The Comorbidity of Conduct Problems and Depression in Childhood and Adolescence

Transcription

1 Clinical Child and Family Psychology Review, Vol. 9, Nos. 3/4, December 2006 (Ó 2006) DOI: /s The Comorbidity of Conduct Problems and Depression in Childhood and Adolescence Jennifer C. Wolff, 1 and Thomas H. Ollendick 1,2 An extensive body of research documents the high prevalence of comorbidity among child and adolescent disorders in general and between conduct problems and depression in particular. These problems co-occur at significantly higher rates than would be expected by chance and their comorbidity may have significant implications for nosology, treatment, and prognosis. Four main hypotheses have been put forth to account for these high rates of comorbidity. First, comorbidity may be a result of shortcomings associated with referral or informant biases. Second, comorbidity may be an artifact of overlapping definitional criteria. Third, one disorder may cause the other disorder by influencing the developmental trajectory and placing an individual at increased risk for further difficulties. Finally, comorbidity between two disorders may be explained by shared underlying causal or risk factors. The purpose of this review is to explore these possibilities, concentrating primarily on the common risk factors of parent psychopathology, emotion regulation, and cognitive biases that may underlie the co-occurrence of these two disorders. Based on our review, we propose a model for the development of comorbidity between these two disorders. KEY WORDS: aggression; child; comorbidity; conduct problems; depression On the surface, the association between conduct problems (including both oppositional defiant disorder and conduct disorder) and major depressive disorder is unexpected given the dissimilarities in symptoms characterizing each of the disorders. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 2000), symptoms associated with oppositional defiant disorder include argumentativeness, loss of temper, and disregard for authority and symptoms of conduct disorder consist of physical fighting, property destruction, and other delinquent acts. Symptoms of depression, on the other hand, are thought to relate more to internalized feelings of 1 Department of Psychology, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA. 2 To whom correspondence should be addressed; tho@ vt.edu sadness as well as loss of energy, apathy, and sleep problems. Given these symptomatic disparities, it is perplexing that comorbid conduct problems and depressive disorders occur at significantly higher rates than would be expected by chance (Capaldi, 1991). The paradox of the apparent distinctiveness of these disorders coupled with their high rates of comorbidity raises the question of how such seemingly distinct disorders come to co-exist in the same individual. The purpose of this review is threefold. First, epidemiological data related to rates of overlap between conduct problems and depression are examined. Second, four possible explanations that might help to inform this co-occurrence are discussed and critically reviewed. Third, based on these findings, a model for the development of comorbidity is presented. The model integrates common causal factors in the development of conduct problems and depression, recognizing their reciprocal relationship. A developmental psychopathology approach serves /06/ /0 Ó 2006 Springer ScienceþBusiness Media, Inc.

2 202 Wolff and Ollendick as the framework for this model and various transactional processes that contribute to comorbidity are discussed. In all, the present review provides a synthesis of the comorbidity between these two disorders and suggests plausible pathways for its occurrence. BACKGROUND AND SIGNIFICANCE Epidemiology Studies of comorbidity between depression and conduct problems suggest that each of these disorders is associated with increased risk for the other. For example, in a meta-analysis completed on child and adolescent community samples, it was reported that % met criteria for oppositional defiant disorder or conduct disorder and % met criteria for depression (Angold and Costello, 1993). In reference to comorbidity, however, % of those with depression also met criteria for oppositional defiant disorder or conduct disorder, whereas % of those with oppositional defiant disorder or conduct disorder also met criteria for depression (Angold and Costello, 1993). Thus, those who have one disorder appear to be at increased risk for the other. Among studies of clinic-referred youth, rates of comorbidity between these two disorders are even higher. In a recent study conducted by Greene et al. (2002), more than 30% of clinically referred children diagnosed with severe major depression also met criteria for conduct problems. Conversely, of those with conduct problems, more than 50% met criteria for major depression. In examining rates of comorbidity as they relate specifically to conduct disorder and oppositional defiant disorder, comorbid depression appears to be more prevalent in those with conduct disorder compared to those with oppositional defiant disorder. For example, in a study of inpatient adolescents, Arredondo and Butler (1994) found that 27% of the adolescents with oppositional defiant disorder (compared to 76% with CD) met the diagnosis of a mood disorder. It is clear that the observed rates of comorbidity in epidemiological surveys and clinical samples exceed those expected by chance alone. As described by Caron and Rutter (1991), the expected rate is obtained by multiplying the base rate of each of the separate conditions. Using the epidemiological survey completed by Anderson et al. (1987) as but one example, 9.2% of 11-year-olds were diagnosed with oppositional defiant disorder or conduct disorder and 1.8% of 11-year-olds met criteria for depression. The expected rate of comorbidity in this sample would be the product of 9.2 and 1.8% or, 0.2%. However, overall rates of comorbidity observed in this study were between 1.5 and 2.9% (95% confidence intervals). Based on these findings, the observed comorbidity of these presumably distinct child psychiatric disorders far exceeds that expected by chance alone. There exist a host of challenges associated with the identification and comparison of prevalence rates across studies, including differences among studies in terms of diagnostic precision and methodology, assessment techniques, the ascertainment method (e.g., community-based or clinic-referred), and distinct characteristics of the samples. The age of the children included in the samples makes comparisons particularly difficult as prevalence rates tend to vary with age. Similarly, gender differences complicate the comparison of these findings as rates are oftentimes found to be different for boys and girls at certain points in their development. Although such limitations exist, the ever-expanding database on this topic has made significant advances in examining rates of comorbidity while largely accounting for such factors. Age of Onset An examination of age of onset of each of these disorders, alone and in combination, serves as an introduction to the possible relationship between conduct problems and depression. Although researchers differ in opinion on the sequence of onset between conduct problems and depression, both conduct disorder and depression tend to increase in prevalence during adolescence (Cohen et al., 1993). As will be discussed shortly, some researchers suggest that conduct problems emerge first and the ensuing social failures experienced by these children and adolescents contribute to the development of depression. Others, however, suggest that depression may emerge first followed by the development of conduct problems as a means of acting out or compensating for some of the internalized feelings associated with depression. Many clinical and community-based studies have found that conduct problems precede rather than follow the development of depression. For example, Biederman et al. (1995) reported that the age at onset for oppositional defiant disorder and conduct disorder was 6 7 years of age, compared to about 8 years of age for depression. Among

