Edited by Shane R. Jimerson, Ph.D.
Contributed to by the Graduate Students in the Counseling, Clinical,
and School Psychology Program at the University of California, Santa Barbara.
Ongoing design and publication of this site is completed by Shane R. Jimerson, Jeff R. Klein and Angela D. Whipple. Please forward comments regarding this site to Shane R. Jimerson. This page was last updated 1.11.02. © 2002
Symptoms
Epidemiology
Etiology
Assessment
Treatment
Authors
Shane R. Jimerson, Ashley Duggan, Angela Whipple and Jeffrey K. Ellens
University of California, Santa Barbara
The authors also note the important contributions of Traci Marx, Sharon Noble and Stacey Peerson who provided information critical to the development of this website
DEPRESSION
During the past decade, as depression is becoming
increasingly evident at younger ages, a great deal of attention has been
directed towards the diagnosis and treatment of depression in children
and adolescents (Birmaher, Ryan, Williamson, & Brent, 1996).
There is a consensus that children and adolescents experience depressed
mood, however, controversy continues to exist when differentiating childhood
from adult depressive disorders. It also must be acknowledged that
a fundamental difference between adults and children is the ongoing developmental
changes that children experience. Because of difficulties in school
settings for depressed children and the high comorbidity with other pathologies,
understanding depression in children is important for school professionals.
Consequently, a clear need exists for an understanding of normative behaviors
as well as the development of diagnostic criteria which are specific for
every childhood and adolescent developmental stage.
Numerous outcome studies have documented several
negative effects of depression on children (Hammen & Compas, 1994;
Birmaher et al., 1996; Kaslow, Deering & Racusin, 1994). Childhood
depression is commonly associated with high incidences of sympomatic comorbidity,
(Angold & Costello, 1993; Birmaher et al., 1996; Hammen & Compas,
1994), wherein, features associated with other disorders are present.
For example, depression and features of anxiety have been found to be correlated
(Weems, Hammond-Laurence, Silverman, & Ferguson, 1997).
Other disorders often observed with depression include conduct/ behavioral
disorders, and substance abuse. Symptomatic comorbidity complicates
both the detection and treatment of depession by “masking” its presence.
The earlier the onset of depression, the poorer the prognosis for the child
(Birmaher et al., 1996; Garrison, Waller, Cuffe, & McKeown, 1997);
remaining undetected (and untreated), childhood depression increases a
child’s risk for substance abuse, suicidal behavior, and poor psychological,
social, and academic functioning (Birmaher et al., 1996; Kaslow et al.,
1994). Additional factors may influence depression as well, including
gender, ethnicity, and social class (Cicchetti & Toth, 1998; Siegel,
Aneshensel, Taub, Cantwell, & others, 1998). In order to more
clearly understand the multiple risk factors of childhood depression, and
in order to better differentiate normative from non-normative developmental
trajectories, the ongoing study of youth depression is vital.
SYMPTOMS
Although the criteria for depression are the
same for children and adolescents as they are for adults, there are unique
developmental challenges and considerations in diagnosing and treating
youth depression. For example, children often have difficulty expressing
or recalling information related to their disorder (Emslie & Mayes,
1999); Due to this complication, it is often critical for purposes of diagnosis
that corroborating information be obtained from parents, school teachers,
and other adults in the child’s life. Another factor that complicates
diagnosis and treatment is the high rate of comorbidity that is characteristic
of childhood depression. Often times depression is not the only diagnosis
warranting clinical attention, and it is important for clinicians to be
sensitive to all mental health needs with which a child presents.
Major Depressive Episode and Dysthymic Disorder
are two distinct classifications for depressive symptoms in the DSM-IV
(1994). The severity and duration of the symptoms distinguish the
two, as noted in Table 1. The core symptoms of a Major Depressive
Episode, as reported in the DSM-IV (1994), are basically the same for children,
adolescents, and adults, despite indications that some characteristic symptoms
may vary with age. The criteria do allow a 1-year duration for children
and adolescents (as opposed to at least 2 years for adults); and permit
the substitution of “irritability” for “depressed mood,” as irritability,
somatic complaints, and social withdrawal are more common symptoms of depression
for children and adolescents.
DSM-IV Criteria for Depressive Disorders
Major Depressive Episode and Dysthymic Disorder are two distinct classifications for depressive symptoms in the DSM-IV (1994). The severity and duration of the symptoms distinguish the two, note below.
The core symptoms of a Major Depressive Episode, as reported in the DSM-IV (1994), are basically the same for children, adolescents, and adults, despite indications that some characteristic symptoms may vary with age. The criteria do allow a 1-year duration for children and adolescents (as opposed to at least 2 years for adults); and permit the substitution of “irritability” for “depressed mood,” as irritability, somatic complaints, and social withdrawal are more common symptoms of depression for children and adolescents.
DSM-IV (1994) Criteria for Major Depressive Episode
A. Five (or more) of the following symptoms have been present
during the same 2-week period and represent a change from previous functioning;
at least one of the symptoms is either (1) depressed mood or (2) loss of
interest or pleasure.
(1) depressed mood most of the day, nearly
every day.
Note: In children
and adolescents, can be irritable mood.
(2) markedly diminished interest or pleasure in all, or almost all activities most of the day, nearly every day.
(3) significant weight loss when not dieting
or weight gain or decrease or increase in appetite nearly every day.
Note: In children, consider failure
to make expected weight gains.
(4) insomnia or hypersomnia nearly every day.
(5) psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
(6) fatigue or loss of energy nearly every day.
(7) feelings of worthlessness or excessive or inappropriate guilt nearly every day (not merely self reproach or guilt about being sick).
(8) diminished ability to think or concentrate, or indecisiveness, nearly every day.
(9) recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
Source. American Psychiatric Association.
(1994). Diagnostic and statistical manual of mental disorders (4th
ed., p. 327). Washington DC: Author.
DSM-IV (1994) Criteria for Dysthymic Disorder
A. Depressed mood for most of the day, for more days than not, as indicated either by subjective account or observation by others, for at least 2 years. Note: In children and adolescents, mood can be irritable and duration must be at least 1 year.
B. Presence, while depressed, of two (or more) of the following:
(1) poor appetite or overeating
(2) insomnia or hypersomnia
(3) low energy or fatigue
(4) low self-esteem
(5) poor concentration or difficulty making decisions
(6) feelings of hopelessness
C. During the 2-year period (1 year for children or adolescents) of the disturbance, the person has never been without the symptoms in Criteria A and B for more than 2 months at a time.
D. No Major Depressive Episode has been present during the first 2 years of the disturbance (1 year for children and adolescents).
E. There has never been a Manic Episode, a Mixed Episode, or a Hypomanic Episode, and criteria have never been met for Cyclothymic Disorder.
F. The disturbance does not occur exclusively during the course of a chronic Psychotic Disorder, such as Schizophrenia or Delusional Disorder.
G. The symptoms are not due to direct physiological effects of a substance or a general medical condition.
H. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
Source. American Psychiatric Association. (1994).
Diagnostic and statistical manual of mental disorders (4th ed., p. 349).
Washington, DC:
Author.
EPIDEMIOLOGY
Researchers have found it difficult to document
the prevalence of depression in children and adolescents due to controversy
about the definition and diagnostic criteria, including unclear distinctions
between symptoms, disorders, and syndromes. The various types of
assessments are not equal in diagnosing depression in all subjects, and
considerable differences have been found in prevalence rates depending
upon the population studied (Hammen & Compas, 1994; Kaslow et al.,
1994). Considering the above, the prevalence of depression in prepubertal
children is estimated at approximately 2% (Carlson, 2000; Institute of
Medicine, 1989). During adolescence the prevalence of depression
increases substantially, with 5% to 10% of adolescents manifesting a major
depressive disorder (Cicchetti, & Toth, 1995). At any given time,
approximately 10% to 15% of children in the general population will report
moderate to severe levels of depressive symptoms (Nolen-Hoeksema et al.,
1992). Prevalence figures are much higher for various groups of referred
and clinical samples of children (Hammen & Compas, 1994). Although
90% of major depressive episodes remit after 1.5 to 2 years, studies have
shown that depression recurs in adulthood for 60% to 70% of depressed children
(Birmaher et al., 1996). Depression is surprisingly common in adolescence,
with recent estimations that approximately 28% of adolescents will have
experienced a Major Depressive Episode by age 19 (35% of young women and
19% of young men) (Lewinsohn, Rohde, & Seeley, 1998). It should
be noted that these prevalence rates compare to the rates in the National
Comorbidity Study (Kessler, McGonagle, Nelson, Hughes, Schwartz, &
Glazer, 1994).
The mean age of onset of first depressive
episodes was approximately 15 years of age in an epidemiological study
of over 1,500 adolescents (Lewinsohn, Clark, Seeley & Rohde, 1994).
It is interesting to note that children who are diagnosed with a comorbid
anxiety disorder have an earlier age of onset (9 to 11 years) of depression
(Hammen & Compas, 1994). Usually gender differences are not reported
in children ages 6 to 12; however, some researchers have found that prior
to puberty (12 years), boys are more likely to be diagnosed with depression
than girls (Angold & Rutter, 1992). Some research suggests (Suesser,
1998) that these prepubescent gender differences may be the result of boys’
greater tendency to utilize externalizing coping styles (i.e. fighting)
when dealing with depression. Externalizing children are more likely
to be targeted, assessed, and consequently diagnosed with depression than
children who utilize an internalizing coping strategy (i.e. social withdrawal).
Additionally, the methods clinicians utilize in their diagnosis may help
determine whether or not a child (especially a young child) is inevitably
diagnosed with depression. Regardless of what the true gender differences
of early childhood depression are, there appears to be a sudden shift in
the aforementioned trend beginning in adolescence (following puberty) in
which the gender ratio shifts, with depression becoming at least twice
as common among females. One study reported even more dramatic gender
differences for adolescent depression finding that girls were four times
more likely to suffer from depression than boys (base rates were 13% and
4%, respectively) (Kashani, Carlson, Beck, & Hoeper, 1987). Clearly,
factors associated with puberty warrant further attention in understanding
the formation of adolescent depression (Clarizio, 1989).
With childhood depression, comorbidity is
the rule rather than the exception. Comorbidity, or the co-occurrence
of two independent diagnoses, has been found to exist in 40% to 70% of
depressed children and adolescents (Birmaher et al., 1996; Hammen &
Compas, 1994). Anxiety, dysthymic and conduct/behavioral disorders,
and substance abuse are the most frequent comorbid diagnoses (Birmaher
et al., 1996; Hammen & Compas, 1994).
