IACAPAP Textbook of Child and Adolescent Mental Health

Chapter

E.1

MOOD DISORDERS

DEPRESSION IN CHILDREN AND
ADOLESCENTS
2015 Edition

Joseph M Rey, Tolulope T Bella-Awusah & Jing Liu

Joseph M Rey MD, PhD,FRANZCP

Professor of Psychiatry, Notre
Dame University Medical
School Sydney & Honorary
Professor, University ofSydney Medical School,
Sydney, Australia
Conflict of interest: none
declared

Tolulope T Bella-Awusah
MBBS(IB), FWACP

Department of Psychiatry,
College of Medicine, Universityof Ibadan & University College
Hospital, Ibadan, Nigeria
Conflict of interest: none
declared

Jing Liu MD

Photo from repowerup.com

Professor & Director, Clinical
Department for Children
and Adolescents, Mental
Health Institute & the Sixth
Hospital, Peking University,
Beijing, China. Vice-President,
Asian Society for Child andAdolescent Psychiatry & Allied
Professions

This publication is intended for professionals training or practicing in mental health and not for the general public. The opinions
expressed are those of the authors and do not necessarily represent the views of the Editor or IACAPAP. This publication seeks todescribe the best treatments and practices based on the scientific evidence available at the time of writing as evaluated by the authorsand may change as a result of new research. Readers need to apply this knowledge to patients in accordance with the guidelines andlaws of their country of practice. Some medications may not be available in some countries and readers should consult the specific drug
information since not all dosages and unwanted effects are mentioned. Organizations, publications and websites are cited or linked toillustrate issues or as a source of further information. This does not mean that authors, the Editor or IACAPAP endorse their content or
recommendations, which should be critically assessed by the reader. Websites may also change or cease to exist.
©IACAPAP 2015. This is an open-access publication under the Creative Commons Attribution Non-commercial License. Use,
distribution and reproduction in any medium are allowed without prior permission provided the original work is properly cited and theuse is non-commercial. Send comments about this e-book or chapter to jmreyATbigpond.net.au
Suggested citation: Rey JM, Bella-Awusah TT, Jing L. Depression in children and adolescents. In Rey JM (ed), IACAPAP e-Textbook
of Child and Adolescent Mental Health. Geneva: International Association for Child and Adolescent Psychiatry and Allied Professions
2015.

Depression E.1

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IACAPAP Textbook of Child and Adolescent Mental HealthMajor depression is an episodic, recurring disorder characterized bypersistent and pervasive sadness or unhappiness, loss of enjoymentof everyday activities, irritability, and associated symptoms such as
negative thinking, lack of energy, difficulty concentrating, and appetite and sleep
disturbances. Manifestations can vary according to age, gender, educational andcultural background. The various subtypes of depression are identified on the basisof symptom severity, pervasiveness, functional impairment, or the presence orabsence of manic episodes or psychotic phenomena. There is still much argument
about whether depression is a dimensional illness—the difference between having
and not having depression is quantitative, a matter of degree, such as in the caseof hypertension—or categorical (i.e., difference is qualitative), and whether there
are several etiologically different types of depression (e.g., melancholic and nonmelancholic).

Conflict of interest: none
declaredAcknowwledgements:
our thanks to Drs Olga
Rusakovskaya (Russia) and
Jenifer Bergen (Australia)
and for their comments

The terms “depression,” “depressive episode,” “depressive disorder” and“clinical depression” will be used throughout the chapter to mean what DSM-5
defines as “major depressive episode” or “major depressive disorder,” and ICD10 “depressive episode” and “recurrent depressive disorder.” Unless otherwise
specified, all the information in this chapter refers to unipolar depression.

EPIDEMIOLOGY
Prevalence varies depending on the population (e.g., country), the period
considered (e.g., last three months, last year, lifetime), informant (e.g., parent, child,both), and criteria used for diagnosis. Most studies concur that about 1% to 2% of
pre-pubertal children and about 5% of adolescents suffer from clinically significant
depression at any one time. The cumulative prevalence (accumulation of new cases
in previously unaffected individuals, also known as lifetime prevalence) is higher.
For example, by the age of 16 years 12% of girls and 7% of boys would have had adepressive disorder at some time in their lives (Costello et al. 2003). Prevalence ofdysthymic disorder is less well known but studies suggest a point prevalence ranging
from 1% to 2% in children and 2% to 8% in adolescents. A further 5% to 10% ofyoung persons have been estimated to exhibit sub-syndromal depression (or minor
depression). Youth with minor depression show some functional impairment,
increased risk of suicide and of developing major depression.

Gender and culture
The ratio of depression in males and females is similar in pre-pubertal
children but becomes about twice as common among females compared withmales during adolescence. Although information is limited, the data available
suggest that rates of depression are higher among patients who suffer from chronic
medical conditions and in particular groups, such as developmentally disabled
or indigenous minority children (e.g., Native Americans, Eskimos, Australian
Aborigines).

Burden of illness
Depression poses a substantial burden to the individual suffering from thisdisorder and to the society at large. Interpersonal relationships are particularly
likely to suffer when someone is depressed—few families and friends are likely
to be untouched by depression. Further, depression is likely to progress into achronic, recurring disease if not treated. The burden of depression is increased
because it appears to be associated with behaviours linked to other chronic diseases

Depression E.1••

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IACAPAP Textbook of Child and Adolescent Mental Healthsuch as smoking, alcohol consumption, physical inactivity and sleep disturbanceamong others, although the nature of the association is still unclear (CDC, 2013).
Specific data on the economic burden of depression in childhood are currently
unavailable. However, assuming a large continuity of the disorder into adulthood,burden is likely to be very substantial. For example, one study estimated that arandomly selected 21-year-old woman with early-onset major depressive disordercould expect future annual earnings that were 12% to 18% lower than those of arandomly selected 21-year-old woman whose onset of depressive disorder occurred
after age 21 or without depression (Berndt et al, 2000).

AGE OF ONSET AND COURSE
Depressed patients can display symptoms of depression at any age; however,the pattern varies slightly according to developmental stage, resulting in differencesin the way depression manifests itself through the lifespan, as highlighted in Table
E.1.1.
Age at onset does not seem to define separate depressive subgroups, butearlier onset is associated with multiple indicators of greater illness burden in
adulthood across a wide range of domains such as never being married, more
impaired social and occupational functioning, poorer quality of life, greater
medical and psychiatric comorbidity, more lifetime depressive episodes and suicide
attempts, and greater symptom severity (Berndt et al, 2000).

Is youth depression
increasing?
Some researchers havesuggested there has beena secular increase in theprevalence of depression
with higher rates among
those born later in the20th century. This is notdefinite for the quality ofthe studies supporting
this finding is suboptimaland more often than not
retrospective. It is possiblethat the perceived increase
may be due to greaterawareness of children’s
symptoms by their parents
or an earlier age of onset.

Although to diagnose clinical depression it is required that symptoms bepresent every day, most of the day for at least two weeks, adolescents, particularly
those who suffer from mild or moderate depression, often have a reactive affect andcan, with effort, hide their symptoms.

Table E.1.1 Differences in the presentation of depression
according to age. These symptoms can all be present at any age
but are more common in the age group specified.
Pre-pubertal
children••••

Irritability (tempertantrums, noncompliance)
Affect is reactive*
Frequently comorbidwith anxiety,behavior problems,and ADHD
Somatic complaints

Adolescents
•
•
•
•
•
•

Irritability (grumpy, hostile,easily frustrated, angry
outbursts)
Affect is reactive*
Hypersomnia
Increased appetite andweight gain
Somatic complaints
Extreme sensitivity torejection (e.g., falsely
perceived putdown or
criticism) resulting, forexample, in difficulties
maintaining relationships.

Adults•••••Anhedonia
Lack of affective
reactivity
Psychomotor agitation
or retardation
Diurnal variation ofmood (worse in themorning)
Early morning waking*Ability to be momentarily cheered up in response to positive events (e.g., visit by peers).

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IACAPAP Textbook of Child and Adolescent Mental Health

CourseSimilar to what happens in adults, clinical depression in youth follows arecurring course. An episode of depression in clinically referred patients lasts 7 to
9 months on average, but it can be shorter in non-referred community samples.
That is, depressive episodes are, on average, a spontaneously remitting illness.
Conversely, there is a 40% probability of recurrence within 2 years. Recurrenceis high even after treatment. For example, participants in the 5-year follow up of
the Treatment of Adolescent Depression Study (TADS) showed that although theimmense majority (96%) of patients recovered from the index episode, after five
years almost half (46%) had a recurrence (Curry et al, 2010).
The likelihood of further episodes in adulthood is up to 60% (Birmaher etal, 1996). Thus, depressive illness should optimally be conceptualized as a chronic
condition with remissions and recurrences. This has important implications for
management, which should seek not only to reduce the duration of the current
depressive episode and lessen its consequences but also to prevent recurrences.
Predictors of recurrence include poorer response to treatment, greater severity,
chronicity, previous episodes, comorbidity, hopelessness, negative cognitive style,family problems, low socioeconomic status, and exposure to abuse or family
conflict (Curry et al, 2010).

SUBTYPES OF DEPRESSION
Subtyping depressive illness is relevant because different types of depression
may have implications for treatment and prognosis. For example, seasonal mooddisorder may specifically respond to light therapy, and treatment of bipolar
depression is different from that of unipolar depression. With the exception of theunipolar/bipolar distinction, many other subtypes (e.g., primary and secondary,endogenous and reactive, neurotic and psychotic) have been proposed over theyears, usually without convincing empirical data or evidence of clinical value.
There are currently differences of opinion about the usefulness of the melancholicvs. non-melancholic dichotomy. Some of these concepts are still popular in somecountries or settings. The most widely used subtypes of depression, irrespective of
their scientific validity, are summarized in Table E.1.2.

ETIOLOGY AND RISK FACTORSThe etiology of depression is complex, multifactorial, and the object of muchacademic argument. As a result, it is not discussed here in detail. Interested readers
may wish to consult the summary by Krishnan and Nestler (2010). Research
has uncovered a multitude of factors associated with the onset, maintenance orrecurrence of depression. This can be confusing or lead to false expectations (e.g.,that dealing with the risk factor may in itself be enough to resolve the depression).
Risk factors that have implications for prevention, detection or treatment are listed
in Table E.1.3.

Affect reactivity
in depressedadolescents“ ‘This morning I will
get out of bed. This
morning I will go toschool. Today I will
finish my maths test. I
will hand in my English
project and during
the lunch break I willsocialize with myfriends. I will laugh,joke and talk with
my friends. I will tell
witty stories about myweekend and before
I know it the schoolday will be over andno one will know how
I am feeling on theinside. Then when
I get home I can goback to bed and nothave to pretend foranyone anymore.’
The words above are froma journal entry I wrote on
April 20, 2000. At the time I
was 14 years old.”
Nathan B. “And Then My

Tears Subsided...”http://www.blackdoginstitute.
org.au/docs/
AndThenMyTearsSubsided.pdf

In summary, depression in youth appears to be the result of complex
interactions between biological vulnerabilities and environmental influences.
Biological vulnerabilities may result from children’s genetic endowment and fromprenatal factors. Environmental influences include children’s family relationships,
cognitive style—most depressed adolescents experience negative thoughts about
themselves, the world or the future that seem to arise spontaneously (automatic
thoughts), which contribute to a negative cognitive style—stressful life events,

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IACAPAP Textbook of Child and Adolescent Mental Health

Table E.1.2. Subtypes of depression relevant to clinical practice.
Unipolar depression

Depression without history of a manic, mixed or hypomanic episode.

Bipolar depression

When there is history of at least one non drug-induced manic, hypomanic ormixed episode.

Psychotic depression

The young person displays hallucinations or delusions in addition tosymptoms of major depression in the absence of other psychotic disorder.

Melancholic depression, major
depression with melancholicfeatures, or melancholia

Episodes are characterized by prominent neurovegetative changes suchas weight loss, psychomotor retardation, marked sleep disturbance, diurnal
mood variation, early morning waking and lack of reactivity. Melancholic
depression is largely equivalent to “endogenous” depression.

Dysthymic disorder or dysthymia

A chronically depressed mood for at least one year but not severe enough toqualify for a diagnosis of depression; symptom-free intervals last less than
two months

Double depression

The depressive episode occurs in a patient already suffering from dysthymia.

Catatonic depression

When the mood disorder presents with symptoms of stupor.

Post-psychotic depression

When it occurs in the course of schizophrenia, often after resolution of theflorid psychotic symptoms

Premenstrual dysphoric disorder

Premenstrual mood changes—dysphoria, tension, irritability, hostility, andlabile mood—that mimic depression. Its nature and validity are still beingargued.

