Electronic copy available at: http://ssrn.com/abstract=1966290

The Dark Side of Social Encounters:Prospects for a Neuroscience of Human Evil

Martin ReimannUniversity of Southern California

Philip G. ZimbardoStanford University

This article discusses how findings from social, cognitive, and affective neurosciencemight contribute to our understanding of human evil. Integrating theories of personalityand social psychology as well as the notions of deindividuation and dehumanizationwith recent neuroscientific insight, the authors elaborate on the nature of human eviland its potential roots in brain systems associated with affective processing andcognitive control.

Keywords: human evil, aggression, deindividuation, dehumanization, social, cognitive, affectiveneuroscience

While much neuroscientific research fo-cuses on the neural basis of positive socialresponses such as empathy, fairness, andtrust, the neural correlates of negative socialencounters are largely unknown. Specifically,what are the neurophysiological substrates ofhuman evil? Or, in other words, which neuralmechanisms underlie this basic social phe-nomenon? For several decades, personalityand social psychology has informed us of twoprocesses that have been named central tohuman evil: deindividuation and dehumaniza-tion (Bandura, 1982; Pines & Solomon, 1977;Zimbardo, 1969; Zimbardo, 2007). Whereasdeindividuation refers to the process that fa-cilitates the perception of others as anony-mous (Zimbardo, 1969), dehumanization is atthe core of much evil, occurring when oneexcludes another from the moral order as ahuman being, or less than human, as animal-like (Zimbardo, 2007). Dehumanization canbe conceptualized as a “cortical cataract,” thatblurs our perception of others as having anysimilarity to our kind or us. It is also a central

process in genocide, mass murder, rape as aterror tactic, and in prejudice.

In this research, we propose how findingsfrom social, cognitive, and affective neurosci-ence might contribute to the study of deindi-viduation and dehumanization and, therefore,at least two aspects of human evil. We outlineseveral ideas advanced by leading neurosci-entists that are provocative and in need offurther experimental testing. We also presenta framework derived from aggression re-search, which might serve for testing of hy-potheses on the neuroscience of human evil.Although the neuroscience of human evil is inits infancy, programmatic research can yieldinteresting insights on one basic form of hu-man social interaction.

While researchers have put forth calls for abetter neural understanding of evil, few inves-tigators have conducted empirical research. Onereason for this inattention may be the absence ofwork that bridges concepts from personality andsocial psychology with insights from neurosci-ence. Such a conceptual integration is the mainobjective of the current research. We start witha general framework rooted in aggression re-search that is relevant to the understanding ofhuman evil. This framework provides a contextfor forming empirical questions and testing hy-potheses on a neuroscience of human evil. Onthe basis of this framework, we develop a pre-liminary model on the neural correlates of dein-dividuation and dehumanization, essential forsubsequent experimental analyses.

This article was published Online First July 18, 2011.Martin Reimann, Department of Psychology, University

of Southern California; Philip G. Zimbardo, PsychologyDepartment, Stanford University.

Correspondence concerning this article should be ad-dressed to Martin Reimann, University of Southern Califor-nia, Department of Psychology, Seeley G. Mudd Building,3620 McClintock Avenue, Los Angeles, CA 90089-1061.E-mail: mreimann@usc.edu

Journal of Neuroscience, Psychology, and Economics © 2011 American Psychological Association2011, Vol. 4, No. 3, 174–180 1937-321X/11/$12.00 DOI: 10.1037/a0024654

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Electronic copy available at: http://ssrn.com/abstract=1966290

A Framework From Aggression Research

We build on extant research on aggression toargue that a unique neural framework underliesthe mechanisms of human evil. Besides con-ducting psychiatric research on the neurobio-logical roots of aggression such as genes andneurotransmitters (e.g., Volavka, 1999), inves-tigators have also focused on the functionalneuroanatomy of aggression. Generally, humanaggression research offers generic concepts onantisocial behavior (Bandura, 1973; Buss, 1961;Buss & Durkee, 1957; Caprara, Barbaranelli, &Zimbardo, 1996), with a number of definitionsand several views of the construct existing inthe literature (for a review on the social, cogni-tive, and affective dimensions of human aggres-sion, see Caprara et al., 1996).