Current Research Regarding Depression Epidemiology
Angold and Costello (1993) discuss depressive
comorbidity in children and adolescents. Their article reviewed a
study that examined comorbidity in children and adolescents experiencing
depression across several recent epidemiological studies. Comorbidity,
in the context of child and adolescent depression, was examined with three
of the common psychiatric disorders of childhood and adolescence:
anxiety disorders, conduct and oppositional disorders, and attention deficit
hyperactivity disorders. The authors addressed four empirical
questions: 1) Is depressive comorbidity more common than expected
by chance in studies of child and adolescent psychopathology. In
the majority of cases, the disorders (anxiety disorders, conduct and oppositional
disorders, and attention deficit hyperactivity) were more common in depressed
children than expected by chance. 2) Is depression associated with
a greater risk of other disorders in general, or do some diagnoses accompany
depression more frequently than do others? Depression co-occurs with
anxiety, conduct and oppositional, and attention deficit disorders more
frequently than with other disorders in general. 3) Are comorbid
disorders found more often in children with depression than depression
is found in children with other diagnoses? There was a high rate
of comorbidity in children and adolescents with major depressive disorders
or dysthymia. Comorbidity with conduct disorder/oppositional defiant
disorder ranged from 21% to 83%; comorbidity with anxiety disorders ranged
from 30% to 75%; and comorbidity with attention deficit disorder ranged
from 0% to 57.1%; and 4) Is comorbidity more common in clinical than in
epidemiological studies of depressed children? Rates of depressive comorbidity
found in community studies were similar to rates found in clinical studies.
While the authors conclude that the specific mechanisms by which comorbidity
occurs are currently obscure they offer several possible substantive explanations
that are worth exploring.
Birmaher, Ryan, Williamson, and Brent (1996)
review the literature published over the last decade on issues pertaining
to early onset depression. These authors note that prevalence rates of
depression in children range from .4% to 2.5%, with a wider range (.4%
to 8.3%) indicated for adolescents. They contend that less information
is available for those with dysthymic disorder, and suggest prevalence
rates of .6% to 1.7% in children, and 1.6% to 8.0% in adolescents.
Although boys and girls manifest symptoms of Major Depressive Disorder
(MDD) equally in childhood, MDD is twice as common in females than in males
during their adolescent years. The mean length of MDD is approximately
seven to nine months in duration. Though virtually 90% of major depressive
episodes remit in 1.5 to 2 years from time of onset, studies consistently
find that MDD is a recurrent condition. The interaction of genetics and
environment are strongly implicated in the onset of MDD. An individual
with a genetic vulnerability is likely to be at increased risk for MDD
when experiencing a stressful environment. Many environmental factors
have been associated with MDD in youths. Parental psychopathology,
poor social support, and stressful life events such as divorce or bereavement
are merely a few of the factors suggested to influence the onset and natural
course of MDD. Beck associates depression with "low self-esteem,
high self-criticism, significant cognitive distortions, and a feeling of
lack of control over negative events." (as cited in Birmaher etal., 1996).
A surprisingly large number of individuals
struggle with difficulties associated with additional psychiatric problems.
Forty to seventy percent of depressed youths have comorbid psychiatric
disorders, with 20 to 50% experiencing two or more comorbid disorders.
Comorbidity is problematic in that it appears to contribute to a more negative
life course. Those with comorbid psychiatric diagnoses that include
MDD are at greater risk for recurrent depression, more enduring depressive
episodes, suicidal behaviors, poorer response to treatment and underutilization
of psychological services. Children and adolescents with depression
frequently suffer in their school performance, as well as in their relationships
with others. Social skills deficits have also shown a significant
correlation with depression, although the direction of relationship is
not as clear (Segrin, 2000). According to Birmaher, Ryan, Williamson,
& Brent (1996), "depression in children and adolescents is also associated
with an increased risk of suicidal behaviors, homicidal ideation, tobacco
use, and abuse of alcohol and other substances during later adolescence."
(p. 1431). Several studies cited by Birmaher et al. suggest that suicide
accounts for a staggering 12% of the total mortality of adolescents.
These authors emphasize the heterogeneous nature of depression. They
imply that its pathogenesis may be complex and varied from one affected
individual to the next.
Cicchetti and Toth (1998) provide a thorough
article on the development of depression in children and adolescents.
Their article presents a developmental psychopathology view of childhood
and adolescent depression, where a multi-level approach is used in examining
the diverse pathways that may lead to depressive disorder. Cicchetti
and Toth (1998) include research that supports current views on the definitions,
epidemiology, clinical characteristics, and gender differences in childhood
depression. The possible relationship between depressed mood and
that of the child’s affect and attachment to a caregiver are also explored.
As such, the ontogenic development of depression is evaluated, including
homeostatic and physiological regulation, the role of affect, attention,
and arousal, the attachment relationship and the self-system. A transactional
model incorporating a social ecological framework is introduced, including
an overview of the microsystem(s), exosystem(s), and macrosystem(s) that
may be involved. These systems include the family, home environment,
neighborhood, school, community-at-large, culture, and societal support.
Prevention, child competence, and therapeutic strategies are promoted,
with an acknowledgement of the larger developmental context as key.
Garrison, Waller, Cuffe, and McKeown (1997)
give evidence for the incidence of major depressive disorder and dysthymia
in young adolescents. They conducted a longitudinal study examining
depression and dysthymia in a sample of junior high and high school students
from one public school district in the southeastern United States.
Data collection included a school screening and diagnostic interview process.
The former procedures consisted of a self-administered questionnaire that
obtained demographic information; the Center for Epidemiologic Studies
Depression Scale (CES-D), with three additional items assessing suicide
intent; a modified Coddington Life Event Schedule for Adolescents (LES-A);
and the Family Adaptability and Cohesion Evaluation Scales (FACES-II).
These instruments evaluated depressive symptomatology/suicidality, stress
from undesirable life events, and level of perceived emotional bonding/individual
autonomy in the family system. Students selected to participate in
the diagnostic interview included individuals whose scores on the CES-D
indicated higher risk for major depressive disorder (MDD), and a random
sample of remaining students from phase one screening. During the
diagnostic interview, an adolescent and his/her parent (typically the mother)
completed separate semi-structured interviews. These included the
Present Episode version of the Schedule for Affective Disorders and Schizophrenia
for School-Age Children (K-SADS), the Children's Global Assessment Scale
(CGAS), and the Hollingshead Two Factor Index of Social Position.
These instruments assessed for psychiatric disorders during the previous
year, level of functional impairment, and household socioeconomic level,
respectively.
Lewinsohn, Rohde, and Seeley, (1998) summarize
current understanding of major depressive disorders (MSD) in adolescents
14 to 18 years old. Results are part of a larger program of research
under the Oregon Adolescent Depression Project. Pheomenology of major
depressive disorder is described in terms of frequency of symptoms of MDD,
cases observed in clinics as compared to the community, and age and gender
difference in symptom presentation. Epidemiology is described in
terms of MDD onset, duration of depressive episodes and time to recurrence,
and the impact of age, gender, and pubertal timing. Occurrence of
suicidal behavior linked to suicide is also discussed. Comorbidity
of depression is described as occurring with dysthemia and other mental
disorders, and implications for high comorbidity are presented. A
psychosocial link with becoming, being, and having been depressed is described
in some detail. An etiologic model of depression is presented, and
assessment and screening options are described. Finally, treatment
and prevention options are compared with regard to efficacy, meeting wants
and needs of depressed adolescents, and responses to different types of
treatment. Conclusions and recommendations covering a broad array
of treatment and intervention options are presented.
Moses (1999) presented information regarding
exposure to violence, depression, and hostility in inner city high school
youth. This article is presented in response to previous findings
that severe stress can have a harmful impact on adolescent emotional adjustment
and has been associated with the development of various forms of psychological
distress. The study examines the prevalence of violence in one population
of students (N = 337) who attend inner city schools. Furthermore,
the relationship between exposure to violence and depression and hostility
among those adolescents was examined. The method included an anonymous
survey where students counted their experiences with traumatic violence,
including witnessing shooting or stabbing of a family member, friend, or
stranger, being raped, being shot or stabbed, and being beaten up/jumped.
Sixty-two percent of students had been exposed to three of the six types
of violence (mean = 3.41). Exposure to different types of violence
showed high multicolinearity. Males had been exposed to more violence
on the whole than females. Exposure to violence was predictive of
hositlity for both males and females, and predictive of depression for
females. Adolescent development and depression within violent exposure
are discussed.
Nolen-Hoeksmea, Girgus, and Seligman (1992)
reviewed a longitudinal study in which the interrelationships among children’s
experiences of depressive symptoms, negative life events, explanatory style,
and helplessness behaviors in social and achievement situations were examined.
The 5-year longitudinal study followed 352 third-grade children assessing
several variable at six month intervals over 5 years. At six month
intervals, the participants were administered the Child Depression Inventory
(CDI), the Children’s Attributional Style Questionnaire (CASQ), and the
Life Events Questionnaire (LEQ). Additionally, the teachers of the students
completed a Student Behavior Checklist (SBC) rating students’ helplessness
behaviors in a variety of situations.
The results of this study revealed differences
in how children in early childhood and middle childhood experienced depressive
symptoms. In early childhood, a pessimistic explanatory style emerged as
a significant predictor of depressive symptoms, while in middle childhood,
a pessimistic explanatory style emerged as a significant predictor of depressive
symptoms, alone and in conjunction with negative events. The study
found that some children repeatedly showed elevated levels of depressive
symptoms, even across the 5-year span of childhood. Additionally,
these children tended to show a constellation of pessimistic thinking and
helplessness behaviors in the classroom and in peer interactions. The article
concluded with suggestions for interventions and prevention programs for
children at risk for developing depression. For example, “family
therapy is the therapy of choice for depressed children” in order to stabilize
the home environment and facilitate the children’s ability to cope with
the remaining stressors. Social skills training was also emphasized to
help children overcome “passivity and helplessness in peer interactions.”
Conclusions
The magnitude of child and adolescent depression
is clearly a major mental health problem. Current research supports
a multifaceted view of childhood and adolescent depression, including social,
family, psychological, developmental, and medical concerns. Children
continue to be diagnosed with depression at increasing levels, and at younger
ages, than ever before, and comorbidity with other disorders is extensive.
Early onset depression interferes with a child’s psychological, social,
and academic functioning, placing him or her at greater risk for problems
such as substance abuse and suicidal behavior (Birmaher et al., 1996; Hammen
& Compas, 1994). A high recurrence rate provides evidence for
a need to help children and adolescents learn prevention strategies for
future use, as well as providing tools for reducing the risk of subsequent
episodes. Moreover, depression in childhood more often than not co-occurs
with other disorders, primarily anxiety, conduct and behavioral disorders.
