Various brain structures have been implicated in the mediation of aggressive behaviour in animals and humans, the most important being the periaqueductal grey ( Brandao et al., 1994 Behbehani, 1995), the hypothalamus ( Andy and Jurko, 1972), the amygdala and associated limbic structures (Dicks et al., 1968 Halgren, 1992 Kling and Brothers, 1992 Rolls, 1992 Aggleton, 1993) and the frontal lobes ( Damasio et al., 1990 Miller et al., 1997 Raine et al., 1998). Obviously, the perception as to whether a stimulus is threatening or not is decisive in the information processing leading to the aggressive behaviour. Apart from the planned and goal-directed aggression often seen in persons with antisocial personality disorder (predatory aggression), most forms of human aggression are thought to be a reaction towards a perceived threat, be it real or not ( Albert et al., 1993). The behaviour itself is less structured and defensive ( Valzelli, 1981). In contrast, defensive aggression is seen typically in the context of high emotional arousal associated with vocalizations and signs of fear or anger. Predatory aggression is characterized phenomenologically as a well-structured and goal-directed behaviour performed in an emotionally calm and concentrated state of mind. However, human data, in agreement with animal research, point to the existence of at least two different phenomenological and neurobiological subtypes of aggression: predatory and defensive aggression ( Goldstein, 1974 Mungas, 1983 Moyer, 1987 Vitiello and Stoff, 1997). One problem with studying aggression is its phenomenological and probably neurobiological heterogeneity, leading to difficulties in assessment and classification. While a history of complex partial seizures is reported to be common in patients with episodic affective aggression ( Bach-Y-Rita et al., 1971 Elliott, 1982), most of the community-based studies did not find an increased prevalence of aggressive behaviour in patients with epilepsy ( Kligman and Goldberg, 1975 Lishman, 1998). The relationship between temporolimbic epilepsy and aggressive behaviour is a particularly controversial issue ( Geschwind, 1975). Human aggression is an important social and clinical problem ( Fenwick, 1986 Saver et al., 1996 Trimble, 1996 Swartz et al., 1998). IED was associated with left-sided or bilateral EEG and MRI abnormalities, low IQ and high scores in depression and anxiety.ĪT2 = amygdala T 2, IED = intermittent explosive disorder Introduction Phenomenology and classification of aggression Another subgroup of aggressive patients (28%) had different left temporal lesions affecting either the amygdala or periamygdaloid structures. However, a significant subgroup of patients (20%) with temporal lobe epilepsy and aggressive behaviour had severe amygdala atrophy in the context of a history of encephalitis. Hippocampal sclerosis was significantly less common in patients with temporal lobe epilepsy and IED. We found no evidence of a higher prevalence of amygdala sclerosis in the aggressive patients. Data from clinical, electrophysiological, neuropsychological and psychometric investigations were obtained, as well as MRI scans for the quantitative assessment of possible amygdala pathology. We investigated 50 patients with temporal lobe epilepsy: 25 with and 25 without a history of IED. With hippocampal sclerosis, in the context of mesial temporal lobe sclerosis, being the most common cause of temporal lobe epilepsy, we hypothesized that the amygdala might be affected by the same pathogenic process in aggressive patients. The amygdala play a crucial role in the affective evaluation of multimodal sensory input and the neurobiological mediation of aggressive behaviour. They are referred to as episodic dyscontrol or, more precisely, as intermittent explosive disorder (IED). Recurrent episodes with interictal affective aggression are a rare but well-recognized problem in patients with temporal lobe epilepsy.
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