One frequently cited definition characterizeshuman aggression as “a response that deliversnoxious stimuli to another organism” (Buss, 1961,p. 1), and a widely used concept of aggressionconsists of seven dimensions: assault, indirect ag-gression, irritability, negativism, resentment, sus-picion, and verbal aggression (Buss & Durkee,1957). However, measurement issues with thisfirst aggression inventory resulted in the intro-duction of a condensed four-factor model ofaggression that includes hostility, anger, verbalaggression, and physical aggression (Buss &Perry, 1992). Hostility consists of ill will and asense of injustice and embodies the cognitivecomponent of behavior. It can be defined as thestubborn refusal to accept proof that the percep-tions of one’s surrounding are false. Anger en-tails physiological arousal (e.g., increased heartrate, blood pressure, and levels of adrenalineand noradrenaline) and preparation for verbaland physical aggression. Anger thus representsthe emotional or affective component of behav-ior. It is also expressed externally and is appar-ent in facial expressions and body language (fora guideline on how to detect subtle anger infacial expressions, see Ekman & Friesen, 2003).Verbal aggression and physical aggression, thethird and fourth components of aggression, bothinvolve attempts to hurt or harm others and, assuch, represent the instrumental or motor com-ponent of behavior (Buss & Perry, 1992).

One prominent incident in medical historymarks a starting point for the neuroscientificstudy of aggression: the case of a nineteenth-century railroad worker, Phineas Gage, who is

best remembered for surviving an accident inwhich an iron rod was driven through his head,damaging large sections of his frontal lobe. Thephotograph in Figure 1 is believed to be one ofPhineas Gage, holding the iron rod (Wilgus &Wilgus, 2009).

After this accident, Phineas Gage’s physiciannoted dramatic changes in his personality, so-cial conduct, judgment, and decision-making(Harlow, 1848, 1868). Gage refused to showrespect for social conventions and offendedother people with profanities, and he also be-came aggressive in his behavior (Harlow,1868). While previous researchers investigatingGage’s case had to rely on Harlow’s notes todraw conclusions, developments in technologyhave allowed more recent researchers to obtainevidence confirming the notion that Gage’s ag-gression was linked to specific frontal lobe dam-ages. Using neuroimaging techniques to exam-ine Gage’s preserved skull, investigators foundthat the lesion Gage experienced affected theprefrontal cortex (Damasio, Grabowski, Frank,Galaburda, & Damasio, 1994). Additionally, re-search in lesion patients as well as healthy in-

Figure 1. A case of frontal lobe damage and aggression:Phineas Gage. Printed with permission of B. Wilgus.

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dividuals undergoing neuroimaging has con-firmed the relationship between frontal lobedamage and aggression. In particular, studieshave shown that patients with prefrontal cor-tex lesions can show disinhibited and sociallyinappropriate behaviors such as aggression(e.g., Rolls, Hornak, Wade, & McGrath,1994). Furthermore, extant neuroimaging re-search has identified functional deactivationin the ventromedial prefrontal cortex of indi-viduals responding to pictures that show ag-gressive behavior (e.g., Pietrini, Guazzelli,Basso, Jaffe, & Grafman, 2000).

Through a content analysis of several neuro-imaging studies, researchers studied the rela-tionship between frontal lobe pathology andaggressive behavior (Bufkin & Luttrell, 2005).Across a number of different neuroimagingmethodologies (including single-photon emis-sion computed tomography, positron emissiontomography, and functional magnetic resonanceimaging), the investigators report a strong linkbetween deficits in frontal functioning and ag-gression. In particular, analyses of specific re-gions in the medial prefrontal cortex revealedthat individuals who were aggressive had sig-nificantly lower prefrontal activity in the orbito-frontal cortex, anterior medial cortex, medialfrontal cortex, and/or superior frontal cortex.The content analysis also identified the tempo-ral lobe and several subcortical structures asbeing involved in aggression, although theseregions were not the focus of most studies in thereview (Bufkin & Luttrell, 2005). Overall, ex-tant research on aggression suggests that de-creased activation of frontal lobe structures,particularly the prefrontal cortex, or lesioning ofthis brain area can be a central cause for aggres-sion, although another review identified theamygdala as a central subcortical structure as-sociated with aggression (Siever, 2008).

