive dominance by upregulating vasopressin gene-expression in the central-medial amygdala. Third, testosterone reduces cortical control over the amygdala, resulting in the general social vigilance that underlies conscious decision making that is beneficial to social status. In sum, testosterone boosts unconscious-reflexive dominance, but can also increase cooperative behaviors depending on the social context. However, both on the level of this reflexive behavior and in conscious decision making, testosterone promotes approach oriented behavior that helps to defend and increase social status
... Moreover, trait anger apparently is highly predictive for social aggression, which is marked by reduced sensitivity to the victim's fearful expression (see [23] for a review). In strong agreement, trait anger is related to reduced amygdala reactivity when perceiving fearful faces [24]. Additionally, trait anger has repeatedly been linked to reward-sensitivity and approach motivation [25,26]. ...
... It must however be noted that, based on the present data, we cannot entirely exclude that trait anger also reduces gaze-imitation towards threat. Indeed, trait anger is associated with reduced amygdala activity when perceiving fearful faces [24], and reduced sensitivity for fearful facial expressions, which is argued to underlie social aggression [23]. The present data are however in favor of increased reward-sensitivity in relation to trait anger, and we therefore assume that the trait anger shift from threat to reward in gaze-imitation is driven by angry individuals imitating happy gaze more strongly, thereby reducing the general imitation bias for fearful gaze-shifts. ...
... Although the correlational analysis shows us that the reduced threat-bias in relation to trait anger is most likely the result of increased gaze-imitation towards reward, we cannot exclude that gaze-imitation towards threat might also be reduced. Both interpretations are supported in the literature23242526, and future research on gaze-imitation should therefore address this issue. In summary, allocation of gaze is reflexively facilitated when an observed gaze-shift is imitated. ...
The gaze of a fearful face silently signals a potential threat's location, while the happy-gaze communicates the location of impending reward. Imitating such gaze-shifts is an automatic form of social interaction that promotes survival of individual and group. Evidence from gaze-cueing studies suggests that covert allocation of attention to another individual's gaze-direction is facilitated when threat is communicated and further enhanced by trait anxiety. We used novel eye-tracking techniques to assess whether dynamic fearful and happy facial expressions actually facilitate automatic gaze-imitation. We show that this actual gaze-imitation effect is stronger when threat is signaled, but not further enhanced by trait anxiety. Instead, trait anger predicts facilitated gaze-imitation to reward, and to reward compared to threat. These results agree with an increasing body of evidence on trait anger sensitivity to reward.
... Several studies show that the amygdala plays a role in anger processing (Alia-Klein et al., 2009, 2020Blair, 2012;Carlson et al., 2010). For example, it has been shown that amygdala activation increases in response to the presentation of angry stimuli (Derntl et al., 2009). ...
Anger and aggression have large impact on people’s safety and the society at large. In order to provide an intervention to minimise aggressive behaviours, it is important to understand the neural and cognitive aspects of anger and aggression. In this systematic review, we investigate the cognitive and neural aspects of anger-related processes, including anger-related behaviours and anger reduction. Using this information, we then review prior existing methods on the treatment of anger-related disorders as well as anger management, including mindfulness and cognitive behavioural therapy. At the cognitive level, our review that anger is associated with excessive attention to anger-related stimuli and impulsivity. At the neural level, anger is associated with abnormal functioning of the amygdala and ventromedial prefrontal cortex. In conclusions, based on cognitive and neural studies, we here argue that mindfulness based cognitive behavioural therapy may be better at reducing anger and aggression than other behavioural treatments, such as cognitive behavioural therapy or mindfulness alone. We provide key information on future research work and best ways to manage anger and reduce aggression. Importantly, future research should investigate how anger related behaviours is acquired and how stress impacts the development of anger.
... L'amygdale droite serait plus en lien avec des comportements de peur et de colère, tandis que l'amygdale gauche serait plus liée aux comportements anti-sociaux et d'agression. Cela rejoint la théorie selon laquelle l'hémisphère droit est impliqué dans les processus d'évitement (Carlson et al., 2010) alors que l'hémisphère gauche est lui plus impliqué dans les processus d'approches (Bobes et al., 2013). De façon similaire il semble que l'amygdale droite soit moins impliquée dans le traitement d'informations émotionnelles positives que l'amygdale gauche. ...
