CHILD AND ADOLESCENT DEPRESSION
From Stress, Vulnerability, and Serious Mental Disorders: Bridging the Gap from Science to Intervention, presented
by the American Society for Adolescent Psychiatry and the University of Texas Southwestern Medical Center
Gabrielle A. Carlson, MD, Professor of Psychiatry and Pediatrics, State University of New York at Stony Brook, and
Director, Child and Adolescent Psychiatry, Stony Brook University School of Medicine
| DUMPS: mnemonic for remembering symptoms of depression in young people; D stands for definite personality
change; child or adolescent who previously has been good student or “nice kid,” gradually or suddenly becomes
defiant, disagreeable, distant, or disorganized; U stands for undesirable drop in grades; adolescent whose grades
fall, eg, from As to Cs over one semester, who starts to avoid school altogether, or who develops “school phobia”;
M stands for morbid preoccupation; eg, adolescent whose compositions dwell on death and disaster, who voices
suicidal thoughts, or who engages in self-destructive behavior; P stands for pessimism and/or psychosis; adolescent
grim, depressed, or demoralized and finds no joy in anything; psychosis not common in adolescents, but does
occur, and often manifested by sudden onset of depressive hallucinations and/or delusions; S stands for somatic
complaints without physical basis; adolescent spends more time in nurse’s office than in classroom
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| Epidemiology: in community samples, depression rare in preschool-age children (<1%), 2% to 4% in school-age
children, and ≈8% in adolescents; in clinical samples, rates higher (in speaker’s clinic, ≈1% in preschool-age children,
15% in school-age children, and 40% in adolescents); rates do not take comorbidity into account; prior to
puberty, rates equal in boys and girls; after puberty, rates increase in girls and decrease in boys (thought to be because
girls respond more to interpersonal events, tend to respond to sad moods with ruminative cognitive style,
and enter puberty earlier, with attendant biologic, psychosocial, and hormonal changes); cohort effect—shows
earlier age of onset with each successive decade after World War II (may be more applicable to comorbid or secondary
depression)
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| Risk factors: prepubertal depression often comorbid with externalizing disorder (eg, attention-deficit/hyperactivity
disorder [ADHD] or oppositional defiant disorder), and risk factors for depression same as those for externalizing
disorders (ie, family discord, parental criminality, and substance abuse); prepubertal group also includes children
with multigenerational family “loading” for anxiety and bipolar disorder; in adolescents, risk factors include early
onset of puberty (especially in girls), substance abuse, decreased supervision, and sleep deprivation
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| Comorbidity: 40% to 70% of depressed youth have comorbid disorder that almost always precedes onset of depression;
20% to 50% have ≥2 comorbid disorders; anxiety disorders—occur in 30% to 80%; separation anxiety
most common in children, social phobia in teens; anxiety disorder precedes onset of depression in about two-thirds
of patients, but does not affect course of depression; learning and language disorders can precipitate depression if
other children treat sufferer unkindly or shun him or her; substance abuse common comorbidity among adolescents,
who often use tobacco, alcohol, or drugs to self-medicate depression
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| Developmental aspects of mood disorders in children: disinhibition, activation, or manic switching more common
in prepubertal children (actual rates controversial, but one study found 10% in prepubescent children, 3% in
teens); in younger children, presenting symptoms usually somatic, and pervasive anhedonia less apparent; visual hallucinations
not uncommon, and speaker has “never known what to make of that; I don’t think they carry the same significance
that they do in older people with psychosis”; she posits that hallucinations in younger children probably not
evidence of psychotic depression; teenagers—irritability prominent symptom; sometimes have atypical depression, in
which they sleep more, eat more, and are lethargic instead of insomniac; by adolescence, psychosis begins to resemble
adult psychosis; in adults, “full-fledged” melancholia and delusions seen
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| Assessment: clinical developmental interview important in understanding historical, contextual, and temporal factors;
determine onset of depression in relationship to other problems; obtain information from patient, parents, and
school; structured interviews can be helpful if therapist good at interviewing and force therapist to ask “all the questions,”
even about things that child or parents do not bring up; ideally, before seeing patient, have child and parents
complete Child and Adolescent Symptom Inventory and Child Behavior Checklist and Report Form (also called
Achenbach Scale); parents may misunderstand intention of questions, so review answers with them; while talking
to parents, have child complete Youth Inventory, depression and anxiety rating scale, and sentence-completion task;
