Adolescent Depression: Challenges and Opportunities

Advances in Pediatrics 53 (2006) 111–163

ADVANCES IN PEDIATRICS Adolescent Depression: Challenges and Opportunities A Review and Current Recommendations for Clinical Practice Brad Jackson, PhDa,b,*, Susan Lurie, MDa,c a

Department of Psychiatry and Behavioral Sciences, The Children’s Hospital, Box 361, 1056 East 19th Avenue, Denver, CO 80218, USA b Private Practice, 1720 South Bellaire, Suite 805, Denver, CO 80222, USA c Department of Psychiatry, University of Colorado Denver Health Sciences Center, 4200 East 9th Avenue, Denver, CO 80262, USA

U

nderstanding and treating adolescent depression is a complex and challenging dilemma for families, providers, educators, and teens themselves. Families are faced with increasing information and misinformation from popular media sources and even celebrities. Black Box warnings declare extreme caution. Choosing a direction in which to proceed has become more challenging. Within crisis, however, emerges greater opportunity to help adolescents and their families understand their struggles, find hope, and recover from depression. Given recent concerns about possible increased suicidality associated with antidepressant medication use in youth, this article provides an overview of the controversy along with detailed approaches for evaluating and managing suicidality with adolescents. The high prevalence of depression and the limited availability of mental health professionals who specialize in work with children and adolescents have put primary care providers on the front line [1]. Research and clinical evidence are presented in this article to support and clarify the current recommendations for assessment, diagnosis, and treatment of adolescent depression. PREVALENCE Lifetime prevalence estimates for major depressive disorder (MDD) by late adolescence are between 20% and 25% [2]. In 2004, approximately 2.2 million adolescents aged 12 to 17 had at least one major depressive episode, with approximately 3.5 million having had at least one major depressive episode in their lifetime [3]. At any given point in time, 3% to 8% of adolescents are *Corresponding author. E-mail address: [email protected] (B. Jackson).

0065-3101/06/$ – see front matter doi:10.1016/j.yapd.2006.04.008

ª 2006 Elsevier Inc. All rights reserved.

112

JACKSON & LURIE

facing MDD, which makes it more common than asthma and most other chronic medical problems for this age group [2,4–6]. The prevalence of depression is increasing, whereas the age of first diagnosis is decreasing [4,7,8]. Reviews indicate that rates of depression demonstrate a concerning rise during adolescence [9,10]. A gender difference in prevalence of depression also emerges in early adolescence that continues through adulthood, with the rates for girls becoming double that for boys [11–15] across numerous cultures and countries [16]. The prevalence of dysthymia runs between 1.6% and 8%. Even when formal diagnostic criteria are not met, it is estimated that 15% of children and adolescents are experiencing elevated depressive symptoms [2,4,5,17,18], which still could have debilitating effects and place the youth at risk for major depression in the future [19,20].

PROGNOSIS Without treatment, an MDD episode for clinically referred youth typically lasts for 7 to 9 months [15,21,22]. Approximately 90% of major depressive episodes remit within 1 to 2 years from onset; however, 6% to 10% of episodes become more persistent [15,21–27]. The fact that most depressive disorders improve, particularly with treatment, is hopeful and important to convey to young people and their families. Among adolescents who participated in the 2004 National Survey on Drug Use and Health, however, only 40.3% of adolescents who reported a major depressive episode in the past year also reported receiving treatment [3]. Teens with health insurance (41.2%) were more likely to have received treatment than teens without (26.9%). Treatment also was more common among white respondents (44.9%) than Hispanics (36.8%) or African Americans (28.9%). It is also important to inform clients of the risk for relapse to help them better prepare and not become more despondent if symptoms recur. Relapse of depression occurs in 20% to 60% of adolescents within 2 years and in up to 70% of adolescents within 5 years [15,21–25,28,29]. The need for intervention is highlighted by the finding that young people with MDD are four times as likely to develop a depressive disorder in adulthood [13]. Having an early onset of depressive symptoms and recurring episodes also can place a young person at risk for increasing episodes with greater severity, duration, and treatment resistance [13]. Dysthymia, by definition, involves a longer duration of symptoms that last on average 3 to 4 years [30–33]. DEVELOPMENTAL COURSE OF DEPRESSION Depression can present with different symptoms across various developmental levels. Younger children may struggle more with anxiety, irritability, and physical complaints [34–36]. Along with irritability, adolescents exhibit depressive

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

113

reactions more similar to adult presentations, including sleep disruption, appetite changes, decreases in functioning, and suicidal ideation [35,36]. It is common for depressed adolescents to experience unexplained physical symptoms, such as headache, stomachache, and fatigue [37]. Depressed youth often present to pediatricians and nurse practitioners with recurrent somatic complaints that cannot be explained medically. The symptoms may seem to escalate in response to life stressors, such as school transitions or even publicized disasters (eg, hurricanes, tsumanis, earthquakes, terrorist attacks); however, specific triggers for symptoms may not always be identifiable. Sadness and depressed mood are normal human reactions to many internal and external experiences. The likelihood for experiencing depressed mood has been estimated at 25% to 40% for adolescent girls and 20% to 35% for adolescent boys [38]. Many youth with depressed mood do not develop a mood disorder [39]. For others, however, depressed mood places them at risk for the development of a depressive disorder [19,40,41]. Even moderate depressive symptoms can disrupt academics, peer interactions, and overall psychosocial functioning [42–44]. Depressive symptoms can contribute to early pregnancy, obesity [45–47], substance use [48], and isolation from peers [23,49]. Each of these difficulties may be influenced by environmental or familial factors that also fuel the depression, such as negative life events, low socioeconomic status, and family psychiatric illness. The treatment of depression may not be the only need [17,50–52]. RISK FACTORS Behavior genetics Evidence from family, twin, and adoption studies supports the role of both genetic and environmental factors in the development of major depression [53–55]. Studies with children, adolescents, and their families support a familial connection that is specific for depression rather than just increased risk for all psychiatric disorders [33,56,57]. Depression in children and adolescents is found to be moderately heritable, with nearly identical heritability estimates for boys and girls [58,59]. The genes implicated for depression risk in boys versus girls are only moderately correlated, however (r ¼ 0.57). This correlation suggests that although the pathways to depression through genetic liability may overlap for both genders, they also differ somewhat for boys and girls [60]. Specific genetic mechanisms, abnormalities, or polymorphisms to account for increased risk for depression have not been determined conclusively [61]. Negative life events also have been found to be partially heritable in children and adolescents [62,63]. The mechanism of heritability and genetic risk remains uncertain, although possibly through the young person’s own actions or personality partially contributing to increased risk for negative interpersonal interactions and stressors [10]. Youth with higher genetic risk seem to be more sensitive to negative environmental events [53,54,64,65]. Finally, measuring the symptom of suicide, monozygotic twins had a significantly higher rate of concordance for suicide than dizygotic twins [66]. Because depression occurs

114

JACKSON & LURIE

from a complex interaction of genetic and environmental contributing factors, a comprehensive assessment and intervention should address individual, family, and social components. Family risk factors The risk for the development of depression is increased by several important family factors. A family history of depression or other mental health disorder is found for 20% to 50% of children and adolescents who experience depression [56,67,68]. Parental depression is an especially strong predictor of depression for adolescents [49,64], as well as other mental health problems, such as anxiety and behavior disorders [23,49,64]. Children of depressed parents are at least three times more likely to have a depressive disorder than children of nondepressed parents. Asking about parental or familial depression can be diagnostically useful with the adolescent patient while also helping to identify relatives who need referral for evaluation and treatment of their own depressive symptoms. Family environmental factors also place certain teens at risk for the development of depression. Among these risk factors are high family conflict, low socioeconomic status, and the death of a parent [4]. On the other end of the socioeconomic spectrum, in affluent families, the pressures for children to achieve and isolation from parents may contribute to depression, anxiety, and substance abuse [69]. It is important to observe and ask about family interactions, particularly how the family and adolescent handle stressors and losses. Depressed adolescents more often indicate negative family life events, such as parental separation or divorce, death of a family member, school problems, health issues, and relationship difficulties with family or peers. Life stressors also can impact parenting and lead to conflicts between caregivers and teens that in turn increase psychiatric risk [70,71]. Evaluating the environmental and family context for depressive symptoms is critical for understanding their origin, meaning, and impact. Gender differences Gender differences in psychopathology emerge more clearly in adolescence, particularly in regards to internalizing symptoms such as depression, anxiety, and eating disorders [72,73]. Prospective longitudinal, national cross-sectional, and prospective community studies support findings that after age 13 more girls than boys reported depressive symptoms and depressed mood [44,74,75], showed clinical depression [76–79], and were diagnosed with clinical depression [2,62,80]. Gender differences in symptom expression also have been found, with girls reacting to depressed mood in a ruminative manner and boys reacting to depressed mood in a more hostile, angry, and behavioral manner [81,82]. It seems that the risk for depressed mood and clinical depression increases at adolescence, particularly so for girls. Depressive disorders are not the only psychiatric disorders that demonstrate a developing pattern of gender differentiation in adolescence. Evidence

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

115

suggests that girls develop anxiety disorders at an earlier age and more frequently than boys [83] and that anxiety disorders often occur before the development of depressive disorders [39,74,76,78,84]. The prevalence of eating disorders is higher for girls than for boys [2,85]. Studies of externalizing behaviors find gender patterns for aggression [10]. Boys develop more overt aggressive behavior through the elementary and latency years than girls [86,87], whereas girls demonstrate more relational aggression than boys, which has been connected to peer rejection, loneliness, and depression [88–90]. The co-occurrence of these psychiatric disorders in adolescence creates a complexity that must be assessed and included in the treatment plan for successful recovery from depression. Pubertal status, timing, and biologic changes When examining developmental transitions, chronologic age may not provide the best benchmark [91]. Among adolescent girls, menarche status [92] and pubertal status have been better predictors for major depression than age [80], with girls reporting increased rates of depressive disorders after Tanner Stage III. The timing of pubertal development is also predictive for internalizing symptoms [72,93]. Early maturing girls have demonstrated an increased risk for the development of major depressive symptoms and panic attacks, substance abuse, disruptive behaviors, and eating disorders [94,95]. Higher prevalence rates for depression have been found in early and late maturing girls, with rates of 30% and 34%, respectively, compared to girls who mature on time (22%) [94]. In research studies that evaluated pubertal girls and examined the relationships between internalizing symptoms and hormone levels for estrogen [96–98], testosterone [97,99], gonadotropin [100,101], and the hypothalamicpituitary-adrenal (HPA) axis [102–105], findings have been mixed. Early stress has been linked to chronic changes in the HPA axis [106,107], which could combine with pubertal changes in HPA axis function to increase vulnerability [72]. Currently, additional studies of the changes in stress and mood responses through puberty are needed to address the complex and interdependent biologic mechanisms [10,72,108]. Body image The physical changes that occur throughout puberty heighten adolescent selfawareness and self-evaluation. More than 80% of adolescent girls between ages 12 and 18 have reported feeling dissatisfied with their body along with 40% of the boys [109–111]. For white girls, this pattern of less satisfaction with their physical appearance than boys begins as early as third grade [112]. Girls are often dissatisfied with their weight even when they are in the normal weight range for their height [113,114], with early maturing girls at increased risk for negative self-evaluation related to body image and weight [115]. Body image dissatisfaction also places girls at increased risk for eating disorders [116,117]. For girls who base their self-worth on physical appearance, low

116

JACKSON & LURIE

self-esteem and high levels of depressed affect are found [112]. Adolescent girls in particular feel bad about their bodies and report decreases in self-esteem that contribute to depressive mood symptoms [10,118]. Low self-esteem is a hallmark depressive symptom and diagnostic criterion. Research supports the importance of specifically addressing an adolescent’s dissatisfaction with aspects of the self and the impact of negative social interactions on the adolescent’s mood and self-perception. Within normative samples, older children and adolescents who report depressed affect also consistently report low self-esteem (r ¼ 0.70–0.80 across numerous studies) [112]. Among clinically depressed inpatient adolescents, 80% of patients who reported depressed affect also indicated low self-worth. When young people were asked to describe their own experience of which comes first, depressed mood or not liking themselves, two distinct groups emerged. Approximately half of the sample described their depressed mood occurring before not liking themselves and it was often triggered by other people through rejection, conflict, and loss. The other half reported not liking something about themselves (eg, appearance, lack of athletic/academic competence, lack of competence in social interactions) and then experiencing depressed mood [119]. In normative and clinical samples, more boys described depressed affect preceding low self-worth, whereas more girls indicated low self-worth preceding depressed mood. This pattern of differences suggests the possibility of different models or pathways connecting low self-worth and depressed mood. Ethnicity Positive and negative reactions to the body changes of puberty may vary across ethnic groups. The increase in negative body image during puberty seemingly occurs more for white girls than African American girls [113,120–124]. In a large, nationally representative sample of girls and boys in fifth through eighth grades, a relationship was found between menarche status and depression symptoms for white girls but not African American girls. In regards to symptoms of depression, pubertal changes may not play as important a role for African American girls as for white girls [72,125]. Two studies found that Hispanic adolescents reported higher levels of depressed mood when compared to African American and white teens [126,127], although significant interaction effects were not found between gender and ethnicity when predicting depressed mood in either study. Early maturing girls of all ethnicities reported the highest levels of depressed mood [127]. The interaction of social and cultural influences must be included when considering the impact of biology at puberty. Substance use Cigarette, alcohol, and substance use was more common among youth who experienced a major depressive episode [3]. Studies suggest that the relationship between depression and smoking is complex and likely bidirectional [128]. Depression is implicated as a risk factor for the initiation of smoking among adolescents, and conversely, smoking has been connected to the development of

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

117

depression, possibly through the impact of nicotine on the central nervous system [129,130]. For this reason, interventions should be directed at simultaneously decreasing depressive symptoms and smoking behavior or initiation among adolescents. Connections between mood and substance use should be explored with adolescents. Victimization and psychopathology Differing rates of sexual abuse victimization for girls and boys have been proposed as contributing to the gender differences in internalizing disorders in adolescence [72,131]. Childhood sexual abuse occurs more often for girls, whereas rates of physical abuse are similar [132] or higher for boys [72,133]. Rates for emotional abuse have been similar for boys and girls [132]. Adolescent girls experienced higher rates of relational victimization, such as hurtful rumors, whereas adolescent boys experienced more overt victimization, such as bullying and physical aggression [134]. Findings regarding the psychological impact of victimization have supported higher rates of major depression in sexually and physically abused girls [135], higher rates of posttraumatic stress disorder (PTSD) for abused girls compared to abused boys [136], and higher likelihood of developing internalizing symptoms for adolescent victims [137]. Victimization among sexual minority youth (ie, gay, lesbian, bisexual, and transgender [GLBT]) also has been described as having an impact on mental health risk and difficulties [138]. Impact of negative events After age 13, research has found a developmental increase in negative life events for boys and girls, but particularly for girls [75,139]. The nature of negative life events also changes at different developmental levels, with preadolescents reporting family stressors, adolescents reporting peer and interpersonal issues, and young adults focusing on academic and achievement events [139,140]. Girls reported more negative events of an interpersonal nature (peers and family), whereas boys reported more negative academic and school events [10,139]. For most people, negative affect, such as anxiety and depression, rises after a negative event occurs [141]. It seems that the initial surge in negative affect hangs on or increases only for individuals who are cognitively vulnerable, for example with depressive or anxious thinking [10,142–144]. Young people with a cognitive style that is ruminative [82,145] or tends toward negative inferences [146,147] are at increased risk for maintaining or increasing depression. This link between stressful life events and depression is bidirectional. Although many negative events occur outside of a person’s control (eg, death of a friend), some negative events occur through some interaction to which a person contributes through his or her behavior, mood, or personality (eg, fight with a friend, romantic breakup) [10]. Studies with depressed adolescents suggest that they experience more negative events to which they partially contribute [148,149]. This pattern of self-generated negative experiences has been

118

JACKSON & LURIE

associated with increases in depression, earlier onset of depression, poorer social skills, personality disordered features, and parental pathology [10,150,151]. An example of this pattern would include a depressed young person excessively seeking approval or reassurance and actually increasing rejection from others [152]. Disasters and mental health Worldwide media coverage has highlighted the devastating impact of natural disasters, terrorism, war, and violence. Many of these events have become a part of our collective cultural experience: Hurricane Katrina, World Trade Center and Pentagon terrorist attacks on 9/11, tsunami devastation in Asia, Columbine High School shootings in Colorado, floods, mudslides, wildfires, plane crashes, kidnappings. The World Psychiatric Association estimates that for every one person who is damaged physically during a disaster, three persons are damaged psychologically [153]. Although most people who encounter trauma or disasters recover well, others develop specific trauma-related psychiatric disorders, including PTSD and trauma-related depression [154]. PTSD after traumatic events is often accompanied by depression [155–158]. Depressive and anxiety disorders may develop after traumatic events, however, even without formal PTSD [159]. PTSD and depression can result without previous psychiatric history [160]. A review of empirical evidence that examined responses to disasters suggested that depression is the second most common psychiatric disorder to emerge [161,162]. Children and adolescents seem to be at particular risk for psychiatric issues after trauma, especially PTSD, depression, and separation anxiety disorder [163,164]. In general, the greater the intensity of the traumatic stressor (ie, direct exposure, threat to life), the more likely psychiatric problems will develop for the individual or group. Even secondary exposure can be traumatic [165]. Several factors particularly experienced with terrorism, such as lack of predictability, possible recurrence, and pervasive loss, can lead to significant psychiatric illness and community distress [160,166,167]. Trauma reactions can result from large-scale disasters and wars but also from the losses and emotional devastation that result from car accidents, house fires, and familial or community violence that affect the adolescent, friends, and loved ones. Mental health issues related to disasters and trauma often present as medical symptoms or contribute to medical illnesses. Medical evaluation can provide the opportunity to assess for symptoms, educate the youth and family about reactions to stressful life events, and refer them for additional services and assistance. The impact of trauma is heightened for youth who already struggle with mental health issues. It is particularly critical to assess directly the impact of traumatic and disastrous events on youth who have depression and mood dysregulation. Early intervention is important to prevent hopelessness, panic, cognitive distortion, and isolation. Previous trauma and lack of family support also place a young person at risk because of increased vulnerability. The secondary

