Empathy is what makes the difference. To test if psychopathic individuals lack this empathic brain activation, the clinic transported 21 and emotional brain regions was much lower in the patients with psychopathy than in the normal subjects. That was my earliest memory that is solid, but I remember it very well. We conclude that insights afforded by the study of psychopathy may provide better the positive relationship between psychopathy and anger experiences. . autobiographical memories and semantic knowledge of emotion prototypes. Previous research indicates that psychopaths are prone to emotional .. relationship between psychopathy and the fading affect bias, we calculated affect .
This also gives others a sense of temporal continuity of, and with us. Imagine the chaos and instability we would experience in our lives if it were not for this sense of continuity? And yet this lack of continuity is precisely one of the defining characteristics of a pathological relationship, where contradictions, dichotomies, and non sequiturs continuously keep us off balance.
The psychopathic personality construct is comprised of traits that fall along and make up the Cluster B continuum, and central to all of these variations of psychopathy is a poverty of emotional experience. Neuro-imaging has revealed that psychopaths have anatomical differences in the paralimbic systems of the brain which deal with the processing and experience of emotion.
What this means is that psychopaths only experience a narrow, primitive, and primordial spectrum of emotion; and what emotions they do experience are very short lived. They are in other words lacking in an emotional memory, which is one of the reasons why psychopaths are notorious for having poor or selective, and contradictory recall; their neurological pathways are not working in tandem.
They have no true or real consistent depth of emotional experience that provides them with an emotional temporal inner story with either themselves or others; they are quite literally empty black holes. Their own inner experience of themselves falls through them in much the same way that their experience of others does. They may be capable of cognitive complexity, but rest assured if they are disordered there is little or no sign of emotional intelligence or nuance that enabled you to follow and keep track of their emotional story with us.
Their script continually changes, or is rewritten and flips in a manner that is severely emotionally disorientating for the victim, leaving us feeling as though we are plucking a never-ending daisy. They are in a sense lacking in a personal story when it comes to emotional relating, bonding, attachment, and intimacy.
We as their partners believed of course that we were living a narrative with them. What we did not comprehend is that everything we shared with them or thought we sharedno matter how significant has absolutely no currency with them whatsoever.
I found it helpful to think about it like this: Imagine you are thirsty and take a glass, you place the glass under the tap and fill it with water, you put the glass to your lips and realise the glass is empty; I could have sworn I just filled the glass under the tap. In an erratic and dramatic manner, their stories are forever changing and lack a smooth seam that charts their transition from emotional position a, to contradictory emotional position b.
Their ever changing scripts to us as victims, made us feel like we had a central role in a very important plot, only to find that the plot had suddenly changed and we were never consulted about it. Our role in the plot suddenly ends and the script we were reading suddenly and abruptly no longer apply. These neurophysiological processes are generally linked to activity in the evolutionarily ancient subcortical structures of the midbrain, striatum, and limbic system most commonly linked to emotion Panksepp, ; Vytal and Hamann, So, for example, the generation of positive excitement is linked to activation in a striatal circuit centered on dopaminergic neurons in the nucleus accumbens Ikemoto and Panksepp,whereas the generation of fear is associated with activity in a circuit involving the periaqueductal gray, anterior and medial hypothalamus, and amygdala LeDoux, In this view, finer gradations of experience result when basic emotions are modulated or elaborated by higher-level cognitive processes controlled by the cerebral cortex, but the emergence of qualitatively distinct emotions is not dependent on these cortically-controlled processes Panksepp, Models that posit emotions to be quantitatively distinct hold that emotions like fear, anger, and happiness are best described as points on one or more core dimensions.
Core dimensions typically proposed to distinguish among emotions are physiological arousal or activation low—high and valence bad—good Bradley et al. Arranged orthogonally, these dimensions form a circumplex upon which emotions can be plotted and quantitatively compared Barrett and Russell, ; Russell and Barrett, ; Colibazzi et al. Positive excitement is plotted as high in arousal and positive in valence, and sadness is low in arousal and negative in valence.
Fear is typically plotted as high arousal and strongly negative, as is anger Russell and Barrett, Further distinctions among emotions are thought to reflect differences in cognitive construals of the events surrounding the basic changes in arousal and valence.
Thus, whether an individual experiences anger or fear which are similar in terms of arousal or valence may be shaped by interpretations of neurophysiological changes in valence and arousal in light of the eliciting stimulus and the individual's idiosyncratic stores of semantic knowledge, memories, and behavioral responses that shape the subjectively experienced state Russell, Under this view, distinctions among experienced emotional states are highly dependent on these cognitively complex processes, which are subserved by a distributed network of regions of the cerebral cortex Lindquist et al.
