Introduction - OISE



Video Game Violence on Adolescent Aggression:

How Exposure to Violence Can Lead to Exhibition of Violence

Introduction

Exposure to video game violence has been linked to increases in aggressive thoughts, feelings, and behaviours in males, females, adults, and adolescents (Anderson & Dill, 2000; Pance & Ballard 2002; Mathews et al. 2005; Barlett et al. 2007). In the 1980s with the advent of video arcades came studies that found a positive correlation between the amount of time spent at the arcade and frequency and intensity of aggressive behaviour as well as reports of delinquency from teachers and parents (Nelson & Carlson 1985; Lin & Lepper 1987; Schutte et.al 1988). In the 1990s studies of game features showed that aggressive behaviour was greater in those competing against (versus cooperating with) peers (Anderson & Morrow, 1995) and in those who played games that contained more frequent and more graphic depictions of injuries (Ballard & Weist, 1996). Most recently, studies have begun to examine first-person-shooter video games (FPSG) in which the player participates from a first-person perspective rather than manipulating an intermediary figure on the screen. Players of FPSG describe themselves as feeling more aggressive than before having played the game (Schneider et al. 2004).

Earlier game controls were buttons that restricted the player’s involvement to the fingers. FPSG controls are model weapons that require whole-body actions in simulated violent acts. For example, common motorcycle street-racing/crashing games require the player to “ride” a model motorbike. Players manipulate the bike along a virtual city street crashing, speeding, and being chased by the police. In a popular military game, players don a helmet that integrates a monitor in the visor that blocks out the real environment completely while the player kills with a model assault rifle. These are two examples of a host of violent FPSG which are popular among adolescents. The increasing realism of these games through first-person perspective and through simulated violent actions warrant concern over the kind of learning resulting from playing these games. Barlett et al. (2007) found a significant increase in aggression during FPSG play and more intense aggression when a model weapon was employed. Specifically, there was a dramatic increase in hostility, physiological arousal, and frustration.

Adolescents experience a wave of neurochemical changes that make them especially reactive to the emotional content of stimuli (Spear, 2003; Monk et al., 2006). This is cause for concern that adolescents may be especially susceptible to FPSG violence. Indeed, Mathews et al. (2005) found that exposure to media violence modified neural activity in normal adolescents to resemble that of adolescents with Conduct Disorder (CD) with aggressive features.

To understand the impact of FPSG violence on adolescent development this paper will draw insight from the General Aggression Model (GAM) and the interactions between SEEKING and RAGE circuits described in Panksepp (1998). The primary focus of this paper are the mechanisms that underlie the relationship between what seems to be an ordinary form of entertainment (FPSG video games) and the documented and rather extraordinary increase in aggressive behaviour of teens with high rates of engagement in this entertainment. I hypothesize a mechanism of kindling which I will refer to as the kindling model of aggression (KMA) and which is based on the kindling model for seizures and depression as discussed in Kramer (1993).

General Aggression Model (GAM) & FPSG

Two parts of GAM are relevant to FPSG exposure. First, GAM states that physiological arousal, feelings, and thoughts that determine the execution of aggressive acts are the products of personal factors (values, attitude, genetic traits, etc.) and environmental factors (exposure to home violence, exposure to media violence, competitive or cooperative contexts, etc.) combined. This is a loop such that the act committed then reenters the loop as an environmental or personal factor in determining the escalation or de-escalation of subsequent behaviours. This looping may explain why studies show that the more time exposed to violent video games, the higher the aggressive feelings, thoughts, arousal, and behaviours (Barlett et al. 2007; Mathews et al. 2005; Nelson & Carlson 1985; Lin & Lepper 1987; Schutte et.al 1988; Anderson & Dill, 2000; Pance & Ballard 2002).

GAM suggests that the damaging effects of aggression-provoking environmental factors (e.g. FPSG exposure) are dampened by strong contrasting personal factors (such as well developed OFC and dorsal ACC control seen in adults) while stronger aggression-promoting personal factors (such as increased HPA sensitivity to cortisol seen in adolescents) would leave one more susceptible to FPSG exposure. That adolescents are greatly attracted to FPSG in addition to research showing changes to cortical control systems in normal teens exposed to media violence (Mathews et al., 2005) support this paper’s focus on effects of video game violence of adolescents. The second part of GAM states that aggressive thoughts infect neutral thoughts through associative memory until widespread networks of hostile thoughts are formed (Anderson et al. 1998). For example, the concept of [man] might at first have calm associations that conjure up images of males, their jobs, or their relationships to other people. However, after associating the concept of [man] with killing, blood, weapons, and enemy in a FPSG, the associations may change such that [man] now elicits hostile thoughts and feelings and gruesome mental representations. For adolescents, whose salience sensitivity? to the emotional content of stimuli is higher than for that of adults, such associations may be held in…”be mediated by…” the hippocampus, activating the amygdala to produce hostile feelings when in the presence of a man. Stress hormones may also be stimulated when experiencing feelings of threat and hostility thereby activating the HPA and triggering the sensation of anger leading to an aggressive act. This reasoning could explain why adolescent aggressive behaviours may extend after the game ends in situations with no obvious connection to the game content.