Seasonal depression, major
depression with seasonal pattern,seasonal affective disorder

The beginning and remission of major depression follow a pattern (for atleast two years) related to specific times of the year, usually onset during
autumn or winter and remission in spring.

Mood disorder not otherwise
specified (NOS)

Significant mood symptoms and impairment that do not meet criteria for a
specific mood disorder often due to mixed presentations (e.g., depressive
and manic symptoms).

Adjustment disorder with depressedmood

Clinically significant depressive symptoms or impairment occur within threemonths of identifiable stressors and do not meet criteria for major depression
or bereavement. It is expected that symptoms will disappear within six
months once stressors have ceased.

Minor depression, subsyndromal
depression, subclinical depression

Depressive symptoms fall short of meeting the criteria for depression (e.g.,
one core symptom, and one to three associated symptoms, and very mild
disability).

and school and neighborhood characteristics. Parental depression is the mostconsistently replicated risk factor for depression in the offspring. Stressful life
events—especially losses—may increase the risk for depression; this risk ishigher if children process loss events (or other stressful life events) using negative
attributions. Parental lack of care and rejection may also be relevant.

COMORBIDITY
Comorbidity, the simultaneous occurrence of two or more distinct illnesses
in the one individual, is a common and complex issue across all child and adolescentmental disorders that has great theoretical and practical implications—for example
for treatment—and is still not well understood.
Data from community surveys suggest that depression comorbid with otherdisorders is frequent in children and adolescents. This is particularly the case inclinic settings because the likelihood of referral is a function of the combined

Depression E.1

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IACAPAP Textbook of Child and Adolescent Mental Healthlikelihood of referral for each disorder separately—the so called Berkson effect.
Patients with comorbid disorders show greater impairment than those with a single
diagnosis. Comorbidity is also associated with worse adult outcomes. For example,
childhood depression comorbid with conduct disorder or substance abuse isassociated with a higher likelihood of severe or violent offending by age 24 thanwhen depression, conduct disorder or substance misuse occur alone (Copeland etal, 2007).
Psychiatric disorders often comorbid with depression include anxiety
disorders, conduct problems, attention deficit hyperactivity disorder (ADHD),
obsessive compulsive disorder, and learning difficulties. An epidemiologicalstudy (Costello et al, 2003) showed that in a three-month period, 28% of theyoung people diagnosed with a depressive disorder also had an anxiety disorder,
7% ADHD, 3% conduct disorder, 3% oppositional defiant disorder, and 1%
substance use disorder. The practical implication is that establishing whether achild shows symptoms of one condition (e.g., depressive illness) is only a first stepin the evaluation; clinicians ought to enquire for symptoms of other conditions as
well.
The link between depression and anxiety is well-known because depressive
and anxiety symptoms often coexist and individuals frequently experience
depressive and anxiety episodes at different times in their lives. Suffering froma depressive episode not only increases the risk of further depressive episodes(homotypic continuity) but also of anxiety disorders (heterotypic continuity).
Depression is frequently comorbid with post-traumatic stress disorder (seechapter F.5). In particular, adolescents are vulnerable to depression and suicidality
in the year following a traumatic event. Mechanisms include so-called survivor guilt(that others died or were severely injured), complicated bereavement, problems incarrying out tasks of daily living owing to impaired concentration or intrusive
memories, and distress arising from chronic anxiety symptoms. Other psychiatriccomplications of traumatic stress that may interact with depression include panic
disorder, other anxiety disorders, disruptive behaviors, dissociative disorder, andsubstance misuse.

Depression and personality style
Personality traits become progressively established during adolescenceand early adulthood and personality styles can influence the presentation and“Masked”
depression
Until the second half ofthe 20th century childhood
depression was largely
believed not to exist. In
the 1950s new theories
emerged postulatingthat depression in thisage group did exist but
did not express itself
as such but through“depressive equivalents”.
These included conduct
problems, hyperactivity,
somatic complaints,
enuresis, and school
problems. That is, children
could be depressed but
expressed their depression
differently from adults—“masked depression”.
The concept of masked
depression was heavily
criticized and subsequently
largely abandoned. By
the 1970’s researchersbegan to show thatchildhood depression did
exist and by and large has
similar symptoms as inadults. While depressedchildren may initiallypresent with a variety ofsymptoms that conceal thedepression (e.g., tantrums,
headaches, tiredness,
problems concentrating) a
competent clinician shouldbe able to uncover the
depression (Carlson &Cantwell, 1980).

Gene-environment interaction: the serotonin transporter gene, childhood maltreatment
and depression.
New Zealand’s Dunedin Health and Development Study followed a cohort of 1,037 children from 3 to 26 years of age carefully
tracking the development of psychiatric disorders, serious life events and other factors such as childhood mistreatment. A
report based on these data concluded that a functional polymorphism of the serotonin transporter gene (5-HTT) moderated
the influence of stressful life events on the development of depression. That is, individuals with the short allele of this gene
were more likely to develop depression in response to severe stressors or maltreatment during childhood, compared to thosewith the long allele exposed to the same experiences (Caspi et al, 2003).
This finding caused much excitement because it seemed to finally prove a plausible gene-environment interaction in thecausation of depression. However, a subsequent meta-analysis concluded that alterations in the serotonin transporter
gene alone or in combination with stressful life events were not associated with an elevated risk of depression (Risch etal, 2009). Another meta-analysis published not long after (Karg et al, 2011) reached the opposite conclusion, while anadditional prospective study—also from New Zealand—failed to confirm such an association (Fergusson et al, 2011). Clearly
more research is needed to resolve this tantalizing issue, which highlights the importance of replication before findings are
accepted, let alone used in clinical practice (e.g., to detect vulnerability for depression).

Depression E.1

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IACAPAP Textbook of Child and Adolescent Mental HealthSocialFamilyPsychological

Biological

TABLE E.1.3. Risk factors and their implications for prevention, detection or treatment
Risk Factor

Implications for prevention, detection ortreatment

Family history of depression

Increase suspicion of depression when there is a positive family
history of depression or suicide.

Parental substance use or
alcohol misuse

Detect and treat parental substance use.

Family history of bipolar
disorderIncrease suspicion that depression might be bipolar. Implications
for pharmacological management.

Female gender

Female adolescents who attend family doctors should bescreened for depression.

Puberty

Depression is much more common in post-pubertal adolescents,
particularly females. Early menarche (<11.5 years) increases therisk. Screen adolescents for depression.

Chronic medical illness

Exclude depression in patient with chronic physical illness or
disability.

Previous history of depression

Relapse-prevention strategies integral part of treatment.

Comorbid psychiatric disorder,
particularly anxiety

Detection and treatment of comorbid psychiatric disorders.

Neurotic or highly emotionaltemperamental style

Detection of individuals at risk and targeted preventive
interventions.

Negative cognitive styles, low
self-esteem

Detection of individuals at risk and targeted preventive
interventions.

TraumaDetection of individuals at risk and targeted preventive
interventions.

Bereavement and losses

Detection of individuals at risk and targeted preventive
interventions.

Abuse, neglect

Targeted preventive interventions such as parenting and abuse
prevention programs.

Negative parenting styles:
rejection, lack of care

Targeted preventive interventions such as parenting programs.

Parental mental disorder

Detection and treatment of mental disorder in parents. Targeted
preventive interventions such as parenting programs andsupport.

Parent-child conflict

Parent education and parenting programs.

Bullying

Bullying prevention programs at school.

Child and adolescentoffenders

Detection of individuals at risk and targeted preventive
interventions.

Institutionalised or fosteredchildren, refugees, homeless,asylum seekers

Detection of individuals at risk and targeted preventive
interventions.

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IACAPAP Textbook of Child and Adolescent Mental Health

AY, a 14-year old Nigerian female, currently in her fourth year in secondary school, was brought to the hospital about fourhours after ingesting a small quantity of a concentrated antiseptic solution with the intention of killing herself. She complainedof having felt sad most of the time over the past 6 months and thinking about death a lot. Her decision to drink the poison
had come after learning that she would have to repeat a year at school. Prior to this, her grades had been progressively
worsening. She felt guilty because her poor school performance was causing a drain in her father’s finances. AY described
longstanding difficulties with falling and staying sleep. She still enjoyed watching TV and playing with her friends, but had
begun to find it increasingly difficult to carry out her household chores because she felt weak and tired. Her family interpreted
this as laziness and she often got scolded or beaten for leaving her chores unfinished. She also felt isolated from herclassmates because of her poor school performance.
AY’s mother had suffered episodes of mental illness in the past and was separated from AY’s father, who had since remarried. AY and her four siblings were living with a paternal aunt because the extended family were afraid that they would
contract mental illness from their mother. Although the mother now lived and worked successfully in another town, AY only
saw her briefly once or twice a year. Her father lived even farther away and she almost never saw him.

manifestation of a depressive illness. This is clearer in adults but it occurs also in
the young. Adolescents’ underlying personality features are amplified when they
are depressed. For example, those who are anxious tend to show higher levels ofanxiety, avoidance and somatic symptoms when depressed (anxious depression),those who are externalizers are likely to show more hostility and irritability.
Borderline personality styles (see Chapter H.5) are particularly relevant todepression as individuals with these traits are dysphoric and extremely sensitive torejection. Their fears of abandonment can be accompanied by intense but usually
brief episodes of sadness, anger, or irritability, which sometimes culminate inincidents of self-harm. Both a depressive disorder and borderline personality traits
or disorder can coexist. Depression may, on the one hand, be misdiagnosed whenadolescents with borderline personality traits present with sadness, irritability, andself-loading. On the other hand, a depressive episode can exaggerate personality
characteristics suggesting that a personality disorder may exist when that is not thecase. In the latter situation, the symptoms of personality disorder would remit once
the individual has recovered from the depressive episode. Diagnosis of personality
disorder should be provisional in a depressed adolescent and made on the bases ofsymptoms and functioning outside of the depressive episode.

Depression and suicidal behavior
Suicide is one of the leading causes of death in adolescents worldwide.
For each completed suicide in adolescents, there are about 100 reported suicide
attempts. Suicidal thoughts are common among the young; about one in six girls
aged 12 to 16 reports having them in the previous six months (one in ten for boys)
but rates in clinic samples are much higher. While suicide is the result of complex
interactions in which individual and psychosocial factors as well as mental healthproblems play a role, there is considerable evidence that depression is the strongest
individual risk factor (although there are exceptions; in some countries such as
China, impulsivity seems to be the strongest risk factor).
About 60% of depressed young people report having thought about suicideand 30% actually attempt suicide. The risk increases if:• There have been suicides in the family• The young person has attempted suicide previously• There are other comorbid psychiatric disorders (e.g., substance abuse),
impulsivity, and aggression

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IACAPAP Textbook of Child and Adolescent Mental Health••

They have access to lethal means (e.g., firearms)
They have experienced negative events (e.g., disciplinary crises, physical orsexual abuse), among others.
Suicidal behaviors and risk need to be carefully evaluated in every depressed young
person (see chapter E.4).

DIAGNOSIS
While diagnosis is not usually difficult, depression in children andadolescents is often not detected or treated. Young people tend to present initiallywith behavioral or physical complaints which may obscure the typical depressive
symptoms seen in adults. Complaints which should alert clinicians to the possibilityof depression include:• Irritability or cranky mood
• Chronic boredom or loss of interest in previously enjoyed leisure activities(for example, dropping out of sporting activities, or dance and music lessons)• Social withdrawal or no longer wanting to “hang out” with friends• Avoiding school• Decline in academic performance• Change in sleep-wake pattern (for example, sleeping in and refusing to go
to school)• Frequent unexplained complaints of feeling sick, headaches, stomach-aches• Development of behavioral problems (such as becoming more defiant,running away from home, bullying others)• Abusing alcohol or other substances.
It is important to ascertain if the current problems represent a change fromthe teenager’s previous level of functioning or character. For example, depression
should be considered in the differential diagnosis in a 14-year-old boy with a sixmonth history of oppositional and conduct symptoms but no previous behavior
problems. Similarly, depression may account for the recent academic failure of a
15-year-old girl who had previously topped her class.

Symptoms ofdepression
Core symptoms:•
Persistent andpervasive sadness or
unhappiness•
Loss of enjoyment of
everyday activities•
Irritability
Associated symptoms:•
Negative thinking andlow self-steem•
Hopelessness•
Unwarranted ideas
of guilt, remorse or
worthlessness•
Suicidal thoughts or
thoughts of death•
Lack of energy,
increased fatigability,
diminished activity,•
Difficulty concentrating,•Appetite disturbance(decrease or increase)•
Sleep problems(insomnia or
hypersomnia).