These models generate distinct predictions to the question of whether a disorder or lesion could result in a single emotion being disabled without affecting the experience of other emotions. The discrete emotions view would argue that a disorder or lesion that resulted in dysfunction in the specific structures subserving a particular emotion could affect the experience of one emotion while leaving others intact.
In contrast, the dimensional view would require either that other emotions that are dimensionally similar to the affected emotion also be affected, or that deficits in a particular emotion would reflect dysfunction in cortically-driven higher-level cognitive processes.
The case of psychopathy lends clear support to notion that fear is qualitatively distinct from other emotions. In psychopathy, the bulk of the clinical and empirical evidence points toward the conclusion that fear responding is uniquely disabled, with other high-arousal positive excitement, anger and negatively valenced anger, disgust emotions remaining intact.
The dimensional view cannot easily explain why in psychopaths the high arousal, negatively valenced state of anger is easily perhaps too easily generated, whereas the high arousal, negatively valenced state of fear is not.
The problem cannot lie in a failure to fully engage neurocognitive systems underlying either the arousal or valence dimension, because psychopaths experience other high-arousal emotions positive excitement as well as other negatively valenced emotions disgust. It also cannot result from some difficulty arising at the interaction of these axes, because anger and fear are highly similar in terms of both dimensions.
Models that substitute a withdrawal—approach axis for a negative—positive axis are no more successful; the two most strongly withdrawal-linked emotions are disgust and fear, and there is no evidence for disgust-based impairments in psychopathy. Can cognitive construals of emotion explain the patterns observed in psychopathy?
Perhaps, one could argue, psychopaths under threat are less likely to construe their negative, high-arousal state as fear and more likely to construe it as anger compared to non-psychopaths.
So, for example, the psychopath whose interview is transcribed above might interpret a pounding heart and churning stomach as the angry response that accompanies a tendency to respond aggressively. Another person might interpret the same body symptoms as the fear that accompanies a tendency to escape or submit. Theoretically, this explanation could explain both the deficits in fear and a concomitant increase in anger in this population. One could argue that, particularly for studies that focus on subjective reports of emotion, group differences in construal underlie the tendency of psychopaths to underreport experiencing fear and overreport experiencing anger.
This argument suffers two shortcomings. First, it is inconsistent with psychophysiological findings of overall reduced arousal during threat anticipation in psychopathy.
As described above, there are two major categories of anger elicitors: The construal argument would require that psychopaths experience arousal in response to threat, but interpret this arousal as anger rather than fear. But the evidence is clear that psychopaths particularly primary psychopaths are no more likely than average to experience physiological arousal under conditions of threat Blackburn and Lee-Evans, —and in fact, as described previously, show reduced physiological responses, including reduced skin conductance, potentiated startle, and corrugator muscle activity.
This suggests that threat anticipation results in neither fear nor anger in this population. Psychopaths are, however, more likely than average to experience anger is in response to frustration Blair, Thus, rather than being chronically likely to construe any high arousal state as anger, psychopaths appear more likely to experience anger primarily in response to frustrated attempts to achieve a reward.
That both frustration-based anger and positive excitement the state that reflects the anticipation of reward are normal or elevated in psychopathy is consistent with the notion that in psychopaths the systems that govern anticipation of reward are functional and perhaps even overactive while the systems that govern threat anticipation are dysfunctional. A further concern is that the construal explanation of emotion leaves unclear why psychopathy might engender such a dramatic shift in emotional experience.
Such a phenomenon is particularly difficult to explain in light of the high heritability coefficient found for psychopathy. Cognitive construals of emotional states are thought to reflect the individual's autobiographical memories and semantic knowledge of emotion prototypes, phenomena that are necessarily a result of learning, rendering it unlikely that the tendency to construe one's emotional response to an event as fear versus anger would itself be heritable.
The pattern of reduced fear responding to anticipated threat observed in psychopathy, then, is more consistent with the view that states like anger and fear reflect biologically coherent and qualitatively distinct responses to particular eliciting stimuli.
Dimensions like valence and arousal are useful means of quantitatively describing differences among subjective feeling states like fear, anger, and positive excitement, but may not accurately reflect the neurobiological origins of those states.
If psychopathy is associated with specific deficits in fear responding, this not only supports the idea that emotions are qualitatively distinct, it supports the corollary that specific neurophysiological processes that support the fear response are also affected.
A key feature of models of discrete emotions is that distinct emotions have dissociable neurophysiological correlates Vytal and Hamann, Ekman has argued: The distinctive features of each emotion, including the changes not just in expression but in memories, imagery, expectations, and other cognitive activities, could not occur without central nervous system organization and direction. There must be unique physiological [CNS] patterns for each emotion p.
