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PubMed1997

Neuroendocrine response to fenfluramine challenge in boys. Associations with aggressive behavior and adverse rearing.

BACKGROUND: There is evidence of relationships among serotonin, aggressive behavior, and a childhood history of socially adverse-rearing conditions. This study examines the prolactin response to fenfluramine hydrochloride challenge in young boys who show clinically significant aggressive behavior or who are raised in a social environment that is conducive to the development of chronic aggression. METHODS: A series of 34 younger brothers of convicted delinquents underwent standardized psychiatric and observation-based assessments of their social-rearing environments that were conducted during home visits. Approximately 2 years later, these boys underwent a reassessment of psychiatric status and an assessment of central serotonergic activity using the fenfluramine challenge procedure. RESULTS: Increasing degrees of aggressive behavior at either assessment were positively correlated with the prolactin response to fenfluramine challenge. Furthermore, adverse-rearing circumstances that were conducive to the development of aggressive behavior also exhibited positive correlations with the prolactin response. This association between adverse rearing and the prolactin response was statistically independent of that between aggression and the prolactin response. CONCLUSION: In young boys, aggressive behavior and social circumstances that are conducive to the development of aggressive behavior are positively correlated with a marker of central serotonergic activity.

Aggression↗
PubMed1997

Fluoxetine and impulsive aggressive behavior in personality-disordered subjects.

BACKGROUND: Evidence of an inverse relationship between central serotonergic (serotonin [5-hydroxytryptamine]) system function and impulsive aggressive behavior has been accumulating for more than 2 decades. If so, pharmacological enhancement of serotonin activity should be expected to reduce impulsive aggressive behavior in subjects in whom this behavior is prominent. METHODS: A double-blind, placebo-controlled trial of the selective serotonin-uptake inhibitor fluoxetine hydrochloride was conducted in 40 nonmajor-depressed, nonbipolar or schizophrenic, DSM-III-R personality-disordered individuals with current histories of impulsive aggressive behavior and irritability. Measures included the Overt Aggression Scale-Modified for Outpatients, Clinical Global Impression Rating of Improvement, and several secondary measures of aggression, depression, and anxiety. RESULTS: Fluoxetine, but not placebo, treatment resulted in a sustained reduction in scores on the Irritability and Aggression subscales of the Overt Aggression Scale-Modified for Outpatients that was first apparent during months 2 and 3 of treatment, respectively. Fluoxetine was superior to placebo in the proportion of "responders" on the Clinical Global Impression Rating of Improvement: first at the end of month 1, and then finally demonstrating a sustained drug-placebo difference from the end of month 2 through the end of month 3 of treatment. These results were not influenced by secondary measures of depression, anxiety, or alcohol use. CONCLUSION: Fluoxetine treatment has an antiaggressive effect on impulsive aggressive individuals with DSM-III-R personality disorder.

Adult↗
PubMed2002

Blunted prefrontal cortical 18fluorodeoxyglucose positron emission tomography response to meta-chlorophenylpiperazine in impulsive aggression.

BACKGROUND: Impulsive aggression is a prevalent problem and yet little is known about its neurobiology. Preclinical and human studies suggest that the orbital frontal cortex and anterior cingulate cortex play an inhibitory role in the regulation of aggression. METHODS: Using positron emission tomography, regional metabolic activity in response to a serotonergic stimulus, meta-chlorophenylpiperazine (m-CPP), was examined in 13 subjects with impulsive aggression and 13 normal controls. The anterior cingulate and medial orbitofrontal regions were hypothesized to respond differentially to m-CPP in patients and controls. In the frontal cortex, regional metabolic glucose response to m-CPP was entered into a group (impulsive aggressive, control) x slice (dorsal, middle, orbital) x position (medial, lateral) x location (anterior, posterior) x hemisphere (right, left) mixed-factorial analysis of variance design. A separate group (impulsive aggressive, controls) x anteroposterior location (Brodmann areas 25, 24, 31, 29) x hemisphere (right, left) analysis of variance was used to examine regional glucose metabolism in the cingulate gyrus. RESULTS: Unlike normal subjects, patients with impulsive aggression did not show activation specifically in the left anteromedial orbital cortex in response to m-CPP. The anterior cingulate, normally activated by m-CPP, was deactivated in patients; in contrast, the posterior cingulate gyrus was activated in patients and deactivated in controls. CONCLUSIONS: The decreased activation of inhibitory regions in patients with impulsive aggression in response to a serotonergic stimulus may contribute to their difficulty in modulating aggressive impulses.

