Haller József, Kruk Menno R
Institute of Experimental Medicine, P.O. Box 67, 1450 Budapest, Hungary.
Neurosci Biobehav Rev. 2006;30(3):292-303. doi: 10.1016/j.neubiorev.2005.01.005.
We review here aggression-related human psychopathologies and propose that human aggressiveness is mainly due to three major factors: (i) brain dysfunction affecting aggression-controlling brain centers (e.g. in certain types of brain lesions, epilepsy, Alzheimer disease, etc.); (ii) hypoarousal associated with chronically low plasma glucocorticoids, which foster violence by diminishing emotional barriers that limit such behaviors (e.g. in conduct disorder and antisocial personality disorder); (iii) hyperarousal which leads to irritability and outbursts (e.g. in depression, intermittent explosive disorder, chronic fatigue, etc.). Different disorders are associated with different types of aggressiveness; e.g. hypoarousal is often associated with instrumental aggression, whereas hyperarousal is associated with uncontrollable outbursts. Many psychological disorders have been simulated in laboratory models, which were used to assess aggressiveness. Little effort was invested, however, in assessing the abnormal dimension of such aggressiveness. We present here three models that appear especially suitable to assess abnormal aspects of rodent aggression: (i) abnormal attack targeting (head, throat, and belly) that is induced by hypoarousal in rats and models violence in hypoarousal-driven human aggression (ii) 'escalated' aggression (increased aggressive response due to frustration or instigation), which models irritability and hyperarousal-driven aggressiveness; and (iii) context-independent attacks induced by hypothalamic stimulation or genetic manipulations. These three models address different aspects of abnormal aggressiveness, and can become extremely useful in three areas: in evaluating and assessing models of human psychopathologies, in studying transgenic animals, and in developing new treatment strategies. Research based on these or similar models do not address aggressiveness in quantitative terms, but follows the development of abnormal aspects, and the possibilities of their specific treatment.
我们在此回顾与攻击行为相关的人类精神病理学，并提出人类攻击性主要归因于三个主要因素：（i）影响攻击行为控制脑区的脑功能障碍（例如在某些类型的脑损伤、癫痫、阿尔茨海默病等中）；（ii）与血浆糖皮质激素长期处于低水平相关的低唤醒状态，这种状态通过削弱限制此类行为的情感障碍来助长暴力行为（例如在品行障碍和反社会人格障碍中）；（iii）导致易怒和爆发的高唤醒状态（例如在抑郁症、间歇性爆发障碍、慢性疲劳等中）。不同的障碍与不同类型的攻击性相关；例如，低唤醒状态通常与工具性攻击相关，而高唤醒状态与无法控制的爆发相关。许多心理障碍已在实验室模型中得到模拟，这些模型被用于评估攻击性。然而，在评估这种攻击性的异常维度方面投入的精力很少。我们在此介绍三种似乎特别适合评估啮齿动物攻击行为异常方面的模型：（i）由大鼠低唤醒状态诱导的异常攻击目标（头部、喉咙和腹部），它模拟低唤醒驱动的人类攻击行为中的暴力；（ii）“升级”攻击（由于挫折或煽动而增加的攻击反应），它模拟易怒和高唤醒驱动的攻击性；以及（iii）由下丘脑刺激或基因操作诱导的与情境无关的攻击。这三种模型解决了异常攻击性的不同方面，并且在三个领域可能会变得极其有用：在评估和评估人类精神病理学模型、研究转基因动物以及开发新的治疗策略方面。基于这些或类似模型的研究并非从定量角度研究攻击性，而是追踪异常方面的发展及其特定治疗的可能性。
