Aggression proneness: Transdiagnostic processes involving negative valence and cognitive systems

Verona, Edelyn; Bresin, Konrad

doi:10.1016/j.ijpsycho.2015.03.008

Cited by 46 publications

(53 citation statements)

References 92 publications

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“…Nonetheless, the WURS includes a host of symptoms related to various elements of aggressiveness, which, based on our factor analysis as well as previous research [Ward et al, ] seem to be of key importance to the phenotype of aADHD, and the ODD measures have also been validated in previous studies of cADHD [Stringaris et al, ; Aebi et al, ]. Our approach may add to the discussion of the Negative Valence System in the Research Domain Criteria (RDoC) of the National Institute of Mental Health (NIMH) of how to conceptualize and operationalize aggressiveness as a dimension across different samples and disorders [Verona and Bresin, ; Veroude et al, ].…”

Section: Discussionmentioning

confidence: 69%

Genome‐wide analyses of aggressiveness in attention‐deficit hyperactivity disorder

Brevik

Donkelaar

Weber

et al. 2016

American J of Med Genetics Pt B

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Aggressiveness is a behavioral trait that has the potential to be harmful to individuals and society. With an estimated heritability of about 40%, genetics is important in its development. We performed an exploratory genome‐wide association (GWA) analysis of childhood aggressiveness in attention deficit hyperactivity disorder (ADHD) to gain insight into the underlying biological processes associated with this trait. Our primary sample consisted of 1,060 adult ADHD patients (aADHD). To further explore the genetic architecture of childhood aggressiveness, we performed enrichment analyses of suggestive genome‐wide associations observed in aADHD among GWA signals of dimensions of oppositionality (defiant/vindictive and irritable dimensions) in childhood ADHD (cADHD). No single polymorphism reached genome‐wide significance (P < 5.00E‐08). The strongest signal in aADHD was observed at rs10826548, within a long noncoding RNA gene (beta = −1.66, standard error (SE) = 0.34, P = 1.07E‐06), closely followed by rs35974940 in the neurotrimin gene (beta = 3.23, SE = 0.67, P = 1.26E‐06). The top GWA SNPs observed in aADHD showed significant enrichment of signals from both the defiant/vindictive dimension (Fisher's P‐value = 2.28E‐06) and the irritable dimension in cADHD (Fisher's P‐value = 0.0061). In sum, our results identify a number of biologically interesting markers possibly underlying childhood aggressiveness and provide targets for further genetic exploration of aggressiveness across psychiatric disorders. © 2016 The Authors. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Published by Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 69%

Genome‐wide analyses of aggressiveness in attention‐deficit hyperactivity disorder

Brevik

Donkelaar

Weber

et al. 2016

American J of Med Genetics Pt B

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“…Studies investigating related topics support the present findings insofar as they showed acute stress to affect selectively different stages of the stream of processing with enhanced N2 amplitude in an oddball task in social drinkers, during action cascading processes, and a change detection task (Ceballos, Giuliano, Wicha, & Graham, ; Sänger, Bechtold, Schoofs, Blaszkewicz, & Wascher, ; Yildiz, Wolf, & Beste, ). Similarly, reduced no‐go/P3 amplitudes are associated with aggression (Verona & Bresin, ). Stress (and, in particular, cortisol) is assumed to promote aggressive behavior (Böhnke, Bertsch, Kruk, Richter, & Naumann, ; Geniole, Carre, & McCormick, ).…”

Section: Discussionmentioning

confidence: 99%

Influence of acute stress on response inhibition in healthy men: An ERP study

et al. 2017

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The current study investigated the influence of acute stress and the resulting cortisol increase on response inhibition and its underlying cortical processes, using EEG. Before and after an acute stressor or a control condition, 39 healthy men performed a go/no-go task while ERPs (N2, P3), reaction times, errors, and salivary cortisol were measured. Acute stress impaired neither accuracy nor reaction times, but differentially affected the neural correlates of response inhibition; namely, stress led to enhanced amplitudes of the N2 difference waves (N2d, no-go minus go), indicating enhanced response inhibition and conflict monitoring. Moreover, participants responding to the stressor with an acute substantial rise in cortisol (high cortisol responders) showed reduced amplitudes of the P3 of the difference waves (P3d, no-go minus go) after the stressor, indicating an impaired evaluation and finalization of the inhibitory process. Our findings indicate that stress leads to a reallocation of cognitive resources to the neural subprocesses of inhibitory control, strengthening premotor response inhibition and the detection of response conflict, while concurrently diminishing the subsequent finalization process within the stream of processing.