Aggression↗
PubMed1998

Defining, measuring, and predicting impulsive aggression: a heuristic model.

Aggression research does not lack data--it lacks a model for integrating data. One of the problems confronting aggression researchers is the extensive body of multidisciplinary data that is difficult to synthesize to generate new directions in research. This paper proposes one solution that starts by asking "what is the minimal number of categories of concepts and measurements which are necessary to describe a person?". The answer is four categories of concepts: biological; cognitive; behavioral; environmental (physical and social). One way of many for integrating these four categories of concepts is a proposed discipline neutral heuristic model that is used herein to compare two different research approaches to the study of impulsive aggression. This comparison identifies clearly the differences in the two approaches with regard to different emphases among the four categories of constructs for each program. Using the model an example of common ground between the two approaches is sought as a basis for extending aggression research. The main conclusion of one of the research programs was that central nervous arousal is related to impulsive aggression. This program demonstrated that phenytoin will reduce impulsive aggressive acts and has an effect on CNS arousal. The other research program on impulsive aggression has been at the forefront in demonstrating the well established inverse relationship between serotonin levels and aggression. The comparison resulted in the suggestion that both serotonin and phenytoin may relate to a common neurochemical substrate which interacts in part to control CNS arousal, especially at the cortical level. The proposed heuristic model made obvious the need to use synthesizing concepts (e.g. information processing or language) which can interrelate multidisciplinary concepts and data from different research programs within the four categories of constructs when comparing interdisciplinary research.

Aggression↗
PubMed2000

Impulsivity, aggression, and serotonin: a molecular psychobiological perspective.

The expression of aggressiveness, which constitutes many facets of behavior, is influenced by a complex interaction of biologic, psychologic, and social variables. Even though individual differences in impulsivity and the behavioral consequences, such as aggression, addiction, and suicidality, are substantially heritable, they ultimately result from an interplay between genetic variations and environmental factors. While formation and integration of multiple neural networks is dependent on the actions of neurotransmitters, such as serotonin (5HT), converging lines of evidence indicate that genetically determined variability in serotonergic gene expression influences complex traits including that of inappropriately aggressive behavior. This contribution reviews studies of major gene effects in inbred and knockout strains of mice with increased aggression-related behavior and discusses the relevance of several serotonergic gene variations in humans which include high aggressiveness as part of the phenotype. Although special emphasis is given to the molecular psychobiology of 5HT in aggression-related behavior in rodents, nonhuman primates, and humans, relevant conceptual and methodological issues in the search for candidate genes for impulsivity and aggressiveness and for the development of mouse models of aggressive and antisocial behavior in humans are also considered.

Aggression↗
PubMed2001

Aggressive behaviors among demented nursing home residents in Japan.

This study investigates the frequency of aggressive behaviors in a sample of elderly nursing home residents with dementia in Japan. Behavioral data were collected on 391 residents using the Cohen-Mansfield Agitation Inventory (CMAI). Data were also gathered on residents' age, sex, and ability to perform self-care. Another scale was used to code the degree of resistance that each resident manifested during bathing, toileting, dressing and eating. In addition, qualitative data were collected from caregivers regarding their main caregiving problems with dementia residents. Findings show that 45.4% of the sample manifested aggressive behavior during the 2-week study period. Men were significantly more likely to manifest physically aggressive behavior, but there was no gender difference for verbal aggression. Age had no relationship to aggressive behavior. Residents who were most dependent in self-care had significantly higher frequencies of aggressive behaviors. Caregivers reported that most aggressive behavior took place during personal care. The majority of caregivers identified verbal agitation rather than physical aggression as their main caregiving problem. This study represents the first time that the CMAI has been translated and used in Japan and the first time empirical data has been collected on the behavior of dementia patients in Japanese nursing homes.

