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One of the most salient features of emotion is the pronounced variability among individuals in their reactions to emotional incentives and in their dispositional mood. Collectively, these individual differences have been described as affective style. Some types of affective style promote more empathic and compassionate behavior than others. Recent research has begun to dissect the constituents of affective style. The search for these components is guided by the neural systems that instantiate emotion and emotion regulation. In this essay, this body of research and theory is applied specifically to positive affect and well-being. The central substrates and peripheral biological correlates of well-being are described. A resilient affective style is associated with high levels of left prefrontal activation, effective modulation of activation in the amygdala and fast recovery in response to negative and stressful events. In peripheral biology, these central patterns are associated with lower levels of basal Cortisol and with higher levels of antibody titers to influenza vaccine. The essay concludes with a consideration of whether these patterns of central and peripheral biology can be modified by training and shifted toward a more salubrious direction.

One of the most salient characteristics of emotion is the remarkable heterogeneity among individuals in how they respond to the same emotionally provocative challenge. Such differences in patterns of emotional reactivity play a crucial role in shaping variations in well-being. While individual differences in emotion processing can be found at many levels of phylogeny, they are particularly pronounced in primates and probably are most extreme in humans. A number of evolutionary theorists have speculated on the adaptive significance of such individual differences (Wilson 1994). While these arguments have never been applied to the domain of emotion and affective style, it is not difficult to develop hypotheses about how such differences might provide advantages to individuals living in groups. Though these distal influences are interesting and important, there is

1 Laboratory for Affective Neuroscience, University of Wisconsin, 1202 West Johnson Street, Madison, WI 53706, USA; e-mail: [email protected]

a paucity of empirical findings that bear on these issues. This essay will mostly focus on the proximal mechanisms that underlie such individual differences, with a focus on well-being. The central substrates of individual differences in components of well-being will be described. The possible influence of the central circuitry of emotion on peripheral biological indices that are relevant to physical health and illness will also be considered. Finally, the concluding section acknowledges the important advances that have recently been made in our understanding of neuroplasticity, and in this section I argue that it would be best to conceptualize emotional characteristics such as happiness as skills that can be trained in ways that are not fundamentally different from other kinds of skill learning.

Affective style refers to consistent individual differences in emotional reactivity and regulation (see Davidson 1998a; Davidson et al. 2000a,b). It is a phrase that is meant to capture a broad array of processes that either singly or in combination modulate an individual's response to emotional challenges, dispositional mood and affect-relevant cognitive processes. Affective style can refer to valence-specific features of emotional reactivity or mood or it can refer to discrete emotion-specific features. Both levels of analysis are equally valid and the choice of level should be dictated by the question posed.

Rapid developments in our understanding of emotion, mood and affective style have come from the study of the neural substrates of these phenomena. The identification of the brain circuitry responsible for different aspects of affective processing has helped to parse the domain of emotion into more elementary constituents in a manner similar to that found in cognitive neuroscience, where an appeal to the brain has facilitated the rapid development of theory and data on the subcomponents of various cognitive processes (see, e.g., Kosslyn and Koenig 1992).

Both lesion and neuroimaging studies provide information primarily about the "where" question, that is, where in the brain are computations related to specific aspects of affective processing occurring? It is important at the outset to consider both the utility of knowing "where" and how such information can provide insight into the "how" question, that is, how might a particular part of the brain instantiate a specific process that is essential to affective style? The brain sciences are now replete with information about the essential nature of specific types of information processing in different regions of the brain. For example, there is evidence to suggest that the dorsolateral prefrontal cortex (DLPFC) is important for maintaining a representation of information on-line in the absence of immediate cues. The neurophysiological basis of this type of information processing has been actively studied in the animal laboratory (e.g., Goldman-Rakic 1996, 2000). If this region of the brain is activated at certain times in the stream of affective information processing, we can develop hypotheses on the basis of extant work about what this territory of the prefrontal cortex (PFC) might be doing during the affective behavior and how it might be doing it. A related consideration is the network of anatomical connectivity to and from a particular brain region. From a consideration of connectivity, insights may be gleaned as to how a particular brain region might react during a particular form of emotional processing. For example, we know that regions of the amygdala have extensive connectivity with cortical territories that can become activated following activation of the amyg dala. In this way, the amygdala can issue a cortical call for further processing in response to potentially threatening stimuli that must be processed further to assess danger. There are prefrontal regions that have extensive anatomical connectivity with the amygdala and they appear to play a modulatory role over amygdala function. Other regions of the amygdala have extensive connections to limbic and brain stem circuits that can modulate behavioral and autonomic outflow. Adjustments in autonomic responses and action tendencies are typical components of emotion.

