ارتباطات اعصاب و غدد و انتقال دهنده عصبی در کودکان مبتلا به رفتار ضد اجتماعی

Abstract When antisocial behavior becomes a persistent pattern that affects diverse domains of children's functioning, psychiatrists refer to oppositional defiant disorder (ODD) or conduct disorder (CD). The term disruptive behavior disorder (DBD) covers both ODD and CD. Research shows that in the absence of effective interventions, the prognosis for DBD children is relatively unfavorable: their disorder can extend into adolescence, manifest itself in delinquency, and convert into other psychiatric symptoms, such as addiction or personality disorders. Although environmental factors have traditionally attracted most attention in explaining the origin and persistence of DBDs, it is important not to overlook the vulnerability of the child in the development of antisocial behavior. Relatively few studies have been conducted on the neurobiological factors involved in the development of DBDs in children. In this paper, we explain how problems in hypothalamic–pituitary–adrenal (HPA) axis and serotonergic system functioning could be important factors in the behavioral problems of DBD children. Low fear of punishment and physiological underactivity may predispose antisocial individuals to seek out stimulation or take risks and may explain poor (social) conditioning and socialization. Findings consistent with this hypothesis are presented. Finally, we explain how stress in general, and adverse early life experiences in particular, could have an impact on the development of the HPA and serotonergic systems. An investigation of the neurobiological factors involved in antisocial behavior disorder might ultimately guide the development of new forms of intervention.

Introduction Antisocial behavior in children can be operationalized in different ways. Antisocial behavior can be defined in terms of psychiatric diagnoses (oppositional defiant disorder (ODD), conduct disorder (CD), or disruptive behavior disorder (DBD); American Psychiatric Association, 1994), in terms of the violation of social or legal norms (delinquency, criminality), or as aggressive behavior (Plomin et al., 1990). These operationalizations are related but not synonymous. Aggression, defined as behavior deliberately aimed at inflicting physical and/or psychological damage on persons or property, represents a problem of significant clinical and social concern. In psychiatry, aggression does not constitute a separate diagnostic entity but appears in several psychopathological conditions, the most important being CD, substance use disorder, neurological disorders involving the frontal and temporal lobes, and personality disorders such as borderline and antisocial personality disorder (American Psychiatric Association DSM-IV, 1994). The term disruptive behavior disorder (DBD) covers both ODD and CD. The prevalence of these disorders is relatively high: 2% for CD and 3.2% for ODD (Lahey et al., 1999). The problem behavior of DBD children is often quite stable and persistent (Offord et al., 1992). Conduct problems in childhood are associated with a host of negative outcomes in adulthood; they predict not only future antisocial behavior (Fombonne et al., 2001), but also substance abuse and dependence in adulthood (Kazdin, 1995), early pregnancy in antisocial girls (Bardone et al., 1998), persistent health problems (Bardone et al., 1998), and depression. Although the short-term effectiveness of intervention strategies (e.g., parent management training, cognitive behavioral therapy) has been demonstrated (Kazdin, 2001), the long-term effectiveness of treatment appears to be limited (Offord and Bennett, 1994). In particular, the high persistence, poor prognosis and limited effectiveness of current treatments of childhood antisocial behavior lend importance to the investigation of the biological correlates of antisocial behavior in childhood. An understanding of these factors in antisocial children should generate hypotheses concerning the underlying neurobiological mechanisms and etiology of antisocial behavior. It is known that both child-specific and environmental factors contribute to the development and maintenance of antisocial behavior. Most interest in research has focused on environmental factors. It is, for example, known that stress in the family (as a consequence of adverse life events), relationship problems between the parents, and depressive symptoms in the mother play a role in this type of problem behavior (Conger et al., 1994). These factors are likely to result in the affective neglect of the child (Erel and Burman, 1995). However, there is an increasing body of evidence that the child him- or herself also plays an important role. The concept of ‘vulnerability’ indicates that certain children have an increased risk of developing psychiatric disorders. This natural disposition is presumably partly biologically determined.

Conclusion Aggressive and antisocial behavior in children is persistent and often difficult to treat. Although behavioral interventions have been shown to be effective in mild forms of these disorders, their effectiveness in more seriously disturbed children is limited. This is partly due to the fact that we lack knowledge of the cognitive and emotional problems of these children and the neurobiological causes of these difficulties. Knowing that this type of problem behavior is persistent and difficult to treat, it is interesting and relevant that HPA axis, ANS and 5-HT disturbances are found in antisocial children because these systems are also implicated in serious antisocial behavior in adults (Van Goozen et al., 2000a). At present, we do not know what causes this pattern of impairments, although it is clear that genetic factors must be involved in the explanation (Caspi et al., 2002 and Foley et al., 2004). An important line of research in animals suggests that early stressful experiences (pre- and perinatal) affect the development of the brain in the first years of life. Knowing that many antisocial children have problematic backgrounds, it seems possible that they have been exposed to severe stress and that these experiences have had a permanent effect on the development of their stress systems, including the HPA axis and the ANS, and the serotonergic system. There is a clear need for long-term follow-up research from a very early age onwards, in order to shed more light on this issue. If it is the case that children with early-onset antisocial behavior are characterized by neurobiological impairments, pharmacological interventions should be taken into consideration as a treatment option. Moreover, one should realize that impairments of HPA axis functioning, such as the ones discussed above, may disrupt the types of cognitive or emotional processing that normally play a critical role in therapeutic interventions. Thus, children with early-onset antisocial behavior and either low basal cortisol levels or attenuated cortisol reactivity may be more effectively treated using pharmacologically based therapies that reinstate normal HPA axis functioning, perhaps as a precursor or an adjunct to psychological forms of treatment. This is clearly an important line of future research. A final point is that the natural tendency to focus on the persistence of the problem of antisocial and violent behavior runs the risk of leading us to ignore the fact that a substantial proportion of disruptive children do not become antisocial adolescents or adults. A study of the neurobiological factors involved in aggression can also play an important role in explaining this observation: there are promising data from a relatively small number of studies showing that neurobiological factors, including those discussed in this paper, differ between those disruptive children who persist and those who desist from engaging in antisocial behavior (e.g., Brennan et al., 1997 and Van de Wiel et al., 2004). Further research on this issue is also urgently needed.