Exploring the link between character, personality disorder, and neuropsychological function.

Personality deviations and deficits in cognitive executive function are common among forensic populations. The present study on incarcerated offenders explored whether there are links between the two domains. Personality was assessed using the Temperament and Character Inventory (TCI). Neuropsychological performance, including visual working memory, attentional set-shifting and planning, were tested with the Cambridge Neuropsychological Test Automated Battery (CANTAB). Subjects with personality disorders scored high on harm avoidance, and low on self-directedness and cooperativeness. Personality disordered offenders did not differ from the comparison groups (offenders without personality disorder, and non-criminal controls) with regard to CANTAB measures of visual working memory (delayed matching to sample, spatial working memory) and planning (Stockings of Cambridge), but they made a larger number of errors on the attentional set-shifting task. Dimensional analysis of the personality and neuropsychological variables revealed significant associations between self-directedness and cooperativeness on the one hand, and attentional set-shifting on the other. Intellectually disabled, non-criminal individuals (marginal mental retardation) who performed poorly on attentional set-shifting also scored low on self-directedness and cooperativeness. The results indicate that poor development of certain personality traits may be associated with deficits in neuropsychological functioning.

A deficit in attentional set-shifting of violent offenders.

BACKGROUND: Recent brain imaging studies suggest that proneness to violence and antisocial behaviour may be associated with dysfunction of the prefrontal cortex. The present study. therefore, examined aspects of prefrontally guided executive functions in a group of criminal violent men. METHODS: Violent offenders undergoing forensic psychiatric examination by court order undertook computerized tasks for planning, visual working memory and attentional set-shifting from the Cambridge Neuropsychological Test Automated Battery. Their performance was compared to that of subjects with marginal mental retardation and normal controls. RESULTS: Violent offenders performed well on tasks for spatial and figurative working memory, as well as on a test for planning. A marked impairment was observed in the attentional set-shifting task: offenders made significantly more errors than the other groups when required to shift attention from one perceptual dimension to another. Reversal learning was also deficient. Correlational analyses within the offender group revealed that poor performance on the perceptual shift problem was associated with fewer errors in tasks for working memory and planning. CONCLUSIONS: The present results suggest that violent offenders show dual impairments in inhibitory cognitive control. First, they are deficient in shifting attention from one category to another. Secondly, the ability to alter behaviour in response to fluctuations in the emotional significance of stimuli is compromised. These deficits might constitute cognitive reflections of the biological prefrontal alterations observed in this group of people.

Behavioral disinhibition following basal forebrain excitotoxin lesions: alcohol consumption, defensive aggression, impulsivity and serotonin levels.

Research on alcoholism have identified a subgroup in which the drinking problem is associated with high rates of violence, an impulsive disposition and signs of reduced serotonin functioning in the brain. The present study reports that male Wistar rats with ibotenic acid-induced (5 micrograms/0.5 microliter) neuron loss in the basal forebrain (ventral striatum, septal area and adjacent structures) showed behavioral and neurochemical signs not unlike this subtype of alcoholics. Thus, rats with this lesion exhibited excessive 6% alcohol drinking in a two-bottle choice test and showed augmentation of certain defensive behaviors, including defensive aggression and increased activity-during signal. In the punished drinking test, a passive avoidance task which taps psychological mechanisms underlying impulsivity [56], experimental rats were not different from sham-operated controls with regard to the number of punished licks, but punishment evoked less disruption of ongoing behavior in subjects with basal forebrain damage. The virtual absence of food hoarding in the face of normal feeding may constitute yet another sign of increased impulsivity, indicating as it does a diminished influence of future rewards on behavior. As expected, in view of ibotenic acid's selectivity for neuronal perikarya, the concentrations of dopamine, serotonin and norepinephrine were normal in the lesioned area. However, the levels of serotonin and norepinephrine in the cortex were reduced. A separate experiment examined the extent to which serotonin depletion alone reproduced the behavioral profile induced by basal forebrain neuron loss. However, measures of alcohol consumption, defensive behavior and impulsivity were not different from controls in rats given intracerebroventricular 5,7-DHT (150 micrograms/20 microliters), except for a modest increase in defensive aggression.

An animal model for type 2 alcoholism? Alcohol consumption and aggressive behavior following lesions in the raphe nuclei, medial hypothalamus, or ventral striatum-septal area.