Limited evidence exists to suggest specific patterns of peripheral nervous system activity that accompany discrete emotions Ekman et al. The availability of non-human animal analogues has made fear one of the best-studied emotions on a neuroanatomical level. On the whole, the empirical data support the idea that the amygdala, along with its efferent projections, is an essential structure for the generation of conditioned fear responses, which account for the majority of experienced fear Davis, Extensive early evidence demonstrated that the amygdala plays a crucial role in the creation of conditioned fear in rodents.
For example, lesions to the amygdala prevent rats from developing a conditioned fear response, like freezing in response to a stimulus that predicts shock Blanchard and Blanchard, Later studies clarified the roles of the various subnuclei of the amygdala, demonstrating that the lateral nucleus is primarily involved in the acquisition of the fear response whereas the central nucleus is involved in both the acquisition and the expression of conditioned fear responses Davis, ; Wilensky et al.
The amygdala's many efferent projections coordinate autonomic and behavioral responses to fear eliciting stimuli. Projections from the central nucleus of the amygdala to the lateral hypothalamus are involved in activating autonomic sympathetic nervous system responses, and projections to the ventrolateral periaqueductal gray direct the expression of behavior responses, such as defensive freezing Davis, ; LeDoux, The amygdala's central role in coordinated fear responding can be demonstrated by electrical stimulation studies showing that complex patterns of behavioral and autonomic changes associated with fear responses result from stimulation of the relevant regions of the amygdala Davis, Heavy reliance on animal models is justified in the study of fear responding and the amygdala given how strongly conserved the amygdala nuclei involved in responding to conditioned threats are across species ranging from reptiles to birds to rodents to primates LeDoux, Ethical and pragmatic considerations prevent experimental paradigms employing electrical stimulation or ablation of the amygdala from being undertaken in human subjects.
However, the advent of neuroimaging technologies have enabled considerable assessments of subcortical responses to a variety of emotional stimuli, enough to provide a basis for seven meta-analyses that have been conducted to assess patterns of brain activation in response to specific emotions Phan et al.
The findings from four of these meta-analyses support the role of the amygdala in human fear responding. Phan and colleagues reviewed 55 PET and fMRI studies including 13 that assessed fear responding and found that fear specifically activated the amygdala relative to other emotions Phan et al. In neither meta-analysis was any other structure observed to be consistently and selectively activated during fear paradigms. Fusar-Poli and colleagues included only fMRI studies assessing responses to emotional faces, but again found heightened amygdala responses to fearful faces relative to other emotional faces Fusar-Poli et al.
Finally, Vytal and Hamann employed a more sensitive meta-analytic method, activation likelihood estimation ALEto analyze the results of 83 PET and fMRI studies of emotion including 37 that assessed fear responding and again found strong support that the amygdala is preferentially active during fear paradigms, and this activation in this region differentiated fear from happiness, sadness, and disgust.
Three recent meta-analyses did not yield findings that fear is preferentially associated with amygdala activation. Two were conducted by Feldman-Barrett and colleagues Kober et al. The authors observed that, bilaterally, the amygdala was the most active brain region during fear perception paradigms although not significantly more active during fear than other emotionsbut that the amygdala was not preferentially active during fear experience paradigms. The selection of studies in this meta-analysis may account in part for the differential findings.
For example, of the nine fear-experience studies included in this analysis, six were conducted by a group that uses primarily IAPS pictures Lang et al.
These meta-analyses also omitted pain anticipation and mood induction tasks included in other meta-analyses that are more directly relevant to fear experience Murphy et al. The third meta-analysis Sergerie et al. This approach yielded results showing amygdala activation that was stronger in response to positive emotional stimuli than to any negative emotional stimuli. Clearly, the conclusions drawn from the various meta-analyses are divergent enough to leave questions remaining as to whether the amygdala is in fact specifically implicated in fear responding.
Can the study of psychopathy clarify the role of the amygdala in fear experience? Perhaps, given the prominence of dysfunctional fear responding in psychopathy, empirical support that amygdala dysfunction underlies aberrant fear responding in psychopathic participants would support the amygdala's role in fear.
And indeed, early hypotheses about the brain basis of psychopathy focused on potential amygdala dysfunction Patrick, ; Blair et al. More recently, the results of both functional and structural neuroimaging studies support these hypotheses.
Several studies have observed that psychopathy is associated with reduced amygdala activation during the viewing of fearful emotional facial expressions but not other expressions like anger, a pattern that is independent of attentional processes Marsh et al. A recent study also found that psychopathy assessed in a community sample was also associated with a failure to exhibit amygdala activation to fear-evoking statements Marsh and Cardinale, b.
Again, no group differences were observed in this task when other emotionally evocative statements were presented. In addition, no main effect of fear stimuli was observed in the amygdala across groups. This suggests that amygdala responses to fear may fail to emerge in neuroimaging studies when the sample contains an unusual proportion of high psychopathy scorers.