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

119

stressors of disaster recovery also can take a toll, such as relocation, negotiating for relief funds or insurance coverage, family unemployment, and changing schools and friends [154]. The meaning attributed to the traumatic event or disaster can influence the psychiatric impact and recovery [154]. For example, negative attributions might include blaming oneself for doing something wrong in the midst of the disaster or causing the trauma (‘‘blaming the victim’’), whereas positive attributions could include recognizing one’s ability to face challenges and handle crises successfully. Adolescents could be at particular risk for self-blame because of their developmental egocentrism. Intervention can be aimed at educating and discussing meanings that engender health and support resiliency. The young person and the family should be connected to developmentally appropriate and empathic support to talk about their reactions, thoughts, and feelings. Response recommendations and materials for providers, families, schools, and communities are available in ‘‘Helping children and adolescents cope with violence and disasters,’’ which is available from the National Institute of Mental Health (www.nimh.nih.gov). SUICIDALITY Depressive disorders increase the risk for suicidal ideation, suicide attempts, and completed suicides. Studies have found that 85% of depressed youth report significant suicidal ideation and 32% report a history of one or more suicide attempts. Suicide is the third leading cause of death among children and adolescents [168]. The rates for suicide increase markedly from children aged 5 to 14 years (0.61 per 100,000) to teens aged 15 to 19 years (7.26 per 100,000) [168]. In the 15- to 19-year-old range, boys had a higher suicide rate than girls, whereas girls had a higher rate of unsuccessful suicide attempts [169–172]. The 2003 National Youth Risk Behavior Survey for grades nine through twelve reported that during the 12 months preceding the survey, 17% of the students had seriously considered suicide, 16.5% made a specific plan, and up to 8.7% had made an attempt [171,173]. Estimates are that 2 million adolescents in the Unites States attempt suicide yearly, with nearly 700,000 receiving medical attention for their attempt [172]. Several factors have been identified as increasing the risk for suicidal behavior and completion [13,174–181]. Frequent suicidal thoughts and previous suicidal behavior are the strongest predictors for suicide attempts and behavior; the more severe the thoughts the greater likelihood for an attempt within the next year. Of the adolescents who completed suicide, 35% to 45% had a previous suicide attempt, which means that the other 50% or more of adolescents who died did not have a known suicide attempt history [172]. A longitudinal follow-up study of clinically depressed adolescents found a completed suicide rate of almost 8% compared to a nondepressed comparison group with no suicide completions [182]. Although adolescent suicide occurs across all races and ethnicities, rates seem to differ between some groups. The lowest adolescent

120

JACKSON & LURIE

suicide rate is found for African American girls, whereas the highest is found among Native American boys. The rate of attempted suicides is higher among Hispanic youth than among African American and white youth. These data may represent isolated subgroups rather than true cultural differences, but assessing cultural background, attitudes, and beliefs is a critical component of the evaluation for suicidality [171,172]. In addition to depressive disorders, youth who attempted or completed suicides commonly carried diagnoses of alcohol or substance abuse, conduct disorder, aggressive behavior, anxiety disorders, psychosis, and bipolar disorders. For girls, panic attacks increased the risk for suicidal ideation and attempt, whereas for boys these risks were increased by aggressive behavior [172]. Adolescents with certain chronic physical disorders also may be at higher risk for suicidal thoughts and behaviors [183]. Beyond diagnoses, several psychosocial, familial, and environmental factors have been identified as increasing risk for suicidal ideation and behavior [4,13,171,172,184]. Risk is increased when there is a family history of psychiatric disorders, particularly depression and suicidality. Neglect and physical, emotional, or sexual abuse significantly increase the risk for suicidal behavior. Losses and conflicts with family, friends, or romantic partners are often triggers for suicidal ideation and behavior, as are school, legal, and physical difficulties. A link between physical fighting and suicide is suggested by findings that youth who had attempted suicide in the past 12 months were four times as likely to report a history of fighting than youths who did not report suicide attempts [185]. Interventions that target violence toward others and violence toward oneself are recommended, possibly even before the transition to high school. Knowing someone who commits suicide increases the risk for depression, anxiety, and one’s own suicidal behavior. The risk for contagion can be increased by media coverage and excessive attention within the weeks after a suicide death [186–188]. The young person may have been handling numerous stressors but finally is ‘‘pushed over the edge’’ by some interpersonal conflict that threatens or removes social support even temporarily. Agitation, impulsivity, and hopelessness increase the risk for suicidal behavior and complicate assessment and safety planning. Alcohol and substance use can increase mood lability, impulsivity, and judgment impairment; alcohol use has been associated with up to 50% of suicides [189]. Engaging youth in the process of developing a realistic safety plan becomes more difficult when they are upset, think nothing will get better, and are unable to demonstrate adequate judgment to be trusted. Exposure to high levels of community violence over a long-term may contribute to emotional and behavior problems adding to suicide risk [190]. Finally, risk for suicide completion is increased by the availability of lethal means within the home, particularly firearms. Firearms have been the leading cause of death for adolescent boys and girls who commit suicide, with more than 90% of suicide attempts with a firearm being fatal [171,191–193]. The most common method for adolescent suicide attempts is taking pills. Statistics from the Centers for Disease Control and Prevention [168] on completed

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

121

suicides in youth aged 13 to 19 found that firearms were the cause of death for 48%, suffocation for 38%, and poisoning for 7.4%. Increased supervision, restriction, and removal of firearms and lethal drugs (prescription and overthe-counter) are necessary to ensure safety for suicidal and at-risk adolescents. GLBT youth report three times the rate of suicidal ideation and suicide attempts. In one statewide survey of seventh to twelfth graders, 28.1% of gay and bisexual boys and 20.5% of lesbian and bisexual girls reported having attempted suicide [194]. Reviews of empirical evidence have not found GLBT youth overrepresented within completed suicides, but high suicide attempts have been found consistently in studies using convenience samples [195– 197]. More recently, these results have been called into question because of methodologic concerns, including reliability of single-item suicide risk assessment and validity when sampling from nonrepresentative settings with youth who are more likely to be in crisis (eg, in shelters or support groups) or at least youth who self-identify earlier and are more visibly out [198,199]. In terms of research, more diverse and representative populations are recommended to include a broader range of youth with same-sex attractions beyond just youth who identify with a sexual minority label. Clinically, follow-up questions are suggested to clarify the nature of the attempt, the seriousness of the intent, and whether the suicidal behavior has required medical attention and been life-threatening. More representative samples have tended to support the higher risk for adjustment difficulties among GLBT youth, however [138,200]. Ongoing research continues to clarify and inform this significant question [138,201]. Most researchers do not suggest that there is anything inherent in GLBT sexual orientation or same-sex attractions that places youth at risk. Rather, they focus on the stigma, discrimination, and victimization that sexual minority youth must face and manage [196]. In a sample of 542 GLBT youth [138], alarmingly high rates of victimization related to sexual orientation were reported, including verbal abuse (81%), threats of physical attack (38%), physical assault (15%), and sexual assault (16%). Past suicide attempts were reported by 37% of the entire sample; more than one fourth of the youth reported ‘‘often or sometimes’’ seriously thinking about suicide. The earlier the youth were aware of their sexual orientation, self-identified as GLBT, and disclosed their orientation or ‘‘came out’’ to others, the higher their rates of lifetime victimization. Past victimization was most closely linked with current mental health problems and suicidal ideation. In our own sample of 134 youth aged 14 to 24 years who were involved in social, support, and campus GLBT groups, harassment and victimization rates related to sexual orientation (ie, bias- or hate-motivated victimization) were similar, with 76% of youth reporting having been called names, 39% being threatened, 26% being physically assaulted, 8% being sexually assaulted, and 4% being stabbed or shot [202]. Almost 50% of the sample indicated experiencing multiple types of harassment because of sexual orientation. Regarding suicidal ideation and behavior, 67% of the youth reported having considered attempting suicide at some point in their life, and 44% of the study participants indicated having actually made a suicide attempt, with

122

JACKSON & LURIE

more youth reporting multiple attempts than single attempts. Sixteen percent of the total sample indicated that their attempt involved injury, poisoning, or overdose that required medical treatment. On a positive note for youth in our sample, higher self-acceptance of one’s sexual orientation predicted higher overall self-worth, brighter mood, and more hopefulness about the future, which, in turn, predicted lower levels of current suicidal ideation. In summary, most sexual minority youth do not attempt suicide and instead demonstrate considerable resilience [198,201]. Careful assessment of experiences of stigmatization, victimization, social support, self-acceptance, depression, and suicidal ideation is highly recommended with this population because of a high-risk minority of GLBT youth. PHENOMENOLOGY OF DEPRESSIVE DISORDERS IN CHILDREN AND ADOLESCENTS BASED ON THE DIAGNOSTIC AND STATISTICAL MANUAL OF MENTAL DISORDERS-IV CLASSIFICATION SYSTEM The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) diagnostic criteria for depressive disorders are the same for children and adolescents as adults, with small exceptions noted in parentheses [203]. Major depressive disorder The DSM-IV defines a major depressive episode as a syndrome in which at least five of the following symptoms have been present during the same 2week period: 1. Depressed mood (for children and adolescents, it also can be an irritable mood) 2. Diminished interest or loss of pleasure in almost all activities 3. Sleep disturbance 4. Weight change or appetite disturbance (for children, it can be failure to achieve expected weight gain) 5. Decreased concentration or indecisiveness 6. Suicidal ideation or thoughts of death 7. Psychomotor agitation or retardation 8. Fatigue or loss of energy 9. Feelings of worthlessness or inappropriate guilt

At least one of the symptoms must be diminished interest/pleasure or depressed mood. The symptoms must cause significant distress or impairment of functioning in social, occupational, or other important areas. The syndrome should not have been precipitated by the direct action of a substance or the result of a medical condition and should not be better explained by bereavement or schizoaffective disorder. The disorder can be rated as mild, moderate, or severe. It also can be noted to be with or without psychotic symptoms that can be mood congruent or incongruent. It can be determined to be in full or partial remission. When the episode has lasted 2 consecutive years, the depression should be diagnosed

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

123

as chronic. The term ‘‘psychotic depression’’ is used when psychotic features (hallucinations and/or delusions) are present during an episode of major depression. The term ‘‘bipolar depression’’ is used when a teen previously was diagnosed with bipolar disorder and the current episode is a depressive one. Dysthymic disorder Dysthymic disorder can be diagnosed when a depressed or irritable mood lasts 1 year or longer (in adults it must be 2 years or longer) and the affected youth is never symptom-free more than 2 months. In addition to a mood disturbance, to diagnose dysthymia at least two of the following symptoms must be present: 1. 2. 3. 4. 5. 6.

Appetite change Sleep change Decreased energy Low self-esteem Difficulty making decisions or poor concentration Feelings of hopelessness

Dysthymia should not be diagnosed if a major depressive episode occurs during the first year of the disturbance, if there is a history of manic, hypomanic, or mixed episodes, if the disorder occurs during the course of a psychotic disorder (eg, schizophrenia), or if it is secondary to use of a substance or general medical condition. Although the symptoms of dysthymia are not as severe as in MDD, they can cause as much, or more, psychosocial impairment [30]. The prognosis for dysthymia is worse than for major depression alone, with substantially longer episodes and a high risk for the development of ‘‘double depression’’ (ie, MDD þ dysthymia). Double depression is a chronic condition that is much more difficult to treat than uncomplicated MDD [23]. Depressive disorder not otherwise specified In the DSM-IV, this category includes disorders with features of depression that do not meet the criteria for a specific mood disorder or adjustment disorder with depressed mood. Examples include depressive episode superimposed on residual schizophrenia, a recurrent, mild depressive disturbance that does not meet criteria for dysthymia, and non–stress-related episodes that do not meet the criteria for a major depressive episode. DSM-IV should be consulted for further details as to the diagnostic criteria for depressive disorders not otherwise specified. In practice, many teens receive the diagnosis of depressive disorder not otherwise specified. Often this is the provisional diagnosis, and as further information is gathered the diagnosis is refined. In many cases, this is the accurate diagnosis, because the teen does not fit into the more formal categories. Patients who are diagnosed with depressive disorder not otherwise specified may have considerable functional impairment.

124

JACKSON & LURIE

Adjustment disorder with depressed mood Patients who have an adjustment disorder develop depressive symptoms and functional impairment within 3 months of an identifiable stressor [203]. They do not have enough symptoms to meet criteria for MDD, however, and by definition, the disorder is self-limited (ie, symptoms do not persist longer than 6 months after the cessation of the stressor). Youth who have adjustment disorder should have close follow-up, and if symptoms do not resolve, alternative diagnoses, including MDD, should be considered. It is important to realize that MDD is often precipitated by stressful events, so if a patient has the appropriate symptoms, even if there is a stressful precipitant, he or she could receive a diagnosis of MDD [65]. Bereavement The symptoms of depression and bereavement may be clinically indistinguishable [204]. The acute phase of uncomplicated bereavement usually remits spontaneously within 6 months to a year. The diagnosis of MDD in bereaved youth also should be considered if bereavement is associated with moderate to severe functional impairment, psychosis, suicidality, and prolonged course. Previous episodes and family history of mood disorder may predispose to depression after bereavement [179]. Seasonal affective disorder The seasonality of mood disorders also can be specified. To diagnose a seasonal mood disorder, a regular temporal relationship should exist between depression and mania and a particular period of the year. A full remission or switching from depression to mania should occur within that characteristic time of the year. An individual should manifest at least two episodes of mood disturbances in the last 2 years. Finally, seasonal episodes should outnumber nonseasonal episodes substantially. Atypical depression A depression also may be identified as having atypical features. Characteristics of this subtype are mood reactivity, exclusion of melancholic and catatonic subtypes, and two or more of the following criteria for a period of at least 2 weeks: 1. 2. 3. 4.

Increase in appetite or significant weight gain Increased sleep Feelings of heaviness in arms or legs A pattern of longstanding rejection sensitivity that extends far beyond the mood disturbance episodes and results in significant social or occupational impairment

Comorbidity Anxiety disorders, disruptive behavior disorders (eg, attention deficit hyperactivity disoder, oppositional defiant disorder, conduct disorder), and

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

125

substance abuse frequently co-occur with depression [9]. Of the children and adolescents who present initially with depressive symptoms, between 5% and 30% subsequently develop bipolar symptoms (eg, mania and hypomania), depending on whether the samples were clinical or epidemiologic [28,41,205– 207]. These patients may have an adverse response to antidepressants and become more irritable or, in some cases, manic. It is not unusual for a teen to have depression and one to two additional DSM-IV Axis 1 diagnoses. Forty percent to 90% of youth who have MDD have other psychiatric diagnoses, with at least 20% to 50% having two or more comorbid diagnoses [23,64,208,209]. The frequency and type of psychiatric comorbidity varies with age. Comorbid substance abuse, conduct disorder, social phobia, and generalized anxiety disorder are more frequent in adolescents, whereas separation anxiety disorder is more common in children [4]. The occurrence of significant comorbidity could be a reason for a pediatrician to consider referring to a child and adolescent psychiatrist or to a substance abuse program. EVALUATION In reality, there is an alarming shortage of child and adolescent psychiatrists nationwide, especially in certain geographic areas [210]. Pediatricians are increasingly being called on to manage depression in teenagers. The goal of this section is to provide general guidelines for pediatricians and highlight situations in which pediatricians may want to refer to a child and adolescent psychiatrist or other mental health provider. Evaluation of depression In the evaluation of adolescents three crucial areas must be covered. The first area involves building the therapeutic alliance with the teenager and family. The second area involves performing a good diagnostic assessment. The third area involves evaluating suicidal risk. It can be difficult to gather all relevant information in the first contact, but a teen should not leave the first visit without suicide risk being assessed. If there are concerns about imminent danger or if a patient cannot contract for safety (see section on suicide safety contracts), he or she should be referred to an emergency room for further evaluation. A key aspect of alliance building is the discussion of confidentiality. The clinician should explain the ground rules regarding when a parent/caregiver is informed of what is discussed with the patient. Suicidal thoughts cannot be kept confidential. Often not taken into account by busy practitioners is the length of time the evaluation may take. There is no substitute for a comprehensive evaluation. If a pediatrician has only a brief appointment available, it is probably wise to schedule a second, longer session or refer to a mental health practitioner, preferably someone with whom the pediatrician has a relationship. Pediatricians may consider referring to a mental health provider based on the complexity of the situation or their own personal comfort dealing with mental health

126

JACKSON & LURIE

issues. Many pediatricians feel more comfortable managing depression if they have ready access to consultation with child psychiatry colleagues. Brent and Birmaher [211] provide some useful guidelines to help primary care physicians determine when to refer to specialty care. Indications for primary physician care include initial episode of depression, recent onset of depression, absence of coexisting conditions, and the ability to make a safety or no-suicide contract. Indications for specialty care include chronic recurrent depression, lack of response to initial course of treatment, coexisting substance abuse, recent suicide attempt, current suicidal ideation with a plan, psychosis, bipolar disorder, high level of family discord, and inability of the family to monitor the patient’s safety. Guidelines for evaluation In its publication ‘‘Practice parameters for the assessment and treatment of children and adolescents with depressive disorders,’’ the American Academy of Child and Adolescent Psychiatry makes several recommendations [4]. Additional clinical points have been added by the authors in italics.












Gather information from multiple sources, including parents/caregivers. Contact is often required with other sources, such as teachers, social services professionals, or a current mental health clinician if involved. Assess comorbidity, psychosocial and academic problems, psychiatric family history, social support, medical and medications history, substance abuse (including nicotine use), and early and recent negative life events (including physical and sexual abuse). Perform a developmentally appropriate mental status examination. Depressed teens can be difficult to engage and are frequently irritable and uncooperative. They can be quite withdrawn. Teens are much more likely to give relevant information once an alliance has been established. It is important to spend some time alone with the teen, because many teens do not share sensitive information in the presence of parents. Using DSM-IV criteria as a guide, teens should be asked about their depressive symptoms and the time course. Suicide risk must be assessed (see the section on suicide assessment). Questions about hypomania and mania, such as decreased need for sleep, inflated selfesteem, and racing thoughts, are important. They should be asked about psychotic symptoms and delusions, anxiety, symptoms of attention deficit and hyperactivity disorder, and substance use, all of which are frequently comorbid. Clinically, once an alliance has been formed, teens should be asked about romantic attachments and sexual activity. Sexually active teenage girls should be asked about the possibility of pregnancy. Be alert to ethnic and cultural factors that may influence the presentation of symptoms and the approach to treatment. Assess level of functional impairment, which guides treatment recommendations.