3 Comorbidity of Conduct Problems and Depression 203 hospitalized girls in another study, the first symptom of conduct disorder was reported to occur at 8.2- years-old and that of depression at 13.5 years (Zoccolillo and Rogers, 1991). By contrast, Kovacs et al. (1988) found that depression was more likely to precede conduct problems. In their study of 8- to 13-year-old children, more depressed children with comorbid conduct disorder developed depression prior to conduct disorder (56%) rather than conduct disorder prior to depression (25%). Thus, it appears that conduct problems may precede depression in some cases but that depression may precede conduct problems in other cases. Overall, studies suggest that the prevalence of comorbidity reaches a peak around middle adolescence (Beyers and Loeber, 2003; Loeber et al., 1994). This phenomenon may be due to the fact that conduct problems tend to decrease as children move out of adolescence and into adulthood while depression tends to increase as children move into adolescence and then on into adulthood. The timing of the overlap in these problems tends to show qualitative differences in the types of behaviors displayed (Loeber et al., 1994). Specifically, when depression occurs in early adolescence, boys with comorbid conduct problems tend to show overt (e.g., bullying, fighting) and covert aggression (e.g., stealing, vandalism, lying), whereas if the overlap emerges in middle- to late-adolescence behaviors are characterized as showing more conflict with authority (e.g., stubbornness, defiance, truancy). Thus, qualitative differences are associated with age of onset of comorbidity. Interestingly, there is some evidence that the age of onset of either comorbid disorder may be later than is typical in non-comorbid individuals. For example, Kovacs et al. (1988) found that the average age of onset for major depression in boys having comorbid conduct problems was 12.2 years, compared to 10.8 years for those with no comorbid condition. This finding may suggest that the presence of one disorder serves a protective function against the development of the second disorder. For our purposes here, it may be the case that children with conduct problems are able to act out their feelings of anger, irritability, or sadness, thus delaying the onset of full-blown depression. An alternate explanation for these findings may be that one disorder masks or conceals the presence of the other; that is, as children receive clinical services for one disorder (in this case conduct problems), the other disorder may become more apparent. This phenomenon would not be unlike the masked depression phenomenon put forth some years ago. Sex Several studies have found sex differences in rates of comorbid conduct problems and depression. In terms of individual disorders, the rate of conduct disorder is considerably higher for adolescent males than for adolescent females (Robins and Price, 1991), whereas the prevalence of depression is higher in adolescent females (Lewinsohn et al., 1993). In a review of child and adolescent population studies, Zoccolillo (1992) found that the co-occurrence of these disorders is most likely to occur in boys in preadolescence, diminishing in late adolescence and into adulthood, but most likely in girls during midadolescence into adulthood. Overall, such studies have demonstrated that co-occurring conduct problems are more likely to occur in males than in females although some have found varying rates depending on the source of the information (Keiley et al., 2003). Interestingly, a greater proportion of girls than boys tend to exhibit an onset of conduct problems during adolescence. Although in the majority of cases adolescent-onset conduct problems tend to be less severe, girls displaying symptoms of adolescent-onset conduct problems seem to show a more severe type of disturbance that is similar in many respects to boys with the childhood-onset pattern (Frick, 1998). Thus, girls with adolescent-onset conduct disorders tend to have high rates of neuropsychological dysfunction and are at high risk for having significantly impaired adult functioning (Moffit, 1993). Some have speculated that this finding may be linked to the concurrent rise of depression in adolescent girls and the deleterious effects of comorbid conduct problems and depression. Along these lines, Loeber and Keenan (1994) hypothesized a paradoxical effect of the child s gender, suggesting that on average the severity of conduct problems in girls is greater than that for boys when the probability of comorbid depression is taken into account. Hence, somewhat surprisingly, the implications of comorbidity may be more profound in girls than boys. Implications of Comorbidity The high prevalence rates of symptom overlap among children and adolescents with conduct problems and depression underscore the importance of examining these comorbid conditions. Quite

4 204 Wolff and Ollendick obviously, the issue of comorbidity raises questions concerning the nosology of disorders. Whether conduct problems with and without comorbid depression (or vice versa) should be considered to be two distinct disorders or as different manifestations of the same condition has important implications for better understanding etiology, disease progression, and treatment response (Biederman et al., 1995). The identification of two distinct but co-existing conditions is important so that each disorder can in turn be treated. On the other hand, different treatment approaches may not be necessary if the symptoms represent the same underlying processes (Biederman et al., 1995). Moreover, this co-occurrence carries important ramifications in terms of the degree of impairment and the course of psychopathology for these children and adolescents. Specifically, those with comorbid conditions are typically more severely impaired than children with either disorder alone (Nottelmann and Jensen, 1994). In combination, these problems may magnify or exacerbate the deleterious effects of either disorder alone and contribute to high levels of psychosocial impairment in various areas of functioning. For example, research demonstrates that risk for suicidality increases in depressed adolescents as a function of pre-existing conduct problems (Capaldi, 1991, 1992). Indeed, a number of studies have demonstrated that comorbid emotional symptoms and conduct problems are common among children and adolescents who commit suicide. Moreover, this risk appears to be higher for girls than boys (Loeber and Keenan, 1994). Longitudinally, youths with both conduct problems and depression are also prone to increased long-term problems in functioning (including adult criminality), compared with depressed-only youth (Capaldi, 1992; Harrington et al., 1991; Kovacs et al., 1988). In one study, Lewinsohn et al. (1995) examined the consequences of comorbidity in a community sample of 1,507 adolescents. Participants with pure and comorbid disorders were compared on six clinical outcome measures. When comparing those diagnosed with major depressive disorder only to those with a major depressive disorder and comorbid disruptive behavior, those with the comorbid disorder were significantly more likely to receive treatment, had poorer global functioning, and had more academic problems. Similarly, when examining those with a disruptive behavior disorder alone compared to those with a behavior disorder and comorbid depression, those with the comorbid condition were more likely to receive treatment, had poorer global functioning, and were more likely to attempt suicide. Thus, comorbidity signaled a poorer clinical profile. Additionally, comorbidity may have implications for the course and treatment of psychopathology. To date, few studies have examined the treatment of youth with comorbid conduct problems and depression (see Rapp and Wodarski, 1997; Rohde et al., 2004). Results of the few medication trials that have examined efficacy in comorbid samples indicate that antidepressant medications may be efficacious for adolescents with comorbid depression. Still, those depressed adolescents with comorbid conduct problems tend to be less responsive to medication than those having other co-occurring disorders (Hughes et al., 1990). In another study investigating the efficacy of the Adolescent Coping with Depression Course (CWD- A), a cognitive behavioral group intervention for adolescent depression, those with comorbid conduct disorder had significantly higher rates of depression recurrence over a 2-year follow-up period (Rohde et al., 2001). In sum, the few studies that have accounted for comorbidity of conduct problems and depression in treatment efficacy studies demonstrate poorer outcomes in those adolescents displaying co-occurring conduct problems and depression. Overall, these findings illustrate the potential implications of comorbidity in terms of nosology, degree of impairment, prognosis, and treatment. While the implications of any single disorder can be profound, the co-occurrence of a second disorder appears to compound and exacerbate the deleterious effects of the individual disorder. OVERVIEW OF PATHWAYS AND CONDITIONS LEADING TO COMORBIDITY Despite the importance of research in this area, studies of comorbidity have largely failed to consider pathways to the development of co-occurring disorders and the conditions under which comorbidity occurs or fails to occur. Moreover, these studies rarely consider the reasons these dual diagnoses occur with such high frequencies. Thus, questions remain as to the origins of comorbidity and the mechanisms that underlie this phenomenon. While at present there is not sufficient evidence to fully answer these questions, the extant literature lends itself to speculation on the onset and causes of developing comorbid psychopathologies.