Conceptual and methodological considerations in the study ofaffective style

Current research on well-being is largely based on the use of self-report measures to make inferences about variation among individuals in type and magnitude of well-being. One important component of neurobiological research on well-being is to begin to dissect well-being into more specific constituents that may underlie the coarse phenomenological descriptions provided by subjects. In addition, research on the neural correlates of well-being may provide an independent biological measure sensitive to variations in well-being that are not subject to the kinds of reporting and judgmental biases commonly found in the self-report measures. For example, researchers have found that questions that precede items asking about well-being can influence a subject's report of well-being. Variations in the weather can similarly affect such reports. These examples illustrate the fact that, when subjects are queried about global well-being, they frequently utilize convenient heuristics to answer such questions and typically do not engage in a systematic integration of utility values over time. It may be that certain parameters of brain function are better repositories of the cumulative experiences that inevitably shape well-being. At the present point in the development of this science, these are mere speculations in search of evidence, but the time is ripe for such evidence to be gathered.

The status of research on well-being is now at a point occupied about a decade ago or more by research on mood and anxiety disorders, though it continues to suffer from some of the same problems. Mood and anxiety disorders are generally conceptualized as being caused or at least accompanied by dysfunctions of emotion. However, what specific affective process is dysfunctional is rarely, if ever, delineated, and nosological schemes for categorizing these disorders do not rely upon the specific nature of the affective dysfunction in question but rather are based upon phenomenological description. Research in my laboratory over the past 15 years has been predicated on the view that more meaningful and rapid progress in understanding the brain bases of mood and anxiety disorders can be achieved if we move to an intermediate level of description that penetrates below the categorical, phenomenologically based classifications of the DSM and seeks to characterize the specific nature of the affective styles that are associated with vulnerability to these forms of psychopathology.

Many of the parameters of affective style, such as the threshold to respond, magnitude of response, latency to peak of response, and recovery function, are features that are often opaque to conscious report, though they may influence the subjective experience of emotion. These parameters of responding can be measured in many different response systems, including both central and peripheral systems. For example, magnitude of response can be measured in a peripheral measure, such as the emotion-modulated startle (Lang 1995), or in a central measure, such as activation in the amygdala assessed with functional magnetic resonance imaging (fMRI). The extent to which coherence across response systems in these parameters is present has not yet been systematically addressed. In previous work, we have argued that variations in some of these parameters in particular response systems are especially relevant to vulnerability to mood, anxiety and other disorders and also to resilience (e.g., Davidson et al. 2000a, b). One of the important developments in emotion research in general and in affective neuroscience in particular is the capacity to objectively measure these parameters of responding. For example, in several studies, we have used the emotion-modulated startle to capture the time course of valence-specific emotion responding (Jackson et al. 2000a; Larson et al. 1998). The startle reflex is controlled by a brainstem circuit that is influenced by activity in forebrain structures. Davis (1992) elegantly dissected the circuitry through which the magnitude of this reflex is modulated during the arousal of fear in rodents, demonstrating that it is via a descending pathway from the central nucleus of the amygdala to the nucleus pontine reticularis in the brain stem that the magnitude of startle is enhanced in response to a conditioned fear cue. Lesions of the central nucleus of the amygdala abolish the fear potentiation of the startle but do not affect the magnitude of the baseline startle. Lang and his colleagues (Vrana et al. 1988) were the first to systematically show that the same basic phenomenon can be produced in humans. They took advantage of the fact that brief acoustic noise bursts produce the eyeblink component of the startle and little else, thus enabling their presentation as innocuous stimuli in the background. By measuring electromyographic activity from the orbicularis oculii muscle with two miniature electrodes under one eye, they were able to quantify the strength of the blink response and show that the magnitude of the blink was greater when subjects were presented with unpleasant pictures in the foreground, compared with the presentation of neutral pictures. Moreover, when subjects were exposed to positive stimuli, the magnitude of startle was actually attenuated relative to a neutral condition (Vrana et al. 1988). This same basic effect has now been reported with many different types of foreground stimuli in several modalities (see Lang 1995, for review).