Given the conspicuous association between aggressive antisocial traits and alcoholism in men, we investigated whether or not a link between defensive aggressive behavior and homecage alcohol consumption could be demonstrated in the laboratory rat. This was accomplished by observing ethanol intake and hyperreactivity towards the experimenter in rats made hyperdefensive by brain lesions. Rats with medial hypothalamic electrocoagulations showed a remarkable degree of hyperdefensiveness, lasting throughout the entire 6-week postoperative period. Alcohol intake, on the other hand, was not different from sham-operated controls when the beverage was offered as a plain 6% solution or in a 0.2% saccharin vehicle. When subjected to the stress of food restriction, which enhances ethanol intake in normal rats, medial hypothalamic subjects actually decreased their alcohol consumption. Electrolytic lesions in the dorsal and median raphe brought about a transient increase in defensive aggression, but no alteration in ethanol drinking. Animals with ibotenic acid-induced extensive lesions to the ventral striatum and septal area were not only viciously aggressive, but also drank considerably more alcohol than controls. Ibotenic acid-lesioned rats did not respond to the saccharin or food-restriction conditions by increasing their alcohol intake further, perhaps because they drank at a maximal rate already during the plain ethanol-phase of the experiment. These observations show that basal forebrain dysfunction in the rat can give rise to excessive alcohol intake and heightened aggression, a constellation of behavioral symptoms observed in male type 2 alcoholics.

In quest for a possible association between heightened social aggression and excessive alcohol drinking in the rat.

Many clinical studies show that a sizeable proportion of male alcoholics are also inclined to act violently and aggressively. Given this association in humans, we asked whether a relationship exists between ethanol intake and aggressive behaviour in laboratory rats. In a first test of the hypothesis, we measured ethanol intake in male rats made aggressive by periodic contacts with sexually active females. Although the males became significantly more aggressive, there was no concomitant enhancement of alcohol consumption. In another experiment, observations of ethanol drinking in lactating rats exhibiting maternal aggression revealed no alteration in ethanol intake relative to nonlactating control females. However, because water intake was substantially elevated in the maternal rats, there was a net decrease in ethanol preference. The final experiment examined aggressiveness in chronically food-restricted male rats. In line with previous studies, this procedure increased ethanol drinking, but it did not enhance aggressive behaviour. It is concluded that, in our rats, there is no apparent association between the level of social aggression and the voluntary intake of ethanol in a two-bottle choice paradigm. The possibility remains, though, that alcohol drinking is better related to other forms of aggression, such as defensive or predatory aggression.

Interaction with pups enhances dopamine release in the ventral striatum of maternal rats: a microdialysis study.

A growing body of evidence suggests that an interference with dopamine (DA) transmission disrupts maternal behavior in the rat. The present brain microdialysis study was therefore conducted to investigate whether infants can modulate ventral striatal DA release in mother rats. There was a significant rise in the extracellular concentrations DA, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) in the ventral striatum when mothers were reunited with their litters following separation overnight. Nursing was the predominant behavior during this phase of the experiment. More active behaviors were elicited by soiling pups with flowerpot earth, and this was accompanied by further increases in DA, DOPAC, HVA, and 5-HIAA. It is suggested that pup-induced stimulation of ventral striatal DA release facilitates parental responses such as pup retrieval.

Peripheral anosmia attenuates female-enhanced aggression in male rats.

It is well established that male rats with prior access to sexually active females show enhanced offensive aggression toward unfamiliar male intruders. The present study assessed the importance of the sense of smell for this facilitatory effect. It was found in 2 independent experiments that anosmia, induced peripherally by surgically removing the olfactory epithelium and cutting the olfactory nerves, reduced baseline levels of offensive aggression and significantly attenuated the female-enhanced aggression effect. It was also found that sexual performance of anosmic rats was context-dependent, in that it was more impaired in the homecage environment than in standard observation cages. In contrast to sham-operated males, the experimental animals showed no preference for estrous over anestrous females in a mate choice test. Anosmic males did not appear more fearful than controls, as assessed in a hyponeophagia test, but they showed less exploratory behavior (rearing and head-dipping) in the hole-board test, and less rearing activity in automated activity boxes.

Female-enhanced aggression in male rats: effects of genital anesthesia, castration, or preoptic lesions.

Male rats that had cohabited with ovariectomized females for 2 weeks became more aggressive toward male intruders after a novel estrous female had been placed in their home cages for a period of 4 hr on the previous day. No increase in aggression was seen in males exposed to anestrous females. Genital anesthesia did not attenuate the female-enhanced aggression effect. By contrast, no enhancement of aggression was observed in long-term castrated males after 24 hr of exposure to estrous females. Rats with bilateral electrolytic lesions in the medial preoptic area showed a normal female-enhanced aggression effect. The observations that exposure to females facilitates aggression in males subjected to genital anesthesia and in males with preoptic lesions raise the possibility that copulatory cues are not always required for the effect.