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Book Title: Treating and Preventing Adolescent Mental Health Disorders
> pp. [15]-[19]
UNDEFINED: AUTHORS
Treating and Preventing Adolescent Mental Health Disorders
Print ISBN 9780195173642, 2005
pp. [15]-[19]
achievement-related goals are at greater risk for depression when they encounter occupational failure. Studies investigating this specific vulnerability hypothesis in children have been supportive (Garber & Kaminski, 2000). In summary, a clear link exists between stress and depression. But by what mechanisms does stress increase an individual's vulnerability to depression? Although stressors often precede mood disorders, not all individuals exposed to stressors become depressed. Thus, there is not a perfect correspondence between exposure to negative life events and the onset of depressive symptoms. How individuals interpret and respond to events and how resilient they are also differentiates who does and does not become depressed. Some of the individual variability is due to differences in appraisals of the meaning of the events with regard to the self and future.
Interpersonal Relationships
Interpersonal perspectives on depression emphasize the importance of the social environment and the development of secure attachments. Vulnerability to depression presumably arises in early family environments in which the children's needs for security, comfort, and acceptance are not met. Bowlby ( 1980) argued that children with caretakers who are consistently accessible and supportive will develop cognitive representations, or “working models,” of the self and others as positive and trustworthy. In contrast, caretakers who are unresponsive or inconsistent will produce insecure attachments leading to working models that include abandonment, self-criticism, and excessive dependency. Such working models may contribute to the development of negative cognitions about self and others, and presumably increase individuals' vulnerability to depression, particularly when exposed to new interpersonal stressors. Reviews of the literature on the relation between the family environment and depression (Beardslee, Versage, & Gladstone, 1998; Rapee, 1997) indicate that families of depressed individuals are characterized by problems with attachment, communication, conflict, cohesion, and social support, as well as poor childrearing practices. Security in attachments helps infants cope
with the environment and a lack of such attachments may lead infants to seek protection by withdrawing from the environment altogether (Bowlby, 1980; Trad, 1994). Two-year-old children with secure attachments have been found to be more cooperative, persistent, and enthusiastic, show more positive affect, and function better overall than those with insecure attachments (Matas, Arend, & Sroufe, 1978). In adolescents, depression has been linked with less secure attachments to parents (Kenny, Moilanen, Lomax, & Brabeck, 1993). Moreover, adolescents undergoing stressful life events are more likely to become depressed if they had insecure attachments to their parents than adolescents with more secure attachments (e.g., Kobak, Cole, Ferenz-Gillies, Fleming, & Gamble, 1993). Beyond attachment, other kinds of dysfunctional family patterns have been found to be associated with depression in children (Rapee, 1997). Serious abuse and neglect interfere with normal expressions of infants' emotions and lead to avoidant or resistant attachments, especially if the mother is the perpetrator of the abuse. Maltreatment also leads to withdrawal behaviors in infants and self-esteem deficits later in childhood (Trad, 1987). The parent–infant relationship is inevitably worsened from such abuse, which in turn puts the infant in higher danger of being abused again (Trad, 1987). Two main parenting dimensions particularly associated with depression in children are acceptance/rejection and psychological control/autonomy (Barber, 1996). In retrospective studies, currently depressed adults recalled their parents as having been critical, rejecting, controlling, and intrusive (Parker, 1993). Currently depressed children have described their parents as authoritarian, controlling, rejecting, and unavailable (Stein et al., 2000), and they tend to perceive their families to be less cohesive and more conflictual than do nondepressed youth (Walker, Garber, & Greene, 1993; although see Asarnow, Carlson, & Guthrie, 1987, for contrary findings). Mothers of depressed children similarly describe themselves as more rejecting, less communicative, and less affectionate than mothers of both normal and psychiatric controls (Puig-Antich et al., 1985a). In observational studies, mothers of depressed children have been described as being
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less rewarding (Cole & Rehm, 1986) and more dominant and controlling than mothers of nondepressed children. Several longitudinal studies have found a significant relation between the family environment and subsequent depressive symptoms (e.g., Barber, 1996; Sheeber, Hops, Alpert, Davis, & Andrews, 1997), whereas others have reported null findings (Burge et al., 1997). Barber ( 1996) showed that children's ratings of parents' psychologically controlling behavior predicted their depressive symptoms, controlling for prior levels of depression, although children's prior depressive symptoms also predicted their ratings of their parents' behavior. Burt, Cohen, and Bjorck ( 1988) found for girls' ratings of family expressiveness predicted depression after controlling for prior depressive symptoms. Other studies have shown that adolescents' reports of family adaptability and cohesion (Garrison, Jackson, Marsteller, McKeown, & Addy, 1990) and perceptions of family support (McFarlane, Bellissimo, & Norman, 1995) contribute to adolescent depressive symptoms, controlling