La sérotonine, un neuromodulateur présent dans la quasi-totalité du système nerveux central, est impliquée dans un grand nombre de processus cognitifs (eg. apprentissage), émotionnels et motivationnels. Son transporteur, une protéine membranaire présynaptique, permet sa recapture et module ainsi l’action de la sérotonine au sein de différents réseaux cérébraux. Cependant, la relation entre le taux de transporteur de la sérotonine et réseaux cérébraux impliqués dans différents aspects du comportement reste mal comprise. Dans cette thèse, nous avons utilisé l’imagerie multimodale, combinant PET et IRMf pour comprendre les liens existants entre le taux de transporteur de la sérotonine et des réseaux impliqués dans les processus de contrôle exécutif de traitement des émotions et d’apprentissage du rang social. Le taux de transporteur libre de la sérotonine a été marqué à l’aide du [11C]-DASB. Dans une première expérience, nous avons étudié le réseau cérébral engagé dans l’apprentissage du rang social lors d’une compétition. Une approche neuro-computationnelle nous a permis de mettre en évidence une modulation de l’apprentissage du rang social par le taux de transporteur de la sérotonine présent dans le noyau dorsal du raphé. De plus, ce taux de transporteur de la sérotonine du raphé module l’activité d’un réseau cérébral impliqué dans cet apprentissage en modulant l'encodage de la valeur choisie.Dans un second temps, nous nous sommes intéressés au réseau soutenant la perception émotionnelle à partir de visages. L’augmentation du taux de transporteur libre de la sérotonine dans le noyau du raphé est associée à une hyperréactivité de l’amygdale lors de la perception d’émotions faciales. De plus, une étude de la connectivité fonctionnelle de l’amygdale en fonction du taux de transporteur dans le noyau du raphé a révélé une augmentation de la connectivité entre l’amygdale et les aires du cortex préfrontal dorsolatéral lors de la visualisation d’émotions au caractère négatif (peur et colère). Finalement, nous avons aussi étudié la modulation de la connectivité fonctionnelle des réseaux exécutifs, de la saillance et du mode par défaut par le taux de transporteur de la sérotonine présent dans le raphé. Seul le réseau du contrôle exécutif, impliqué dans les processus attentionnels et mnésiques révèle une augmentation de sa connectivité globale avec la diminution de la disponibilité en transporteur au niveau du raphé. Dans leur ensemble, ces résultats montrent que la disponibilité en transporteur sérotoninergique dans le raphé module, l’apprentissage de la hiérarchie de rang, la sensibilité aux stimuli extérieurs tels que les émotions, ainsi que le contrôle exécutif et leurs réseaux cérébraux respectifs. L’étude de ces relations revêt donc une importance sociétale et clinique du fait du lien fort entre le système sérotoninergique et les troubles anxieux
... The copyright holder for this preprint this version posted October 15, 2020. ; https://doi.org/10.1101/2020.10.14.338863 doi: bioRxiv preprint 2018; Wang et al., 2017;Carré et al., 2012;Carlson, Greenberg & Mujica-Parodi, 2010) and its connectivity with the prefrontal cortices (Beyer et al., 2014;Fulwiler et al., 2012) based on a priori theoretical and empirical work (LeDoux, 1996;Marsh & Blair, 2008). While other studies have individually reported a number of brain regions beyond the amygdala associated with trait anger, such as the thalamus (Alia- Klein et al., 2018;Herpertz et al., 2017), striatum (da Cunha-Bang et al., 2017, and anterior cingulate cortex (Repple et al., 2018), our analysis demonstrates that all of these neural sites reflect individual differences in trait anger with regards to the amygdala. ...
Past research on the brain correlates of trait anger has been limited by small sample sizes, a focus on relatively few regions-of-interest, and poor test-retest reliability of functional brain measures. To address these limitations, we conducted a data-driven analysis of variability in connectome-wide general functional connectivity, which has good test-retest reliability, in a sample of 1,048 young adult volunteers. Multi-dimensional matrix regression analysis showed that individual differences in self-reported trait anger maps onto variability in the whole-brain functional connectivity patterns of three brain regions that serve action-related functions: bilateral supplementary motor area (SMA) and the right lateral frontal pole. Follow-up seed-based analysis confirmed that high trait anger is associated with hyperconnectivity between these three regions and the somatomotor network as well as hyperconnectivity and hypoconnectivity between SMA and default mode and visual networks, respectively. Supplementary targeted analyses based on theoretical and empirical grounds further revealed that high trait anger is associated with hyperconnectivity between the amygdala and dorsomedial prefrontal cortex, dorsal anterior cingulate cortex, and striatum. These patterns suggest that the dispositional tendency to more easily experience frustration and anger is associated with variability in the functional connectivity of brain networks supporting somatomotor, affective, self-referential, and visual information processes. The emergence of action-related brain regions from our connectome-wide analysis is consistent with trait anger as reflecting a greater propensity to provoked action.
... This suggestion receives support with respect to threat and social provocation. Work with healthy participants has reported that a predisposition to anger is positively associated with the amygdala responding to masked fearful expressions [84]. Moreover, patients with psychiatric disorders at increased risk for reactive aggression and irritability (BPD, IED and DMDD) show hyper-amygdala responsiveness to threat [85 -87]. ...
Empathy and anger are two social emotions that modulate an individual's risk for aggression. Empathy is an emotional reaction to another individual's emotional state. Anger is an emotional reaction to threat, frustration or social provocation. Reduced empathy, seen in psychopathy, increases the risk for goal-directed aggression. Atypically increased anger (i.e. irritability), seen in conditions like disruptive mood dysregulation disorder and borderline personality disorder, increases the risk for reactive aggression. In this paper, I will outline core neurocognitive functions that correspond to empathy and which are compromised in individuals with psychopathic traits. In addition, I will outline neurocognitive functions involved in either the generation or regulation of anger and which are compromised in psychiatric conditions at increased risk for irritability/reactive aggression. It can be hoped that improved understanding of empathy and anger will lead to better assessment tools and improved interventions to reduce aggression risk.
