Human Aggressive Behavior Research Articles

Anger attacks in depression

Anger, hostility and irritability are frequently observed among patients with unipolar depressive disorders. Approximately one-third of depressed outpatients present with "anger attacks," sudden spells of anger accompanied by symptoms of autonomic activation such as tachycardia, sweating, hot flashes, and tightness of the chest. Depressed patients with anger attacks are significantly more anxious and hostile and they are more likely to meet criteria for avoidant, dependent, borderline, narcissistic, and antisocial personality disorders than depressed patients without anger attacks. Several studies suggest that antidepressant treatment of anger attacks in depression is safe and effective. Anger attacks disappear in 53-71% of depressed outpatients treated with antidepressants such as fluoxetine, sertraline, and imipramine. In addition, the rate of emergence of anger attacks after treatment with fluoxetine (6-7%) is no different from the rates observed after treatment with sertraline (8%) and imipramine (10%), and lower than the rate with placebo (20%). Finally, since the central serotonergic neurotransmitter system is known to be involved in the modulation of aggressive behavior in animals and humans, one can hypothesize that antidepressants which affect this system may be particularly effective in depressed patients with anger attacks.

The serotonin hypothesis of aggression revisited

Many contemporary theorists believe serotonin (5-HT) neurotransmitter functioning plays a role in the regulation of human aggressive behavior. We argue that the evidence supporting this 5-HT hypothesis of human aggression is less compelling than commonly assumed, due to 1. (a) conflicting study results, and 2. (b) significant methodological limitations of existing studies. Recent models that integrate the role of psychological and contextual variables in 5-HT-associated aggression are reviewed. The need to incorporate psychometrically sound measures of aggression in 5-HT studies, to use experimental and longitudinal designs, and to test hypotheses drawn from multifactorial models in future research is advocated.

Biopsychosoc1al approaches to understanding human aggression: The first 30 years

Theorists and researchers have long been aware of the potential utility of multi-dimensional explanations of human behavior, including human aggressive behavior. Biopsychosocial models are multidimensional explanations that attempt to provide a framework for understanding how biologic, contextual, and individual difference variables combine to influence human behavior. In this paper, the rationale for giving contemporary investigators a forum to discuss research findings on aggressive behavior from a biopsychosocial perspective is developed. The advantages and potential shortcomings of viewing aggressive behavior from a biopsychosocial perspective are briefly discussed.

Differential effects of ethanol on feline rage and predatory attack behavior: an underlying neural mechanism.

Previous studies have shown that, at certain dose levels, ethanol can exert a powerful, facilitatory effect on aggressive behavior in both animals and humans. In the cat, however, it was discovered that ethanol differentially alters two forms of aggression that are common to this species. Defensive rage behavior is significantly enhanced, whereas predatory attack behavior is suppressed by ethanol administration. One possible mechanism governing alcohol's potentiation of defensive rage behavior is that it acts on the descending pathway from the medial hypothalamus to the midbrain periaqueductal gray (PAG)-an essential pathway for the expression of defensive rage behavior that uses excitatory amino acids as a neurotransmitter. This hypothesis is supported by the finding that the excitatory effects of alcohol on defensive rage behavior are blocked by administration of the N-methyl-D-aspartate antagonist alpha-2-amino-7-phosphoheptanoic acid (AP-7) when microinjected into the periaqueductal gray, a primary neuronal target of descending fibers from the medial hypothalamus that mediate the expression of defensive rage behavior. Thus, the present study establishes for the first time a specific component of the neural circuit for defensive rage behavior over which the potentiating effects of ethanol are mediated.

Physiological responses to d-fenfluramine and ipsapirone challenge correlate with indices of aggression in males with personality disorder.

Hormonal responses to challenge with the 5-HT2A/2C probe d-fenfluramine and hormonal and thermal responses to challenge with the 5-HT1A probe ipsapirone were correlated with self-report and historical assessments of aggression in a pilot sample of eight male personality-disordered individuals. Prolactin responses to d-fenfluramine and cortisol responses to ipsapirone challenge were inversely correlated with self-reported assaultiveness. Thermal responses to ipsapirone were inversely correlated with a historical assessment of aggression. Since none of these physiological indices of 5-HT system function were intercorrelated, it is possible that simultaneous assessment of these 5-HT indices may yield a more comprehensive assessment of the relationship between central 5-HT system function and aggressive behavior in humans.

Reduction in serotonin 5HT2 receptor binding on platelets of delinquent adolescents.