This comorbidity can further impede normative child development, which
may result in a more negative life course (Hammen & Compas, 1994; Birmaher
et al., 1996; Angold & Costello, 1993). Attempting to account
for the biological, environmental, and developmental influences on the
pathogenesis of depression is a complex and challenging task. To
facilitate this understanding, distinctions are necessary in evaluating
variables that cause, maintain, or are merely associated with childhood
depression, so that appropriate prevention and intervention measures may
be implemented with this high-risk population.
ETIOLOGY
What one sees as the etiology, the cause or
origin, of any disorder depends on the lens through which one views psychopathology.
From a medical orientation, disorder result from organic dysfunction; from
a behavior model, abnormal behavior has been learned; from a psychodynamic
perspective, interpersonal forces are key; and from a social framework,
a person's relationship within the social system is examined (Wicks-Nelson
& Israel 1996). For depression, single risk factors can rarely
be conceived as resulting in depressive outcomes. Instead, the biological,
psychosocial, and social systems may be considered within a larger framework
for explaining the etiology of depression. This section presents
explanations as they are summarized in research articles and web sites
and offers a developmental framework to include more than one etiological
perspective.
Although the medical model is prominent today,
many consider the etiology of various psychopathologies to be multidimensional,
commanding the consideration of the multiple factors that influence a person's
life and development. Since many different factors can lead to psychopathology
for different individuals, the etiology of a given disorder is perhaps
best understood by looking at [but etiology may be] the interaction or
transaction between these multiple variables over time (Cicchetti, Nurcombe
& Garber, 1992). The following discussion presents various explanations
of the etiology of childhood depression; however, we urge the reader to
begin thinking about how these variables may interact with one another
throughout development, and the ways in which they put a child at risk
for depression.
Although the explanations provided below help
researchers and practitioners understand the etiology of depression
as it relates to specific etiological models, a developmental perspective
suggests: 1) the manifestation of depression varies with age [across ages
as it is displayed]; 2) how individuals experience depression internally
varies greatly from one individual to the next [that depression varies
across individuals as it is experienced]; and 3) the context of ongoing
development changes must be considered and the causes of depression understood
within the child’s developmental level. With this in mind, aspects
unique to childhood should also be considered within a developmental perspective
in order to understand the etiology of depression, and to insure that etiology
is not be limited to a single perspective.
Biological Influences
Reynolds (1992) conducted an extensive review
of the literature and found several persuasive biological models in the
etiological structure of depression. Many of these models focus on
brain neurochemistry, specifically on the role neurotransmitters play in
the etiology of depression. Research has discovered that insufficient
levels of chemicals such as norepinephrine and serotonin in the brain lead
to a depressed state. More recently, however, attention has been
directed toward growth hormone secretion and sleep disturbance in children
and adolescents.
Neuroendocrine research claims that a relationship
exists between hypothalamic-pituitary-adrenal axis function and childhood
depression. Literature suggests that individuals with depression have higher
levels of a hydrocortisone, cortisol, in their system, a hormone manufactured
by the adrenal gland. This controversial model has spawned a proliferation
of research in the study of adolescent and childhood depression.
Both the American Psychiatric Association Task Force on Laboratory Tests
in Psychiatry and the World Health Organization state the inconclusive
nature of these hypotheses at this time.
Field, Fox, Pickens, & Nawarocki (1995) provide evidence
of brain activity related to depression. The brain electrical
activity of adolescent mothers and their infants were studied using an
electroencephalogram (EEG) technique. A sample of 32 infants were
studied, evenly split by gender, with a mean age of 4.8 months. All
were full-term at birth and without medical complications. The mothers
were right-handed, single, had lower socio-economic status. This
sample included only two ethnicities: Hispanic (35%) and African-American
(65%). All mothers were evaluated for depression both neonatally
and when their infants were between three and six months of age.
It was found that depressed mothers and their infants displayed right frontal
asymmetry. These findings parallel those of inhibited infants and
children, and chronically depressed adults who exhibit depressed affect
as well. The authors suggest that further research is needed to determine
if these EEG patterns are indicative of current or chronic mood states.
Steingard (2000) recently conducted a review
of research on the neuroscience of childhood and adolescent depression
that included scientific studies spanning more than a decade. According
to Steingard, recent endocrine studies show inconsistent results; one of
the studies under review found higher rates of depression among children
with high levels of nocturnal growth hormone secretion, however, these
results were not replicated by subsequent researchers. Recently,
sleep studies have gained much attention in the childhood and adolescent
depression literature. It has been noted by several authors that
children with a tendency toward reduced REM latency will be more likely
to show signs of depression in subsequent years than normal controls.
But as the author warns, such REM sleep patterns are also seen in children
exposed to stressful life events and so results should be interpreted with
caution. Neuroimaging studies, especially magnetic resonance imaging
(MRI) studies show promise in helping us understand the etiology of childhood
depression.
One reason for the current popularity of MRI’s
is that they do not require radionucleotide exposure common of other neuroimaging
techniques and, thus, repeated scanning using MRI’s appears to be safe
for use with developing children. Results of MRI neuroimaging show
that children suffering from depression have decreased frontal lobe volume
when compared with normal age mates. The author states that future
MRI studies will more clearly identify the psychophisiological markers
of depression; this will, in turn, facilitate our ability to identify individuals
at risk for developing depression and allow us to predict patient response
to treatment.
Apter et al. (1999) provide evidence for increased
cholesterol as a possible biologic risk factor in depression. Their
study was undertaken to examine the relationship between serum cholesterol
levels and suicidal behaviors in adolescent psychiatric inpatients.
Any association between serum cholesterol and measures of suicidal behavior,
impulsivity, aggression, anxiety, and depression was also examined.
Individuals admitted to an adolescent inpatient unit were assessed for
their suicidal behavior, violence, impulsivity, and depression. Serum
cholesterol for individuals admitted for suicidal tendencies were compared
with serum cholesterol for individuals admitted for other reasons.
Serum cholesterol levels were significantly higher among patients who were
suicidal than those who were admitted for other reasons. Within the
suicidal group, serum cholesterol was found to have a negative correlation
with the degree of suicidal behavior. Implications for associations
between cholesterol and suicidal tendencies are presented, and the usefulness
of understanding serum cholesterol as a possible risk factor in depression
is presented.
Genetic Influences
Recently, the focus of empirical studies and
literature reviews on child and adolescent phychopathology has moved beyond
documenting the prevalence of, and risk factors for individual disorders,
as these data are reasonably well documented. O’Connor, McGuire,
Reiss, Hetherington, and Plomin (1998) extend previous research documenting
the prevalence of depression by studying the patterns of co-occurring disorders.
Specifically, the highlight the consistently high rates of co-occurring
dimension of phychopathology, particuarly between internalizing and externalizing
disorders. Using a sample of same-sex adolescent siblings between
10 and 18 years of age consisting of monozygotic and dizygotic twins, full,
siblings, half siblings, and unrelated siblings. Their research indicates
a significant proportion of variability in depressive symptoms and antisocial
behavior is attributed to genetic influence. The authors also discuss
the role of environmental influences as predictors. Results are discussed
in terms of the genetic influence of child and adolescent phychopathology.
Cichetti and Toth (1995) provide an extensive
review that covers a broad span of issues, including the role of genetics
on depression. Timed biological events, which are genetically released,
create challenges at each and every developmental phase. Therefore,
genetic factors "contribute sources of vulnerability" as well as "resilience
to the probabilistic unfolding of unipolar and bipolar illnesses".
There has been a tremendous body of literature that has demonstrated that
mood disorders occur more commonly among the relatives of depressed persons
than in the general population. The empirical literature reveals
that the greater the percentage of genes shared with the proband (i.e.,
the affected individual), the greater the chance that the relative will
be similarly affected by a mood disorder. Additionally, there is
an increased rate of affective disorder in the biological relatives and
not in the adopted relatives of the adoptees that have been found in on-going
adoption studies. Following this, twin studies of affective illness
have consistently revealed the concordance rates for monozygotic (MZ) twins
to be substantially higher than in dizygotic (DZ) twins, leading one to
conclude that a genetic "trigger" may exist for clinical depression.
Genetic markers can be viewed as risk traits.
Although genetic research has provided strong evidence for the existence
of specific genes that may increase the probability of developing a mental
disorder, such as major depression, these genetic markers are not guarantees
that depression will develop. What must be included in this equation
is the protective, or resilience, factors that each person may possess.
Therefore, a multifactorial model of risk is supported; such that environmental
factors play in either protecting or triggering a depression. That is,
environmental experiences may be more critical than genes in increasing
an individual's liability to depression. Collaboration between the fields
of molecular genetics and developmental psychopathologist would allow much
needed research in this arena. Future work for developmental geneticist
would be necessary to uncover the ontogenetic processes whereby "genetic
and environmental factors conspire to orchestrate normal and abnormal patterns
of adaptation". It would be especially helpful to identify the factors
that turn particular genes on and off during phases of development.
Similarly, Eley & Stevenson present a
primarily genetic explanation for risk of depression. Their
research utilizes self-reported anxiety and depression symptoms in children
and adolescents have been shown to be heritable, and are also highly correlated.
This study set out to ascertain to what extent the genetic and environmental
factors that influence anxiety symptoms also influence depression symptoms,
and whether these are the same in children and adolescents, and males and
females. Twins age 8-16 years old completed the measures of depression.
There were significant effects of age and sex on the variance and on the
variance and covariance between these two types of symptoms. The
authors conclude that genetic influences on anxiety and depression were
shared for all 4 groups, a finding that has been consistently demonstrated
for adults.
Thapar and McGuffin (1998) provide evidence
for genetic influence on depressive symptoms. Their study utilized
monozygotic and dyzygotic twin subjects to test the hypothesis that genetic
factors influence the same life events that influence depression.
Also, these genetic factors are thought to mediate the association between
the life events and the depression. Mothers rated depression and
life events for 270 twin pairs 8- to 17-years-old. It was found that
depression and some life events, such as number of events and their negative
impact, share a common genetic influence. A portion of the association
between depression and life events was best explained by both genes and
the environment. Bivariate genetic model fitting indicated that the
covariation between life events and depression was best explained by a
common environmental factor. Due to the limitations of the study,
directionality of the results is impossible to determine. As such,
it is difficult to evaluate if life events predated the depression or vice
versa. These results point out the need for longitudinal studies
as well as the necessity of larger sample sizes.
Environmental Influences
With regard to the family, an important environmental
influence on children and adolescents, Chasin, Pitts, DeLucia, and Todd
(1999) suggest the importance of family influences on depression.