some children who are reluctant to talk about their problems may be willing to write about them
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 | Look for: psychiatric and medical problems; severity; suicidality; comorbidity; psychosocial stressors; cognitive
ability; use information to determine whether child sick enough to need hospitalization; decide what needs to be
treated first, or whether conditions can be treated simultaneously (depression and substance abuse probably
should be treated first)
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| Neurobiologic correlates: in some respects, childhood and adolescent depression similar to adult depression, and
in other respects, different; children do not seem to have same neurobiologic response to various probes (eg, cortisol
secretion, corticotropin stimulation, serotonin probes, immunity indices) as adults, and response to probes may
differ even between children and adolescents; known that neurobiologic systems implicated in depression not fully
developed in children and teens, but more research needed to understand developmental differences between child,
adolescent, and adult mood disorders
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| Genetics: monozygotic and dizygotic twin studies seem to show genetic diathesis to depression, although when information
collected from parents, results differ from those obtained from their child (ie, information provided by
parents indicates depression very heritable, but information provided by child indicates more environmental and
psychosocial influences); however, “clearly it’s a familial disorder”; studies show that offspring of depressed
parents 3 times more likely to develop depression and that early-onset parental depression increases risk of offspring
having depression, compared to psychiatric and nonpsychiatric controls
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| Psychosocial stressors that contribute to development of depression include: divorce; loss; penetrating sexual
abuse; certain medical conditions; learning disabilities; poverty; expressed emotion; living with parent who is
highly judgmental and critical; also, some temperaments seem more prone to development of depression
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| Outcomes: children usually do not spend entire day moping, but when asked about depressive symptoms, often report
that they occur more days than not during week; episodes can last 6 to 9 mo; although remission rate high, relapse
rate also high; likelihood of developing adult depression greater if individual has depression in adolescence
than in childhood; 4% to 49% of children with early-onset depression go on to develop bipolar disorder (“that’s a
lot of slippage”), but speaker believes it is probably 10% to 20%; risk factors include acute severe depression, psychomotor-retarded
depression with psychosis, family history of bipolar disorder, and possibly pharmacologically
induced mania; adverse outcomes include suicide, drug and alcohol abuse, social impairment, school dropout, and
adult depression
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| Treatments: empirically supported treatments include cog-nitive behavioral therapy (CBT), interpersonal psychotherapy
(IPT), selective serotonin reuptake inhibitors (SSRIs; mostly fluoxetine), and electroconvulsive therapy
(ECT)
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| CBT: based on premise that changing thoughts and behavior improves mood (“cognitive restructuring”); remission
rates good but, for unknown reasons, some studies show better outcomes than others
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| IPT: focuses on interpersonal issues such as recent loss, interpersonal roles and difficulties, role transitions, and personal
values; teaches effective communicating; outcomes favorable, but studies small
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| Medications: select medication by severity of depression; in most studies, the more severe the depression, the less
likely it is to respond to CBT or IPT; important considerations include how other family members feel about having
child or adolescent on medication, recurrence or chronicity of depression, failure to respond to psychotherapy,
unavailability of therapist trained in psychotherapy, and psychosocial stressors that might interfere with medication
use; begin with psychoeducation of patient and family; discuss treatment options and supportive evidence;
visits more intense at beginning of therapy, can be less intense after child responds; reassess treatment at regular
intervals—if no response or partial response by 6 wk, decide whether to continue current treatment regimen or to
change; may take up to 12 wk to get robust response to antidepressant; establish targets and measure progress
with rating scales; extensive medical work-up not necessary unless history suggests it; probably wise to obtain
baseline blood tests and thyroid levels; dose ranges wider for children and adolescents than for adults; no data indicating
differences in side effects based on sex; monitor child for bipolar switching and for suicide risk; other issues
include child’s age, presence of comor-bidities, level of premorbid functioning, family competence, where
medication used, and cost and availability of medication
