The Meaning of Aggression - Essay Sample

Introduction

Aggression can be categorized in many ways. For instance, it can be classified based on the cause of aggression (such as medical-related causes), the mode of aggression (e.g. indirect, direct, or verbal aggression), and the target of aggression (other-directed or self-directed). The most widely employed classification of aggression is impulsive versus premeditated aggression. In premeditated aggression, the individual's behavior is planned and not linked to frustration or response to any threat in the environment. This type of aggression has also been described as proactive, instrumental, or predatory (Blair, 2004, p. 198). This type of aggression is not always accompanied by autonomic arousal and is planned with clear goals in the mind of the individual performing the act. Conversely, impulsive aggression is linked to high levels of autonomic arousal and precipitation linked to negative emotions, especially fear and anger (Meloy, 2006, p. 539). This type of aggression is a response to perceived to perceived stress (Meloy, 2006, p. 539).

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It can also be described as a persistent pattern of antisocial and aggressive behaviors that violate social norms and rights of other individuals, and that is part of the general class of Disruptive Behavioral Disorders. These disorders are at high prevalence at the adolescent stage of development and are highly prevalent in the male population with health cost implications to the family, the society, and the public health (Romeo et al., 2006, p. 547). Current estimates suggest that aggression is found in at least 3.6% of males and 1.5% of the females (Erskine et al., 2013, p. 1263) and has been established to lead to about 6 million years living with a disability (Erskine et al., 2014, p. 328).

Findings of past empirical studies have linked the neural basis of aggression to many factors. Some of these factors include hypo-activation of amygdala responses, increased left-sided amygdala activation in sight of threats, prefrontal cortical lesions leading to disinhibited aggression, damage to ventromedial prefrontal cortex, the presence of frontal lobe injuries such as orbitofrontal cortex. Additionally, decreased volume of prefrontal gray matter leads to aggression. Lastly, lesions in the medial amygdala and anterior hypothalamus lead to aggressive behaviors. On the other hand, electrical stimulation of the anterior hypothalamus, the amygdala, and the ventromedial hypothalamus have been associated with elevated levels of aggressive behaviors.

Causes of Aggression

Amygdala and Prefrontal Cortex

The neurological underpinnings of aggression have been extensively studied in empirical studies. For example, it has been reported that reactive aggression is attributable to abnormal activations in areas instrumental in promoting the regulation of emotions and emotional reactivity in adolescents with conduct disorders compared with their counterparts without the disorder. Other studies have also associated aggressive behaviors, such as conduct problems, to hypo-activation of amygdala responses which results in abnormal emotional reactivity processing characterized by sadness in aggression compared to controls (Passamonti et al., 2010, p. 729). On the other hand, other studies have linked aggression to hyperactivity of the amygdala, especially elevated left-sided amygdala activation when exposed to negative images (Herpertz et al., 2008, p. 781).

Empirical studies on anger and aggression have revealed the vital role of the prefrontal cortex underpinning aggression (Erskine et al. 2014, p. 429). For instance, Erskine et al. (2014, p. 429) reported that the underlying basis of repeated occurrence of aggression is associated with failure of "top-down" control systems in the prefrontal cortex to modulate aggressive behaviors that are activated by anger-provoking stimuli.

Cortex and Its Role in Aggression

The crucial role played by the prefrontal control in aggression, and antisocial behaviors were first discovered in the context prefrontal cortical lesions leading to disinhibited aggression. These lesions arise due to metabolic disturbances, tumors, and trauma affecting the prefrontal cortex. A key example of disinhibition is commonly explained with reference to Phineas Gage, a railroad employee who underwent injury involving penetration of the skull by a tamping rod which reached the orbital frontal cortex. Consequently, Phineas Gage showed increased anger, irritability, and decreased social judgement. It has also been established that decreased real-world competence arises when the ventromedial prefrontal cortex is damaged leading to severely disrupted emotion. Specifically, according to Anderson et al. (2006, p. 224), damage to the ventromedial prefrontal region leads to disrupted emotion leading to impairment of real-world competencies. In their study, Anderson et al. (2006, p. 224) established that both adult-onset and childhood-onset damage to ventromedial prefrontal region lead to the same level of severity of long-term impairments regarding diminished real-world competence.

It has also been reported that individuals with frontal lobe injuries, including orbitofrontal cortex, are more inclined towards physically intimidating others and using threats in conflict situations. Specifically, Grafman et al. (1996, p. 1231) reported that patients exhibiting frontal ventromedial lesions have higher aggression or violence tendencies than controls and patients with lesions in other brain areas. Additionally, higher violence and aggression scores in patients with frontal ventromedial lesions were found to engage in verbal conflicts rather than in physical assaults. The presence of aggression and violence in these patients were not linked to the total size of the lesion.

