This page uses content from Wikipedia and is licensed under CC BY-SA.
|Specialty||Psychiatry, pediatrics, clinical psychology|
Conduct disorder (CD) is a mental disorder diagnosed in childhood or adolescence that presents itself through a repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate norms are violated. These behaviors are often referred to as "antisocial behaviors." It is often seen as the precursor to antisocial personality disorder, which is per definition not diagnosed until the individual is 18 years old.
Conduct disorder is estimated to affect 51.1 million people globally as of 2013.
One of the symptoms of conduct disorder is a lower level of fear. Research performed on the impact of toddlers exposed to fear and distress shows that negative emotionality (fear) predicts toddlers' empathy-related response to distress. The findings support that if a caregiver is able to respond to infant cues, the toddler has a better ability to respond to fear and distress. If a child does not learn how to handle fear or distress the child will be more likely to lash out at other children. If the caregiver is able to provide therapeutic intervention teaching children at risk better empathy skills, the child will have a lower incident level of conduct disorder.
Currently, two possible developmental courses are thought to lead to conduct disorder. The first is known as the "childhood-onset type" and occurs when conduct disorder symptoms are present before the age of 10 years. This course is often linked to a more persistent life course and more pervasive behaviors. Specifically, children in this group have greater levels of ADHD symptoms, neuropsychological deficits, more academic problems, increased family dysfunction, and higher likelihood of aggression and violence.
There is debate among professionals regarding the validity and appropriateness of diagnosing young children with conduct disorder. The characteristics of the diagnosis are commonly seen in young children who are referred to mental health professionals. A premature diagnosis made in young children, and thus labeling an individual, may be inappropriate. It is also argued that some children may not in fact have conduct disorder, but are engaging in developmentally appropriate disruptive behavior.
The second developmental course is known as the "adolescent-onset type" and occurs when conduct disorder symptoms are present after the age of 10 years. Individuals with adolescent-onset conduct disorder exhibit less impairment than those with the childhood-onset type and are not characterized by similar psychopathology. At times, these individuals will remit in their deviant patterns before adulthood. Research has shown that there is a greater number of children with adolescent-onset conduct disorder than those with childhood-onset, suggesting that adolescent-onset conduct disorder is an exaggeration of developmental behaviors that are typically seen in adolescence, such as rebellion against authority figures and rejection of conventional values. However, this argument is not established and empirical research suggests that these subgroups are not as valid as once thought.
In addition to these two courses that are recognized by the DSM-IV-TR, there appears to be a relationship among oppositional defiant disorder, conduct disorder and antisocial personality disorder. Specifically, research has demonstrated continuity in the disorders such that conduct disorder is often diagnosed in children who have been previously diagnosed with oppositional defiant disorder, and most adults with antisocial personality disorder were previously diagnosed with conduct disorder. For example, some research has shown that 90% of children diagnosed with conduct disorder had a previous diagnosis of oppositional defiant disorder. Moreover, both disorders share relevant risk factors and disruptive behaviors, suggesting that oppositional defiant disorder is a developmental precursor and milder variant of conduct disorder. However, this is not to say that this trajectory occurs in all individuals. In fact, only about 25% of children with oppositional defiant disorder will receive a later diagnosis of conduct disorder. Correspondingly, there is an established link between conduct disorder and the diagnosis of antisocial personality disorder as an adult. In fact, the current diagnostic criteria for antisocial personality disorder require a conduct disorder diagnosis before the age of 15. However, again, only 25-40% of youths with conduct disorder will develop antisocial personality disorder. Nonetheless, many of the individuals who do not meet full criteria for antisocial personality disorder still exhibit a pattern of social and personal impairments or antisocial behaviors. These developmental trajectories suggest the existence of antisocial pathways in certain individuals, which have important implications for both research and treatment.
Children with conduct disorder have a high risk of developing other adjustment problems. Specifically, risk factors associated with conduct disorder and the effects of conduct disorder symptomatology on a child's psychosocial context have been linked to overlap with other psychological disorders. In this way, there seems to be reciprocal effects of comorbidity with certain disorders, leading to increased overall risk for these youth.
ADHD is the condition most commonly associated with conduct disorders, with approximately 25-30% of boys and 50-55% of girls with conduct disorder having a comorbid ADHD diagnosis. While it is unlikely that ADHD alone is a risk factor for developing conduct disorder, children who exhibit hyperactivity and impulsivity along with aggression is associated with the early onset of conduct problems. Moreover, children with comorbid conduct disorder and ADHD show more severe aggression.