5 Comorbidity of Conduct Problems and Depression 205 Certainly, without due consideration of particular mechanisms in the development of comorbid diagnoses, little can be done to effectively prevent the development of further psychopathology. With this problem in mind, the literature suggests four possible explanations for comorbidity (Angold et al., 1999; Caron and Rutter, 1991; Seligman and Ollendick, 1998). First, it may be that comorbidity is a methodological artifact based on shortcomings associated with referral biases and the use of multiple informants. Second, although conduct problems and depression are believed to be two distinct constructs, the extent of overlapping definitional criteria may produce inflated rates of comorbidity. Third, one disorder may cause or put an individual at increased risk for the second disorder. Fourth, two disorders can be comorbid because they share underlying risk factors. It is important to note that the first two explanations suggest that comorbidity is the result of methodological flaws, whereas the second two explanations suggest that comorbidity is due to the nature of the two disorders. Each of these explanations will be explored briefly as they relate to the relationship between conduct problems and depression in children and adolescents. While an exhaustive review of this vast literature was not undertaken, the present review is illustrative of the findings. METHODOLOGICAL ARTIFACT? Some have suggested that comorbidity is a methodological artifact rather than a real psychopathological phenomenon (see Angold et al., 1999). In particular, those who question high rates of comorbidity have suggested that the effects of referral bias, clinician bias, and the use of multiple informants, may inflate rates of co-occurrence among clinical disorders. As was noted earlier, past studies of comorbidity were often based on clinic samples. Since they were not population-based surveys, these results were likely to be subject to referral biases and Berkson s bias, producing higher comorbidity rates in the clinic population than those in the general population (Angold et al., 1999). According to Berkson s bias, whenever less than all subjects with a particular disorder are referred, selected samples will contain a disproportionately large proportion of patients showing multiple problems and probable comorbidity. As illustrated earlier, this bias is presumably because the referral likelihood for subjects with more than one disorder will be a function of the combined likelihood of referral for either disorder separately (Caron and Rutter, 1991). In addition, comorbidity diagnosed in clinic settings may simply reflect more extensive psychopathology in those referred to such settings as compared to those in the general population (Nottelmann and Jensen, 1995). For example, clinic-referred individuals may have more severe symptomatology, be more impaired, and come from families that generally feel more overwhelmed by their children s problems, as compared to those who do not seek treatment for psychological symptoms (Angold et al., 1999). Another potential source of methodological error is clinician bias. Previous work has related rates of comorbidity to clinical interviewers who might be more attuned to the possibility of multiple disorders (Angold and Costello, 1993). Moreover, it was suggested that parents, teachers, and children may be similarly sensitized in that reporting one problem may make them more sensitive to other problems and hence more likely to report another disorder. However, this possibility has received little support; especially with the widespread use of structured interviews. In fact, it is hypothesized that the opposite effect may be true that comorbidity may actually be underreported in instances that clinical interviewers are not open to the possibility of alternate explanations for emerging symptoms (e.g., clinicians assume that internalizing and externalizing disorders cannot co-exist). The increased use of multiple informants has also raised questions regarding the legitimacy of comorbidity. In particular, reliance on multiple informants frequently results in varying opinions and interpretations of problem behaviors (Youngstrom et al., 2003). Combining information from various sources often requires employing some rule for making decisions. Typically, this means using the or rule that if either the parent or child endorses the disorder, it is considered present. However, this rule raises the possibility that different informants may have different interpretations of the same behavior or may view different behaviors as being typical of the child based on the environment where they observe the child (e.g., home, school, with peers). For example, a parent might view the behavior as oppositional, whereas the child might indicate feeling depressed, leading to disparity in diagnostic labels (and increased likelihood of comorbidity). In one recent study, different decision rules resulted in the classification of anywhere from 5 to 74% of the participants classified as having comorbid internalizing and

6 206 Wolff and Ollendick externalizing symptoms (Youngstrom et al., 2003). Such difficulties with reconciling discrepancies between reporters may lead to inflated rates of comorbidity (Jensen et al., 1999). However, Angold et al. (1999) proposed several reasons that the use of multiple informants alone does not explain the high rates of comorbidity. First, Angold and colleagues highlight the finding that adult studies that frequently rely on single reporters (primarily self-report) also find high rates of comorbidity. Second, those child studies using only selfreport have reported similar rates of comorbidity as those using multiple informants. Third, in many studies comparing differences in the number of comorbid diagnoses reported by parents, children, or both informants, no significant differences were found (e.g., Jensen et al., 1995, 1999), which stand in contrast to the findings of Youngstrom and colleagues (2003). Together, these findings discredit the argument that comorbidity is the result of the use of multiple informants. In fact, estimates of co-occurrence may be more accurate when based on multiple sources of information, because studies have suggested that a single reporter may be biased and that multiple informants yield a more complete picture of the child (Ollendick and Hersen, 1993). In summary, it appears that comorbidity is not the result of some methodological flaw. Increased use of community-based samples and multiple informants has primarily ruled out the possibility that systematic errors in studies of comorbidity are responsible for the high prevalence rates observed in numerous studies. Such findings suggest that comorbidity is a real phenomenon and an area in need of further research. FLAWS IN CURRENT NOSOLOGIES? It is possible that the co-occurrence of these problems is so common that the distinctiveness of the purportedly separate diagnostic entities should be questioned. In the past, some have suggested that comorbidity arises because these conditions reflect a general syndrome reflecting the individual s generalized vulnerability to psychiatric disorder that is manifest in comorbidity between different types of the same disorder (Zoccolillo, 1992). Conversely, several authors have pointed out that comorbidity could be due to the fact that individual non-specific symptoms may be shared by disparate diagnoses (e.g., Caron and Rutter, 1991), with the result that a certain amount of overlap is built into the diagnostic system (Angold et al., 1999). In other words, these disorders are not actually comorbid at greater than chance levels, but they appear to be so because of lack of specificity in the diagnostic nomenclature. To examine this possibility, it is first necessary to examine DSM-IV criteria for different disorders and compare the specific symptoms associated with each disorder. In comparing conduct disorder and depression, the criteria for these disorders do not seem to overlap, at least on the surface. On the other hand, it is known that irritability is common in childhood depressive disorders and that several symptoms of oppositional defiant disorder appear to be related to irritability (e.g., often loses temper). Irritability, frustration, and angry outbursts are either primary or secondary features of ODD (APA, 2000). Furthermore, a tendency to display intense and negative emotions is an important aspect of the difficult temperament that has been linked to the development of both conduct problems and depression. In effect, the presence of one disorder partially fulfills the criteria for a second disorder, and thus, in operational terms, implies the existence of the second disorder. If such an effect was the sole cause of the apparent comorbidity between the two disorders, then the coexistence of the two disorders would be present only in those manifesting the shared symptoms and not in those whose disorders did not involve such symptoms (Angold and Costello, 1993). Along these lines, one study controlled for these overlapping symptoms (using subtraction and proportion methods) in 341 clinically referred children and then reevaluated each child s diagnosis (Biederman et al., 1995). Eliminating these overlapping symptoms ( angry mood for depression) failed to reduce elevated rates of comorbidity between these problems. Such findings suggest that comorbidity is not just an artifact of overlapping diagnostic criteria. Although some minor overlap may be perceived, the vast majority of the criteria offer an acceptable level of specificity to distinguish the disorders. The diagnoses for each of the disorders require multiple symptoms, making this explanation an unlikely candidate for explaining the co-occurrence of disorders (Zoccolillo, 1992). Moreover, if poorly delineated criteria were an explanation, then comorbidity should decrease as the number of conduct disorder symptoms increases, in fact, the opposite occurs (Robins and Price, 1991). That is, the more symptoms of conduct disorder, the less likely the occurrence of depression. In fact, the opposite pattern is obtained. This finding suggests that comorbidity is a real

7 Comorbidity of Conduct Problems and Depression 207 phenomenon rather than a methodological or definitional flaw. In sum, definitional or criteria-based flaws are not a viable explanation for the co-existence of conduct problems and depression. In general, the literature suggests that conduct problems and depression are distinct entities. Moreover, similarities in diagnostic criteria do not appear to account for high rates of comorbidity. Put simply, empirical evidence demonstrates that symptom overlap and developmental explanations do not account for high rates of comorbidity. DOES THE COURSE OF ONE DISORDER AFFECT THE OCCURRENCE OF THE OTHER DISORDER? A third possible explanation for the overlap of conduct problems and depression is that comorbidity occurs because one disorder causes or puts an individual at risk for the other. Three such types of association may occur between these disorders (Fergusson et al., 1996). First, conduct problems may be a direct cause of affective disorder (e.g., Capaldi 1991, 1992; Capaldi and Stoolmiller, 1999). Second, depression may be a direct cause of conduct disorder (Kovacs et al., 1988; Puig-Antich, 1982). Third, conduct problems and depression may be reciprocally related so that they influence one another in a simultaneous and transactive fashion. In other words, while conduct problems increase the risk for depression, depression in turn, leads to symptoms of conduct problems. As suggested by Seligman and Ollendick (1998), for any of these direct causal assumptions to be true, it must be shown that one disorder temporally precedes the other and puts an individual at elevated risk for the development of the second disorder. Conduct Problems Preceding Depression As mentioned previously, the age of onset for conduct problems typically precedes the age of onset for depression (Biederman et al., 1995; Nock et al., 2006; Zoccolillo and Rogers, 1991). In fact, the National Comorbidity Survey Replication study found that conduct disorder precedes depression in 72% of cases (Nock et al., 2006). Moreover, those with both active and remitted conduct disorder had significantly higher risk for developing depression later in life suggesting that conduct problems may be a marker of risk for subsequent psychopathology. It has been theorized that the progression of conduct problems into depression is related to the chain reaction of developmental failures experienced by youth with conduct problems (Capaldi 1991, 1992; Capaldi and Stoolmiller, 1999; Patterson et al., 1992). Specifically, the combination of lack of competence and negative reactions from others may result in pervasive failures in adaptation that subsequently contributes to a child s vulnerability to the onset of depressive symptoms (Capaldi and Stoolmiller, 1999). For example, higher levels of conduct problems are associated with peer rejection, problems in the parent child relationship, and failure to develop academic skills (e.g., Capaldi, 1991). Such consequences often affect social development and contribute to associations with deviant peers, negative attitudes, and may in turn contribute to depressed mood. In a longitudinal study, Capaldi (1992) found that boys with high conduct problems at Grade 6 reported significantly higher depressed mood symptoms at Grade 8. Some have hypothesized that one cause of this phenomenon may be that the social consequences of antisocial behavior may increase with age. Social consequences in adolescence (e.g., poor family relations, academic underachievement) may become more costly for the individual as they enter a stage when peer relationships become increasingly important. However, controlling for prior depressed mood, conduct problems at Grade 8 did not predict higher levels of depressed mood at Grade 12 (Capaldi and Stoolmiller, 1999). Beyers and Loeber (2003) suggest that this pattern of results may indicate that the effect of conduct problems on later depressed mood may be limited to early adolescence or select transition periods. Depression Preceding Conduct Problems However, a subset of studies has found the reverse to be true. At the forefront of this alternate position is the work of Kovacs et al. (1988) who found that in the majority of cases involving comorbid depression and conduct disorder, depression was diagnosed first. This early study followed depressed children ages 8 13 over several years. Over the course of the study, 23% developed conduct disorder. Of these comorbid cases, 56% of participants developed depression prior to conduct disorder while 25% developed conduct disorder prior to depression. While these results demonstrate that, at