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| More on medications: if patient has history of mania or bipolar disorder, start with mood stabilizer; if evidence of
psychosis, start with antipsychotic agent (currently, more data available for atypical than typical antipsychotics);
fluoxetine—SSRI with most consistent positive response; start teenagers at 10 mg/day, younger children at 5
mg/day; doses can be increased up to 60 to 80 mg/day; if no response, switch to another SSRI or to bupropion
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| Treatment of Adolescent Depression Study (TADS): showed children who received combined CBT and fluoxetine
treatment did best, but not much difference between combination and fluoxetine alone; CBT and placebo similar;
at end of study, 80% of patients no longer met criteria for depression, but while response rate “wasn’t bad,” remission
rate “wasn’t so hot”; absolute benefit for combined treatment 35%, for fluoxetine alone 26%, and for
CBT alone 7%; few other studies exist in children and adolescents
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| Summary of continuation treatment: 90% of children and adolescents recovered from index episode of depression
over 1 to 2 yr, whether or not they received medication; risk for recurrence appeared to be greater in patients who
stopped fluoxetine or sertraline, compared to those who continued medication
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| How to treat: residual symptoms shown to predict relapse; longer initial treatment results in fewer residual symptoms;
general consensus to treat 4 to 6 mo after initial treatment; most suggest full-dose continuation treatment
for 6 to 9 mo; if child has multiple depressions, full-dose continuation treatment for up to 5 yr
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| No or partial remission: may be due to patients not taking medications; check for noncompliance, parental depression,
cohort substance abuse, comorbid conditions, undiagnosed mixed states, medical conditions, and rapid drug
metabolism
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| Electroconvulsive therapy: no controlled trials, but many literature reviews suggest ECT helpful for patient who
is very depressed or very manic, or who did not respond to medication trial; no absolute contraindications; assessment
must include psychiatric, medical, and cognitive factors before ECT, and at 3 and 6 mo after ECT; obtain informed
consent
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| Adverse events associated with treatment: include activation and behavioral disinhibition, symptoms of which
include irritability, hyperactivity, inappropriate behavior, euphoria, akithisia, agitation, and suicidality; if symptoms
stop when medication dose lowered or discontinued, then side effects probably from medication; suicide
rates tend to be higher in younger children than in teenagers and higher in teenagers than in adults; activation
rates vary with SSRI, but overall rates ≈10% in younger children and 3% to 4% in teens
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| Serotonin syndrome: some people think activation rep-resents mild serotonin syndrome; activation, nausea,
diarrhea, dizziness, and chills relatively common; serotonin syndrome can be fatal and needs to be monitored
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| Conclusions: monitor suicide risk; educate family and patient; provide explanatory models; treat parent if depressed;
find appropriate therapeutic environment at home, in classroom, or out of home if necessary; develop realistic
expectations (“control what you can control”); identify and use patient resources; teach mastery experiences
(accomplishing small tasks important); encourage generation of alternative beliefs; encourage appropriate expression
of thoughts and feelings
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Suggested Reading
Carlson GA et al: What is new in bipolar disorder and major depressive disorder in children and adolescents. Child Adolesc
Psychiatr Clin N Am 11:xv, 2002; Carlson GA: Mania and ADHD: comorbidity or confusion. J Affect Disord
51:177, 1998; Carlson GA: The challenge of diagnosing depression in childhood and adolescence. J Affect Disord 61 Suppl
1:3, 2000; Cheung AH et al: Review of the efficacy and safety of antidepressants in youth depression. J Child Psychol
Psychiatry 46:735, 2005; Daviss WB et al: Bupropion sustained release in adolescents with comorbid attention-deficit/hyperactivity
disorder and depression. J Am Acad Child Adolesc Psychiatry 40:307, 2001; Emslie GJ et al: Fluoxetine in
child and adolescent depression: acute and maintenance treatment. Depress Anxiety 7:32, 1998; Emslie GJ 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 43:1397, 2004; Emslie GJ et al: Venlafaxine ER for the treatment of pediatric subjects
with depression: results of two placebo-controlled trials. J Am Acad Child Adolesc Psychiatry 46:479, 2007; Findling RL
et al: The relevance of pharmacokinetic studies in designing efficacy trials in juvenile major depression. J Child Adolesc Psychopharmacol
16:131, 2006; Hughes CW et al: Texas Children's Medication Algorithm Project: update from Texas Consensus
Conference Panel on Medication Treatment of Childhood Major Depressive Disorder. J Am Acad Child Adolesc
Psychiatry 46:667, 2007; Kaufman J et al: Are child-, adolescent-, and adult-onset depression one and the same disorder?