Although definitions are similar, in this section we largely follow the DSM5 because ICD-10 criteria are more ambiguous. To make a diagnosis of depression
in practice requires the presence of:
•
•
•
•
•

Core symptoms
Some associated symptoms (usually four should be present)
Pervasiveness (symptoms must be present every day, most of the day)Duration (for at least two weeks)
Symptoms must cause impairment in functioning or significant subjective
distress, and• Symptoms are not the manifestation of the effects of a substance or anothermedical condition.
The core symptoms are sadness, unhappiness or irritability, and anhedonia.
Irritability is the most ambiguous because it can be present in a wide range ofpsychiatric conditions (e.g., oppositional defiant disorder, obsessive compulsive
disorder, bipolar illness).

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Associated symptoms include:
•
•
•
•
•
•
•

Significant weight or appetite change (when not dieting)
Insomnia or hypersomnia
Psychomotor agitation or retardation
Fatigue or loss of energy
Feelings of worthlessness or excessive or inappropriate guilt
Diminished ability to think or concentrate or indecisiveness, andRecurrent thoughts of death or suicide.
A key aspect in the assessment of any depressed youth is the evaluation ofrisk, particularly of suicide and homicide (see Chapter E.4). The outcome of therisk assessment will have an important bearing on management, for example indeciding the best setting (e.g., inpatient, outpatient) in which to treat the patient.

Informant
Parents and teachers tend to under-estimate depressive feelings inchildren while young persons may overestimate them. Additionally, reports
and questionnaire data from different informants often disagree. This does notnecessarily imply untruthfulness—it often reflects observers’ difficulty interpretingchildren’s emotions and behavior, and their limited knowledge of the child (e.g.,teachers observe the young person’s behavior and emotions in the classroom but
not at home or in social situations). Hence, it is essential to interview the child,often on several occasions, to obtain an accurate picture of how the young person
is feeling. Integrating information from several sources, a key clinical skill, is often
difficult in this context. However, contrary to what happens with other conditions
such as conduct disorder or ADHD, clinicians should give more weight to theyoung person’s report when diagnosing depression, though information fromparents and teachers should also be considered.

Severity

To make a diagnosis ofdepression in practicerequires:•the presence of core
symptoms•
some associatedsymptoms•
pervasiveness(symptoms must bepresent every day,most of the day)•duration (for at least
two weeks)•functional impairment
or significant subjective
distress.

Evaluating the severity of a depressive episode is important because treatment
guidelines use severity as one of the yardsticks to indicate what treatment should
Table E.1.4. Assessing the severity of a depressive episode(DSM-IV)
Mild••

Five depressive
symptoms (at least
one core symptom)
Mild impairment infunctioning (distressedby the symptoms,
some difficulty incontinuing withordinary work andsocial activities, which
can be done with extra
effort).

Depression E.1

Moderate••

Six or seven symptoms(at least one core
symptom)
Considerable difficulty incontinuing with school
work, social and family
activities.

Severe••••More than seven
depressive symptoms
Hallucinations ordelusions can bepresent (psychotic
depression)
Severe impairment
in most aspects offunctioning (home,school, social)Significant risk ofsuicide is often
present.

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IACAPAP Textbook of Child and Adolescent Mental Healthbe administered first. However, current definitions of severity are inadequate;
assessment of severity is largely based on clinical consensus and largely relies on theskills and experience of the clinician. Table E.1.4 provides guidance about assessing
severity. Depression rating scales can also assist in this assessment (see Table E.1.6).
Apart from depressive symptoms and impairment, other factors (e.g., risk
to self or others) influence decisions about treatment, particularly about which
treatment setting is more appropriate. For example, an adolescent with highsuicide risk may require hospitalization while another with an otherwise similarly
severe depression but with low risk of suicide may not.

DIFFERENTIAL DIAGNOSIS
Sadness and unhappiness are components of normal human experience,
particularly following losses and disappointments. Sometimes, however, thesefeelings are so intense and persistent that individuals are unable to function at
the level to which they are accustomed. It is in these situations that the labels

Table E.1.5. Distinguishing between normal adolescent behavior
and depression.
Adolescent with clinicaldepression

Normal adolescent•

In spite of some “angst”*,
moodiness and other difficulties,
they show no significant andenduring change in behavior.

•

There is a change from previous
behavior (e.g., became sad, irritable,lost interest in everyday activities,
dramatic response to perceived slights
or rejections, frequent complaints ofboredom)•

Although they can be sad andtearful at times, this usually occurs
in response to life events and isshort-lived.

•

Core depressive symptoms (sadness oranhedonia) are present every day, mostof the day for at least two weeks•

No significant change infunctioning.

•

Deterioration from previous functioning(e.g., not coping at school, drop inmarks, stopping previously enjoyedactivities). They take longer to complete
homework and class work than
before and it takes more effort; school
performance may decline. Withdraw into
themselves, their room or the Internet
at the expense of previously enjoyedfriendships and other social activities.

•

Thoughts of death and suicide are
infrequent.

•Suicidal thoughts (“life is not worth
living,” “I may be better off dead”) andattempts are common.

•

Risk behaviors, such as•
May start engaging in uncharacteristic,
reckless driving, drinking, anddangerous or high-risk behaviors,
experimentation with sex aresuch as reckless driving, out-of-control
common but usually contained
drinking, and thoughtless, unsafe sex.
within reasonable limits for thatadolescent’s character.
*Anguish, fear, anxiety. “Angst” is often used to describe the intense feelings ofapprehension, anxiety or inner turmoil that adolescents experience.

Depression E.1

11IACAPAP Textbook of Child and Adolescent Mental Healthof “clinical depression”, “major depression”, “depressive illness” or “melancholia”
are applied. People in everyday life speak about being “depressed”, meaning thatthey feel unhappy, down or sad. The issue therefore is how to distinguish clinicaldepression on the one hand, from the normal ups and downs of adolescents’ lives
and, on the other hand, from conditions that may mimic depression.

Depression and normal adolescent behavior
One of the most common concerns voiced by clinicians when diagnosing
depression is: how can we distinguish normal adolescent behavior from that of adepressed youth? This is because teenagers are often perceived as normally being
moody, irritable, anhedonic, and bored. Table E.1.5 lists some of the differences.

Physical illness or medication
A variety of medical conditions, treatments and substances can mimic
depression in children and adolescents. These include (the list is not exhaustive):• Medications: isotretinoin, corticosteroids and stimulants (e.g.,amphtetamines, methylphenidate)• Substances of abuse: amphetamines, cocaine, marijuana, solvents• Infections: acquired immunodeficiency syndrome (AIDS), monucleosis,
influenza• Neurologic disorders: epilepsy, migraine, traumatic brain injury• Endocrine: Addison’s disease, Cushing’s disease, hypopituitarism, thyroid
disorders.

Unipolar or bipolar?
One of the key diagnostic issues when dealing with a depressive episode
is to ascertain whether it is unipolar or bipolar because of its implications fortreatment. Although the clinical picture can be exactly the same in both, there arecharacteristics that increase suspicion that a depressive episode may be bipolar, suchas a family history of bipolar disorder and the presence of psychotic symptoms or
catatonia. However, a bipolar disorder diagnosis should not be made unless there
is history of at least one non drug-induced manic, hypomanic or mixed episode.
Detecting depression
Depression in adolescents is often not identified by parents, teachers and medical
practitioners, sometimes with tragic consequences. Hannah Modra, a 17-year-old brightand successful student confided her recently developed depressive symptoms to her diary.
Although her caring and well educated family realized that something was wrong, they did
not understand what, and how serious it potentially was. In her mother’s words:

Click on the picture to watch
The Girl Less Likely (30minutes), an excellent
documentary about one
adolescent’s depression.

“I still could see that there was something not completely right about Hannah but I
had no clue. I didn’t know what it was or what I could do about it or what I should do
about it. And so on the 29th of January I said, ‘Look, why don’t I just take you to thedoctor?’ The doctor didn’t really know her. Hannah wasn’t saying much, she was justsitting there. And the doctor thought probably a girl of this age, you know, it’s often
something to do with, you know, iron deficiency or anemia. So we went off and had
her blood taken and then we were coming back home and Hannah said, ‘Mum, I
know it’s not anything to do with my blood.’ But I didn’t think anything more of it. You
know maybe I could have said to her, ‘Well what is it Hannah?’ You know, but I didn’t
say that. I didn’t ask that question, you know, and she didn’t give me an answer. And
I thought she was just saying ‘I’m okay’.”

Hannah, who in retrospect had clear symptoms of depression, killed herself the following day(Australian Broadcasting Corporation, 2008).

Depression E.1

12IACAPAP Textbook of Child and Adolescent Mental Health

Suspicion will encourage conducting a more thorough history looking for manicor hypomanic symptoms in the past. The unipolar-bipolar distinction is mademore difficult because bipolar illnesses often start with an episode of depression inchildhood or adolescence without previous history of manic symptoms.

Substance use disorders
Given the frequency of substance use among adolescents it is always
important to clarify whether depressive symptoms are etiologically related to theingestion of substances such as amphetamines, cocaine, marijuana, and solvents.
For example, amphetamine withdrawal can present (particularly after episodes ofintense use—“speed run”) with a picture of dysphoria, fatigue, sleep disturbanceand psychomotor retardation (“crash”) that can be very similar to depression. It
is expected that symptoms would disappear after a few days of abstinence when
they are substance-induced. If depressive symptoms persist or precede the onsetof substance use, one would suspect that a depressive disorder is present andcomorbid with substance use.

Schizophrenia
When adolescents present with depressive symptoms as well as hallucinations
or delusions it is important to clarify whether schizophrenia or psychotic depressionis the appropriate diagnosis. Features suggestive of psychotic depression include afamily history of depression or bipolar disorder, relatively rapid onset without aprodromal period, the presence of mood congruent hallucinations (e.g., a voice
telling the patient he is bad or that he should kill himself ) or delusions (e.g., ofsin, poverty, imminent disaster, the belief that she is a witch and has caused harm
to others). In spite of these differences, distinguishing between the two conditions
can be difficult in practice. For example, it is not uncommon for the dysphoria andself-neglect of a prodromal stage of schizophrenia to be misdiagnosed as depression.
Often, only the passage of time (course) helps to solve the diagnostic problem.
In circumstances in which there is some doubt, rather than making a diagnosisof psychotic depression or schizophrenia, it may be preferable to diagnose “first
episode psychosis” and leave making a final diagnosis for later, when the course of
the illness is clearer or more information becomes available.

ADHD and disruptive behavior disorders
Irritability and demoralization are very common symptoms in children—
particularly pre-pubertal children—who suffer from ADHD, oppositional defiant
disorder or conduct problems, often in a context of significant family dysfunction,
poverty, neglect, foster care, or institutionalization. In these cases it is difficult toestablish whether demoralization is the result of the child’s plight or a manifestationof clinical depression. If symptoms meet criteria for depression, a comorbid
diagnosis of depression (i.e., two diagnoses) is encouraged by the DSM system.
The ICD system, on the other hand, recommends making only one diagnosis:
mixed disorder of conduct and emotions or depressive conduct disorder. At this point,
the advantages of one approach over the other are unclear, although research showsthat children with both conduct problems and depression grow up resembling
more closely children with conduct disorder than those with depression.

Stigma“Fear ofembarrassment and
pride are keeping
me both from the
medication andcounsellors. However
I could be a great
help to others if I tried
out these things andreported things thatworked and things
that didn’t work to
the public. Everyone
would know I have adepression weakness
but I would be helping
myself and others”(Australian Broadcasting
Corporation, 2008).
Adolescents are selfconscious about theirmental health and often
consider depression a signof weakness or a character
flaw. Stigma makes
diagnosis and treatment
more difficult.

Adjustment disorder with depressed mood and bereavement
Clinicians often diagnose adjustment disorder when the onset of symptoms
occurs following a significant life event. This is correct only if clinically significant

Depression E.1

13

IACAPAP Textbook of Child and Adolescent Mental Healthdepressive symptoms or impairment occur within three months of identifiable
stressors and do not meet criteria for major depression or bereavement. In the caseof adjustment disorder, it is also expected that symptoms will disappear within six
months once stressors have ceased.
Bereavement can present with a clinical picture very similar to a depressive
episode but depression should not be diagnosed unless symptoms are severe,
persistent, and incapacitating (e.g., inappropriate and persistent guilt, morbid
preoccupation with worthlessness, significant impairment of functioning).
Symptoms of grief tend to decrease over days or weeks, are often associatedwith thoughts or reminders of the deceased, are not as pervasive as in the case ofmajor depression, may be accompanied by periods of positive emotions and evenhumor, and—contrary to what happens in major depression in which feelings ofworthlessness are common—self-esteem is generally preserved.

