Impulsive Aggressive Individuals Research Articles

Neuronal responses in social-emotional information processing in impulsive aggressive individuals.

How we perceive and interpret signals from others' behavior, known as social-emotional information processing (SEIP), is key when responding to social threat. Impulsively aggressive individuals, behaviorally, demonstrate impaired SEIP for encoding relevant social stimuli, attribution of intent of the other person in the interaction, and responding negatively to potentially threatening social situations. In this study, we sought to explore how neural processing differs between healthy controls (HC) and individuals with impulsive aggressive behavior (individuals with Intermittent Explosive Disorder, I-IED), during a validated SEIP paradigm. Forty-five adults (19 I-IED, 26 HC) participants underwent a validated SEIP tasks during an fMRI scan. The task utilized video clips depicting a socially ambiguous, but possibly aggressive (AGG), act by one person to another and control video clips in which where possibly aggressive act does not occur (CON). Behavioral anomalies in SEIP are also manifest in altered neural activation in distributed networks/brain regions in each phase of SEIP examined. Overall, neural responses during the SEIP paradigm were characterized as reduced discrimination of the AGG vs. CON videos for I-IEDs compared to HCs. These data suggest the presence of compromised neural circuits underlying impaired social cognition in individuals with IED and highlights potential neural targets of intervention for impaired social cognition in I-IED and other behavioral disorders as well.

Dysfunction of pre-attentive information processing in impulsive aggressive individuals: acoustic startle-response and P50 study

Dysfunction of pre-attentive information processing in impulsive aggressive individuals: acoustic startle-response and P50 study

Mild Traumatic Brain Injury and Aggression, Impulsivity, and History of Other- and Self-Directed Aggression.

Mild traumatic brain injury (mTBI) is highly prevalent, with an estimated occurrence in the United States of more than 1.3 million per year. While one consequence of mTBI is impulsive aggressive behavior, very few studies have examined the relationship between history of mTBI and aggressive behavior in impulsively aggressive individuals. The authors examined the relationship between history of mTBI in a healthy control group (HC; N=453), a control group with psychiatric disorders (PC; N=486), and individuals with intermittent explosive disorder (IED; N=695), a disorder of primary impulsive aggression. Results demonstrated that IED study participants were significantly more likely to have a history of mTBI (with or without history of a brief loss of consciousness [LOC]) compared with both HC and PC participants. A similar observation was made with regard to self-directed aggression (i.e., suicidal or self-injurious behavior), although group differences were only among those with mTBI with LOC. For both other- and self-directed aggression variables, the authors observed a stepwise increase in dimensional aggression and impulsivity scores across participants as a function of mTBI history. Given that impulsive aggressive behavior begins very early in life, these data are consistent with the hypothesis that lifelong presence of an impulsive aggressive temperament places impulsive aggressive individuals in circumstances that put them at greater risk for mTBI compared with other individuals with and without nonimpulsive aggressive psychopathology.

Emotional processing and frontal asymmetry in impulsive aggressive individuals

Right frontal cortical activity, thought to reflect increased activity in withdrawal-related systems, has been observed in angry and anxious samples. The current study attempted to examine this effect in impulsive aggressive individuals (IAs) and nonaggressive controls. Impulsive aggression is a reactive violent response characterized by loss of behavioral control and previous physiological studies have found IAs have sensory and informational processing deficits. In Study 1, undergraduate volunteers (n=10 IAs, n=14 controls) completed a resting EEG and IAs showed more right frontal cortical activity than controls at rest. In Study 2, we replicated this result with undergraduate males (n=15 IAs, n=15 controls) and demonstrated that not only did IAs have more right frontal activity at rest than controls, controls were able to switch between the behavioral inhibition system (BIS) and behavioral activation system (BAS) depending on exposure to affective stimuli, whereas IAs could not. Results indicated IAs likely have an overactive BIS, and thus have difficulty recognizing emotional stimuli, suggesting a dysfunction in emotional arousal. Future directions are discussed.

Developmental predictors of an impulsive‐aggressive phenotype

In hamsters, individual differences in offensive aggression are associated with impulsive choice, leading to the characterization of a distinct impulsive-aggressive phenotype. This study had two goals: to determine the developmental trajectory of the maturation of this phenotype and to address its parental lineage. Interestingly, individuals most aggressive as adults were less likely to attack in early puberty. However, looking at the transition of agonistic behavior from play fighting to adult aggression, impulsive-aggressive individuals were less likely to engage in play fighting attacks and more likely to engage in more mature agonistic behavior. Additionally, parental lineages were compared for the aggressive responses expressed by their adult offspring. Most impulsive-aggressive individuals were offspring of few select males, which were more likely to produce this phenotype, without an association with females or specific litters. These findings identify an abnormal and accelerated development of agonistic behavior in impulsive-aggressive individuals and a likelihood of heritability.