for prior symptom levels. In addition, maternal hostile child-rearing attitudes have been found to significantly predict increases in children's de-pressive symptoms (Katainen, Raikkonen, Keskivaara, & Keltikangas-Jarvinen, 1999). Using observational data of parental warmth, hostility, and disciplinary skills, Ge et al. ( 1994) reported that increases in adolescent internalizing symptoms were predicted by lower levels of parental warmth and higher levels of maternal hostility. In this same sample, Rueter, Scaramella, Wallace, and Conger ( 1999) found that escalating parent–adolescent conflict predicted increases in adolescent internalizing symptoms, which in turn increased the risk of the onset of internalizing disorders. Depressed children also have significant peer difficulties and social skills deficits (Altmann & Gotlib, 1988). Self-reported depression significantly correlates with teachers' reports of peer rejection in children (Rudolph, Hammen, & Burge, 1994). In laboratory studies, children with depressive symptoms were rated by their peers more negatively than were children without symptoms (Peterson, Mullins, & Ridley-Johnson, 1985). French, Conrad, and Turner
( 1995) noted that rejection by peers predicted higher levels of self-reported depressive symptoms among antisocial, but not among non-antisocial youth. Panak and Garber ( 1992) found a significant relation between peer-rated rejection and self-reported depression, and this relation was mediated by perceived rejection. Kistner, Balthazor, Risi, and Burton ( 1999) similarly found that perceived rejection predicted increases in depressive symptoms during middle childhood. Finally, in a longitudinal study of children in sixth grade, Nolan, Flynn, and Garber ( 2003) found that a composite measure of rejection by peers, family, and teachers significantly predicted depressive symptoms across 3 years. Thus, depression in children is associated with high levels of interpersonal conflict and rejection from various members in their social domain. Finally, relationships between depressed parents and their children have also consistently been found to be disrupted. Depressed parents report more conflict and less coherence in their families (Billings & Moos, 1983), are less involved and affectionate with their children, and experience poorer communication in parent–child relationships than nondepressed parents (Weissman, Paykel, Siegel, & Klerman, 1971). Moreover, depressed mothers tend to feel more hostile toward their children and less positive and competent about their parenting than do well mothers (Webster-Stratton & Hammond, 1988). Observations of depressed mothers interacting with their children reveal that these mothers are more negative (Lovejoy, 1991), more controlling (Kochanska, Kuczynski, Radke-Yarrow, & Welsh, 1987), and less responsive and affectively involved (Cohn & Tronick, 1989) and use less productive communications (Gordon et al., 1989). Depressed mothers spend less time talking to and touching their infants and show more negative affect in their interactions with their infants who themselves show less positive affect, less activity, and more frequent protests (Field, 1995). Parental depression can also lead to disturbed attachment behavior and an inability by the infant to regulate emotions, thereby putting the infant at greater risk for developing depression (Gaensbauer, Harmon, Cytryn, & McKnew, 1984). Offspring of depressed parents have more
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insecure attachments than do offspring of well mothers (DeMulder & Radke-Yarrow, 1991; Teti, Gelfand, Messinger, & Isabella, 1995). Moreover, insecurely attached offspring of depressed mothers tend to have difficulties in their relationships with peers (Rubin, Booth, Zahn-Waxler, Cummings, & Wilkinson, 1991). Finally, negative reciprocal interaction patterns have been observed between depressed mothers and their children (Radke-Yarrow, Nottelman, Martinez, Fox, & Belmont, 1992). In summary, two important findings emerge regarding the link between interpersonal vulnerability and depression. First, families with a depressed member tend to be characterized by less support and more conflict, and such family dysfunction increases children's risk of developing depression. Second, depressed individuals are themselves more interpersonally difficult, which results in greater problems in their social network. Thus, the link between interpersonal vulnerability and depression likely is bidirectional (Gotlib & Hammen, 1992). Longitudinal studies examining the contribution of family dysfunction, parent–child conflict, peer difficulties, and interpersonal rejection to increases in and maintenance of depressive symptoms in children have shown both that social problems temporally precede depression, and that depression contributes to interpersonal difficulties. Moreover, interpersonal difficulties appear to persist after depressive symptoms have remitted (Puig-Antich et al. 1985b). In addition, social adversities such as persistent poor friendships, low involvement of fathers, negative attitudes by family members, and stressful family environments can contribute to the maintenance or relapse of depressive disorders in youth (e.g., Asarnow, Goldstein, Tompson, & Guthrie, 1993). The interpersonal environment clearly is an important and sometimes stressful context in which children develop schema about themselves and others, which can then serve as a vulnerability to depression. In addition, children's own reactions to these environments can exacerbate and perpetuate negative social exchanges, which furthers the interpersonal vicious cycle, thereby resulting in more rejection and depression. Thus, a transactional model of mutual influence probably best characterizes the associa
tion between depressed individuals and their social environment.
