Impairments in some brain regions and a lack of aggression regulation

Started by Volunto, Feb 07, 2023, 06:52 PM

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Before further analysis of the neurophysiology of aggression inhibition, we should divide it into proactive (instrumental) and reactive (affective) forms. Reactive aggression arises as a reaction of the subject to a certain stimulus (including a threat stimulus that can lead to self-defense) or as a result of frustration. In turn, proactive aggression consists in achieving a certain positive result by resorting to aggressive actions; it is a planned and motivated act of harming the victim.

The amygdala plays the main role in the regulation of aggression, being involved in the formation of emotions and conditioned reflex reactions, as well as the ventromedial prefrontal cortex (or orbitofrontal cortex), which is involved in the decision-making process. Together, they regulate the neural circuit that mediates reactive aggression (this network includes the medial hypothalamus and periaqueductal gray) and regulates the subcortical systems that respond to threats (among them, the basal ganglia, including the striatum). Both impairments of the amygdala and the orbitofrontal cortex can lead to an increase in the level of reactive aggression. At the same time, the orbitofrontal cortex does not inhibit reactive aggression but only increases or decreases the chance of triggering this process, depending on the surrounding social signals. The neural circuit that mediates proactive aggression is regulated by the amygdala (it includes the temporal lobe, which processes information, as well as the striatum and premotor cortex, which are necessary for the implementation of actual behavior).

Psychopaths are characterized by an increased level of proactive aggression. They also show impairments in empathic response and regulation of fear-related behavior, which are the result of amygdala dysfunction. But psychopaths are not like other patients with amygdala dysfunction. Other functions of the amygdala, such as the formation of incentive and reward associations and certain aspects of social cognition, are only mildly or not impaired at all in individuals with psychopathy. The reason for this may be the presence of a genetic anomaly, which, instead of leading to extensive dysfunction of the amygdala, acts pointwise, disrupting the work of individual neurotransmitters.

Let us now turn to a framework for understanding conduct disorder, which confirms that it is the dysfunction of the amygdala and ventromedial prefrontal cortex that leads to disorders associated with aggressive behavior. Traits of psychopathy and CU-traits are associated with reduced emotional empathy. This is a result of reduced sensitivity of these brain regions to distress cues (as we know, the observation of signals such as expressions of sadness, fear, and pain from other people leads to direct activation of the violence inhibitor in humans).

Based on this framework, we get the following: genetic factors lead to decreased amygdala responsiveness, which in turn reduces the empathic response, and this is the cause of aggression from CU-traits, antisocial behavior, and instrumental aggression. Another cause of antisocial behavior and instrumental aggression, as well as under-regulated responses to social provocations and reactive aggression based on frustration, is an impairment in the ability to make decisions, which in turn comes from decreased responsiveness of the striatum and ventromedial prefrontal cortex. Genetic influence also plays a significant role here. In addition, the occurrence of dysfunction in one of the brain regions is associated with dysfunctions in others. Thus, with decreased responsiveness of the amygdala, one would expect decreased responsiveness of the striatum and ventromedial prefrontal cortex. Environmental factors such as trauma, exposure to abuse, and neglect in upbringing only play a role in increased amygdala responsiveness, resulting in greater sensitivity to threats. However, even here genetic influence is involved, as it is present in all the components considered by this framework.

From the neurophysiological evidence, it is also worth noting that measurement of the binding potential of 5-HT1B receptors using positron emission tomography demonstrated its lower level in the anterior cingulate cortex, orbitofrontal cortex, and striatum in people with a high level of aggressive traits. At the same time, in the case of the striatum, the connection with psychopathic traits was also found.

Finally, we should also note that one of the studies showed that the stability in reactive aggression from childhood to adolescence could be explained by genetic (48%), shared (11%), and nonshared (41%) environmental influences, whereas the continuity in proactive aggression was primarily genetically (85%) mediated. According to a study of the genetic risk of psychopathy in 7-year-old children, the presence of both сallous-unemotional traits and antisocial behavior has an extremely high level of heredity - 81%. At the same time, if children have only antisocial behavior, a moderate level of heredity is observed - 30% [80]. The difference between these two groups of children lies in the fact that the members of the first group, who have сallous-unemotional traits, are capable precisely of deliberate antisocial behavior and violence. They have a high risk of developing psychopathy and violent criminality in adulthood and are also difficult to educate. Their condition is more aggravated than the condition of children from the second group, whose behavior problems are not so serious and long-term. It is also worth mentioning that at an older age, a strong genetically mediated stability of сallous-unemotional traits is still preserved. Thus, between 17 and 24 years it is 58%.