Clarifying relations between dispositional aggression and brain potential response: Overlapping and distinct contributions of impulsivity and stress reactivity

Impulsive-aggressive individuals exhibit deficits in amplitude of the P3 brain potential response, however, it remains unclear how separable dispositional traits account for this association. The current study sought to clarify the basis of this association by examining contributions of trait impulsiveness and stress reactivity to the observed relationship between dispositional aggression and amplitude of the P3 brain potential response in a visual novelty-oddball procedure. A significant negative association was found between aggressiveness and amplitude of P3 response to both target and novel stimuli over frontal–central scalp sites. Impulsivity showed a parallel inverse relationship with P3 amplitude, attributable to its overlap with dispositional aggression. In contrast, stress reactivity did not exhibit a zero-order association with P3 amplitude, but modestly predicted P3 in a positive direction after accounting for its overlap with aggression. Results are discussed in terms of their implications for individual difference variables and brain processes underlying impulsive-aggressive behavior.

A Double-Blind, Randomized, Placebo-Controlled Trial of Fluoxetine in Patients With Intermittent Explosive Disorder

Intermittent explosive disorder (IED) is a disorder of impulsive aggression that affects as many as 7.3% of the U.S. population during some period of life. Since central serotonergic (5-HT) system dysfunction is related to impulsive aggressive behavior, pharmacologic enhancement of 5-HT activity should reduce impulsive aggressive behavior in individuals with IED. A double-blind, randomized, placebo-controlled trial of the selective 5-HT uptake inhibitor fluoxetine was conducted in 100 individuals with IED (research diagnostic criteria) and current histories of impulsive aggressive behavior. The primary efficacy measure was the aggression score from the Overt Aggression Scale-Modified (OAS-M) for Outpatient Use. Secondary efficacy measures included the irritability score from the OAS-M and the Clinical Global Impressions-Improvement scale (CGI-I) score. The study took place between July 1990 and July 1999. Fluoxetine treatment resulted in a sustained reduction in OAS-M aggression, and OAS-M irritability scores, apparent as early as week 2 (p < .01 for aggression and p < .001 for irritability at endpoint). Fluoxetine was also superior to placebo in the proportion of responders on the CGI-I (p < .001). Closer examination of the data revealed that full or partial remission of impulsive aggressive behaviors, as reflected by the A criteria for IED, occurred in 46% of fluoxetine-treated subjects. Fluoxetine did not exert an antidepressant or antianxiety effect, and its effects on impulsive aggression were not influenced by presence of current symptoms of depression or anxiety. Fluoxetine treatment has a clear antiaggressive effect in impulsive aggressive individuals with IED. However, while fluoxetine's antiaggressive effects appear robust, they lead to full or partial remission of IED in less than 50% of subjects treated with fluoxetine.

The role of serotonin in impulsive and aggressive behaviors associated with epilepsy-like neuronal hyperexcitability in the amygdala

Neuronal hyperexcitability in limbic areas, especially the amygdala, is a significant underlying mechanism associated with complex partial seizures (CPS). CPS may be comorbid with emotional disturbances, especially major mood disorders, anxiety, and aggression. Anticonvulsant medications such as phenytoin are also mood-stabilizing, and have been used for treatment of behavioral dyscontrol in impulsive aggressive individuals. Because the amygdala has important functional roles in epilepsy, emotion, and behavioral control, there may be common biological mechanisms involving neuronal excitability that contribute to both seizure activity and psychopathology. This review examines physiological mechanisms in the amygdala that regulate neuronal excitability and discusses how this may underlie, in part, disturbances in emotional behavior.

Premeditated aggression: clinical assessment and cognitive psychophysiology

Aggressive behavior has traditionally been classified into two distinct subtypes: an affective, impulsive aggressive display or a planned, predatory aggressive act. While a number of investigations have examined the clinical and physiological correlates in impulsive aggressive individuals, very little research has been conducted on those individuals engaging in predominantly premeditated aggressive acts. The present study compared a group of premeditated aggressive psychiatric outpatients with a group of normal, non-aggressive control subjects on personality, neuropsychological and cognitive psychophysiological measures. Consistent with previous work, premeditated aggressors did not differ significantly from controls on most measures of neuropsychological and psychophysiological function. Premeditated aggressors did show significant personality pathology scoring higher on measures of impulsivity, verbal and physical aggression, anger, hostility, psychoticism and neuroticism. Overall, these results suggest a distinctive personality style that is associated with aggressive behavior. With respect to this and previous work, it is suggested that the physiological aspects of behavioral control play a key role in the type of aggressive behavior displayed.

