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Food intake is essential for survival, but maladaptive patterns of intake, possibly encoded by a preexisting vulnerability coupled with the influence of environmental variables, can modify the reward value of food. Impulsivity, a predisposition toward rapid unplanned reactions to stimuli, is one of the multifaceted determinants underlying the etiology of dysregulated eating and its evolving pathogenesis. The medial prefrontal cortex (mPFC) is a major neural director of reward-driven behavior and impulsivity. Compromised signaling between the mPFC and nucleus accumbens shell (NAcSh) is thought to underlie the cognitive inability to withhold prepotent responses (motor impulsivity) and binge intake of high-fat food (HFF) seen in binge eating disorder. To explore the relationship between motor impulsivity and binge-like eating in rodents, we identified high (HI) and low impulsive (LI) rats in the 1-choice serial reaction time task and employed a rat model of binge-like eating behavior. HFF binge rats consumed significantly greater calories relative to control rats maintained on continual access to standard food or HFF. HI rats repeatedly exhibited significantly higher bingeing on HFF vs. LI rats. Next, we employed dual viral vector chemogenetic technology which allows for the targeted and isolated modulation of ventral mPFC (vmPFC) neurons that project to the NAcSh. Chemogenetic activation of the vmPFC to NAcSh pathway significantly suppressed motor impulsivity and binge-like intake for high-fat food. Thus, inherent motor impulsivity and binge-like eating are linked and the vmPFC to NAcSh pathway serves as a 'brake' over both behaviors.

Impulsivity and the attentional orienting response to cocaine-associated cues ( cue reactivity ) promote relapse in cocaine-use disorder (CUD). A time-dependent escalation of cue reactivity ( incubation ) occurs during extended, forced abstinence from cocaine self-administration in rats. The investigational serotonin (5-HT) 5-HT 2A receptor (5-HT 2A R) antagonist/inverse agonist M100907 suppresses impulsive action , or the inability to withhold premature responses, and cocaine-seeking behaviors. The present preclinical study was designed to establish the potential for repurposing the Food and Drug Administration-approved selective 5-HT 2A R antagonist/inverse agonist pimavanserin as a therapeutic agent to forestall relapse vulnerability in CUD. In male Sprague-Dawley rats, pimavanserin suppressed impulsive action ( premature responses ) measured in the 1-choice serial reaction time (1-CSRT) task, similarly to M100907. We also used the 1-CSRT task to establish baseline levels of impulsive action before cocaine self-administration and evaluation of cue reactivity (lever presses reinforced by the discrete cue complex previously paired with cocaine delivery). We observed an incubation of cocaine cue reactivity between day 1 and day 30 of forced abstinence from cocaine self-administration. Baseline levels of impulsive action predicted incubated levels of cocaine cue reactivity in late abstinence. We also found that baseline impulsive action predicted the effectiveness of pimavanserin to suppress incubated cue reactivity in late abstinence from cocaine self-administration at doses that were ineffective in early abstinence. These data suggest that integration of clinical measures of impulsive action may inform refined, personalized pharmacotherapeutic intervention for the treatment of relapse vulnerability in CUD., (U.S. Government work not protected by U.S. copyright.)

Background and Objectives: Substance misuse is increasing in the older population, which may have differing effects on behavior compared to younger substance participants. Differences in trait and state impulsivity were assessed in younger and older cocaine-dependent participants., Methods: Thirty-one younger cocaine-dependent participants (n = 31) and 21 older cocaine-dependent participants (n = 21) were assessed using the Barrett Impulsiveness Scale-11 and the Immediate Memory Task., Results: Younger participants showed higher trait impulsivity than older participants (p =.027). However, older participants demonstrated higher state impulsivity than younger participants (p =.018)., Conclusion: Higher state impulsivity in older cocaine participants suggests that cocaine use may have accelerating effects on the aging brain., Scientific Significance: This preliminary study adds the limited research on how cocaine use affects normal aging. Current treatments are based on younger adults, therefore the needs of older adults should be taken into consideration and studied more. (Am J Addict 2018;27:557-559)., (© 2018 American Academy of Addiction Psychiatry.)

Objective: To determine if elevated rapid-response impulsivity after blast exposure (as a putative marker of ventral prefrontal cortex [vPFC] damage) is predictive of future elevated affective symptomatology in blast-exposed service members., Design: Longitudinal design with neurocognitive testing at initial assessment and 1-year follow-up assessment of psychiatric symptomatology by telephone interview., Setting: Veterans Administration medical centers and postdeployment assessment centers at military bases., Participants: Blast-exposed U.S. military personnel (N=84) ages 19 to 39 years old., Interventions: Not applicable., Main Outcome Measures: Center for Epidemiological Studies-Depression Scale (CES-D) scores, Posttraumatic Stress Disorder Checklist Version 5 (PCL-5) scores, and Alcohol Use Disorders Identification Test-C (AUDIT-C) scores at the 12-month follow-up telephone interview., Results: After controlling for age and affective symptom scores reported at the initial assessment, commission errors on the Continuous Performance Test-II of the initial assessment were predictive of higher symptom scores on the CES-D and PCL-5 at follow-up, but were not predictive of AUDIT-C scores., Conclusions: Elevated rapid-response impulsivity, as a behavioral marker of reduced top-down frontocortical control, is a risk factor for elevated mood and posttraumatic stress disorder symptoms over time in blast-exposed individuals. Future longitudinal studies with predeployment neurobehavioral testing could enable attribution of this relation to blast-related vPFC damage., (Copyright © 2017 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.)

In military populations, traumatic brain injury (TBI) also holds potential to increase impulsivity and impair mood regulation due to blast injury effects on ventral frontal cortex - to put military personnel at risk for suicide or substance abuse. We assessed a linkage between depression and impaired behavioral inhibition in 117 blast-exposed service members (SM) and veterans with post-concussion syndrome (PCS), where PCS was defined using a Rivermead Postconcussive Symptom Questionnaire (RPQ) modified to clarify whether each symptom worsened compared to pre-blast. Center for Epidemiological Studies-Depression Scale (CES-D) scores, PTSD Checklist 5 (PCL-5) scores, and RPQ raw subscale scores correlated positively with commission and perseverative errors on the continuous performance test II (CPT-II). In contrast, the number of RPQ symptoms ostensibly worsened post-blast did not correlate with impulsive errors on the CPT-II. These data replicate earlier findings that link increased affective symptomatology to impaired behavior inhibition in military TBI populations, but where additional effects on impulsivity from the blast itself remain equivocal., (Published by Elsevier Ireland Ltd.)