The view that mania in younger people is extremely rare or nonexistent has been increasingly challenged by many case reports and by large-scale community surveys of adults; for example, Akiskal et al. ( 1985), in a case series of adolescent relatives of “classic” adult bipolar patients, found that despite frank symptoms of depression and mania and frequent mental health contacts, none of these youth had been diagnosed with an affective disorder. Weller, Weller, Tucker, and Fristad ( 1986) reviewed over 200 articles published between the years of 1809 and 1982 and identified 157 cases that would likely be considered manic by modern standards. However, approximately half of those subjects retrospectively diagnosed as manic according to DSM-III criteria were not considered so at the time of referral. More recently, Wozniak et al. ( 1999) reported that 16% of psychiatrically referred prepubertal children satisfied diagnostic criteria for bipolar disorder. Biederman et al. ( 1996) reported that a sizeable minority of children with ADHD has bipolar disorder. These reports suggested that mania in children/adolescents (pediatric mania) may not be rare, but difficult to diagnose. Despite continued debate and controversy over the validity of the diagnosis of mania in children (Biederman, 1998; Klein, Pine, & Klein, 1998), there is a growing consensus that many seriously disturbed children are afflicted with severe affective dysregulation and high levels of agitation, aggression, and dyscontrol that may be early bipolar disorder. These issues have received increased scientific attention, as evidenced by the scheduling of two NIMH workshops on bipolar disorder in children and adolescents and in exhaustive reviews that have supported the validity of the disorder in youth (Faedda et al., 1995; Geller and Luby, 1997; Weller, Weller, & Fristad, 1995). The NIMH Strategic Research Plan for Mood Disorder Research recommended the establishment of a multisite network program on pediatric onset bipolar disorder (Costello et al., 2002).
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Agreement on what constitutes the first presentation of bipolar illness is critical for epidemiologic studies to obtain the true age of onset and estimate of prevalence and risk. The following questions need to be addressed: Does pediatric bipolar disorder differ from the adult form? What are the early signs and symptoms? What is the relationship of ADHD and other disruptive disorders to juvenile onset bipolar disorder? Answers to these questions are complicated by the uncertainty about the duration of a manic episode; that stems from the fact that youth more frequently report manic symptoms that persist only a few hours or days (Carlson and Kelly, 1998; Geller et al., 1995), and therefore do not fulfill adult criteria.
Differentiating Prepubertal and Adolescent Onset
In April 2000, the NIMH convened a meeting of experts to discuss diagnostic issues impeding research on children/adolescents bipolar disorder. There was general agreement that a diagnosis of bipolar disorder, using DSM criteria, is possible in prepubertal children. Children fall into two categories: (1) those who clearly have a bipolar disorder (because they meet DSM-IV criteria for bipolar I [the classic form of the illness characterized by recurring episodes of mania and depression] or bipolar II (A form of the illness characterized by milder episodes of hypomania that alternate with depression) and (2) those who may be bipolar but do not completely fit the adult phenotype defined in DSM-IV but suffer from severe mood disturbances and symptoms of bipolar disorder and are highly impaired. Currently, severely ill children with an impaired mood disturbance, but not meeting full DSM-IV criteria for bipolar I or II, are not included in research studies of bipolar disorder because of the perceived uncertainty of their diagnosis. It was recommended that “bipolar-NOS” (not otherwise specified) could be used as a “working diagnosis” for advancing research on this broader phenotype, as long as the children are well described (with particular attention to symptoms of ADHD). Because available diagnostic instruments may not generate a reliable and
replicable diagnosis of bipolar-NOS, it was recommended that careful assessment include all of the behaviors that are impairing (Leibenluft et al., 2003).