The possible involvement of serotonin receptors of the 5HT2 type in aggressive behavior was studied in juvenile delinquents. A group of 28 delinquent adolescents (13-18 years old) who had committed violent crimes was compared with a group of age matched controls. Subjects were drug and medication free during the study. 5HT2 receptors were labeled on platelet membranes using tritiated ketanserin. Receptor binding in the delinquent adolescents was significantly lower than in age matched controls. Mean +/- SD of 76 controls was 32.3 +/- 14.2 fm/mg, compared to 16.6 +/- 8.2 fm/mg in 28 delinquents (P < 0.002, Student's t-test). These results support a role for serotonin in general and 5HT2 receptors in particular in human aggressive behavior.

EVidence for dorsolateral and orbital prefrontal cortical involvement in the expression of aggressive behavior

Numerous studies have implicated the role of the prefrontal cortex in the expression of aggressive behavior, However, the nature of this relationship remains poorly understood. As such, the purpose of this article is to review both the animal and human literature pertaining to prefrontal cortical functioning and aggression in an attempt to help clarify this relationship. Particular attention is paid to differentiating the functions of the dorsolateral and the orbital regions of the prefrontal cortex in the expression of aggression. Evidence was garnered from four different types of studies: 1) those examining aggressive behavior in animals following ablations to the prefrontal cortex; 2) those examining aggressive behavior in humans following surgical and accidental lesions to the prefrontal cortex; 3) those examining prefrontal cortical functioning in individuals with psychiatric disorders characterized by aggression; and 4) those relating prefrontal cortical functioning to human aggressive behavior in laboratory situations. The general conclusion of this article is that the dorsolateral region of the prefrontal cortex is more likely to be involved in the expression of physical aggression whereas the orbital region is more likely to be involved in the expression of what is termed herein 'disinhibited-nonaggressive' behavior.

The effects of alcohol on free-operant aggressive behavior.

Although strong correlations between alcohol use and the frequency and intensity of social aggression have been observed in many populations, the relationship between these two events remains complex. Aggressive behavior is not always associated with alcohol or drug use, and substantial amounts of alcohol are consumed in social settings without the occurrence of violent or aggressive behavior. The relationship between alcohol and human aggressive behavior has been investigated using a free-operant procedure developed from the experimental tradition of behavioral pharmacology. The reliability of the free-operant procedure is evidenced by the similarity in experimental outcomes across laboratories using similar experimental procedures. Evidence for the validity of the procedure comes from recent studies with populations varying in histories of violent behavior, as well as from similarities in the outcome of studies using different experimental paradigms. Recent studies indicate clearly that both antecedent and consequent variables, such as the schedule of provocation and the response requirement for both aggressive and nonaggressive behavior, as well as the social context in which provocation occurs, influence the relationship between alcohol and aggressive behavior. The implications of the role of contextual factors for social policy regarding violence and alcohol use are discussed.

Role of serotonin in human aggressive behaviour

This study aimed to evaluate a peripheral serotonergic marker, 3H-imipramine (3H-IMI) binding to platelet membranes, in a group of severely aggressive subjects (A), institutionalized since childhood for mental retardation, as compared with suicide attempters (S) and healthy controls (H). The maximum binding capacity of 3H-IMI to platelet membranes was statistically lower in (A) and (S) than in (H). In addition, a statistically significant difference was observed between the Bmax values of aggressive subjects and those of suicide attempters. No changes in the dissociation constant (Kd) of IMI binding were observed. These data provide further supporting evidence for the hypothesis of an abnormality of the 5HT system in aggressive behaviour and suggest that such an abnormality, as reflected by platelet markers, is more severe in suicide attempters. © 1993 Wiley-Liss, Inc.

Aggressive behavior: from laboratory to clinic. Quo vadit?

This article sets forth two theses: (1) that animal models of aggressive behavior have utility in fostering and guiding human aggression research; and (2) that clinical violence research should now focus on the severely and repetitively aggressive patients for study and therapeutic research. Animal models are reviewed in terms of typology; studies of temperament; the role of sensory cues; neuroanatomy, neurochemistry, and neuroendocrinology; studies of stress; and studies of social conditions. Examples are presented that have implications and potential utility for human research. Clinical approaches to the study of human aggressive behavior are examined and five suggestions are made to enhance the efficacy and utility of clinically relevant aggression research.

Aggressive behavior following exposure to cholinesterase inhibitors

The authors report four instances of significant, essentially unprovoked aggressive behavior, including two homicides, following exposure to cholinesterase inhibitors. No subject had a history of violent behavior, antisocial personality, or major psychiatric or neurologic disorder. After anticholinesterase exposure ceased, all showed sincere remorse for their actions, and none has since engaged in aggressive or psychopathologic behavior. Well-controlled experimentation in animals suggests that enhanced activation of hypothalamic cholinergic receptors may underlie aggressive behavior in humans exposed to cholinesterase inhibitors. A relationship between cholinesterase inhibitors and aggression has important implications for public health, raising the possibility of unappreciated neurotoxic influences on behavior.

