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Perpetual conduct problems are witnessed in kids in recent years; such problems had been associated with averse social and economic outcomes, and are an indication of future psychological disorders in adulthood (Hawes, Price, & Dadds, 2014). Research into conduct problems progressed and is currently more informative in its criterion of diagnosis. The 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013) distinguished Conduct Disorder (CD) from Oppositional Defiant Disorder (ODD) based on emerging evidence that the two are separate disorders. Whereas ODD was considered a developmental precursor to CD in the past, recent research suggested that only 56% of ODD symptoms precede CD symptoms and factor analytic studies revealed that they load on distinct separate factors (Rowe, Costello, Angold, Copeland, & Maughand, 2010; Loeber, Burke, & Pardini, 2009). This distinction is essential in this paper as it suggests differential treatment in ODD and CD, highlighting the use of updated literature in the discussion of treatment methods.
CD is a more severe disorder than ODD because it concerns the infringement of the basic rights of others and the violation of societal norms, often causing hurt to others. The prevalence rate of CD ranges from about 2% – 10% and is consistent across various countries and their cultures. Sadly, few children receive appropriate treatment for CD (American Psychiatric Association, 2013) or respond to traditional treatment methods (Kyranides, Fanti, Katsimicha, & Georgiou, 2017). A recent study revealed that the newly-specified Callous-Unemotional (CU) trait in DSM-5 predicts poor treatment outcomes (Hawes et al., 2014). CU traits are characterized by lack of guilt, lack of empathy, and bland affect; those with CU traits are prone to severe and chronic antisocial behaviours, and a range of negative behavioural patterns (Hawes et al., 2014).
Current research has investigated various treatment effects on CD with CU traits. As such, this paper evaluates CD based on DSM-5 – its diagnostic criteria, aetiology, and treatment methods – from a biopsychosocial perspective, consistent with current pathological practices. The literature reviewed are from the last ten years to ensure the integrity of updated findings in treatment procedures.
The DSM-5 diagnoses CD when “repetitive and persistent pattern of behaviour in which the basic rights of others or major age-appropriate societal norms or rules are violated” (American Psychiatric Association, 2013, p. 469), manifested by three of the 15 behaviours in the last one year, of which one must be present in the past six months. The 15 behavioural criteria is grouped into four categories: Aggression to people and animals, destruction of property, deceitfulness or theft, and serious violations of rules. Furthermore, the behaviours must cause significant impairment in social, academic, or occupational functioning. The individual must be above 18 years old and criteria for antisocial personality disorder are not met (American Psychiatric Association, 2013).
There are three subtypes of CD, namely the childhood-onset type, adolescent-onset type, and unspecified onset. Childhood-onset type is characterized by the appearance of at least one symptom of CD before 10 years old, while no CD symptoms appear prior to age 10 in adolescent-onset type. Finally, symptoms are met for CD but there is insufficient information to determine the age of onset for the unspecified onset type. CU traits are included into diagnostic criteria as a specifier “with limited prosocial emotions”, characterized by 1) lack of remorse or guilt, 2) callous – lack of empathy, 3) unconcerned about performance, 4) shallow or deficient affect (American Psychiatric Association, 2013).
Individuals with childhood-onset CD were reported to be more aggressive, have poorer social relationships, and have persistent antisocial behaviours into adulthood than adolescent-onset CD. Therefore, childhood-onset CD tends to have more serious repercussions and social impairment than the other subtypes of CD. Also, individuals with CU traits are more likely to have a childhood-onset type CD and more severe behavioural symptoms (American Psychiatric Association, 2013), hinting to a possible causal relationship between CU traits and CD – especially early in childhood – but the direction of causality remains elusive. Other factors that contribute to CD have been identified from the domains of genetics, environmental, and biology.
The aetiology of CD consist of complex interactions from the individual’s biopsychosocial context. From a genetic standpoint, Moffitt (2005) review of twin studies found that antisocial behaviours was about 50% heritable. Furthermore, recent advances in neuroimaging studies showed structural abnormalities in children with CD. Fairchild and colleagues (2013) found reduced bilateral anterior insula and right striatal grey matter volumes in female adolescent with CD, those with CU traits were found to have a positive correlation with bilateral orbitofrontal cortex volume, while aggressive symptoms were negatively correlated with right dorsolateral prefrontal cortex (dlPFC) volume. These results were largely consistent with previous studies of male adolescent with CD (Fairchild et al., 2011; Matthys, Vanderschuren, & Schutter, 2013). The associated functions and implications of the brain structures are summarized in Table 1. Additionally, structural abnormalities in late childhood or early adolescence were found to be similar with adult populations with psychopathy (Breeden, Cardinale, Lozier, VanMeter, & Marsh, 2015), suggesting the continuity of disorders into adulthood.
Note. Information summarized from Fairchild et al.’s (2013) and Matthys et al.’s (2013) review.
Moffitt (2005) further postulated the genetic-environment interaction in the development of antisocial behaviours. Consistent with the diathesis-stress model of psychopathological framework (Kring, Johnson, Davison, & Neale, 2015), a child may be predisposed (inherited genes) to have antisocial tendencies and the environment may be the trigger that manifests such tendencies in terms of behaviour, thereby developing CD. The family unit has been extensively studied upon as a contributing factor to CD. Poor parenting patterns, lack of familial affection, or abuse were predictive factors of the development of CD (Elizur, Somech, & Vinokur, 2016; Hawes et al., 2014). These factors were conceptualized with social learning theory which focuses on parents as models for the child (Hawes et al., 2014). Also, peer relations may bring risk of rejection and reinforcement towards deviant behaviours (Dishion & Tipsord, 2011); such peer relationships may stem from the child’s school wherein normative-aged peers interact on a frequent basis. While CU traits were found to be mainly genetic, the environment can precipitate or trigger the expression of the genetic vulnerability of the child in the development of CD (Hawes et al., 2014). In sum, while CD may be biologically-predisposed, the environment constitutes a significant role in the expression of the disorder.