8 208 Wolff and Ollendick times, depression precedes conduct problems, the sample used for the study was small and does not permit ready generalizations. Moreover, the sample was selected based on a diagnosis of depression, which may have increased the likelihood of reporting a subsequent diagnosis of conduct problems. If the reverse had been true (i.e., the sample was selected based on diagnosis of conduct problems) they may have been more likely to find subsequent diagnoses of depression. Hence, limitations of this study render the results difficult to interpret. Another way to examine the progression from one disorder to another is to look at the effects of treatment for one disorder on the other disorder. For example, in one study, Puig-Antich (1982) found that clinic-referred children who met criteria for major depression often exhibited comorbid conduct problems. Moreover, symptoms of conduct problems improved when depression remitted. The study initially sought to examine the effectiveness of imipramine in pre-pubertal major depressive disorder. Clinical observations during the 5-week imipramine trial and during follow-up thereafter indicated that successful outcome of participants mood disorder was followed by alleviation of conduct disorder behaviors in the majority of the participants. However, these results should also be interpreted cautiously since no pure conduct problem control group was included, and because contrary results have been reported elsewhere, albeit in somewhat older samples (Harrington et al., 1991). It should also be noted that Patterson et al. s (1992) model further predicts that as children progress to later stages, the depressed mood resulting from earlier antisocial behavior and its negative consequences is expected to precede more delinquent behaviors. For instance, it has been found that depressed mood in boys is associated with escalation to more serious and varied kinds of delinquent behavior (Beyers and Loeber, 2003; Loeber et al., 1994). Basically, a transactional model is hypothesized in which conduct problems give rise to depression which, in turn, contributes to more delinquent acts. Alternately, it has been suggested that youth with depression may develop conduct problems as the irritability associated with depression becomes more severe. Difficulties regulating the irritability and negative affect associated with depression may contribute to increased conflict with others, oppositionality, and subsequent acting out behaviors. Such an explanation warrants further study as do additional mechanisms that may explain the progress from depression to conduct problems as the literature in this area is limited. Suggesting Common Ground More recent studies have proposed a dynamic link between conduct problems and depression that occurs concurrently and prospectively (Lahey et al., 2002). In examining 7- to 12-year old boys (at Wave 1) over a 7-year period, wave-to-wave changes were paralleled by correlated changes in the number of symptoms of depression. In other words, higher levels of CD in Wave 1 were accompanied by higher average levels of depression symptoms in Wave 1. Moreover, these symptoms remained relatively stable across waves two to seven. Thus, the findings suggest that when depression increases from one wave to the next, it is accompanied by concurrent increases in conduct problems and vice versa. In a similar longitudinal investigation, Beyers and Loeber (2003) examined relations between depressed mood and delinquency while controlling for common risk factors. Results indicated that depressed mood predicted concurrent delinquent acts, while at the same time delinquent acts predicted depressed mood. However, the relationship implicated was not a symmetrical one. In fact, depressed mood had a more robust effect on delinquency than delinquency had on depression. Hence, these findings suggest that while one disorder may predict the other, depression may have a stronger effect on conduct problems such that delinquent acts increase at a higher than would be expected rate. While such studies illustrate the relationship between conduct problems and depression in boys, there remains a lack of research on this issue in girls. Thus, little is known about the dynamics of these disorders as they relate to females. Finally, the work of Fergusson et al. (1996) offers an alternate explanation for the relationship between these dimensions. Specifically, he posits that the relationship between these disorders relates to risk factors common to both disorders. Structural equation modeling suggested that a substantial component of the comorbidity between conduct and affective disorders arose because the risk factors associated with the development of conduct problems overlapped with the risk factors for adolescent affective disorders. In particular, of the shared variance between conduct disorder and affective disorders, more than two thirds was accounted for by common risk factors. Accordingly, results suggested

9 Comorbidity of Conduct Problems and Depression 209 that the link between the two disorders was not a direct relationship, but an indirect one accounted for by other factors. It should be noted that research on the temporal ordering of these problems is limited and several factors have been neglected. First, research is hindered by the lack of longitudinal investigations of this topic. Even those longitudinal studies that have explored this topic have tended to cover a relatively brief period of time. Second, differences in the sequalae of disorders for males and females have not been adequately examined. Third, several studies have focussed on the onset of disorders without accounting for the emergence of early symptomotology. For example, a depressed child may begin to display temper outbursts, but may not meet full criteria for oppositional defiant disorder. While the onset of a disorder serves as one marker of comorbidity, it may be useful for clinical purposes to consider co-occurring symptoms that may subsequently develop into a second disorder. Finally, research in this area has failed to identify various mechanisms for risk as well as moderators in this relationship. For example, severity of the initial disorder may be a primary predictor of which individuals subsequently develop a second disorder. Along these lines, Nock et al. (2006) found that conduct-disordered individuals with increased symptom number and severity were more likely to develop a second disorder. Further elucidation of such factors is needed. An alternate explanation for these findings may be that because conduct problems have extremely deleterious effects on interactions between children and their adult caretakers, parents and teachers may be more likely to recognize symptoms of conduct problems as opposed to depression. Thus, children with conduct problems may be more likely to present to clinic settings for this reason, and symptoms of co-occurring depression may be overlooked by parent or teacher raters. Accordingly, it may be that depression precedes conduct problems in more cases than the previously reviewed studies suggest. In brief, however, findings demonstrate that in the majority of cases depressive symptoms tend to emerge after the onset of conduct problems. In a smaller proportion of cases, depression seems to occur earlier than the onset of conduct problems, although these findings may be tainted by referral biases. Moreover, studies suggest a reciprocal relationship, as a rise in one disorder is often associated with an increase in the other. Still, based on the work of Ferguson et al. (1996), it appears that much of the relationship between conduct problems and depression may be explained by their common risk factors, as will be discussed next. Research on the mechanisms that may explain the path from one disorder to another is limited and warrants further investigation. COMMON RISKS? The final explanation for high rates of comorbidity between conduct problems and depression involves the presence of common risk factors. Questions of vulnerabilities, risk factors, and familial (genetic and environmental) transmission that involve adolescent characteristics and the familial and extra-familial context in which development takes place remain at the forefront of research on comorbidity. As Caron and Rutter (1991) noted some years ago, antecedent causal factors may lead to comorbidity in two ways. First, the risk factors for one disorder may be the same as the risk factors for the other disorder. Second, even though two disorders may have apparently different risk factors, these risk factors may correlate with each other. In both instances, the comorbidity between disorders arises because the risk factors and life pathways that lead to one disorder overlap or correlate with the risk factors and life pathways that lead to the other disorder. In general, research has shown support for the inter-correlation and overlap of risk factors between conduct problems and depression (e.g., Fergusson et al., 1996). Such findings suggest that the risk factors and life pathways that lead to increased risk of conduct disorder have much in common with the risk factors and life pathways that contribute to depression. There are many levels of risk factors, including child, family, school, peer, neighborhood, and culture, which may contribute to comorbidity. Moreover, a number of common genetic, biological, physiological, psychological, environmental, and social factors may be implicated in the development of comorbidity. While a plethora of possibilities exists, the present review selectively examined the common risk factors of parental psychopathology, emotion regulation, and emerging cognitive biases and sought to find common and unique aspects of this risk; as such, it was not intended to be an exhaustive review of all of the aforementioned possibilities. These risk factors were chosen because they illustrate both shared and unique sources of overlap in the symptoms associated with conduct problems and depression. However, it is also important to keep in mind that despite the presence of various risk factors, many