A feature of multiple neuropsychiatric disorders is motor impulsivity. Recent studies have implicated serotonin (5-HT) systems in medial prefrontal cortex (mPFC) in mediating individual differences in motor impulsivity, notably the 5-HT2AR receptor (5-HT2AR) and 5-HT2CR. We investigated the hypothesis that differences in the ratio of 5-HT2AR:5-HT2CR protein expression in mPFC would predict the individual level of motor impulsivity and that the engineered loss of the 5-HT2CR would result in high motor impulsivity concomitant with elevated 5-HT2AR expression and pharmacological sensitivity to the selective 5-HT2AR antagonist M100907. High and low impulsive rats were identified in a 1-choice serial reaction time task. Native protein levels of the 5-HT2AR and the 5-HT2CR predicted the intensity of motor impulsivity and the 5-HT2AR:5-HT2CR ratio in mPFC positively correlated with levels of premature responses in individual outbred rats. The possibility that the 5-HT2AR and 5-HT2CR act in concert to control motor impulsivity is supported by the observation that high phenotypic motor impulsivity associated with a diminished mPFC synaptosomal 5-HT2AR:5-HT2CR protein:protein interaction. Knockdown of mPFC 5-HT2CR resulted in increased motor impulsivity and triggered a functional disruption of the local 5-HT2AR:5-HT2CR balance as evidenced by a compensatory upregulation of 5-HT2AR protein expression and a leftward shift in the potency of M100907 to suppress impulsive behavior. We infer that there is an interactive relationship between the mPFC 5-HT2AR and 5-HT2CR, and that a 5-HT2AR:5-HT2CR imbalance may be a functionally relevant mechanism underlying motor impulsivity.

Impulsivity is an important feature of multiple neuropsychiatric disorders, and individual variation in the degree of inherent impulsivity could play a role in the generation or exacerbation of problematic behaviors. Serotonin (5-HT) actions at the 5-HT2AR receptor (5-HT2AR) promote and 5-HT2AR antagonists suppress impulsive action (the inability to withhold premature responses; motor impulsivity) upon systemic administration or microinfusion directly into the medial prefrontal cortex (mPFC), a node in the corticostriatal circuit that is thought to play a role in the regulation of impulsive action. We hypothesized that the functional capacity of the 5-HT2AR, which is governed by its expression, localization, and protein/protein interactions (eg, postsynaptic density 95 (PSD95)), may drive the predisposition to inherent impulsive action. Stable high-impulsive (HI) and low-impulsive (LI) phenotypes were identified from an outbred rodent population with the 1-choice serial reaction time (1-CSRT) task. HI rats exhibited a greater head-twitch response following administration of the preferential 5-HT2AR agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) and were more sensitive to the effects of the selective 5-HT2AR antagonist M100907 to suppress impulsive action relative to LI rats. A positive correlation was observed between levels of premature responses and 5-HT2AR binding density in frontal cortex ([(3)H]-ketanserin radioligand binding). Elevated mPFC 5-HT2AR protein expression concomitant with augmented association of the 5-HT2AR with PSD95 differentiated HI from LI rats. The observed differential sensitivity of HI and LI rats to 5-HT2AR ligands and associated distinct 5-HT2AR protein profiles provide evidence that spontaneously occurring individual differences in impulsive action reflect variation in the cortical 5-HT2AR system.

Impulsivity is a multifaceted construct that is a core feature of multiple psychiatric conditions and personality disorders. However, progress in understanding and treating impulsivity is limited by a lack of precision and consistency in its definition and assessment. Rapid-response impulsivity (RRI) represents a tendency toward immediate action that occurs with diminished forethought and is out of context with the present demands of the environment. Experts from the International Society for Research on Impulsivity (InSRI) met to discuss and evaluate RRI measures in terms of reliability, sensitivity, and validity, with the goal of helping researchers and clinicians make informed decisions about the use and interpretation of findings from RRI measures. Their recommendations are described in this article. Commonly used clinical and preclinical RRI tasks are described, and considerations are provided to guide task selection. Tasks measuring two conceptually and neurobiologically distinct types of RRI, "refraining from action initiation" (RAI) and "stopping an ongoing action" (SOA) are described. RAI and SOA tasks capture distinct aspects of RRI that may relate to distinct clinical outcomes. The InSRI group recommends that (a) selection of RRI measures should be informed by careful consideration of the strengths, limitations, and practical considerations of the available measures; (b) researchers use both RAI and SOA tasks in RRI studies to allow for direct comparison of RRI types and examination of their associations with clinically relevant measures; and (c) similar considerations be made for human and nonhuman studies in an effort to harmonize and integrate preclinical and clinical research., ((c) 2015 APA, all rights reserved).)

Impulsivity critically relates to many psychiatric disorders. Given the multifaceted construct that impulsivity represents, defining core aspects of impulsivity is vital for the assessment and understanding of clinical conditions. Choice impulsivity (CI), involving the preferential selection of smaller sooner rewards over larger later rewards, represents one important type of impulsivity. The International Society for Research on Impulsivity (InSRI) convened to discuss the definition and assessment of CI and provide recommendations regarding measurement across species. Commonly used preclinical and clinical CI behavioral tasks are described, and considerations for each task are provided to guide CI task selection. Differences in assessment of CI (self-report, behavioral) and calculating CI indices (e.g., area-under-the-curve, indifference point, and steepness of discounting curve) are discussed along with properties of specific behavioral tasks used in preclinical and clinical settings. The InSRI group recommends inclusion of measures of CI in human studies examining impulsivity. Animal studies examining impulsivity should also include assessments of CI and these measures should be harmonized in accordance with human studies of the disorders being modeled in the preclinical investigations. The choice of specific CI measures to be included should be based on the goals of the study and existing preclinical and clinical literature using established CI measures., ((c) 2015 APA, all rights reserved).)

Alcohol-related aggression is a complex and problematic phenomenon with profound public health consequences. We examined neural correlates potentially moderating the relationship between human aggressive behavior and chronic alcohol use. Thirteen subjects meeting DSM-IV criteria for past alcohol-dependence in remission (AD) and 13 matched healthy controls (CONT) participated in an fMRI study adapted from a laboratory model of human aggressive behavior (Point Subtraction Aggression Paradigm, or PSAP). Blood oxygen level dependent (BOLD) activation was measured during bouts of operationally defined aggressive behavior, during postprovocation periods, and during monetary-reinforced behavior. Whole brain voxelwise random-effects analyses found group differences in brain regions relevant to chronic alcohol use and aggressive behavior (e.g., emotional and behavioral control). Behaviorally, AD subjects responded on both the aggressive response and monetary response options at significantly higher rates than CONT. Whole brain voxelwise random-effects analyses revealed significant group differences in response to provocation (monetary subtractions), with CONT subjects showing greater activation in frontal and prefrontal cortex, thalamus, and hippocampus. Collapsing data across all subjects, regression analyses of postprovocation brain activation on aggressive response rate revealed significant positive regression slopes in precentral gyrus and parietal cortex; and significant negative regression slopes in orbitofrontal cortex, prefrontal cortex, caudate, thalamus, and middle temporal gyrus. In these collapsed analyses, response to provocation and aggressive behavior were associated with activation in brain regions subserving inhibitory and emotional control, sensorimotor integration, and goal directed motor activity., ((PsycINFO Database Record (c) 2015 APA, all rights reserved).)