Most adolescents encounter times of sadness and depressed mood that they often can describe and share. Studies have found that youth can report accurately on their own depressed mood and symptoms [212]. Studies suggest

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

127

that children and adolescents more often share internalizing symptoms, such as depressed mood and suicidal ideation, whereas parents report externalizing symptoms, such as behavior problems, irritable mood, and changes in eating, sleeping, and energy level [10,213]. Clinical experience suggests that adolescents respond best to direct and honest questioning. A young person may not use the word ‘‘depressed’’ per se. Instead the interviewer might address feeling down, sad, tearful, bored, irritable, edgy, or crabby. Two questions are recommended by the US Preventive Services Task Force to screen for depression in adults: (1) Over the past 2 weeks have you ever felt down, depressed, or hopeless? (2) Have you felt little interest or pleasure in doing things? [13]. Screening for depression Several screening measures are available to assess for depressive symptoms. These measures can be used to validate concerns from an interview or to determine when further follow-up evaluation is recommended. They can be administered easily in a pediatrician’s office. Beck Depression Inventory An updated version of the original Beck Depression Inventory, the Beck Depression Inventory-II (BDI-II) is a self-report scale of 21 items that tap depressive symptoms, such as agitation, concentration difficulties, and loss of energy [214,215]. Items use a Likert rating scale for severity or frequency of various symptoms and behaviors. The BDI-II is designed to assess the presence and severity of depressive symptoms for adolescents and adults beginning at age 13. A more recent version was developed for assessing depression in medical patients. The Beck Depression Inventory for Primary Care is a seven-item self-report scale that covers cognitive and affective symptoms of depression [216]. For children aged 7 to 18, the Beck Youth Inventories, 2nd Edition, are designed to assist in the early identification of emotional and social impairment through five scales that assess depression, anxiety, anger, behavior disruption, and self-concept [217]. It takes 5 to 10 minutes to complete each. Scores and profiles can be compared to age and gender norms that are ethnically and socioeconomically representative of the US population. (This information is available from the Psychological Corporation at www.psychcorp.com.) Children’s Depression Inventory The Children’s Depression Inventory (CDI) was designed for school-aged children and adolescents [218]. The CDI is a self-report measure with 27 items that allow an evaluator to assess and quantify depressive symptoms of MDD or dysthymia. Respondents are asked to choose among three options on each item to describe their experience for the past 2 weeks. The scale provides a total score and five empirically derived factor scores that address negative mood, interpersonal problems, ineffectiveness, anhedonia, and negative self-esteem. Repeated administrations can help to track changes in symptoms over time. The

128

JACKSON & LURIE

CDI also comes in a short form with 10 items for brief assessment and screening. CDI Parent and CDI Teacher Forms capture observable symptoms of depression and provide a total score and subscale scores for emotional and functional problems. The CDI is appropriate for youth aged 7 to 17. (It is available from Psychological Assessment Resources, Inc. at www.parinc.com.) Reynolds Adolescent Depression Inventory The Reynolds Adolescent Depression Inventory-2 (RADS-2) is a self-report measure with 30 items that evaluate depressive symptoms along the subscale dimensions of dysphoric mood, anhedonia/negative affect, negative self-evaluation, and somatic complaints [219]. The test takes 5 to 10 minutes to complete and can be hand scored and interpreted. Scores can be mapped onto the summary and profile form, which allows comparisons between the subscale scores and determines the level of severity for symptoms (ie, normal, mild, moderate, or severe). The total score captures the overall level of depressive symptoms and can be compared to an empirically derived cutoff score to determine clinical significance and risk for depressive disorders. Six critical items also help to identify youth who have concerning levels of depression, even if the overall score is below the clinical cutoff. Norms were restandardized for gender and ethnicity based on 2000 US Census data. The scale is designed for youth aged 11 to 20. (It is available from Psychological Assessment Resources, Inc. at www.parinc.com.) Several structured clinical/diagnostic interview formats also exist but are generally used only in clinical research projects because of the length of time for administration and the training required to standardize the procedures. These more comprehensive diagnostic tools assess depressive mood disorders and comorbid symptoms and disorders. They include the Children’s Schedule for Affective Disorders and Schizophrenia (K-SADS) [220,221], the Diagnostic Interview for Children and Adolescents (DICA) [222], and the NIMH Diagnostic Interview Schedule for Children, Version 4 (DISC-IV) [223]. Medications and underlying medical conditions associated with depression A teen always should have a medical evaluation as part of a complete psychiatric evaluation to help rule out underlying medical conditions [224]. Any medical concerns that were raised by an adolescent as part of the history taking should be addressed during the physical examination [37]. Organic causes that might mimic depressive disorders fall into several general categories: medications, infections, endocrine disorders, tumors, neurologic disorders, and miscellaneous disorders [225]. It is important to review all medications (prescribed or over-the-counter) or substance use, including alcohol and nicotine, that may cause depressive symptoms or mood changes [37]. Medications that may lead to depression include beta-blockers, corticosteroids, clonidine, accutane, and oral contraceptives (although the data on oral contraceptives are somewhat unclear) [226]. Infections include infectious mononucleosis, HIV, influenza, and hepatitis. Endocrine disorders include diabetes,

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

129

Cushing’s disease, Addison’s disease, hypo- and hyperthyroidism, hyperparathyroidism, and hypopituitarism. Neurologic disorders include epilepsy, postconcussion syndrome, cerebrovascular accident, multiple sclerosis, and Huntington’s disease. Miscellaneous causes include anemia, lupus and electrolyte abnormalities (hypokalemia, hyponatremia), Wilson’s disease, porphyria, and renal disease. Initial evaluation probably should include a complete blood count with differential, electrolytes, including blood glucose, blood urea and nitrogen (BUN), creatinine, liver function tests (LFT’s) and thyroid stimulating hormone (TSH). Adolescents who have chronic medical disorders may struggle with a combination of physical and emotional symptoms that complicate diagnosis and treatment [37]. In cases in which emotional and behavioral difficulties are interwoven with somatic concerns (eg, depression, chronic pain, noncompliant diabetes or asthma), we have found that a treatment team composed of medical and mental health professionals can be more effective and supportive to the youth and the family, who are often struggling with how best to respond. With appropriate permission from the teen and family, frequent communication and occasional staffing meetings, conference calls, or confidential emails among the various providers are critical to ensure coordinated and responsive care. This method also helps to identify when youth need higher levels of care, such as day treatment or inpatient hospitalization because of decreases in functioning, grave disability, or safety concerns. Cultural issues The meaning and presentation of depressive symptoms can be influenced by an adolescent’s cultural environment. It is not uncommon for depression to be experienced and described in terms of somatic complaints rather than emotions. Presenting with physical concerns may be more culturally appropriate for some adolescents and their families. Within the context of discussing somatic symptoms, emotional issues might be explored and understood more fully [227]. Beliefs and stigma regarding mental health issues within certain cultures also may impact an adolescent’s willingness to address depression directly and accept certain types of treatment options [228]. Providers must educate themselves and seek consultation regarding culturally appropriate assessments and interventions. The goal is to assist adolescents and families in a manner that is culturally respectful and provides the best chance for improvement. Evaluation of suicidality Assessing for suicidal ideation and preventing suicidal behavior are critical roles for any provider who works with depressed youth. All adolescents with depressive symptoms should be evaluated for suicidal ideation and intent [184]. Reaching the point of suicidality suggests that a young person’s situation or emotional state has become overwhelming or unbearable. In general when asked about suicidal thoughts and behavior in a direct but respectful manner, adolescents will respond openly. These questions can demonstrate a physician’s desire to understand a young person’s experience and be helpful.

130

JACKSON & LURIE

Research does not indicate that asking about suicide precipitates the behavior [184]. It is important to address thoughts or feelings of wanting to give up, not be around any longer, or have everything end. This questioning should be followed by asking whether the youth ever felt so overwhelmed that they thought about or tried to hurt themselves. One example of a question is ‘‘Some people get so overwhelmed or depressed that they think about hurting themselves or wish they were dead. Have you ever felt that bad?’’ It is appropriate to ask adolescents directly if they have thought about or tried to kill themselves and whether they might have or had a plan in mind [13]. This plan or action might have included placing themselves in harm’s way (eg, driving unsafely) with the hope that something hurtful or deadly might occur. ‘‘Do you find yourself doing things that are particularly risky where you might be seriously hurt or die?’’ Positive responses to any of these questions should be discussed further regarding how recent, intense, frequent, and specific the thoughts and feelings have been. If a young person states that he or she has a suicidal plan, detailed information should be gathered about the proposed method, time, place, and available means (eg, access to medication, weapons, firearms) [184]. The more specific the information, the more targeted the treatment and safety planning can be. Items from several standardized questionnaires could help young people to respond in written form, which allows follow-up discussion to focus on critical items that address mood and safety. Most of the standardized depression inventories have questions about suicidal ideation and behavior, such as the Beck Depression Inventory, 2nd Edition, the Childhood Depression Inventory, and the Reynolds Depression Inventory, 2nd Edition. The Suicidal Ideation Questionnaire (which is available at www.parinc.com) could be filled out by an adolescent or even used to develop a set of standardized screening questions that are asked verbally and used to complete the form (Suicidal Ideation Questionnaire for grades 10–12 and Suicidal Ideation Questionnaire-JR for grades 7–9) [229]. Self-injurious behaviors, such as cutting and burning, often occur as a way to relieve psychological tension, manage emotions, prevent dissociation, punish oneself, or gain a sense of control [230–233]. Although self-injurious behavior is typically distinguished from suicidal behavior in its function, self-injurers still can be at significant risk and can make suicide attempts [171,234]. Careful evaluation of the self-injurious behaviors and their functions is necessary to determine the level of risk and the appropriate intervention. Additional information on self-injurious behavior is available from SAFE Alternatives (www.selfinjury. com, 1-800-DONTCUT) or www.aacap.org. Safety contracting Suicidal ideation usually suggests an overwhelming state of emotion that creates or intensifies hopelessness and short circuits problem-solving abilities, such that self-harm or death seems to be the only solution. Safety contracting can help to clarify that other options are always available and that support is

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

131

available to assist a young person when problems become too confusing or overwhelming to handle. The safety contract should include the following major parts: (1) an agreement to not harm oneself or attempt suicide, (2) a list of safe alternatives that a young person could try to manage emotions, and (3) a list of safe people whom an adolescent can contact for help if she or he becomes suicidal (eg, a clinician, parent, suicide hotline, or hospital). The US Department of Health and Human Services through Substance Abuse and Mental Health Services Administration (www.samhsa.gov) sponsors the toll-free National Suicide Prevention Lifeline (www.suicidepreventionlifeline.org), on which callers are connected to suicide prevention and mental health service providers in their area for immediate assistance (1-800-273-TALK [8255]). A young person’s ability to generate and agree to certain strategies and safe alternatives also helps to determine his or her level of insight and readiness to ask for help and stay safe. Agreements that seem too easy or too difficult suggest that a young person might be trying to end the discussion prematurely or not have the skills necessary to face current circumstances without a more intensive treatment plan. Although confidentiality is important in working with adolescents, ensuring a young person’s safety allows an exception to that agreement legally and ethically. Comprehensive evaluation should include information from caregivers, parents, and other family members, if possible, to assess symptoms and risk accurately. Safety contracts also help to clarify what family members, parents, caregivers, and professionals are willing and able to provide for an adolescent when help is sought. The safety contract is between the adolescent and the provider but also between the adolescent and caregivers or parents. The agreement must satisfy and alleviate the concerns of all the parties to be workable. The accessibility of clinicians and supportive adults should be determined as part of the contracting process so that assistance is available for the adolescent and family from some source at all times. Safety contracts alone are not adequate to prevent suicide, but they are a tool for developing safer alternative plans of action. Ongoing assessment of suicidal ideation and behavior must occur at each visit with a provider. Regular monitoring of attendance for treatment, following up on missed appointments, and revisiting the safety plan are advised [13]. Urgent psychiatric evaluation and intensive treatment Evaluating and treating the complex psychological system within which suicidal ideation and behavior occur may require consultation with mental health care professionals. When an adolescent presents at high or moderate risk for suicide or has made an attempt, urgent evaluation should be arranged with a mental health care professional immediately. Emergency rooms or sameday appointments should be used for urgent assessment and treatment planning [184]. A multidisciplinary evaluation of medical stability and mental status is important. Families should take the opportunity to assess the home environment and safeguard or remove risks, such as access to firearms, medications (prescription and over-the-counter), and possibly vehicles [4,13].

JACKSON & LURIE

132

Sometimes adolescents or their support system have become too overwhelmed to remain safe and psychiatric hospitalization is required to ensure an adolescent’s safety. Admission also may be warranted because of the lethality of a suicide plan or attempt, the secrecy or unexpectedness of the attempt, or the careful preparation associated with an attempt. Hospitalization stays have become progressively briefer and focus on diagnostic assessment, stabilization, safety, and aftercare treatment planning. Partial hospitalization, day treatment, intensive outpatient, and in-home therapy also provide more intensive services when an adolescent’s support system becomes overwhelmed. Partial hospitalization and day treatment programs typically include intensive group therapies along with individual therapy, family therapy, and medication evaluation and monitoring. Group interaction can help adolescents to practice safer alternative coping strategies within a therapeutic environment. Evenings and weekends at home allow a young person, family members, and the treatment team opportunities to assess responses to stress, demonstrate safety, and adjust the treatment plan, support, and possibly medication more rapidly. Families and providers often must make choices for treatment in the context of managed care. Treatment involves helping families determine the accessibility of various treatment options and facilities along with negotiating health and mental health insurance issues. With permission from the adolescent and family, aftercare treatment should include the referral sources (eg, pediatricians, school personnel, or religious organizations), because they were involved in the initial assessment, have an ongoing relationship, and can support compliance with follow-up treatment [235]. TREATMENT Before treatment recommendations are provided, it seems important to begin with a discussion of recent developments in the field of child and adolescent psychopharmacology. Important shifts have taken place since 2003. The current concerns with antidepressants











In October 2004, the US Food and Drug Administration (FDA) recommended a Black Box warning regarding risk for suicidality in children and adolescents who are being treated with antidepressants. Earlier advisories concerning antidepressant use were released by the US FDA and other regulatory agencies worldwide, beginning in 2003. The concern for increased suicidality contrasts strongly with recent data that suggest that there has been a decrease in suicide, associated with the more widespread use of selective serotonin reuptake inhibitors (SSRIs). The American Academy of Child and Adolescent Psychiatry (AACAP) expressed concern that the Black Box warning could prevent some patients from seeking or receiving appropriate treatment. Complicating the issue, less than one third of the randomized studies of antidepressants for depressed youth have shown efficacy. Critics are concerned about modest, if any, efficacy and whether the risk/benefit ratio for these medications is acceptable, especially given the heightened concerns about suicidality.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

133

Background to the current debate An excellent overview is available through the AACAP website (www.aacap. org) detailing the concerns with antidepressant use and the responses by the US FDA and other regulatory agencies [236]. Beginning with the availability of tricyclic antidepressants in the 1960s, the concept that suicidality could emerge with initiation of treatment has been recognized [237]. This concept was revisited in 1990 with the publication of a case series that involved adult patients who appeared to become suicidal as a result of being treated with fluoxetine [238]. This issue was debated by the US FDA’s Psychopharmacologic Drugs Advisory Committee in 1991 [239], which noted the existence of treatment-emergent suicidality. Several mechanisms were proposed to account for its occurrence, including worsening of depression, induction of conditions (eg, akathisia, anxiety, panic, or insomnia) that can lead to suicidal behavior, and stage shifts in patients with bipolar disorder. They evaluated the existing clinical trial database in adults exposed to fluoxetine, and because the results were reassuring with respect to antidepressant-induced suicidality, the Psychopharmacologic Drugs Advisory Committee took no action at that time [239,240]. There were no significant controlled data on fluoxetine use in children and adolescents available at that time. The notion did, however, persist that some patients, including children and adolescents, may be at unique risk for treatment-emergent suicidality with fluoxetine [241–246]. The FDA Black Box warning Over the past few years there has been renewed interest in the possible risk of suicide with antidepressants (SSRIs and the new non-SSRIs) in the treatment of depressed children and adolescents [236]. In June 2003, the United Kingdom’s Medicines and Healthcare Products Regulatory Agency, the equivalent of the US FDA, recommended that paroxetine not be used in children and adolescents younger than age 18 who were being treated for depression. This recommendation was based on a reanalysis of data for the use of paroxetine in depression, which showed a signal for increased suicidal ideation. The US FDA also issued a talk paper in June advising against the use of paroxetine in children and adolescents. The clinical trial data for paroxetine and other antidepressants were subsequently re-examined for adverse events related to suicidality. Drug regulatory agencies worldwide took action, either discouraging the use of antidepressants in children and adolescents or introducing substantial warnings into product labeling. In October 2003, the US FDA issued a public health advisory and talk paper that alerted physicians to reports of suicidal thinking (and suicide attempts) in clinical studies of various antidepressants in pediatric patients with MDD. In October 2004, the US FDA recommended adding a Black Box warning of suicidality in children and adolescents, making the related changes to the warnings and precautions sections, and providing a medication guide to be given to patients whenever antidepressants are dispensed.