Their study tested the specificity of parent
alcoholism effects on young adult alcohol and drug abuse/dependence,
anxiety, and depression, and tested whether adolescent symptoms and substance
use mediated the effects of living with an alcoholic parent. Using structured
interviews, the researchers suggest unique effects of parent alcoholism
on young adult substance abuse/dependence diagnoses over and above the
effects of other parental psychopathology. There was some evidence of parent
alcoholism effects on young adult depression and of maternal alcoholism
effects on young adult anxiety, although these were not found consistently
across subsamples. Mediational models suggested that parent alcoholism
effects could be partially (but not totally) explained by adolescent externalizing
symptoms.
Whether the context is a child with depression,
or a child with depressed parents, the family environment plays a role
in both the onset and maintenance of childhood depression. Kaslow,
Deering, and Rucasin (1994) present an extensive literature review that
hightlights numerous family variables and patterns associated with, but
not causing, childhood depression, as well as the ways in which these factors
may interact to sustain a child's depression. Family variables associated
with childhood depression are parental psychopathology, divorce, low SES,
negative life circumstances including loss, abuse, or neglect, and low
levels of social support. Families with depressed children have been
found to be less cohesive and supportive, less able to communicate effectively,
have less secure parental attachment, and more conflictual relationships,
more controlling and critical parents (leading to feelings of helplessness
in depressed children), and higher levels of expressed emotion (hostility,
criticism, and overinvolvement) than do the families of nondepressed peers.
Siblings play a role in the development of depression, as problematic sibling
relationships have been associated with greater depression, and a positive
sibling relationship may mediate depression.
Children of depressed parents are at high
risk for childhood depression. Parental depression may be transferred
to children by way of genetic predisposition, maladaptive parent-child
interactions, and marital conflicts. Specifically, maternal depression
negatively affects a child's functioning, parenting styles, and interactional
patterns. Taking into account all of the above mentioned factors,
family environments may interact with childhood depression in various ways
that contribute to the onset and maintenance of childhood depression.
From a systems perspective, families reinforce the child's depression.
A family dynamics perspective suggests a "subtle reciprocity" between childhood
depression and family dynamics; for example, a certain family environment
may not be a 'good fit' for a child predisposed to depression. The
authors do not contend that family variables and interaction patterns are
the only or primary contributors in the etiology and development of childhood
depression; but rather that it is one variable that should be considered
in conjunction with developmental, social, and/or biological factors.
Hamilton et. al., (1997) studied 49 children
with either depression, schizophrenia, or no clinical diagnosis, to see
if differences existed in their social, academic and/or behavioral functioning.
In addition, they investigated the influence of transactional family behavior
on child competence in these domains. Statistical analyses showed
that the children with depression and their non-clinical cohort functioned
comparably in academic performance. No impaired cognitive functioning
was evidenced by the students who were depressed. However, a significant
difference was noted in the social domain, with the depressed children
demonstrating poorer social functioning than their non-clinical peers.
No distinctions could be made between the children with depression and
the children with schizophrenia in this domain. This finding is important,
when we consider that the problem only compounds as the child reaches adolescence
and adulthood. It is important to note, however, that the children who
participated in this study were inpatients, and that the severity of their
psychiatric illness may not allow for generalization to children with depression
in the community. In other words, although a child may experience
depression, s/he will not necessarily have dysfunctional interpersonal
interactions.
Another important finding in the study showed
a relationship between family transactional patterns and child adjustment.
They found that children from parents who use more negative interactional
styles demonstrated poorer social competence and more behavioral problems
than those whose parents interact with them in a more benign manner.
Conversely, children with parents who engaged them in a more positive manner
showed better social and behavioral competence. This study found
a relationship between parenting behavior and child social and behavioral
competence. It does not reveal whether the parents' negative interactional
style caused the child's depression, whether the parents' negative interactional
style evolved in response to the child's depressive characteristics, or
whether the two components of the family system interact to maintain and
perpetuate the child's depressive symptoms. Even without the certain
identification of the causal agent, it seems evident that the family system
needs to be altered in the treatment of childhood depression.
Segrin (2000) provides an in-depth conceptualization
of the role that social skills deficits play in childhood and adolescent
depression. His perspective, which draws from the work of such authors
as Coyne and Lewinsohn, posits that there are [at least] three ways to
understand the relationship between depression and social skills: 1) poor
social skills as the cause of depression; 2) depression as the cause of
poor social skills; and 3) poor social skills as a risk factor to the development
of depression. While much of the available literature has focused
on adult populations, there appears to be an emerging body of literature
that demonstrates the relationship between poor social skills and depression
in children as well. However, Segrin’s evaluation of the literature
failed to determine the direction of the correlation between the development
of depression and social skills deficits. While some evidence supports
the notion that social skills deficits are a risk factor in the development
of depression, most studies provide inconclusive evidence as to directionality.
More longitudinal studies of childhood and adolescent depression would
facilitate our understanding of the temporal ordering of social skills
deficits and depression. Additionally, utilizing an approach that
considers the interaction between social skills and other risk factors
might enhance our ability to predict the onset of depression. In
the meantime, it appears that the question “Do social skills deficits cause
depression or vice-versa” remains – at least for the moment – unanswered.
Parent Influences
Downey and Coyne (1990) provide an integrative
review of children of depressed parents. Among women of child-bearing
age, depression, is a highly prevalent disorder, with approximately 8%-12%
of mothers exhibiting clinical depression at any given time. A child's
adjustment is likely to reflect the type of depression, the degree of family
stress and marital discord experienced, and the parent's level of symptomology
and social impairment. This article is an extensive, integrative review
on various literatures on the adjustment of children of depressed parents,
difficulties in the parent-child interaction in these families and contextual
factors that may play a role in child adjustment. In earlier studies, children
of depressed parents were used as the controls in high-risk research on
children of schizophrenic parents. This earlier work led to the serendipitous
finding that children of depressed parents were equally at risk for childhood
disturbance (especially mood disorders) as the children of schizophrenic
parents. Subsequent studies have found that children of depressed parents
are at risk for a full range of adjustment problems and at specific risk
for clinical depression.
Not surprisingly, maternal depression is associated
with difficulties in parenting; depressed mothers view the role of parenting
less positively than do control mothers. In addition to experiencing
greater feelings of depression and hostility towards the parenting role,
a depressed mother's behavior and affective expression is constricted and
her speech is flat as compared to control group mothers. Depressed
parents respond less positively, less frequently, and less quickly to their
children's efforts to engage their attention. Difficulties are found beginning
in infancy in the delayed speech patterns of infants of depressed parents.
In school-aged children, the adjustment problems emerge in peer, teacher
and observer reports demonstrating children experiencing difficulties across
social and academic settings. Furthermore, parents who are clinically
depressed show heightened levels of child-directed hostility and negatively,
and their attempts to control child behavior are marked by coercion rather
than by negotiation. The authors conclude by stating, "there is a distinct
and consistent mother-bashing quality to much of this body of work."
While depression in parents is clearly associated with adjustment and mood
disorders in children, the specificity and origin of this association is
not clearly established.
Parent influence may vary by social class,
and the types of social support available for parents, according to Mathiesen,
Tambs, & Dalgard (1999). This study identified risk and protective
factors for anxiety and depression among mothers of toddlers. Mothers
with 18-mo-old children completed a questionnaire designed to examine the
affect of socioeconomic and demographic factors, somatic health problems,
negative life events, chronic strain and social support on symptoms of
anxiety and depression. There was a moderate negative effect of negative
life events and chronic strain and a moderate protective effect of social
support on the symptom level, but no interaction effects were found between
the risk and protective factors. Behavior problems among the children clearly
seemed to affect the mothers' symptom level. The symptom level varied with
background factors. The largest effect of background factors seemed to
be indirect, mediated through their effect on the risk and protective factors.
Although problems with children's behavior and child care arrangements
were observed to have a strong impact on the mothers' symptom level, the
frequencies of such problems appeared to be less dependent on socioeconomic
conditions than did other types of strain.
Environmental Influences
Monroe, Rohde, Seeley, and Lewinsohn examine
life events and depression among adolescents. Specifically, risk
as the result of a recent romantic break-up was examined as a predictor
of 1st onset versus recurrence of MDD. Results indicated a heightened likelihood
of 1st onset of MDD during adolescence if a recent break-up had been reported;
in contrast, a recent break-up did not predict recurrence of depression.
These results held for both genders and remained significant after controlling
for gender. Implications of these findings and subsequent research directions
are discussed.
Tulisalo and Aro (2000) conducted a study
to determine the effects of parental remarriage on depression in young
adults. Considering the vast number of children and adolescents that
will go through a divorce, and considering that many of these individuals’
parents will enter a second marriage, exploring the ways in which parental
remarriage moderates depression is a pertinent research question.
The authors distributed questionnaires to 2,194 9th grade students (mean
age 15.9 years) in a small Finnish city. Six years after the original
questionnaires had been completed, another questionnaire was sent to the
same cohort of students. Now 22-years-old, there were 210 females
and 146 males who had been through a divorce, half of which also experienced
the remarriage of one or both of their parents. Contrary to expectations,
results of the study indicated that mothers’ remarriage did not result
in an increase in depressive symptomatology. There was, however,
a significant relationship between fathers’ remarriage and depressive symptoms
of both boys and girls; boys displayed a decrease in signs of depression,
while girls harbored an increasing number of depressive symptoms.
The authors discuss the limitations of the present study and highlight
the fact that the original design was not intended to study the impact
of remarriage. Additionally, considering that the results tended
to conflict preexisting research in the area, the reader is encouraged
to exercise caution in interpretation.
Abuse
Pearce and Pezzot-Pearce (1997) provides a
comprehensive description of individual difficulties and psychotherapy
strategies that can be used to assess and treat children who have suffered
various types of abuse and neglect. Child maltreatment can be regarded
as one of several variables that may contribute to childhood depression.
Pearce & Pezzot-Pearce outline the various methodological difficulties
in this type of research demonstrating how difficult it is to define and
characterize children exposed to different types of maltreatment; not to
mention, problems with subject selection, research design and control groups.
The chapter provides an overview of attachment theory including a discussion
of the organizations of maltreated children following some of the work
of the Minnesota Mother-Child Interaction Project, which is a prospective,
longitudinal study of the development of a sample of high-risk children
(see Egeland, 1991). This chapter further reviews the emotional and
behavioral self-regulation of maltreated children including a thorough
discussion of externalizing problems (i.e., physical aggression & sexualized
behaviors) as well as internalizing problems (i.e., depression & posttraumatic
stress disorder).
Maltreated children are at a significant risk
for the development of a number of problems, including insecure attachment,
poor emotional and behavioral self-regulatory skills, lowered cognitive
functioning, poorer adaptation to school, and language delays. Depression,
viewed as a manifestation of disturbances in self-regulation, is associated
with various types of maltreatment. The authors review a number of
studies in which depressive symptomology is correlated with sexually abused
children. All of the reviewed studies found higher rates of depression
in sexually abused children and also higher rates of suicide. Furthermore,
not only is depression the most common symptom reported in children and
adolescents who have been molested, but these elevated depressive symptoms
have been found to carry well into adulthood (see Briere, 1992).