Somatic marker theory (Damasio, 1994,1996; Damasio, Tranel, & Damasio, 1991;Reimann & Bechara, 2010) provides the theo-retical basis of the relationship between theventromedial prefrontal cortex and other brainareas, which include both brain stem structures(i.e., hypothalamus and periaqueductal gray)and the amygdala. According to this theory,emotion-related signals (i.e., somatic markers,also sometimes termed bodily markers), whichare indexed changes in the visceral state (e.g.,changes in heart rate, blood pressure, gut mo-

tility, and glandular secretion), interact withcognitive processes. These changes in the vis-ceral state can be considered a form of antici-pation of the bodily impact of events in theworld that allows an organism to maximize thesurvival value of particular situations. Thesesituations could promote homeostasis, such asan opportunity to engage in social interaction,as well as events that disrupt homeostasis, suchas a signal of deindividuation (e.g., beingtreated anonymously rather than as an individ-ual) or dehumanization (e.g., a serious threat ofbeing excluded as a human being). Overall,these visceral responses are one component of abroader emotional response system that alsoincludes changes in the endocrine and skeleto-motor systems, and within the brain (Damasio,1994).

Somatic marker theory further proposes sev-eral neural structures that studies have shown tobe key components of the neural circuitry un-derlying somatic state activation. The amygdalaand the ventromedial prefrontal cortex region(i.e., medial frontal and orbitofrontal cortex) arecritical structures for triggering somatic states.Whereas the amygdala seems to be more im-portant for triggering somatic states from emo-tional events that occur in the external environ-ment, the ventromedial prefrontal cortex regionseems to be more vital for triggering somaticstates from the internal cortical environment ofmemories and knowledge (Bechara & Damasio,2005).

Toward a Neuroscience of Human Evil

In personality and social psychology, twoprocesses have been named central to humanevil: deindividuation and dehumanization (Ban-dura, 1982; Pines & Solomon, 1977; Zimbardo,1969; Zimbardo, 2007). The deindividuationand dehumanization phenomena offer a frame-work for explaining the antisocial behavior ofaggressive crowds, such as hooligans and thelynch mob (Postmes, Spears, & Lea, 1998).Deindividuation theory has also been applied tohelp explain antisocial behavior in computer-mediated communication (Kiesler, Siegel, &McGuire, 1984; Kiesler & Sproull, 1992) andgroup decision support systems (Jessup, Con-nolly, & Tansik, 1990; for a history and meta-analysis of deindividuation theory, see Postmeset al., 1998).

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Deindividuation

The idea of deindividuation goes back to thework of Le Bon (1897), was reintroduced byFestinger, Pepitone, and Newcomb (1952), andthen extended and developed by Zimbardo(1969). The term refers to the process that fa-cilitates the perception of others as lacking inpersonal identity (Pines & Solomon, 1977), andpeople engaging in deindividuation treat othersas anonymous, not as individuals (Zimbardo,2007). Deindividuation also includes processesthat encourage a person to mask his or heridentity in various ways, thereby reducing asense of personal accountability. Decades ofresearch have demonstrated that deindividua-tion strongly predicts the odds of antisocial be-havior such as aggression. Social circumstancesthat promote anonymity increase the probabilityof eliciting antisocial behaviors when individu-als perceive they have permission to be hostileor aggressive or to break social norms. Deindi-viduation can result from a variety of factors inaddition to anonymity and loss of personal ac-countability, including sensory overload, un-structured situations, and substance abuse.

Social psychologists have long recognizedthe crucial role of anonymity in antisocial be-havior. Beginning with the Stanford Prison Ex-periment in 1971 (Haney, Banks, & Zimbardo,1973), numerous studies have demonstrated thata feeling of anonymity can often cause antiso-cial behavior. In the Stanford Prison Experi-ment, physically fit and mentally stable youngmen were randomly assigned to play the roleseither of “guard” or “prisoner” for two weeks inthe basement of the psychology department ofStanford University. With the cooperation ofthe local police department, prisoners were un-expectedly arrested, brought to the police sta-tion for finger printing and registration, and thenplaced in a detention cell. After being blind-folded, each prisoner was guided to the mockprison at Stanford University. To promote ano-nymity of the subjects, each group was issuedidentical uniforms and identification numbersreplaced their names. Guards’ uniforms con-sisted of plain khaki shirts and trousers, whistle,wooden baton, and reflecting sunglasses, thelast making eye contact impossible. Prisoners’uniforms were loose-fitting muslin smocks withidentification numbers on the front and back andrubber sandals. No underwear was worn under

the smocks and a chain and lock were placedaround one ankle. After only 6 days, the experi-ment had to be stopped because the behavior ofthe guards toward the prisoners had become in-creasingly aggressive and the prisoners were ex-periencing severe emotional distress. Since thisexperiment, research on deindividuation hasbeen interpreted as suggesting that any situa-tion that makes individuals feel anonymousand reduces their sense of personal account-ability can potentially lead to evil behavior.