134

JACKSON & LURIE

Before issuing this warning, the US FDA conducted a meta-analysis of suicide attempts and ideation in all antidepressant placebo controlled trials, published and unpublished [247]. In all, 24 trials were included in the analysis, 15 of which were designed to examine MDD. Only 8 of the 24 trials previously were published in the peer-reviewed medical literature [236]. Among the findings were the following data:






There were no completed suicides in any subject, either on placebo or medication, in any of the randomized trials of antidepressants in youth Suicide-related events (ideation or preparation or attempt) occurred in 2% of patients on placebo and 4% of patients on medication when data for all drugs were pooled There was no significant difference for drug and placebo for any of the medications individually, in terms of suicide-related events, except for venlafaxine, for which the signal seemed to be stronger

Although the US FDA analysis was methodologically well done, there were clear limitations, not the least being that the studies included in the meta-analysis were not designed to examine suicidality [248]. In adolescents, suicidal ideation and attempts are remarkably frequent (as reviewed in the section on suicidality). In a recent psychotherapy trial for adolescent depression, even without the use of medication the incidence of emergent suicidality was 12.5% [249]. Self-reported suicidality at intake seemed to predict emergent suicidality in this study. Is there a decrease in suicide with the more widespread use of selective serotonin reuptake inhibitors? Several recent studies support this notion. A study by Olfson and colleagues [250] examined increased SSRI use between 1990 and 2000 within a geographic region. There was a significant correlation with decreased adolescent death by completed suicide within the same region. This finding suggests that SSRIs are protective against suicide or that the conversion from tricyclic antidepressants to SSRIs decreased the rate of suicide. World Health Organization data show a decline in adolescent suicide coinciding with the introduction of SSRIs in other countries and in the United States [250–252]. Valuck and colleagues [253] examined data from 24,119 adolescents with first diagnosis of major depression. They found that treatment for at least 6 months with antidepressant medication reduced the likelihood of a suicide attempt compared to 2 months of treatment. Most recently, Simon and colleagues [254] reviewed computerized health plan records of more than 65,000 adults and teens on antidepressants and reported on suicide attempts in this sample. The risk of suicide attempt was highest in the month before starting antidepressant treatment and declined progressively after starting medication. When the ten new antidepressants included in the US FDA advisory were compared to older drugs, an increase in risk after starting treatment was seen only for the older drugs. Adolescents constituted a small portion of the sample. In this study, risk of serious suicide attempt was four times as high as in adults, but the pattern over time was similar for the two groups.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

135

Evidence from toxicology studies does not support the notion of increased suicidal behavior with SSRIs. In a study of 49 completed adolescent suicides in Utah, none of the youth tested positive for SSRIs at the time of death [255]. In another study of 66 completed suicides in New York City from 1993 to 1998, in which a subgroup of 54 had serum toxicologic analysis for antidepressants at autopsy, imipramine was detected in only 2 people and fluoxetine was detected in only 2 people [256]. One is left with the obvious question of whether the suicide rate would have been lower had more of these individuals been treated with SSRIs. Has antidepressant use in children and adolescents declined recently? The AACAP expressed concern that some patients might be less likely to seek or receive appropriate treatment because of the Black Box warning [257]. The concern has been well founded. Over the last 2 years, there has been a significant decline in antidepressant prescriptions dispensed to youth aged 18 and younger [258]. The dataset provided by NDC Health Inc. shows a statistically significant drop in prescribing of nearly 20% in this age group. Data from the United Kingdom also suggest that fewer children and adolescents have been prescribed antidepressants in the primary care setting since 2003 [259]. The public health consequences of this change are unknown, but the AACAP and American Psychiatric Association urge close monitoring of the situation [260]. Do antidepressants work in children and teenagers? Excellent reviews of all randomized, placebo-controlled antidepressant trials with SSRIs and other third-generation antidepressants have been published by Ryan [248], Cheung and colleagues [261], and the American College of Neuorpsychopharmacology [262]. Fluoxetine has demonstrated efficacy in three trials [263–265] and citalopram in one trial [266]. Fluoxetine remains the only antidepressant with a US FDA indication for the treatment of depression in youth, because the US FDA requires two positive studies to win approval for indication. Two sertraline studies in depressed children and adolescents were conducted [267]. Neither study, considered separately, reached statistical significance. When all data from both studies were combined, sertraline was significantly better than placebo. The combined results were not considered by the US FDA to be positive. Some data show that paroxetine [268,269] and venlafaxine [270] may have efficacy in adolescents when they are separated out as a group from children. Warnings, however, were sent to practitioners in August 2003 by Wyeth, the makers of venlafaxine, about possible increased hostility/suicidality with that medication [236]. Data suggest that there is no evidence to support the efficacy of tricyclic antidepressants in children [271]. There is marginal evidence to support the use of tricyclics in adolescent depression, although the magnitude of effect is likely to be modest at best.

136

JACKSON & LURIE

There have been two negative studies of mirtazepine [272], one negative study of escitalopram [273], two other negative studies of paroxetine [274,275], two negative studies of venlafaxine [276], and two negative studies of nefazodone [272,277] (although one demonstrated efficacy on a secondary outcome measure). One question raised by the outcome of the SSRI randomized controlled trials is why fluoxetine has shown efficacy in all three studies and other SSRIs mostly do not [262]. If the antidepressant effect is caused by the SSRI action, one would expect that an antidepressant effect should be common to this class of drugs. It is possible that the longer half-life of fluoxetine would mitigate the effects of missed doses, potentially a greater problem in youth because of more rapid drug metabolism [262]. Other answers may lie in the study design, study population, and interpretation of their outcomes [261,262]. The lack of efficacy of the tricyclic antidepressants and the new non-SSRI antidepressants in general as a class lends credence to the notion that it is the SSRI action, combined with the absence of other pharmacologic effects (eg, on the noradrenergic system), that is crucial for an antidepressant effect in children and adolescents [262]. It is possible that the differential maturation of brain regulatory systems in youth accounts for the specificity of positive treatment response with SSRIs [278]. Pediatric antidepressant drug trials may fail for different reasons in addition to lack of efficacy [236,262]. Antidepressant efficacy is difficult to establish given the high placebo response rate in many trials. Placebo response rates can also differ widely from study to study [261]. Other factors that may contribute to the difficulty demonstrating efficacy include developmental issues in pediatric patients, such as age of puberty, maturity of neural circuitry, and metabolic differences. The fact that antidepressants do not unambiguously demonstrate efficacy in children and adolescents is contrary to clinicians’ experiences with antidepressants in this population [279]. There is a great need for well-controlled clinical trials to address definitively the issue of efficacy of antidepressants in youth and the concern about suicidality. The American College of Neuropsychopharmacology Task Force suggests the need for head-to-head studies that compare other antidepressants to fluoxetine, which has documented efficacy [262]. It is important to note that in the adult literature, up to 50% of antidepressant trials for MDD did not demonstrate efficacy [261]. Frequently up to four to five trials are conducted to achieve the required two trials for a US FDA indication [261]. By contrast with MDD, in which most studies have been negative, SSRI treatment of obsessive-compulsive disorder and anxiety disorders in youths seems robustly better than placebo treatment [280–283]. PATIENT EDUCATION Before a treatment course is selected, it is recommended that time be spent on psychoeducation for teens and caregivers. This important step in treatment is often overlooked. Pressured schedules do not always allow for time to ensure

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

137

that families and patients have the necessary understanding of the condition. Treatment that starts off on a sound footing is likely to proceed more smoothly with better adherence to the regimen and better alliance with the teen and family. Educating and recruiting patients as partners in treatment have been shown to be essential factors in primary care for improving depression outcomes in adults. This is the appropriate time to address the issue of stigma. Adolescents are often relieved to hear that depression is common and that it is considered a medical illness, not a reflection of weak character [37]. It is helpful for patients and families to understand that although recovery from depression is likely to occur, improvement usually happens in small increments. It may be several weeks or months before returning to baseline emotional functioning. Hopelessness may predict withdrawal from treatment and suicidal behavior [284]; thus it is important to address the matter clinically. The primary care provider is the ideal person to address the somatic complaints that are so common with depression. It can be more reassuring for families and teens to hear from the pediatrician, rather than the child psychiatrist, about how depression affects mind and body and to have their lingering concerns about underlying medical illness allayed. This is also an excellent time for pediatricians to talk to patients about other basic lifestyle interventions, such as exercise [285] and sleep hygiene, which have been shown to help depressive symptoms [37]. Once these topics and other questions brought up by the family have been addressed, the stage has been set for a productive discussion of treatment options. TREATMENT OPTIONS A biopsychosocial approach should be used in treating a depressed adolescent. Such an approach includes psychotherapy and medication management, while addressing academic and school placement issues, social skills, and family functioning [224]. Opinions vary regarding whether psychotherapy or medication should be offered first and whether they should be offered in combination. Psychotherapy and medication management are reviewed in further detail later. Treatment is conventionally thought of as occurring in three stages: (1) the initial or acute phase, (2) the continuation phase, and (3) the maintenance phase. Initial or acute treatment phase In practice, some teens present with occasional, mild symptoms but no functional impairment. In this situation it is clinically reasonable to monitor and not necessarily refer for treatment. A follow-up assessment 3 to 4 weeks later is important. The family should be encouraged to return sooner, however, if symptoms become more severe. Psychotherapy should be mentioned as an option. Some teens, even those who do not demonstrate functional impairment, are interested in engaging in therapy and should be encouraged to do so. The importance of a thorough evaluation cannot be stressed enough. Even teens who at first report few symptoms may provide information of a more severe picture after further and more detailed questioning.

138

JACKSON & LURIE

Mild to moderate depression These recommendations rely heavily on AACAP’s practice parameters [4] and incorporate more recent recommendations from the Treatment for Adolescents with Depression Study (TADS) [265]. For mild to moderate depression, which is noncomplicated, an initial trial of psychotherapy is recommended. Cognitive behavioral therapy (CBT) and interpersonal psychotherapy (IPT) have documented efficacy in clinical trials (see later discussion) and should be tried for at least 6 to 12 weeks. Other forms of therapy, such as psychodynamic therapy and family therapy, have been found to be effective and are used clinically. Many factors, such as clinician availability and family/teen preference, may influence the choice of therapy. If there is no or only partial response after an adequate trial of therapy, consideration should be given to the addition of an SSRI. Factors associated with the partial response should be examined, such as discomfort with the particular form of therapy or therapist or an ongoing stressor. Some teens or families may be opposed to psychotherapy and request medication as first line. Based on the results of the TADS (see later discussion) this would be a reasonable choice for moderate depression. If a patient has any of the following conditions, psychotherapy alone may not be sufficient: bipolar disorder, psychosis, chronic treatment resistant depression, and seasonal affective disorder (SAD). Patients who have bipolar disorder probably require a mood stabilizer or an antipsychotic agent or both. Patients who have psychosis require an antipsychotic agent, treatment-resistant patients require different antidepressants or combination treatment, and patients with clear SAD can benefit from light therapy. It is probably best for most of these patients to be referred to a child and adolescent psychiatrist. Moderate to severe depression For moderate to severe depression, based on the results of the TADS, many teens would be best served by combination treatment. The TADS is the first, and currently the only published randomized, controlled trial that looked at pharmacologic treatment (fluoxetine), psychotherapy (CBT), and their combination for depressed adolescents with moderate to severe depression [265]. The results of the acute treatment phase showed that the combination of fluoxetine with CBT produced the greatest improvement in symptoms of MDD (71% response). Fluoxetine alone also was effective (61% response). This difference was not statistically significant; however, the combination treatment did result in statistically significantly more rapid symptom relief. CBT alone was not statistically more effective than placebo. The study findings suggest that for moderate to severe depression, fluoxetine alone or combined with CBT is effective treatment and that CBT alone is not. (CBT can vary greatly in quality and does have documented efficacy in other trials. It can be a powerful treatment, although it is unclear why it proved disappointing in the TADS trial. Generalizations about CBT cannot be made from this study alone.)

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

139

Although combination treatment is the first recommendation, it may not be available in certain geographic areas. Some teens refuse therapy but are willing to take medication. Based on the results of the TADS, it would be reasonable to recommend treatment with an SSRI without psychotherapy for moderate depression. If at all possible, however, it is best to include psychotherapy. There is evidence that the environmental and social problems associated with MDD remain when a patient’s mood has been stabilized with medication-only treatment. Prescribing guidelines for teenagers From 1995/1996 to 2001/2002 there was a 2.6-fold increase in the number of prescriptions for SSRIs for children and adolescents [286]. Most of this increase involved off-label use, with no reliable evidence of safety and efficacy. The increased scrutiny of antidepressant use in children and adolescents since 2003 has brought about, in some minds, a necessary correction, and practitioners are strongly advised to use evidence-based treatments. The AACAP, American Psychiatric Association, and the American Academy of Pediatrics support the continued use of SSRIs, but they emphasize careful monitoring. At the time of writing, fluoxetine is the only SSRI with a US FDA indication for the treatment of depression in teenagers. For new patients, fluoxetine should be considered the first-line medication for the treatment of depression given the strong evidence for its efficacy in children and teenagers [262,287]. There is also some evidence that citalopram [266] and sertraline [267] are effective in this population, although this evidence is not considered to be as robust. These medications could be considered second-line treatments and would be recommended if a patient failed an adequate trial of fluoxetine or is not able to tolerate the medication [287]. Citalopram and sertraline are sometimes used as first-line treatments if there is a strong family/teen preference (eg, many relatives with depression have done well on one of these medications) or if there is a need for an SSRI with a shorter half-life than fluoxetine. See Box 1 for prescribing guidelines. Teens who are already on another antidepressant (SSRI or non-SSRI), and responding well need not be taken off the medication. There is little evidence that tricyclic agents are effective in teenagers, and they are not recommended. It should be emphasized that these are the recommendations at the time of writing. It is likely that as the results of more well-designed randomized, controlled trials become available, other antidepressants may gain US FDA indications for the treatment of depression in children and adolescents. There is no need for laboratory tests or an electrocardiogram before starting an SSRI, and no medical monitoring is required. As mentioned in the assessment section, however, it is important to rule out possible underlying medical causes. The Texas Children’s Medication Algorithm project The Texas Consensus Conference Panel developed an algorithm for the medication treatment of childhood MDD [288]. This algorithm addressed routine

140

JACKSON & LURIE

Box 1: Initial treatment dose guidelines Week 1 Fluoxetine or citalopram, 10 mg, every morning Sertraline, 50 mg, every morning or every evening Weeks 2–4 Fluoxetine or citalopram, 20 mg, every morning Sertraline, 100 mg, every morning or every evening Weeks 5–8 If response is inadequate, increase fluoxetine or citalopram to 30 or 40 mg every morning (as long as patient has been on 20 mg for at least 4 weeks) Increase sertraline to 150–200 mg every morning or every evening (as long as patient has been on 100 mg for at least 4 weeks). Dosing for sertraline is approximate and can be done in smaller increments (eg, 25–50 mg per day every 3–5 days as tolerated to reach a dose of 100 mg per day by weeks 2–4. If there is a good response to a lower dose (eg, 10 mg of fluoxetine or citalopram or 50–100 mg of sertraline), it is reasonable to hold the dose at that level and monitor If teen experiences significant side effects, titration should be slower. (See section on side effects with SSRIs.) Adverse reactions to antidepressants are most likely to occur early in the course of treatment. It may be appropriate to adjust the dose, change to a different SSRI from the group of three mentioned previously, or stop using the medication. If no response is observed by 6–8 weeks, it would be reasonable to switch to another SSRI (eg, fluoxetine, citalopram, or sertraline). Dosing instructions are not given herein for other SSRIs or newer generation antidepressants because they are not recommended as first-line agents. They may be useful in treatment-resistant depression, but it could be an indication for referral—or at least consultation—with a child and adolescent psychiatrist. Dosing guidelines are available in a comprehensive article for primary care providers by Richardson and Katzenellenbogen [37].

treatment of depression and treatment-resistant depression. These recommendations were made 6 years ago, before the current body of knowledge had accumulated. A revision of this algorithm has been submitted for publication [289]. In the revised version they recommend fluoxetine, sertraline, and citalopram as first-line treatments for uncomplicated major depression, emphasizing that most data exists on the efficacy of fluoxetine. Paroxetine and escitalopram have been removed from this list of first-line medications but can be considered at a later stage. Tricyclic agents were previously considered to be treatment options for resistant depression, but they have been removed from the list. There

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

141

is an increased focus on assessment and additional recommendations about integrating psychotherapy. Side effects with selective serotonin reuptake inhibitors SSRIs offer the advantage of having fewer anticholinergic effects, less sedation, less weight gain, and fewer cardiac effects than the tricyclic antidepressants. In adults, side effects reported in association with the SSRIs include gastrointestinal difficulties (nausea, vomiting, diarrhea), central nervous system effects (agitation, extrapyramidal symptoms, hyperkinesias, disinhibition, jitteriness, headache, dizziness, insomnia, occasionally somnolence and fatigue, and tremor). This pattern also occurs in children and adolescents [290,291]. Sexual dysfunction is thought to occur in adolescents, but there is not enough information currently available [292]. Slowing of growth has been reported [293,294], as have easy bruising and epistaxis [295]. Discontinuation symptoms including dizziness, nausea, paraesthesias, tremor, anxiety, and dysphoria have been described. These are most acute with agents with short half-lives, such as paroxetine and venlafaxine, and minimal with fluoxetine. SSRIs also can be associated with behavioral activation/disinhibition and induction of mania [296–298]. An increase in motor activity may be more common in children and adolescents than adults [298]. All antidepressants can induce mania in patients with underlying bipolar disorder, and this effect is not unique to children and adolescents. Whether such activation/disinhibition is related to suicidal ideation or increases the risk of self-injurious acts is unclear. The SSRIs inhibit, to varying degrees, the metabolism of several medications that are metabolized by the cytochrome P450 isoenzymes (eg, tricyclics, antipsychotics, antiarrhythmics, benzodiazepines, carbamazepine, theophylline, and warfarin) [291,299]. The SSRIs bind tightly to plasma proteins and may interfere with other protein-bound drugs (eg, warfarin, digitoxin), which causes a shift in plasma concentrations that can potentially result in adverse effects. Interaction with other SSRIs, and particularly monoamine oxidase inhibitors (rarely used), also may induce the serotonergic syndrome, which is marked by agitation, confusion, and hyperthermia. Monitoring guidelines Careful monitoring by physicians and parents of an adolescent’s mental health and behavioral status while on antidepressants is critically important. The US FDA recommends weekly visits in the first 4 weeks of antidepressant initiation. The AACAP and the American Psychiatric Association believe that the frequency and nature of the monitoring should be individualized to the needs of the child and family. It would be reasonable to see an adolescent 2 to 3 weeks after starting treatment if the family were reliable and would call to report concerns. An excellent guide for physicians and families is available on the website www.ParentsMedGuide.org. These guidelines are prepared by the American Psychiatric Association and AACAP. These guidelines recommend enlisting

142

JACKSON & LURIE

the parents/guardians in the responsibility of monitoring. Families should contact the physician if the patient exhibits any of the following behaviors:




Expresses new or more frequent thoughts of wanting to die or engages in selfdestructive behavior Shows signs of increased anxiety/panic, agitation, aggressiveness, or impulsivity Experiences involuntary restlessness (akathisia) or an extreme degree of unwarranted elation or energy accompanied by fast, driven speech and unrealistic plans or goals

Medical and mental health providers should convey to parents the importance of consulting with a physician before changing or stopping their child’s medication. Continuation treatment phase If there is a positive response to medication, continue for at least 6 to 12 months after symptom remission to reduce risk of relapse [4]. During a naturalistic follow-up of children and adolescents who participated in a trial of acute fluoxetine treatment, 40% of patients who had recovered from an MDD experienced recurrence within 1 year [300]. In a recent study, Emslie and colleagues [301] demonstrated that mean time to relapse was significantly longer for persons who remained on fluoxetine (20–60 mg) than individuals who were on fluoxetine and then randomized to placebo. The goal of treatment is remission. Most studies that document the efficacy of SSRIs do not look at remission as the endpoint. For instance, in the TADS, although 71% of patients who received the combination treatment were considered improved, only 35% were judged to be in remission [289]. A response that falls short of remission is suboptimal and is often still associated with disabling symptoms. Remission is associated with lower rates of relapse, low risk of suicide and alcohol/drug abuse, and lack of disabling symptoms [302]. Additional risk factors for relapse are psychosis, increased psychosocial stressors, comorbid psychiatric disorders, and poor or failed treatment compliance [23,25]. Maintenance treatment The main goal of the maintenance phase is to foster healthy growth and development and prevent relapse or recurrence. This phase may extend from 1 year to indefinitely and is typically conducted in at least monthly or quarterly visits, depending on the situation. The literature on maintenance treatment in children and adolescents is sparse. In a recent letter to the editor, Hamilton and Bridge [303] reported that 78% of teenagers with MDD who were enrolled in a treatment study relapsed in the 5-year follow-up period. Many of these patients were not engaged in active treatments (medication or therapy), although they were available to them. They suggested that clinicians should actively seek ways to engage adolescents in specific evidence-based treatments with an alliance lasting 1 to several years. The AACAP practice parameters recommend that the psychotherapeutic or pharmacologic treatments that were efficacious to induce the remission of the acute