Therefore, depression is an important risk factor to consider for children
who have been maltreated in any way.
Kaufman, Birmaher, Dahl, Bridge, & Ryan
(1998) evaluated the first- and second-degree relatives of 26 depressed
adolescents (13 of which were abused) compared to the relatives of 27 normal
control children. The first-degree relatives totaled 104 (25 depressed-abused,
29 depressed-nonabused, and 50 normal control) and the second-degree relatives
totaled 503 (127 depressed-abused, 117 depressed-nonabused, and 259 normal
control). It was found that the first-degree relatives of depressed-abused
adolescents had nine times the odds for depression over the first-degree
relatives of the normal control adolescents. In addition, the
odds for other disorders, such as alcoholism and anti-social personality,
were found to be three to nine times that for the control group.
A similar pattern was found for the second-degree relatives. No differences
were found between the abused/nonabused groups. These findings are
consistent with previous research and suggest that depression, and related
disorders, have a biological component. Further research is needed
to replicate and extend these findings.
Brown, Cohen, Johnson, and Smailes (1999)
provide additional evidence for the role of abuse in youth depression.
Investigated the magnitude and independence of the effects of childhood
neglect, physical abuse, and sexual abuse on adolescent and adult depression
and suicidal behavior. 776 randomly selected children was studied from
a mean age of 5 years to adulthood in 1975, 1983, 1986, and 1992 during
a 17-yr period. Assessments included a range of child, family, and environmental
risks and psychiatric disorders. A history of abuse was determined by official
abuse records and by retrospective self-report in early adulthood on 639
youths. Attrition rate since 1983 has been less than 5%. Adolescents and
young adults with a history of childhood maltreatment were 3 times more
likely to become depressed or suicidal compared with individuals without
such a history. Adverse contextual factors, including family environment,
parent and child characteristics, accounted for much of the increased risk
for depressive disorders and suicide attempts in adolescence but not in
adulthood. The effects of childhood sexual abuse were largest and most
independent of associated factors. Risk of repeated suicide attempts was
8 times greater for youths with a sexual abuse history.
Social Identity
Safren and Heimberg (1999) examined factors related to depression, hopelessness, and suicide risk in gay, lesbian, and bisexual adolescents, compared with demographically similar heterosexual adolescents. Sexual minority adolescents reported greater depression, hopelessness, and past and present suicide risk than did heterosexual adolescents. However, when controlling for other psychological predictors of present distress, significant differences between the 2 samples disappeared. For past suicide risk scores, the effects of sexual orientation were reduced, but still significant, when accounting for the other predictor variables. These results suggest that environmental factors associated with sexual orientation, which can be targeted and changed through prevention and intervention efforts, play a major role in predicting distress in this population.
Transactional Model Explanation
A transactional perspective suggests that depression
as a pathology does not occur in isolation, but rather as the result of
various factors operating together. Cicchetti and Toth (1995) provide
an exhaustive review of affective disorders and a comprehensive understanding
of clinical depression from a transactional approach. A transactional
model states that an illness does not occur in isolation, by one process
alone, but rather is the result of various factors operating together.
A transactional model specifies that the interrelationships between the
organization of developmental domains (biological, socioemotional, cognitive,
representational) and the environment in which the individual resides (family,
school, community) exert a bi-directional influence on the individual.
Understanding an individual child's risk and protective factors may be
the appropriate lens through which to understand a transactional model
of psychopathology. Rutter (1990) has cautioned that risk, vulnerability,
and protective factors do not cause (emphasis added) pathological outcomes
per se, but rather indicate more complex processes and mechanisms that
will affect an individual's adaptation. The ways in which risk and
protective factors exert themselves depend on the developmental period
within which the individual is developing.
Viewing childhood depression from a transactional
model allows us to see how the child and the environment are mutually influenced
as the child evolves. The bi-directional transactions will continue
to influence the child, and the environment in which the child resides,
allowing for continued variations in the organization of the child as development
unfolds. For a child who is experiencing clinical depression, an
understanding of the child's current world in terms of his/her protective
and risk factors is an important beginning. For example, a child
who is the product of depressed parents may possess a unique set of risk
and protective factors, while another child who has undergone chemotherapy
may face a completely different set of factors; each child may warrant
a diagnosis of clinical depression but the etiologies leading to each child’s
depression differ drastically. A transactional model would allow
each child's unique set of circumstances to explain the his/her current
functioning.
Consistent with the transactional model described
above, the developmental perspective of psychopathology maintains that
no single cause determines pathology. Rather, many risks and protective
factors interact with one another to influence a person’s development over
time. Due to these complex interactions, there is no singular pathway
common to all individuals with negative outcomes. Maladaptation is
an outcome that can unfold differently for everyone; in the same way that
competence does, through successive interactions with the environment (Sroufe,
1997). A disorder also changes throughout development, manifesting
itself differently at various stages of development. A child’s age
and (more importantly) developmental level, then, becomes a very important
question to a developmental psychopathologist; because whether a behavior
is regarded as normal or pathological depends on where it occurs in the
developmental sequence (Cicchetti, Nurcombe, & Garber, 1992).
The developmental perspective provides a comprehensive
and integrative way of conceptualizing the etiology and course of childhood
depression. Unlike other models, this view accounts for the various
genetic, biological and environmental factors that have been identified
as differentially and interactively putting a child at risk for depression
(Sroufe, 1997). Depression is viewed as a state that develops over time,
not as an intractable trait [something] that a child is simply inherits
at birth. For example, an adolescent with insecure attachment (one
known risk factor for depression) may react maladaptively to a life stress
situation, thereby learning poor problem skills that will negatively affect
subsequent interactions with the environment. This pattern may eventually
lead this individual to the experience of depression (Kovak, Sudler, &
Gamble, 1992). When viewed as a "snowball effect" (i.e. transactional)
it is easy to see how detrimental early onset depression can be to a child's
development. Since early childhood is such a critical period in development,
the onset of depression is especially detrimental. Psychopathology
at such a young age can result in the formation of negative cognitive styles
and in decreases in cognitive flexibility. Such a combination can
be catastrophic to a child’s subsequent development.
In addition to acknowledging the various factors
that influence depression, the developmental perspective also acknowledges
the ongoing developmental changes characteristic of childhood. Clearly
a child's depressive symptoms will vary with his/her developmental level
of cognitive ability, psychosocial functioning, emotional awareness and
psychosexual maturity (e.g. puberty) (Cicchetti, Nurcombe & Garber,
1992). For example, depression during childhood and adolescence may
be manifested as "irritable" mood rather than the depressed mood of an
adult (DSM-IV). Such developmental considerations are especially essential
for diagnosing youth depression. From a developmental perspective,
pathology is defined as the extent to which children's' behaviors reflect
deviations from normal developmental processes at different ages. Crying
hourly, for example, at age one has different implications than this same
behavior at age thirteen.
Conclusion
As with many disorders, the etiology of depression
is not well understood. Although some adhere to a specific orientation,
it seems that the etiology of depression is multidimensional. A plethora
of factors have been identified as putting a child at risk for depression,
however, none of these factors alone seem to lead to depression for all
individuals. Studies of biological factors, such as neurotransmitter
and hormone levels, as causes of depression have led to inconclusive results;
genetic explanations cannot account for depression without the effect of
the environment; environmental factors including family variables and interaction
patterns, parent variables including maternal depression, and abuse all
play a part in the development of depression, but no single one of these
factors fully explains the development of childhood depression.
The developmental perspective, consistent with the transactional
model and multifactorial orientation of depression is integrative, comprehensive,
and likely to better explain the etiology of depression than could any
single model in isolation. The developmental perspective also provides
a more complex understanding of the etiology and considers numerous risk
factors that interact over time to create multiple pathways to depression.
It is also the most comprehensive model in that it recognizes developmental
changes that will undoubtedly affect the experience of depression for children.
It is important to consider that depression may manifest itself differently
at different developmental stages and the extent to which behaviors deviate
from normal developmental processes at any given age. In viewing
depression as an outcome that develops, the developmental perspective takes
an important first step in eliminating the notion that pathology exists
solely within the child; such a perspective emphasizes the synergistic
impact that biology, genetics, and the environment can have on the etiology
and manifestation of childhood depression.
Assessment
The proper and objective assessment of childhood and adolescent
depression is the first step in moving toward a comprehensive treatment
process (McConaughy, Milling & Martin, 1992). Only trained professionals
or clinicians should perform assessments as these individuals have an understanding
of normative and non-normative behaviors (Cicchetti & Toth, 1998).
For instance, it is common for children and adolescent to experience short
episodes of sadness and disappointment. However, these episodes generally
do not meet the criteria contained in the Diagnostic and Statistical Manual
of Mental Disorders (DSM-IV). From a developmental perspective, multiple
assessments that account for developmental concerns are crucial in the
diagnosis of depression (Milling & Martin, 1992). This not only
allows for a more complete picture of the child’s behavior within multiple
domains, but also includes information from the child, the child’s parent(s),
clinician, and possibly even teachers and peers (McConaughy, 1992).
Even if a youth does not fully meet the criteria for depression, professional
attention may still be warranted in order to prevent clinical depression
or possible suicide (Cicchetti & Toth, 1998).
Assessments for depression primarily include interviews and questionnaires.
More specifically, assessments include child self-report measures, parent
report measures, teacher scales, peer nominations, clinical interviews,
and semi-structured interviews (Kaslow & Rehm, 1991). Essau,
Hamik-Larson, Crocker, and Petermann (1999) state, “When choosing an assessment
approach for measuring depressive disorder, important considerations are
the reliability and validity of the instruments.” The measurements for
depression listed below are empirically-based and are capable of being
verified or disproven through observation or experiment (McConaughy, 1992).
All scales contain explicit instructions, multiple items, and result in
a score that is compared against clinically established cutoffs.
Each measurement has been tested for validity and reliability (Kaslow &
Rehm, 1991).
Table of Assessment Instruments and References:
ASSESSMENT INSTRUMENT REFERENCE
Children’s Depression Inventory (CDI; Kovacs & Beck, 1977)
Children’s Depression Scale (CDS; Tisher & Lang, 1983)
Depression Adjective Checklist (C-DACL; Sokologg & Lubin,
1983)
Center for Epidemiological Depression Studies’ Depression Scale Modified
for Children (CES-DC; Weissman, Orvaschel, & Padian, 1980)
Reynolds Adolescent Depression Scale (RADS; Reynolds, 1986)
Children’s Depression Scale Revised (CDS-R; Reynolds, Anderson,
& Bartell, 1985)
Modified Zung (M-Zung; Lefkowitz & Tesiny, 1980).