Finally, a fear-conditioning paradigm found that psychopaths' failure to exhibit skin conductance responses during the task was accompanied by reduced activation in the amygdala and functionally connected regions of the cortex, such as orbitofrontal cortex and insula Birbaumer et al. These patterns of dysfunction may stem from structural abnormalities in the amygdala, which have also been observed in psychopathy.
Structural abnormalities across multiple nuclei in the amygdala have been observed in psychopathy Yang et al. Yang and colleagues observed not only significant bilateral volume reductions in the amygdalae of adult psychopaths relative to controls controls, but also surface deformations in the vicinity of the amygdala's basolateral, lateral, cortical, and central nuclei.
Ermer and colleagues identified gray matter reductions in adult psychopaths' amygdalae, in addition to other paralimbic regions such as parahippocampal gyrus Ermer et al.
It should be noted that how specific nuclei of the amygdala are involved in psychopathy is not yet clear, in part due to insufficient spatial resolution of functional imaging scan. Various hypotheses have been proposed regarding the role of discrete nuclei in psychopathic symptoms Blair, a ; Moul et al. On the whole, the results of these studies directly link amygdala dysfunction to observed deficits in fear responding in psychopathy.
But perhaps the most compelling evidence that amygdala dysfunction underlies fear deficits in psychopathy emerges from the results of paradigms testing fear responding in psychopaths and individuals with lesions to the amygdala. As previously described, psychopathy has been found to impair anticipatory skin-conductance responses Lykken, ; Aniskiewicz, ; Herpertz et al.
Striking parallels to these deficits can be found in studies of individuals with amygdala damage. In these individuals, comparable impairments in each of these fear paradigms have also been observed Table 1. Comparison of deficits observed in samples with psychopathy and amygdala lesions.
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Because amygdala dysfunction has been observed in psychopathy during several of these tasks, and because amygdala lesions impair performance in all of them, these patterns generate a compelling case for the role of the amygdala specifically in fear responding. Consistent with this, researchers studying one patient with bilateral amygdala damage SM clarify that she has not only striking deficits in fear responding, but these deficits are limited to fear responding: SM's reaction to fear-inducing stimuli was not characterized by a loss of responsiveness, but rather manifested as a heightened arousal and interest in the face of a near-complete lack of avoidance and caution … Our findings suggest that the amygdala's role in the induction and experience of emotion is specific to fear.
To say that SM is emotionless or unable to feel emotion is simply false. Her emotional deficit is primarily circumscribed to the behaviors and experiences that characterize a state of fear Feinstein et al. The clear correspondence between patterns of fear dysfunction observed in psychopathy and following amygdala lesions, in the absence of other clear emotional deficits, provides strong support for the specific involvement of the amygdala in fear.
Dysfunction in the amygdala, whether via acquired lesion or developmental psychopathology, impairs fear-related processes while leaving other forms of emotion, such as anger, positive excitement, and disgust, largely intact.
In answer to our second question, then, research in psychopathy suggests that the amygdala—or, more likely, specific populations of neurons within the amygdala LeDoux, —plays a critical role in generating fear but does not appear to be critical for other emotions like positive excitement and anger.
The findings reviewed thus far suggest answers to a third question of ongoing interest in psychology and neuroscience: As we have seen, the evidence is clear that psychopathy is associated with deficits in the experience of fear but not other emotions. Psychopathic individuals show reduced physiological responding during anticipation of an aversive event, are less apt to adapt their behavior in response to punishment, and report reduced subjective fear.
In some psychopaths the experience of fear may be essentially absent but, in keeping with the idea that psychopathy is a continuum rather than a taxon, fear is likely muted to varying degrees rather than absent in most individuals with psychopathic traits.
Finally, psychopathy impairs the recognition of others' fear. Three meta-analyses have now demonstrated that psychopathy impairs recognition of fearful facial expressions in the face, body, and voice Marsh and Blair, ; Wilson et al. Marsh and Blair found that responses to fear are impaired to a significantly greater degree than any other emotion, and Dawel et al.
In addition, psychopathy impairs the ability to identify the circumstances under which others would experience fear, such as in response to threats of harm Marsh and Cardinale, a.
The parallels between psychopathic deficits in emotional experience and emotion recognition are striking. The emotion that psychopaths appear not to feel strongly—fear—is the same emotion that they have the most difficulty recognizing in others.
Associations between the experience and recognition of emotion have previously been observed for a number of emotions, including fear Buchanan et al. These data suggest the possibility of a basic empathic failure in psychopaths—they have great difficulty understanding an emotion in others that they themselves do not feel or at least, do not feel strongly.