Cocaine dependence is associated with increased impulsivity in humans. Both cocaine dependence and impulsive behavior are under the regulatory control of cortico-striatal networks. One behavioral laboratory measure of impulsivity is response inhibition (ability to withhold a prepotent response) in which altered patterns of regional brain activation during executive tasks in service of normal performance are frequently found in cocaine dependent (CD) subjects studied with functional magnetic resonance imaging (fMRI). However, little is known about aberrations in specific directional neuronal connectivity in CD subjects. The present study employed fMRI-based dynamic causal modeling (DCM) to study the effective (directional) neuronal connectivity associated with response inhibition in CD subjects, elicited under performance of a Go/NoGo task with two levels of NoGo difficulty (Easy and Hard). The performance on the Go/NoGo task was not significantly different between CD subjects and controls. The DCM analysis revealed that prefrontal-striatal connectivity was modulated (influenced) during the NoGo conditions for both groups. The effective connectivity from left (L) anterior cingulate cortex (ACC) to L caudate was similarly modulated during the Easy NoGo condition for both groups. During the Hard NoGo condition in controls, the effective connectivity from right (R) dorsolateral prefrontal cortex (DLPFC) to L caudate became more positive, and the effective connectivity from R ventrolateral prefrontal cortex (VLPFC) to L caudate became more negative. In CD subjects, the effective connectivity from L ACC to L caudate became more negative during the Hard NoGo conditions. These results indicate that during Hard NoGo trials in CD subjects, the ACC rather than DLPFC or VLPFC influenced caudate during response inhibition.

Impulsivity and sensation seeking are stimulus-oriented traits. Because they differ in degree of intention and planning, they may have distinct neurophysiological mechanisms. Impulsivity is prominent in bipolar disorder, and may be related to pre-attentional information filtering and stimulus-orientation. We investigated specificity of relationships between impulsivity and sensitivity to stimulus intensity in bipolar disorder and controls, using intensity-sensitivity of auditory evoked potentials. Seventy-six subjects (37 healthy controls, 39 with bipolar disorder) were administered an intensity-sensitivity paradigm. Additional measures included Barratt Impulsiveness Scale (BIS-11) and Eysenck Impulsivity and Venturesomeness scores. State-dependent rapid-response impulsivity was measured using the Immediate Memory Task. Intensity-sensitivities of the auditory evoked P1N1, N1P2, P1, N1, and P2 potentials were assessed as the slope of amplitude relative to loudness. Analyses used general linear models (GLM) with impulsivity-related measures as dependent variables and age, gender, education, and diagnosis as dependent variables. BIS-11 total, motor, and attentional impulsivity scores correlated positively with pre-attentional N1 and P1N1 intensity-sensitivity slopes in bipolar disorder, but not in controls. BIS-11 nonplanning and Eysenck Venturesomeness scores did not correlate with intensity-sensitivity. Intensity-sensitivity slopes did not correlate with rapid-response impulsivity. Correlations between N1 or P1N1 slopes and BIS-11 scores in bipolar disorder were not affected by age, education, WAIS, treatment, symptoms, or gender. Trait impulsivity in bipolar disorder may be related to poorly modulated stimulus-driven late pre-attentional responses to stimuli, potentially resulting in exaggerated responses to intense stimuli even before conscious awareness. Components of trait impulsivity are physiologically heterogenous relative to intensity-sensitivity., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

The multidimensional construct of impulsivity is implicated in all phases of the addiction cycle. Substance dependent individuals (SDIs) demonstrate elevated impulsivity on both trait and laboratory tests of neurobehavioral impulsivity; however our understanding of the relationship between these different aspects of impulsivity in users of different classes of drugs remains rudimentary. The goal of this study was to assess for commonalities and differences in the relationships between trait and neurobehavioral impulsivity in heroin and amphetamine addicts. Participants included 58 amphetamine dependent (ADIs) and 74 heroin dependent individuals (HDIs) in protracted abstinence. We conducted Principal Component Analyses (PCA) on two self-report trait and six neurobehavioral measures of impulsivity, which resulted in two trait impulsivity (action, planning) and four neurobehavioral impulsivity composites (discriminability, response inhibition efficiency, decision-making efficiency, quality of decision-making). Multiple regression analyses were used to determine whether neurobehavioral impulsivity is predicted by trait impulsivity and drug type. The analyses revealed a significant interaction between drug type and trait action impulsivity on response inhibition efficiency, which showed opposite relationships for ADIs and HDIs. Specifically, increased trait action impulsivity was associated with worse response inhibition efficiency in ADIs, but with better efficiency in HDIs. These results challenge the unitary account of drug addiction and contribute to a growing body of literature that reveals important behavioral, cognitive, and neurobiological differences between users of different classes of drugs., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Impulsivity and compulsivity represent useful conceptualizations that involve dissociable cognitive functions, which are mediated by neuroanatomically and neurochemically distinct components of cortico-subcortical circuitry. The constructs were historically viewed as diametrically opposed, with impulsivity being associated with risk-seeking and compulsivity with harm-avoidance. However, they are increasingly recognized to be linked by shared neuropsychological mechanisms involving dysfunctional inhibition of thoughts and behaviors. In this article, we selectively review new developments in the investigation of the neurocognition of impulsivity and compulsivity in humans, in order to advance our understanding of the pathophysiology of impulsive, compulsive, and addictive disorders and indicate new directions for research.

Early responses to stimuli can be measured by sensory evoked potentials (EP) using repeated identical stimuli, S1 and S2. Response to S1 may represent efficient stimulus detection, while suppression of response to S2 may represent inhibition. Early responses to stimuli may be related to impulsivity. We compared EP reflecting stimulus detection and inhibition in bipolar disorder and healthy controls, and investigated relationships to impulsivity. Subjects were 48 healthy controls without family histories of mood disorder and 48 with bipolar disorder. EP were measured as latencies and amplitudes for auditory P50 (pre-attentional), N100 (initial direction of attention) and P200 (initial conscious awareness), using a paired-click paradigm, with identical stimuli 0.5 s apart. Impulsivity was measured by questionnaire and by laboratory tests for inability to suppress responses to stimuli or to delay response for a reward. Analyses used general linear models. S1 amplitudes for P50, N100, and P200, and gating of N100 and P200, were lower in bipolar disorder than in controls. P50 S1 amplitude correlated with accurate laboratory-task responding, and S2 amplitude correlated with impulsive task performance and fast reaction times, in bipolar disorder. N100 and P200 EP did not correlate with impulsivity. These findings were independent of symptoms, treatment, or substance-use history. EPs were not related to questionnaire-measured or reward-based impulsivity. Bipolar I disorder is characterized by reduced pre-attentional and early attentional stimulus registration relative to controls. Within bipolar disorder, rapid-response impulsivity correlates with impaired pre-attentional response suppression. These results imply specific relationships between ERP-measured response inhibition and rapid-response impulsivity., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Rationale: Rapid-response impulsivity, characterized by inability to withhold response to a stimulus until it is adequately appraised, is associated with risky behavior and may be increased in a state-dependent manner by norepinephrine., Objective: We assessed effects of yohimbine, which increases norepinephrine release by blocking alpha-2 noradrenergic receptors, on plasma catecholamine metabolites, blood pressure, subjective symptoms, and laboratory-measured rapid-response impulsivity., Methods: Subjects were 23 healthy controls recruited from the community, with normal physical examination and ECG, and negative history for hypertension, cardiovascular illness, and axis I or II disorder. Blood pressure, pulse, and behavioral measures were obtained before and periodically after 0.4 mg/kg oral yohimbine or placebo in a randomized, counterbalanced design. Metabolites of norepinephrine [3-methoxy-4-hydroxyphenylglycol (MHPG) and vanillylmandelic acid (VMA)] and dopamine [homovanillic acid (HVA)] were measured by high-pressure liquid chromatography with electrochemical detection. Rapid-response impulsivity was measured by commission errors and reaction times on the immediate memory task (IMT), a continuous performance test designed to measure impulsivity and attention., Results: Yohimbine increased plasma MHPG and VMA but not HVA. Yohimbine increased systolic and diastolic blood pressure and pulse rate. On the IMT, yohimbine increased impulsive errors and impulsive response bias and accelerated reaction times. Yohimbine-associated increase in plasma MHPG correlated with increased impulsive response rates. Time courses varied; effects on blood pressure generally preceded those on metabolites and test performance., Conclusions: These effects are consistent with increased rapid-response impulsivity after pharmacological noradrenergic stimulation in healthy controls. Labile noradrenergic responses, or increased sensitivity to norepinephrine, may increase risk for impulsive behavior.