There are various available treatment options for CD, but a full discussion is beyond the scope of this paper. Two psychosocial methods – the Parent Management Training Oregon Model (PMTO; Patterson, Reid, Jones, & Conger, as cited in Eyberg, Nelson, & Boggs, 2008) and the Multisystemic Therapy (MST; Henggeler & Lee, as cited in Eyberg et al., 2008) – and pharmacotherapy methods will be evaluated.
PMTO. The PMTO is a behavioural parent-training procedure that teaches behavioural principles to parents for the management of their child’s behaviours. Therapists typically meet with the parents on a weekly basis and are on telephone contact. The time of the treatment varies but generally the treatment requires 10 one-hour sessions and twice-weekly telephone contacts. Overall, studies reviewed found the treatment efficacious in reducing disruptive behaviours (Eyberg et al., 2008). However, several limitations can be identified.
The PMTO assumes that parents are cooperative and willing to incorporate the techniques into their handling of the child. The therapists are not directly in contact with the child therefore there is no control of the delivery of behavioural techniques untoward the child. Also, the high commitment of parents having to attend the training programs may discourage families to continue with the treatment. Lastly, PMTO does not consider the psychopathological status of the parents. As CD can be hereditary, it is cautionary to ensure the mental state of the parents, especially when parents are the only medium involved in the direct treatment of the child.
MST. The MST is an improvement of the PMT wherein a combination of treatment procedures is utilized to provide structured family-and-community-based intervention. The goal of the treatment is to promote responsible behaviour and minimizing the need to send the child outside of home. The multi-dimensional treatment includes cognitive-behavioural techniques, behaviour therapies, parent training, family therapies, and pharmacological methods (Eyberg et al., 2008). The MST recognizes the influence of the external environment unto the child, while simultaneously acknowledge the biological abnormalities. Figure 1 illustrates the therapy framework of the MST. Overall, review of the outcome of MST demonstrated showed superiority to alternative treatment methods (Eyberg et al., 2008).
Figure 1. Multisystemic Treatment (MST). This figure illustrates the relative influence (with the nearest to centre having the most influence) of factors affecting the child.
While the MST is a comprehensive treatment procedure that targets the child’s disorder, it may exhaust too much resources on the family for the treatment of the child, especially low-income families. The child will be subjected to treatment at all levels of his/her social environment, and it is contentious that an environment filled with intervention is a healthy one for the child’s development. Furthermore, the social support provided at the community level can differ vastly in different states or countries, thus there is no standardized method of support at this level. Granted, perhaps proper guidelines and structure in such comprehensive intervention can ensure the smooth transition into a healthy adulthood for the child.
Medication treatments for CD remains limited. Studies using medication as treatment typically focused on aggressive symptoms (Eyberg et al., 2008). There are four main categories of medication – antipsychotics, stimulants, alpha agonists, and mood-stabilizing drugs that target specific symptoms of CD. No compelling evidence of pharmacotherapy as an efficient treatment method was found, however research suggests that medication be used as an auxiliary treatment method that targets specific behaviours, mainly aggression (Eyberg, 2008; Findling, 2016). Studies further suggest adverse side-effects of using medication, hence cautioning against its use (Hambly, Khan, McDermott, Bor, & Haywood, 2016). Intuitively, pharmacotherapy for CD is best used with caution and remains a lesser alternative for treatment to CD. However, its use may augment treatment such as in MST and may be a last option if other psychosocial methods fail. Overall, psychosocial treatment, MST, is the best option.
This paper presented DSM-5 diagnostic criteria, aetiology, and treatment options for CD. While research into CD has been extensive, several questions remain. Firstly, the arbitrary age of 10 years old in the distinction between childhood-onset and adolescent-onset of CD. This criterion is the same as DSM-4, which was set in 1993. Agreeably, Moffitt and colleagues (2008) argued that research might have been updated and the age criterion might be subjected to change. Moreover, forcefully dichotomizing variables have been contended from a statistical viewpoint (Altman & Royston, 2006). Since there might be differential treatment as the severity of the subtypes differ (childhood-onset type being more severe), future studies may wish to thoroughly examine this distinction of CD subtypes to ensure proper treatment.
Secondly, does CU traits lead to the development of CD or otherwise? Research consistently demonstrated that CD with CU traits lead to more adverse outcomes and persistence into adulthood; CU traits were demonstrated to be genetically predisposed, thereby alluding to personality factors of an individual. Moffitt (2005) proposed that personality factors of an individual influences one’s interaction with the environment, in turn affecting the development of CD for those who are genetically predisposed. Conversely, it can be argued that the symptoms of CD lead to the formation of CU traits when a child does not function normally in his social environment, possibly leading to interpersonal and psychological issues. Indeed, the co-occurrence of depressive, anxiety, and substance-related disorders remain high (American Psychiatric Association, 2013). Plausibly, CD may induce the formation of CU traits due to impaired social functioning. Hence, future studies may look at the direction of causality, if any, for a better prognosis or early prevention.
In all, there appears to be complex interactions between the individual and the environment in the aetiology and treatment procedures of CD. A biopsychosocial perspective in research of pathological disorder remains imperative as medical practitioners require more extensive research to make informed decisions about treating CD. Perhaps with a greater understanding of CD, the future generation can see a reduction in the prevalence of this disorder and minimize impact on the social and economic front.
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