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

143

episode should be used for maintenance therapy [4]. They also recommend that patients who are maintained only on medication should be offered psychotherapy to help them cope with the psychosocial sequelae of the depression. It is important to note that the long-term effects of antidepressant medications on the maturation and development of children have not been studied. The clinician and the patient’s family should weigh the risks and benefits of maintenance antidepressants against the possible consequences of relapse [4]. One would be more likely to maintain an adolescent on medication if there had been several episodes of MDD, severe symptoms with significant impairment of functioning, or serious suicide attempts. Teens who have dysthymia or double depression are good candidates for maintenance treatment. On the other hand, if there has been a good recovery after an episode of uncomplicated MDD, one might consider tapering the medication 6 to 12 months after symptom remission. PSYCHOTHERAPY The AACAP recommends that psychotherapy be included as part of the treatment approach for depressed adolescents, particularly given the associated psychosocial difficulties [4]. Initial treatment goals are to ensure the safety of adolescents and establish a therapeutic alliance with young persons and their families. Psychoeducation is an important component to include in any intervention to help adolescents and families increase their understanding of symptoms, reduce self-blame, increase treatment adherence, identify familial mood disorders, predict struggles in recovery, and reduce blame for symptoms (eg, irritability, anhedonia) that may affect others [13,304–306]. It can be useful clinically to ask who is the most worried or concerned in the family. It may help to determine a course of treatment that assists not only the adolescent but also family members who care and want to help. An adolescent’s depression is often of concern to the caregivers but also to younger children who are a part of the family environment and who are impacted by the strain this illness can place on the family system as a whole, and they may feel powerless to help a brother or sister relieve sadness and remain safe. Educational materials should be developmentally and culturally appropriate for adolescents and families. With appropriate permission to share information, education and support also may be needed in the school or community to help attain services or advocate for an adolescent’s treatment needs. Psychotherapy is recommended for the treatment of adolescent depression [4]. In this section, we highlight CBT and IPT, which have the most empirical validation along with family therapy, which is often an essential treatment component for teenagers. Cognitive behavioral therapy [307–313] Cognitive theories of depression suggest that depressed individuals are more likely to interpret life events with a negative bias, to differentially notice negative information that supports their negative expectations and world view

144

JACKSON & LURIE

[314], and to make negative inferences about the causes and consequences, often in a self-blaming attributional manner [10,315]. Empirical research supports this theoretical approach for predicting prospective changes in depression among children and adolescents [10,42,144]. Low self-esteem and high self-criticism, negative attributional styles, and cognitive distortions can contribute to the development of depression for adolescents [316]. Identifying and targeting these thinking styles and errors is important for interrupting the self-reinforcing nature of depressive thinking. Cognitive theorists believe that the depressed person has developed maladaptive reaction patterns that must be unlearned [311]. The symptoms of depression (eg, depressed mood, isolation, suicidal ideation) become the targets of the intervention rather than addressing underlying conflicts or personality issues. The goal is to teach skills to manage and reduce depressive thoughts, moods, and behaviors. CBT focuses on identifying and modifying the negative, distorted thought patterns that underlie and maintain depression. For example, in the Coping with Depression for Adolescents (CWD-A) course (www. kpchr.org/public/acwd/acwd.html and www.feelbetter.org) teens are taught to monitor and control their mood through a diary, identify positive and negative thoughts that affect their mood, challenge unrealistic or irrational thoughts that support negativity and hopelessness, problem solve conflicts through better social skills and negotiation, actively relax, and schedule positive, life-affirming activities [310,311,317,318]. It has been recommended that CBT with adolescent girls also focus on cognitive vulnerability in the areas of physical appearance and body image [10]. On an optional basis, parents of depressed adolescents can participate in a parallel course in which they learn the basic skills being taught to their children and how to apply advanced skills to benefit themselves and their family [319]. Among psychotherapeutic treatment approaches for depression in adolescence, CBT has found the greatest empirical support [307,318]. In outcome research with randomized assignment to treatment groups, CBT consistently provides greater relief from depressive symptoms than the waitlist control. In some studies, CBT outperforms family and nondirective supportive therapies [313,320,321], whereas others have seen similar efficacy when compared to alternative treatments [312,322]. Early improvements after treatment with CBT have suggested that a particular strength for CBT might be in speeding up improvement for teens. Comparison treatments, such as systemic family therapy and relaxation training, eventually may catch up and provide equal treatment efficacy, however [307]. Monthly follow-up sessions of CBT may help solidify the skills that were learned and prevent relapse of depressive symptoms [323]. Interpersonal psychotherapy The development of social relationships, including close friendships and romantic relationships, is a hallmark of adolescent development. Social anxiety, poor social relationships, and social skills deficits can contribute to the

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

145

development of depressive symptoms in adolescence. IPT focuses on the ways depression becomes interwoven within an adolescent’s interpersonal relationships [324–326]. The goals are to enhance communication skills within significant relationships and decrease depressive symptoms. Coping within interpersonal relationships is improved through greater self-understanding, problem solving, and communication [13]. Specifically designed for adolescents, IPT-A provides an active treatment approach that focuses on psychoeducation and building competencies. Adolescents are encouraged to become increasingly active through the course of treatment taking more control of their progress. The course of treatment involves 12 weeks of therapy sessions with intermittent phone contacts. A parent/caregiver component also addresses the family changes that occur with adolescent development and role transitions. Four problem areas are highlighted in the treatment: grief, interpersonal role disputes, role transitions, and interpersonal deficits. IPT-A adds a fifth problem area that specifically supports single-parent families with a depressed adolescent. Objectives are also tailored to address adolescent interpersonal issues, such as autonomy, individuation, romantic relationships, and peer pressure. An interpersonal inventory is used to interview adolescents about important relationships with a goal of identifying the interpersonal issues that might be contributing to depressive symptomatology (eg, relationship changes, negative life events). Modifications are made when the treatment must address parental depression, alternative family constellations, treatment noncompliance, crisis, and suicidality. Treatment manuals with detailed scripts and clinical examples are available to guide the sessions [324]. In randomized trials, IPT-A participants reported significantly fewer depressive symptoms, met depression recovery criteria, and had improved social relationships, particularly with peers and romantic partners, when compared to members of a clinical monitoring control group [326]. Additional supportive research has been conducted with samples in which IPT was modified to increase cultural sensitivity for depressed Puerto Rican adolescents [327]. IPT seems to reduce depressive symptoms while enhancing social relationships, which could protect against future depressive episodes and promote greater overall health. Family therapy Depression affects not only an individual adolescent but also the family and social network. In a family therapy approach, the entire family system is included as the client [320,328–332]. The therapist initially helps the family to clarify concerns, worries, and fears that have led them to treatment. An attempt is made to help the family re-examine the problems and symptoms as issues for the entire family system rather than just the adolescent; the whole family is needed to help solve this problem together. The family is assisted in identifying dysfunctional patterns of communicating and behaving together that might contribute to mood changes in the family. Education is provided regarding depression and parenting strategies. With this enhanced awareness, families

146

JACKSON & LURIE

then focus on changing family patterns through better communication, problem solving together, and trying out new ways of interacting. As an example of family interactions that could contribute to mood changes, parents have been found to discuss emotional issues more with daughters than sons [333]. In another study, mothers were found to discuss sadness more with daughters and anger more with sons [334]. Although this pattern may be changing over time in various cultures, family therapy would focus on educating and teaching skills to support the family’s discussion of emotional experiences that could in turn help children and teenagers become more skilled and comfortable in recognizing and managing their emotions before depression emerges or intensifies. Additional therapies In addition to these more widely studied and empirically supported therapies for depression, other psychotherapies have been used extensively in the treatment of children and youth. Group therapy can provide opportunities for depressed youth to become more educated about their illness, gain support, understanding, and social skills practice with peers, and be challenged through group dynamics to make changes for themselves. Older adolescents also might benefit from dialectical behavior therapy (DBT) to address self-harm urges, chronic suicidality, and personality features that can complicate the treatment and recovery from depression [335,336]. Group and individual dialectical behavior therapy teaches skills to resolve conflict in relationships and manage negative affective states. An adolescent modification, DBT-A, has been developed for suicidal adolescents with borderline personality features [337,338]. With each of these therapies, an adolescent’s motivation and readiness for change are also important to assess. Additional education may be needed to help youth and their families evaluate the degree of concern and their openness to change at the current time. Maintaining a connection and alliance with the young person and their family is critical during this time of ambivalence. When an adolescent is more prepared to enter treatment, the likelihood of success also may be higher [339]. In the treatment of depression related to trauma, CBT can increase skills for managing anxiety and depression. Art therapy, group therapy, and exposure protocols have been used in the treatment of PTSD. Eye movement desensitization and reprocessing (EMDR) has come into vogue as a treatment for trauma experiences. Eye movement desensitization and reprocessing involves imaginal exposure to a target traumatic event, replacement of negative cognitions, and repetitive lateral eye movements or sounds [340]. Meta-analyses suggest that similar treatment results can be attained through conventional behavioral therapy, CBTs, and eye movement desensitization and reprocessing [341]. Brief psychotherapy soon after catastrophic events can help reduce PTSD symptoms and prevent increases in depressive symptoms [342]. Within clinical practice, most therapists use components of several therapy approaches. Interventions can be tailored to match an adolescent’s and family’s belief systems while addressing the most pressing psychological needs. The

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

147

response of an adolescent to treatment also can guide the integration of various techniques and approaches [4]. Finally, even after stabilization of acute symptoms, some ongoing therapeutic intervention is recommended for 1 to 3 years for adolescents with multiple major depressive episodes to prevent relapse and address the psychosocial impact of their depression [4]. SUMMARY Many aspects of the treatment for adolescent depression are still uncertain. However, our body of knowledge continues to accumulate, and our approaches continue to be refined. When we remember that 40 years ago the field was still arguing about the existence of depression in youth, it is clear that significant progress has been made. Recent controversies have provided another opportunity to step back and re-evaluate. Given the chronicity, morbidity, and mortality associated with adolescent depression, the risks of doing nothing are too great [343]. Evidence-based research has provided us with some direction during this unsettling time. After careful reviews, the major professional organizations representing pediatric medicine and psychiatry all support the continued use of SSRI antidepressant medications but emphasize close monitoring. The debates also have heightened interest in effective psychotherapy approaches, particularly CBT and IPT. Given the risk for suicidality in depressed adolescents, assessment and management of safety concerns remain critical, regardless of medication usage. Above all, it is most important that we remain hopeful about our ability to guide adolescents and families through the struggles with depression toward recovery. Information resources The following is a list of organizations with websites that contain resource information and publications for adolescents and families regarding depression American Academy of Child and Adolescent Psychiatry (www.aacap.org) National Institute of Mental Health (www.nimh.nih.gov) American Psychiatric Association (www.psych.org) American Psychological Association (www.apa.org) US Department of Health and Human Services, Substance Abuse and Mental Health Services Administration (SAMHSA) National Mental Health Information Center (www.mentalhealth.org) American Academy of Pediatrics (www.aap.org).

References [1] Rushton JL, Clark SJ, Freed GL. Primary care role in the management of childhood depression: a comparison of pediatricians and family physicians. Pediatrics 2000;105(4 Pt 2): 957–62. [2] Lewinsohn PM, Hops H, Roberts RE, et al. Adolescent psychopathology: I. Prevalence and incidence of depression and other DSM-III-R disorders in high school students. J Abnorm Psychol 1993;102(1):133–44. [3] Office of Applied Studies, Substance Abuse and Mental Health Services Administration. Depression among adolescents. In: National survey on drug use and health report.

148

JACKSON & LURIE

Washington, DC: Office of Applied Studies, Substance Abuse and Mental Health Services Administration; 2005. [4] American Academy of Child and Adolescent Psychiatry. Practice parameters for the assessment and treatment of children and adolescents with depressive disorders. J Am Acad Child Adolesc Psychiatry 1998;37(10 Suppl):63S–83S. [5] US Department of Health and Human Services. Mental health: a report of the Surgeon General. Rockville (MD): US Department of Health and Human Services; 1999. [6] Lock J, Walker LR, Rickert VI, et al. Suicidality in adolescents being treated with antidepressant medications and the black box label: position paper of the Society for Adolescent Medicine. J Adolesc Health 2005;36(1):92–3. [7] Kovacs M, Gatsonis C. Secular trends in age at onset of major depressive disorder in a clinical sample of children. J Psychiatr Res 1994;28(3):319–29. [8] Ryan ND, Williamson DE, Iyengar S, et al. A secular increase in child and adolescent onset affective disorder. J Am Acad Child Adolesc Psychiatry 1992;31(4):600–5. [9] Angold A, Costello EJ, Erkanli A. Comorbidity. J Child Psychol Psychiatry 1999;40(1): 57–87. [10] Hankin BL, Abramson LY. Development of gender differences in depression: an elaborated cognitive vulnerability-transactional stress theory. Psychol Bull 2001;127(6):773–96. [11] Nolen-Hoeksema S. Sex differences in depression. Stanford (CA): Stanford University Press; 1990. [12] Avenevoli S, Steinberg L. The continuity of depression across the adolescent transition. In: Reese HW, Kail R, editors. Advances in child development and behavior. San Diego (CA): Academic Press; 2001. p. 139–73. [13] Hatcher-Kay C, King CA. Depression and suicide. Pediatr Rev 2003;24(11):363–71. [14] Fleming JE, Offord DR. Epidemiology of childhood depressive disorders: a critical review. J Am Acad Child Adolesc Psychiatry 1990;29(4):571–80. [15] Lewinsohn PM, Clarke GN, Seeley JR, et al. Major depression in community adolescents: age at onset, episode duration, and time to recurrence. J Am Acad Child Adolesc Psychiatry 1994;33(6):809–18. [16] Weissman MM, Bland RC, Canino GJ, et al. Cross-national epidemiology of major depression and bipolar disorder. JAMA 1996;276(4):293–9. [17] Lewinsohn PM, Roberts RE, Seeley JR, et al. Adolescent psychopathology: II. Psychosocial risk factors for depression. J Abnorm Psychol 1994;103(2):302–15. [18] Garrison CZ, Addy CL, Jackson KL, et al. Major depressive disorder and dysthymia in young adolescents. Am J Epidemiol 1992;135(7):792–802. [19] Pine DS, Cohen E, Cohen P, et al. Adolescent depressive symptoms as predictors of adult depression: moodiness or mood disorder? Am J Psychiatry 1999;156(1):133–5 [20] Lewinsohn PM, Solomon A, Seeley JR, et al. Clinical implications of ‘‘subthreshold’’ depressive symptoms. J Abnorm Psychol 2000;109(2):345–51. [21] McCauley E, Myers K, Mitchell J, et al. Depression in young people: initial presentation and clinical course. J Am Acad Child Adolesc Psychiatry 1993;32(4):714–22. [22] Kovacs M, Feinberg TL, Crouse-Novak MA, et al. Depressive disorders in childhood. I. A longitudinal prospective study of characteristics and recovery. Arch Gen Psychiatry 1984;41(3):229–37. [23] Kovacs M. Presentation and course of major depressive disorder during childhood and later years of the life span. J Am Acad Child Adolesc Psychiatry 1996;35(6): 705–15. [24] Kovacs M, Feinberg TL, Crouse-Novak M, et al. Depressive disorders in childhood. II. A longitudinal study of the risk for a subsequent major depression. Arch Gen Psychiatry 1984;41(7):643–9. [25] Emslie GJ, Rush AJ, Weinberg WA, et al. Recurrence of major depressive disorder in hospitalized children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6): 785–92.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

149

[26] Harrington R, Fudge H, Rutter M, et al. Adult outcomes of childhood and adolescent depression: II. Links with antisocial disorders. J Am Acad Child Adolesc Psychiatry 1991;30(3):434–9. [27] Rohde P, Lewinsohn PM, Seeley JR. Are adolescents changed by an episode of major depression? J Am Acad Child Adolesc Psychiatry 1994;33(9):1289–98 [28] Rao U, Ryan ND, Birmaher B, et al. Unipolar depression in adolescents: clinical outcome in adulthood. J Am Acad Child Adolesc Psychiatry 1995;34(5):566–78. [29] Fleming JE, Boyle MH, Offord DR. The outcome of adolescent depression in the Ontario Child Health Study follow-up. J Am Acad Child Adolesc Psychiatry 1993;32(1): 28–33. [30] Kovacs M, Akiskal HS, Gatsonis C, et al. Childhood-onset dysthymic disorder: clinical features and prospective naturalistic outcome. Arch Gen Psychiatry 1994;51(5):365–74. [31] Lewinsohn PM, Rohde P, Seeley JR, et al. Comorbidity of unipolar depression: I. Major depression with dysthymia. J Abnorm Psychol 1991;100(2):205–13. [32] Keller MB, Beardslee W, Lavori PW, et al. Course of major depression in non-referred adolescents: a retrospective study. J Affect Disord 1988;15(3):235–43. [33] Kovacs M, Obrosky DS, Gatsonis C, et al. First-episode major depressive and dysthymic disorder in childhood: clinical and sociodemographic factors in recovery. J Am Acad Child Adolesc Psychiatry 1997;36(6):777–84. [34] Chambers WJ, Puig-Antich J, Tabrizi MA, et al. Psychotic symptoms in prepubertal major depressive disorder. Arch Gen Psychiatry 1982;39(8):921–7. [35] Mitchell J, McCauley E, Burke PM, et al. Phenomenology of depression in children and adolescents. J Am Acad Child Adolesc Psychiatry 1988;27(1):12–20. [36] Ryan ND, Puig-Antich J, Ambrosini P, et al. The clinical picture of major depression in children and adolescents. Arch Gen Psychiatry 1987;44(10):854–61. [37] Richardson LP, Katzenellenbogen R. Childhood and adolescent depression: the role of primary care providers in diagnosis and treatment. Curr Probl Pediatr Adolesc Health Care 2005;35(1):6–24. [38] Petersen AC, Compas BE, Brooks-Gunn J, et al. Depression in adolescence. Am Psychol 1993;48(2):155–68. [39] Pine DS, Cohen P, Gurley D, et al. The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Arch Gen Psychiatry 1998;55(1):56–64. [40] Harrington R, Fudge H, Rutter M, et al. Adult outcomes of childhood and adolescent depression. I. Psychiatric status. Arch Gen Psychiatry 1990;47(5):465–73. [41] Weissman MM, Wolk S, Wickramaratne P, et al. Children with prepubertal-onset major depressive disorder and anxiety grown up. Arch Gen Psychiatry 1999;56(9):794–801. [42] Nolen-Hoeksema S, Girgus JS, Seligman ME. Predictors and consequences of childhood depressive symptoms: a 5-year longitudinal study. J Abnorm Psychol 1992;101(3): 405–22. [43] Gotlib IH, Lewinsohn PM, Seeley JR. Symptoms versus a diagnosis of depression: differences in psychosocial functioning. J Consult Clin Psychol 1995;63(1):90–100. [44] Petersen AC, Sarigiani PA, Kennedy RE. Adolescent depression: Why more girls? J Youth Adolesc 1991;20(2):247–71 [45] Richardson LP, Davis R, Poulton R, et al. A longitudinal evaluation of adolescent depression and adult obesity. Arch Pediatr Adolesc Med 2003;157(8):739–45. [46] Whitaker RC, Wright JA, Pepe MS, et al. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997;337(13):869–73. [47] Pine DS, Goldstein RB, Wolk S, et al. The association between childhood depression and adulthood body mass index. Pediatrics 2001;107(5):1049–56. [48] Brown RA, Lewinsohn PM, Seeley JR, et al. Cigarette smoking, major depression, and other psychiatric disorders among adolescents. J Am Acad Child Adolesc Psychiatry 1996;35(12):1602–10.