Activities of Daily Living↗
PubMed2003

Aggressive behavior in schizophrenia is associated with the low enzyme activity COMT polymorphism: a replication study.

We have previously reported that increased aggressive behavior in schizophrenic patients may be associated with a polymorphism at codon 158 of the catechol O-methyltransferase (COMT) gene that encodes a low enzyme activity variant. The finding has been replicated by one group, but not others. The discordant findings could be due to statistical errors or methodological issues in the assessment of aggressive/violent behavior. Consequently, additional studies are needed. Patients with schizophrenia (SZ) were assessed for violent behavior using the Lifetime History of Aggression (LHA) scale, an 11-item questionnaire that includes Aggression, Self-Directed Aggression, and Consequences/Antisocial Behavior subscales. DNA was genotyped for the COMT 158 polymorphism, as well as a functional polymorphism in the monoamine oxidase A (MAOA) gene promoter. Similar to our previously reported findings, a statistically significant association was found between aggressive behavior in SZ and the COMT 158 polymorphism; mean LHA scores were higher in subjects homozygous for 158Met, the low enzyme activity COMT variant (F(2,105) = 5.616, P = 0.005). Analysis of the major LHA subscales revealed that the association with 158Met was due to high scores on the Aggression, and Self-Directed Aggression subscales, but not the Consequences/Antisocial Behavior subscale. No significant association was detected for the MAOA gene alone. Our findings provide further support that COMT is a modifying gene that plays a role in determining interindividual variability in the proclivity for outward and self-directed aggressive behavior found in some schizophrenic patients.

Aggression↗
PubMed2002

Childhood predictors of adult criminality: are all risk factors reflected in childhood aggressiveness?

BACKGROUND: Early aggressive behaviour is one of the best predictors of adult criminality. AIM: To assess the degree to which family background variables, parental beliefs and behaviour and child intelligence predict child aggression and adult criminality. METHOD: Data were used from the Colombia County Longitudinal Study, a longitudinal study of 856 children in third grade in New York, in 1959-60. Adult measures of criminal behaviour, child measures taken at age eight, child peer-nominated aggression, child's peer-nominated popularity, child's IQ and parental measures at eight years were used. RESULTS: Aggressive children were less intelligent, less popular, rejected more by their parents, had parents who believed in punishment, were less identified with their parents' self-image and were less likely to express guilt. As adults, more aggressive children with parents who were less well educated, experienced more marital disharmony and who seldom attended church were most at risk for arrest. However, after the effect of early aggression was controlled, most effects disappeared and only parents having a strong belief in punishment added significantly to risk of arrest by age 30; the only fact that then reduced the risk of arrest was having parents who attended church often. Both parental authoritarianism and child IQ reduced the risk of conviction for arrested children. DISCUSSION: Level of aggression at age eight is the best predictor of criminal events over the next 22 years. A clear implication is that the risk for criminality is affected by much that happens to a boy before he is eight years old. Preventive interventions need to target risk factors that appear to influence the development of early aggression.

Adolescent↗
PubMed2004

Sodium valproate in aggressive behaviour in dementia: a twelve-week open label follow-up study.