Aggression, impulsivity, and psychopathic traits are prominent in both antisocial personality disorder (ASPD) and substance use disorders (SUD), but have rarely been examined collectively. The authors' results show that all three variables were elevated in adults with comorbid ASPD/SUD, relative to SUD-only and control subjects.

Background: Interactions between characteristics of bipolar and Axis II cluster B disorders are clinically and diagnostically challenging. Characteristics associated with personality disorders may be dimensional aspects of bipolar disorder. We investigated relationships among antisocial personality disorder (ASPD) or borderline personality disorder symptoms, impulsivity, and course of illness in bipolar disorder., Methods: Subjects with bipolar disorder were recruited from the community. Diagnosis was by structured clinical interview for DSM-IV (SCID-I and -II), psychiatric symptom assessment by the change version of the schedule for affective disorders and schizophrenia (SADS-C), severity of Axis II symptoms by ASPD and borderline personality disorder SCID-II symptoms, and impulsivity by the Barratt impulsiveness scale (BIS-11)., Results: ASPD and borderline symptoms were not related to clinical state or affective symptoms. Borderline symptoms correlated with BIS-11 impulsivity scores, and predicted history of suicide attempts independently of the relationship to impulsivity. ASPD symptoms were more strongly related to course of illness, including early onset, frequent episodes, and substance-related disorders. These effects persisted after allowance for gender and substance-use disorder history., Conclusions: Personality disorder symptoms appear to be dimensional, trait-like characteristics of bipolar disorder. ASPD and Borderline symptoms are differentially related to impulsivity and course of illness., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Limited information is available on the relationship between antisocial personality disorder (ASPD) and early filtering, or gating, of information, even though this could contribute to the repeatedly reported impairment in ASPD of higher-order information processing. In order to investigate early filtering in ASPD, we compared electrophysiological measures of auditory sensory gating assessed by the paired-click paradigm in males with ASPD (n = 37) to healthy controls (n = 28). Stimulus encoding was measured by P50, N100, and P200 auditory evoked potentials; auditory sensory gating (ASG) was measured by a reduction in amplitude of evoked potentials following click repetition. Effects were studied of co-existing past alcohol or drug use disorders, ASPD symptom counts, and trait impulsivity. Controls and ASPD did not differ in P50, N100, or P200 amplitude or ASG. Past alcohol or drug use disorders had no effect. In controls, impulsivity related to improved P50 and P200 gating. In ASPD, P50 or N100 gating was impaired with more symptoms or increased impulsivity, respectively, suggesting impaired early filtering of irrelevant information. In controls the relationship between P50 and P200 gating and impulsivity was reversed, suggesting better gating with higher impulsivity scores. This could reflect different roles of ASG in behavioral regulation in controls versus ASPD., (Published by Elsevier Ltd.)

Background: Bipolar disorder and antisocial personality disorder (ASPD) overlap in clinical characteristics and behavioral consequences. Impulsivity is prominent in both, but there is little information on how specific mechanisms of impulsivity differentiate, bridge, or underlie the disorders., Methods: Subjects, all males, were controls (n = 46), bipolar disorder without cluster B personality disorder (n = 21), ASPD without bipolar disorder (n = 50), and bipolar disorder with ASPD (n = 16). Impulsivity measures were the Immediate Memory Task (IMT), a continuous performance test of response inhibition measuring ability to evaluate a stimulus before responding, and the Two-Choice Impulsivity Paradigm (TCIP), a choice between smaller-sooner and larger-later reward. Data were analyzed using general linear models analysis., Results: Subjects with bipolar disorder had fewer IMT correct detections and slower reaction times than controls. Reaction times were faster with combined diagnoses than in bipolar disorder alone. TCIP responding in either diagnosis alone resembled controls, but was more impulsive in combined disorders. These differences persisted after correction for age and education, which had significant independent effects. In combined ASPD and bipolar disorder, increased reaction speed, impulsive response bias, and reward-delay impulsivity occurred independent of substance-use disorder history., Conclusions: Impulsivity was increased in the combined disorders over either disorder alone. Results were consistent with at least partially distinct mechanisms of impulsivity in ASPD and bipolar disorder. Compensatory mechanisms for impulsivity in uncomplicated ASPD or bipolar disorder appear to be compromised or lost when the disorders are combined., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Alterations in the balance of functional activity within the serotonin [5-hydroxytryptamine (5-HT)] system are hypothesized to underlie impulse control. Cocaine-dependent subjects consistently show greater impulsivity relative to nondrug using control subjects. Preclinical studies suggest that the 5-HT(2A) receptor (5-HT(2A)R) contributes to the regulation of impulsive behavior and also mediates some of the behavioral effects of cocaine. We hypothesized that the selective 5-HT(2A)R antagonist M100907 would reduce inherent levels of impulsivity and attenuate impulsive responding induced by cocaine in two animal models of impulsivity, the differential reinforcement of low rate (DRL) task and the one-choice serial reaction time (1-CSRT) task. M100907 reduced rates of responding in the DRL task and premature responding in the 1-CSRT task. Conversely, cocaine disrupted rates of responding in the DRL task and increased premature responding in the 1-CSRT task. M100907 attenuated cocaine-induced increases in specific markers of behavioral disinhibition in the DRL and 1-CSRT tasks. These results suggest that the 5-HT(2A)R regulates inherent impulsivity, and that blockade of the 5-HT(2A)R alleviates specific aspects of elevated levels of impulsivity induced by cocaine exposure. These data point to the 5-HT(2A)R as an important regulatory substrate in impulse control.