Kiddie-SADS Epidemiologic Version (K-SADS-E; Orvaschel &
Puig-Antich, 1987)
Kiddie- SADS Present Episode (K-SADS-P; revised by Puig-Antich
& Ryan, 1986)
NIMH Diagnostic Interview Schedule for Children (DISC; National
Institute of Mental Health, 1992)
Bellevue Index of Depression (BID; Petti, 1978)
Interview Schedule for Children (ISC; Kovacs, 1981)
Children’s Affective Rating Scale (CARS; Kovacs, 1981)
Children’s Depression Rating Scale - Revised (CDRS-R; Poznanski et
al., 1984)
Hamilton Depression Rating Scale (HDRS; Hamilton, 1960, 1967)
School Aged Depression Listed Interview (SADLI; Petti & Law,
1982)
Dysthymic Check List (DCL; Fine, Moretti, Haley, &
Marriage, 1984)
Diagnostic Interview Schedule for Children (DISC; Costello, Edelbrock,
Dulcan, Kales, & Klavic, 1984)
Diagnostic Interview for Children and Adolescents (DICA; Herjanic,
Herjanic, Brown, & Wheatt, 1975)
Child Assessment Schedule (CAS; Hodges, McKnew, Cytryn, Stern,
& Kline, 1982)
Child Behavior Checklist (CBCL; CBCL/4-18; Achenbach & Edelbrock,
1983)
Personality Inventory for Children Depression Scale
(PIC; Wirt, Lachar, Klinedinst, & Seat, 1977)
Peer Nomination Inventory for Depression (Lefkowitz & Tesiny,
1980)
Major Methods of Assessment
Self-report measures are useful for evaluating the severity of
depressive symptoms, but do not provide a complete assessment of depression.
Self-report measures of depression for children and adolescents include:
Children’s Depression Inventory (CDI; Kovacs & Beck, 1977), Children’s
Depression Scale (CDS; Tisher & Lang, 1983), Depression Self-Rating
Scale (DSRS; Birleson, 1981), Depression Adjective Checklist (C-DACL; Sokologg
& Lubin, 1983), Center for Epidemiological Depression Studies’ Depression
Scale Modified for Children, (CES-DC; Weissman, Orvaschel, & Padian,
1980), Reynolds Adolescent Depression Scale (RADS; Reynolds, 1986), Children’s
Depression Scale Revised (CDS-R; Reynolds, Anderson, & Bartell, 1985),
and the Modified Zung (M-Zung; Lefkowitz & Tesiny, 1980). Benefits
of using self-report measures include their ability [Self-report measures
allow children] to describe [provide] subjective internal experiences that
only the child him/herself has access to, and the relative ease with which
self-report measures can be administered and scored. However, the
limitations of self-report measures include assumed cognitive, language,
and reading skills that may exceed a given child’s abilities. Thus,
care should be taken to consider the child’s level of development and age
when administering self-report measures of childhood depression.
Structured interviews are commonly used in the diagnosis of depressive
syndromes. Such interviews include: Kiddie-SADS Epidemiologic
Version (K-SADS-E; Orvaschel & Puig-Antich, 1987), Kiddie- SADS Present
Episode (K-SADS-P; revised by Puig-Antich & Ryan, 1986), NIMH Diagnostic
Interview Schedule for Children (DISC; National Institute of Mental Health,
1992), Bellevue Index of Depression (BID; Petti, 1978), and the Interview
Schedule for Children (ISC; Kovacs, 1981). Structured interviews
provide a consensus of multiple perspectives and can allow the interviewer
to observe behavior in addition to asking questions, providing a rich description
of the depression. However, interviews may be time consuming, and
therefore cumbersome in terms of resources.
Similarly, clinical interviews are also used to evaluate depressive
symptoms. Clinical interviews include the Children’s Affective Rating
Scale (CARS; Kovacs, 1981), Children’s Depression Rating Scale Revised
(CDRS-R; Poznanski et al., 1984), Hamilton Depression Rating Scale (HDRS;
Hamilton, 1960, 1967), School Aged Depression Listed Interview (SADLI;
Petti & Law, 1982), Dysthymic Check List (DCL; Fine, Moretti, Haley,
& Marriage, 1984), Diagnostic Interview Schedule for Children (DISC;
Costello, Edelbrock, Dulcan, Kales, & Klavic, 1984), Diagnostic Interview
for Children and Adolescents (DICA; Herjanic, Herjanic, Brown, & Wheatt,
1975), and the Child Assessment Schedule (CAS; Hodges, McKnew, Cytryn,
Stern, & Kline, 1982).
A parent report or another informant important to the child or
adolescent’s world may provide information to assess depression.
The most commonly used methods employing informants include the Child Behavior
Checklist (CBCL; CBCL/4-18; Achenbach & Edelbrock, 1983), and the Personality
Inventory for Children Depression Scale (PIC; Wirt, Lachar, Klinedinst,
& Seat, 1977). When peers are the informants, the assessment
instrument would likely include the Peer Nomination Inventory for Depression
(Lefkowitz & Tesiny, 1980). Although informants can provide valid
descriptions of a child’s behavior in social and school settings, informants
are not able to provide information about the child or adolescent’s internal
state.
Current Research
Current research supports the importance of multiple assessment
in depression. A developmental perspective highlights the relevance
of various perspectives accounting for growth within the child or adolescent.
Articles presented provide evidence of self-report, interviews, and parent
reports on symptoms of depression.
Questionnaires
Reynolds, & Mazza, J. (1998) examine the validity and
reliability of a relatively new self-report depression assessment, the
Reynolds Adolescent Depression Scale (RADS; Reynolds, 1986). This
scale is intended for use with adolescents from 12 to 18 years of age and
consists of 30 self-report items geared to identify depressive symptoms
according to the Diagnostic and Statistical Manual for Mental Disorders,
Third Edition (DSM-III; American Psychiatric Association, 1980).
It was noted within the article that few changes have been made for depression
symptomology in subsequent editions of the DSM.
The participants (N=89) were in 6th, 7th, or 8th grade at a parochial
school in Brooklyn, NY. The age and gender breakdown were as follows:
36 males and 53 females with a total mean age of 12.53 years. The
ethnicity of the sample was 71% African-American, 20% Hispanic American,
1% Caucasian, and 8% other. The RADS was administered to the participants
on the same day. They were interviewed separately within one to five
weeks later with the Hamilton Depression Rating Scale (HDRS; Hamilton,
1960, 1967), which is a clinical interview. A second administration
of the RADS was given just prior to the interview to evaluate test-retest
reliability. The participants were then assigned to one of two groups
(“clinically depressed” and “not depressed”) based on the assessment results.
Statistical analyses were then performed to evaluate validity and reliability.
Researchers found that the internal consistency reliability was high (.91)
as was the test-retest reliability (.87). The criterion-related validity
was measured by the correlation coefficient between the HDRS and the second
administration of the RADS and was considered strong. The authors
conclude that overall the validity and reliability of the RADS is high.
This self-report measure is relatively easy to use and can be completed
in about 10 minutes by most adolescents.
From a more broad measurement perspective, Lonigan, Hooe, David,
and Kistner (1999) provide a model of positive affect (PA) and negative
affect (NA) model of anxiety and depression as an investigation of the
measurement of PA and NA and the relation between PA and NA and levels
of adjustment in children and youth. A confirmatory factor analysis was
used in this study to examine the structure of self-reported affect and
its relation to depressive and anxious symptoms in school children (4th
to 11th grade). Results supported a 2-factor orthogonal model that was
invariant across age and sex. Support for the expected pattern of relations
between NA and PA with symptoms of depression and anxiety was strong for
the older sample (M = 14.2 years) but weaker for the younger sample (M
= 10.3 years). Results also provide preliminary support for the reliability
and validity of the Positive and Negative Affect Schedule for children.
Chorpita, Yim, Moffitt, Umemoto, and Francis (2000) revised the
Spence Children’s Anxiety Scale (SCAS) so that the measure included items
designed to assess child and adolescent depression. The authors believed,
due to the high rates of comorbidity between anxiety and depression, that
incorporating items to assess depression made good intuitive sense.
Additionally, since items added corresponded to DSM-IV criteria for major
depression, the Revised Child Anxiety and Depression Scale (RCADS) also
enhanced the clinical utility of the original measure. The revised
scale was administered to a sample of 1641 children and adolescents ranging
in age from 3rd to 12th grade. Results of the study indicate that
the RCADS has high structural validity, reliability, retest reliability,
internal consistency, and convergent and discriminant validity. The
RCADS also showed good convergence with the Children’s Depression Inventory
(CDI), a widely accepted assessment instrument for child and adolescent
depression. The authors believe that the RCADS has several advantages
over the SCAS including its close association with DSM-IV criteria for
childhood disorders and its ability to assess both anxiety and depression
in children and adolescents. Other advantages of the RCADS, including
its suitability for use in clinical and research settings are discussed.
With regard to self-report, Prince, Reischies, Beekman, Fuhrer, Jonker,
Kivela, Lawlor, Lobo, Magnusson, Fichter, Van Oyen, Roelands, Skoog, Turrina,
and Copeland, describe the development of the Euro-D. This study
aimed to derive from these instruments a common depression symptoms scale,
the EURO-D, to allow comparison of risk factor profiles between centers.
Common items were identified from the instruments. Algorithms for fitting
items to the GMS were derived by observation of item correspondence or
expert opinion. The resulting 12-item scale was checked for internal consistency,
criterion validity and uniformity of factor-analytic profile. The EURO-D
is internally consistent, capturing the essence of its parent instrument.
A two-factor solution seemed appropriate: depression, fearfulness and wishing
to die loaded on the first factor (affective suffering), and loss of interest,
poor concentration and lack of enjoyment on the second (motivation). It
is concluded that the EURO-D scale should permit valid comparison of risk-factor
associations between centres, even if between-centre
variation remains difficult to attribute.
Mathiesen, Tambs, Dalgard (1999) identified risk and protective
factors for anxiety and depression among mothers of toddlers. A population-based
sample of 92 mothers (aged 19-46 yrs) with 18-mo-old children completed
a questionnaire designed to examine the impact of socioeconomic and demographic
factors, somatic health problems, negative life events, chronic strain
and social support on symptoms of anxiety and depression. There was a moderate
aversive effect of negative life events and chronic strain and a moderate
protective effect of social support on the symptom level, but no interaction
effects were found between the risk and protective factors. Behavior problems
among the children clearly seemed to affect the mothers' symptom level.
The symptom level varied with background factors like the mothers' education,
employment status, and age, even after controlling for the effect of strain
and social support. The largest effect of background factors seemed to
be indirect, mediated through their effect on the risk and protective factors.