This article is part of the theme issue ‘Diverse perspectives on diversity: multi-disciplinary approaches to taxonomies of individual differences’.
... Performing this task in conjunction with fMRI has revealed that the amygdala is more active in response to masked fearful versus masked happy faces, again suggesting the amygdala plays a role in detecting important stimuli without the need for conscious awareness (Whalen et al., 1998). Findings of amygdala activity to masked threats have subsequently been replicated numerous times (Armony, Corbo, Clement, & Brunet, 2005;Carlson, Greenberg, & Mujica-Parodi, 2010;Carlson, Reinke, & Habib, 2009;Liddell et al., 2005;Morris, Ohman, & Dolan, 1998, 1999Rauch et al., 2000;Sheline et al., 2001;Suslow et al., 2006;Whalen et al., 2004;L. E. Williams, Bargh, Nocera, & Gray, 2009; L. M. Williams et al., 2005). ...
Emotions contain appraisal, reactivity, and feeling stages that serve evolutionarily adaptive functions. Although emotional processing is adaptive, it can also be advantageous to regulate one’s emotional response. In this chapter, we introduce the neural mechanisms associated with emotional appraisal, reactivity, feeling, and regulation. Given the great breadth of possible emotional behaviors and experiences, we only provide an abbreviated introduction into the neural mechanisms of emotion. The chapter summarizes early research assessing deficits in emotional processing following localized brain damage to more modern research using functional neuroimaging techniques. The reviewed literature illustrates that emotion is not a singular process and the neural substrate of emotion is not a singular region.
... Further, the severity of CU traits was inversely correlated with the connectivity of the amygdala with the vmPFC ) These findings are consistent with the critical role of the amygdala as an interface between the perception of social stimuli and the triggering of emotional reactions (Adolphs 2010). Hypoactivation of the amygdala during encoding of fearful faces in youth with CU traits could reflect an impairment of social perception; specifically, reduced capacity to recognize salient distress cues, a factor that decreases aggression in healthy populations Carlson et al. 2010). This interpretation is consistent with the findings of impaired social perception and problem-solving in aggressive children (Lochman and Dodge 1994). ...
Objective:
We present the rationale and design of a randomized controlled trial of cognitive-behavioral therapy (CBT) for aggression in children and adolescents, which is conducted in response to the National Institute of Mental Health (NIMH) Research Domain Criteria (RDoC) approach initiative. Specifically, the study is focused on the brain-behavior associations within the RDoC construct of frustrative non-reward. On the behavioral level, this construct is defined by reactions elicited in response to withdrawal or prevention of reward, most notably reactive aggression. This study is designed to test the functional magnetic resonance (fMRI) and electrophysiological (EEG) correlates of aggression and its reduction after CBT.
Methods:
Eighty children and adolescents with high levels of aggression across multiple traditional diagnostic categories, ages 8-16, will be randomly assigned to receive 12 sessions of CBT or 12 sessions of supportive psychotherapy. Clinical outcomes will be measured by the ratings of aggressive behavior collected at baseline, midpoint, and endpoint evaluations, and by the Improvement Score of the Clinical Global Impressions Scale assigned by an independent evaluator (blinded rater). Subjects will also perform a frustration-induction Go-NoGo task and a task of emotional face perception during fMRI scanning and EEG recording at baseline and endpoint.
Results:
Consistent with the NIMH strategic research priorities, if functional neuroimaging and EEG variables can identify subjects who respond to CBT for aggression, this can provide a neuroscience-based classification scheme that will improve treatment outcomes for children and adolescents with aggressive behavior.
Conclusions:
Demonstrating that a change in the key nodes of the emotion regulation circuitry is associated with a reduction of reactive aggression will provide evidence to support the validity of the frustrative non-reward construct.
... In addition, experiments involving punishment contingencies during human social interaction paradigms reported activation in the amygdala, the DLPFC, and the dorsal striatum (de Quervain et al., 2004;Fehr & Rockenbach, 2004;Kahn et al., 2002;Rilling & Sanfey, 2011). Neuroimaging studies that experimentally induced anger in humans demonstrated increased activation in the DLPFC and OFC (Carlson, Greenberg, & Mujica-Parodi, 2010;Kimbrell et al., 1999). Two fMRI studies that explicitly measured operationally defined aggressive behavior reported BOLD activation in the medial frontal gyrus and caudate (Kramer et al., 2007(Kramer et al., , 2011. ...