RATING SCALES
There are numerous rating scales for child and adolescent depression. The
clinician-administered Hamilton Rating Scale for Depression is the most widely used
to rate adult depression but its usage in children and adolescents has not been
extensive. The Children’s Depression Rating Scale (CDRS) (Poznanski & Mokros,
1996) is also clinician-administered and was specifically developed for the young.
This proprietary scale has been used in major treatment trials such as the TADS
(Curry et al, 2010). There are also interview-based diagnostic instruments, such as
The Child and Adolescent Psychiatric Assessment (CAPA) (Angold & Costello, 2000)
which are mostly used in research.
The most widely used rating scales are self-rating, most having child,parent, and teacher versions. Since rating scales cannot validly be used to make adiagnosis—which requires an assessment interview by a competent clinician and,
optimally, interviewing key informants—these instruments are mostly used forscreening purposes (e.g., in schools or among people considered at risk) or to assess
response to treatment over time (outcome). Increasingly, they are being modified
to be completed by the young person using computers, smart phones, and tablets(Stevens et al, 2008).

Manic switching
The rate of switching
to hypomania or mania
in young people withdepression is higher inyouth than in adults, withsome researchers claiming
rates as high as 40%.
However, in the TADS
five-year follow up only 6%
developed a bipolar illness
after five years (Curry et al,2010). It can be concluded
from this and other studies
that bipolar disorder will
occur in about 10% ofdepressed adolescents.
Rates may be higher if
there is a family historyof bipolar disorder andin childrren who suffer amanic switch when treatedwith antidepressants.

Overall, self-report scales seem to be of limited use in pre-pubertal children
but more helpful in adolescents. The impact of new technologies, such as smart
phones, has not been fully exploited and may increase their utility. The majority ofthese scales are proprietary and costly but none has demonstrated a clear superiority
over the others. Table E.1.6 lists some of the scales that are free of charge forclinical use; some are available in several languages.

TREATMENT
It is necessary to aim high, that is, seeking to achieve full remission ofsymptoms and a return to the premorbid level of functioning (recovery). Anything
less is a suboptimal outcome because persistence of depressive symptoms increases
the likelihood of poorer psychosocial functioning, suicide and other problems(e.g., substance abuse), as well as relapse and recurrence.
In most cases it is good practice to involve the young person’s parents
in the evaluation and treatment process (for example, in discussions about thetreatment options available and their relative risks and benefits) but the degree

Depression E.1

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IACAPAP Textbook of Child and Adolescent Mental Health

Table E.1.6. Selected scales to rate depressive symptoms that are in the public domain
or freely available for clinical use.
Scale

Rater

CES-DC:
Center for Epidemiologic
Studies-Depression Scale(Faulstich et al, 1986)

MFQ:
Mood and Feelings
Questionnaire (Angold etal, 1995)

DSRS:
Depression Self-Rating
Scale (Birleson, 1981)

KADS:
Kutcher Adolescent
Depression Scale(Brooks et al., 2003)

PHQ-A:

Comments

Self, parent(Children,
adolescents)•

There are questions about its specificity measuring depressive
symptoms (as opposed to distress).

Self, parent, teacher(Children,
adolescents)•

Free for clinical or research use, with permission.

Self(Children,
adolescents)•

Available in several languages•

Few studies

Self(Adolescents)•

Two versions with 6 and 11 items respectively.

•

The 6-item KADS is designed for use in institutional settings(such as schools or primary care settings) where it can be used
as a screening tool to identify young people at risk for depression
or by trained health care providers (such as public healthnurses, primary care physicians) or educators (such as guidancecounselors) to help evaluate young people who are in distressor who have been identified as possibly having a mental healthproblem. It is currently available in English, French, Chinese,
German, Spanish, Portuguese, Korean, and Polish.

•

The 11-ITEM KADS is available in English, Portuguese, andTurkish.

Self (adolescent)•A short questionnaire developed as part of the PRIME-MD
package funded by Pfizer.

Self (adolescent),parent, teacher•

Measures overall psychopathology but a subscale can be used toscreen for depression risk.

•

Reasonably sensitive and specific when screening “probable”
depressive illness.

•

Can be completed by the young person on-line and get
immediate feedback at http://www.youthinmind.info/UK/sdqonline/
Self/StartSelf.php

Patient Health
QuestionnairesAdolescent (Johnson etal, 2002)

SDQ:
Strengths and Difficulties
Questionnaire (Goodman
et al., 2000)

Click on the picture to access the
National Institute for Health and ClinicalExcellence (NICE) (2005) guideline.

Depression E.1

15

IACAPAP Textbook of Child and Adolescent Mental Healthof involvement will depend on the young person’s age, stage of development,
their wishes and circumstances, and the culture of the country. Taking time to do
this will strengthen the therapeutic relationship, improve adherence to treatment
and outcome. It is always recommended to monitor regularly the severity of thedepression using a rating scale (e.g., one of those listed in Table E.1.6). Suicide
risk should also be evaluated regularly and not just at the first assessment interview
because suicide risk fluctuates.
Watchful waiting is an approach to managing illnesses in which time isallowed to pass before further treatment is considered. Watchful waiting is often
used in conditions with a high likelihood of self-resolution or where the risks oftreatment may outweigh the benefits (e.g., prostate cancer). A key component ofwatchful waiting is the use of explicit rules to ensure a timely transition to anotherform of management, if necessary. The National Institute for Health and ClinicalExcellence (NICE) (2005) guideline introduced watchful waiting as a strategy “forchildren and young people with diagnosed mild depression who do not want anintervention or who, in the opinion of the healthcare professional, may recoverwith no intervention, a further assessment should be arranged, normally within 2
weeks”. It is important to note that watchful waiting does not mean no-treatment.
During the watchful waiting period, treatment should take place as described in
the supportive management section below.

The aims of treatment
are to:•Reduce the symptoms
and impairment to aminimum•
Shorten the depressive
episode, and•Prevent recurrences.

Supportive management
The American Academy of Child and Adolescent Psychiatry (AACAP)
practice parameter (Birmaher et al, 2007) indicates that instead of medication“it is reasonable, in a patient with a mild or brief depression, mild psychosocial
impairment, and the absence of clinically significant suicidality or psychosis,
to begin treatment with education, support, and case management related toenvironmental stressors in the family and school. It is expected to observe response
after 4 to 6 weeks of supportive therapy.” That is, education, support, and casemanagement—supportive management—is a valid, widely used but poorly
researched treatment option.
Many patients seek help following a crisis (e.g., a suicide attempt); in these
emotionally-charged circumstances symptoms tend to be exacerbated. Dealing
with the crisis itself may be enough to settle the perceived depression, particularly
in primary care settings. As part of the supportive management, seeing theadolescent—and parents, if appropriate—on two or three occasions allows fora more thorough assessment of the illness and of factors maintaining it, and to
discuss treatment options, risks and side effects in more detail. Thus, supportive
management/watchful waiting are useful strategies when suicide risk is low anddepression not severe.

Psychosocial interventions

Click on the picture to accessthe American Academy ofChild & Adolescent Psychitry
practice parameter on
depressive disorders (2007).

Psychosocial interventions (summarized in Table E.1.7), in particularcognitive behavior therapy (CBT) and interpersonal psychotherapy (IPT), appear
to be effective in the treatment of mild to moderate depression although the number
and quality of studies examining specific therapies is limited. The optimal numberof CBT and IPT sessions is not known. Most studies report using weekly one-hoursessions for 8 to 16 weeks, though booster sessions may improve outcomes andreduce recurrence. In practice the number of sessions can be tailored to patients’needs, severity of the illness and other relevant factors.

Depression E.1

16

IACAPAP Textbook of Child and Adolescent Mental HealthThough antidepressants achieve better results in the short term, differencesin outcome between the various psychosocial interventions and with antidepressant
medication tend to disappear after 24-36 weeks (TADS Team, 2007). The qualityof the therapist (trained therapists vs. paraprofessionals) as well as the strength ofthe patient-therapist alliance seem to be relevant factors for response in all thepsychotherapies.

Cognitive behavior therapy (CBT)CBT is based on the assumption that depressed mood is associated with anindividual’s behavior and thoughts, and that changing behavioral and cognitive
patterns will lead to a reduction in depressive feelings and improved functioning.
Individuals are exposed to a range of stressors and respond automatically to themwith feelings; in depressed adolescents these automatic responses are unrealisticallynegative — often cataclysmic: “no one likes me”; “I am good for nothing”. These
depressed thoughts and subsequent actions make them feel worse, often generating
a downward spiral: unhappy feelings leading to unrealistically negative thoughts
and behaviors. The aim of treatment is to turn back this vicious cycle by learning (a)that one’s feelings, thoughts, and actions are interconnected, and (b) by developing
strategies for more positive patterns of thinking and behaving, which in turn leadto more positive feelings (Langer et al, 2009).

Click on the picture to view abrief description of CBT and
IPT by Neal Ryan MD.

The first goal of CBT is to help patients identify links between mood,thoughts and activities in their lives (e.g., speaking to a friend on the phone
resulting in an improvement in mood) and challenge some of their negative
beliefs; at the same time the number of activities is increased using strategies suchas scheduling enjoyable activities. Optimally, this requires using a mood diary (seeFigure E.1.1). Another goal is to help the patient discriminate between helpful andunhelpful thoughts, to develop strategies for generating more helpful thoughts,
and to practice using helpful thought patterns in response to stressful situations(cognitive restructuring). The third goal is to equip the young person with skills tobuild and maintain relationships, undermined by the adolescent’s depression, by
training in social skills, communication and assertiveness.

Interpersonal psychotherapy (IPT)Interpersonal psychotherapy stresses the importance of interpersonal
relationships and that people experience distress when disruptions occur in theirsignificant attachments. This results in a loss of social support that causes ormaintains depressive feelings. IPT therapists do not probe into the adolescent’s
past, focusing instead on current interpersonal conflicts, targeting depressedadolescents’ interpersonal skills to improve their relationships (Mufson et al, 2009).
IPT has many commonalities with CBT. For example, the goals are to linkmood with interpersonal events happening at the time, to provide psychoeducation
about depression, and to encourage prticipation in enjoyable activities (especiallyat school) as a means to feeling better. However, the focus is on interpersonal
issues (e.g., examining and modifying maladaptive communication patterns andinterpersonal interactions) and on teaching the adolescent how to deal with themconstructively.
In recent years mindfulness techniques are often added to CBT and IPT
programs with growing evidence of effectiveness in the treatment of depression
and to prevent recurrences. Mindfulness is a technique in which individuals

Depression E.1

17

IACAPAP Textbook of Child and Adolescent Mental Healthfocus their awareness on the present moment, while calmly acknowledging andaccepting one’s feelings, thoughts, and bodily sensations. Click here [http://www.
blackdoginstitute.org.au/docs/10.MindfulnessinEverydayLife.pdf ] to access some
mindfulness exercises in everyday life.

Medication
Antidepressant drugs and their efficacy are summarized in Table E.1.8.
Antidepressants are an important weapon for treating depression in the young,however several antidepressants that are effective in adults are not effective in youth(e.g., tricyclic antidepressants) or too risky to use in this age group (e.g., MAOIs)—
highlighting the issue that empirical data obtained in adult treatment trials cannot
necessarily be generalized to children and adolescents. The placebo effect, if
anything, is stronger among children and adolescents than in adults, severity ofthe depressive episode being an important consideration: antidepressants are notmore effective than placebo in mild depression but appear to be more effective
when depression is severe.

Click on the image to view aclip explaining mindfulness(18:05)

A key aspect of prescribing and of obtaining informed consent is to discusswith the patient, and family if appropriate the:•Reasons for the medication•

Possible adverse effects (including emerging or escalating suicidal thinking,nervousness, agitation, irritability, and mood instability)•

Need to take medication as prescribed, and•Delayed action of antidepressants (to dampen expectations of immediate
benefit).

Table E.1.7. Summary of evidence of effectiveness of psychosocial therapies forunipolar depression.
Treatment

Comments

Cognitive behavior therapy
(CBT)

•
•

Some evidence showing that individual CBT (8 to 16 one-hour weekly sessions) is
effective in the short term.
Differences between CBT and medication usually disappear by 12 months.

Interpersonal
psychotherapy (IPT)•Some evidence showing that IPT is effective in the short term.

Psychodynamic(psychoanalytic)
psychotherapy••

Very few studies but some evidence that it might be effective.
Requires longer duration of treatment (e.g., one year)

Family therapy••More effective than no treatment. Unclear how effective it is in comparison toother treatments.
May be particularly useful in cases with family conflict or disharmony.

Group therapies (mostly
CBT-based)••

Evidence is limited and results conflicting.
Mostly used as a preventive intervention for at-risk individuals.