Grafman et al. (2011, p. 8) carried out a study to establish the changes in brain activation when an individual is engaged in imagined physical aggression and also examined the thickness of cortex of healthy male adolescents aged 14 to 17 years. Findings of this study showed that imagined aggression is linked to decreased activation in the ventromedial prefrontal cortex and elevated activity in the visual cortex. Grafman et al. (2011, p. 8) further discussed the social-cognitive mechanisms that explain the influence of aggressive situation cues on decreased activation of the ventromedial prefrontal cortex. The researchers posited that the ventromedial prefrontal cortex reenacts the social event knowledge based on simulation mechanisms.

Because the ventromedial prefrontal cortex has reciprocal linkages with brain regions that are linked to processing of emotional information (amygdala), higher-order sensory processing (temporal visual association areas), reward processing (basal ganglia), and memory (hippocampus), it is highly adapted to seize the reward and affective value that accompanies experiences in social situations (Grafman et al., 2011, p. 8). For instance, when a person experiences aggression in real life, such as through media, the ventromedial prefrontal cortex captures various examples of such situations leading to the establishment of a summary representation that comprises of a multi-modal representation found all over the brain's association and modality-precise regions. The summary representation is the basis of the cognitive structure needed to develop traits involved in organizing and guiding a person's prospective behavior in future social interactions (Grafman et al., 2011, p. 8).

Structural Imaging Studies

Structural imaging studies have revealed natural variation in volumes and shapes of brain structures, unlike lesion studies which evaluate the impact of the injury to specific brain regions. The decreased prefrontal gray matter that probably underpins aberrant development are found in people with antisocial personality disorder and are often linked to autonomic deficits. A substantial decrease in the volume of brain structures has also been found in the right anterior cingulate cortex and left orbital frontal cortex of such patients mostly seen in Brodmann's area 24.

Hypothalamus and Aggression

Studies carried out in animals have also been vital in understanding the neurological basis of aggression. Most of these studies have involved non-human primates and rodents and have largely been carried out using lesion studies. In these studies, lesions found in the medial amygdala and anterior hypothalamus have been linked to decreased aggressive behaviors. This means that these areas are vital for aggression response. Conversely, electrically stimulating the anterior hypothalamus, the amygdala, and the ventromedial hypothalamus has been established to lead to increased aggressive behaviors.

Moreover, electrically stimulating the periaqueductal gray or the anterior hypothalamus in cats have been also found to lead to defensive behaviors similar to those that are naturally shown by animals or people when they are threatened. Furthermore, a diverse range of prefrontal cortex regions has been linked to aggression network, specifically the orbitofrontal cortex. According to Machado and Bachevalier (2006, p. 761), lesions occurring in the orbitofrontal cortex have been established to play a significant role in the development of aggressive behaviors, indicating that these regions are involved in the regulating aggressive behaviors through inhibitory control function.

Experiments involved human beings have further confirmed the importance of lesions in the development and expression of aggression. Specifically, human lesion and brain injury studies have established the same results as those found in animal studies. Lesions occurring in the orbitofrontal cortex in human beings have linked to elevated levels of reactive aggression in people known to have 'acquired sociopathy.' Similarly, frontal brain injuries involving orbitofrontal cortex has been found to lead to enhanced aggressive activity than those occurring in other regions of frontal brain injury. Likewise, lesions to neighboring ventromedial prefrontal cortex have been linked to elevated aggression in veterans than in veterans with lesions to other areas and to healthy controls. Similarly, high levels of aggressive behaviors that occur after the removal or injury to the orbitofrontal cortex and the ventromedial prefrontal cortex indicate that these regions are involved in the regulation of aggressive responses, such that higher arousal in these areas result in stronger suppression of an aggressive response.

Neuroimaging Studies

The advances in neuroimaging studies have also resulted in a convergence of evidence concerning findings of animal models of aggressive behaviors and lesion studies in human beings. Specifically, neuroimaging has revealed that elevated levels of reactive aggression are associated with high levels of responsivity, especially within the amygdala, when a person is watching threatening images or negatively valenced ones compared to non-threatening faces. Conversely, other studies have linked the presence of increased aggression to the activation of insular cortex following exposure to angry faces. The hypothalamus, insular cortex, and amygdala constitute the limbic system responsible for the processing of threat and salience (Gilam and Hendler, 2017, p. 257).

Moreover, neuroimaging studies have established increased ventromedial prefrontal cortex and orbitofrontal cortex activity during aggression for a healthy developing adult but a decline in activity in people with high levels of reactive aggression. Overall, aggression has been found to depend on limbic areas such as the periaqueductal gray, hypothalamus, and amygdala (Panksepp, 2004, p. 196), with the ventromedial prefrontal cortex and orbitofrontal cortex (the prefrontal...