While neuroscientific research on deindividu-ation is nonexistent in the literature, extant neu-roimaging research investigating how socialgestures affect brain activation provides somelimited clues to potential neural markers asso-ciated with deindividuation. In a recent study,participants underwent functional MRI whileviewing various social gestures, including fas-cist saluting or simple waving (Knutson, Mc-Clellan, & Grafman, 2008). The investigatorsfound that highly provocative social gestures(i.e., fascist saluting) compared to less provoc-ative but still socially meaningful gestures (i.e.,waving) are associated with activation in themedial prefrontal cortex, among other areas.The researchers also compared brain activationof participants viewing multiple gesturing ac-tors with activation while viewing a single ges-turing actor and found an involvement of thefrontal lobe for viewing multiple gesturing ac-tors. However, results were ambiguous as towhether this effect was due to participants beingdeindividuated because they felt they were ananonymous member of a group with a resultingloss in personal accountability (as argued bythese investigators) or whether this effect wasdue to the perception of many different motormovements.

Dehumanization

Dehumanization occurs when one personconsiders others to be excluded from the moralorder of being a human being (Zimbardo, 2007).It involves the denial of uniquely human attri-butes and is often accompanied by contemptand disgust and by a tendency to explain others’behavior in terms of one’s own desires ratherthan cognitive states (Haslam, 2006). Dehu-manization is at the core of human evil, becauseit depicts a person as less than human. It occursin a variety of stressful human encounters, such

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as when a large flow of people has to be man-aged or processed efficiently (Bandura, 1977;Pines & Solomon, 1977; Zimbardo, 1969), andcan be considered an everyday social phenom-enon (Haslam, 2006).

Some pioneering neuroimaging research hasexamined dehumanization. In particular, a re-cent neuroimaging study reports decreasedbrain activation in the medial prefrontal cortexand increased activation in the amygdala andthe insula when participants viewed pictures ofstereotypically hostile and stereotypically in-competent groups (Harris & Fiske, 2006). Theinvestigators used functional MRI in a between-subjects design, showing photographs of socialgroups to one group and pictures of objects toanother group. Results demonstrated that per-ceiving extreme out-groups (e.g., homeless peo-ple and drug addicts) results in decreased me-dial frontal cortex activation and increasedamygdala and insula activation. The authorsargue that these extreme out-groups may beperceived as less than human, or dehumanized(Harris & Fiske, 2006). This finding suggeststhat when humans dehumanize others, less me-dial prefrontal cortex activation but moreamygdala and insula activation is involved. Insum, these findings point in the same directionas previous neuroscientific research on aggres-sion, which predicts less activation in the ven-

tromedial prefrontal cortex in association withaggressive behavior. The results are also in linewith the case of Phineas Gage, which revealedthat ventromedial prefrontal cortex lesioningcan result in a loss of “cognitive control” andthe rise of aggressive behavior.

Although drawing conclusions regarding theneurophysiological markers of deindividuationand dehumanization would be premature, extantresearch on aggression points toward the pre-frontal cortex as a crucial mechanism in humanevil. Besides the prefrontal cortex, prior studieshave named other subcortical brain regions,such as the amygdala, as being important. Weborrow from somatic marker theory (Damasio,1994, 1996; Damasio et al., 1991; Reimann &Bechara, 2010) to derive a preliminary model ofdeindividuation and dehumanization, their poten-tial neural correlates, and downstream aggression.As Figure 2 shows, being deindividuated and/ordehumanized could potentially involve a networkof brain areas, including the ventromedial prefron-tal cortex, the amygdala, and brainstem structures(i.e., hypothalamus and periaqueductal gray). Asreviewed above, somatic marker theory predictsthat the amygdala is more important for trigger-ing somatic states from emotional events thatoccur in the environment and that the ventro-medial prefrontal cortex region is more vital fortriggering somatic states from memories and

Figure 2. A preliminary model of neurophysiological and behavioral correlates of deindi-viduation and dehumanization. Note. (1) Ventromedial prefrontal cortex, (2) amygdala, (3)brainstem structures, and (4) visceral responses such as changes in heart rate, blood pressure,gut motility, and glandular secretion.

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knowledge (Bechara & Damasio, 2005). In ad-dition, deindividuation and dehumanizationcould involve visceral responses, such aschanges in heart rate, blood pressure, gut mo-tility, and glandular secretion, which couldserve as important somatic markers for evaluat-ing social encounters and for controlling ag-gressive behavior.