150

JACKSON & LURIE

[49] Birmaher B, Ryan ND, Williamson DE, et al. Childhood and adolescent depression: a review of the past 10 years. Part II. J Am Acad Child Adolesc Psychiatry 1996;35(12): 1575–83. [50] Warner V, Mufson L, Weissman MM. Offspring at high and low risk for depression and anxiety: mechanisms of psychiatric disorder. J Am Acad Child Adolesc Psychiatry 1995;34(6):786–97. [51] Asarnow JR, Goldstein MJ, Tompson M, et al. One-year outcomes of depressive disorders in child psychiatric in-patients: evaluation of the prognostic power of a brief measure of expressed emotion. J Child Psychol Psychiatry 1993;34(2):129–37. [52] Asarnow JR, Tompson M, Hamilton EB, et al. Family-expressed emotion, childhood-onset depression, and childhood-onset schizophrenia spectrum disorders: is expressed emotion a nonspecific correlate of child psychopathology or a specific risk factor for depression? J Abnorm Child Psychol 1994;22(2):129–46 [53] Kendler KS. Genetic epidemiology in psychiatry: taking both genes and environment seriously. Arch Gen Psychiatry 1995;52(11):895–9. [54] Plomin R. The Emanuel Miller Memorial Lecture 1993: genetic research and identification of environmental influences. J Child Psychol Psychiatry 1994;35(5):817–34. [55] Eaves LJ, Silberg JL, Meyer JM, et al. Genetics and developmental psychopathology: II. The main effects of genes and environment on behavioral problems in the Virginia twin study of adolescent behavioral development. J Child Psychol Psychiatry 1997;38(8): 965–80. [56] Puig-Antich J, Goetz D, Davies M, et al. A controlled family history study of prepubertal major depressive disorder. Arch Gen Psychiatry 1989;46(5):406–18. [57] Klein DN, Lewinshon PM, Seeley JR, et al. A family study of major depressive disorder in a community sample of adolescents. Arch Gen Psychiatry 2001;58(1):13–20. [58] Rutter M, Silberg J, O’Connor T, et al. Genetics and child psychiatry: I Advances in quantitative and molecular genetics. J Child Psychol Psychiatry 1999;40(1):3–18. [59] Rutter M, Silberg J, O’Connor T, et al. Genetics and child psychiatry: II Empirical research findings. J Child Psychol Psychiatry 1999;40(1):19–55. [60] Kendler KS, Prescott CA. A population-based twin study of lifetime major depression in men and women. Arch Gen Psychiatry 1999;56(1):39–44. [61] Waslick BD, Kandel R, Kakouros A. Depression in children and adolescents: an overview. In: Shaffer D, Waslick BD, editors. The many faces of depression in children and adolescents. Washington, DC: American Psychiatric Publishing; 2002. p. 1–36. [62] Silberg J, Pickles A, Rutter M, et al. The influence of genetic factors and life stress on depression among adolescent girls. Arch Gen Psychiatry 1999;56(3):225–32. [63] Thapar A, Harold G, McGuffin P. Life events and depressive symptoms in childhood: –genes or shared adversity? A research note. J Child Psychol Psychiatry 1998;39(8):1153–8. [64] Birmaher B, Ryan ND, Williamson DE, et al. Childhood and adolescent depression: a review of the past 10 years. Part I. J Am Acad Child Adolesc Psychiatry 1996;35(11): 1427–39. [65] Garber J, Hilsman R. Cognitions, stress, and depression in children and adolescents. Child Adolesc Psychiatr Clin N Am 1992;1(1):129–67. [66] Roy A, Segal NL, Centerwall BS, et al. Suicide in twins. Arch Gen Psychiatry 1991;48(1): 29–32. [67] Kovacs M, Devlin B, Pollock M, et al. A controlled family history study of childhood-onset depressive disorder. Arch Gen Psychiatry 1997;54(7):613–23. [68] Williamson DE, Ryan ND, Birmaher B, et al. A case-control family history study of depression in adolescents. J Am Acad Child Adolesc Psychiatry 1995;34(12):1596–607. [69] Luthar SS. The culture of affluence: psychological costs of material wealth. Child Dev 2003;74(6):1581–93. [70] Downey G, Coyne JC. Children of depressed parents: an integrative review. Psychol Bull 1990;108(1):50–76.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

151

[71] Mufson L, Moreau D, Weissman MM, et al. Modification of interpersonal psychotherapy with depressed adolescents (IPT-A): phase I and II studies. J Am Acad Child Adolesc Psychiatry 1994;33(5):695–705. [72] Hayward C, Sanborn K. Puberty and the emergence of gender differences in psychopathology. J Adolesc Health 2002;30(4 Suppl):49–58. [73] Hayward C. Gender differences at puberty. New York: Cambridge University Press; 2003. [74] Cole DA, Martin JM, Peeke LA, et al. Children’s over- and underestimation of academic competence: a longitudinal study of gender differences, depression, and anxiety. Child Dev 1999;70(2):459–73. [75] Ge X, Lorenz FO, Conger RD, et al. Trajectories of stressful life events and depressive symptoms during adolescence. Dev Psychol 1994;30(4):467–83. [76] Cohen P, Cohen J, Kasen S, et al. An epidemiological study of disorders in late childhood and adolescence: I. Age- and gender-specific prevalence. J Child Psychol Psychiatry 1993;34(6):851–67. [77] Hankin BL, Abramson LY, Moffitt TE, et al. Development of depression from preadolescence to young adulthood: emerging gender differences in a 10-year longitudinal study. J Abnorm Psychol 1998;107(1):128–40. [78] Reinherz HZ, Giaconia RM, Lefkowitz ES, et al. Prevalence of psychiatric disorders in a community population of older adolescents. J Am Acad Child Adolesc Psychiatry 1993;32(2):369–77. [79] Weissman MM, Warner V, Wickramaratne P, et al. Offspring of depressed parents: 10 years later. Arch Gen Psychiatry 1997;54(10):932–40. [80] Angold A, Costello EJ, Worthman CM. Puberty and depression: the roles of age, pubertal status and pubertal timing. Psychol Med 1998;28(1):51–61. [81] Gjerde PF. Alternative pathways to chronic depressive symptoms in young adults: gender differences in developmental trajectories. Child Dev 1995;66(5):1277–300. [82] Broderick PC. Early adolescent gender differences in the use of ruminative and distracting coping strategies. J Early Adoles 1998;18(2):173–91. [83] Lewinsohn PM, Gotlib IH, Lewinsohn M, et al. Gender differences in anxiety disorders and anxiety symptoms in adolescents. J Abnorm Psychol 1998;107(1):109–17. [84] Kovacs M, Devlin B. Internalizing disorders in childhood. J Child Psychol Psychiatry 1998;39(1):47–63. [85] Steiner H, Lock J. Anorexia nervosa and bulimia nervosa in children and adolescents: a review of the past 10 years. J Am Acad Child Adolesc Psychiatry 1998;37(4):352–9. [86] Keiley MK, Bates JE, Dodge KA, et al. A cross-domain growth analysis: externalizing and internalizing behaviors during 8 years of childhood. J Abnorm Child Psychol 2000;28(2): 161–79. [87] Loeber R, Keenan K. Interaction between conduct disorder and its comorbid conditions: effects of age and gender. Clin Psychol Rev 1994;14(6):497–523. [88] Crick NR, Grotpeter JK. Relational aggression, gender, and social-psychological adjustment. Child Dev 1995;66(3):710–22. [89] Crick NR, Werner NE, Casas JF, et al. Childhood aggression and gender: a new look at an old problem. In: Bernstein D, editor. Gender and motivation. (p). Lincoln (NE): University of Nebraska Press; 1999. p. 75–141. [90] Rys GS, Bear GG. Relational aggression and peer relations: gender and developmental issues. Merrill Palmer Q 1997;43(1):87–106. [91] Rutter M. Age as an ambiguous variable in developmental research: some epidemiological considerations from developmental psychopathology. Int J Behav Dev 1989;12(1): 1–34. [92] Patton GC, Hibbert ME, Carlin J, et al. Menarche and the onset of depression and anxiety in Victoria, Australia. J Epidemiol Community Health 1996;50(6):661–6. [93] Ge X, Conger RD, Elder GH Jr. Coming of age too early: pubertal influences on girls’ vulnerability to psychological distress. Child Dev 1996;67(6):3386–400.

152

JACKSON & LURIE

[94] Graber JA, Lewinsohn PM, Seeley JR, et al. Is psychopathology associated with the timing of pubertal development? J Am Acad Child Adolesc Psychiatry 1997;36(12):1768–76. [95] Hayward C, Killen JD, Wilson DM, et al. Psychiatric risk associated with early puberty in adolescent girls. J Am Acad Child Adolesc Psychiatry 1997;36(2):255–62. [96] Brooks-Gunn J, Warren MP. Biological and social contributions to negative affect in young adolescent girls. Child Dev 1989;60(1):40–55. [97] Angold A, Costello EJ, Erkanli A, et al. Pubertal changes in hormone levels and depression in girls. Psychol Med 1999;29(5):1043–53. [98] Paikoff RL, Brooks-Gunn J, Warren MP. Effects of girls’ hormonal status on depressive and aggressive symptoms over the course of one year. J Youth Adolesc 1991;20(2): 191–215. [99] Susman EJ, Dorn LD, Chrousos GP. Negative affect and hormone levels in young adolescents: concurrent and predictive perspectives. J Youth Adolesc 1991;20(2):167–90. [100] Slap GB, Khalid N, Paikoff RL, et al. Evolving self-image, pubertal manifestations, and pubertal hormones: preliminary findings in young adolescent girls. J Adolesc Health 1994;15(4):327–35. [101] Nottelmann ED, Susman EJ, Inoff-Germain G, et al. Developmental processes in early adolescence: relationships between adolescent adjustment problems and chronologic age, pubertal stage, and puberty-related serum hormone levels. J Pediatr 1987;110(3):473–80. [102] Goodyer IM, Herbert J, Tamplin A, et al. Recent life events, cortisol, dehydroepiandrosterone and the onset of major depression in high-risk adolescents. Br J Psychiatry 2000;177: 499–504. [103] Goodyer IM, Herbert J, Tamplin A, et al. First-episode major depression in adolescents: affective, cognitive and endocrine characteristics of risk status and predictors of onset. Br J Psychiatry 2000;176:142–9. [104] Susman EJ, Inoff-Germain G, Nottelmann ED, et al. Hormones, emotional dispositions, and aggressive attributes in young adolescents. Child Dev 1987;58(4):1114–34. [105] Susman EJ, Nottelmann ED, Inoff-Germain G, et al. Hormonal influences on aspects of psychological development during adolescence. J Adolesc Health Care 1987;8(6): 492–504. [106] Weiss EL, Longhurst JG, Mazure CM. Childhood sexual abuse as a risk factor for depression in women: psychosocial and neurobiological correlates. Am J Psychiatry 1999; 156(6):816–28. [107] Meaney MJ, Diorio J, Francis D, et al. Early environmental regulation of forebrain glucocorticoid receptor gene expression: implications for adrenocortical responses to stress. Dev Neurosci 1996;18(1–2):49–72. [108] Brooks-Gunn J, Graber JA, Paikoff RL. Studying links between hormones and negative affect: models and measures. J Res Adolesc 1994;4(4):469–86. [109] Kostanski M, Gullone E. Adolescent body image dissatisfaction: relationships with selfesteem, anxiety, and depression controlling for body mass. J Child Psychol Psychiatry 1998;39(2):255–62. [110] Paxton SJ, Wertheim EH, Gibbons K, et al. Body image satisfaction, dieting beliefs, and weight loss behaviors in adolescent girls and boys. J Youth Adolesc 1991;20(3):361–79. [111] Wertheim EH, Paxton SJ, Maude D, et al. Psychosocial predictors of weight loss behaviors and binge eating in adolescent girls and boys. Int J Eat Disord 1992;12(2):151–60. [112] Harter S. The construction of the self: a developmental perspective. New York: Guilford Press; 1999. [113] Casper RC, Offer D. Weight and dieting concerns in adolescents: fashion or symptom? Pediatrics 1990;86(3):384–90. [114] Drewnowski A, Yee DK. Men and body image: are males satisfied with their body weight? Psychosom Med 1987;49(6):626–34. [115] Graber JA, Brooks-Gunn J, Paikoff RL, et al. Prediction of eating problems: an 8-year study of adolescent girls. Dev Psychol 1994;30(6):823–34.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

153

[116] Stice E, et al. Age of onset for binge eating and purging during late adolescence: a 4-year survival analysis. J Abnorm Psychol 1998;107(4):671–5. [117] Stice E, Hayward C, Cameron RP, et al. Body-image and eating disturbances predict onset of depression among female adolescents: a longitudinal study. J Abnorm Psychol 2000;109(3):438–44. [118] Wichstrom L. The emergence of gender difference in depressed mood during adolescence: the role of intensified gender socialization. Dev Psychol 1999;35(1):232–45. [119] Harter S, Jackson BK. Young adolescents’ perceptions of the link between low self-worth and depressed affect. J Early Adolesc 1993;13(4):383–407. [120] Parker S, Nichter M, Vuckovic N, et al. Body image and weight concerns among African American and white adolescent females: differences that make a difference. Hum Organ 1995;54(2):103–14. [121] Dolan BM, Lacey J, Evans C. Eating behaviour and attitudes to weight and shape in British women from three ethnic groups. Br J Psychiatry 1990;157:523–8. [122] Felts W, Parrillo AV, Chenier T, et al. Adolescents’ perceptions of relative weight and selfreported weight-loss activities: analysis of 1990 YRBS national data. J Adolesc Health 1996;18(1):20–6. [123] Rucker CE, Cash TF. Body images, body-size perceptions, and eating behaviors among African-American and white college women. Int J Eat Disord 1992;12(3):291–9. [124] Halpern CT, et al. Effects of body fat on weight concerns, dating, and sexual activity: a longitudinal analysis of black and white adolescent girls. Dev Psychol 1999;35(3):721–36. [125] Hayward C, Gotlib IH, Schraedley PK, et al. Ethnic differences in the association between pubertal status and symptoms of depression in adolescent girls. J Adolesc Health 1999;25(2):143–9. [126] Schraedley PK, Gotlib IH, Hayward C. Gender differences in correlates of depressive symptoms in adolescents. J Adolesc Health 1999;25(2):98–108. [127] Siegel JM, Aneshensel CS, Taub B, et al. Adolescent depressed mood in a multiethnic sample. J Youth Adolesc 1998;27(4):413–27. [128] Paperwalla KN, Levin TT, Weiner J, et al. Smoking and depression. Med Clin North Am 2004;88(6):1483–94. [129] Goodman E, Capitman J. Depressive symptoms and cigarette smoking among teens. Pediatrics 2000;106(4):748–55. [130] Wu LT, Anthony JC. Tobacco smoking and depressed mood in late childhood and early adolescence. Am J Public Health 1999;89(12):1837–40. [131] Cutler SE, Nolen-Hoeksema S. Accounting for sex differences in depression through female victimization: childhood sexual abuse. Sex Roles 1991;24(7–8):425–38. [132] Kaplan SJ, Pelcovitz D, Labruna V. Child and adolescent abuse and neglect research: a review of the past 10 years. Part I: Physical and emotional abuse and neglect. J Am Acad Child Adolesc Psychiatry 1999;38(10):1214–22. [133] MacMillan HL, Fleming JE, Trocme N, et al. Prevalence of child physical and sexual abuse in the community: results from the Ontario Health Supplement. JAMA 1997; 278(2):131–5. [134] Crick NR, Bigbee MA. Relational and overt forms of peer victimization: a multiinformant approach. J Consult Clin Psychol 1998;66(2):337–47. [135] Silverman AB, Reinherz HZ, Giaconia RM. The long-term sequelae of child and adolescent abuse: a longitudinal community study. Child Abuse Negl 1996;20(8):709–23. [136] Boney-McCoy S, Finkelhor D. Is youth victimization related to trauma symptoms and depression after controlling for prior symptoms and family relationships? A longitudinal, prospective study. J Consult Clin Psychol 1996;64(6):1406–16. [137] Feiring C, Taska L, Lewis M. Age and gender differences in children’s and adolescents’ adaptation to sexual abuse. Child Abuse Negl 1999;23(2):115–28. [138] D’Augelli AR. Developmental and contextual factors and mental health among lesbian, gay, and bisexual youths. In: Omoto AM, Kurtzman HS, editors. Sexual orientation and

154

[139]

[140]

[141]

[142]

[143] [144] [145] [146]

[147]

[148]

[149]

[150] [151]

[152] [153] [154]

[155]

[156]

[157]