INTRODUCTION: Short-term randomised clinical trials on valproate in distinct types of disturbed behaviour in dementia showed no effects on aggressive behaviour. OBJECTIVES: To assess the course of disturbed behaviour during medium term treatment with sodium valproate for aggressive behaviour. DESIGN: An open label observational 12-week follow-up study consecutive to a preceding randomised control trial; assessments at 4-week interval. SETTING: A psychogeriatric medium-stay ward at a psychiatric teaching hospital and psychogeriatric nursing home wards. PARTICIPANTS: Patients who completed a preceding randomised placebo controlled clinical trial on sodium valproate in aggressive behaviour in dementia were included. INTERVENTION: The starting dose of sodium valproate was 2 x 6 ml of a 40 mg/ml suspension (daily defined dose of 480 mg). The patient's regular physicians managed all treatment decisions, including decisions on dosage and plasma level measurements of sodium valproate and decisions regarding discontinuation. Co-medication was allowed and any change in prescription was recorded. MEASUREMENTS: The Social Dysfunction and Aggression Scale-9 (SDAS-9), the Behaviour Observation scales for Intramural Psychogeriatrics (in Dutch: Gedragsobservatieschaal voor Intramurale Psychogeriatrie (GIP) and the Clinical Global Impression of aggressive behaviour (CGI) were performed at the last week of each 4-week interval. RESULTS: Data of 39 patients (F=24 and M=15) were analysed. At week 12 compared to week 0 mean sodium valproate prescriptions were higher; aggressive behaviour as measured by the SDAS-9 improved. Non-social behaviour, apathetic behaviour, disoriented behaviour and distorted memory improved, but rebellious behaviour increased as measured by the GIP. Seven patients died during this study. LIMITATIONS OF THE STUDY: Open label observational design; absence of placebo/reference prescription; no systematic measurements of sodium valproate plasma levels and the allowance of psychotropic co-medication. CONCLUSION: Low dose sodium valproate may be effective reducing a broad range of types of disturbed behaviours in aggressive demented patients. The high death rate underlines the fragility of demented patients with aggressive behaviour.

Aged↗
PubMed1996

Progesterone does not inhibit aggression induced by testosterone metabolites in castrated male mice.

Sufficient data exist indicating that testosterone (T) or metabolites of T, i.e., dihydrotestosterone (DHT) and estrogen (E), induce aggressive behavior. The effects of T have also been shown to be suppressed by concurrent administration of progesterone (P). It is unknown if the effects of P are exerted on T directly or upon the T metabolites. The objective of this experiment was to evaluate the inhibitory effects of P on aggression induced by T and T metabolites. Seven male mice were randomly allocated to one of the following treatment groups: castration (C), C + T, C + 5 alpha-dihydrotestosterone (DHT), C + estrogen (E), C + DHT + E (DE), T + P, and DE + P. The males were then placed with androgenized females in three 10-min trials to determine the effects of each treatment on hormone induced aggression. The degree of aggressive behavior displayed was measured by number of trials where attacks occurred (N), mean latency to attack (L), frequency of attacks (AF), duration of attacks (D), and a composite index score (INDEX). All androgen treated groups showed significantly higher degrees of aggression compared to C and T + P animals. P inhibited aggression in T-treated males but did not inhibit aggression in the DE treated group. The data suggest that P inhibits the aggressive effects of T by acting on receptors of the metabolite-producing enzymes or by direct competitive binding for 5 alpha-reductase.

Aggression↗
PubMed1996

Effects of testosterone and 7 alpha-methyl-19-nortestosterone (MENT) on sexual and aggressive behaviors in two inbred strains of male mice.

Behavioral and endocrine effects of a synthetic androgen, 7 alpha-methyl-19-nortestosterone (MENT), which is not 5 alpha-reduced to dihydrotestosterone, were compared to those of testosterone in two inbred strains of male mice, C57BL/6J and DBA/2J, in two experiments. In the first experiment, seminal vesicle (SV) weights, kidney weights, and circulating steroid levels were examined in castrated mice treated with three doses of testosterone (3.125, 12.5, or 50 micrograms/day) or four doses of MENT (1, 4, 16, or 64 micrograms/day) for 2 weeks to determine the optimal replacement levels of the two androgens for behavioral studies. Both testosterone and MENT dose-dependently increased the SV weights that were greatly reduced, in both strains, by castration. MENT was more effective than testosterone in increasing SV weights, fully restoring them to intact levels in both strains, at the dose of 4 micrograms/day. At the dose of 12.5 micrograms/day, testosterone restored the SV weights completely in C57BL/6J and up to 80% in DBA/2J mice. DBA/2J mice were more sensitive than C57BL/6J mice to both androgens, as measured by kidney weights, although circulating levels of either steroid were very similar between the two strains of mice. In the second experiment, we investigated the effects of testosterone (12.5 micrograms/day) and MENT (4 micrograms/day) on sexual and aggressive behaviors. In each strain, MENT-treated and testosterone-treated mice showed similar numbers of mounts or intromissions. MENT was equally effective as testosterone to fully (C57BL/6J) or partially (DBA/2J) restore sexual behaviors as well as the SV weights to the intact levels. In contrast, MENT-treated mice of both strains were much less aggressive than testosterone-treated mice. In both C57BL/6J and DBA/2J mice, testosterone fully restored aggression to the intact levels as measured by aggression latency, number of aggressive bouts, and duration of aggression, whereas aggressive behaviors of the MENT-treated groups were not different from those of the castrated control groups. These results suggest that MENT can restore both male sexual behaviors and reproductive organ weights as effectively as testosterone, at one-third of the testosterone dose, without stimulating male aggressive behaviors.