Self-help (e.g., relaxation,
educational leaflets orbooks, support groups)••

Data are limited and with conflicting results.
Growing interest in CBT-based internet-delivered self-help but little evidence ofeffectiveness as yet.
Psycho-education is usually included as part of clinical treatment.

•

Depression E.1

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IACAPAP Textbook of Child and Adolescent Mental Health

MOOD

Figure E.1.1. Example of a completed mood chart.
MONDAYTUESDAYWEDNESDAY

THURSDAYFRIDAY

SATURDAYSUNDAY

AM

2

1

4

1

3

6

5

PM

4

3

2

2

5

6

7

SchoolGot bullied

School
Bad mark;
could not do
the work in
maths

SchoolSpent sometime with afriendSchoolCaughtsmoking:
detention

SchoolSlept inPlayed tennis

Visitedgrandmother in
hospitalComputergames
Took dog fora walkComputergames
Homework

Computergames
Argument withsisterHelped dad withgardening

Visited goodfriendTook dog for walk

ACTIVITIESAMPMComputer
Went to see
games
movie with
Argument withfriends
motherWrite down the relevant activities in each day (morning and afternoon) and rate your mood from 0 (very unhappy), to 5(neither happy nor unhappy), to 10 (very happy). Use all the range of ratings.

Good practice also recommends reviewing the patient at weekly intervals(personally or, when this is not possible, over the phone) for the first month once
medication is prescribed. These reviews allow further supportive management andmonitoring of side effects and response (by the administration at each visit of adepression rating scale).
Under-treatment—not enough medication or not for long enough—is acommon error in clinical practice. Although it is important to start with a low
dose, the amount of medication should be gradually increased until symptoms
lessen or side effects appear, keeping in mind that there is wide individual variationin the dose of medication required.

Side effects of medication
Since antidepressants other than SSRIs will rarely be used in youth, onlyside effects of SSRIs are discussed in detail. In the case of TCAs, anticholinergicside effects and cardiac toxicity are the main ones, while hypertensive crises are themain risk for MAOIs.

Suicidality
It has been suggested that, paradoxically, SSRIs may induce suicidal behavior
in the young. Ascertaining whether this is true is not easy because depression also
increases suicide risk. So far, data are contradictory. On the one hand, pharmacoepidemiological and ecological studies suggest that increased use of SSRIs may
have resulted not on an increase but on a lessening in youth suicide. On the other
hand, a review by the FDA of controlled trials with more than 4400 children andadolescents showed a robust if small (2%) short-term increase in the incidence ofsuicidality (suicidal thoughts, attempts) in those receiving antidepressants, mostly
SSRIs, compared with placebo. There were no suicides. This resulted in the FDA
and regulatory bodies in other countries warning of this risk. The mechanisms
underlying this phenomenon are unclear. SSRIs can induce akathisia, agitation,

Depression E.1“A typical CBT session
begins by collaboratively
setting an agenda forthe session, reviewing
homework from theprevious week, teachingand practicing the current
cognitive-behavioral skill,addressing crises andissues that have arisen in
the youth’s life over theprevious week, helping
the youth to summarize
the skills that havebeen learned during thesession, and allocating
practice/homeworkassignments” (Langer etal, 2009).

19

IACAPAP Textbook of Child and Adolescent Mental HealthHelping adolescents solve problems in a structured way
1.
2.
3.
4.
5.
6.

“What’s the problem?” — ask the teenager to write it down.
List all possible solutions — brainstorm and list all possible solutions. The teenager
should write down all the solutions they can think of without evaluating them (i.e.,
both good and bad solutions).
Take each possible solution on the list and think about the pros and cons.
Ask the teenager to choose the best or most practical solution.
Work out how to implement the best solution and the resources needed. You may
need to rehearse the difficult steps with the teenager.
After the teenager has carried out the chosen solution, review and praise all efforts.
If the solution did not work, go through the steps again and identify an alternative
solution.

irritability and disinhibition. Like other antidepressants, SSRIs can also trigger amanic switch.
The implications of these findings are that patients need to be warned ofthis risk and clinicians ought to put in place strategies to manage it such as weekly
reviews during the first month of treatment, and educating patient and family
about detecting changes in behavior (e.g., agitation, thoughts of self-harm) once
medication is started.

Other side effects
SSRIs are also associated with higher rates of agitation, akathisia, nightmares
and sleep disturbance, gastrointestinal problems, weight gain, sexual dysfunction(reduced sexual desire, difficulty reaching orgasm, inability to maintain an erection)and increased risk of bleeding. Most of these side effects are dose-related and canbe controlled by reducing the dose.
Depending on the half-life of the specific SSRI, stopping treatment abruptly
or missing several doses can cause withdrawal symptoms, also called discontinuation
syndrome, including: nausea, headaches, dizziness, and flu-like symptoms(infrequent with fluoxetine, very common with paroxetine). Abrupt cessation may
also increase the likelihood of relapse or recurrence.

Antidepressant use in pregnancy
The use of SSRIs (the other antidepressants are not usually recommended
in the young) during pregnancy is an important issue due to reports of SSRIs
being associated with teratogenicity, spontaneous abortion and premature labor,
low birth weight, and pulmonary hypertension. The evidence is conflicting but
the weight of it suggests that properly used SSRIs are safe. Thus, most treatment
guidelines state that these concerns should not prevent prescription of SSRIs (withthe exception of paroxetine) for the treatment of major depression in pregnancy
once the potential benefits outweigh the risks, taking into account that depression
during pregnancy carries its own dangers. Paroxetine should not be used becauseof an association with both major malformations and cardiac abnormalities(Bellantuono et al, 2007). Bellantuono C, Migliarese G, Gentile S (2007).
Serotonin reuptake inhibitors in pregnancy and the risk of major malformations:
A systematic review. Human Psychopharmacology, 22:121–128.

Depression E.1

Click on the picture to watch
how SSRIs and MAOIs work

Placebo response
and severity ofdepression
One of the most puzzling
aspects of the treatment
of depression is the highrate of placebo response,
estimated at 50% to 60%
in RCTs examining thepharmacological treatmentof clinical depression
in youth. A review of
RCTs found that placebo
response was higher inchildren than adolescents,
among those with milder
depression, and increased
with the number of centers
participating in the study(Bridge et al., 2009).
Effectiveness ofantidepressants does
not seem to increase
with growing severity
but placebo response
decreases. That is,placebo response
is similar to that of
medication in cases of mild
depression, while placebo
response is clearly
inferior to medication insevere depression. For
example in TADS, inwhich participants wereseverely depressed, at
12 weeks, 35% of thosetaking placebo had
responded comparedwith 61% of thosetreated with fluoxetine.
Similar results have beenreported in adults. This is
one of the reasons why
antidepressants are notusually recommended asa first line of treatment inmild depression.

20

IACAPAP Textbook of Child and Adolescent Mental Health

Table E.1.8. Summary of evidence of effectiveness of antidepressant drugs for unipolar
depression.
Treatment

Comments••

Tricyclic antidepressant (TCAs):
Amitriptyline, clomipramine,
desipramine, dosulepin, doxepin,
imipramine, lofepramine, nortriptyline,
protriptyline, trimipramine•

Tetracyclic antidepressants(TeCAs):Amoxapine, maprotiline, mianserin,mirtazapine•

Selective serotonin reuptake
inhibitors (SSRIs):
−
−
−
−
−
−

citalopram
escitalopram
fluoxetine
fluvoxamine
paroxetine
sertraline

•
•
•

•
•
•
•

•

•

•

•

No evidence of superiority vs. placebo for any of them,
particularly in pre-pubertal children
Significant side effects (anticholinergic, QT prolongation)
Toxic (cardiotoxic) in overdose (with the exception of mirtazapine)
To be avoided in children and adolescents

As a group, SSRIs are more effective than placebo, particularly
in adolescents with severe depression
Few side effects but may increase suicidality
Fluoxetine is the best studied and has the best evidence ofeffectiveness. Approved by the FDA and EMEA* for those aged 8
years or older.
Sertraline, citalopram, escitalopram: less robust evidence ofeffectiveness, though they may be effective in patients who did
not respond to fluoxetine (Brent et al, 2008). Escitalopram has
been approved by the FDA for adolescent depression
Paroxetine: appears not to be effective in youth and shows moreside effects than the other SSRIs. Short half-life easily resulting
in withdrawal symptoms; use not recommended.

Serotonin-norepinephrine
reuptake inhibitors (SNRIs):
Venlafaxine, desvenlafaxine,
duloxetine, milnacipran,
Levomilnacipran•

Monoamine oxidase inhibitors(MAOIs):Isocarboxazid, moclobemide,
phenelzine, selegiline, tranylcypromine,pirlindole•••No evidence of effectiveness in the young
Significant risk of side effects due to non-compliance with dietary
restrictions
To be avoided in children and adolescents

Other antidepressants:
agomelatin, buspirone, nefazodone,
vilazodone, vortioxetine.

•

Evidence of effectiveness in this age group is lacking.

•

One study showed that venlafaxine is as effective as SSRIs inpatients with treatment-resistant depression but has a worse
side-effect profile (Brent et al, 2008). Not recommended in youth.
No consistent evidence about the others.

*EMEA: European Medicines Agency
Antidepressant benefit and risk of suicidality
Across antidepressants, mainly SSRIs, a meta-analysis including 15 depression RCTs reported numbers needed to treat(NNT) that ranged from 4 (for fluoxetine) to 20 (for nefazodone) and a pooled average of 10 (Bridge et al, 2007). That is, four
depressed youth will need to be treated with fluoxetine for one to get better due to treatment (as opposed to other factors
such as the placebo effect or natural course of the illness).
The same meta-analysis reported number needed to treat to harm (NNH) ─ defined as emerging suicidal behavior ─ that
ranged from 112 (across 13 depression trials) to 200 (across 6 OCD trials) and to 143 (across 6 non-OCD anxiety disordertrials), with a pooled average of 143. That is, 112 depressed adolescents will need to be treated with antidepressants for one
to develop suicidal behavior attributable to the treatment. In summary, across indications, benefits of antidepressants appear
to be much greater than risks from suicidal ideation/suicide attempt.

Depression E.1

21

IACAPAP Textbook of Child and Adolescent Mental HealthPharmacogenomics and individualized treatment
Antidepressants are of moderate effectiveness overall but there is wide variation between patients in their response to
individual antidepressants. Clinical characteristics (e.g., whether there is melancholia or not) have not been helpful indicatorsof antidepressant response. The only option currently available is trial and error (i.e., try an antidepressant, if it does not work,
try another), which is time consuming and cumbersome.
It is well known that when parents respond well to one antidepressant drug, children are also likely to respond to thesame drug. As a result there is growing interest in detecting gene variants (e.g., serotonin transporter, norepinephrinetransporter) that may be associated with response to antidepressants. This situation is further compounded because
antidepressants are metabolized by enzymes that vary considerably from person to person. For example, cytochrome P450
(CYP) 2D6 is instrumental in the metabolism of many antidepressants but more than 74 allelic variants of the CYP2D6 gene
have been found, and the number is still growing. This results in CYP2D6 activity varying considerably within a populationfrom “ultra-rapid”, to “extensive”, to “intermediate”, to “poor” metabolizers. Distribution of these alleles also varies between
ethnic groups. Clinical consequences of CYP2D6 polymorphism can be either the occurrence of adverse drug effects or lackof response. There is an expectation that genetic testing may in the future help choosing the right antidepressant for a given
individual. Thus far this is not possible.

Physical treatments
Physical treatments are summarized in Table E.1.9. Besides medication,
several physical treatments are used in the management of depression in children
and adolescents. Of these, electroconvulsive therapy (ECT) has been administered
to the young for about 60 years—described as “lifesaving” in some cases—and has aplace in the armamentarium to treat depression. However, there are no controlled
trials in youth (they pose significant ethical challenges) and there is no wide
agreement on when ECT should be used, whether reasonably early in the courseof treatment (e.g., if antidepressants are not tolerated), as a last resort, or never. Thislargely reflects individual countries’ attitude towards ECT, which has been severely
stigmatized due to ECT having been used occasionally as a means of politicalcontrol, negative media portrayals, or misuse by some psychiatrists. As a result,many states place legal restrictions on its use—some countries (e.g., Slovenia) haveeven outlawed its use.
More recently, transcranial magnetic stimulation (TMS) has been used inyoung people but it can only be considered an experimental treatment at this time.
For more details see Walter and Ghaziuddin (2009). Light therapy has been used
for seasonal mood disorders with some success.

Complementary and alternative medicine treatments

Toxicity
Toxicity—death due toacute poisoning by asingle drug, with or without
ingestion of alcohol—ismuch lower among the
SSRIs (1.3 deaths per
million prescriptions) thanwith TCAs (34.8), and
MAOIs (20.0). That is,
toxicity is 27 times higher
for TCAs than SSRIs.
Toxicity of venlafaxine isquite high (13.2) (Buckley& McManus, 2002).