Conduct disorder is also highly associated with both substance use and abuse. Children with conduct disorder have an earlier onset of substance use, as compared to their peers, and also tend to use multiple substances. However, substance use disorders themselves can directly or indirectly cause conduct disorder like traits in about half of adolescents who have a substance use disorder. As mentioned above, it seems that there is a transactional relationship between substance use and conduct problems, such that aggressive behaviors increase substance use, which leads to increased aggressive behavior.
Substance use in conduct disorder can lead to antisocial behavior in adulthood.
While the cause of conduct disorder is complicated by an intricate interplay of biological and environmental factors, identifying underlying mechanisms is crucial for obtaining accurate assessment and implementing effective treatment. These mechanisms serve as the fundamental building blocks on which evidence-based treatments are developed. Despite the complexities, several domains have been implicated in the development of conduct disorder including cognitive variables, neurological factors, intraindividual factors, familial and peer influences, and wider contextual factors. These factors may also vary based on the age of onset, with different variables related to early (e.g., neurodevelopmental basis) and adolescent (e.g., social/peer relationships) onset.
The development of conduct disorder is not immutable or predetermined. A number of interactive risk and protective factors exist that can influence and change outcomes, and in most cases conduct disorder develops due to an interaction and gradual accumulation of risk factors. In addition to the risk factors identified under cause, several other variables place youth at increased risk for developing the disorder, including child physical abuse and prenatal alcohol abuse and maternal smoking during pregnancy. Protective factors have also been identified, and most notably include high IQ, being female, positive social orientations, good coping skills, and supportive family and community relationships.
However, a mere correlation between a particular risk factor and a later developmental outcome (such as conduct disorder) cannot be taken as definitive evidence for a causal link. Co-variation between two variables can arise, for instance, if they represent age-specific expressions of similar underlying genetic factors. For example, the tendency to smoke during pregnancy (SDP) is subject to substantial genetic influence (D'Onofrio et al., 2007), as is conduct disorder. Thus, the genes that dispose the mother to SDP may also dispose the child to CD following mitotic transmission. Indeed, Rice et al. (2009) found that in mother-fetus pairs that were not genetically related (by virtue of in-vitro fertilisation), no link between SDP and later conduct problems arose. Thus, the distinction between causality and correlation is an important consideration.[full citation needed]
While language impairments are most common, approximately 20-25% of youth with conduct disorder have some type of learning disability. Although the relationship between the disorders is complex, it seems as if learning disabilities result from a combination of ADHD, a history of academic difficulty and failure, and long-standing socialization difficulties with family and peers. However, confounding variables, such as language deficits, SES disadvantage, or neurodevelopmental delay also need to be considered in this relationship, as they could help explain some of the association between conduct disorder and learning problems.
In terms of cognitive function, intelligence and cognitive deficits are common amongst youths with conduct disorder, particularly those with early-onset and have intelligence quotients (IQ) one standard deviation below the mean and severe deficits in verbal reasoning and executive function. Executive function difficulties may manifest in terms of one's ability to shift between tasks, plan as well as organize, and also inhibit a prepotent response. These findings hold true even after taking into account other variables such as socioeconomic status (SES), and education. However, IQ and executive function deficits are only one piece of the puzzle, and the magnitude of their influence is increased during transactional processes with environmental factors.
Beyond difficulties in executive function, neurological research on youth with conduct disorder also demonstrate differences in brain anatomy and function that reflect the behaviors and mental anomalies associated in conduct disorder. Compared to normal controls, youths with early and adolescent onset of conduct disorder displayed reduced responses in brain regions associated with social behavior (i.e., amygdala, ventromedial prefrontal cortex, insula, and orbitofrontal cortex). In addition, youths with conduct disorder also demonstrated less responsiveness in the orbitofrontal regions of the brain during a stimulus-reinforcement and reward task. This provides a neural explanation for why youths with conduct disorder may be more likely to repeat poor decision making patterns. Lastly, youths with conduct disorder display a reduction in grey matter volume in the amygdala, which may account for the fear conditioning deficits. This reduction has been linked to difficulty processing social emotional stimuli, regardless of the age of onset. Aside from the differences in neuroanatomy and activation patterns between youth with conduct disorder and controls, neurochemical profiles also vary between groups. Individuals with conduct disorder are characterized as having reduced serotonin and cortisol levels (e.g., reduced hypothalamic-pituitary-adrenal (HPA) axis), as well as reduced autonomic nervous system (ANS) functioning. These reductions are associated with the inability to regulate mood and impulsive behaviors, weakened signals of anxiety and fear, and decreased self-esteem. Taken together, these findings may account for some of the variance in the psychological and behavioral patterns of youth with conduct disorder.