SEEKING-RAGE (affective) and SEEKING-aggression (non-affective) Interactions

Panksepp (1998) makes a distinction between SEEKING and RAGE systems. However, he counters that distinction several times with examples that show how RAGE can be triggered by bodily irritation, physical restriction, or anything that produces frustration. This author suggests that neural substraits of anger and the SEEKING system should be linked or shared. Panksepp (1998) believes that, “unfulfilled expectancies within the SEEKING system activate the neural patterns of frustration…reward and expectation mismatches may promote anger by downward neural influences that arouse RAGE circuits.” (p. 189). His schema (Panksepp, 1998, p. 192) places SEEKING at the root of aggression. That is, goal-seeking (assumed to originate in circuits containing the lateral hypothalamus and medial forebrain, i.e., ventral striatum) stimulate the frontal and temporal cortices to set up expectations of the outcome of that seeking. Moyer’s (1976) aggression taxonomy distinguishes types of aggressive acts based on their specific behavioural functions such as maternal aggression, intermale aggression, predatory aggression, and so on (Panksepp, 1998). In some of these – such as predatory aggression and intermale aggression – the SEEKING goal itself is the aggressive act and so anger is at first not a function of this type of aggression. After setting up expectations of outcome of SEEKING goals, the frontal and temporal cortices also appraise situations and emotional states for reward attainment (ie. expectations fulfilled) as well as appraising when rewards are not attained. When the latter occurs there is an expectancy-outcome mismatch that produces the sensation of frustration that activates the RAGE system, producing affective attack. Moyer’s irritable aggression is one example of RAGE-aggression. RAGE-aggression can also be provoked in aggression that began as non-affective (e.g. predatory aggression) if the process towards goal attainment is interrupted or if the process is prolonged beyond the expected time to attain the goal.

Others have also implied that SEEKING is not exclusive but rather influences RAGE activity as well as non-affective aggression (Van Goozen et al., 2007; Dill & Anderson 1995; Barlett 2007). These authors state recent support for causal links between frustration and aggression that was suggested years ago in the frustration-aggression hypothesis (Dollard et al. 1939).

Since it seems the SEEKING-aggression (non-affective)..I wish you wouldn’t call it non-affective. Surely there is affect involved in predation or sexual competition. It’s just that the affect isn’t anger per se…. and SEEKING-RAGE-aggression (affective) relationships are applicable to any aggressive act, FPSG-related aggression should…or “could”… also be explained by both aggression-seeking (where the goal is to perform an aggressive act) and by frustration (where goals are interrupted). Goal-seeking is intrinsic in game performance with expectations encompassing everything from winning points, to obtaining social status, to avoiding “game over”, to even how one expects to feel physically and emotionally while playing the game and after it is over. Examples of FPSG-aggression as a function of aggression-seeking might include violence committed in the virtual environment and the play-fighting with peers. Examples of FPSG-aggression as a function of frustration might include performance errors leading to loss of points or “game over” (indirect RAGE link) and could also stem from physical irritation caused, for instance, by people repeatedly bumping into the player as they walk by (direct RAGE link).

Adolescent Susceptibility to FPSG-induced Aggression

Before the game begins, personal factors determine the responsivity of a typical adolescent to FPSG violence. Younger adolescents undergo a shift in DA input from mesolimbic regions to the PFC and this reduction in mesolimbic DA has been linked to reward-deficiency syndrome (Spear, 2003). Although this syndrome may not be clinically present, younger adolescents may still experience a special attraction to game novelty, simulated risk and violence, and the elation that comes from competition with peers or with the virtual opponents.

Increase in DA to mesocortical regions occurs around the same time that glutamine excitatory drive decreases (Spear, 2003) which can affect serotonergic (5-HT) systems (Van Goozen et al., 2007). Changes to DA and 5-HT during adolescence have been implicated in mental health and conduct. Disruptions to 5-HT affects HPA axis responsivity to cortisol resulting in stress while disruptions to 5-HT input to hypothalamic, frontal, hippocampal, amygdala, and striatal regions can precipitate aggression (Van Goozen et al., 2007).