We have exploited the emotion-modulated startle to begin to characterize the time course of affective responding, or what I have referred to as affective chro-nometry (Davidson 1998a). By inserting acoustic noise probes at different latencies before and after a critical emotional stimulus is presented, both the anticipatory limb as well as the recovery limb of the response can be measured. And, by utilizing paradigms in the MRI scanner that were first studied in the psychophysi-ology laboratory, the neural circuitry underlying the different phases of affective processing can be interrogated with fMRI. Our current work in this area has emphasized the importance of the recovery function following negative events for vulnerability to certain forms of psychopathology as well as for resilience. We have argued that the failure to rapidly recover following a negative event can be a crucial ingredient of vulnerability to both anxiety and mood disorders, particu larly when such a style is combined with frequent exposure to negative events over a sustained period of time. The failure to adequately recover would result in sustained elevations in multiple systems that are activated in response to negative events. On the other hand, the capacity for rapid recovery following negative events may define an important ingredient of resilience. We have defined resilience as the maintenance of high levels of positive affect and well-being in the face of significant adversity. It is not that resilient individuals never experience negative affect, but rather that the negative affect does not persist. Such individuals are able to profit from the information provided by the negative affect, and their capacity for "meaning making" in response to such events may be part and parcel of their ability to show rapid decrements in various biological systems following exposure to a negative or stressful event (see, e.g., Geise-Davis and Spiegel 2003).

Neural substrates ofemotion and affective style

In this section, a brief overview is provided of core components of the circuitry that instantiates some important aspects of emotion and affective style, with an emphasis on prefrontal cortex and the amygdala. It is not meant to be an exhaustive review but rather will present selected highlights to illustrate some of the key advances that have been made recently.

Emotion and affective style are governed by a circuit that includes the following structures and likely others as well: dorsolateral prefrontal cortex (DLPFC), ventromedial PFC (vmPFC), orbitofrontal cortex (OFC), amygdala, hippocampus, anterior cingulate cortex (ACC) and insular cortex. It is argued that different subprocesses are instantiated in each of these structures and that they normally work together to process, generate and regulate emotional information and emotional behavior.

Prefrontal cortex

A large corpus of data at both the animal and human levels implicates various sectors of the PFC in emotion. The PFC is not a homogeneous zone of tissue but rather has been differentiated on the basis of both cytoarchitectonic and functional considerations. The three subdivisions of the primate PFC that have been consistently distinguished are the DLPFC, vmPFC, and OFC. In addition, there appear to be important functional differences between the left and right sides within some of these sectors.

The case for the differential importance of left and right PFC sectors for emotional processing was first made systematically in a series of studies on patients with unilateral cortical damage (Gainotti 1972; Robinson et al. 1984; Sackeim et al. 1982). These findings, as well as more modern efforts to examine mood consequences of unilateral prefrontal damage, have been extensively reviewed by Davidson (2004) and thus will not be considered here.

A growing corpus of evidence in normal intact humans is consistent with the findings derived from the lesion evidence. Davidson and his colleagues have reported that induced positive and negative affective states shift the asymmetry in prefrontal brain electrical activity in lawful ways. For example, film-induced negative affect increases relative right-sided prefrontal and anterior temporal activation (Davidson et al. 1990), whereas induced positive affect elicits an opposite pattern of asymmetric activation. Similar findings have been obtained by others (e.g., Ahern and Schwartz 1985; Jones and Fox 1992).

Using a cued reaction time paradigm with monetary incentives, Sobotka et al. (1992) first reported that, in the anticipatory interval between the cue and the response, EEG differences were observed between reward and punishment trials, with greater left-sided frontal activation observed in response to the former compared with the latter trial type. In a more recent study, Miller and Tomarken (2001) replicated and extended this basic effect and very recently, we (Shackman et al. 2003) replicated the Miller and Tomarken effect, showing that reward trials produced significantly greater left prefrontal activation in the anticipatory interval compared with no incentive trials. In addition to these studies that manipulated phasic emotion, we will review in the next section a body of evidence that supports the conclusion that individual differences in baseline levels of asymmetric activation in these brain regions are lawfully related to variations in dispositional affective style. Using an extended picture presentation paradigm designed to evoke longer-duration changes in mood (Sutton et al. 1997a), we measured regional glucose metabolism with positron emission tomography (PET) to ascertain whether similar patterns of anterior asymmetry would be present using this very different and more precise method to assess regional brain activity (Sutton et al. 1997b). During the production of negative affect, we observed right-sided increases in metabolic rate in anterior orbital, inferior frontal, middle and superior frontal gyri, whereas the production of positive affect was associated with a pattern of predominantly left-sided metabolic increases in the pre- and postcentral gyri. Using PET to measure regional cerebral blood flow, Hugdahl and his colleagues (1995; Hugdahl 1998) reported a widespread zone of increased blood flow in the right PFC, including the orbitofrontal and dorsolateral cortices and inferior and superior cortices, during the extinction phase, after aversive learning had occurred, compared with the habituation phase, prior to the presentation of the experimental contingencies.

