Kavoussi R, Armstead P, Coccaro E
Clinical Neuroscience Research Unit, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania, USA.
Psychiatr Clin North Am. 1997 Jun;20(2):395-403. doi: 10.1016/s0193-953x(05)70319-1.
As noted previously, it is likely that the tendency to lash out verbally or physically at others is influenced by an interaction among multiple complex biologic factors. We need to investigate how these systems interact with each other to develop a more thorough understanding of the brain's influence over aggressive behavior. We are at a very early stage in our understanding of the neurobiology of aggression. There are no simple tools for studying the complex neurophysiology of the human brain. The studies cited in this article include techniques limited in their utility. As our technologies improve, discovering a more thorough picture of the brain's influence over aggressive behavior may be possible. For example, functional neuroimaging may help to localize abnormal neurotransmitter functioning in the brains of individuals with impulsive aggressive behavior. Our technologies are beginning to reveal the differential effects of subsystems of neurotransmitter regulation. Subtypes of serotonin receptors may differentially mediate impulsive aggressive behaviors. Animal studies suggest that 5-HT 1A receptor stimulation results in a decrease in aggressive behavior. As noted previously, aggressive personality-disordered patients show a blunted prolactin response to the 5-HT1A agonist buspirone. Antagonism of 5-HT 2 receptors appears to decrease aggression, and this effect may explain the ability of newer antipsychotic agents (which, unlike older antipsychotic medications, block 5-HT 2 receptors) to produce a dramatic reduction in aggression and agitation independent of effects on psychotic symptoms. Neglecting psychosocial factors in the causes of aggressive behavior would also be naive. Although environmental factors account for much of the predisposition to aggression, there have been few systematic studies to explore the relationship between life experiences and aggression. In addition, there have been no well-designed studies of the interaction between biology and an individual's environment in the genesis of aggressive behavior. There is some evidence of an association between childhood abuse and neglect and adult antisocial personality disorder, but this relationship might be merely an artifact of the genetic relationship between parental and offspring antisocial personality disorder. As we discussed in the introduction, one of the biggest hurdles in the study of the neurobiology of aggression is the lack of a consensus on definitions. "Intermittent Explosive Disorder" is the only category in DSM-IV that directly addresses individuals with problems with aggression, but the criteria are vague and only focus on a handful of the many patients who exhibit problems with aggressive behavior. It is our hope that investigators in this field can work together toward developing more precise and encompassing diagnostic criteria to study effectively both the neurobiology and treatment of these disorders.
如前所述,对他人进行言语或身体攻击的倾向很可能受到多种复杂生物因素相互作用的影响。我们需要研究这些系统如何相互作用,以便更全面地理解大脑对攻击行为的影响。我们对攻击行为的神经生物学的理解尚处于非常早期的阶段。目前还没有简单的工具来研究人类大脑复杂的神经生理学。本文引用的研究包括一些实用性有限的技术。随着我们技术的进步,有可能更全面地了解大脑对攻击行为的影响。例如,功能性神经成像可能有助于定位冲动攻击行为个体大脑中异常的神经递质功能。我们的技术开始揭示神经递质调节子系统的不同作用。血清素受体亚型可能对冲动攻击行为有不同的介导作用。动物研究表明,刺激5-HT 1A受体会导致攻击行为减少。如前所述,患有攻击性人格障碍的患者对5-HT1A激动剂丁螺环酮的催乳素反应迟钝。拮抗5-HT 2受体似乎可以减少攻击行为,这种作用可能解释了新型抗精神病药物(与旧型抗精神病药物不同,它们能阻断5-HT 2受体)能够独立于对精神病症状的影响而显著减少攻击行为和激动情绪的能力。忽视攻击行为成因中的社会心理因素也是幼稚的。虽然环境因素在很大程度上导致了攻击行为的易感性,但很少有系统的研究来探讨生活经历与攻击行为之间的关系。此外,在攻击行为的发生过程中,关于生物学与个体环境之间相互作用的研究设计得都不完善。有一些证据表明童年期受虐待和被忽视与成人反社会人格障碍之间存在关联,但这种关系可能仅仅是父母与后代反社会人格障碍之间遗传关系的一种表现。正如我们在引言中所讨论的,攻击行为神经生物学研究中最大的障碍之一是在定义上缺乏共识。“间歇性爆发障碍”是《精神疾病诊断与统计手册》第四版中唯一直接针对有攻击行为问题个体的类别,但标准模糊,且只关注了众多表现出攻击行为问题患者中的一小部分。我们希望该领域的研究人员能够共同努力,制定更精确、更全面的诊断标准,以便有效地研究这些障碍的神经生物学和治疗方法。