Background: Cocaine-dependent subjects show attentional bias to cocaine-related stimuli, increased impulsivity on questionnaires, and impaired inhibitory control (one component of impulsivity on behavioral tasks). However, the relationship between attentional bias, impulsivity, and inhibitory control in cocaine-dependent subjects is unknown., Objective: To investigate the relationship between attentional bias to cocaine-related stimuli, impulsivity, and inhibitory control in cocaine dependence., Methods: This study employed the cocaine Stroop task to measure attentional bias to cocaine-related stimuli, immediate memory task (IMT) to measure inhibitory control, and Barratt Impulsiveness Scale version 11 to measure impulsivity. Thirty-two controls and 37 cocaine-dependent subjects were recruited through newspaper advertisement., Results: Cocaine-dependent subjects had higher attentional bias to cocaine-related words, higher scores for Barratt Impulsiveness Scale, and higher commission error rate on the IMT than controls. The attentional bias was positively correlated with the commission error rate on the IMT in the cocaine-dependent subjects but not in control subjects., Conclusions: Cocaine-dependent subjects showed attentional bias to cocaine-related words, increased impulsivity, and poor inhibitory control compared with controls. The attentional bias was associated with inhibitory control in cocaine-dependent subjects but not in control subjects., Scientific Significance: Our findings suggest that cocaine-dependent subjects with poor inhibitory control may show higher attentional bias to cocaine-related words compared with controls and those with better inhibitory control., (Copyright © Informa Healthcare USA, Inc.)

Objective: Criminal behavior in bipolar disorder may be related to substance use disorders, personality disorders, or other comorbidities potentially related to impulsivity. We investigated relationships among impulsivity, antisocial personality disorder (ASPD) or borderline personality disorder symptoms, substance use disorder, course of illness, and history of criminal behavior in bipolar disorder., Methods: A total of 112 subjects with bipolar disorder were recruited from the community. Diagnosis was by Structured Clinical Interview for DSM-IV (SCID-I and SCID-II); psychiatric symptom assessment by the Change version of the Schedule for Affective Disorders and Schizophrenia (SADS-C); severity of Axis II symptoms by ASPD and borderline personality disorder SCID-II symptoms; and impulsivity by questionnaire and response inhibition measures., Results: A total of 29 subjects self-reported histories of criminal conviction. Compared to other subjects, those with convictions had more ASPD symptoms, less education, more substance use disorder, more suicide attempt history, and a more recurrent course with propensity toward mania. They had increased impulsivity as reflected by impaired response inhibition, but did not differ in questionnaire-measured impulsivity. On logit analysis, impaired response inhibition and ASPD symptoms, but not substance use disorder, were significantly associated with criminal history. Subjects convicted for violent crimes were not more impulsive than those convicted for nonviolent crimes., Conclusions: In this community sample, a self-reported history of criminal behavior is related to ASPD symptoms, a recurrent and predominately manic course of illness, and impaired response inhibition in bipolar disorder, independent of current clinical state., (© 2011 John Wiley and Sons A/S.)

Alcohol misuse and dependence, and many of its accompanying psychological problems, are associated with heightened levels of impulsivity that both accelerate the development of clinically significant illness and complicate clinical outcome. This article reviews recent developments in our understanding of impulsivity as they relate to brain circuitry that might underlie these comorbid factors, focusing upon the clinical features of substance use (and dependence), bipolar disorder, and pathological gambling. Individuals who are affected by these disorders exhibit problems in several domains of impulsive behavior including deficient response or "motor" control, and the tolerance of prolonged delays prior to larger rewards at the expense of smaller rewards ("delay-discounting"). These populations, like alcoholic dependents, also exhibit impairments in risky decision-making that may reflect dysfunction of monoamine and catecholamine pathways. However, several areas of uncertainty exist including the specificity of impairments across disorders and the relationship between impulse control problems and altered evaluation of reward outcomes underlying observed impairments in action selection.

Impulsivity and decision making are associated on a theoretical level in that impaired planning is a component of both. However, few studies have examined the relationship between measures of decision making and impulsivity in clinical populations. The purpose of this study was to compare cocaine-dependent subjects to controls on a measure of decision making (the Iowa Gambling Task or IGT), a questionnaire measure of impulsivity (the Barratt Impulsiveness Scale or BIS-11) and a measure of behavioural inhibition (the immediate memory task or IMT), and to examine the interrelationship among these measures. Results of the study showed that cocaine-dependent subjects made more disadvantageous choices on the IGT, had higher scores on the BIS and more commission errors on the IMT. Cognitive model analysis showed that choice consistency factors on the IGT differed between cocaine-dependent subjects and controls. However, there was no significant correlation between IGT performance and the BIS total score or subscales or IMT commission errors. These results suggest that in cocaine-dependent subjects there is little overlap between decision making as measured by the IGT and impulsivity/behavioural inhibition as measured by the BIS and IMT., (Copyright 2009 Elsevier Ltd. All rights reserved.)

Objective: We investigated trait impulsivity in bipolar disorder and antisocial personality disorder (ASPD) with respect to severity and course of illness., Method: Subjects included 78 controls, 34 ASPD, 61 bipolar disorder without Axis II disorder, and 24 bipolar disorder with ASPD, by Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (SCID-I and -II). Data were analyzed using general linear model and probit analysis., Results: Barratt Impulsiveness Scale (BIS-11) scores were higher in ASPD (effect sizes 0.5-0.8) or bipolar disorder (effect size 1.45) than in controls. Subjects with both had more suicide attempts and previous episodes than bipolar disorder alone, and more substance-use disorders and suicide attempts than ASPD alone. BIS-11 scores were not related to severity of crimes., Conclusion: Impulsivity was higher in bipolar disorder with or without ASPD than in ASPD alone, and higher in ASPD than in controls. Adverse effects of bipolar disorder in ASPD, but not of ASPD in bipolar disorder, were accounted for by increased impulsivity.

Background: Impulsive behavior is a prominent characteristic of antisocial personality disorder. Impulsivity is a complex construct, however, representing distinct domains of cognition and action. Leading models refer to impulsivity as an inability to evaluate a stimulus fully before responding to it (rapid-response impulsivity), and as an inability to delay responding despite a larger reward (reward-delay impulsivity). We investigated these models in terms of the diagnosis and severity of antisocial personality disorder., Methods: Thirty-four male subjects on probation/parole who met DSM-IV criteria for ASPD, and 30 male healthy comparison subjects, matched by ethnicity, were recruited from the community. The Barratt Impulsiveness Scale (BIS-11) provided an integrated measure of trait impulsivity. Rapid-response impulsivity was assessed using the Immediate Memory Task (IMT), a continuous performance test. Reward delay impulsivity was assessed using the Two-choice Impulsivity Paradigm (TCIP), where subjects had the choice of smaller-sooner or larger-delayed rewards, and the Single Key Impulsivity Paradigm (SKIP), a free-operant responding task., Results: Compared to controls, subjects with ASPD had higher BIS-11 scores (Effect Size (E.S.)=0.95). They had slower reaction times to IMT commission errors (E.S.=0.45). Correct detections, a measure of attention, were identical to controls. On the SKIP, they had a shorter maximum delay for reward (E.S.=0.76), but this was not significant after correction for age and education. The groups did not differ on impulsive choices on the TCIP (E.S.<0.1). On probit analysis with age and education as additional independent variables, BIS-11 score, IMT reaction time to a commission error, and IMT positive response bias contributed significantly to diagnosis of ASPD; SKIP delay for reward did not. Severity of ASPD, assessed by the number of ASPD symptoms endorsed on the SCID-II, correlated significantly with commission errors (impulsive responses) on the IMT, and with liberal IMT response bias. This relationship persisted with correction for age and education., Discussion: These results suggest that ASPD is characterized by increased rapid-response impulsivity. Aspects of impulsivity related to reward-delay or attention appear relatively intact.