Adolescents can become emotionally aroused during FPSG. Monk et al. (2006) show combined amygdala, OFC, and ACC activity in a goal-directed task indicating high salience of emotional content of stimuli particularly for adolescents. Since emotional arousal facilitates learning/structural reorganization, adolescents may be more susceptible to the influence of violence.

Finally, obtaining the rewarding effects of the game features (risk, violence, novelty, competition, and social status) is a key reason for engaging in game play and is evidence of the activation of SEEKING circuits. Thus, adolescents’ neural settings are primed for aggression via the SEEKING-interruption-frustration-aggression link even before the game begins.

Cortical Control

Violent video games activate SEEKING of rewarding sensations of the game features mentioned above and of game-specific rewards such as gaining points, moving up levels of difficulty, continuing play/ avoiding “game over”, etc. Additional expectations about one’s performance, the game script, and the anticipated excitement of engaging in play and perhaps of winning create more opportunities for interrupted SEEKING activity. Since goal-seeking appears to be inherent in game performance, frustration and aggression may be a function of FPSG.

Neural structures of the SEEKING system include the lateral hypothalamus and medial frontal cortex (Panksepp, 1998).….but more importantly the ventral striatum (part of the basal ganglia) Expectations (goals) and whether those expectations have been met (rewards) or not met (leading to the sensation of frustration) are processed in frontal and temporal cortices (e.g. PFC, OFC). The PFC is involved in appraising goals and emotions to evaluate whether getting angry and acting out are “worth it” or whether to reappraise the situation and set new goals that promote calming down. The PFC interacts with the ACC which now determines the messages that will be sent to the amygdala, brainstem, and motor cortex to escalate or deescalate emotions and behaviours that satisfy the PFC’s latest revised goals. Via vertical integration, the behaviours and emotions set into action by the ACC also influence the continued reappraisals of the PFC during this cyclical cortical control process.

The amygdala connects via the hypothalamus (involved in the SEEKING system and thus indicating the structural neural link between SEEKING and RAGE) to the PAG which connects to reflexive motor outputs (Panksepp, 1998). Therefore stress response of the hypothalamus should directly activate the dorsal PAG causing rage-aggression.….mostly correct…but it isn’t “stress” until it runs downstream from the HPTH to the ANS… This may occur during game play (e.g. if controls malfunction resulting in performance errors) and may also occur outside of the game (according to GAM’s aggressive networks theory). Stimulus-bound emotional reactions of the amygdala should also activate RAGE circuits and again according to GAM’s aggressive networks theory, anger-eliciting stimuli do not necessarily need to have direct links with the FPSG. Escalatory signals to the amygdala by the PFC via the ACC may also eventually lead to affective-attack both during and outside of the game.

A certain amount of aggression is accepted in the arcade and in certain peer groups. Mathew’s (2005) study showed decreased ACC activity in teens with high media violence exposure. Therefore, adolescents that practice not inhibiting aggressive behaviours in games and among aggressive peers may have difficulty activating the dorsal ACC when in situations where this conduct is unacceptable.

Kindling Model of Aggression (KMA)

“Kindling” generally refers to the way sparks from a heat source can ignite small pieces of flammable material like dry grass and this small heat can eventually spread to engulf large tree limbs and even entire forests in a blazing fire. The analogy was originally used to explain the tendency for seizures to recur with decreasing stimulation and to eventually spread across brain areas that were not directly stimulated. This idea was later used to model the neurological processes of depression (Kramer, 1993). Stress hormones are implicated in cell death and other structural reorganization via its effects on physiological and psychological functioning that can lead to depression (Kramer, 1993). Repeated and prolonged stress has been linked with higher levels of depression. In accordance with kindling principles, one becomes sensitized to stress which can be triggered by direct and associated stimuli. Stress “carves out” neural paths that allow triggers to easily and frequently activate episodes of depression. As mentioned before, adolescence is associated with increased sensitivity of the HPA-axis to stress, increase in cortisol secretion, occurrence of depression, and higher salience to emotional qualities of stimuli. KMA proposes that these combined factors promote proliferation and pruning of synapses and cellular reorganization in general and in particular for FPSG-induced stress. FPSG may stimulate cortisol when frustration or anxiety occurs, or even in the mere effort to avoid frustration (e.g. avoid “game over”) or avoid acting on aggressive impulses (ie. self-regulation processes). FPSG stress may contribute to the kind of learning that constitutes kindling thereby increasing aggression during play and then spreading to real-life situations.

