Past research suggests an association between reactive aggression and alexithymia, but neural mechanisms underlying this association remain unknown. Furthermore, the relationship between proactive aggression and alexithymia remains untested. This study aimed to: (1) test whether alexithymia is more related to reactive than proactive aggression; and (2) determine whether amygdala, insula, and/or anterior cingulate cortical (ACC) volume could be neurobiological mechanisms for this association. One hundred and fifty-six community males completed the Reactive-Proactive Aggression Questionnaire and the Toronto Alexithymia Scale. Amygdala, insula, and ACC volumes were assessed using MRI. Alexithymia was positively associated with reactive but not proactive aggression. Alexithymia was positively and bilaterally associated with amygdala and anterior cingulate volumes. Reactive aggression was positively associated with right amygdala volume. Controlling for right amygdala volume rendered the alexithymia-reactive aggression relationship non-significant. Results suggest that increased right amygdala volume is a common neurobiological denominator for both alexithymia and reactive aggression. Findings suggest that greater right hemisphere activation may reflect a vulnerability to negative affect, which in turn predisposes to experiencing negative emotions leading to increased aggression. Findings are among the first to explicate the nature of the alexithymia-aggression relationship, with potential clinical implications.
There is a growing literature on biological explanations of antisocial and criminal behavior. This paper provides a selective review of three specific biological factors – psychophysiology (with the focus on blunted heart rate and skin conductance), brain mechanisms (with a focus on structural and functional aberrations of the prefrontal cortex, amygdala, and striatum), and genetics (with an emphasis on gene-environment and gene-gene interactions). Overall, understanding the role of biology in antisocial and criminal behavior may help increase the explanatory power of current research and theories, as well as inform policy and treatment options.
Increased aggression and impulsivity represent a key component of several psychiatric disorders, including substance use disorder, which is often associated with deficient prefrontal brain activation. Thus, innovative tools to increase cognitive control are highly warranted.
The current study investigates the potential of transcranial direct current stimulation (tDCS), a tool to modulate cortical activation, to increase cognitive control in individuals with a high potential for impulsive and aggressive behavior.
In a double-blind, sham-controlled study, we applied anodal tDCS over the right dorsolateral prefrontal cortex in an all-male sample of alcohol dependent patients (AD), tobacco users (TU) and healthy controls (HC) who completed the Taylor Aggression Paradigm and Stop Signal Task twice.
While there were no observable effects of tDCS in controls, results revealed altered aggressive behavior in AD following active stimulation. Specifically, these individuals did not show the standard increase in aggression over time seen in the other groups. Furthermore, improved response inhibition was found in AD and TU following active but not sham stimulation.
Our study demonstrates that prefrontal tDCS improves our laboratory measure of impulse control in at-risk groups, illustrating the importance of sample characteristics such as nicotine intake and personality traits for understanding the effects of brain stimulation.
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