Use of complementary and alternative medicine treatments (CAM) is
widespread (see Chapter J.2). For example, St John’s wort is one of the mostcommonly prescribed antidepressants for children in Germany. A host of CAM
interventions have been recommended or used for the treatment of depression
but hardly any are supported by credible evidence of effectiveness, particularly
in children and adolescents. This is compounded by the fact that CAM remedies
have to satisfy less rigorous efficacy and safety criteria than prescription drugs. For
example, they lack standardized preparation and are more prone to contamination,
adulteration and inaccurate dosage, among other problems. While cliniciansrecognize patients’ and families’ interest in CAM therapies, often do not feel
comfortable asking about, discussing, or recommending them. Nevertheless acompetent clinical evaluation should include routine questioning about CAM
usage. An open, informed stance by the treating clinician often leads to disclosure,acknowledgement of patients’ dislikes and beliefs, and better patient educationand outcomes. Alternative medicine treatments are summarized in Table E.1.10.

Depression E.1

22IACAPAP Textbook of Child and Adolescent Mental Health

MANAGING ACUTE DEPRESSIVE EPISODES
Unipolar depressive episode
Currently treatment of unipolar depressive episodes in youth is largely guided
by their severity. Following initial assessment clinicians should contact children
and young people with depression who do not attend follow-up appointments.
•

Mild severity: supportive management or psychosocial treatment, if
available. If no response after 4 to 6 weeks: CBT, IPT or medication•

Moderate severity: supportive management or psychosocial treatment,
if available; in some cases (e.g., patient preference, non-availability ofpsychosocial treatment), medication. Medication should be used also if
patients do not benefit from 4 to 6 weeks of supportive management or
psychosocial treatment•

Severe: psychosocial treatment and antidepressant medication•

Psychotic depression: as per severe depression but adding a second generation
antipsychotic.

Bipolar depressive episode (see also Chapter E.2)
There is little evidence available to guide treatment in young people.
Recommendations are therefore extrapolated from adult data (Frye, 2011):•

Initial treatment (first line) would usually be lithium carbonate or quetiapine

Table E.1.9. Summary of evidence of effectiveness for physicaltreatments for unipolar depression.
Treatment

Comments

Electroconvulsive
Therapy (ECT)

•
•
•
•
•

ECT is rarely used in this age group. It would appear to
be of comparable efficacy as in adults
Used in severe depression when other treatments havefailed or are not tolerated
ECT should not be used in pre-pubertal children except
in the most extreme circumstances
Few side effects, retrograde amnesia being the main one
Use subject to legal restrictions in some countries

Transcranial
magnetic stimulation
(TMS)

•
•
•

Few studies, but early results promising
Experimental treatment at this stage
Side effects are generally mild and transient, mostly
headache and scalp pain

Light therapy•

Data limited, but includes controlled trials reporting
positive results
Used for seasonal mood disorder. Suggestions that it
may also be effective in non-seasonal mood disorder(e.g., in older patients)
Few adverse effects••

Depression E.1

Serotonin syndrome
Serotonin syndrome is apotentially serious toxic
effect resulting from too
much serotonin. It has
been observed in overdoseof (a) a single agent(usually an SSRI), (b) withthe simultaneous use of
two drugs that increase
serotonin levels orserotonergic transmission(e.g., monoamine oxidase
inhibitors or moclobemide
used with any drugthat inhibits re-uptakeof serotonin such as
SSRIs and some tricyclic
antidepressants), or (c)by failing to observean adequate washout
period when switchingantidepressants. Risky
situations include
polypharmacy, use of overthe-counter or alternative
medicine substancessuch as St John’s wort,
or of illicit drugs such as
ecstasy.
Clinical features ofserotonin syndrome
include:•••Mental: confusion,agitation, hypomania,
hyperactivity,
restlessness
Neuromuscular:
clonus (spontaneous,
inducible orocular), hypertonia,
hyperreflexia, ataxia,
tremor (hypertonia andclonus are symmetricaland more obvious
in lower limbs to
begin with). Clonus
is the most importantdistinguishing feature
in diagnosis.
Autonomic:
hyperthermia,
sweating, tachycardia,
hypertension,
mydriasis, flushing,shivering23

IACAPAP Textbook of Child and Adolescent Mental Health

Table E.1.10. Summary of evidence of effectiveness of alternative treatments forunipolar depression.
Treatment

Comments

St John’s wort (hypericum)

•

•

•
•

Many RCTs in adult patients, mostly with mild depression. Results inconsistent—
larger, better designed studies with more severely depressed patients show
negative results more often than smaller ones with mildly depressed patients. Verylimited data for children.
Hypericum might be as beneficial as antidepressants in mild depression.
Few adverse effects
Significant risk of interaction with a wide range of prescribed medications due toactivation of the cytochrome P450 system

Omega-3 fatty acids•••

Several RCTs in adults of heterogeneous quality but few in young people
Not clear yet whether they are effective
Few, minor side effects

S-Adenosyl Methionine(SAMe)•

Trials of inconsistent quality show that SAMe might be as effective as TCAs in
adults. No evidence for children.

Exercise•

Some evidence of a specific benefit in mildly depressed older patents. No definite
evidence in youth•

Second line treatments would be:(a) A combination of lithium or valproate with an SSRI(b) Olanzapine and an SSRI, or(c) Lamotrigine.

•

There is no evidence that antidepressants alone (without a mood stabilizer)
are helpful and are not recommended due to risk of a manic switch or of
induction of rapid cycling.
Lithium and valproate should be avoided in women of childbearing age(teratogenic).

•

Which antidepressant?
•

•
•

•

Choice of antidepressant should be guided by two considerations:effectiveness and safety. As a group, SSRIs are the safest antidepressants; ofthese, fluoxetine has the best evidence of effectiveness in this age group.
Response or non-response or adverse effects of treatment during a previous
episode will influence the choice of medication for the current episode.
Start with 10mg of fluoxetine. If well tolerated, increase dose to 20mg
after one week; 20mg is usually sufficient for pre-pubertal children. In
adolescents, dose may need to be increased to 30 or 40mg if they do notrespond adequately to 20mg and is well tolerated, although 20mg would
suffice in most cases.
If fluoxetine is not well tolerated or there are other reasons for not using it,
try another SSRI (e.g., sertraline or escitalopram).

Duration of treatment
It is widely accepted that stopping treatment early (e.g., after 8 to 12 weeks),
when the patient is getting better, often results in relapse. Clinical wisdom suggests

Depression E.1

24

IACAPAP Textbook of Child and Adolescent Mental Healththat treatment should continue for at least six months after recovery. When ceasing
antidepressants, it should be done gradually and not abruptly to avoid withdrawal
or cessation phenomena, common in all antidepressants but particularly in SSRIs
with short half-life.

The patient does not improve
The majority of patients recover; with ongoing treatment, improvement
continuing after 12 weeks. For example, in the TADS follow up study, 88% had
recovered by two years and 96% by five years (Curry et al, 2010). However, this also
shows that a small minority of patients do not recover (see Figure E.2.2). Before
considering a patient partial-responder, non-responder or treatment-resistant it isimperative to review all potential factors that may have contributed to the patient’s
poor response; these are listed in Table E.1.11. For example, a child’s depression
was not improving; further assessment showed the mother to be depressed;
treating the mother’s depression resulted in an improvement in the child as well.
A clinical review in an adolescent who was not getting better showed short periodsof hypomanic symptoms and a grandfather who suffered from bipolar disorder;
treatment with lithium carbonate resulted in an improvement of symptoms.
One of the key issues is to ascertain whether the patient has been treatedwith an effective antidepressant at the appropriate dose (e.g., 40mg of fluoxetine)
and for long enough (e.g., 12 weeks). Inadequate dosage can also be due to poor
adherence to treatment, willful or accidental.

Treatment resistance
Despite the importance of this matter there is very limited empirical dataon treatment-resistant depression in youth and no agreed definition. Birmaher
and colleagues (2009) proposed the following definition of treatment resistance: ayouth whose symptoms of depression and functional impairment persist after 8-12
weeks of optimal pharmacological treatment or 8-16 sessions of IPT or CBT and afurther 8-12 weeks of an alternative antidepressant or augmentation therapy withother medications or evidence-based psychotherapy. That is, treatment resistanceshould be diagnosed only after two trials of evidence-based treatment at an adequate
dose and for an appropriate duration (e.g., 12 weeks).
Figure E.2.2 Recovery and recurrence: TADS participants after five
years (Curry J et al. 2010).

Depression E.1

25

IACAPAP Textbook of Child and Adolescent Mental HealthOnce treatment resistance has been confirmed, several options are available(following clinical wisdom and extrapolation of adult data, although none isbacked by evidence). These include optimization, switching, augmentation, and
ECT. An important practical aspect is that changes to treatment should be madeone at a time; otherwise it will be difficult to ascertain which change resulted in
the improvement.

Optimization isincreasing the medication(or psychotherapy) toa maximum dose or
lengthening the duration oftreatment. This is the firststrategy to consider when
patients do not improve
unless the patient has side
effects or is reluctant tocontinue the treatment.

There is little empirical data to guide us on the advantages of switchingversus augmentation, although it would appear that switching from fluoxetine toanother SSRI or to venlafaxine results in response in about one third of the patients,
consistent with data from adults (Brent et al, 2008). However, those treated withvenlafaxine showed more side effects. This suggests that if switching is the chosen
option, the initial switch should be to another SSRI rather than venlafaxine.

Augmenting the current
treatment is done by adding
another type of medication(e.g., lithium, another classof antidepressant) or, if notalready administered, byadding CBT or IPT.

Treatment setting
Most depressed young people should optimally receive ambulatory
treatment, which minimizes disruption to school attendance, family and social
relationships and stigma. Inpatient care may be justified when patients’ safety
cannot be guaranteed (e.g., high suicide risk), depression is very severe (e.g., severe
psychotic symptoms), or there is a lack of response. In the last case, admission tohospital may allow for a more accurate assessment of the reasons for non-response
and to monitor adherence and changes in treatment more closely.

Switching means
stopping or cross-tapering(reducing gradually) one
medication while the otheris gradually introduced.
The switch can be: (a) to
a different compound of
the same class (e.g., an
SSRI for another SSRI),(b) to a different class ofantidepressant (e.g., a
SSRI to a SNRI), or (c) to
psychotherapy.

RECURRENT DEPRESSION
It has already been highlighted that depression in the young is an illness thattends to recur. In the TADS follow up, for example, almost half (47%) of those
who recovered had a recurrence by 5 years. Adolescents who had responded poorly
in the short term, females and those with comorbid anxiety disorder were more
likely to have a new episode. However, recurrence rates were the same irrespectiveof the treatment provided (e.g., those who received fluoxetine combined with
CBT did not seem to obtain an extra benefit) (Curry et al, 2010). Treatment of a

Table Table E.1.11. Factors associated with partial or no response to treatment.
Patient
•
•
•
•
•
•
•
•
•
•

Younger age
Severe depression
Poor short-term
response
Poorer functioning
Appetite or weight
disturbanceSleep disturbancePoor adherence
Comorbid psychiatric ormedical conditions
Side effects
Medications (e.gsteroids)

Depression E.1

Family•••••Maternal depression
Lack of cooperation
Unreliability
Mistreatment, conflict
Psychopathology (e.g.,
drug and alcohol)

Environment
•
•
•
•
•

Bullying
Stressors
Dysfunctional schoolor neighborhood
Antisocial peer group
Cultural/ethnic issues

Clinician••••Misdiagnosis
Inappropriate treatment(non-evidence-based
treatment, inadequate
dose or not for longenough)Non-recognition of side
effects
Poor doctor-patienttherapeutic relationship26

IACAPAP Textbook of Child and Adolescent Mental Healthrecurrence should be the same as for the acute episode. Frequent recurrences may
require ongoing treatment with an antidepressant.

TREATING DEPRESSION COMORBID WITH OTHERDISORERS
Treating depression in youth comorbid with other psychiatric disorders (e.g.,anxiety, ADHD) requires particular skill. One would seek to alleviate symptomsof the most severe disorder first and symptom change should be monitored withspecific rating scales and not by assessing global functioning alone:• If at all possible, begin with a single medication.
• Make one medication change or addition at a time and allow adequate time
for response and dose adjustment.
• A change in medication may be warranted after 4 to 8 weeks of treatment if
there is no or minimal response in spite of an adequate dose. If there is some
response, continue with the medication making sure the dose is adequate.
• If symptoms persist after the administration of two evidence-based
treatments, follow the protocol for treatment-resistant depression.
• If use of multiple medications is clinically warranted (e.g., to treat the
comorbidities), you must be aware of and monitor potential interactions.