10 210 Wolff and Ollendick individuals demonstrate great resilience and do not go on to display comorbid psychopathology. Parental Psychopathology Previous research has indicated that children of parents with various forms of psychopathology are at increased risk for many psychological problems including conduct problems and depression. Since a complete discussion is beyond the scope of this paper, only the primary conclusions that can be drawn from this literature will be presented. For parents of children with conduct problems, high rates of parental depression, antisocial personality disorder, and substance abuse have consistently been reported (e.g., Frick et al., 1992). Depression, particularly in mothers, has been linked to child conduct problems in several studies (e.g., Phares and Compas, 1992). In general, depressed mothers are more negative in their interactions with children than non-depressed mothers. They appear to use more physical punishment, are more verbally aversive, monitor and supervise their children s activities less effectively, engage in fewer affectionate interactions with their children, and respond to their children with less warmth (see McMahon and Wells, 1998). Such parenting practices may in turn contribute to coercive interactions between the parent and child and result in more opportunities for the child to engage in more conduct problems behaviors. High rates of parental antisocial personality disorder have also been reported for parents of children referred for conduct problems (e.g., Lahey et al., 1988). Although some studies have found an association between maternal antisocial behavior and child conduct problems, research has consistently shown that the association is stronger between father and child (e.g., Frick et al., 1992). Additional studies have also pointed to increased risk of conduct problems associated with parental alcoholism and other substance use (e.g., Loeber et al., 1995). Similarly, estimates of the incidence of depression in the children of depressed parents range from 14% to almost 50% (see Trad, 1987). In fact, several studies have found that depression in one member of a family magnifies the risk of depression twofold (e.g., Williamson et al., 1995). As reviewed by Stark et al. (2000), the offspring of depressed parents are more likely to develop depression if the parent s depression had an early onset, has been recurrent, or if the parent was repeatedly hospitalized. Hammen (1991) has also noted that the severity of a child s depression is related to their mother s experiencing more depression. In addition to this risk factor for depression, other studies have implicated the role of parental alcoholism (e.g., Puig-Antich, 1989). Thus, children of depressed or substance abusing parents are at increased risk for depression. A few studies have examined the relationship between comorbid conduct disorder and depression in youth and psychopathology among family members. For instance, Puig-Antich (1989) studied the family history of 95 prepubertal probands (aged 6 12 years). Results showed that depression in the probands correlated with high family prevalence of depression and alcoholism. However, results further indicated that when family members of depressed children had low rates of depression, the children were more likely to exhibit comorbid conduct disorder (in comparison to those with high family rates of depression). This finding suggests that when family members have not experienced depression, these children may be more likely to act out their internalized feelings. In addition, Williamson et al. (1995) found that the rate of antisocial personality disorder among relatives of youth with depression and conduct disorder was elevated compared with the rate among relatives of youth with depression only. Thus, comorbid children are more likely to have family members with antisocial personality disorder. Although family factors are often considered to be primarily psychosocial in nature, such variables contain both genetic and environmental influences. For example, O Connor et al. (1998) demonstrated that genetic factors accounted for approximately half of the variance in the overlap of depression and antisocial symptoms. In terms of environmental influences, research has also linked parent depression to lower levels of nurturance and affection as well as greater control, hostility, and conflict (see Jewell and Stark, 2003 for review). Although space considerations preclude a thorough presentation of such mechanisms, the role of such processes should be recognized. Unfortunately, the majority of studies have tended to examine the role of parent psychopathology in isolation. This decision presents several problems. First, when family characteristics are examined, they usually focus on single childhood conditions, either by excluding potential participants who have other forms of psychopathology or by ignoring potential co-occurring conditions (Marmorstein and Iancono, 2004). Thus, little is known about the role of parental psychopathology as it relates to co-occurring disorders

11 Comorbidity of Conduct Problems and Depression 211 in their offspring. Second, looking at these factors in isolation does not allow for the examination of how risk factors operate together in placing a child at risk for psychopathology. Third, because family risk factors are often interconnected with one another, their independent examination is probably confounded by these overlapping variables (Frick et al., 1992). In other words, although factors such as parental psychopathology may explain part of the variance in the development of child psychopathology, they do little to explain the mechanisms of change underlying their development (e.g., dynamics in the parent child relationship, parenting techniques). Overall, those studies that have looked at comorbidity as it relates to parental psychopathology point to the common risks of parental depression (particularly in the mother) and substance abuse (primarily in the father) and the distinct risk factor of paternal antisocial personality disorder for conduct problems. Risks for comorbidity appear to be similar to those with conduct problems with at least one distinction. Specifically, research has demonstrated that when a mismatch occurs between parent and child where the child demonstrates depression, but the parent does not, the child may be at increased risk for the development of comorbid conduct problems and depression. Thus, it may be that families showing goodness-of-fit between parent and child psychopathology are less prone to having a child with a comorbid presentation. Such a possibility remains to be empirically verified however. Emotion Regulation Emotion regulation deficits also have ties to both conduct problems and depression. In discussing this risk factor, it is necessary to first define emotion regulation. For purposes of this review, emotion regulation is conceptualized as the internal and external processes involved in initiating, maintaining, and modulating the occurrence, intensity, and expression of emotions to accomplish one s goals (see Eisenberg et al., 1997; Grolnick et al., 1996). Based on the work of Block and Block (1980), it has been argued that children with externalizing problems are undercontrolled in their expression of affect, whereas those with internalizing problems are overly controlled or constrained in their expression of emotions. For example, in contrasting those with various styles of emotion regulation (i.e., highly inhibited, optimal regulation, undercontrolled) to those with varying levels of negative emotionality (i.e., moderately high, moderately low), Eisenberg et al. (2000) hypothesized that the interaction of these variables would result in differences in adjustment and quality of social behavior. Results indicated that negative emotionality was a general risk factor related to both internalizing and externalizing disorders. In addition, regulatory undercontrol was a predictor of externalizing behavior problems, whereas regulatory overcontrol (e.g., behavioral inhibition) predicted internalizing problems. In another study, Eisenberg et al. (2001) examined emotion regulation in children with internalizing and externalizing problem behaviors. Based on parent and teacher reports as well as observations during several behavioral tasks, various similarities and differences emerged between groups. In general, children with externalizing problems, compared with children with internalizing problems and non-disordered children were more prone to anger, impulsivity, and low regulation. Children with internalizing symptoms were prone to sadness, low impulsivity, and were more regulated on measures of attentional and inhibitory control. Those children that were comorbid in the study showed a similar presentation as those with externalizing behaviors. Specifically, comorbid children were higher on anger and impulsivity, but lower on attentional regulation and inhibitory control. It is important to recognize that emotion regulation involves both physiological and behavioral components, both of which are expected to influence pathways to child psychopathology. It has been argued, for example (see Eisenberg et al., 2001), that the Behavioral Inhibition System (BIS) and the Behavioral Activation System (BAS), with connections to the limbic system, may underlie high and low levels of regulatory control. For example, BIS has been implicated in behaviors related to overcontrol (e.g., social withdrawal), whereas low BIS and/or high BAS are associated with more externalizing behaviors including impulsivity (Gray, 1987). Others have pointed to regulatory differences related to right and/or left frontal asymmetry, although findings are somewhat contradictory at this time (e.g., Forbes et al., 2006). Along these lines, Cole et al. (1996) examined expressive and physiological aspects of emotion regulation during a negative mood induction in preschoolers with varying degrees of behavior problems. Findings indicated that at follow-up, inexpressive children had higher rates of both externalizing and internalizing disorders while expressive children had higher rates of externalizing disorders. Moreover,