Alcohol-related aggression is a complex and problematic phenomenon with profound public health consequences. We examined neural correlates potentially moderating the relationship between human aggressive behavior and chronic alcohol use. Thirteen subjects meeting DSM-IV criteria for past alcohol-dependence in remission (AD) and 13 matched healthy controls (CONT) participated in an fMRI study adapted from a laboratory model of human aggressive behavior (Point Subtraction Aggression Paradigm, or PSAP). Blood oxygen level dependent (BOLD) activation was measured during bouts of operationally defined aggressive behavior, during postprovocation periods, and during monetary-reinforced behavior. Whole brain voxelwise random-effects analyses found group differences in brain regions relevant to chronic alcohol use and aggressive behavior (e.g., emotional and behavioral control). Behaviorally, AD subjects responded on both the aggressive response and monetary response options at significantly higher rates than CONT. Whole brain voxelwise random-effects analyses revealed significant group differences in response to provocation (monetary subtractions), with CONT subjects showing greater activation in frontal and prefrontal cortex, thalamus, and hippocampus. Collapsing data across all subjects, regression analyses of postprovocation brain activation on aggressive response rate revealed significant positive regression slopes in precentral gyrus and parietal cortex; and significant negative regression slopes in orbitofrontal cortex, prefrontal cortex, caudate, thalamus, and middle temporal gyrus. In these collapsed analyses, response to provocation and aggressive behavior were associated with activation in brain regions subserving inhibitory and emotional control, sensorimotor integration, and goal directed motor activity. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
... In healthy individuals, the amygdala activates both to consciously (Morris et al. 1996) and nonconsciously (Liddell et al. 2005; Whalen et al. 1998) processed fearful faces. The extent to which the amygdala is activated in response to fearful faces in any given individual correlates with a number of dispositions including anxiety (Etkin et al. 2004) and aggression (Carlson et al. 2010). In addition to the recognition of fearful expressions, the amygdala is also necessary for the experience of fear (Feinstein et al. 2011) and the facilitation of perceptual processing by fearful facial expressions (Vuilleumier et al. 2004). ...
Fearful facial expressions are salient nonverbal social cues that signal the existence of potential threat within the environment. These threat signals capture spatial attention both when processed consciously (unmasked) and nonconsciously (masked). Studies using masked fearful faces have most reliably found speeded orienting towards their location, but delayed disengagement from this location has also been observed. Surprisingly however, the extent to which orienting and disengagement processes underlie modulations in spatial attention to conscious/unmasked fearful faces has yet to be explored. Here, participants performed an unmasked and masked fearful face dot-probe task, which included a baseline condition to assess attentional orienting and disengagement effects. We found that both unmasked and masked fearful faces capture spatial attention through facilitated orienting and delayed disengagement. These results provide new evidence that consciously and nonconsciously processed social expressions of fear facilitate attention through similar mechanisms.
... In particular , fearful facial expressions automatically elicit shifts in visuospatial attention towards their location (Pourtois, Grandjean, Sander, & Vuilleumier, 2004) even when awareness of these faces has been restricted by backward masking 1 (Carlson & Reinke, 2008; Fox, 2002). This fear-elicited modulation in spatial attention serves to preferentially enhance visual cortical processing at the location of potential threat (Carlson & Reinke, 2010; Carlson, Reinke, LaMontagne, & Habib, 2011; Pourtois et al., 2004), which prepares an individual for additional threat at this location. ...
Fearful facial expressions convey threat-related information and automatically elicit modulations in spatial attention. The eye-region appears to be a particularly important feature for recognising and responding to fearful faces. However, it is unknown as to whether or not fearful eyes initiate modulations in spatial attention. In the current study, three dot-probe experiments with fearful and neutral eye stimuli were performed. The results of Experiment 1 demonstrate that fearful eyes capture spatial attention through facilitated attentional orienting to threat and delayed attentional disengagement from threat. In Experiments 2 and 3, these attentional effects were replicated, while ruling out the influence of overall size/shape and brightness differences between fearful and neutral eyes, respectively. Thus, fearful eye-whites appear to be a salient feature of fearful facial expressions that elicit modulations in spatial attention.
... Consistent with these models, accumulating evidence suggests that the amygdala detects and evaluates nonconscious representations of visual threat (Morris et al. 1998; Whalen et al. 1998; Liddell et al. 2005), which are likely relayed via the pulvinar nucleus of the thalamus and the superior colliculus (Morris et al. 1999Morris et al. , 2001 Liddell et al. 2005 ). Furthermore, amygdala reactivity to nonconscious threat is elevated in a variety of negative affect-related dispositions such as anxiety (Etkin et al. 2004), depression (Sheline et al. 2001), anger (Carlson et al. 2010), and post-traumatic stress disorder (Rauch et al. 2000; Armony et al. 2005). More recent research has linked the facilitation of spatial attention by nonconscious threats to an amygdala–ACC network ( ), in which amygdala reactivity is positively coupled with ACC activity. ...