In other words, teens at first will experience stress from game performance, expectation-reward appraisals, effortful emotional-regulation of frustrations that may arise, and so forth. While experiencing this stress, they practice reacting in the arcade setting with virtual violence and rough-housing with peers, and sometimes with anger. The longer and more frequently teens engage in FPSG, the greater the sensitivity to stress. The greater the sensitivity to stress, the less stressing triggers needed to provoke an aggressive response. At the same time there is also that aspect of kindling where triggers of aggression may not have any obvious connection to FPSG. Together, all this translates into increasing aggression in daily life outside of the arcade.

Summary…more like “Conclusion”

No explicit information was found that distinguishes the types of aggression that increased in adolescents with high exposure to FPSG. With the rationales made in this paper I can only speculate that of Moyer’s taxonomy, affective attack, predatory, intermale, territorial aggression, sex-related, fear-induced and irritable aggression all are influenced. by FPSG violence. It is probable that adolescent HPA sensitivity to cortisol resulting in greater experience of stress not only has a kindling effect on adolescent depression but also on aggression when combined with exposure to violent video games. Emotional and physiological arousal during FPSG produced by higher salience to emotional features of stimuli promotes synaptic shaping of the sort that can be viewed as kindling. With more exposure to FPSG comes more stress resulting from expectation-fulfillment mismatches and from the effort to avoid frustration and disappointment. Stress is notorious for its ability to cause structural changes and for carving-out information pathways that facilitate repeated stress and neural changes. FPSG-induced kindling may cause neural activity in normal teens to resemble those in adolescents with CD. That would include under-activation of the left amygdala and right dorsal ACC (Sterzer et al., 2007). Impaired amygdala functioning translates into difficulty using social cues to help regulate emotion, misinterpretation of threats, fear and other negative responses, or inability to experience emotions like fear or empathy that suppress the desire to act aggressively. Since the ACC is integral in the communication between several mesocortical and mesolimbic structures, reduced ACC activation means that conflict and error-monitoring ability is also reduced as well as overall emotion processing including emotion regulation. These are the problems found in clinical diagnoses with aggressive features. Mathews et al. (2005) showed that normal adolescents’ neural functions during an inhibitory task resembled those with CD when they had as high or higher amounts of media violence exposure. This is a reason to speculate that the increase in aggression with exposure to FPSG violence may indeed be explained by a form of kindling that could result in entrenchment of aggressive pathways in the SEEKING and RAGE circuits as well as damage to amygdala and ACC and other areas involved in behavioural inhibition.

The scope of this paper was limited to suggestions of the mechanisms behind the rise in aggressive behaviour in adolescents who engage frequently and for longer periods in FPSG. Several additional issues remain to be explored. If stress (from frustration, anger, and the effort to avoid these) can lead to structural reorganization promoting more sensitivity to stress and increasing the number of triggers of stress, then would adolescents with symptoms of clinical depression (also theorized to result from stress kindling) be more susceptible to the aggressive effects of FPSG? Conversely would those who live in less stressful environments and have genetically less stressed personalities exhibit less aggressiveness than others? Could it be that FPSGs attract one of these types of adolescents? Is the speculated structural damage persistent or reversible once frequency of FPSG play diminishes? Do adults who have spent more time in childhood and adolescence playing FPSGs differ from those with less exposure in terms of behavioural inhibition and efficiency of emotional-regulation when expectations of the SEEKING system are unfulfilled? The answers to these questions will tell us whether we need more than just age-ratings on video games as exists now. They will give us the information we need to make truly safe choices in entertainment for our youth.

Comments:

Splendid paper. I commented a lot more than I usually do because I was very intrigued. To summarize, I think that you worked very hard to bring together a lot of different neural and psychological constructs to fashion a truly comprehensive paper, presenting an original and persuasive model. I’m very impressed by the originality of the work. And by the precision, detail, and sophistication of the writing itself. The level of detail was admirable! And a lot of the neurobiology was accurate, though not all of it. You are showing a real, workable, and rich knowledge base in an area in which you were no expert at the start of the term, and that’s impressive! As I say, the writing itself was refined and polished, making the meanings come through with clarity and precision. But one kind of weakness that showed up a few times was a sort of squishing together of important points into a very condensed sentence or two. By doing this, you missed some of the logic completely, got some of your points confused, and generally did more harm than good. It’s better to limit the scope and number of propositions you are putting out, but to explicate each one patiently and clearly. That’s one way to figure out whether you really know what you’re trying to say, or whether it’s not clear enough in your own mind to leave for another time. In any case, you tried to put so much into one 12-page paper, it was nearly impossible to do each point justice. It might have been better to restrict yourself to something a little less comprehensive, so that you could provide adequate discussion of the main points.

Paper: A/A+

References

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