12 212 Wolff and Ollendick inexpressive children had the highest heart rate, lowest vagal tone, and smallest autonomic nervous system (ANS) change during negative mood induction. Highly expressive children had the slowest heart rate, highest vagal tone, and largest ANS change. Such physiological differences in the two groups may suggest different emotion regulation strategies between the groups. For example, inexpressive children may not show external reactivity (e.g., show facial response), but they may focus internally on distress. Based on these results, the authors suggest that inexpressive children with disruptive behavior may be at increased risk for subsequently developing comorbid depression. However, because the study did not follow these children past first grade, this possibility was not fully explored. It is also necessary to consider the means by which emotion regulation might lead to emotional or behavioral problems. In some cases, problems in emotion regulation (e.g., over/undercontrol) may directly influence the child s propensity to display conduct problems or depression (Frick and Morris, 2004). For example, a child with low regulatory abilities may be quick to show anger and act aggressively or a child who is overcontrolled may be quick to internalize feelings of sadness and to withdraw. However, emotion regulation may also affect the development of these behaviors through indirect means (Frick and Morris, 2004). Mechanisms such as parenting style, social cognitive skills, and peer relations may mediate the relationship between emotion regulation and the development of these disorders. Finally, it should be recognized the majority of research in this area discusses internalizing/externalizing disorders rather than conduct problems and depression in particular. Therefore, the present discussion is somewhat speculative as it is not known if these descriptions apply to the primary disorders in question. Although those disorders that comprise internalizing disorders (anxiety and depression) and externalizing disorders (attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder, and conduct disorder) bare many relations to one another, there are clear distinctions in the presentation of each. Thus, although these findings are assumed to relate to conduct problems and depression, their generalizability to distinct disorders remains unknown. Cognitive Deficits and Distortions Researchers have also identified cognitive deficits and distortions as a link between conduct problems and depression. Specifically, the role of social information processing and schemata in aggressive and depressive youth represents a general common risk factor between these two groups. While there are many similarities in the type of distortions and deficits displayed by these children, there are also distinct differences in the processing patterns and basic schemata of those with each type of psychopathology. Research exploring various knowledge structures, or schemata, tend to differentiate these two groups of children. In general, aggressive children are thought to possess inflated self-concepts, underestimate their social rejection, and show a hostile attribution bias (see Rudolph and Clark, 2001 for review). Conversely, the negatively biased schemata of depressed children contribute to negative views of the self, current circumstances, and the future (Beck, 1967). In particular, according to learned helplessness theories of depression (Abramson et al., 1978), depressed individuals tend to attribute the causes of negative events to stable, global, and internal factors. In comparing the conceptions of self and peers in youth with aggression, depression, or a combination of the two, Rudolph and Clark (2001) demonstrated that children in the depressed and depressed-aggressive groups demonstrated more negative conceptions of both self and peers than did non-symptomatic and aggressive children. Aggressive children, on the other hand, demonstrated a self-enhancement bias. Thus, depressed and comorbid individuals appear to hold negative views of the self, whereas aggressive individuals show more inflated ideas of the self. In addressing the role of social information processing, Dodge s model of the steps children engage in before enacting social behaviors provides a framework for discussion. As reviewed by Dodge (1993), this dynamic model of steps includes encoding and interpreting social stimuli as well as generating and evaluating responses before enacting a behavior. Deficits and distortions at any one of these steps may independently contribute to the development of conduct problems and/or depression (e.g., Quiggle et al., 1992). Indeed, as reviewed by Dodge (1993), studies of social information processing in children with conduct problems and depression indicate general and specific difficulties at each stage of processing. In the first step, encoding social cues, individuals must pay attention to as many relevant cues as possible in an unbiased manner. For aggressive children, research demonstrates both deficits and distortions

13 Comorbidity of Conduct Problems and Depression 213 related to the coding of social stimuli. Specifically, aggressive boys have been found to encode fewer cues than non-aggressive boys before making attributions about another s intent (Dodge and Newman, 1981) and their encoding tends to be systematically biased toward hostile cues (Crick and Dodge, 1996). Conversely, those with depression tend to attend to negative cues about the self particularly in response to situations involving affiliative loss or failure (Beck, 1967). Thus, both children with conduct problems and depression demonstrate biases in coding. However, those with conduct problems show biases toward encoding hostile acts, whereas depressed children are primed to attend to failure, loss, and negative self-reference (Dodge, 1993). The second step of processing involves the mental representation and interpretation of the encoded cues. Research shows that children with conduct problems show a hostile attribution bias as they tend to selectively attend to or misperceive hostile cues in social interactions (Crick and Dodge, 1996; Dodge and Frame, 1982). Again at this stage, depressed children tend to make internal, stable, and global attributions for negative events (e.g., Abramson et al., 1978). Using the Children s Attributional Style Questionnaire, several studies have replicated this finding (e.g., Abela, 2001). Additional studies have shown that depressed children also demonstrate hostile attribution bias. In comparing those with aggression and depression, one study (Quiggle et al., 1992) showed that aggressive children who showed a hostile attributional bias were more likely to report that they would engage in aggressive behavior and indicated that aggression would be easy for them. However, depressed children were more likely to attribute negative situations to internal, stable, and global causes. In the third step, children access one or more possible behavioral responses from long-term memory or construct a novel response. Both the quantity and the quality of responses generated at this stage have been studied. Aggressive boys tend to generate a fewer number of responses than popular boys (Richard and Dodge, 1982). Moreover, they tend to show proportionately more aggressive responses (Dodge, 1980). Comparatively less research has examined response generation in depressed children. However, one of the few studies to examine this issue found that depressed children generated more irrelevant responses to problems (Quiggle et al., 1992). In the fourth step, children evaluate the previously accessed or constructed responses and select the most positively evaluated response for enactment. A number of factors are involved in children s evaluations of responses including the moral ( good versus bad ) acceptability of a response and the degree of confidence children have in their ability to enact each response (i.e., self-efficacy). Aggressive children judge aggression to be less morally bad than other children (Deluty, 1983). Aggressive children are also more confident in their ability to aggress than their non-aggressive counterparts (Quiggle et al., 1992). Depressed children, on the other hand, tend to expect more positive outcomes for withdrawal (Quiggle et al., 1992). In one of the few studies to evaluate information processing in comorbid aggressive and depressed children, Quiggle and colleagues (1992) found that those having both conduct problems and depression demonstrated processing characteristics similar to both subgroups. In other words, comorbid children showed the cognitive patterns of both the aggressive and depressive subgroups in an additive manner. The only seemingly unique difference in the comorbid group emerged on response generation when comorbid children tended to generate more purely affective responses to negative situations. The authors suggest that comorbid children become more frustrated than non-comorbid individuals when they do not obtain their desired goal. In turn, they feel more angry and helpless, similar to their depressed peers. However, they may focus more on the anger and frustration rather than the helplessness. Thus, they may be less likely than those with depression alone to give up or withdraw. Instead, they might continue to be frustrated and aggressive. Such an account, however, is only speculative. Summary of Common Risk Factors While this review has indicated several factors common to both conduct problems and depression, it is necessary to point out that while such studies have shown that these factors are correlates of each disorder, sufficient evidence has not been offered to show that they are causal risk factors antecedent to the onset of the disorders. Even when studies do take a longitudinal approach, they typically follow these children for only a short period of time. In addition, these studies often follow children at quite young ages before they have even reached the period of greatest risk for comorbidity (see Seligman and Ollendick, 1998). Since knowledge of causal risk factors relies heavily on the results of experimental