... Consistent with these models, accumulating evidence suggests that the amygdala detects and evaluates nonconscious representations of visual threat (Morris et al. 1998; Whalen et al. 1998; Liddell et al. 2005), which are likely relayed via the pulvinar nucleus of the thalamus and the superior colliculus (Morris et al. 1999Morris et al. , 2001 Liddell et al. 2005 ). Furthermore, amygdala reactivity to nonconscious threat is elevated in a variety of negative affect-related dispositions such as anxiety (Etkin et al. 2004), depression (Sheline et al. 2001), anger (Carlson et al. 2010), and post-traumatic stress disorder (Rauch et al. 2000; Armony et al. 2005). More recent research has linked the facilitation of spatial attention by nonconscious threats to an amygdala–ACC network ( ), in which amygdala reactivity is positively coupled with ACC activity. ...
... Consistent with these models, accumulating evidence suggests that the amygdala detects and evaluates nonconscious representations of visual threat (Morris et al. 1998; Whalen et al. 1998; Liddell et al. 2005), which are likely relayed via the pulvinar nucleus of the thalamus and the superior colliculus (Morris et al. 1999Morris et al. , 2001 Liddell et al. 2005 ). Furthermore, amygdala reactivity to nonconscious threat is elevated in a variety of negative affect-related dispositions such as anxiety (Etkin et al. 2004), depression (Sheline et al. 2001), anger (Carlson et al. 2010), and post-traumatic stress disorder (Rauch et al. 2000; Armony et al. 2005). More recent research has linked the facilitation of spatial attention by nonconscious threats to an amygdala–ACC network ( ), in which amygdala reactivity is positively coupled with ACC activity. ...
Cognitive processing biases, such as increased attention to threat, are gaining recognition as causal factors in anxiety. Yet, little is known about the anatomical pathway by which threat biases cognition and how genetic factors might influence the integrity of this pathway, and thus, behavior. For 40 normative adults, we reconstructed the entire amygdalo-prefrontal white matter tract (uncinate fasciculus) using diffusion tensor weighted MRI and probabilistic tractography to test the hypothesis that greater fiber integrity correlates with greater nonconscious attention bias to threat as measured by a backward masked dot-probe task. We used path analysis to investigate the relationship between brain-derived nerve growth factor genotype, uncinate fasciculus integrity, and attention bias behavior. Greater structural integrity of the amygdalo-prefrontal tract correlates with facilitated attention bias to nonconscious threat. Genetic variability associated with brain-derived nerve growth factor appears to influence the microstructure of this pathway and, in turn, attention bias to nonconscious threat. These results suggest that the integrity of amygdalo-prefrontal projections underlie nonconscious attention bias to threat and mediate genetic influence on attention bias behavior. Prefrontal cognition and attentional processing in high bias individuals appear to be heavily influenced by nonconscious threat signals relayed via the uncinate fasciculus.
... Trait anger is a reliable predictor of reactive aggression (Bettencourt et al., 2006). Congruently, amygdala reactivity is positively correlated with trait anger in normal individuals (Carlson et al., 2010;Carre et al., 2012). In chronically violent subjects, the amygdala hyper-reactivity extends to neutral faces (Pardini and Phillips, 2010), which highly aggressive individuals tend to perceive as negatively valence (Best et al., 2002). ...
Amygdala structural and functional abnormalities have been associated to reactive aggression in previous studies. However,
the possible linkage of these two types of anomalies has not been examined. We hypothesized that they would coincide in the
same localizations, would be correlated in intensity and would be mediated by reactive aggression personality traits. Here
violent (n = 25) and non-violent (n = 29) men were recruited on the basis of their reactive aggression. Callous-unemotional (CU) traits were also assessed. Gray
matter concentration (gmC) and reactivity to fearful and neutral facial expressions were measured in dorsal and ventral amygdala
partitions. The difference between responses to fearful and neutral facial expressions was calculated (F/N-difference). Violent
individuals exhibited a smaller F/N-difference and gmC in the left dorsal amygdala, where a significant coincidence was found
in a conjunction analysis. Moreover, the left amygdala F/N-difference and gmC were correlated to each other, an effect mediated
by reactive aggression but not by CU. The F/N-difference was caused by increased reactivity to neutral faces. This suggests
that anatomical anomalies within local circuitry (and not only altered input) may underlie the amygdala hyper-reactivity to
social signals which is characteristic of reactive aggression.
... Moreover, there are data from work with healthy populations that also support this suggestion. Thus, a predisposition to anger has been positively associated with an increased amygdala response to masked fearful expressions [23] and even the presentation of the word "no" [24]. Moreover, an increased predisposition to anger has also been positively associated with increased amygdala volume [25].i ...
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 posttraumatic 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 nonsocial frustrating situations. WIREs Cogn Sci 2012, 3:65–74. doi: 10.1002/wcs.154
For further resources related to this article, please visit the WIREs website.
This article is a U.S. Government work, and as such, is in the public domain in the United States of America.
... Each trial started with a target picture with a duration of 26 ms. (A duration of 33 ms is generally used in this paradigm (eg, Carlson et al, 2010; Childress et al, 2008), and is considered 'unseen'. However, we noticed in a pilot study that specifically sexual stimuli are still detectable at a 33 ms duration, whereas at 26 ms, emotionally negative, neutral, and sexual pictures were all detected at below chance level.) ...