Although problems with children's behavior and child care arrangements
were observed to have a strong impact on the mothers' symptom level, the
frequencies of such problems appeared to be less dependent on socioeconomic
conditions than did other types of strain.
Winter, Steer, Jones-Hicks, and Beck (1999) investigated the
psychometric characteristics of the Beck Depression Inventory for Primary
Care (BDI-PC) among adolescents (aged 12-17 yrs) scheduled for health maintenance
examinations, and determined the effectiveness of the BDI-PC in screening
the adolescents for Mental Disorders-IV (DSM-IV) major depression disorders
(MDD). The BDI-PC was administered to 50 male and 50 female adolescents
who received pediatric health maintenance examinations. The diagnosis of
MDD was established with the Mood Module from the Primary Care Evaluation
of Mental Disorders. Results showed that the internal consistency of the
BDI-PC was high (Cronbach alpha = .88), and it was not significantly associated
with gender, ethnicity, age, or having a medical disorder. A cutoff score
of >=4 had both 91% sensitivity and specificity rates for identifying adolescents
with and without MDD. Results show the BDI-PC to be a useful instrument
for screening for clinical depression in adolescents receiving routine
medical examinations.
Interviews
From a pharmacology perspective, Emslie and Mayes (1999)
discuss the epidemiology, diagnosis, and treatment of major depressive
disorder (MDD) in childhood and adolescence. Although the criteria for
MDD are the same for children and adolescents as for adults, some challenges
exist in ascertaining the diagnosis. Children often have difficulty in
expressing or recalling information regarding their disorder; therefore,
multiple informants must often be used to obtain this information. Additionally,
comorbid diagnoses are common in early onset depression, making diagnosis
more difficult. The treatment of depression in this population is multi-modal,
including the patient, parents, and school, and is aimed at shortening
the episode of depression. Treatment, which is individualized based on
need, may include psychotherapy, family therapy or education, and pharmacological
treatment.
Pine, Cohen, Cohen, and Brook (1999) examined the relationship between
sub-clinical depressive symptoms in adolescence and major depressive episodes
in adulthood. A sample of 776 young people (aged 9-26 yrs) received psychiatric
assessments in 1983, 1985, and 1992. Among adolescents not meeting criteria
for majordepression, the authors estimated the magnitude of the association
between subclinical adolescent depressive symptoms and adult major depression.
Symptoms of major depression in adolescence strongly predicted an adult
episode of major depression: having depressive symptoms more than two-standard-deviations
above the mean in number predicted a twofold to three-fold greater risk
for an adult major depressive episode. Symptoms of depression in adolescence
strongly predict an episode of major depression in adulthood, even among
adolescents without major depression.
Parker, Gladstone, Mitchell, Wilhelm, and Roy (2000) conducted
a study to examine the relationship between early adverse events and depression
in adulthood. The authors hypothesized that exposure to events that
mirrored traumatic events of the individual’s childhood would result in
higher levels of depression in adult subjects. That is, early adverse
experiences create a vulnerability to depression when the individual is
exposed to similar circumstances in adulthood. The authors also posit
that this vulnerability may be cognitively mediated; negative cognitive
schemas that are formed in childhood may re-surface in the face of similar
events in adulthood.
A sample of 96 clinically depressed adults were given a detailed clinical
interview as well as questionnaires to assess a link between early adverse
experiences and depression in adulthood. The clinical interview focused
on life events immediately preceding the current episode of depression
and subjects were asked to identify the most relevant/pertinent “key” that
led to their current depression. The questionnaire, which was incorporated
into the clinical interview, asked subjects to reveal the extent to which
their parent or parents were critical, physically violent, verbally abusive,
overprotective, avoidant and a host of other negative attributes.
Finally, the subjects were asked to identify how the most detrimental attribute
of their parents “affected” them (i.e. made them feel rejected, criticized,
abused, etc). Results indicate that early adverse experiences do
tend to influence the development of negative cognitive schemas that can
be reactivated in adulthood. However, the results did not support
the hypothesis that exposure to events that “mirror” the traumatic experiences
of their childhood reactivates negative schemas that consequently lead
to an episode of depression. The authors discuss the methodological
shortcomings of the present study in an attempt to explain the lack of
significant findings and make suggestions for future research.
Comparison between questionnaires and interviews
Boyle, Offord, Racine, Szatmari, Sanford, and Fleming (1997)
evaluated a structured interview and a checklist against criteria from
the Diagnostic and Statistical Manual for Mental Disorders, Third Edition
- Revised (DSM-III-R; American Psychiatric Association, 1987) in order
to determine the reliability and validity of the measures. The initial
sample of children (N=1751) and their parents and teachers were given the
Ontario Child Health Study scales (OCHS; Boyle et al., 1987). A stratified
random sample of the participants were then selected for an intensive follow-up.
This group of children (N=251) filled out the OCHS scales a second time
for test-retest reliability. The revised version of the NIMH Diagnostic
Interview Schedule for Children and Adolescents (DICA-R; Shaffer et al.,
1996) was administered to parent-child dyads. The order of the interview
and scale completion was randomized.
Researchers found that reliability was relatively high (.70)
for major depressive disorder (MDD) from the structured interview.
Reliability was lower for the OCHS (.27). Convergent and discriminant
validity were comparable for both assessments. As the results would
indicate, a multiple assessment approach is supported as the interview
was more reliable than the self-report scale. Again, surveys or checklists
may be a good starting point, however, a clinical or structured interview
remains important to adequately assess depression.
Kasius, Ferdinand, van den Berg, & Verhulst (1997) explain
and compare parent report and structured interviews as two diagnostic approaches
within the fields of psychology and psychiatry. The clinical-diagnostic
approach primarily utilizes critieria from the Diagnostic and Statistical
Manual of Mental Disorder (DSM; American Psychiatric Association, 1994)
and can be described as “top-down,” where decisions are made about what
should be included based on consensus among experts. This framework
primarily utilizes the clinical interview for diagnostic purposes.
On the other hand, the empirical-quantitative approach uses psychometric
measures and procedures to diagnose mental disorders. This approach
can be thought of as “ground up” due to the use of rating scales that are
based on norms and distributions of scores within populations, with attention
given to reliability and validity issues.
The purpose of this study was to evaluate the relationship between
the two approaches. Participants (N=231) were obtained from a sample
of families who were referred to one outpatient facility in the Netherlands.
The gender and mean age of this sample was split as follows: 148 boys (mean
age = 10.4 years) and 83 girls (mean age = 10.6 years). The parents,
usually the mother (78%), filled out the Child Behavior Checklist (CBCL;
Achenbach, 1991). This measure achieved good reliability and validity
in the Dutch translation (Verhulst, Berden, & Sanders-Wondstra, 1985),
similar to that found by Achenbach (1991). The parent then participated
in a structured interview (NIMH Diagnostic Interview Schedule for Children
and Parent; DISC-P; NIMH, 1992).
Researchers found that most DSM-III-R diagnoses were predicted
by more than one CBCL scale independent from other scales. In particular,
the Anxious/Depressed Scale (CBCL) was most strongly related with the Generalized
Anxiety Disorder and Overanxious Disorder (DSM-III-R). The authors
conclude that the clinical-diagnostic approach and the empirical-quantitative
approach converge, but not to the extent that one can replace the other.
It was suggested that both should be used in combination to better capture
the complexity of behaviors presented by children and adolescents.
Fristad, Emery, and Beck, (1997) describe the ways self-report
alone may lead to lack of generalizability and predictive validity.
The Children’s Depression Inventory (CDI; Kovacs & Beck, 1977) is frequently
used as a self-report diagnostic tool for depression in children.
It is inexpensive and easy to administer, score, and interpret. However,
this rating scale was intended to be used in conjunction wit other assessments,
such as structured or clinical interviews (Fristad, Emery, & Beck,
1997). With this in mind, the authors evaluated published studies
from May 1993 to May 1995 in order to determine how the CDI was utilized.
A total of 133 articles were found which involved the diagnosing
of childhood depression. It was found that the CDI was used in 75%
of the studies that used a self-report assessment. Of these studies,
34% (46) used the CDI without a clinical or structured interview to determine
the diagnosis. In 44% of the studies in which the CDI was used in
isolation it was also found that the participants who scored highly were
referred to as “depressed,” with no clear cautionary statement about the
limitations of the CDI scale. Generalizability of the findings was
also not clearly addressed. The authors conclude that the CDI should
be used within an assessment strategy that includes multiple measures,
including a structured or clinical interview. A “multiple gating”
procedure was also noted, where the self-report measures could potentially
be used to screen large pools of potential participants (Kendall, Cantwell,
& Kazdin, 1989). The measure would then be given again to the
high-scoring participants in addition to utilizing a structured or clinical
interview. This “multiple gating” sequence would most likely prevent
misuse of self-report measures, including the CDI.
Stark (1990) also recommends a “Multiple Gate Assessment Model”
in assessing child and adolescent depression. The first step in such
a model is to use the Children’s Depression Inventory (CDI) as a screening
instrument. Benefits of using the CDI as the initial screening device
include: the ease with which the CDI can be administered to large groups
of children simultaneously; the short amount of time involved in completing
this paper-and-pencil, self-report measure; and the ease with which the
CDI can be scored and interpreted. Children who score higher than
19 (the recommended cutoff score) move on to the next stage, or “gate,”
of multiple gate assessment, while those who score below 19 receive no
further assessment. Additionally, any child who endorses a suicide
question (i.e. “I want to kill myself”) should be interviewed immediately
following the administration and should also remain in the group of children
participating in the second assessment phase. The next step in the
multiple gate model is to re-administer the CDI to children who scored
above 19 on the first administration and to children who endorsed a suicide
question. Again, children who score above 19 move on to the next
phase of the assessment while those scoring under 19 are excluded.
The third phase involves interviewing each remaining child with an instrument
such as the K-SADS. At this point in the model, it is up to the clinician
to determine the severity of the child’s depression and to make treatment
recommendations. In one of Stark’s research studies, just 43% of
children who scored above 19 on both administrations of the CDI exhibited
the full criteria necessary for a diagnosis of depression. However,
in spite of the fact that the CDI does result in a large number of false
positives, utilizing 2 administrations of the measure has been shown to
reduce the number of children administered the K-SADS by more than 37%;
thus, the multiple gate assessment model can greatly reduce the time spent
on more lengthy assessment measures like the K-SADS without sacrificing
accuracy in diagnosis.
Self-report measures suggest differences among cultures and youth
assesssment, as Manson, Ackerson, Dick, Baron (1999) report using psychometric
characteristics of the Center for Epidemiologic Studies Depression Scale
(CESD) as investigated with American Indian boarding school students (N
= 188; Grades 9-22). The CESD showed good internal consistency (alpha =
.82). Its dimensional structure was different from that described for adults,
both Indian and non-Indian. Of the Indian students, 58% were classified
as depressed, using the standard cutoff score of 16 or more, consistent
with past studies of this age group. Alternative scoring methods were considered,
based on persistence of symptoms as well as derived Diagnostic and Statistical
Manual of Mental Disorders (DSM-III) and Research Diagnostic Criteria algorithms.