14 214 Wolff and Ollendick trials as opposed to observational or even longitudinal research the present findings fall short of demonstrating a causal link. Moreover, a clear paucity of research fails to explain how such common factors relate to comorbid individuals. While ample findings have demonstrated correlates of each disorder alone, the current research lends itself largely only to speculation as to how these issues might present in comorbid individuals. INITIAL CONCLUSIONS The above discussion explored various aspects of comorbidity, focussing on potential explanations for the overlap of conduct problems and depression. Various methodological flaws, including Berkson s bias and the use of multiple informants, were explored as possible explanatory factors. However, the fact that similar rates of comorbidity have been found in nonclinical samples primarily ruled out this possibility. The previous discussion also entertained the idea that the presence of shared diagnostic criteria may explain the covariance of these disorders. However, examination of the symptom criteria for conduct problems and depression showed that criterion overlap is minimal and this factor alone does not account for comorbidity. Next, the potential causal roles between conduct problems and depression were discussed. Although only tentative conclusions may be drawn, the literature suggests that in the vast majority of individuals, conduct problems develop prior to depression, although in other individuals the reverse may be true. Thus, it appears that conduct problems exert a main effect on depression and vice versa. Finally, various common risk factors for the two disorders were explored. The review of the literature demonstrated that conduct problems and depression have common (e.g., maternal depression) and unique risk factors (e.g., parental antisocial personality disorder). Thus, the co-occurrence of these disorders may be explained, in part, by their overlapping risk factors. Still, there remains a lack of research on the presentation of these risk factors in comorbid individuals. Thus, a model by which these factors might develop in comorbid individuals is next proposed. MODEL FOR THE DEVELOPMENT OF COMORBIDITY Many of the factors reviewed above are interrelated and serve to compound one another though a complex network of factors. These variables influence one another and influence relations between risk factors and problem behaviors. Unfortunately, the majority of studies on risk factors stop at the point of identifying these common variables. While a number of factors have been identified, far less is known about the mechanisms by which they operate (Rutter, 1997). Studies continue to provide retrospective, correlational results that are not able to explain how these factors influence the development of psychopathology. While identifying these factors is an appropriate first step, little can be done in terms of interventions without knowing how these factors interrelate and how they operate upon one another. Indeed, knowing what characteristics or events precede the onset of comorbid disorders does not adequately explain the mechanisms by which these risk factors lead to the development of a specific disorder. To account for this limitation, investigators are increasingly incorporating a developmental psychopathology framework to address the full array of features associated with these disorders (Toth and Cicchetti, 1999). Developmental Psychopathology The goal of developmental psychopathology is to integrate often disparate fields of study into an interdisciplinary perspective that informs efforts to prevent and ameliorate maladaptation and psychopathology across the lifespan, (Toth and Cicchetti, 1999, p. 16). Under this framework, the organization of specific problem behaviors is considered in the context of a series of age- and stage-relevant tasks, which are important to adaptation over time. The role of isolated risk factors and causal pathways in the development of child and adolescent psychopathology are considered within a transactional context involving the growing child and his/her environment. Based on this framework, the individual child and their environment are intricately intertwined in the development of child psychopathology. Thus, the following discussion considers the dynamic development of comorbidity as it emerges over time and integrates the aforementioned risk factors into this theoretical framework for understanding the etiology of conduct disorder and depression. The model is, of course, tentative since firm empirical support for the various connections is not yet available. Overview of Model The proposed model (see Figure 1) builds upon the work of Fergusson et al. (1996) and Weiss et al.

15 Comorbidity of Conduct Problems and Depression 215 Fig. 1. Model for the development of comorbid conduct problems and depression (adapted from Fergusson et al., 1996). (1998) to explain the development of comorbid conduct problems and depression. As noted earlier, Fergusson and colleagues sought to explain how common risk factors account for relations between conduct problems and affective disorders over time. Basically, common risk factors were expected to account for the relationship between these disorders. However, this model did not explain the exegesis of the initial disorder or account for unique risk factors. Moreover, when tested, the common risks in this model did not fully account for comorbidity as hypothesized. It is suggested that the work of Weiss et al. (1998) may serve as a practical addition to this model with a focus on common and unique features of psychological disorders. These authors argued that it might be useful to conceptualize childhood disorders in terms of generality and specificity. Weiss and colleagues combined these factors into a conceptual and data-analytic model for characterizing different features of childhood psychopathology. Specifically, the model pooled these factors in an additive manor resulting in the following equation: Expression of Syndrome = Common Features + Broadband- Specific Features + Error [Individual Differences]. While this model may account for the expression and differentiation of a single disorder, it does not account for the expression of comorbidity and the interaction between disorders. In other words, the model shows how disorders may be distinct from one another, but it does not explain how such distinct characteristics may coexist in the same individual. For these reasons, a modified model is needed to account for comorbidity. In general, our model suggests common and unique risk factors that might account for the initial onset and interaction between disorders as well as risk factors which may lead to comorbidity. The model accounts for the development and maintenance of conduct problems and depression (alone and in combination), the interconnectedness of various common and unique risk factors, and the direct and indirect relations between these disorders over time. In this vein, the model (adapted from Fergusson et al., 1996 and Weiss et al., 1998) assumes that 1. The child s level of conduct problems at Time 1 is a function of the unique and common risk factors that contribute to the development of this disorder. 2. The child s level of depression at Time 1 is a function of the unique and common risk factors that contribute to the development of this disorder. 3. Conduct problems and depression are reciprocally related so that one disorder increases the child s risk for the second disorder (at Times 1 and 2) and vice versa. 4. The child s level of conduct problems at Time 2 is a function of his or her preexisting level of conduct problems and depression at Time 1 and known unique and common risk factors for conduct problems. 5. The child s level of depression at Time 2 is a function of his or her preexisting level of depression and conduct problems at Time 1 and the unique and common risk factors for depression. 6. Common risk factors may influence the development of conduct problems and/or depression at Times 1 and 2. In sum, the model allows for several potential pathways to comorbidity. To be considered a common risk factor, a variable must be shown to significantly relate to both conduct problems and depression. To be defined as a unique risk factor, a variable must discriminate between conduct problems and depression, showing significant correlation with only one of the disorders, but not the other. Accordingly, common risk factors are related to the development of conduct problems, depression, or their comorbid condition, while unique risk factors serve to differentiate conduct problems and depression. The existence of these disorders (alone or in combination) is considered a byproduct of these various risk factors as they influence the child s development over time.

