Aggressiveness is an integral part of social behavior. The emergence of this trait early in life enables the individual to secure a position in the family and later in an ever- widening social circle. Individual differences are noteworthy. Timidity, for example, is a persistent trait recognized in infancy (Kagan). Males tend to be more aggressive than females. The degree to which excessively aggressive behavior is tolerated varies in different cultures. In most civilized societies, tantrums, rage reactions, and outbursts of violence and destructiveness are not condoned and one of the principal objectives of child rearing and education is the suppression and sublimation of such behavior. The rate at which this developmental process proceeds varies from one individual to another. In some males and the cognitively impaired, it is not complete until 25 to 30 years of age; the deviant behavior results in sociopathy (see Chap. 28). Undoubtedly, from our own casual and others’ more systematic observations, aggressiveness is an inherited tendency.
Seemingly groundless outbreaks of unbridled and disorganized rage may rarely represent the initial or main manifestation of disease. A patient with these symptoms may, with little provocation, change from a reasonable state to one of the wildest rage, with a blindly furious impulse to violence and destruction. In such states, the patient appears out of contact with reality and is impervious to all argument or pleading. There are examples also of a dissociation of affect and behavior in which the patient may spit, cry out, attack, or bite without seeming to be angry. This is especially true of the developmentally delayed.
All the human and animal data point to an origin of aggressiveness, anger, and rage in the temporal lobes and particularly in the amygdala. In humans, stimulation of the medial amygdaloid nuclei, through depth electrodes, evokes a display of anger, whereas stimulation of the lateral nuclei does not; destruction of the amygdaloid complex bilaterally reportedly reduces aggressiveness (Kiloh; Narabayashi et al). In an unintended experiment in a patient with Parkinson disease, Bejjani and colleagues found that aggressive behavior could be induced by stimulation of the posteromedial hypothalamus. As with the comparable elicitation of depression from an aberrant electrode in the substantia nigra that was reported by the same group, it is not clear whether the effect was because of changes induced in adjacent neuronal pathways or if the physiologic response was the result of excitatory or inhibitory neuronal activity in the hypothalamus.
Sex hormones influence the activity of these temporal lobe circuits; testosterone promotes aggressiveness and estradiol suppresses it, suggesting an explanation for sex differences in the disposition to anger. Surprisingly, propranolol and lithium have benefited such patients more than haloperidol, other neuroleptics, or sedatives.
Animal studies have corroborated observations in humans. As mentioned in the introductory section, bilateral removal of the amygdaloid nuclei in the macaque greatly reduces the expressions of both fear and anger. Electrical stimulation in or near the amygdala of the unanesthetized cat yields a variety of motor and vegetative responses. One of these has been referred to as the fear or flight response, in which the animal appears frightened, and runs away and hides; another is the anger or defense reaction, characterized by growling, hissing, and piloerection. However, structures other than the amygdaloid nuclei are also involved in these reactions. Lesions in the ventromedial nuclei of the hypothalamus (which receive abundant input from the amygdaloid nuclei) have been shown to cause aggressive behavior, and bilateral ablation of Brodmann area 24 (rostral cingulate gyrus) has produced the opposite state—tameness and reduced aggressiveness—at least in some species.