Aggression↗
PubMed1997

Effects of alcohol on human aggression. Validity of proposed explanations.

In the present review, meta-analytic procedures were used to test the validity of three explanations of alcohol-related aggression: physiological disinhibition, expectancy, and indirect cause. According to the physiological disinhibition explanation, alcohol increases aggression directly by anesthetizing the center of the brain that normally inhibits aggressive responding. According to the expectancy explanation, alcohol increases aggression because people expect it to. According to the indirect cause explanation, alcohol increases aggression by causing changes within the person that increase the probability of aggression (e.g., by reducing intellectual functioning). The results from the review were inconsistent with the physiological disinhibition and expectancy explanations, but were consistent with the indirect cause explanation. Experimental manipulations that increased aggression (e.g., provocations, frustrations, aggressive cues) had a stronger effect on intoxicated participants than on sober participants.

Aggression↗
PubMed1997

Alcohol, GABAA-benzodiazepine receptor complex, and aggression.

Neurobiological investigations have become productive since experimental protocols were developed that engender large increases in aggressive behavior after acute alcohol challenges in individual experimental animals. Recent developments extended the heightened aggressive behavior to rats that self-administered alcohol shortly before the social confrontation. Quantitative ethological analysis revealed that alcohol prolongs "bursts" of aggressive acts and displays and disrupts communication between the aggressive animal and the opponent who defends, submits, or flees. Pharmacological modulation of the GABAA receptor with benzodiazepine agonists and neuroactive steroids results in dose-dependent biphasic changes in aggressive behavior that mimic the dose-effect function of alcohol; benzodiazepines potentiate the aggression-heightening effects of alcohol as well as the behaviorally suppressive effects; and antagonists at benzodiazepine receptors prevented the aggression-heightening effects of alcohol. The maturational and experiential origins for potentially distinctive GABAA receptor characteristics in individuals who exhibit heightened aggressive behavior await identification.

Aggression↗
PubMed1986

Effects of d-amphetamine on human aggressive behavior.

Male research subjects were administered placebo and three doses of d-amphetamine (5, 10 and 20 mg/70 kg) in a laboratory situation which provided both aggressive and non-aggressive response options. The non-aggressive response was button pressing maintained by presentation of points exchangeable for money at the end of the session. The aggressive response was button pressing on a separate manipulanda which ostensibly subtracted points from a fictitious partner. Aggressive responding was elicited by subtracting points from the research subjects which was attributed to the fictitious partner. d-Amphetamine increased both aggressive and non-aggressive responding, particularly at 5 and 10 mg/70 kg. At the highest dose (20 mg/70 kg), aggressive responding decreased to levels similar to those observed during placebo sessions, while monetary reinforced responding remained elevated.

Adolescent↗
PubMed1984

Involvement of adenosine receptor activities in aggressive responses produced by clonidine in mice.