16 216 Wolff and Ollendick Risk Factors Although at first glance, and as evidenced by our review, there appears to be a great deal of overlap in factors related to the onset of conduct problems and depression. However, our review also illustrates how these can be broken down into common and unique factors. For example, while both groups have difficulty regulating emotion, the review of the literature demonstrates that those with externalizing problems are undercontrolled while those with internalizing problems are overcontrolled (e.g., Eisenberg et al., 2001). Moreover, the previous discussion of risk factors serves as an example of how these factors may interrelate in a transactional manner. For example, parent psychopathology may give rise to negative self-concepts, which may, in turn lead to depression in the child. Furthermore, the depression in the child may lead to more depression in the parent as the parent may, for example, question their parenting abilities if the child develops behavior problems. Thus, a cycle in which parent and child influence one another s psychopathology is suggested. Overall, according to the model, common risk factors give rise to either disorder, while unique factors differentiate between these conditions. Various combinations of these unique and common risk factors may contribute to comorbidity. Following the onset of conduct problems or depression, the model further posits that conduct problems may exert a main effect on depression (or vice versa) or one disorder might exert an indirect effect on the other through common risk factors. The direct link between conduct problems and depression in the present model is maintained for two reasons. First, given the number of risk factors believed to be related to these disorders, it seems that it is not likely that the correlation between the disorders will be fully explained by common risk factors. If for example, any one of these factors is not appropriately included in the model then the mediation of this relationship will not be complete. While Fergusson et al. (1996) attempted to explain this relationship through indirect means they were only successful in explaining part of the variance in the co-occurrence of disorders. Second, and more importantly, this direct relationship is maintained in the current model since several studies have shown that one disorder may place an individual at increased risk for comorbidity (e.g., Capaldi, 1991). The nature of the relationship between conduct problems and depression appears to be a reciprocal one in which there is somewhat of a cyclical pattern with one giving rise to the other and vice versa. Accordingly, each disorder places an individual at risk for the development of the other disorder. However, the interaction between these two disorders does not necessarily have to be symmetrical in that one disorder affects the other to the same degree as the other (Loeber and Keenan, 1994). Based on the reviewed literature, it seems quite probable that conduct problems increase the risk of depression more than the reverse direction. Although the exact mechanisms by which these processes take place are not known, several theories have been presented. In particular, children may progress from depression to conduct problems as a means of acting out their internalized feelings. Related to the idea of masked depression, depressed children may become aggressive as a means of externalizing some of the feelings, particularly of sadness, that they experience. Others have suggested that depression may lead to conduct problems through cognitive debilitation in the midst of frustrating situations (Greene and Doyle, 1999). Children experiencing the irritability and distractibility associated with depression may have increased difficulty thinking through various situations and responding appropriately. For example, depression might in some cases impair an individuals concern about the adverse consequences of their actions, thereby increasing risk for conduct problems (Lilienfeld, 2003). Moreover, the negative affect that is associated with depression may by annoying or irritating to others and, in turn, may have negative effects on relationships with significant others in the child s life which may contribute to greater conflict with others (Oland and Shaw, 2005). Such pathways from depression to conduct problems are worthy of consideration in the development of comorbidity. In terms of the path from conduct problems to depression, it is believed that as hypothesized by Patterson and colleagues (1992), the adverse consequences and life circumstances associated with conduct problems may lead to more depressed thoughts such as negative views of the self, current circumstances, and the future. As mentioned previously, specific social and academic problems that are often seen as byproducts of conduct problems include academic underachievement, peer rejection, problems in parent child relationship, and/or legal difficulties (Capaldi, 1991). The accumulation of negative reactions from others coupled with failures in various realms of functioning may subsequently increase a

17 Comorbidity of Conduct Problems and Depression 217 child s vulnerability to depression. Thus, it appears that there are of number of possibilities to explain the path from conduct problems to depression. Summary In sum, the proposed model incorporates common and unique factors related to the development of comorbidity over time. Both direct and indirect relationships between conduct problems and depression have been reviewed and incorporated into this framework. A significant drawback of this model is its neglect of risk factors that might be unique to comorbid individuals. While the model allows for risk factors of conduct problems and depression to be compiled in an additive manner, it does not account for variations in these factors which may be unique to children with comorbid disorders. Still, those studies that have examined risk factors in comorbid individuals seem to suggest the risk factors for comorbidity consist of a compilation of factors related to both conduct problems and depression, and that separate factors may not exist. It should be reiterated that despite the presence of various risk factors, many individuals demonstrate great resilience and do not go on to display psychopathology. This resilience may reside in the presence of a number of factors in the child s life that may counteract these risk factors. For example, an easy temperament, high level of intelligence, or the presence of positive social support may mitigate the relationship between the aforementioned risk factors and subsequent psychopathology within the proposed model. Finally, while the proposed model is believed to elucidate relationships between conduct problems and depression, it is recognized that these processes remain speculative at this time and await empirical verification. However, in as much as the proposed model helps to elucidate the interconnectedness of various factors, the heuristic utility of the model is that it brings a developmental perspective on psychopathology and provides a framework for integrating various mechanisms of risk. IMPLICATIONS FOR CLINICAL RESEARCH AND PRACTICE Based on the review of the literature and proposed model, suggestions for future research and practice are warranted. First, in terms of research, it is important for studies to use techniques that reduce artifactual comorbidity. As has been reviewed, various methodological techniques (e.g., use of clinical samples or multiple informants) may over inflate rates of comorbidity. To address some of these issues, it is recommended that studies make use of general population samples. In addition, to reduce error rates based on the use of multiple informants, it is suggested that discrepancies between reporters be resolved by a trained clinician rather than the so-called OR rule (Jensen, 2003). Since some informants may be more reliable or accurate than others, the resolution of this issue by a third, expert party seems to be a better option. An alternate solution to the use of multiple informants involves the application of confirmatory factor analyses to data from two informants (e.g., Keiley et al., 2003). It is believed that in employing such techniques, researchers may be better able to concentrate on true cases of comorbidity. Next, to address the temporal ordering of disorders and the possibility that one may give rise to the other, a greater emphasis on longitudinal investigations is needed. While conduct problems tend to precede depression in the majority of cases, further research is needed to elucidate the nature of these relationships. Investigations of these disorders over time may clarify the developmental course of these disorders as they tend to wax and wane over time (Caron and Rutter, 1991; Loeber and Keenan, 1994). Such studies allow for better elucidation of various antecedent risks and outcomes of the disorders as well as mechanisms which may explain the path from conduct problems into depression or vice versa. To date, research on such mechanisms and predictors of comorbidity have been limited. Along these lines, it is hoped that the presently proposed model may lend itself to longitudinal research. It is believed that this model lends itself to the integration of various risk factors and examination of the processes by which comorbidity develops. Accordingly, various mediating and moderating variables in the development of comorbidity must be thoroughly delineated. In particular, the risk factors reviewed in this study merit further investigation as parental psychopathology, emotion regulation, and maladaptive cognitions place individuals at risk for the development of both disorders. Specifically, greater delineation of the common and unique aspects of these risk factors that may contribute to one or both disorders is needed.

18 218 Wolff and Ollendick In terms of clinical practice implications, the high prevalence of comorbid conduct problems and depression highlight the need for interventions specific to this population. It is also hoped that prevention research in this area may be benefitted by the proposed model as specific common and unique risk factors for these disorders are identified and targeted. Identifying these early risk factors may help clinicians to identify individuals who are at risk for comorbidity and to develop more appropriate interventions which include prevention efforts focussing on one or both disorders. For example, as early differences in emotion regulation are identified, prevention programs may be designed to target these children before the onset of one or both disorders. Moreover, because comorbid children and adolescents demonstrate poor treatment outcomes (e.g., Hughes et al., 1990; Rohde et al., 2001) more research must identify effective treatment modalities for these individuals. Indeed, while research has provided us with some empirically based guidelines for treating these disorders alone, much less is known about effective means of treating those having symptoms of both disorders. In fact, presently no empirically supported treatments have been developed for youth who present with these cooccurring conditions (Ollendick and King, 2004). Given the high rates of comorbidity between these disorders, it is all the more important to account for treatment variables specific to these individuals in order to determine what treatments work best for which individuals under which circumstances. In the mean time, because the literature suggests that co-varying conduct problems and depression often present more similar to pure conduct problem behaviors than to pure depression, it is hypothesized that treatments targeting the risks associated with co-occurrence may most productively apply treatments found to be effective for conduct problems. Future research should explore not only the efficacy of such treatments for children with co-occurring conduct problems and depression, but also the efficacy of treatments tailored to the distinct characteristics of these comorbid individuals. CONCLUSIONS Clearly, the study of comorbidity and its development remain in their embryonic state (Loeber et al., 2000, p. 1475). Although comorbidity has been documented in many epidemiological and longitudinal studies, the risks and mechanisms related to its etiology and development are yet to be fully delineated (Caron and Rutter, 1991). 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