In the case of deindividuation, a decrease inactivation of the ventromedial prefrontal cortexcould possibly result from a “feeling” of ano-nymity and a loss of personal accountability,because somatic states are not triggered bymemories and knowledge of social norms and,thus, lead to disinhibited, antisocial behaviors.In the case of dehumanization, decreased ven-tromedial prefrontal cortex activation could alsobe accompanied by an increase in amygdalaactivation (Harris & Fiske, 2006). Being ex-cluded from the moral order of human beings(that is, being dehumanized) could pose an im-mediate threat that leads to increased processingin the amygdala, which in turn triggers somaticstates in the viscera via the brainstem.

Conclusion

With the goal of better understanding coreprocesses of human evil, this analysis bringstogether several disparate themes from person-ality and social psychology as well as social,cognitive, and affective neuroscience. The pros-pects for a neuroscience of human evil arepromising. Applying ideas from investigationsof aggression as well as preliminary findingsfrom neuroimaging studies of deindividuationand dehumanization may guide the develop-ment of future hypotheses that test the cognitiveand affective mechanisms underlying humanevil.

Of the many issues within this domain ofresearch, the most pressing is the need for em-pirical testing. Here, the differentiation betweendeindividuation and dehumanization in terms offunctional neuroanatomy will pose certainmethodological challenges. Are the same or dif-ferent neural processes involved for deindividu-ation and dehumanization, and to what extent?Another interesting issue worth pursuing is thedistinction between the person who deindividu-ates and/or dehumanizes and the one beingdeindividuated and/or dehumanized. Reportsfrom the Stanford Prison Experiment state that

both guards and prisoners showed negative,hostile, and affrontive attitudes and behaviorswhen encountering each other (Haney et al.,1973). Thus, does it matter, in terms of theunderlying neural mechanisms, which perspec-tive one takes—the perspective of the guard orthe perspective of the prisoner? Could even theguards, who were obviously in power, be sub-ject to the same neural mechanisms because oftheir uniform appearance, which resulted in an-onymity and loss of personal accountability? Inaddition to addressing these questions, otherworthwhile investigations include the causalitybetween deindividuation/dehumanization, brainmechanisms, and aggressive behaviors. Re-searchers could also examine the possible me-diating role of these brain processes in therelationship between deindividuation and dehu-manization and aggression.

Beyond using functional neuroimaging inhealthy individuals, researchers should alsoconduct experimental work in patients withbrain damage. While functional neuroimagingstudies will yield a broader picture of the neuralprocesses underlying deindividuation and dehu-manization, lesion studies could focus on pre-frontal cortex patients and, therefore, help tofurther pinpoint a brain area that seems to beimplicated in human evil. Moreover, investigat-ing the neural correlates of human evil mayadvance existing areas of inquiry, such as ag-gression research and somatic marker theory,and also reveal new findings and further re-search questions.

References

Bandura, A. (1973). Aggression: A social learninganalysis. Englewood Cliffs, NJ: Prentice Hall.

Bandura, A. (1977). Self-efficacy: Toward a unifyingtheory of behavioral change. Psychological Re-view, 84, 191–215.

Bandura, A. (1982). Self-efficacy mechanism in hu-man agency. American Psychologist, 37, 122–147.

Bechara, A., & Damasio, A. R. (2005). The somaticmarker hypothesis: A neural theory of economicdecision. Games and Economic Behavior, 52,336–372.

Bufkin, J. L., & Luttrell, V. R. (2005). Neuroimagingstudies of aggressive and violent behavior.Trauma, Violence, & Abuse, 6, 176–191.

Buss, A. H. (1961). The psychology of aggression.New York, NY: Wiley.

179NEUROSCIENCE OF HUMAN EVIL

Buss, A. H., & Durkee, A. (1957). An inventory forassessing different kinds of hostility. Journal ofConsulting Psychology, 21, 343–349.

Buss, A. H., & Perry, M. (1992). The aggressionquestionnaire. Journal of Personality and SocialPsychology, 63, 452–459.

Caprara, G. V., Barbaranelli, C., & Zimbardo, P.(1996). Understanding the complexity of humanaggression: Affective, cognitive, and social dimen-sions of individual differences in propensity to-ward aggression. European Journal of Personal-ity, 10, 133–155.

Damasio, A. R. (1994). Descartes’ error: Emotion,reason, and the human brain. New York, NY:Putnam.