Other investigators have used clinical groups to induce a stronger form of negative affect in the laboratory than is possible with normal controls. One common strategy for evoking anxiety among anxious patients in the laboratory is to present them with specific types of stimuli that are known to provoke their anxiety (e.g., pictures of spiders for spider phobics; making a public speech for social phobics). Davidson and colleagues (2000d), in a study using brain electrical activity measures, have recently found that when social phobics anticipate making a public speech, they show large increases in right-sided anterior activation. Pooling across data from three separate anxiety-disordered groups that were studied with PET, Rauch and his colleagues (1997) found two regions of the PFC that were consistently activated across groups: the right inferior PFC and right medial orbital PFC.

The ventromedial PFC has been implicated in the anticipation of future positive and negative affective consequences. Bechara and his colleagues (1994) reported that patients with bilateral lesions of the ventromedial PFC have difficulty anticipating future positive or negative consequences, although immediately available rewards and punishments do influence their behavior. Such patients show decreased levels of electrodermal activity in anticipation of a risky choice compared with controls, whereas controls exhibit such an autonomic change before they explicitlyknow that it is a risky choice (Bechara et al. 1996,1997,1999).

The findings from the lesion method - when the effects of small unilateral lesions are examined - and from neuroimaging studies in normal subjects and patients with anxiety disorders converge on the conclusion that increases in right-sided activation in various sectors of the PFC are associated with increased negative affect. Less evidence is available for the domain of positive affect, in part because positive affect is much harder to elicit in the laboratory and because of the negativity bias (see Cacioppo and Gardner 1999; Taylor 1991). This latter phenomenon refers to the general tendency of organisms to react more strongly to negative compared to positive stimuli, perhaps as a consequence of evolutionary pressures to avoid harm.

Systematic studies designed to disentangle the specific role played by various sectors of the PFC in emotion are lacking. Many theoretical accounts of emotion assign it an important role in guiding action and organizing behavior toward the acquisition of motivationally significant goals (e.g.,Frijda 1994; Levenson 1994). This process requires that the organism have some means of representing affect in the absence ofimmediately present rewards and punishments and other affective incentives. It is likely that the PFC plays a key role in this process (see Wata-nabe 1996). Damage to certain sectors of the PFC impairs an individual's capacity to anticipate future affective outcomes and consequently results in an inability to guide behavior in an adaptive fashion. Such damage is not likely to disrupt an individual's responding to immediate cues for reward and punishment, only the anticipation before and maintenance after an affective cue is presented. This proposal can be tested using current neuroimaging methods (e.g., fMRI) but has not yet been rigorously evaluated. With regard to the different functional roles of the dorsolateral, orbitofrontal and ventromedial sectors of the PFC, Davidson and Irwin (1999) suggested, on the basis of considering both human and animal studies, that the ventromedial sector is most likely involved in the representation of elementary positive and negative affective states in the absence of immediately present incentives. The ventromedial sector also has strong anatomical reciprocity with the amygdala and thus appears to play an important role in modulating activity in the amygdala, thereby contributing to the regulation of emotion. The orbitofrontal sector has most firmly been linked to rapid learning and unlearning of stimulus-incentive associations and has been particularly implicated in reversal learning (Rolls 1999). Therefore, the orbitofrontal sector is also likely key to understanding aspects of emotion regulation (see Davidson et al. 2000b). One critical component of emotion regulation is the relearning of stimulus-incentive associations that might have been previously maladaptive, a process likely requiring the orbitofrontal cortex. The dorsolateral sector is most directly involved in the representation of goal states toward which more elementary positive and negative states are directed.


A large corpus of research at both the animal and human levels has established the importance of the amygdala for emotional processes (LeDoux 1996; Cahill and McGaugh 1998; Aggleton 1993; Davis and Whalen 2001). Since many reviews of the animal literature have appeared recently, a detailed description of these studies will not be presented here. LeDoux and his colleagues marshaled a large corpus of compelling evidence to suggest that the amygdala is necessary for the establishment of conditioned fear. Whether the amygdala is necessary for the expression of that fear following learning and whether the amygdala is the actual locus of where the learned information is stored are still matters of some controversy (see Cahill et al. 1999; Fanselow and LeDoux 1999). The classic view of amygdala damage in non-human primates resulting in major affective disturbances - as expressed in the Kluver-Bucy syndrome, where the animal exhibits abnormal approach, hyper-orality and sexuality, and little fear - is now thought to be a function of damage elsewhere in the medial temporal lobe. When very selective excitotoxic lesions of the amygdala are made that preserve fibers of passage, nothing resembling the Kluver-Bucy syndrome is observed (Kalin et al. 2001). The upshot of this diverse array of findings is to suggest a more limited role for the amygdala in certain forms of emotional learning, though the human data imply a more heterogeneous contribution.