Background: Pathological impulsivity in bipolar disorder could be related to deficiencies in mechanisms involved in attention or response inhibition. We investigated these mechanisms in subjects with bipolar disorder and examined relationships to severity of course of illness, use of medication, affective state, age, education, and gender. We measured two complementary aspects of response inhibition: attention-based and reward-based., Methods: Subjects with bipolar disorder (n=112) and healthy controls (n=71) were recruited from the community. Diagnoses were rendered using the SCID for DSMIV. Impulsivity-related measures included the Immediate Memory Task (IMT), a form of the Continuous Performance Task, and the Single Key Impulsivity Paradigm (SKIP), an operant procedure measuring ability to delay responding for a reward., Results: Subjects with bipolar disorder had fewer correct detections (Effect Size (ES)=0.5), prolonged reaction times (ES=0.88), and decreased discriminability (ES=0.57) on the IMT compared to controls. History of frequent episodes, substance use disorders, or suicide attempts predicted faster reaction times, especially to a commission error. Subjects with bipolar disorder who also met criteria for an Axis II disorder had fewer correct detections, more commission errors relative to correct detections, and poorer discriminability on the IMT than other subjects with bipolar disorder. Subjects with bipolar disorder made more responses on the SKIP than did controls (ES=0.5), with a shorter maximum delay (ES=0.62), consistent with inability to delay reward. Probit analysis showed that faster reaction time to a commission error on the IMT was associated with history of substance use disorder, suicide attempt, or many previous episodes. Effects of medication or affective state did not account for these differences., Discussion: Bipolar disorder was associated with impairment in attention and response inhibition, encompassing impaired inhibition of rapid responses and an inability to delay reward, and resulting in impulsivity. Response inhibition mechanisms are impaired further in subjects with more severe complications of illness.

Background: Substance abuse continues to be a major public health problem. Keeping substance abusers in treatment is a challenge, and researchers continue to investigate ways to increase retention., Objective: The aim of this study was to investigate the relationship between impulsivity in substance abusers and length of stay in the context of therapeutic community., Methods: The Barratt Impulsiveness Scale- 11 (BIS-11) was used to assess impulsivity in 138 substance abusers at admission and at nine months in a therapeutic community., Results: Impulsivity significantly decreased in subjects who completed nine months in the therapeutic community. Legal stipulation increased length of stay, on average, by three months. On admission, female participants were on average more impulsive than their male counterparts., Conclusion: Impulsivity decreased in subjects who remained in therapeutic community for nine months although self-reported impulsivity at baseline did not seem to be associated with retention., Scientific Significance: Therapeutic community factors contribute to a decrease in self-reported impulsivity and these factors might be enhanced to increase retention in therapeutic community.

Introduction: Impulsivity, a component of the initiation of action, may have a central role in the clinical biology of affective disorders. Impulsivity appears clearly to be related to mania. Despite its relationship to suicidal behavior, relationships between impulsivity and depression have been studied less than those with mania. Impulsivity is a complex construct, and it may be related differently to depression and to mania., Methods: In subjects with bipolar disorder, we investigated impulsivity in relationship to affective symptoms. Trait-like impulsivity was assessed with the Barratt Impulsiveness Scale (BIS-11). Affective symptoms were measured using the Change version of the Schedule for Affective Disorders and Schizophrenia (SADS-C). Measures were compared using analysis of variance, multiple regression and factor analysis., Results: Impulsivity, as measured by the BIS, was related differentially to measures of depression and mania. Total and attentional impulsivity correlated independently with depression and mania scores. Motor impulsivity correlated with mania scores, while nonplanning impulsivity correlated with depression scores. These relationships were strongest in subjects who had never met criteria for a substance use disorder. Among manic symptoms, visible hyperactivity correlated most strongly with BIS scores, regardless of clinical state. Among depressive symptoms, hopelessness, anhedonia, and suicidality correlated most strongly with BIS scores., Conclusions: Depression and mania are differentially related to impulsivity. Impulsivity is related more strongly to measures of activity or motivation than to depressive or manic affect. The relationship between impulsivity and hopelessness may be an important factor in risk for suicide.

This study extends the use of the Impulsive/Premeditated Aggression Scale for subtyping aggressive behavior among adolescents with Conduct Disorder. Of the Conduct Disorder symptoms, aggression has the strongest prognostic and treatment implications. While aggression is a complex construct, convergent evidence supports a dichotomy of impulsive and premeditated aggressive subtypes that are qualitatively different from one another in terms of phenomenology and neurobiology. Previous attempts at measuring subtypes of aggression in children and adults are not clearly generalizable to adolescents. Sixty-six adolescents completed a questionnaire for characterizing aggression (Impulsive/Premeditated Aggression Scale), along with standard measures of personality and general functioning. Principal components analysis demonstrated two stable factors of aggression with good internal consistency and construct validity. Compared to the premeditated aggression factor, the impulsive aggression factor was associated with a broader range of personality, thought, emotional, and social problems. As in the adult and child literature, characterization of aggressive behavior into two subtypes appears to be relevant to understanding individual differences among adolescents with Conduct Disorder.

The correlation between scores on the Barratt Impulsiveness Scale (BIS) and activation measured by functional magnetic resonance imaging in a dorsolateral prefrontal cortical (DLPFC) activating task was examined in 15 MDMA-using subjects and 19 controls. A significant correlation between BIS scores and DLPFC activation was found, supporting a role for the DLPFC in BIS-measured impulsivity.

Background: State-dependent changes in impulsivity may be related to norepinephrine. To examine possible relationships between norepinephrine and acute changes in impulsivity, we measured effects of yohimbine, which increases norepinephrine release by blocking alpha-2 noradrenergic receptors, on laboratory-measured impulsivity in healthy subjects without psychiatric or substance-use disorders., Methods: Impulsivity was assessed using the Immediate and Delayed Memory Tasks (IMT-DMT), derived from the Continuous Performance Test, before and after placebo or two doses of yohimbine, given 4 days apart. Blood pressure was monitored, and psychiatric symptoms were measured using self-rated visual analog scales., Results: Yohimbine was associated with a dose-related increase in impulsive IMT commission errors, with an increase of > 50% relative to baseline at the higher dose. The activation factor of the Internal State Scale was increased at the same dose., Conclusions: These results are consistent with increased impulsivity in normal subjects given yohimbine, possibly related to increased norepinephrine.