Impulsive aggression and central serotonergic system function in humans: an example of a dimensional brain-behavior relationship.

A dimensional relationship between central serotonergic (5-HT) system function and indices of suicidal and impulsive aggressive behaviors has been suggested by more than a decade of research in patients with psychiatric disorders. This paper reviews a series of studies conducted in healthy male individuals and in male patients with major mood and/or personality disorder involving pharmacochallenge and neurochemical strategies designed to explore the role of central 5-HT system function in the regulation of suicidal and impulsive aggressive behavior in humans. The results of these studies suggest that reduced overall central 5-HT function in the limbic-hypothalamic system is associated with suicidal and/or impulsive aggressive behaviors in patients with major mood and/or personality disorders and that diminished 5-HT post-synaptic receptor function in this brain region may be an important biological correlate of these behaviors.

Neurochemical and Psychopharmacologic Aspects of Aggressive Behavior

The clinical treatment of violent behavior shows a remarkable congruence with preclinical research concerning the modulations of central neurotransmitter systems and their influence upon human aggressive behavior. Moreover, systematic alterations of central neurotransmitter activity in patients offer substantial promise of increasing the successful biological modification of violent behavior.

Effects of provocation and alcohol on human aggressive behavior

Effects of provoking stimuli on human aggressive behavior and on the relationship between alcohol and aggressive behavior were measured. Four adult males manipulated pushbuttons that produced points on their own counters (redeemable for money) or ostensibly subtracted points (money) from the counters of fictitious persons described as participating in the same study at other locations. During five 10-min components, frequency and intensity of point subtractions, ostensibly controlled by another person, were manipulated. Each subject was repeatedly exposed to alcohol doses (0.25, 0.5 and 0.75 g/kg of 95% ethanol) over time using a repeated measures design. Aggressive responding was affected by provocation intensity and frequency. The highest dose of alcohol produced selective increases in aggressive responding; however, no interactions between alcohol effects and provocation conditions were observed.

Effects of secobarbital on human aggressive behavior

Effects of secobarbital on human aggressive behavior

Alcohol and human aggressive behavior: The effects of provocation: Thomas H. Kelly. Veterans Administration Medical Center, Shreveport, LA; Don R. Cherek. Dept. of Psychiatry, Louisiana State University Medical Center; and Joel L. Steinberg. Veterans Administration Medical Center, Shreveport, LA

Alcohol and human aggressive behavior: The effects of provocation: Thomas H. Kelly. Veterans Administration Medical Center, Shreveport, LA; Don R. Cherek. Dept. of Psychiatry, Louisiana State University Medical Center; and Joel L. Steinberg. Veterans Administration Medical Center, Shreveport, LA

A guide to the literature on aggressive behavior

A guide to the literature on aggressive behavior

Evolution and the nonlegal equivalent of aggressive criminal behavior

Within the framework of modern evolutionary theory, arguments are reviewed that the nonlegal equivalent of aggressive criminal behavior may have evolved by natural selection among mammals, particularly primates, as part of their overall approach to reproduction. If so, the commission of aggressive crimes (or their nonlegal equivalent) by humans, and even efforts to prevent fellow social group members from being victimized by aggressive crimes, may also be partially explainable in natural selection terms. The plausibility of this deduction was explored, first, by specifying the three elements that a human act must have to be regarded as an aggressive crime. Summarily, these were that (1) injury to a victim must be a likely result of the act, (2) the act must be intended, and (3) the act must elicit negative responses from those witnessing it. The primate behavior literature was examined for evidence that some behavior of nonhumans met all three conditions. Affirmative results were obtained. Therefore, while further research is in order, human aggressive criminal behavior, as well as human efforts to control it, seem to have close parallels in other primates. This would be consistent with the notion that aggressive criminal behavior (along with its condemnation by fellow group members) is part of a social system produced and sustained by natural selection.

Effects of D-amphetamine on human aggressive behavior: D. R. Cherek, J. L. Steinberg and T. H. Kelly. Louisiana State University School of Medicine in Shreveport, LA

Effects of D-amphetamine on human aggressive behavior: D. R. Cherek, J. L. Steinberg and T. H. Kelly. Louisiana State University School of Medicine in Shreveport, LA

Regular or decaffeinated coffee and subsequent human aggressive behavior

A new methodology was used to study the effects of coffee on human aggressive behavior in a laboratory situation. Aggressive responding was elicited by subtracting money from the research subjects, an action which was attributed to a fictitious person. Regular coffee compared to decaffeinated coffee produced decreases in aggressive responses, but increased nonaggressive monetary reinforced responding. Thus, the suppressing effect of regular coffee on aggressive responding was not due to a nonspecific depressant action.