While the number of patients with discrete lesions of the amygdala is small, they have provided unique information on the role of this structure in emotional processing. Several studies have now reported specific impairments in the recognition of facial expressions of fear in patients with restricted amygdala damage (Adolphs et al. 1995; 1996; Broks et al. 1998; Calder et al. 1996). Interestingly, in a very recent report, Adolphs and his colleagues (2005) specifically identified a failure to gaze normally at the eye region of the face as the proximal cause of the deficit in fear face recognition in patient SM, a patient with bilateral destruction of the amygdala. Recognition of facial signs of other emotions has been found to be mostly intact. In a study that required subjects to make judgments about the trustworthiness and approachability of unfamiliar adults from facial photographs, patients with bilateral amygdala damage judged the unfamiliar individuals to be more approachable and trustworthy than did control subjects (Adolphs et al. 1998). Recognition of vocal signs of fear and anger was found to be impaired in a patient with bilateral amygdala damage (Scott et al. 1997), suggesting that this deficit is not restricted to facial expressions. Other researchers (Bechara et al. 1995) have demonstrated that aversive autonomic conditioning is impaired in a patient with amygdala damage despite the fact that the patient showed normal declarative knowledge of the conditioning contingencies. Collectively, these findings from patients with selective bilateral destruction of the amygdala suggest specific impairments on tasks that tap aspects of negative emotion processing. Most of the studies have focused on the perceptual side, where the data clearly show the amygdala to be important for the recognition of cues of threat or danger. The conditioning data also indicate that the amygdala may be necessary for acquiring new implicit autonomic learning of stimulus-punishment contingencies. In one of the few studies to examine the role of the amygdala in the expression of already learned emotional responses, Angrilli and colleagues (1996) reported on a patient with a benign tumor of the right amygdala in a study that used startle magnitude in response to an acoustic probe measured from orbicularis oculi. Among control subjects, they observed the well-known effect of startle potentiation during the presentation of aversive stimuli. In the patient with right amygdala damage, no startle potentiation was observed in response to aversive versus neutral stimuli. These findings suggest that the amygdala might be necessary for the expression of already learned negative affect.

Since 1995, a growing number of studies using PET and fMRI to investigate the role of the amygdala in emotional processes have begun to appear. Many studies have reported activation of the amygdala detected with either PET or fMRI when anxiety-disordered patients have been exposed to their specific anxiety-provoking stimuli compared with control stimuli (e.g., Breiter et al. 1996b; Rauch et al. 1996). When social phobics were exposed to neutral faces, they showed activation of the amygdala comparable to what was observed in both the phobics and controls in response to aversive compared with neutral odors (Birbaumer et al. 1998). Consistent with the human lesion data, a number of studies have now reported activation of the amygdala in response to facial expressions of fear compared with neutral, happy or disgust control faces (Morris et al. 1996; Phillips et al. 1997). In the fMRI study by Brieter et al. (1996 a), they observed rapid habituation of the amygdala response, which may provide an important clue to the time-limited function of the amygdala in the stream of affective information processing. Whalen and his colleagues (1998) observed activation of the amygdala in response to masked fear faces that were not consciously perceived. Unpleasant compared with neutral and pleasant pictures have also been found to activate the amygdala (Irwin et al. 1996). Finally, a number of studies have reported activation of the amygdala during early phases of aversive conditioning (Buchel et al. 1998; LaBar et al. 1998). Amygdala activation in response to several other experimental procedures for inducing negative affect has been reported, including unsolvable anagrams of the sort used to induce learned helplessness (Schneider et al. 1996), aversive olfactory cues (Zald and Pardo 1997) and aversive gustatory stimuli (Zald et al. 1998). Other data on individual differences in amygdala activation and their relation to affective style will be treated in the next section. The issues of whether the amygdala responds preferentially to aversive versus appetitive stimuli, is functionally asymmetric, and is required for both the initial learning and subsequent expression of negative emotional associations have not yet been adequately resolved and are considered in detail elsewhere (Davidson and Irwin 1999), though some data clearly suggest that the amygdala does activate in response to appetitive stimuli (Hamman et al. 2002). It should be noted that one fMRI study (Zalla et al. 2000) found differential activation of the left and right amygdala to winning and losing money, with the left amygdala showing increased activation to winning more money whereas the right amygdala showed increased activation in response to the parametric manipulation of losing money. Systematic examination of asymmetries in amygdala activation and function in appetitive and aversive contexts should be performed in light of these data. In several recent reviews, Whalen (Davis and Whalen 2001) has argued that a major function of the amygdala is the detection of ambiguity and the issuing of a call for further processing when ambiguous information is presented. I will return to this claim later in this chapter, when the issue of individual differences is addressed.