JACKSON & LURIE

mental health: examining identity and development in lesbian and bisexual people. Washington, DC: American Psychological Association; 2006. p. 37–53. Rudolph KD, Hammen C. Age and gender as determinants of stress exposure, generation, and reactions in youngsters: a transactional perspective. Child Dev 1999;70(3): 660–77. Wagner BM, Compas BE. Gender, instrumentality, and expressivity: moderators of the relation between stress and psychological symptoms during adolescence. Am J Community Psychol 1990;18(3):383–406. Compas BE, Grant KE, Ey S. Psychosocial stress and child and adolescent depression: can we be more specific? In: Reynolds WM, Johnston HF, editors. Handbook of depression in children and adolescents. New York: Plenum Press; 1994. p. 509–23. Metalsky GI, Halberstadt LJ, Abramson LY. Vulnerability to depressive mood reactions: toward a more powerful test of the diathesis-stress and causal mediation components of the reformulated theory of depression. J Pers Soc Psychol 1987;52(2):386–93. Ralph JA, Mineka S. Attributional style and self-esteem: the prediction of emotional distress following a midterm exam. J Abnorm Psychol 1998;107(2):203–15. Hankin BL, Abramson LY, Siler M. A prospective test of the hopelessness theory of depression in adolescence. Cognit Ther Res 2001;25(5):607–32. Schwartz JA, Koenig LJ. Response styles and negative affect among adolescents. Cognit Ther Res 1996;20(1):13–36. Metalsky GI, Joiner TE Jr, Hardin TS, et al. Depressive reactions to failure in a naturalistic setting: a test of the hopelessness and self-esteem theories of depression. J Abnorm Psychol 1993;102(1):101–9. Robinson NS, Garber J, Hilsman R. Cognitions and stress: direct and moderating effects on depressive versus externalizing symptoms during the junior high school transition. J Abnorm Psychol 1995;104(3):453–63. Daley SE, Hammen C, Burge D, et al. Predictors of the generation of episodic stress: a longitudinal study of late adolescent women. J Abnorm Psychol 1997;106(2): 251–9. Williamson DE, Birmaher B, Anderson BP, et al. Stressful life events in depressed adolescents: the role of dependent events during the depressive episode. J Am Acad Child Adolesc Psychiatry 1995;34(5):591–8. Kendler KS, Karkowski LM, Prescott CA. Causal relationship between stressful life events and the onset of major depression. Am J Psychiatry 1999;156(6):837–48. Hammen C. The emergence of an interpersonal approach to depression. In: Joiner T, Coyne JC, editors. The interactional nature of depression: advances in interpersonal approaches. Washington, DC: American Psychological Association; 1999. p. 21–35. Joiner T, Coyne JC. The interactional nature of depression: advances in interpersonal approaches. Washington, DC: American Psychological Association; 1999. Lopez-Ibor JJ, Christodoulou G, Maj M, et al. Disasters and mental health. New York: John Wiley & Sons; 2005. Fullerton CS, Ursano RJ. Psychological and psychopathological consequences of disasters. In: Lopez-Ibor JJ, Christodoulou G, Maj M, et al, editors. Disasters and mental health. New York: John Wiley & Sons; 2005. p. 13–36. March JS, Amaya-Jackson L, Terry R, et al. Posttraumatic symptomatology in children and adolescents after an industrial fire. J Am Acad Child Adolesc Psychiatry 1997;36(8): 1080–8. Pfefferbaum B, Nawaz S, Kearns LJ. Posttraumatic stress disorder in children: implications for assessment, prevention, and referral in primary care. J Okla State Med Assoc 1999;92(7):309–15. Lipschitz DS, Winegar RK, Hartnick E, et al. Posttraumatic stress disorder in hospitalized adolescents: psychiatric comorbidity and clinical correlates. J Am Acad Child Adolesc Psychiatry 1999;38(4):385–92.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

155

[158] Ackerman PT, Newton JE, McPherson WB, et al. Prevalence of post traumatic stress disorder and other psychiatric diagnoses in three groups of abused children (sexual, physical, and both). Child Abuse Negl 1998;22(8):759–74. [159] Green BL. Traumatic stress and disaster: mental health effects and factors influencing adaptation. In: Mak FL, Nadelson CC, editors. International review of psychiatry. Washington, DC: American Psychological Association; 1996. p. 476. [160] North CS, Nixon SJ, Shariat S, et al. Psychiatric disorders among survivors of the Oklahoma City bombing. JAMA 1999;282(8):755–62. [161] Norris FH, Friedman MJ, Watson PJ. 60,000 disaster victims speak: Part II. Summary and implications of the disaster mental health research. Psychiatry: Interpersonal and Biological Processes 2002;65(3):240–60. [162] Norris FH, Friedman MJ, Watson PJ, et al. 60,000 disaster victims speak: Part I. An empirical review of the empirical literature, 1981–2001. Psychiatry: Interpersonal and Biological Processes 2002;65(3):207–39. [163] Pynoos RS, Steinberg AM, Goenjian A. Traumatic stress in childhood and adolescence: recent developments and current controversies. In: van der Kolk BA, McFarlane AC, Weisaeth L, editors. Traumatic stress: the effects of overwhelming experience on mind. New York: Guilford Press; 1996. p. 331–58. [164] Pynoos RS. Exposure to catastrophic violence and disaster in childhood. In: Pfeffer CR, editor. Severe stress and mental disturbance in children. Washington, DC: American Psychiatric Association; 1996. p. 181–208. [165] Lengua LJ, Long AC, Smith KI, et al. Pre-attack symptomatology and temperament as predictors of children’s responses to the September 11 terrorist attacks. J Child Psychol Psychiatry 2005;46(6):631–45. [166] Fullerton CS, Ursano RJ, Norwood AE, et al. Trauma, terrorism, and disaster. In: Ursano RJ, Fullerton CS, Norwood AE, editors. Terrorism and disaster: individual and community mental health interventions. New York: Cambridge University Press; 1993. p. 1–20. [167] Ursano RJ, Fullerton CS, Norwood AE, editors. Terrorism and disaster: individual and community mental health interventions. New York: Cambridge University Press; 2003. [168] National Center for Injury Prevention and Control. Injury mortality reports. Available at: http://www.cdc.gov/ncipc/wisqars. Accessed January 15, 2006. [169] Centers for Disease Control and Prevention. Death rates from 72 selected causes by 5-year age groups, race, and sex: United States, 1979–1997. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Health Statistics; 1999. [170] Centers for Disease Control and Prevention. Youth risk behavior surveillance, United States, 2001. Mortality and Morbidity Review 2002;53:1–64. [171] Berman AL, Jobes DA, Silverman MM. Adolescent suicide: assessment and intervention. 2nd edition. Washington, DC: American Psychological Association; 2006. [172] Summary of the practice parameters for the assessment and treatment of children and adolescents with suicidal behavior. J Am Acad Child Adolesc Psychiatry 2001;40(4): 495–9. [173] Grunbaum JA, Kann L, Kinchen S, et al. Youth risk behavior surveillance: United States, 2003. MMWR Surveill Summ 2004;53(2):1–96. [174] Lewinsohn PM, Rohde P, Seeley JR. Psychosocial characteristics of adolescents with a history of suicide attempt. J Am Acad Child Adolesc Psychiatry 1993;32(1):60–8. [175] Fergusson DM, Lynskey MT, Horwood LJ. Childhood sexual abuse and psychiatric disorder in young adulthood: I. Prevalence of sexual abuse and factors associated with sexual abuse. J Am Acad Child Adolesc Psychiatry 1996;35(10):1355–64. [176] Brent DA, Perper JA, Allman CJ. Alcohol, firearms, and suicide among youth: temporal trends in Allegheny County, Pennsylvania, 1960 to 1983. JAMA 1987;257(24):3369–72. [177] Brent DA. Risk factors for adolescent suicide and suicidal behavior: mental and substance abuse disorders, family environmental factors, and life stress. Suicide Life Threat Behav 1995;25(Suppl):52–63.

156

JACKSON & LURIE

[178] Brent DA, Perper JA, Moritz G, et al. Psychiatric risk factors for adolescent suicide: a casecontrol study. J Am Acad Child Adolesc Psychiatry 1993;32(3):521–9. [179] Brent DA, Perper JA, Moritz G, et al. Psychiatric sequelae to the loss of an adolescent peer to suicide. J Am Acad Child Adolesc Psychiatry 1993;32(3):509–17. [180] Brent DA, Johnson BA, Perper J, et al. Personality disorder, personality traits, impulsive violence, and completed suicide in adolescents. J Am Acad Child Adolesc Psychiatry 1994;33(8):1080–6. [181] Pfeffer CR, Klerman GL, Hurt SW, et al. Suicidal children grow up: rates and psychosocial risk factors for suicide attempts during follow-up. J Am Acad Child Adolesc Psychiatry 1993;32(1):106–13. [182] Weissman MM, Wolk S, Goldstein RB, et al. Depressed adolescents grown up. JAMA 1999;281(18):1707–13. [183] Hodgman CH, McAnarney ER. Adolescent depression and suicide: rising problems. Hosp Pract (Off Ed) 1992;27(4):73–6, 81, 84–5. [184] Committee on Adolescents, American Academy of Pediatrics. Suicide and suicide attempts in adolescents. Pediatrics 2000;105(4 Pt 1):871–4. [185] Centers for Disease Control and Prevention. Suicide attempts and physical fighting among high school students, United States, 2001. Morbidity and Mortality Weekly Review 2004;53(22):474–6. [186] Bollen KA, Phillips DP. Imitative suicides: a national study of the effects of television news stories. Am Sociol Rev 1982;47(6):802–9. [187] Gould MS, Wallenstein S, Kleinman M. Time-space clustering of teenage suicide. Am J Epidemiol 1990;131(1):71–8. [188] Phillips DP, Carstensen LL. Clustering of teenage suicides after television news stories about suicide. N Engl J Med 1986;315(11):685–9. [189] Frances RJ, Franklin J, Flavin DK. Suicide and alcoholism. Am J Drug Alcohol Abuse 1987;13(3):327–41. [190] Cooley-Quille MR, Turner SM, Beidel DC. Emotional impact of children’s exposure to community violence: a preliminary study. J Am Acad Child Adolesc Psychiatry 1995;34(10): 1362–8. [191] American Academy of Pediatrics Committee on Injury and Poison Prevention. Firearm injuries affecting the pediatric population. Pediatrics 1992;89(4 Pt 2):788–90. [192] American Academy of Pediatrics Committee on Adolescence. Firearms and adolescents. Pediatrics 1992;89(4 Pt 2):784–7. [193] Kachur SP, Potter LB, James SP, et al. Suicide in the Unites States: 1980–1992. Violence surveillance. Atlanta (GA): National Center for Injury Prevention and Control; 1995. [194] Remafedi G, French S, Story M, et al. The relationship between suicide risk and sexual orientation: results of a population-based study. Am J Public Health 1998;88(1): 57–60. [195] Gould MS, Greenberg T, Velting DM, et al. Youth suicide risk and preventive interventions: a review of the past 10 years. J Am Acad Child Adolesc Psychiatry 2003;42(4):386–405. [196] McDaniel JS, Purcell D, D’Augelli AR. The relationship between sexual orientation and risk for suicide: research findings and future directions for research and prevention. Suicide Life Threat Behav 2001;31(Suppl):84–105. [197] Russell ST. Sexual minority youth and suicide risk. Am Behav Sci 2003;46(9):1241–57. [198] Savin-Williams RC. Suicide attempts among sexual-minority youths: population and measurement issues. J Consult Clin Psychol 2001;69(6):983–91. [199] Savin-Williams RC. A critique of research on sexual-minority youths. J Adolesc 2001;24(1):5–13. [200] Lewinsohn PM, Rohde P, Seeley JR. Adolescent suicidal ideation and attempts: prevalence, risk factors, and clinical implications. Clin Psychol Sci Pract 1996;3(1):25–46. [201] Savin-Williams RC, Ream GL. Suicide attempts among sexual-minority male youth. J Clin Child Adolesc Psychol 2003;32(4):509–22.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

157

[202] Jackson BK. Predictors and outcomes of self-acceptance among lesbian, gay, and bisexual youth. Dissertation Abstracts International: Section B: The Sciences and Engineering 2000;60(9-B):4930. [203] Diagnostic and statistical manual of mental disorders. 4th edition. Washington, DC: American Psychiatric Association; 1994. [204] Weller RA, Weller EB, Fristad MA, et al. Depression in recently bereaved prepubertal children. Am J Psychiatry 1991;148(11):1536–40. [205] Geller B, Fox LW, Clark KA. Rate and predictors of prepubertal bipolarity during follow-up of 6- to 12-year-old depressed children. J Am Acad Child Adolesc Psychiatry 1994;33(4): 461–8. [206] Lewinsohn PM, Klein DN, Seeley JR. Bipolar disorders in a community sample of older adolescents: prevalence, phenomenology, comorbidity, and course. J Am Acad Child Adolesc Psychiatry 1995;34(4):454–63. [207] Birmaher B, Arbelaez C, Brent D. Course and outcome of child and adolescent major depressive disorder. Child Adolesc Psychiatr Clin N Am 2002;11(3): 619–38. [208] Goodyer IM, Herbert J, Secher SM, et al. Short-term outcome of major depression: I. Comorbidity and severity at presentation as predictors of persistent disorder. J Am Acad Child Adolesc Psychiatry 1997;36(2):179–87. [209] Rohde P, Lewinsohn PM, Seeley JR. Comorbidity of unipolar depression: II. Comorbidity with other mental disorders in adolescents and adults. J Abnorm Psychol 1991;100(2): 214–22. [210] Kim WJ. Child and adolescent psychiatry workforce: a critical shortage and national challenge. Acad Psychiatry 2003;27(4):277–82. [211] Brent DA, Birmaher B. Clinical practice: adolescent depression. N Engl J Med 2002;347(9):667–71. [212] Kazdin AE. Informant variability in the assessment of childhood depression. In: Reynolds WM, Johnston HF, editors. Handbook of depression in children and adolescents. New York: Plenum Press; 1994. p. 249–71. [213] Costello EJ, Edelbrock CS, Costello AJ. Validity of the NIMH diagnostic interview schedule for children: a comparison between psychiatric and pediatric referrals. J Abnorm Child Psychol 1985;13(4):579–95. [214] Beck AT, Steer RA, Brown GK. Manual for the Beck depression inventory. 2nd edition. San Antonio (TX): The Psychological Corporation; 1996. [215] Beck A, Ward C, Mendelson M, et al. An inventory for measuring depression. Arch Gen Psychiatry 1961;4:561–71. [216] Beck AT, Guth D, Steer RA, et al. Screening for major depression disorders in medical inpatients with the Beck depression inventory for primary care. Behav Res Ther 1997;35(8): 785–91. [217] Beck JS, Beck AT, Jolly JB. Beck youth inventories. 2nd edition. San Antonio (TX): Harcourt Assessment; 2005. [218] Kovacs M. The children’s depression inventory (CDI). Psychopharmacol Bull 1985;21(4): 995–8. [219] Reynolds WM. Reynolds adolescent depression scale professional manual. 2nd edition. Odessa (FL): Psychological Assessment Resources; 2002. [220] Ambrosini PJ. Historical development and present status of the schedule for affective disorders and schizophrenia for school-age children (K-SADS). J Am Acad Child Adolesc Psychiatry 2000;39(1):49–58. [221] Kaufman J, Birmaher B, Brent D, et al. Schedule for affective disorders and schizophrenia for school-age children-present and lifetime version (K-SADS-PL): initial reliability and validity data. J Am Acad Child Adolesc Psychiatry 1997;36(7):980–8. [222] Reich W. Diagnostic interview for children and adolescents (DICA). J Am Acad Child Adolesc Psychiatry 2000;39(1):59–66.

158

JACKSON & LURIE

[223] Shaffer D, Fisher P, Lucas CP, et al. NIMH diagnostic interview schedule for children version IV (NIMH DISC-IV): description, differences from previous versions, and reliability of some common diagnoses. J Am Acad Child Adolesc Psychiatry 2000;39(1): 28–38. [224] Lewis M. Child and adolescent psychiatry: a comprehensive textbook. 3rd edition. Philadelphia: Lippincott Williams & Wilkins; 2002. [225] Wise MG, Rundell JR. Concise guide to consultation psychiatry. Washington, DC: American Psychiatric Press; 1988. [226] Oinonen KA, Mazmanian D. To what extent do oral contraceptives influence mood and affect? J Affect Disord 2002;70(3):229–40 [227] Lin KM, Cheung F. Mental health issues for Asian Americans. Psychiatr Serv 1999;50(6): 774–80. [228] US Department of Health and Human Services. Mental health: culture, race, and ethnicity. In: A supplement to mental health: a report to the surgeon general. Rockville (MD): US Department of Health and Human Services; 2001. [229] Reynolds WM. Suicidal ideation questionnaire: professional manual. Odessa (FL): Psychological Assessment Resources; 1987. [230] Favazza AR. Why patients mutilate themselves. Hosp Community Psychiatry 1989;40(2): 137–45. [231] Walsh BW, Rosen P. Self-mutilation and contagion: an empirical test. Am J Psychiatry 1985;142(1):119–20. [232] Conterio K, Lader W, Bloom J. Bodily harm: the breakthrough healing program for selfinjurers. New York: Hyperion; 1998. [233] Robinson KR, Jackson BK, Hagman JO. Not just cutting calories: assessment and treatment of self-injurious-behavior for individuals with eating disorders. International conference on eating disorders. Orlando (FL): Academy for Eating Disorders; 2004. [234] Schroeder SR, Oster-Granite ML, Thompson T. Self-injurious behavior: gene-brain-behavior relationships. Washington, DC: American Psychological Association; 2002. [235] Hawton K. Suicide and attempted suicide among children and adolescents. Thousand Oaks (CA): Sage Publications; 1986. [236] Council on Scientific Affairs. Safety and efficacy of selective serotonin reuptake inhibitors (SSRIs) in children and adolescents. Washington, DC: American Academy of Child and Adolescent Psychiatry; 2005. [237] Laughren TP. Background comments for February 2, 2004 meeting of Psychopharmacological Drugs Advisory Committee and pediatric subcommittee of the anti-infective drugs advisory committee. Available at: http://www.fda.gov/ohrms/dockets/ac/04/briefing/ 2004-4065b1-04-Tab02-Laughren-Jan5.pdf. Accessed February 18, 2006. [238] Teicher MH, Glod C, Cole JO. Emergence of intense suicidal preoccupation during fluoxetine treatment. Am J Psychiatry 1990;147(2):207–10. [239] Department of Health and Human Services, Public Health Service, Food and Drug Administration. Psychopharmacological drugs advisory committee, 1991. Available at: http://www.fda.gov/ohrms/dockets/ac/prozac/2443T1.pdf. Accessed February 18, 2006. [240] Beasley CM Jr, Dornseif BE, Bosomworth JC, et al. Fluoxetine and suicide: a meta-analysis of controlled trials of treatment for depression. BMJ 1991;303(6804):685–92. [241] Masand P, Gupta S, Dewan M. Suicidal ideation related to fluoxetine treatment. N Engl J Med 1991;324(6):420. [242] Rothschild AJ, Locke CA. Reexposure to fluoxetine after serious suicide attempts by three patients: the role of akathisia. J Clin Psychiatry 1991;52(12):491–3. [243] Wirshing WC, Van Putten T, Rosenberg J, et al. Fluoxetine, akathisia, and suicidality: is there a causal connection? Arch Gen Psychiatry 1992;49(7):580–1 [244] Lane RM. SSRI-induced extrapyramidal side-effects and akathisia: implications for treatment. J Psychopharmacol 1998;12(2):192–214.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