Dopaminergic medication influences conscious processing of rewarding stimuli, and is associated with impulsive-compulsive behaviors, such as hypersexuality. Previous studies have shown that subconscious subliminal presentation of sexual stimuli activates brain areas known to be part of the 'reward system'. In this study, it was hypothesized that dopamine modulates activation in key areas of the reward system, such as the nucleus accumbens, during subconscious processing of sexual stimuli. Young healthy males (n=53) were randomly assigned to two experimental groups or a control group, and were administered a dopamine antagonist (haloperidol), a dopamine agonist (levodopa), or placebo. Brain activation was assessed during a backward-masking task with subliminally presented sexual stimuli. Results showed that levodopa significantly enhanced the activation in the nucleus accumbens and dorsal anterior cingulate when subliminal sexual stimuli were shown, whereas haloperidol decreased activations in those areas. Dopamine thus enhances activations in regions thought to regulate 'wanting' in response to potentially rewarding sexual stimuli that are not consciously perceived. This running start of the reward system might explain the pull of rewards in individuals with compulsive reward-seeking behaviors such as hypersexuality and patients who receive dopaminergic medication.
... Thus, early preconscious attention biases to threat appear to influence states of worry and stress reactivity, which may be associated with elevated ACC volume. In addition to anxiety, other negative emotion-related individual differences and/or disorders, may have hyper-vigilance to threat, exaggerated amygdala activity, and abnormal ACC volumes, such as post-traumatic stress disorder, depression, and heightened trait anger (Bryant and Harvey, 1997; Carlson et al., 2010a; Kasai et al., 2008; Kitayama et al., 2006; Mogg and Bradley, 2005; Mogg et al., 1995; Rauch et al., 2000 Rauch et al., , 2003 Sheline et al., 2001; van Honk et al., 2001a van Honk et al., , 2001b). Taken together, these results highlight the close relationship between the disposition for negative emotionrelated traits, the amygdala–ACC network, and biased attention to threat. ...
An important aspect of the fear response is the allocation of spatial attention toward threatening stimuli. This response is so powerful that modulations in spatial attention can occur automatically without conscious awareness. Functional neuroimaging research suggests that the amygdala and anterior cingulate cortex (ACC) form a network involved in the rapid orienting of attention to threat. A hyper-responsive attention bias to threat is a common component of anxiety disorders. Yet, little is known of how individual differences in underlying brain morphometry relate to variability in attention bias to threat. Here, we performed two experiments using dot-probe tasks that measured individuals' attention bias to backward masked fearful faces. We collected whole-brain structural magnetic resonance images and used voxel-based morphometry to measure brain morphometry. We tested the hypothesis that reduced gray matter within the amygdala and ACC would be associated with reduced attention bias to threat. In Experiment 1, we found that backward masked fearful faces captured spatial attention and that elevated attention bias to masked threat was associated with greater ACC gray matter volumes. In Experiment 2, this association was replicated in a separate sample. Thus, we provide initial and replicating evidence that ACC gray matter volume is correlated with biased attention to threat. Importantly, we demonstrate that variability in affective attention bias within the healthy population is associated with ACC morphometry. This result opens the door for future research into the underlying brain morphometry associated with attention bias in clinically anxious populations.
Fearful facial expressions are important social indicators of environmental threat. Among the various features of a fearful face, the eyes appear to be particularly important for recognizing and responding to these social cues. One way in which fearful faces facilitate observers’ behavior is by automatically capturing attention. This is true for both consciously and nonconsciously processed fearful faces. Recent research suggests that consciously processed fearful eyes alone are sufficient to capture observers’ attention. However, it is unknown as to whether or not nonconsciously processed, backward masked, fearful eyes are sufficient to facilitate spatial attention. To test this possibility, two dot-probe experiments with masked fearful eye stimuli were performed. In Experiment 1, we found that, relative to scrambled eyes, masked fearful eyes facilitate attentional orienting and delay attentional disengagement. In Experiment 2, we replicated this effect when comparing backward masked fearful to neutral eyes. Thus, the data suggest that nonconscious fearful eyes facilitate spatial attention through facilitated orienting and delayed disengagement.
