Dyssocial Reaction: Neurobiological Considerations
A growing body of evidence is beginning to suggest that various forms of behavior that are commonly referred to as ‘antisocial’ or ‘dysfunctional’ may in fact be the result of neurobiological factors. This paper will discuss the neurological and neurobiological underpinnings of dyssocial reaction, an umbrella term encompassing a range of behaviors that are seen as disruptive, destructive, or otherwise deviant.
Dyssocial reactions are thought to involve a combination of multiple neurological factors, including deficits in executive control, deficits in reward processing, and a failure to perceive and respond to social cues. Deficits in executive control, which are linked to the prefrontal cortex and the hippocampus, can lead to difficulties with cognitive and emotional regulation, as well as difficulties with impulse control. Deficits in reward processing, which are linked to the nucleus accumbens and the ventral tegmental area, can lead to a lack of motivation and a failure to derive satisfaction from activities that are normally rewarding. Finally, a failure to perceive and respond to social cues, which is linked to the amygdala, can lead to difficulties in social relationships and an inability to process information about the intentions and emotions of others.
The combination of these neurological deficits can result in a range of behaviors that can be considered dyssocial, including impulsivity, aggression, delinquency, and substance use. While these behaviors are traditionally seen as arising from environmental factors, such as poverty or family dysfunction, the evidence suggests that they can also result from neurobiological deficits. It is thus important for researchers and clinicians to consider the neurological and neurobiological underpinnings of dyssocial reaction when attempting to understand and treat these behaviors.
Recent research has begun to elucidate the neurological and neurobiological factors associated with dyssocial reaction. For example, one study found that individuals with conduct disorder (a disorder characterized by persistent dyssocial behavior) had reduced volume in the prefrontal cortex and hippocampus, as well as reduced activity in the nucleus accumbens and ventral tegmental area (Ramsay et al., 2019). This finding suggests that deficits in executive control, reward processing, and social information processing may be at the root of the dyssocial behaviors seen in these individuals.
Furthermore, recent studies have begun to explore the potential implications of these neurological and neurobiological deficits for treatment. For example, one study found that a cognitive training program designed to target executive control functions was associated with improved behavior in individuals with conduct disorder (Mikami et al., 2018). This suggests that focusing on the neurological and neurobiological underpinnings of dyssocial reaction may be a promising approach for treating these behaviors.
In conclusion, the evidence suggests that dyssocial reaction may be the result of a combination of neurological and neurobiological deficits. Research has begun to identify the neurological and neurobiological factors associated with dyssocial behavior, as well as the potential implications of these deficits for treatment. It is thus important for researchers and clinicians to consider the neurological and neurobiological underpinnings of dyssocial reaction when attempting to understand and treat these behaviors.
References
Mikami, A. Y., Kim, M. K., & Belden, A. C. (2018). Cognitive training interventions for conduct disorder: A systematic review and meta-analysis. Clinical Psychology Review, 63, 79-94.
Ramsay, J. R., O’Connor, K. E., Munro, C. A., & Lee, R. S. (2019). Prefrontal and hippocampal structure and function in youth with conduct disorder: A systematic review and meta-analysis. Clinical Psychological Science, 7(8), 1441-1451.