A double-blind placebo-controlled crossover study of phenytoin in individuals with impulsive aggression

The present study examines the behavioral and psychophysiological effects of phenytoin (PHT) in individuals who display impulsive-aggressive outbursts. In a double-blind placebo-controlled crossover design, individuals meeting previously established criteria for impulsive aggression were administered PHT and placebo during separate 6-week conditions. The efficacy measures used were the Overt Aggression Scale (OAS) and the Profile of Mood States (POMS). Psychophysiological measures (evoked potentials) were taken at baseline and at the end of each 6-week condition. Photic stimulation was used to evoke the mid-latency P1–N1–P2 waveform complex. Analysis indicated a significant decrease in the frequency of impulsive-aggressive outbursts during PHT administration compared to baseline and placebo. Analysis of the psychophysiological data showed significantly increased P1 amplitude and significantly longer N1 latency during PHT administration. In addition, a reduction in N1 amplitude during PHT administration was also suggested. These findings indicate reparation of physiological abnormalities previously observed in impulsive-aggressive individuals and imply more efficient sensory processing and effective orienting of attention. Taken together, these results provide insight as to the physiological mechanisms by which PHT serves to ameliorate impulsive-aggressive behavior.

Mid-latency evoked potentials in self-reported impulsive aggression

The present study was conducted to examine psychophysiological differences in arousability among individuals who display impulsive aggressive outbursts. Amplitude and latency for the mid-latency evoked potentials (P1, N1 and P2) were obtained at scalp electrode sites. The evoking stimuli were three intensities (low, medium, high) of photic stimulation. Compared to non-aggressive controls, impulsive aggressive subjects showed significantly reduced P1 amplitude, which is indicative of an inefficient sensory gating mechanism. In addition, these subjects exhibited significantly larger N1 amplitude implying an enhanced orienting of attention to stimuli. Impulsive aggressive subjects also exhibited shorter P1, N1 and P2 peak latency. These results suggest that impulsive aggressive individuals may display quicker orienting and processing of stimuli in an attempt to compensate for low resting arousal levels. Finally, impulsive aggressive subjects augmented the P1–N1 component more frequently than controls, which is consistent with previous studies examining impulsivity and sensation seeking. Together, these findings extend previous work concerning the underlying physiology of impulsive aggression. It has been suggested that impulsive aggressive individuals may attempt to compensate for low resting arousal levels by engaging in stimulus seeking behaviors. Accordingly, the present findings imply similar physiological compensatory responses as demonstrated by heightened orienting of attention, processing and arousability. In addition, a compromised sensory gating system in impulsive aggressors may exacerbate such circumstances, and lead to later cognitive processing deficits.

P300 under standard and surprise conditions in self-reported impulsive aggression

1. 1. The purpose of the present study was to determine the cognitive psychophysiological correlates of impulsive aggression in a “high” functioning sample: college students. 2. 2. Visual P300 was measured during a standard oddball task and a surprise task that included unexpected low probability stimuli. 3. 3. Results indicated significantly reduced P300 amplitude and prolonged latency for impulsive aggressive subjects to target stimuli on the standard task. Target amplitude differences where further augmented under conditions involving unexpected stimuli although no significant latency differences were observed. The topography of P300 amplitude to unexpected stimuli differed from that of the target. 4. 4. Topographic group differences found for unexpected stimuli are suggestive of cognitive processing deficits previously demonstrated using neuropsychological techniques in impulsive aggressive individuals.

Irritability and impulsiveness: relationship to self-reported impulsive aggression

Impulsive aggressive behavior was assessed in a group of 214 college students through self-report. All subjects completed the Anger Attack Questionnaire, Buss-Durkee Hostility Inventory (BDHI) and the Barratt Impulsiveness Questionnaire (BIS-11). Fifty-one subjects (24%) were classified as impulsive aggressive. Analysis of the BDHI and BIS-11 found that impulsive aggressive subjects scored significantly higher than nonaggressives on impulsiveness (BIS-11) and all subscales of the BDHI with the exception of Negativism and Suspicion. Correlation analysis demonstrated that impulsiveness and BDHI Irritability were significantly correlated with number of impulsive aggressive episodes in the previous month, while BDHI Assault was not. Impulsiveness was also found to be significantly related to BDHI Irritability but not to BDHI Assault. Irritability assesses an explosive, uncontrolled type of hostility; assault on the other hand assesses more of a provoked or retaliatory type of hostility which is not likely to be related to impulse control or impulsive aggression. The results of this study clearly demonstrate the usefulness of self-report data in the assessment of impulsive aggressive behavior. BDHI Irritability and BIS-11 impulsiveness both appear to be measuring similar aspects of behavioral control. It is suggested that the BDHI Irritability and BIS-11 scales may be useful in the identification of impulsive aggressive individuals early in their contact with the criminal justice and/or mental health systems.

Amygdaloid nucleus syndrome and dehumanization syndrome.

Through statistical tests 3 groups of impulsive-aggressive patients were studied: group 1, 100 individuals with temporal dysrhythmia; group 2, 18 individuals with temporal dysrhythmia submitted either to group analytical therapy or to psychoanalysis; group 3, 25 impulsive-aggressive individuals. Moreover the author differentiates between the amygdaloid nucleus and dehumanization syndromes, through psychoanalytical or psychiatric studies, and stresses the importance of the molding periods in relation to social factors (frustration-aggression-injustice). Amygdalotomy of the hippocampus was suggested in special cases.