Interacting with others is crucial for human fitness. In the past decade, there has been a growing interest for oxytocin (OXT) and its implication in social behavior. In the first section of this work we show that peripheral and central concentrations of OXT are correlated. Peripheral and central OXT are also correlated with subjects’ extraversion and with the volume of amygdala and hippocampus, two brain regions important for the regulation of social behavior. Interestingly, we show that OXT intake increases the subjective perception of subjects’ sociability. These findings suggest that OXT can be considered a biomarker of social behavior, thus opening the possibility of using this hormone in the screening process of psychiatric disorder like Autism. In a second section, we focused on the central action of OXT and in particular its interaction with another neurotransmitter also essential for social behavior: the serotonin (5-HT). We assessed OXT effect on the central serotoninergic activity in healthy subjects using the Positon Emission Tomography (PET) thanks to a radiotracer ([18-F]MPPF) specific for the 5-HT1A receptors and known to be localised in brain regions important for social processing. Our results show that oxytocin administration increases MPPF binding potential (BP) in raphe nuclei, right amygdala, hippocampus and orbitofrontal cortex. Interestingly, Asperger patients showed a decrease in MPPF BP in these regions compared to controls. This difference disappeared after oxytocin. These results strengthen the role of oxytocin in social behavior and underline the therapeutic potential of this neuromodulator for psychiatric disorders implicating both serotonin and oxytocin dysfunctions
While the amygdalar role in fear conditioning is well established, it also appears to be involved in a wide spectrum of other functions concerning emotional information. For example, the amygdala is thought to be involved in guiding spatial attention to emotionally relevant information such as the eye region in faces, and it gets activated differentially during different tasks. Here, we propose that the guidance of feature-based attention is the basis for the involvement of the amygdala in these seemingly disparate functions. Feature-based attention usually precedes spatial attention, and performing different tasks usually requires attending to different features. Although to date, no experiments have specifically tested the amygdalar role in feature-based attention, studies showing that the amygdala responds to simple elements, and findings of amygdalar involvement in non-spatial forms of attention hint at such a role. Our hypothesis that the amygdala guides feature-based attention builds on earlier proposals that the amygdala guides spatial attention and assesses biological relevance, but it is more specific and accounts for the failure to find amygdalar activation when spatial cues guide attention. Our hypothesis results in the testable prediction that the amygdala is involved when searching for stimuli based on their feature information, but not when searching for stimuli based on spatial cues.
This article provides a review of research on the hemispheric specialization in emotional processing during the past 40 years and the theoretical models derived from the conceptual analysis of these results. The publications reviewed here were collected to better appreciate the cortical lateralization of emotional perception (visual and auditory), expression (facial and prosodic), and experience. Four major models of emotional processing are discussed--the Right Hemisphere, Valence, Approach-Withdrawal, and Behavioral Inhibition System-Behavioral Activation System models. Observing the relative merits and limitations of these models, a new direction for exploration is offered. Specifically, to better appreciate the strength and direction (i.e., approach versus withdrawal) of experienced emotions, it is recommended that state "dominance" be evaluated in the context of asymmetrical activation of left-frontal (dominance) versus right-frontal (submission) brain regions.
Individuals with disorders marked by antisocial behavior frequently show deficits in recognizing displays of facial affect. Antisociality may be associated with specific deficits in identifying fearful expressions, which would implicate dysfunction in neural structures that subserve fearful expression processing. A meta-analysis of 20 studies was conducted to assess: (a) if antisocial populations show any consistent deficits in recognizing six emotional expressions; (b) beyond any generalized impairment, whether specific fear recognition deficits are apparent; and (c) if deficits in fear recognition are a function of task difficulty. Results show a robust link between antisocial behavior and specific deficits in recognizing fearful expressions. This impairment cannot be attributed solely to task difficulty. These results suggest dysfunction among antisocial individuals in specified neural substrates, namely the amygdala, involved in processing fearful facial affect.
In 1872, Darwin (1965) observed that anger (rage) was a powerful emotion that motivated “animals of all kinds, and their progenitors before them, when attacked or threatened by an enemy, to fight and protect themselves” (p. 74). Anger is reflected in facial expressions (e.g., reddened face, clenched teeth), muscular tension, and accelerated heart rate, and it differs from rage “only in degree, and there is no marked distinction in their characteristics” (Darwin, 1965, p. 244).
Keywords:
anger;
aggression;
hostility;
STAXI;
emotion;
personality;
anger expression;
anger control
Studies in animals have shown that the amygdala receives highly processed visual input, contains neurons that respond selectively to faces, and that it participates in emotion and social behaviour. Although studies in epileptic patients support its role in emotion, determination of the amygdala's function in humans has been hampered by the rarity of patients with selective amygdala lesions. Here, with the help of one such rare patient, we report findings that suggest the human amygdala may be indispensable to: (1) recognize fear in facial expressions; (2) recognize multiple emotions in a single facial expression; but (3) is not required to recognize personal identity from faces. These results suggest that damage restricted to the amygdala causes very specific recognition impairments, and thus constrains the broad notion that the amygdala is involved in emotion.
Facial expressions of emotion are increasingly being used in neuroscience as probes for functional imaging and as stimuli for studying hemispheric specialization for face and emotion processing. Available facial stimuli are 2-dimensional and therefore, their orientation is fixed and poorly suited for examining asymmetries, they are often obtained under poorly specified conditions, usually posed, lack ethnic diversity, and are of restricted age range. We describe a method for accurately acquiring and reconstructing the geometry of the human face and for display of this reconstruction in a 3-dimensional format. We applied the method in a sample of 70 actors and 69 actresses expressing happiness, sadness, anger, fear and disgust, as well as neutral expressions. Each emotion was expressed under three levels of intensity and under both posed and evoked conditions. Resulting images are of high technical quality and are accurately identified by raters. The stimuli can be downloaded in digital form as 'movies' where angle and orientation can be manipulated for inclusion in functional imaging probes or in tests that can be administered as measures of individual differences in facial emotion processing. The database of emotional expressions can also be used as a standard for comparison with clinical populations.