A behavioral study was made of the mechanisms underlying the aggressive behavior induced by high doses of clonidine in mice. The frequency of clonidine-induced aggressive responses such as attacking and biting was increased dose-dependently from 10 to 50 mg/kg. Aggressive behavior induced by clonidine at doses of 10-30 mg/kg was potentiated under conditions of isolation and food deprivation for 24 h. Clonidine (30 mg/kg)-induced aggressive behavior was attenuated by adenosine (10 mg/kg IP) or dipyridamole (10 mg/kg IP), but markedly antagonized by combined pretreatment with both drugs. The behavior was strongly reduced by potent adenosine analogs, such as N6-cyclohexyl adenosine (CHA, 0.1 and 0.2 mg/kg IP) and N6-(L-phenyl isopropyl) adenosine (L-PIA, 0.2 mg/kg IP), but conversely was potentiated by phentolamine (10 mg/kg IP) or theophylline (10 mg/kg IP). Diazepam (2.5 mg/kg IP) and Ro15-1788 (2.5 mg/kg IP), a benzodiazepine receptor antagonist, also blocked the aggressive behavior. The inhibition by CHA (0.2 mg/kg IP) or diazepam (2.5 mg/kg) of clonidine-induced aggression was not antagonized by additional pretreatment with bicuculline (2 mg/kg IP). The aggressive response to apomorphine (8 mg/kg IP) was not affected by those drugs which inhibited the response to clonidine. The results suggest that the aggressive behavior evoked by high doses of clonidine, but not that by apomorphine, involves a blockade of adenosine receptors.

Adenosine↗
PubMed1987

Attention and social problem solving as correlates of aggression in preschool males.

This study examined the relationship between two cognitive processing variables--attention and social problem solving--and aggression in preschool-age boys. The 43 participants were administered two selective attention tasks that assess children's tendency to focus on aggressive versus cooperative social situations, the Preschool Interpersonal Problem Solving Test developed by Shure and Spivack, and the information and block design subtests of the Wechsler Preschool and Primary Scale of Intelligence. Aggressive behavior was measured by teacher ratings and observational data. Results indicated that, in contrast to their nonaggressive peers, aggressive preschool boys tend to focus their attention on aggressive social interactions in their environment. They also provide aggressive solutions to hypothetical interpersonal conflict situations more often than their less aggressive peers. Intelligence does not appear to play a mediating role in these relationships. Implications of these results for understanding and remediating aggressive behavior in young boys are discussed.

Aggression↗
PubMed1981

Developmental patterns of aggressive and withdrawn behavior in childhood: a possible method for identifying preschizophrenics.

The generality of results from high-risk studies of the children of schizophrenics may be limited. Studies of preschizophrenics suggest that an alternative approach to the identification of populations at risk involves the selection of children high on aggression and withdrawal. Aggressive children, withdrawn children, aggressive-withdrawn children, and nondeviant controls were identified by peer ratings of 4,110 children in grades 1, 4, and 7. The probability of identifying aggressive withdrawn subjects decreased as grade level increased, while the probability of identifying aggressive subjects and withdrawn subjects increased with age. Peer-rated likability of the aggressive-withdrawn group decreased systematically as grade level increased, in contrast to likability scores for other groups. Teachers rated the aggressive-withdrawn group as more deviant on scales of external reliance, inattention-withdrawal, unable to change tasks easily, and slow to complete work. Mothers described this group as more deviant on scales of distractibility, pathological use of senses, and need for adult contact. These results suggest that especially at older ages, children who are both aggressive and withdrawn represent a less mature, less socially skilled group that is potentially at risk for poor adjustment later in life.

Aggression↗
PubMed1990

Acute and chronic effects of cocaine on isolation-induced aggression in mice.

The purpose of the present study was to investigate the effects of acute and chronic cocaine administration on aggressive behaviour in mice. The animals were made more aggressive by individual housing for a period of 6 weeks. Group-housed anosmic conspecifics which were not aggressive were used as intruder controls. In acute studies, cocaine induced no significant change in aggressive behaviour at low doses (0.5-5 mg/kg) but significantly decreased aggressive behaviour after doses of 10 and 20 mg/kg. Cocaine increased the isolation-induced aggressive behaviour in mice when they were injected twice daily for a week with low doses of 0.5 or 1 mg/kg. In particular, the latency to first attack was significantly decreased by the drug and the frequency of attack towards the non-aggressive intruder was dramatically increased. Higher cocaine doses (10 or 20 mg/kg) under the described treatment regimen decreased these agonistic repertories. Tolerance did not develop to the anti-aggressive effects of high doses of cocaine on continued treatment.

Aggression↗