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    Antisocial Disorders

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    Submitted by: Ronald Toro

    Abstract

    Transdiagnostic causal variables have been identified that have allowed understanding the origin and maintenance of psychopathologies in parsimonious explanatory models of antisocial disorders. However, it is necessary to systematize the information published in the last decade. The main findings indicated that at a structural level there is a general psychopathological factor (psychopathy or externalizing), non-emotional callousness and impulsivity from behavioral inhibition and activation systems, and negative affect traits as base structures. In the emotional level, the study found a risk component from emotional dysregulation and experiential avoidance. In the cognitive level, a key role of anger-rumination and violent ideation as explanatory variables of antisocial disorders. We concluded that the interaction of these identified variables makes it possible to generate an evidence-based transdiagnostic model.

    1. Introduction

    Antisocial disorders (ADs) are characterized by alterations in impulse control, emotional dysregulation and behavioral problems, manifested in behaviors that violate the rights of others such as delinquency, property damage, aggression, and conflicts with accepted social norms and authority figures[1][2]. ADs have been analyzed from a dimensional spectrum made up of a group of psychopathologies, which are organized according to their common etiologies and symptoms, resulting in the externalizing spectrum[3]. In DSM 5[2], they appear in the group of ADs of childhood, adolescence, and adulthood, which includes conduct disorders (including specification: with limited pro-social emotions), intermittent explosive disorder and antisocial personality disorder, in addition to antisocial behavior in the child or adolescent located in other disorders associated with disruptive or impulsive behavior.

    It is possible to develop models that guide the understanding of the origin and maintenance, from the common variables called transdiagnostic by using a spectrum as an indicator of AD in psychopathology research, following a dimensional perspective of the processes and factors underlying the different disorders. The transdiagnostic model (TM) “consists of understanding mental disorders based on a range of etiopathogenic cognitive and behavioral processes that are the cause or maintain most of the mental disorders or consistent groups of mental disorders” ([4], p.187).

    This model has developed research based on the symptoms and processes underlying mental illness, following a limited range of common symptoms, or diagnoses with multiple processes, or others, with single universal and multiple processes[5]. The transdiagnostic approach to multiple processes seeks the least number of key mechanisms with the greatest explanatory power in the understanding of different comorbid externalizing psychopathological disorders[6]. To this end, variables have been suggested that have generated new lines of research and intervention in AD, such as cognitive rumination, emotional dysregulation (ED), behavioral activation and inhibition systems, among others. However, this research around a transdiagnostic model is still limited in its development and scope; although the studies still have small samples and the available intervention protocols are scarce, more research is needed on its efficacy in the different comorbid problems—especially antisocial ones since they have focused on internalizing ones such as anxiety and depression[7].

    In the adolescent and young adult population, an empirically reviewed TM requires a stance that allows for the integration of various levels of analysis that has an impact on efforts focused on the promotion and prevention of these problems[8]. When identifying the interactions between the variables of vulnerability that increase the risk of AD at these ages, whether emotional, cognitive, biological, and contextual, it is possible to propose a TM that allows for the prediction of future incremental risk in symptomatic severity. These transdiagnostic approaches are found in studies on impulsivity and addictive disorders within the framework of the research domain criteria (RDoC), which seeks to develop a multidimensional explanatory model at the bio-behavioral level ranging from the molecular, genetic to the behavioral[9]. Among the advances for a TM are studies on inhibitory control and reward systems as motivational mechanisms at the structural level.

    In turn, reports with a transdiagnostic scope from the RDoC framework, have stood out for presenting genetic and psychophysiological variables and in models of traits oriented towards broad range factors such as externalizing or psychopathic factors. For example, recent studies have reported that adolescence and adulthood are characterized by significant changes in gray matter structure - volume - and genes associated with reward-seeking (DRD2, DRD4, DAT1, OPRM1, COMT). It leads to increases in impulsivity, especially in people with heavy drinking problems[10]. Increases derived from the interaction of genes and development explain variations in accelerated sensorimotor maturation for the cortex (high and low executive control, reward evaluation, and working memory)[10][11]. In other studies, psychopathy has generated advances in the understanding of the spectrum of AD, which is characterized by difficulties in establishing genuine interpersonal relationships, superficial affection, and chronic antisocial behavior[12]. Psychopathy also has been considered a continuum from primary psychopathy (emotional deficit) to secondary psychopathy (pathological level) with uninhibited profiles and interpersonal problems[13], aggressive behavior with anger dysregulation, and emotional withdrawal[14].

    However, despite extant evidence suggesting a strong association between various variables and the externalizing problems, it is necessary to go deeper into these transdiagnostic variables. It is imperative to analyze the interaction between transdiagnostic variables at the different levels, as suggested by the RDoC framework, allowing their integration into an explanatory TM of the AD. Thus, this study was aimed at identifying, through a systematic review, the transdiagnostic variables and their interaction at the structural, emotional, and cognitive levels in the studies comprising the spectrum of AD in adolescence and youth.

    2. Conclusions

    Advances are made for the consolidation of a transdiagnosis model framed in the guidelines of the RDoC project for externalizing psychopathologies in adolescents and young people. Within the framework of a general psychopathological factor, in the case of an AD model, this is a general psychopathic or externalizing factor, in which the variables are integrated as fundamental structures of the inhibition and activation systems and negative affect as a trait. There is more evidence for these variables, and they may be associated with subsequent experiential avoidance, ED, anger rumination, and violent ideation.

    It is necessary to develop new directions around the development of a transdiagnostic model for AD. Firstly, measures of change must be incorporated through longitudinal studies, either with a model of developmental trajectories or models that allow a prospective analysis taking into account the variables reported in this review, since this type of psychopathology, variations in behavior, contexts and other variables such as gender, can generate limitations in the development of a complete model of these problems.

    3. Clinical Implications

    The clinical implications of this study are the development of new directions of a transdiagnostic model in which the identified variables are submitted together. The approach should maintain the transdiagnostic approach of the multiple processes, that is, the search for the least number of key mechanisms with the greatest explanatory power for the understanding of comorbid disorders[6]. Also, having a transdiagnostic model that has been empirically reviewed will solve the limited progress made in this field by following a position that allows for the integration of various levels of analysis of theoretical and empirical knowledge that will have an impact on efforts to promote and prevent these problems[8]. Ultimately, this will favor the development of temporarily less costly treatments, and thus will allow for the promotion of prevention alternatives in directions other than those currently available.

    The entry is from 10.3390/ijerph17093036

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