Brain imaging studies find evidence of prefrontal cortical dysfunction in cocaine-dependent subjects. Similarly, cocaine-dependent subjects have problems with behaviors related to executive function and impulsivity. Since prefrontal cortical axonal tracts cross between hemispheres in the corpus callosum, it is possible that white matter integrity in the corpus callosum could also be diminished in cocaine-dependent subjects. The purpose of this study was to compare corpus callosum white matter integrity as measured by the fractional anisotropy (FA) on diffusion tensor imaging (DTI) between 18 cocaine-dependent subjects and 18 healthy controls. The Barratt Impulsiveness Scale (BIS-11) and a continuous performance test: the Immediate and Delayed Memory Task (IMT/DMT) were also collected. Results of the DTI showed significantly reduced FA in the genu and rostral body of the anterior corpus callosum in cocaine-dependent subjects compared to controls. Cocaine-dependent subjects also had significantly higher BIS-11 scores, greater impulsive (commission) errors, and reduced ability to discriminate target from catch stimuli (discriminability) on the IMT/DMT. Within cocaine dependent subjects there was a significant negative correlation between FA in the anterior corpus callosum and behavioral laboratory measured impulsivity, and there was a positive correlation between FA and discriminability. The finding that reduced integrity of anterior corpus callosum white matter in cocaine users is related to impaired impulse control and reduced ability to discriminate between target and catch stimuli is consistent with prior theories regarding frontal cortical involvement in impaired inhibitory control in cocaine-dependent subjects.

Previous studies report reduced amplitude of the P300 event-related potential in cocaine-dependent individuals. Cocaine dependence is also associated with increased impulsivity, possibly due to deficits in cognitive function that are associated with reduced P300 amplitude. In the current study, the relationship between cocaine dependence, impulsivity, and P300 amplitude were examined. An auditory oddball event-related potential task along with self-report (Barratt Impulsiveness Scale version 11) and behavioral laboratory (Immediate and Delayed Memory Task) measures of impulsivity were assessed in healthy controls (n = 14) and subjects who met DSM-IV criteria for current cocaine dependence (n = 17). P300 amplitude was reduced and self-reported and behavioral laboratory impulsivity scores were elevated among the cocaine-dependent group compared to controls. There was a positive correlation between the questionnaire and behavioral laboratory measures of impulsivity, and a negative correlation between impulsivity measures and P300 amplitude. The correlation between self-reported impulsivity scores and P300 amplitude remained after taking into account the number of childhood conduct disorder symptoms. This study supports the hypothesis that the basic neurophysiology responsible for the P300 amplitude in cocaine-dependent individuals is associated with impulsivity independent of a history of childhood conduct disorder symptoms.

Background: Behavioral impulsivity paradigms vary widely and studies using these measures have typically relied on a single measure used in isolation. As a result, comparisons between measures are difficult, with little consensus regarding which method may be most sensitive to individual impulsivity differences of different populations., Method: A single testing session of each of four different impulsivity tasks was completed by two groups of adolescents aged 13-17: hospitalized inpatients with disruptive behavior disorders (DBD; n = 22) and controls (n = 22). Tasks included two rapid-decision (IMT/DMT and GoStop) and two reward-directed (TC and SKIP) impulsivity paradigms. Behavioral testing took place within 3 days of hospitalization for the adolescents with DBD., Results: Compared to controls, the DBD group exhibited higher commission error rates, lower inhibited response rates after a stop-signal, and twice as many reward-directed responses even after IQ differences between the groups were taken into account. When the four paradigms were compared, effect-size calculations indicated that the two rapid-decision paradigms were more sensitive to group differences than the reward-directed tasks., Conclusions: Despite the initiation of pharmacotherapy within the first 3 days of hospitalization, in contrast to the control group, the adolescents with DBD performed consistently with what has been operationally defined as impulsivity. Based on these results, these tasks appear to measure similar, but unique components of the impulsivity construct. With further study, laboratory behavioral paradigms may prove to be useful additions to current clinical diagnostic and treatment procedures in a variety of psychiatric populations.

This study is one in a series investigating the relationship between impulsive behavior on a Continuous Performance Test (i.e., the Immediate and Delayed Memory Task) and other cognitive deficits measured by clinical instruments. Forty-two adolescents were selected for two groups, controls and hospitalized patients with disruptive behavior disorders. Each adolescent completed the Immediate and Delayed Memory Task and the Benton Visual Retention Test. Our main findings were that, even when controlling for IQ, the Immediate and Delayed Memory Task commission errors were associated with adverse Benton performance, but only in the patient group. These results may be explained by a shared association between processes of impulsivity and other deficits of executive control that may interfere with successful performance of the Benton.

Continuous Performance Tests (CPTs) provide information on attentional processing and impulsive behavior. The results of previous research that used self-report measures have provided evidence for familial transmission (through genetic and/or environmental influences) of impulsive characteristics. The authors of the present study examined whether the impulsive behavioral parameters that are measured by the CPT also share familial relationships. The researchers asked 26 healthy parent-adolescent pairs to complete the Immediate and Delayed Memory Tasks (IMT/DMT; D. M. Dougherty, 1999; D. M. Dougherty, D. M. Marsh, & C. W. Mathias, 2002), a modified CPT (B. A. Cornblatt, N. J. Risch, G. Faris, D. Friedman, & L. Erlenmeyer-Kimling, 1988; H. E. Rosvold, A. Mirsky, I. Sarason, E. D. Breansome, Jr., & L. H. Beck, 1956), and the Barratt Impulsiveness Scale (BIS; J. H. Patton, M. S. Stanford, & E. S. Barratt, 1995), a self-report measure. The main findings can be summarized as follows: (a) commission errors (but not correct detections) on the IMT and DMT were correlated between parents and their adolescent children, (b) adolescents emitted a higher proportion of commission errors than did their parents, and (c) self-reported impulsivity (i.e., BIS) was correlated with commission errors for parents, but not for adolescents. The findings of this study support the use of an objective behavioral measure of impulsivity to assess familial relationships of impulsivity.

Several previous studies show a relationship between impulsivity and substance abuse; however, it is unclear whether the increased impulsivity seen in substance dependent groups is specifically related to substance abuse, or if it is due to concomitant antisocial personality disorder (ASPD) or aggression. The issue of whether impulsivity is specifically related to substance abuse is important since it has a bearing on risk factors for development of substance abuse. To determine whether cocaine dependent subjects show increased impulsivity independent of ASPD, the Barratt impulsiveness scale (BIS-11), a delayed reward laboratory measure of impulsivity, and the life history of aggression scale were administered to 49 cocaine dependent subjects and 25 controls. Results showed that cocaine dependent subjects with ASPD were more impulsive and aggressive than controls, but cocaine dependent subjects without ASPD were also more impulsive compared to controls. Controlling for aggression history, cocaine dependent subjects without ASPD continued to have elevated impulsivity as measured by the BIS-11, but not the delayed reward task. This study supports the hypothesis that the increased impulsivity as measured by the BIS-11 in cocaine dependent individuals is not exclusively due to concomitant increases in aggression or ASPD.

