Abstract：
Scholars have established subcategories of aggressive behavior in order to better understand this construct. Specifically, a classification based on motivational underpinnings makes it possible to differentiate between reactive and proactive aggression. Whereas reactive aggression is characterized by emotional lability, which means it is prone to impulsive reactions after provocation, proactive aggression is driven by low emotionality and high levels of instrumentality to obtain benefits. Some authors have conceived these two types as having a dichotomous nature, but others argue against this conceptualization, considering a complementary model more suitable. Hence, neuroscientific research might help to clarify discussions about their nature because biological markers do not present the same biases as psychological instruments.
The main objective of this study was to carry out a systematic review of studies that assess underlying biological markers (e.g., genes, brain, psychophysiological, and hormonal) of reactive and proactive aggression.
To carry out this review, we followed PRISMA quality criteria for reviews, using five digital databases complemented by hand-searching.
The reading of 3993 abstracts led to the final inclusion of 157 papers that met all the inclusion criteria. The studies included allow us to conclude that heritability accounted for approximately 45% of the explained variance in both types of aggression, with 60% shared by both, especially, for overt and physical expression forms, and 10% specific to each type. Regarding allelic risk factors, whereas low functioning variants affecting serotonin transport and monoaminoxidase increased the risk of reactive aggression, high functioning variants were associated with proactive aggression. Furthermore, brain analysis revealed an overlap between the two types of aggression and alterations in the volume of the amygdala and temporal cortex. Moreover, high activation of the medial prefrontal cortex (PFC) facilitated proneness to both types of aggression equally. Whereas stimulation of the right ventrolateral (VLPFC) and dorsolateral (DLPFC) reduced proneness to aggression, inhibition of the left DLPFC increased it. Finally, psychophysiological and hormonal correlates in general did not clearly differentiate between the two types because they were equally related to each type (e.g., low basal cortisol and vagal variability in response to acute stress) CONCLUSIONS: This study reinforces the complementary model of both types of aggression instead of a dichotomous model. Additionally, this review also offers background about several treatments (i.e., pharmacological, non-invasive brain techniques…) to reduce aggression proneness.
The main objective of this study was to carry out a systematic review of studies that assess underlying biological markers (e.g., genes, brain, psychophysiological, and hormonal) of reactive and proactive aggression.
To carry out this review, we followed PRISMA quality criteria for reviews, using five digital databases complemented by hand-searching.
The reading of 3993 abstracts led to the final inclusion of 157 papers that met all the inclusion criteria. The studies included allow us to conclude that heritability accounted for approximately 45% of the explained variance in both types of aggression, with 60% shared by both, especially, for overt and physical expression forms, and 10% specific to each type. Regarding allelic risk factors, whereas low functioning variants affecting serotonin transport and monoaminoxidase increased the risk of reactive aggression, high functioning variants were associated with proactive aggression. Furthermore, brain analysis revealed an overlap between the two types of aggression and alterations in the volume of the amygdala and temporal cortex. Moreover, high activation of the medial prefrontal cortex (PFC) facilitated proneness to both types of aggression equally. Whereas stimulation of the right ventrolateral (VLPFC) and dorsolateral (DLPFC) reduced proneness to aggression, inhibition of the left DLPFC increased it. Finally, psychophysiological and hormonal correlates in general did not clearly differentiate between the two types because they were equally related to each type (e.g., low basal cortisol and vagal variability in response to acute stress) CONCLUSIONS: This study reinforces the complementary model of both types of aggression instead of a dichotomous model. Additionally, this review also offers background about several treatments (i.e., pharmacological, non-invasive brain techniques…) to reduce aggression proneness.
摘要：
为了更好地理解这种结构，学者们已经建立了攻击性行为的子类别。具体来说,基于动机基础的分类可以区分反应性和主动性侵略。而反应性侵略的特征是情绪不稳定，这意味着它在挑衅后容易发生冲动反应，积极主动的侵略是由低情绪化和高水平的获取利益的工具驱动的。一些作者认为这两种类型具有二分法性质，但是其他人反对这种概念化，考虑一个更合适的互补模型。因此，神经科学研究可能有助于澄清有关其性质的讨论，因为生物标记物与心理学工具不存在相同的偏见。
本研究的主要目的是对评估潜在生物学标记的研究进行系统综述（例如，基因，大脑,心理生理学，和荷尔蒙）的反应性和主动性侵略。
为了进行这项审查，我们遵循PRISMA质量标准进行审查，使用五个数字数据库，辅以手工搜索。
阅读了3993篇摘要，最终纳入了符合所有纳入标准的157篇论文。这些研究使我们能够得出结论，在这两种类型的攻击中，遗传力约占解释方差的45％。两者共有60%，尤其是,对于公开的和物理的表达形式，和10%特定于每种类型。关于等位基因风险因素，而影响5-羟色胺转运和单氨氧化酶的低功能变体增加了反应性攻击的风险，高功能变异与主动攻击相关.此外，大脑分析显示，两种类型的攻击与杏仁核和颞叶皮层体积的改变之间存在重叠。此外，内侧前额叶皮层（PFC）的高度激活同样促进了两种攻击的倾向性。右腹外侧（VLPFC）和背外侧（DLPFC）的刺激降低了攻击的倾向性，左侧DLPFC的抑制增加了它。最后,心理生理学和激素相关性通常没有明确区分这两种类型，因为它们与每种类型的相关性相同(例如，对急性应激的低基础皮质醇和迷走神经变异性）结论：这项研究加强了两种类型侵略的互补模型，而不是二分法模型。此外,这篇综述还提供了几种治疗方法的背景(即，药理学,非侵入性大脑技术...)以减少攻击性倾向。
本研究的主要目的是对评估潜在生物学标记的研究进行系统综述（例如，基因，大脑,心理生理学，和荷尔蒙）的反应性和主动性侵略。
为了进行这项审查，我们遵循PRISMA质量标准进行审查，使用五个数字数据库，辅以手工搜索。
阅读了3993篇摘要，最终纳入了符合所有纳入标准的157篇论文。这些研究使我们能够得出结论，在这两种类型的攻击中，遗传力约占解释方差的45％。两者共有60%，尤其是,对于公开的和物理的表达形式，和10%特定于每种类型。关于等位基因风险因素，而影响5-羟色胺转运和单氨氧化酶的低功能变体增加了反应性攻击的风险，高功能变异与主动攻击相关.此外，大脑分析显示，两种类型的攻击与杏仁核和颞叶皮层体积的改变之间存在重叠。此外，内侧前额叶皮层（PFC）的高度激活同样促进了两种攻击的倾向性。右腹外侧（VLPFC）和背外侧（DLPFC）的刺激降低了攻击的倾向性，左侧DLPFC的抑制增加了它。最后,心理生理学和激素相关性通常没有明确区分这两种类型，因为它们与每种类型的相关性相同(例如，对急性应激的低基础皮质醇和迷走神经变异性）结论：这项研究加强了两种类型侵略的互补模型，而不是二分法模型。此外,这篇综述还提供了几种治疗方法的背景(即，药理学,非侵入性大脑技术...)以减少攻击性倾向。