Substance use
Depression comorbid with substance use disorder poses particular challenges
and getting parents involved constructively in these efforts is critical. Because of
the increased risk of harm, implementing a safety plan when first assessing theadolescent and higher vigilance throughout treatment are very important. This
may include education regarding safe sex, sexually transmitted diseases including
HIV, contraception and about the additive impact of depression and substanceuse on these risks. It is necessary to emphasize that drugs and alcohol are notacceptable treatments for depression; they may appear to relieve symptoms in the
short term but will make the depression worse in the longer term.
Treatment should be integrated; that is, concurrent rather than sequential.
For example, do not wait for abstinence from drugs before starting antidepressanttreatment. Psychotherapies such as family therapy, motivation-enhancement
therapy and CBT should also be administered concurrently.
Managing a patient with a substance use disorder may require collecting
laboratory specimens such as urine drug screens regularly. In that case you should
know in advance—usually after discussion with the adolescent—to whom you
will inform of the results, under what circumstances, and how you will use that
information (see Chapters G.1, G.2 and G.3).

Depression in the intellectually disabled
Depression is difficult to diagnose and under-recognized in the intellectuallydisabled. No reliable data on the prevalence of depression in children withintellectual disability (mental retardation) exists, although there are suggestions thatit may be several times more common than in the general population. Depressed,
intellectually disabled youth usually show a sad or miserable facial expression,
crying and irritability, loss of interest in usual activities or stereotypical interests,
and appetite and sleep disturbances in the context of a change from previous

Depression E.1

Combining
antidepressant
medication and CBTThe TADS showed thatcombining an SSRI
(fluoxetine) and CBT was
better than fluoxetine or
CBT alone. Results indepressed adults alsosuggest that adding
CBT to antidepressant
medication results inhigher improvement rates.
As a consequence, manytreatment guidelines
recommend the use of an
SSRI combined with CBT
as the treatment of choice
for severe depression in theyoung.
A meta-analysis (Dubicka B
et al, 2010) addressed thequestion of whether CBT
confers additional benefit toantidepressant treatment inadolescents with unipolar
depression. Results
showed no evidence of anadvantage when combining
antidepressants and CBTover medication alone fordepressive symptoms,
suicidality and global
improvement after acutetreatment or at follow-up.
The combined treatment
did result in a greater
reduction in impairment
in the short-term (at 12
weeks). These results,
therefore, challenge
current wisdom but willneed replication. However,some specific groups ofyoung people may benefit
from the combination.
Evidence is emerging
that a combination of anantidepressant with CBT
may be more effective
than other interventionsin adolescents who had
failed to respond to an
appropriate course of anantidepressant.

27

IACAPAP Textbook of Child and Adolescent Mental Healthbehavior. Reduced food intake or food refusal, slowed movements, impaired selfcare, and catatonia are suggestive of depression in those more severely disabled.
Adolescents with mild intellectual disability are often able to report on theirinternal world and to describe depressive symptoms such as sadness, hopelessness,and suicidal thinking. Information from parents, caregivers, teachers, and respite
workers is important.
Given that there is no empirical evidence referring specifically to thetreatment of intellectually disabled children and adolescents with depression,
recommended management is the same as for non-intellectually disabled youth
with the appropriate adjustments (e.g., cognitive aspects are often inappropriate).
Consent to treatment issues, particularly to invasive treatment (such as ECT) pose
particular problems in these patients.

Depression comorbid with physical illness
Depression is common among young people with chronic physical illness
and its impact on their quality of life is considerable. According to Ortiz-Aguayo
and Campo (2009) “rather than being just another disorder suffered by a physicallyill child, the relationship between physical disease and depression is often complex
and bidirectional.” As a result recognition and diagnosis of depression in chronicallyill children is often a challenge because there is the risk of misattributing symptomsof the physical disease (e.g., fatigue, poor sleep or appetite) to a mood disorder andvice versa. Evaluation of changes in functioning is essential.
While treatment is as described for depressive episodes in other youth,
medication is particularly well suited to the management of depression in medical
settings but also has drawbacks, such as increased likelihood of adverse events anddrug interactions, requiring careful tailoring. For example, SSRIs may increase
the risk of gastrointestinal bleeding in children with coagulation disorders or in
combination with non-steroid anti-inflammatory drugs.

CROSS-CULTURAL PERSPECTIVESDo all youth, regardless of their culture, experience depression and its
manifestations similarly or does it vary according to cultural background? There
are many obstacles to answering this question. The well documented lack of
epidemiological data about childhood mental disorders in the developing worldis one. Accordingly, research is limited, unreliable and compounded by variations
in diagnostic practices. While cultural considerations in the assessment, diagnosis,
and treatment of childhood depression are necessary, it is difficult to disentangle
what is biological, what is cultural, and what is due to service issues. For example, it
has been suggested the reported increase in rates of childhood depression in North
America and Europe may only reflect a lowering of the threshold for diagnosis,
while the higher rate of suicide among Chinese young women compared withmen as well as its weaker association with depression seem to be largely due
to easy access to pesticides and poor access to emergency medical care in rural
Chinese communities. Though not specifically relating to depressive symptoms
but to behavior and emotional symptoms in general, data available suggest thatdifferences within groups in one society can be greater than differences between
societies (Achenbach et al, 2008).
There are many case reports about cultural differences in the manifestation ofdepression. For example, depressive symptoms in Afghanistan are similar to those

Depression E.1

28

IACAPAP Textbook of Child and Adolescent Mental Healthin other countries but in Afghanistan the majority of depressed patients express
passive death wishes rather than active suicidal thoughts. Despite suggestions that ahigher incidence of guilt feelings in Western countries is due to the influence of the
Judeo-Christian religion, when different religions are compared, the presence orabsence of guilt feelings is associated with the level of education and the degree ofdepression rather than with religious background (Inal-Emiroglu & Diler, 2009).
Japanese patients do not describe depression in the same way as Americans, nor
do they express feelings in the same way. For the Japanese, concrete images fromnature allow personal emotions to be expressed impersonally; as a result, they often
lack a personal reference or connection when expressing emotions. Rather thanas feelings of guilt or low mood, depression is frequently experienced in somatic
terms in Hispanic populations. Clinicians must be aware that depressed Hispanic
youth may present with headaches, gastrointestinal and cardiovascular symptoms,
or complaints of “nerves”. Many Chinese people when depressed do not reportfeeling sad; they complain of boredom, feelings of inner pressure, pain, dizziness,and fatigue and often find a diagnosis of depression morally unacceptable andmeaningless.

BARRIERS IN THE IMPLEMENTATION OF EVIDENCEBASED CARE IN LOW-INCOME COUNTRIESThere are numerous barriers to the implementation of evidence-based carefor depression in developing countries (for more detail see Inal-Emiroglu & Diler,2009). This is most concerning because the proportion of the population younger
than 18 years is much higher in low income than in affluent nations.
Barriers to care exist in all countries but more so in low-income ones.
Besides issues such as transportation and the capacity to pay for services, the dearthof professionals, including allied health, trained in this area is a global problem.
Not only there are few child and adolescent psychiatrists but also the profession
is not formally recognized as specialty in many countries, even in some developed
nations. The number of child psychiatrists per million people was estimated around2006 to be 21 in the United States, 2.8 in Singapore, 2.5 in Hong Kong and 0.5 in
Malaysia. With few exceptions, the number of child and adolescent psychiatrists is
negligible in most African, Eastern Mediterranean, Southeast Asian, and Western
Pacific countries. This also applies to child psychologists, social workers and nurses
trained in this area, and to the services available. Gaps are often filled by religious
figures (i.e., priests, imams) and healers (see Chapter J.2). Inpatient facilities forchildren and adolescents do not exist in many countries even developed ones.

According to Kleinman(2004), “culture

confounds diagnosis
and management by
influencing not only
the experience ofdepression, but also
the seeking of help,
patient-practitioner
communication, andprofessional practice.
Culture also affects theinteraction of risk factors
with social supports andprotective psychologicalfactors that contributeto depression in thefirst place. Culture may
even turn out to create
distinctive environments
for gene expression andphysiological reaction,
resulting in a local
biology of depression:
research alreadyshows that persons
from various ethnic
backgrounds metabolize
antidepressant drugs indistinct ways.”

Countries in Central and Eastern Europe deserve special mention. They
comprise 30 new democracies with a population of around 400 million that had
been under communist regimes for 50 to 70 years and have moved to democraticsystems of government towards the end of the 20th century (see Chapter J.10).
These Central and Eastern European countries had developed a unique systemof mental health care driven by Soviet ideology, which focused in residential
institutions reflecting state policies based on the social exclusion of vulnerable
groups. The usual solution was to institutionalize children when families werein crisis or if children developed problems. Ignoring psychosocial factors was theconsequence of believing that psychosocial problems had been successfully solvedby the Soviet political system. These attitudes and structures are gradually changing(Puras, 2009).

Depression E.1

29

IACAPAP Textbook of Child and Adolescent Mental HealthParents’, teachers’ and health professionals’ knowledge of, and attitudes
towards depression may lead to delayed or inappropriate help-seeking, or may
hamper adherence to clinicians’ recommendations. In general, knowledge about
depression in developing countries is limited, emotional problems being viewed as
more stigmatizing—a sign of weakness, contagious—in some cultures than others.
However, stigma appears to be a more significant barrier to treatment in high income
than in low income countries. Perceptions of depression are often inconsistent.
For example a survey suggested that Turkish people identified depression as an
illness, perceived it as a social problem, believed that depression could be treatedwith drugs but had little knowledge about medications and treatment and weredoubtful about society’s acceptance of depressed patients (Inal-Emiroglu & Diler,2009). Training primary care doctors on the diagnosis and treatment of depression
may be the best way to improve treatment.
Access to psychosocial treatments in developing countries is very poor
due to lack of trained professionals, so it is access to medication. The WHO’s(2010) list of essential medicines for pediatric patients only includes fluoxetine,
while for adults it only includes fluoxetine and amitriptyline for the treatment ofmood disorders, as well as lithium carbonate, carbamazepine, and valproic acid forbipolar disorder. Less than half of the countries in the world provide some formof subsidy for medication. Even if medication is prescribed, follow up is likely to
be inadequate.

PREVENTION
The goal of prevention is to decrease the likelihood of depressive symptoms
and disorders from developing in a population (universal intervention). There areother, more targeted, preventative options that may be more useful, for example
early intervention with individuals with subclinical levels of depressive symptoms,
seeking to reduce these symptoms and prevent the development of a full blown
depressive episode: selective (if the target participants have significant risk factors) orindicated prevention (when individuals already show subclinical levels of depressive
symptoms). Table E.1.3 lists key risk factors and implications for prevention.
Overall, outcome of prevention programs has been mixed. Targeted (selective
and indicated) programs show small to moderate effect sizes but greater than thoseof universal programs, which have been found to be largely ineffective. The mostefficacious programs focus on cognitive restructuring, social problem-solving,interpersonal communication skills, coping, and assertiveness training individuallyor in groups. Prevention programs are typically conducted with groups of children
or adolescents in school or clinic settings (Garber 2009; US Preventive Services
Task Force, 2009). One approach that seems to have achieved more success is
the Coping with Depression Course for Adolescents. The program consists of eight
weekly 90-minute group sessions followed by six continuation sessions. In one
study the program showed significant sustained effects compared with usual carein preventing the onset of depressive episodes in youth at risk over a 3-year period(Beardslee et al, 2013).

Depression E.1

Barriers refer to:•
Resources: trained
personnel, services
available, cost•

Cultural issues:
perceptions ofdepression, stigma•

Use of medication

Project CATCH-IT
This is a free internet-based
intervention developed by
the University of Chicago.
The purpose is to help teachresiliency to teenagers
and young adults using
a cognitive behaviouralmodel to reduce the risk
developing depression.
Initial research suggeststhat it may be effective. To
access the program click on
the picture below.