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“…Ces résultats correspondent au profil d'activation cérébrale caractéristique des individus violents et antisociaux, dans lequel est observée une activité réduite des régions préfrontales accompagnées d'une activité accrue des régions sous-corticales (limbiques) (Raine et al, 1998). En effet, Verona & Bresin (2015) ont récemment rapporté que les personnes manifestant un haut niveau d'agressivité (comportement associé au Facteur 2) présentent un contrôle de l'inhibition perturbé (amplitude P300 réduite lors de la condition No-go), seulement lors de contextes émotionnels saillants. Par conséquent, alors que la désinhibition et les déficits du fonctionnement préfrontal pourraient constituer la vulnérabilité centrale à l'émergence de différentes manifestations antisociales, les perturbations affectives du contrôle cognitif prédisposeraient les individus présentant des traits impulsifs et antisociaux à certaines manifestations spécifiques telles que l'agressivité et la violence.…”

Section: Resultsunclassified

Interactions cognition-émotion et personnalité psychopathique : des trajectoires distinctes vers les comportements antisociaux et violents

Verona

2016

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Les chercheurs ont depuis longtemps reconnu l’hétérogénéité des individus présentant des comportements antisociaux et violents. Or, l’étude de la personnalité psychopathique (ou psychopathie), par l’examen de ses différentes facettes, peut aider à mieux comprendre cette hétérogénéité. Plus particulièrement, la distinction entre les corrélats des traits interpersonnels et affectifs (Facteur 1) et ceux des traits impulsifs et antisociaux (Facteur 2) de la psychopathie suggère l’existence d’au moins deux trajectoires pouvant mener aux comportements antisociaux. Basée sur diverses études en neurosciences cognitives et affectives, nous proposons une revue ciblée, non exhaustive, des travaux identifiant les mécanismes biopsychologiques impliqués dans ces deux trajectoires, avec une attention particulière accordée aux études utilisant la méthode des potentiels évoqués (PE). Plus spécifiquement, nous présentons une série d’études portant sur les processus cognitifs et affectifs permettant de distinguer, parmi un groupe de délinquants, ceux ayant des traits psychopathiques élevés, en mettant en évidence les altérations des interactions entre émotion et cognition associées à chaque facteur de la psychopathie. L’ensemble de ces résultats mène aux conclusions suivantes. Le Facteur 1, associé à une réponse émotionnelle diminuée exacerbée par des anomalies attentionnelles, correspond à un profil de délinquance caractérisé par des conduites délibérées et une insensibilité émotionnelle. À l’opposé, le Facteur 2 comporte des dérégulations émotionnelles et comportementales, de même que des troubles de contrôle cognitif, particulièrement en contexte émotionnel. Les implications de l’identification de ces processus étiologiques seront ensuite présentées dans la perspective d’une meilleure compréhension des comportements violents et antisociaux.Researchers have long acknowledged heterogeneity among persons who exhibit antisocial and violent behaviours. The study of psychopathic personality or psychopathy can help elucidate this heterogeneity through examination of the different facets that constitute this disorder. In particular, the distinct correlates of the interpersonal-affective traits (Factor 1) and the impulsive-antisocial traits (Factor 2) of psychopathy suggest at least two possible pathways to antisocial behaviours. Building on basic studies in cognitive and affective neuroscience, we provide a focused, non-comprehensive review of work identifying the biopsychological mechanisms involved in these two pathways, with special attention to studies using event-related potential (ERP) methods. In specific, a series of studies are discussed which examined affective and cognitive processes that may distinguish offenders high on psychopathic traits from other offenders, with emphasis on alterations in emotion-cognition interactions related to each factor of psychopathy. The set of findings reviewed highlight a central conclusion: Factor 1 represents a pathway involving reduced emotional responding, exacerbated by attentional abnorma...

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Aggression proneness: Transdiagnostic processes involving negative valence and cognitive systems

Cited by 46 publications

References 92 publications

Genome‐wide analyses of aggressiveness in attention‐deficit hyperactivity disorder

Genome‐wide analyses of aggressiveness in attention‐deficit hyperactivity disorder

Influence of acute stress on response inhibition in healthy men: An ERP study

Interactions cognition-émotion et personnalité psychopathique : des trajectoires distinctes vers les comportements antisociaux et violents

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