It has been established that individuals who score high on measures of psychopathy demonstrate difficulty when performing tasks requiring the interpretation of other's emotional states. The aim of this study was to elucidate the relation of emotion and cognition to individual differences on a standard psychopathy personality inventory (PPI) among a nonpsychiatric population.
Twenty participants completed the PPI. Following survey completion, a mean split of their scores on the emotional-interpersonal factor was performed, and participants were placed into a high or low group. Functional magnetic resonance imaging data were collected while participants performed a recognition task that required attention be given to either the affect or identity of target stimuli.
No significant behavioral differences were found. In response to the affect recognition task, significant differences between high- and low-scoring subjects were observed in several subregions of the frontal cortex, as well as the amygdala. No significant differences were found between the groups in response to the identity recognition condition.
Results indicate that participants scoring high on the PPI, although not behaviorally distinct, demonstrate a significantly different pattern of neural activity (as measured by blood oxygen level-dependent contrast)in response to tasks that require affective processing. The results suggest a unique neural signature associated with personality differences in a nonpsychiatric population.
We examined whether consciously undetected fear signals engage a collateral brainstem pathway to the amygdala and prefrontal cortex in the intact human brain, using functional neuroimaging. 'Blindsight' lesion patients can respond to visual fear signals independently from conscious experience, suggesting that these signals reach the amygdala via a direct pathway that bypasses the primary visual cortex. Electrophysiological evidence points to concomitant involvement of prefrontal regions in automatic orienting to subliminal signals of fear, which may reflect innervation arising from brainstem arousal systems. To approximate blindsight in 22 healthy subjects, facial signals of fear were presented briefly (16.7 ms) and masked such that conscious detection was prevented. Results revealed that subliminal fear signals elicited activity in the brainstem region encompassing the superior colliculus and locus coeruleus, pulvinar and amygdala, and in fronto-temporal regions associated with orienting. These findings suggest that crude sensory input from the superior colliculo-pulvinar visual pathway to the amygdala may allow for sufficient appraisal of fear signals to innervate the locus coeruleus. The engagement of the locus coeruleus could explain the observation of diffuse fronto-temporal cortical activity, given its role in evoking collateral ascending noradrenergic efferents to the subcortical amygdala and prefrontal cortex. This network may represent an evolutionary adaptive neural 'alarm' system for rapid alerting to sources of threat, without the need for conscious appraisal.
Brain imaging studies in humans have shown that face processing in several areas is modulated by the affective significance of faces, particularly with fearful expressions, but also with other social signals such gaze direction. Here we review haemodynamic and electrical neuroimaging results indicating that activity in the face-selective fusiform cortex may be enhanced by emotional (fearful) expressions, without explicit voluntary control, and presumably through direct feedback connections from the amygdala. fMRI studies show that these increased responses in fusiform cortex to fearful faces are abolished by amygdala damage in the ipsilateral hemisphere, despite preserved effects of voluntary attention on fusiform; whereas emotional increases can still arise despite deficits in attention or awareness following parietal damage, and appear relatively unaffected by pharmacological increases in cholinergic stimulation. Fear-related modulations of face processing driven by amygdala signals may implicate not only fusiform cortex, but also earlier visual areas in occipital cortex (e.g., V1) and other distant regions involved in social, cognitive, or somatic responses (e.g., superior temporal sulcus, cingulate, or parietal areas). In the temporal domain, evoked-potentials show a widespread time-course of emotional face perception, with some increases in the amplitude of responses recorded over both occipital and frontal regions for fearful relative to neutral faces (as well as in the amygdala and orbitofrontal cortex, when using intracranial recordings), but with different latencies post-stimulus onset. Early emotional responses may arise around 120ms, prior to a full visual categorization stage indexed by the face-selective N170 component, possibly reflecting rapid emotion processing based on crude visual cues in faces. Other electrical components arise at later latencies and involve more sustained activities, probably generated in associative or supramodal brain areas, and resulting in part from the modulatory signals received from amygdala. Altogether, these fMRI and ERP results demonstrate that emotion face perception is a complex process that cannot be related to a single neural event taking place in a single brain regions, but rather implicates an interactive network with distributed activity in time and space. Moreover, although traditional models in cognitive neuropsychology have often considered that facial expression and facial identity are processed along two separate pathways, evidence from fMRI and ERPs suggests instead that emotional processing can strongly affect brain systems responsible for face recognition and memory. The functional implications of these interactions remain to be fully explored, but might play an important role in the normal development of face processing skills and in some neuropsychiatric disorders.
Manual for the State-Trait Anxiety Inventory (Self-Evaluation Questionnaire)
- C D Spielberger
- R L Gorsuch
- R E Lushene
Spielberger, C.D., Gorsuch, R.L., Lushene, R.E., 1970. Manual for the State-Trait Anxiety
Inventory (Self-Evaluation Questionnaire). Consulting Psychology Press, Palo Alto, CA.