Biol Psychiatry 49:980, 2001; Keller MB et al: Efficacy of paroxetine in the treatment of adolescent major depression: a
randomized, controlled trial. J Am Acad Child Adolesc Psychiatry 40:762, 2001; Kim-Cohen J et al: Prior juvenile diagnoses
in adults with mental disorder: developmental follow-back of a prospective-longitudinal cohort. Arch Gen Psychiatry
60:709, 2003; Klein DN et al: Toward guidelines for evidence-based assessment of depression in children and adolescents. J
Clin Child Adolesc Psychol 34:412, 2005; March J et al: Fluoxetine, cognitive-behavioral therapy, and their combination
for adolescents with depression: Treatment for Adolescents With Depression Study (TADS) randomized controlled trial. JAMA
292:807, 2004; Rice F et al: The genetic aetiology of childhood depression: a review. J Child Psychol Psychiatry 43:65,
2002; Rutter M et al: Continuities and discontinuities in psychopathology between childhood and adult life. J Child Psychol
Psychiatry 47:276, 2006; Wagner KD et al: An open-label trial of divalproex in children and adolescents with bipolar
disorder. J Am Acad Child Adolesc Psychiatry 41:1224, 2002; Weiss B et al: Developmental differences in the phenomenology
of depression. Dev Psychopathol 15:403, 2003.
Educational Objectives
| The goal of this program is to improve diagnosis and treatment of child and adolescent depression. After hearing and
assimilating this program, the clinician will be better able to:
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| Use the mnemonic “DUMPS” to remember the symptoms of depression in young people.
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| List the risk factors for development of depression in young people.
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| Discuss the developmental aspects of mood disorders in children and adolescents.
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| Assess children and adolescents for depression.
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| Describe treatment options, including cognitive behavioral therapy, interpersonal psychotherapy, medications,
and electroconvulsive therapy, for children and adolescents with depression.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, the Audio-Digest Foundation requires all faculty members to disclose
relevant financial relationships within the past 12 months that might create any personal conflict of interest. Any identified
conflicts were resolved to ensure that this educational activity promotes quality in health care education and not a
proprietary business or commercial interest. For this program, Dr. Carlson disclosed she is a speaker for Shire and Lilly; is a
consultant for Lilly, Janssen, Bristol-Myers Squibb, and Otsuka; and does contracted research for Lilly, Janssen, BMS, Otsuka,
and Sanofi-Aventis.
Acknowledgements
Dr Carlson was recorded at Stress, Vulnerability and Serious Mental Disorders: Bridging the Gap from Science to Intervention,
held March 8-11, 2007, and sponsored by the American Society for Adolescent Psychiatry and the University of
Texas Southwestern Medical Center. The Audio-Digest Foundation thanks Dr. Carlson and the sponsors for their cooperation
in the production of this program.
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