Pediatric mania tends to be chronic and continuous rather than episodic and acute (Carl-son, 1983; Carlson, 1984; Feinstein and Wol-pert, 1973; McGlashan, 1988). In a recent review of the past 10 years of research on pediatric mania, Geller and Luby ( 1997) concluded that childhood-onset mania is a nonepisodic, chronic, rapid-cycling, mixed manic state. Wozniak, Biederman, Kiely, et al. ( 1995) also found that the overwhelming majority of 43 children from an outpatient psychopharmacology clinic who met diagnostic criteria for mania on structured diagnostic interview had a chronic and mixed presentation. Carlson, Bromet, and Sievers ( 2000) reported that early-onset manics were more likely to have comorbid behavior disorders in childhood and, compared to adult-onset cases of mania, to have fewer episodes of remission over a 2-year period. A review by McElroy et al. ( 1997) described “mixed mania,” which affects 20%–30% of adults with mania. Subjects with mixed mania tend to have a chronic course, absence of discrete episodes, onset of the disorder in childhood and adolescence, a high rate of suicide, poor response to treatment, and an early history of neuropsychological deficits highly suggestive of ADHD. Determination of the adult course of pediatric mania awaits data from longitudinal studies with larger samples. Presently, the same criteria defined in the DSM-IV-TR to diagnose bipolar disorder in adults are used for adolescents, as follows:
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A distinct period of abnormally and persistently elevated, expansive, or irritable mood, lasting at least 1 week (or any duration if hospitalization is necessary)
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During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree:
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Inflated self-esteem or grandiosity
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More talkative than usual or pressure to keep talking
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Flight of ideas or subjective experience that thoughts are racing
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Increase in goal-directed activity
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Excessive involvement in pleasurable activities that have a high potential for painful consequences
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In addition, the symptoms do not meet the criteria of a mixed mood episode, in which both criteria for a manic episode and for MDD (except for duration) are met with symptoms nearly every day during at least a 1-week period. For hypomania, the elevated or irritable mood lasts for 4 days. The mood disturbance causes significant impairment and is not better accounted for by other psychiatric disorders or medical conditions. The DSM IV-TR notes that adolescents are more likely to exhibit psychotic features and may be associated with school difficulties, substance abuse, and antisocial behavior. It also notes that a significant minority of adolescents have a long-standing pattern of behavior problems that may represent an extended prodomal phase to bipolar disorder or, in fact, may represent a distinct disorder.
Epidemiological data on juvenile bipolar disorder must be seen within the context of these diagnostic uncertainties. The 1980s Epidemiologic Catchment Area study (ECA), based on over 18,000 adults ages 18 and over for five U.S. communities, provided the first community-based data using modern diagnostic criteria and the first epidemiologic clue about the youth onset of bipolar disorder (Robins & Price, 1991) (Table 1.3). The lifetime prevalence of bipolar disorder was about 1/100, with few gender differences in rates and an overall median age of onset of 18 years. The 1990 National Comorbidity Survey (NCS) included a representative national sample in the
United States of over 8,000 subjects ages 15 to 54 (Kessler et al., 1994) and provided the best currently available epidemiologic information. The younger age included in the NCS was based on the ECA findings that many psychiatric disorders have a young age of onset. The overall lifetime prevalence of bipolar I disorder in the full sample was 1.7% (median age of onset, 21 years); in the sample ages 15 to 17 it was 1.3% with equal gender rates. Both the ECA and the NCS suggested that onset of bipolar disorder in adolescence and childhood is common. In the 1990s, the Cross-National Collaborative Group was formed to directly compare rates and risk of psychiatric disorders by standardizing analysis to overcome the problem of disparate data among studies. Seven countries (U.S., Canada, Puerto Rico, Germany, Taiwan, Korea, and New Zealand) provided data on bipolar disorder (Table 1.4). The lifetime prevalence rates for bipolar I ranged from 0.3% in Taiwan to 1.5% in New Zealand (Weissman et al., 1996), with equal gender ratios across sites (with the exception of Korea) and median ages of onset of 18 to 25 years. Efforts have been made to study children and adolescents directly in epidemiologic studies. Table 1.5 presents the prevalence rates from these efforts. There is considerable variability across these studies in the age ranges, diagnostic methods, and diagnostic criteria. All of these differences affect prevalence rates and may account for discordant findings. The Methodological Epidemiologic Catchment Area study (MECA) was conducted in a population-based sample of children and adolescents (Shaffer, unpublished observations). Probability household samples of 1,285 youth aged 9 to 17 years were selected at four sites (Atlanta, Georgia; New Haven, Connecticut; Westchester County, New York; and Puerto Rico; see Lahey et al., 1996 for methods). Data were collected for both children and their parents. The current (6-month) prevalence for mania was 1.2% and for hypomania was 0.6% (unpublished); 4.5% of youth with suicide ideation and 7.1% with suicide attempts had mania, compared to 0.9% of those who had neither suicide ideation nor attempts (Gould et al., 1998). Significant associations between bipolar disorder
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doi:10.1093/9780195173642.003.0002
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