159

[245] King RA, Riddle MA, Chappell PB, et al. Emergence of self-destructive phenomena in children and adolescents during fluoxetine treatment. J Am Acad Child Adolesc Psychiatry 1991;30(2):179–86. [246] Lipinski JF Jr, Mallya G, Zimmerman P, et al. Fluoxetine-induced akathisia: clinical and theoretical implications. J Clin Psychiatry 1989;50(9):339–42. [247] Hammad T. Review and evaluation of clinical data. Available at: http://www.fda. gov/ohrms/dockets/ac/04/briefing/2004-4065b1-10-TAB08-Hammads-Review.pdf. Accessed February 18, 2006. [248] Ryan ND. Treatment of depression in children and adolescents. Lancet 2005;366(9489): 933–40. [249] Bridge JA, Barbe RP, Birmaher B, et al. Emergent suicidality in a clinical psychotherapy trial for adolescent depression. Am J Psychiatry 2005;162(11):2173–5. [250] Olfson M, Shaffer D, Marcus SC, et al. Relationship between antidepressant medication treatment and suicide in adolescents. Arch Gen Psychiatry 2003;60(10):978–82. [251] Carlsten A, Waern M, Ekedahl A, et al. Antidepressant medication and suicide in Sweden. Pharmacoepidemiol Drug Saf 2001;10(6):525–30. [252] Ohberg A, Vuori E, Klaukka T, et al. Antidepressants and suicide mortality. J Affect Disord 1998;50(2–3):225–33. [253] Valuck RJ, Libby AM, Sills MR, et al. Antidepressant treatment and risk of suicide attempt by adolescents with major depressive disorder: a propensity-adjusted retrospective cohort study. CNS Drugs 2004;18(15):1119–32. [254] Simon GE, Savarino J, Operskalski B, et al. Suicide risk during antidepressant treatment. Am J Psychiatry 2006;163(1):41–7. [255] Gray D, Moskos M, Keller T. Utah youth suicide study new findings. Presented at the Annual Meeting of the American Association of Suicidology. Sante Fe, NM, 2003. [256] Leon AC, Marzuk PM, Tardiff K, et al. Paroxetine, other antidepressants, and youth suicide in New York City: 1993 through 1998. J Clin Psychiatry 2004;65(7):915–8. [257] AACAP. AACAP advises child and adolescent psychiatrists on antidepressants. Available at: www.aacap.org. Accessed February 2, 2006. [258] Rosack J. New data show declines in antidepressant prescribing. Psychiatric News, September 9, 2005. p. 1. [259] Murray ML, Thompson M, Santosh PJ, et al. Effects of the committee on safety of medicines advice on antidepressant prescribing to children and adolescents in the UK. Drug Saf 2005;28(12):1151–7. [260] American Psychiatric Association, American Academy of Child and Adolescent Psychiatry. Letter to the commissioner of the FDA. Available at: www.aacap.org. Accessed February 2, 2006. [261] Cheung AH, Emslie GJ, Mayes TL. Review of the efficacy and safety of antidepressants in youth depression. J Child Psychol Psychiatry 2005;46(7):735–54. [262] Mann JJ, Emslie G, Baldessarini RJ, et al. ACNP task force report on SSRIs and suicidal behavior in youth. Neuropsychopharmacology 2006;31(3):473–92. [263] Emslie GJ, Rush AJ, Weinberg WA, et al. A double-blind, randomized, placebo-controlled trial of fluoxetine in children and adolescents with depression. Arch Gen Psychiatry 1997;54(11):1031–7. [264] Emslie GJ, Heiligenstein JH, Wagner KD, et al. Fluoxetine for acute treatment of depression in children and adolescents: a placebo-controlled, randomized clinical trial. J Am Acad Child Adolesc Psychiatry 2002;41(10):1205–15. [265] March J, Silva S, Petrycki S, et al. Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: treatment for adolescents with depression study (TADS) randomized controlled trial. JAMA 2004;292(7):807–20. [266] Wagner KD, Robb AS, Findling RL, et al. A randomized, placebo-controlled trial of citalopram for the treatment of major depression in children and adolescents. Am J Psychiatry 2004;161(6):1079–83.

160

JACKSON & LURIE

[267] Wagner KD, Ambrosini P, Rynn M, et al. Efficacy of sertraline in the treatment of children and adolescents with major depressive disorder: two randomized controlled trials. JAMA 2003;290(8):1033–41. [268] Brent DA. Is the medication bottle for pediatric and adolescent depression half-full or half-empty? [editorial] J Adolesc Health 2005;37(6):431–3. [269] Keller MB, Ryan ND, Strober M, et al. Efficacy of paroxetine in the treatment of adolescent major depression: a randomized, controlled trial. J Am Acad Child Adolesc Psychiatry 2001;40(7):762–72. [270] Emslie GJ, Findling RL, Yeung PP, et al. Efficacy and safety of venlafaxine ER in children and adolescents with major depressive disorder. New York: American Psychiatric Association; 2004. [271] Hazell P, O’Connell D, Heathcote D, et al. Tricyclic drugs for depression in children and adolescents. Cochrane Database Syst Rev 2002;2:CD002317. [272] Dubitsky GM. Review and evaluation of clinical data: placebo-controlled antidepressant studies in pediatric patients. Available at: http://www.fda.gov/ohrms/dockets/ac/04/ briefing/2004-4065b1-08-TAB06-Dubitsky-Review.pdf. Accessed February 18, 2006. [273] Wagner K. Poster presentation. Presented at the meeting of the American Academy of Child and Adolescent Psychiatry. Washington, DC, October 2004. [274] Emslie G. Presented at the Annual Meeting of the American Academy of Child and Adolescent Psychiatry. Washington, DC, October 2004. [275] Milin R. Presented at the Annual Meeting of the American Academy of Child and Adolescent Psychiatry. Chicago, October 1999. [276] Emslie G. Poster presentation. Presented at the Annual Meeting of the American Academy of Child and Adolescent Psychiatry. Washington, DC, October 2004. [277] Emslie G, Findling RL, Rynn MA, et al. Efficacy and safety of nefazodone in the treatment of adolescents with major depressive disorder. [abstract]. J Child Adolesc Psychopharmacol 2002;12:299. [278] Strober M, DeAntonio M, Schmidt-Lackner S, et al. The pharmacotherapy of depressive illness in adolescents: an open-label comparison of fluoxetine with imipramine-treated historical controls. J Clin Psychiatry 1999;60(3):164–9. [279] Emslie GJ, Ryan ND, Wagner KD. Major depressive disorder in children and adolescents: clinical trial design and antidepressant efficacy. J Clin Psychiatry 2005;66(Suppl 7):14–20. [280] Birmaher B, Axelson DA, Monk K, et al. Fluoxetine for the treatment of childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry 2003;42(4):415–23. [281] The Research Unit on Pediatric Psychopharmacology Anxiety Study Group. Fluvoxamine for the treatment of anxiety disorders in children and adolescents. N Engl J Med 2001;344(17):1279–85. [282] Flament MF, Rapoport JL, Berg CJ, et al. Clomipramine treatment of childhood obsessivecompulsive disorder: a double-blind controlled study. Arch Gen Psychiatry 1985;42(10): 977–83. [283] Blomhoff S, Haug TT, Hellstrom K, et al. Randomised controlled general practice trial of sertraline, exposure therapy and combined treatment in generalised social phobia. Br J Psychiatry 2001;179:23–30. [284] Brent DA, Kolko DJ, Birmaher B, et al. Predictors of treatment efficacy in a clinical trial of three psychosocial treatments for adolescent depression. J Am Acad Child Adolesc Psychiatry 1998;37(9):906–14. [285] Paluska SA, Schwenk TL. Physical activity and mental health: current concepts. Sports Med 2000;29(3):167–80. [286] Ma J, Lee KV, Stafford RS. Depression treatment during outpatient visits by US children and adolescents. J Adolesc Health 2005;37(6):434–42. [287] Scahill L, Hamrin V, Pachler ME. The use of selective serotonin reuptake inhibitors in children and adolescents with major depression. J Child Adolesc Psychiatr Nurs 2005; 18(2):86–9.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

161

[288] Hughes CW, Emslie GJ, Crismon ML, et al. The Texas children’s medication algorithm project: report of the Texas Consensus Conference Panel on medication treatment of childhood major depressive disorder. J Am Acad Child Adolesc Psychiatry 1999;38(11): 1442–54. [289] Emslie G. Evidence-based psychopharmacological treatment using SSRI’s and other antidepressants in children and teens considering regulatory concerns. In: Psychopharmacology Update Institute. New York: American Academy of Child and Adolescent Psychiatry; 2006. [290] Varley CK. Psychopharmacological treatment of major depressive disorder in children and adolescents. JAMA 2003;290(8):1091–3. [291] Leonard HL, March J, Rickler KC, et al. Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6): 725–36. [292] Scharko AM. Selective serotonin reuptake inhibitor-induced sexual dysfunction in adolescents: a review. J Am Acad Child Adolesc Psychiatry 2004;43(9):1071–9. [293] Nilsson M, Joliat MJ, Miner CM, et al. Safety of subchronic treatment with fluoxetine for major depressive disorder in children and adolescents. J Child Adolesc Psychopharmacol 2004;14(3):412–7. [294] Weintrob N, Cohen D, Klipper-Aurbach Y, et al. Decreased growth during therapy with selective serotonin reuptake inhibitors. Arch Pediatr Adolesc Med 2002;156(7): 696–701. [295] Lake MB, Birmaher B, Wassick S, et al. Bleeding and selective serotonin reuptake inhibitors in childhood and adolescence. J Child Adolesc Psychopharmacol 2000;10(1):35–8. [296] Walkup J, Labellarte M. Complications of SSRI treatment. J Child Adolesc Psychopharmacol 2001;11(1):1–4. [297] Go FS, Malley EE, Birmaher B, et al. Manic behaviors associated with fluoxetine in three 12- to 18-year-olds with obsessive-compulsive disorder. J Child Adolesc Psychopharmacol 1998;8(1):73–80. [298] Guile JM. Sertraline-induced behavioral activation during the treatment of an adolescent with major depression. J Child Adolesc Psychopharmacol 1996;6(4):281–5. [299] Preskorn S. Targeted pharmacotherapy in depression management: comparative pharmacokinetics of fluoxetine, paroxetine and sertraline. Int Clin Psychopharmacol 1994; 9(Suppl 3):13–9. [300] Emslie GJ, Rush AJ, Weinberg WA, et al. Fluoxetine in child and adolescent depression: acute and maintenance treatment. Depress Anxiety 1998;7(1):32–9. [301] Emslie GJ, Heiligenstein JH, Hoog SL, et al. Fluoxetine treatment for prevention of relapse of depression in children and adolescents: a double-blind, placebo-controlled study. J Am Acad Child Adolesc Psychiatry 2004;43(11):1397–405. [302] Trivedi MH, Rush AJ, Wisniewski SR, et al. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry 2006;163(1):28–40. [303] Hamilton J, Bridge J. Supportive psychotherapy, SSRIs, and MDD. J Am Acad Child Adolesc Psychiatry 2006;45(1):6–7. [304] Beardslee WR, Salt P, Versage EM, et al. Sustained change in parents receiving preventive interventions for families with depression. Am J Psychiatry 1997;154(4):510–5. [305] Beardslee WR, Wright EJ, Salt P, et al. Examination of children’s responses to two preventive intervention strategies over time. J Am Acad Child Adolesc Psychiatry 1997;36(2): 196–204. [306] Brent DA, Poling K, McKain B, et al. A psychoeducational program for families of affectively ill children and adolescents. J Am Acad Child Adolesc Psychiatry 1993;32(4): 770–4. [307] Weisz JR. Psychotherapy for children and adolescents: evidence-based treatments and case examples. New York: Cambridge University Press; 2004.

162

JACKSON & LURIE

[308] Kazdin AE, Weisz JR. Evidence-based psychotherapies for children and adolescents. New York: Guilford Press; 2003. [309] Lewinsohn PM, Clarke GN, Hops H, et al. Cognitive-behavioral treatment for depressed adolescents. Behavior Therapy 1990;21(4):385–401. [310] Clarke GN, Lewinsohn PM, Hops H. Student workbook: adolescent coping with depression course. Eugene (OR): Castalia Publishing Co.; 1990. [311] Clarke GN, Lewinsohn PM, Hops H. Leader’s manual for adolescent groups: adolescent coping with depression course. Eugene (OR): Castalia Publishing Co.; 1990. [312] Reynolds WM, Coats KI. A comparison of cognitive-behavioral therapy and relaxation training for the treatment of depression in adolescents. J Consult Clin Psychol 1986; 54(5):653–60. [313] Wood A, Harrington R, Moore A. Controlled trial of a brief cognitive-behavioural intervention in adolescent patients with depressive disorders. J Child Psychol Psychiatry 1996;37(6):737–46. [314] Beck AT. Cognitive models of depression. Journal of Cognitive Psychotherapy 1987;1(1): 5–37. [315] Abramson LY, Metalsky GI, Alloy LB. Hopelessness depression: a theory-based subtype of depression. Psychol Rev 1989;96(2):358–72. [316] Beasley PJ, Beardslee WR. Depression in the adolescent patient. Adolesc Med 1998;9(2): 351–62. [317] Clarke GN, Lewinsohn PM, Hops H. Instructor’s manual for the adolescent coping with depression course. Available at: www.kpchr.org/public/acwd/acwd.html. Accessed January 15, 2006. [318] Clarke GN, DeBar LL, Lewinsohn PM. Cognitive-behavioral group treatment for adolescent depression. In: Kazdin AE, Weisz JR, editors. Evidence-based psychotherapies for children and adolescents. New York: Guilford Press; 2003. p. 120–34. [319] Lewinsohn PM, Rohde P, Hops H, et al. The coping with depression course: adolescent version. Instructor’s manual for the parent course. Available at: www.kpchr.org/public/ acwd/acwd.html. Accessed February 21, 2006. [320] Brent DA, Holder D, Kolko D, et al. A clinical psychotherapy trial for adolescent depression comparing cognitive, family, and supportive therapy. Arch Gen Psychiatry 1997;54(9): 877–85. [321] Weersing V, Brent DA. Cognitive-behavioral therapy for adolescent depression: comparative efficacy, mediation, moderation and effectiveness. In: Kazdin AE, Weisz JR, editors. Evidence-based psychotherapies for children and adolescents. New York: Guilford Press; 2003. p. 135–47. [322] Vostanis P, Feehan C, Grattan E, et al. A randomised controlled out-patient trial of cognitive-behavioural treatment for children and adolescents with depression: 9-month followup. J Affect Disord 1996;40(1–2):105–16. [323] Kroll L, Harrington R, Jayson D, et al. Pilot study of continuation cognitive-behavioral therapy for major depression in adolescent psychiatric patients. J Am Acad Child Adolesc Psychiatry 1996;35(9):1156–61. [324] Mufson L, Dorta KP, Moreau D, et al. Interpersonal psychotherapy for depressed adolescents. 2nd edition. New York: Guilford Press; 2004. [325] Mufson L, Dorta KP. Interpersonal psychotherapy for depressed adolescents. In: Kazdin AE, Weisz JR, editors. Evidence-based psychotherapies for children and adolescents. New York: Guilford Press; 2003. p. 148–64. [326] Mufson L, Weissman MM, Moreau D, et al. Efficacy of interpersonal psychotherapy for depressed adolescents. Arch Gen Psychiatry 1999;56(6):573–9. [327] Rossello J, Bernal G. The efficacy of cognitive-behavioral and interpersonal treatments for depression in Puerto Rican adolescents. J Consult Clin Psychol 1999;67(5):734–45. [328] Alexander JF, Parsons BV. Functional family therapy: principles and procedures. Monterey (CA): Brooks/Cole; 1992.

UNDERSTANDING & TREATING ADOLESCENT DEPRESSION

163

[329] Sexton TL, Alexander JF. Functional family therapy: a mature clinical model for working with at-risk adolescents and their families. In: Sexton TL, Weeks GR, Robbins MS, editors. Handbook of family therapy: the science and practice of working with families and couples. New York: Brunner-Routledge; 2003. p. 323–48. [330] Robin AL, Foster SL. Negotiating parent-adolescent conflict: a behavioral-family systems approach. New York: Guilford Press; 1989. [331] Haley J. Problem-solving therapy. 2nd edition. San Francisco (CA): Jossey-Bass; 1987. [332] Minuchin S. Families and family therapy. Cambridge (MA): Harvard University; 1974. [333] Brody LR, Hall JA. Gender and emotion. In: Lewis M, Haviland JM, editors. Handbook of emotions. New York: Guilford Press; 1993. p. 447–60. [334] Fivush R. Gender and emotion in mother-child conversations about the past. Journal of Narrative and Life History 1991;1(4):325–41. [335] Linehan MM. The empirical basis of dialectical behavior therapy: development of new treatments versus evaluation of existing treatments. Clin Psychol Sci Pract 2000;7(1): 113–9. [336] Linehan MM. Cognitive-behavioral treatment of borderline personality disorder. New York: Guilford Press; 1993. [337] Miller AL. Dialectical behavior therapy: a new treatment approach for suicidal adolescents. Am J Psychother 1999;53(3):413–7. [338] Miller AL, Rathus JH, Linehan MM, et al. Dialectical behavior therapy adapted for suicidal adolescents. Journal of Practical Psychiatry and Behavioral Health 1997;3:78–86. [339] Miller WR, Rollnick S. Motivational interviewing: preparing people for change. 2nd edition. New York: Guilford Press; 1992. [340] Shapiro F. Eye movement desensitization: a new treatment for post-traumatic stress disorder. J Behav Ther Exp Psychiatry 1989;20(3):211–7. [341] Van Etten ML, Taylor S. Comparative efficacy of treatments for posttraumatic stress disorder: a meta-analysis. Clin Psychol Psychother 1998;5:126–45. [342] Goenjian AK, Karayan I, Pynoos RS, et al. Outcome of psychotherapy among early adolescents after trauma. Am J Psychiatry 1997;154(4):536–42. [343] Richmond TK, Rosen DS. The treatment of adolescent depression in the era of the black box warning. Curr Opin Pediatr 2005;17(4):466–72.