Background: Impulsivity is prominent in psychiatric disorders. Two dominant models of impulsivity are the reward-discounting model, where impulsivity is defined as inability to wait for a larger reward, and the rapid-response model, where impulsivity is defined as responding without adequate assessment of context. We have compared the role of these models of impulsivity in human psychopathology, based on the hypothesis that rapid-response impulsivity would be more strongly related to other aspects of psychopathology and to impulsivity as described by questionnaires., Methods: We investigated relationships between personality and laboratory measures of impulsivity, and between these measures and clinical characteristics, in parents of adolescent subjects with disruptive behavioral disorders (DBDs) and matched control subjects. Diagnoses were rendered using the Structured Interview for DSM-IV. The Barratt Impulsiveness Scale (BIS) was used as a trait measure of impulsivity. Rapid-response impulsivity was assessed using a form of the Continuous Performance Test, the Immediate Memory-Delayed Memory Task (IMT/DMT). Reward-delay impulsivity was measured using two tasks where subjects could choose between smaller immediate or larger delayed rewards., Results: Rapid-response, but not reward-delay impulsivity, was significantly higher in subjects with lifetime Axis I or Axis II diagnoses. Scores on the BIS were elevated in subjects with Axis I diagnoses and correlated significantly with both rapid-response and reward-delay tests, but more strongly with the former. Multiple regression showed that rapid-response, but not reward-delay performance or intelligence quotient, contributed significantly to BIS scores. Correlations were similar in parents of control subjects and of DBD subjects., Conclusions: These data suggest that measures of rapid-response impulsivity and of reward-delay impulsivity are both related to impulsivity as a personality characteristic. The relationship appears stronger, however, for rapid-response impulsivity, as measured by the IMT/DMT. Laboratory and personality measures of impulsivity appear to be related to risk of psychopathology.

To determine whether impulsivity was related to severity of drug use and treatment outcome, 50 cocaine dependent subjects underwent baseline measures of severity of current cocaine use and the Barratt Impulsiveness Scale (BIS-11). The hypothesis of the study was that there would be a significant correlation between impulsivity and cocaine use severity. As predicted, there was a significant correlation between BIS-11 total scores and self-reported average daily cocaine use as well as cocaine withdrawal symptoms. A subset of 35 patients underwent a 12-week double-blind placebo controlled trial of buspirone and group therapy. Subjects with high baseline impulsivity remained in the study a significantly shorter period than did subjects with lower baseline impulsivity. This study shows that impulsivity is a significant predictor of cocaine use and treatment retention, and suggests the need for targeting impulsivity in cocaine dependence treatment.

A correlation between elevated testosterone and aggressive behavior has been demonstrated in animals and to a lesser degree in humans, primarily in the context of dominance. Some aggression, namely non-premeditated aggression, is characterized by impaired impulse control. Real-world aggressive histories and self-reported impulsivity have correlated with commission errors (failures to withhold responses to nontarget stimuli) in versions of the continuous performance test (CPT). To begin exploring whether testosterone may play a role in aggression due more to a direct relationship with impaired impulse control, we related plasma total testosterone concentrations of 27 psychiatrically healthy women to commission errors in two variants of the CPT - with and without interstimulus distracters. Controlling for age and IQ, testosterone did not relate to rates of correct detections in either task, but correlated positively with commission errors in the distracter CPT variant. In light of the fact previous studies find commission errors on the CPT are associated with impulsivity, the results of this study support a positive relationship between testosterone and impulsivity.

To characterize how severe negative affect in women is reflected in objective measures of aggression and impulsivity, the aggressive and impulsive behavior of 14 hospitalized women with borderline personality disorder (BPD) was compared with that of 17 controls. In an impulsivity task, subjects experienced two sets of 50 trials during which they could choose a smaller, immediate monetary reward or a larger but progressively delayed reward. In a separate task (PSAP), subjects earned monetary reinforcers with repeated button presses, and were provoked by the subtraction of money which was blamed on a fictitious other participant. Subjects could respond by ostensibly subtracting money from the fictitious subject (the aggressive response). While selection frequency of the short-delay responses was similar in patients and controls, BPD patients responded to avoid longer delay of reward across trials, and had higher Barratt Impulsiveness Scale total scores and attentional subscale scores. BPD patients responded to the money losses with roughly three times as many aggressive responses as controls and had higher Buss-Durkee Hostility Inventory (BDHI), Brown History of Violence, and Retrospective Overt Aggression Scale scores than controls. Aggressive responding rates correlated positively with BDHI scores. These results extend previous findings that negative affect in women is reflected in laboratory behavioral measures.

Impulsivity was contrasted between 32 subjects with a history of drug-dependence (DRUG+) and 26 subjects with no drug use history (DRUG-) using both behavioral and self-report measures. The hypothesis was that the DRUG+ group would be more impulsive than the DRUG- group. Subjects in the DRUG+ group self-reported more of a tendency toward impulsivity than the DRUG- group in the situations posed in questionnaires. In the behavioural paradigm involving a choice between a smaller intermediate reward and a larger but delayed reward, DRUG+ subjects selected the impulsive option more often, but these differences were not significant. The DRUG+ and DRUG- groups did differ on the mean delay interval for the larger reward, indicating less ability to tolerate longer delays for the larger reward. A frequency distribution of delay intervals for the larger reward indicated that DRUG+ subjects were more likely to maintain very short intervals and less likely to maintain longer intervals.

Males parolees were recruited into a laboratory study to determine the relationship between their previous criminal history (violent versus nonviolent), and behavioral and psychometric measures of impulsivity. During sessions, subjects were given two response options defined as: 1) an impulsive choice--small monetary reward after a short fixed delay; and 2) a self-control choice--a larger monetary reward after a variable longer delay. Based upon an extensive experimental literature in animals and humans related to delay of gratification, the degree of impulsivity was defined as the proportion of trials on which the subject selected the impulsive option. Our results indicated that the violent subjects selected the impulsive option significantly more often than the nonviolent parolees. The number of impulsive responses parolees emitted was significantly correlated with the number of aggressive responses reported in an earlier paper. This study provides support for the relationship between impulsivity and aggression among male parolees.

1. 10 male cocaine dependent patients and 10 sex matched controls were administered several behavioral measures of aggression including the Buss-Durkee Hostility Inventory, and The Brown-Goodwin Life History of Aggression. 2. All subjects were also administered a buspirone neuroendocrine challenge as a measure of serotonin function. 3. The cocaine dependent subjects were significantly more aggressive than the controls. 4. There was a significant correlation between the growth hormone response to buspirone and behavioral measures of aggression in the cocaine dependent subjects, but not in the controls. 5. There was no difference in the overall growth hormone response between the controls and cocaine dependent subjects, possibly due to differences in metabolism of buspirone. 6. This study supports a role for serotonin in aggression in cocaine dependent subjects.