The guiding principles forprevention (Garber 2009)are:•

Keep it simple•

Keep it interesting, and•Make it relevant

30IACAPAP Textbook of Child and Adolescent Mental Health

REFERENCES

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Australian Broadcasting Corporation. The Girl Less Likely. 15
September 2008.
Beardslee WR, Brent DA, Weersing VR et al (2013). Preventionof depression in at-risk adolescents: Longer-term effects,
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Birleson P. The validity of depressive disorder in childhood andthe development of a self-rating scale: A research report.
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Issues. Practice parameter for the assessment andtreatment of children and adolescents with depressive
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Birmaher B, Brent D. Treatment resistant depression. In Rey
JM, Birmaher B (eds). Treating Child and Adolescent
Depression. Philadelphia: Lippincott Williams & Wilkins
2009:209-219.
Birmaher B, Ryan ND, Williamson DE et al. Childhood andadolescent depression: a review of the past 10 years. Part
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Psychiatry, 1996; 35:1427-1439.
Brent D, Emslie G, Clarke G et al. Switching to another SSRI
or to venlafaxine with or without cognitive behavioral
therapy for adolescents with SSRI-resistantdepression.
The TORDIA randomized controlled trial. JAMA, 2008;
299:901-913.
Bridge JA, Birmaher B, Iyengar S et al. Placebo response inrandomized controlled trials of antidepressants forpediatric major depressive disorder. American Journal of
Psychiatry, 2009;166: 42–49.
Bridge JA, Iyengar S, Salary CB et al. Clinical response and risk
for reported suicidal ideation and suicide attempts inpediatric antidepressant treatment. A meta-analysis ofrandomized controlled trials. JAMA, 2007; 297:16831996.
Brooks SJ, Krulewicz S, Kutcher S. The Kutcher Adolescent
Depression Scale: Assessment of its evaluative properties
over the course of an 8–week pediatric pharmacotherapy
trial. Journal of Child and Adolescent Psychopharmacology,
2003; 13:337–349.

Depression E.1

Buckley NA, McManus PR. Fatal toxicity of serotoninergic andother antidepressant drugs: analysis of United Kingdom
mortality data. BMJ 2002;325:1332–1333.
Carlson GA, Cantwell DP. Unmasking masked depression inchildren and adolescents. American Journal of Psychiatry
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Caspi A, Sugden K, Moffitt TE et al. Influence of life stresson depression: moderation by a polymorphism in the
5-HTT gene. Science. 2003; 18;301(5631):386-389.
Copeland WE, Miller-Johnson S, Keeler G et al. Childhood
psychiatric disorders and young adult crime: A
prospective, population-based study. American Journal of
Psychiatry, 2007; 164:1668–1675.
Costello EJ, Mustillo S, Erkanli A et al. Prevalence anddevelopment of psychiatric disorders in childhood andadolescence. Archives of General Psychiatry 2003; 60:837844.
Curry J, Silva S, Rohde P, Ginsburg G et al. Recovery andrecurrence following treatment for adolescent major
depression. Archives of General Psychiatry 2010.
Published online November 1, 2010. doi:10.1001/
archgenpsychiatry.2010.150.
Dubicka B, Elvins R, Roberts C et al. Combined treatment withcognitive behavioural therapy in adolescent depression:
meta-analysis. The British Journal of Psychiatry, 2010;
197: 433-440.
Faulstich ME, Carey MP, Ruggiero L et al. Assessment ofdepression in childhood and adolescence: An evaluationof the Center for Epidemiological Studies Depression
Scale for Children (CES-DC). American Journal of
Psychiatry, 1986; 143(8):1024–1027.
Fergusson DM, Horwood LJ, Miller AL, Kennedy MA. Life
stress, 5-HTTLPR and mental disorder: findings froma 30-year longitudinal study. The British Journal of
Psychiatry 2011;198:129-135.
Frye MA. Bipolar disorder. A focus on depression. New England
Journal of Medicine, 2011;364:51-59.
Garber J. Prevention of depression and early intervention with
sub-clinical depression. In Rey JM, Birmaher B (eds).
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Lippincott Williams & Wilkins 2009:274-294.
Goodman R, Ford T, Simmons H et al. Using the Strengths andDifficulties Questionnaire (SDQ) to screen for childpsychiatric disorders in a community sample. The British
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Inal-Emiroglu FN, Diler RS. International views and treatment
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IACAPAP Textbook of Child and Adolescent Mental HealthJohnson JG, Harris ES, Spitzer RL et al. The Patient Health
Questionnaire for Adolescents: Validation of an
instrument for the assessment of mental disorders among
adolescent primary care patients. Journal of Adolescent
Health. 2002;30:196-204.
Kleinman A. Culture and depression. New England Journal of
Medicine, 2004; 351:951-953.
Karg K, Burmeister M, Shedden K, Sen S. The serotonintransporter promoter variant (5-HTTLPR), stress,and depression meta-analysis revisited: Evidence ofgenetic moderation. Archives of General Psychiatry.
Published online January 3, 2011. doi:10.1001/
archgenpsychiatry.2010.189
Krishnan V, Nestler EJ. Linking molecules to mood: new insight
into the biology of depression. American Journal of
Psychiatry 2010; 167:1305–1320.
Langer DA, Chiu A, Asarnow JR. How to use CBT foryouth depression: A guide to implementation. In Rey
JM, Birmaher B (eds). Treating Child and Adolescent
Depression. Philadelphia: Lippincott Williams & Wilkins
2009:100-113.
Mufson L, Verdeli H, Clougherty KF et al. How to useinterpersonal psychotherapy for depressed adolescents(IPT-A). In Rey JM, Birmaher B (eds). Treating Childand Adolescent Depression. Philadelphia: Lippincott
Williams & Wilkins 2009:114-127.
Nathan B. “And Then My Tears Subsided...”National Institute for Health and Clinical Excellence. Depressionin Children and Young People: Identification andManagement in Primary, Community and Secondary
Care. National Clinical Practice Guideline Number 28.
Leicester, UK: The British Psychological Society 2005.
Ortiz-Aguayo R, Campo JV. Treating depression in children
and adolescents with chronic physical illness. In Rey
JM, Birmaher B (eds). Treating Child and Adolescent
Depression. Philadelphia: Lippincott Williams & Wilkins
2009:295-309.

Depression E.1

Puras D. Development of child mental health services in Central
and Eastern Europe. IACAPAP Bulletin, 2009; 24:9-10.
Poznanski E, Mokros H. Children’s Depression Rating Scale–
Revised Manual. Los Angeles, CA: Western Psychological
Services; 1996.
Rey JM. How to use complementary and alternative medicine
treatments. In Rey JM, Birmaher B (eds). Treating Childand Adolescent Depression. Philadelphia: Lippincott
Williams & Wilkins 2009:151-161.
Risch N, Herrell R. Lehner T at al. Interaction between theserotonin transporter gene (5-HTTLPR), stressful life
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2009; 301:2462-2471.
Stevens J, Kelleher KJ, Gardner W et al. Trial of computerized
screening for adolescent behavioral concerns. Pediatrics
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2010.

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IACAPAP Textbook of Child and Adolescent Mental HealthAppendix E.1.1
SELF-DIRECTED LEARNING EXERCISES AND SELF-ASSESSMENT•

Interview a child or adolescent who is complaining of depressive symptoms.

•

Write a letter to the family doctor or referring agent summarizing the above case(formulation), including a provisional diagnosis and a management plan (as per Chapter
A.10).

•

Watch the documentary The Girl Less Likely (30 Minutes) http://www.abc.net.au/
austory/specials/leastlikely/default.htm and write a summary (less than one page inlength) highlighting the main issues raised.

•

What are the important medical causes of depressive symptoms that should beconsidered before making a diagnosis of major depression? (see page 12)•

Write short summary describing risk factors for depression (see Table E.1.3 on page 7).

•

Describe and contrast the appropriate management of mild, moderate and severe
unipolar depression (see page 23).

•

Describe the difference between the treatment of unipolar depression and bipolar
depression and the reasons for it (see Page 23 and 24).

MCQ E.1.1
What class of medicationis the first line treatment for severe
depression OR moderate depression
unresponsive to psychotherapy in children
and adolescents?
A. Monoamine oxidase inhibitors
B. Selective serotonin reuptake inhibitors
C. Serotonin norepinephrine reuptake
inhibitors
D. Tetracyclic antidepressantsE. Tricyclic antidepressants
MCQ E.1.2
Fluoxetine in the treatment ofdepression in children and adolescents:
A. Is the best studied and has the best
evidence of effectiveness
B. Is a Selective Norepinephrine
Reuptake Inhibitor
C. Shows more side effects than the other
SSRIs
D. Is a Monoamine Oxidase Inhibitor

MCQ E.1.3
Paroxetine in the treatment
of depression in youth:
A. Has a longer half-life than otherselective serotonin reuptake inhibitors
B. Has been shown to be as effective asother antidepressants
C. Has more side effects than otherselective serotonin reuptake inhibitors
D. Has no withdrawal symptoms
E. Is less likely to cause a serotonergic
syndrome
MCQ E.1.4
All of the following
substances are known to mimic
depression in children and adolescents
except:A. Corticosteroids
B. Isotretinoin
C. Marijuana
D. Solvents
E. Tetracyclines

E. Is a Tricyclic antidepressant

Depression E.1

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IACAPAP Textbook of Child and Adolescent Mental Health

MCQ E.1.5
The prevalence ofdepression in children and adolescents:
A. Is lower in teenage girls than teenage
boys

MCQ E.1.9
All of the following should
increase suspicion that a depressive
episode is part of a bipolar disorder
except:B. Is higher in patients who suffer fromchronic medical conditions

A. Catatonic symptoms

C. Is lower in indigenous minority children

C. Family history of bipolar disorder

D. Is lower in adolescence than inchildhood

D. Manic switch after treatment withantidepressants

E. Is the same from country to country

E. Psychotic symptoms.

MCQ E.1.6
The course of depression inchildren and adolescents:
A. Generally does not have recurring
episodesB. Is likely to be better with earlier onset
C. Is likely to continue in adulthood
D. Is not similar to that of adults
E. On average, episodes do notspontaneously remit.
MCQ E.1.7
Predictors of depression
recurrence in children and adolescence
do not include which of the following?
A. Comorbidity
B. Greater hopelessness
C. High socioeconomic status

B. Comorbid thyroid disease

Q E.1.10
Parental depression is themost consistently replicated risk factor for
depression in the offspring.
True or false?
Q E.1.11
Diagnosis of personality
disorder should be provisional in a
depressed adolescent and made on thebases of symptoms and functioning
outside of the depressive episode.
True or false?
MCQ E.1.12 Which of the following
psychosocial therapies has evidence thatit can be effective for mild to moderate
depression in as few as 8 to 16 sessions?

D. Negative cognitive style

A. Cognitive Behavioral Therapy

E. Previous episodes

B. Family therapy

MCQ E.1.8
All of the following medical
conditions are known to mimic depressionin children and adolescents except:
A. Acquired Immunodeficiency Syndrome(AIDS)
B. Pyloric Stenosis
C. Mononucleosis
D. Thyroid Disease
E. Migraine

C. Group therapies
D. Psychodynamic (psychoanalytic)
psychotherapy
E. Self-help
MCQ E.1.13 While antidepressants tend
to achieve better results in the shortterm, differences between medication andtherapy tend to disappear after:
A. 2-5 weeks
B. 6-10 weeks
C. 11-18 weeks
D. 19-23 weeks
E. 24-36 weeks

Depression E.1

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IACAPAP Textbook of Child and Adolescent Mental Health

MCQ E.1.14 The most importantdistinguishing feature in the diagnosis ofserotonin syndrome is:

MCQ E.1.16 First line therapy for abipolar depressive episode in a young
teenager usually is:

A. Ataxia

A. An antidepressant

B. Bradycardia

B. Lamotrigine

C. Clonus

C. Lithium carbonate or quetiapine

D. Confusion

D. Olanzapine and an antidepressant

E. Diarrhea

E. Valproate and an antidepressant

MCQ E.1.15 In a unipolar depressive
episode of mild severity in a 10-year-old,the appropriate first intervention is:
A. Anti-depressants
B. Electroconvulsive therapy
C. S-adenosyl methionine
D. Second generation antipsychotic
E. Supportive management or
psychosocial treatment

Depression E.1

Q E.1.17
Antidepressant treatment
in an adolescent for a first episode of
unipolar depression should be:
A. Continued for at least 6 months after
recoveryB. Continued indefinitely
C. Continued until recovery
D. Stopped after 6 months
E. Stopped after 8 weeks

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IACAPAP Textbook of Child and Adolescent Mental HealthANSWERS•

MCQ E.1.1: B; see page 18,19 & 21.

•

MCQ E.1.2: A; see page 21.

•

MCQ E.1.3: C; see Table E.1.8 on page 21•

MCQ E.1.4: E; see page 12•

MCQ E.1.5: B; see page 2-3.

•

MCQ E.1.6: C; see page 3-4.

•

MCQ E.1.7: C; see page 4.

•

MCQ E.1.8: B; see page 12•

MCQ E.1.9: B; see page 12•

Q E.1.10: True; see page 5•

Q E.1.11: True; see page 8•

MCQ E.1.12: A; see page 16•

MCQ E.1.13; E; see page 17•

MCQ E.1.14: C; see page 23•

MCQ E.1.15: E; see page 16•

MCQ E.1.16: C; see page 23•

Q E.1.17: A; see page 24-25.

Depression E.1

36