These findings raise the question concerning the "optimal" pattern of amygdala function for well-being. Based upon evidence reviewed below in the context of individual differences, we will argue that low basal levels of amygdala activation in conjunction with situationally appropriate responding, effective top-down regulation and rapid recovery characterize a pattern that is consistent with high levels of well-being.

What are individual differences in PFC and amygdala activations associated with?

In both infants (Davidson and Fox 1989) and adults (Davidson and Tomarken 1989), there are large individual differences in baseline electrophysiological measures of prefrontal activation, and such individual variation is associated with differences in aspects of affective reactivity. In infants, Davidson and Fox (1989) reported that 10-month-old babies who cried in response to maternal separation were more likely to have less left- and greater right-sided prefrontal activation during a preceding resting baseline compared with infants who did not cry in response to this challenge. In adults, we first noted that the phasic influence of positive and negative emotion elicitors (e.g., film clips) on measures of prefrontal activation asymmetry appeared to be superimposed upon more tonic individual differences in the direction and absolute magnitude of asymmetry (Davidson and Tomarken 1989).

During our initial explorations of this phenomenon, we needed to determine if baseline electrophysiological measures of prefrontal asymmetry were reliable and stable over time and thus could be used as a trait-like measure. Tomarken et al. (1992) recorded baseline brain electrical activity from 90 normal subjects on two occasions separated by approximately three weeks and found excellent internal consistency reliability and adequate test-retest stability for metrics of prefrontal activation asymmetry over this time period.

On the basis of our prior data and theory, we reasoned that extreme left- and extreme right-frontally activated subjects would show systematic differences in dispositional positive and negative affect. We administered the trait version of the Positive and Negative Affect Scales (PANAS; Watson et al. 1988) to examine this question and found that the left-frontally activated subjects reported more positive and less negative affect than their right-frontally activated counterparts (Tomarken et al. 1992; see Fig. 1). More recently (Sutton and Davidson 1997), we showed that scores on a self-report measure designed to operationalize Gray's concepts of Behavioral Inhibition and Behavioral Activation (the BIS/BAS scales; Carver and White 1994) were even more strongly predicted by electrophysiological measures of prefrontal asymmetry than were scores on the PANAS scales. Subjects with greater left-sided prefrontal activation reported more relative BAS to BIS activity compared with subjects exhibiting more right-sided prefrontal activation.

In a very recent study, we extended these early findings and found that baseline measures of asymmetric prefrontal activation predicted reports of well-being

Positive Affect

Negative Affect

Fig. 1. Dispositional positive affect (from scores on the PANAS-General Positive Affect Scale) in subjects who were classified as extreme and stable left-frontally active (N=14) and extreme and stable right-frontally active (N=13) on the basis of electrophysiological measures of baseline activation asymmetries on two occasions separated by three weeks. Error bars denote standard error ofthe mean (Tomarken et al. 1992).

Positive Affect

Negative Affect

Fig. 1. Dispositional positive affect (from scores on the PANAS-General Positive Affect Scale) in subjects who were classified as extreme and stable left-frontally active (N=14) and extreme and stable right-frontally active (N=13) on the basis of electrophysiological measures of baseline activation asymmetries on two occasions separated by three weeks. Error bars denote standard error ofthe mean (Tomarken et al. 1992).

Baseline EEG Asymmetry (FC4-FC3) and Psychological Well-being: Self-Acceptance

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Anxiety and Panic Attacks

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Suffering from Anxiety or Panic Attacks? Discover The Secrets to Stop Attacks in Their Tracks! Your heart is racing so fast and you don’t know why, at least not at first. Then your chest tightens and you feel like you are having a heart attack. All of a sudden, you start sweating and getting jittery.

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