Damasio, A. R. (1996). The somatic marker hypoth-esis and the possible functions of the prefrontalcortex. Philosophical Transactions of the RoyalSociety B: Biological Sciences, 351, 1413–1420.

Damasio, A. R., Tranel, D., & Damasio, H. (1991).Somatic markers and the guidance of behavior:Theory and preliminary testing. In H. S. Levin,H. M. Eisenberg, & A. L. Benton (Eds.), Frontallobe function and dysfunction (pp. 217–229). NewYork, NY: Oxford University Press.

Damasio, H., Grabowski, T., Frank, R., Galaburda,A. M., & Damasio, A. R. (1994). The return ofPhineas Gage: Clues about the brain from the skullof a famous patient. Science, 264, 1102–1105.

Ekman, P., & Friesen, W. V. (2003). Unmasking theface: A guide to recognizing emotions from facialclues. Cambridge, MA: Malor Books.

Festinger, L., Pepitone, A., & Newcomb, T. (1952).Some consequences of de-individuation in agroup. Journal of Abnormal and Social Psychol-ogy, 47, 382–389.

Haney, C., Banks, C., & Zimbardo, P. G. (1973).Interpersonal dynamics in a simulated prison. In-ternational Journal of Criminology & Penology, 1,69–97.

Harlow, J. M. (1848). Passage of an iron rod throughthe head. Boston Medical and Surgical Jour-nal, 39, 389–393.

Harlow, J. M. (1868). Recovery from the passage ofan iron bar through the head. Publications of theMassachusetts Medical Society 2, 327–347.

Harris, L. T., & Fiske, S. T. (2006). Dehumanizingthe lowest of the low: Neuroimaging responses toextreme out-groups. Psychological Science, 17,847–853.

Haslam, N. (2006). Dehumanization: An integrativereview. Personality and Social Psychology Re-view, 10, 252–264.

Jessup, L. M., Connolly, T., & Tansik, D. A. (1990).Toward a theory of automated group work: The

deindividuating effects of anonymity. Small GroupResearch, 21, 333–348.

Kiesler, S., Siegel, J., & McGuire, T. W. (1984).Social psychological aspects of computer-medi-ated interaction. American Psychologist, 39, 1123–1134.

Kiesler, S., & Sproull, L. (1992). Group decisionmaking and communication technology. Organi-zational Behavior and Human Decision Pro-cesses, 52, 96–123.

Knutson, K. M., McClellan, E. M., & Grafman, J.(2008). Observing social gestures: An fMRI study.Experimental Brain Research, 188, 187–198.

Le Bon, G. (1897). The crows: A study of popularmind. New York, NY: The Macmillan Company.

Pietrini, P., Guazzelli, M., Basso, G., Jaffe, K., &Grafman, J. (2000). Neural correlates of imaginalaggressive behavior assessed by positron emissiontomography in healthy subjects. American Journalof Psychiatry, 157, 1772.

Pines, A., & Solomon, T. (1977). Perception of selfas a mediator in the dehumanization process. Per-sonality and Social Psychology Bulletin, 3, 219.

Postmes, T., Spears, R., & Lea, M. (1998). Breachingor building social boundaries?: Side-effects ofcomputer-mediated communication. Communica-tion Research, 25, 689–715.

Reimann, M., & Bechara, A. (2010). The somaticmarker framework as a neurological theory of de-cision-making: Review, conceptual comparisons,and future neuroeconomic research. Journal ofEconomic Psychology, 31, 767–776.

Rolls, E., Hornak, J., Wade, D., & McGrath, J.(1994). Emotion-related learning in patients withsocial and emotional changes associated with fron-tal lobe damage. Journal of Neurology, Neurosur-gery & Psychiatry, 57, 1518.

Siever, L. J. (2008). Neurobiology of aggression andviolence. American Journal of Psychiatry, 165,429–442.

Volavka, J. (1999). The neurobiology of violence: Anupdate. Journal of Neuropsychiatry and ClinicalNeurosciences, 11, 307.

Wilgus, J., & Wilgus, B. (2009). Face to face withPhineas Gage. Journal of the History of the Neu-rosciences, 18, 340–345.

Zimbardo, P. (1969). The human choice: Individua-tion, reason, and order versus deindividuation, im-pulse, and chaos. In W. J. Arnold & D. Levine(Eds.), Nebraska symposium on motivation (pp.237–307): University of Nebraska Press.

Zimbardo, P. G. (2007). The Lucifer effect: Under-standing why good people turn evil. New York,NY: Random House.

180 REIMANN AND ZIMBARDO