Aside from findings related to neurological and neurochemical profiles of youth with conduct disorder, intraindividual factors such as genetics may also be relevant. Having a sibling or parent with conduct disorder increases the likelihood of having the disorder, with a heritability rate of .53. There also tends to be a stronger genetic link for individuals with childhood-onset compared to adolescent onset. In addition, youth with conduct disorder also exhibit polymorphism in the monoamine oxidase A gene, low resting heart rates, and increased testosterone.
Elements of the family and social environment may also play a role in the development and maintenance of conduct disorder. For instance, antisocial behavior suggestive of conduct disorder is associated with single parent status, parental divorce, large family size, and young age of mothers. However, these factors are difficult to tease apart from other demographic variables that are known to be linked with conduct disorder, including poverty and low socioeconomic status. Family functioning and parent-child interactions also play a substantial role in childhood aggression and conduct disorder, with low levels of parental involvement, inadequate supervision, and unpredictable discipline practices reinforcing youth's defiant behaviors. Peer influences have also been related to the development of antisocial behavior in youth, particularly peer rejection in childhood and association with deviant peers. Peer rejection is not only a marker of a number of externalizing disorders, but also a contributing factor for the continuity of the disorders over time. Hinshaw and Lee (2003) also explain that association with deviant peers has been thought to influence the development of conduct disorder in two ways: 1) a “selection” process whereby youth with aggressive characteristics choose deviant friends, and 2) a “facilitation” process whereby deviant peer networks bolster patterns of antisocial behavior. In a separate study by Bonin and colleagues, parenting programs were shown to positively affect child behavior and reduce costs to the public sector.
In addition to the individual and social factors associated with conduct disorder, research has highlighted the importance of environment and context in youth with antisocial behavior. However, it is important to note that these are not static factors, but rather transactional in nature (e.g., individuals are influenced by and also influence their environment). For instance, neighborhood safety and exposure to violence has been studied in conjunction with conduct disorder, but it is not simply the case that youth with aggressive tendencies reside in violent neighborhoods. Transactional models propose that youth may resort to violence more often as a result of exposure to community violence, but their predisposition towards violence also contributes to neighborhood climate.
Conduct disorder is classified in the fourth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM). It is diagnosed based on a prolonged pattern of antisocial behaviour such as serious violation of laws and social norms and rules in people younger than the age of 18. Similar criteria are used in those over the age of 18 for the diagnosis of antisocial personality disorder. No proposed revisions for the main criteria of conduct disorder exist in the DSM-5; there is a recommendation by the work group to add an additional specifier for callous and unemotional traits. According to DSM-5 criteria for conduct disorder, there are four categories that could be present in the child's behavior: aggression to people and animals, destruction of property, deceitfulness or theft, and serious violation of rules.
Almost all adolescents who have a substance use disorder have conduct disorder-like traits, but after successful treatment of the substance use disorder, about half of these adolescents no longer display conduct disorder-like symptoms. Therefore, it is important to exclude a substance-induced cause and instead address the substance use disorder prior to making a psychiatric diagnosis of conduct disorder.
The most effective treatment for an individual with conduct disorder is one that seeks to integrate individual, school, and family settings. Additionally, treatment should also seek to address familial conflict such as marital discord or maternal depression.
About 25-40% of youths diagnosed with conduct disorder qualify for a diagnosis of antisocial personality disorder when they reach adulthood. For those that do not develop ASPD, most still exhibit social dysfunction in adult life.
Conduct disorder is estimated to affect 51.1 million people globally as of 2013. The percentage of children affected by conduct disorder is estimates to range from 1-10%. However, among incarcerated youth or youth in juvenile detention facilities, rates of conduct disorder are between 23% and 87%.
The majority of research on conduct disorder suggests that there are a significantly greater number of males than females with the diagnosis, with some reports demonstrating a threefold to fourfold difference in prevalence. However, this difference may be somewhat biased by the diagnostic criteria which focus on more overt behaviors, such as aggression and fighting, which are more often exhibited by males. Females are more likely to be characterized by covert behaviors, such as stealing or running away. Moreover, conduct disorder in females is linked to several negative outcomes, such as antisocial personality disorder and early pregnancy, suggesting that sex differences in disruptive behaviors need to be more fully understood.
Research on racial or cultural differences on the prevalence or presentation of conduct disorder is limited. However, it appears that African-American youth are more often diagnosed with conduct disorder, while Asian-American youth are about one-third as likely to develop conduct disorder when compared to White American youth.