Major gender differences were observed in the prevalence of reported symptoms
as well as patterns of endorsement for certain CESD items. The CESD should
be used with caution with American Indian adolescents, given the observed
variation in its dimensional structure and uncertainty regarding appropriate
cutoff scores.
Often, child and informant reports are provided concurrently,
as Mulhern, Fairclough, Smith, and Douglas (1999) discuss. They investigated
the incidence of depressive symptoms and their covariates in 99 child cancer
patients (aged 8-26 yrs) and their mothers. Classification of depressed
children was highly dependent on the informant and instrument used. Separate
multiple regression analyses of the mother's and nurse's ratings of the
child's level of depression, the child's self-report on the Child Depression
Inventory, and the mother's responses to the ChildBehavior Checklist depression
scales revealed different statistical models for each method of assessment.
However, increased severity of the mother's self-report of depressive symptoms
on the Beck Depression Inventory, which was predicted by low perceived
social support and hospitalization of her child, was associated with higher
levels of child depression on all child- and parent-report measures.
Developmental Perspective
Unfortunately, developmental concerns are not always addressed
well in assessments, regardless of approach (clinical-diagnostic or empirical-quantitative).
Often distinctions are generally made between the categories of “children”
and “adolescent,” however both categories contain large age ranges, often
overlap, and are used inconsistently from measurement to measurement.
For instance, the developmental trajectory of a 12-year-old is often very
different from that of a 16-year-old, yet both are considered to be adolescents.
This hold true for the “child” category as well, as a six-year-old experiences
a much different world than that of a ten-year-old. Many developmental
theorists, such as Piaget, would categorize these two children in different
cognitive stages, yet as with the adolescents, the two would be assessed
with identical assessments and measured against the same diagnostic criteria.
The developmental issues set forth here may be the result of
a “developmental continuity myth,” where it is thought that the symptoms
of psychopathology are similar regardless of age (Shirk, 1988). This
can be actively seen in the many adaptations of adult criteria, assessments,
and measures that are then applied to children and adolescents. In
the end, it is critical that old lenses and frameworks are challenged with
new research so that developmental changes across the lifetime are accurately
and adequately considered.
Another dangerous assumption that is commonly made by professionals
in the field is that children of various racial and ethnic identifications
can be adequately, validly, and reliably assessed by standard assessment
measures. There are many reasons that this assumption is quite ill-founded.
Garcia Coll and Garrido (2000) contend that minority children growing up
in this country have a qualitatively different experience than their White
counterparts, and that such divergent experiences predisposes them to more
risks of developing a psychopathology. For example, the authors state,
“It is our position that the systematic exclusion from critical resources
and power experienced by many minority populations places these children
and their families on less favorable developmental pathways from the very
beginning. By not having access to good prenatal care, by being exposed
to environmental toxins in utero and thereafter, and by experiencing on
a day-to-day basis the cumulative effects of other poverty-related factors
(such as limited nutrition, exposure to violence in local communities,
parental un- or underemployment, inadequate housing, etc.), these children
are placed at a higher risk for developmental psychopathology.” The
result of these factors tends to be the over-pathologizing of minority
youth in this country using instruments that are considered to be standard
measures by most. The additional fact that the vast majority of assessment
measures have been constructed using relatively homogenous samples of middle
class adults should make professionals extremely cautious when employing
adaptations of such adult measures in working with any child; hence, the
validity of such measures in assessing children from ethnic minority groups
is even more questionable. Symptoms of depression (or any other psychopathology
for that matter) may have very different meaning depending on the context
within which they are displayed. A child who grows despondent
and loses interest in things he/she used to take pleasure in (i.e. playing
with friends at a nearby park) may be displaying an adaptive response to
an abusive parent who beats the child when he/she returns from play, not
suffering from Major Depressive Disorder in the conventional sense.
What we as professionals have labeled as the syndrome of depression may
be just as adaptive given one set of circumstances as it is harmful in
another context. This logic highlights the importance of multiple
assessment procedures in assessment and diagnosis of child and adolescent
depression. We have more to gain from understanding the context within
which a given child’s depression developed than we do from the diagnosis
of depression alone. Until future research allows for the development
of assessment devices that are sensitive to racial and ethnic diversity,
there is no substitute for analysis of pertinent contextual factors of
childhood depression.
Children may not have the vocabulary to talk about negative feelings
and, as such, may express their feelings through behavior. Younger individuals
with depression are may show phobias, separation anxiety disorder, somatic
complaints and behavior problems. With psychotic depression, children are
more likely to report hallucinations. Older adolescents and adults with
psychotic depression may have delusions. An additional developmental
consideration is that children may display irritable symptoms rather than
typical “sadness” associated with adult depression. This is an important
consideration in the assessment and diagnosis of childhood depression.
Optimal Assessment Strategy
As was seen in the literature and current research, multiple
assessments are key for diagnosing psychopathology, particularly that of
depression. Because of developmental concerns and the range of symptoms,
it may take more time to diagnose depression in a child than it does to
diagnose an adult. The diagnostic process from a developmental perspective
includes interviews of both parents the child. Parents are more likely
to report outward signs of depression, but the child may be more aware
of experiences the parents do not recognize. Additionally, school
and other outside reports are useful, as they are less subject to the parents’
agendas. A report of the developmental history and information about
the existence of other conditions would be helpful in assessment as well.
Self-report scales, in addition to a clinical or structured interview,
would provide the cornerstone of a proper assessment strategy. One
advantage of self report, quantitative assessment is that they can be graded
in the same way every time for all patients and situations, so the information
is useful for making comparisons, and therefore for assessing the effect
of treatment on the patient. However, as previously stated, there
is danger in making broad-based comparisons between groups of children
and adolescents in that such an approach assumes homogeneity across ethnic
and racial groups. Thus, quantitative self-report measures, although
helpful under some circumstances, is not indicated in all situations.
No scale can yield as much information as a frank personal interview.
The clinical interview [would] takes advantage of at least [the] two assessment
approaches, clinical-diagnostic and empirical-quantitative, in order to
converge on a more informed diagnosis. In the clinical environment,
an initial screening with self-report scales may be indicated in order
to assess large groups of referred clients in a less time-consuming or
expensive manner. A structured or clinical interview can then be
used to confirm the initial diagnosis or give one pause to review assessment
strategies. However, professionals are cautioned to err on the side
of producing false positives so that children and adolescents have access
to the professional assistance that they need in order to cope with clinical
depression. It is more ethical to over-diagnose and, thus, offer
treatment to children with sub-clinical levels of depression than it is
to under-diagnose and fail to treat youth suffering from the disorder.
Moreover, such a strategy may serve as an effective intervention for children
who may be on a developmental pathway leading to depression.
I. TREATMENT
Because it has only been in the past two decades
that the concept of childhood depression has come to be accepted, most
research on treatment of depressed children is recent. The narrow
range of treatment options that include developmental considerations is
likely a product of the complexity of depressive symptoms within child
and adolescent life changes. It should also be noted that methods
of assessing child and adolescent depression are evolving to include ways
the expression of depression differ with developmental level.
Just as treatment for a headache will be different
if one goes to an acupuncturist, a pediatrician, or an herbalist, so too
will the treatment of childhood depression differ depending on the professional
consulted. Treatments logically go hand in hand with a professional's model
for viewing psychopathology and conceptualization of the etiology of a
disorder. If one chooses to see a psychiatrist, for example, where
the medical model is the perspective and etiology is viewed as biological,
pharmacology (drugs) are likely be a component of the treatment.
A cognitive-behaviorist, perceiving that depression is learned, will likely
want to change the behavior by replacing faulty cognitions. In addition,
certain cultural and/or religious beliefs may lead one to seek treatment
from someone other than a psychologist or psychiatrist, and again, the
treatment will reflect that person's framework for viewing depression.
In Western psychology, the two most common
treatments for childhood depression are pharmacology and psychosocial treatments,
namely cognitive-behavioral interventions (Stark, Sommer, Bowen, Goetz,
Doxey, & Vaughn, 1997). Approaches to pharmacology and psychosocial
treatments are reviewed below. Since most professionals currently
agree that the etiology of childhood depression is multifactorial, optimal
treatments must be multimodal (considering and incorporating aspects from
various models of depression).
Pharmacology Treatments
According to Stark, Bronik, Wong, Wells, and
Ostrander (2000), there is literally no evidence that antidepressant medications
work better than a placebo in the treatment of child and adolescent depression.
However, as the authors point out, the use of antidepressant medications
for youth depression has gained widespread acceptance in the field.
In fact, Stark, Laurent, Livingston, Boswell, and Swearer (1999) stated,
“Despite the lack of empirical evidence for the efficacy of antidepressants,
they are so commonly used with depressed youngsters that many consider
them to be the standard of care.” In spite of the lack of empirically
supported research documenting the efficacy of pharmacological treatments
for youth depression, the authors outline a current trend called polymedicating
that may show promise. According to Stark and his colleagues, “Proponents
of this approach believe that one medication may potentiate the effectiveness
of the other medication. There is some literature that suggests that
adolescents who are non-responsive to an antidepressant may respond favorably
to augmentation of the antidepressant with lithium.” The authors
discuss alternative augmentation strategies and provide and outline of
the considerations a psychiatrists might make in determining whether a
given child was appropriate for augmentation procedures.
A literature review conducted by Hammen, Rudolph,
Weisz, Rao, and Burge (1999) revealed a significant lack of research focusing
on treatments specific to childhood depression. Although studies
examining child and adolescent depression were plentiful, the authors were
hard-pressed to locate research focusing on children alone. In fact,
only 2 controlled studies using clinical samples of depressed children
were identified – neither of which presented results specifically for children.
The authors’ review of the literature on pharmacological treatments revealed
that tricyclic antidepressant (TCAs) treatment of child and adolescent
depression show mostly insignificant results. In all studies reviewed,
the authors reported that placebo treatments were as effective as TCAs
treatments of youth depression. The authors remarked that one study
examining the effectiveness of flouxetine in reducing depressive symptomatology
demonstrated modest advantages over placebo, with just 31% of patients
demonstrating symptom remission. The authors discuss the role of
methodological limitations including small sample size, brevity of treatment,
and sample heterogeneity and provide an overview of a developmental model
that they recommend as an alternative to current treatment approaches.
Bostic, Wilens, Spencer, and Biederman, (1999)
provide a literature and research review of depression and related treatments.
Specifically, they describe depression in children and adolescents in terms
of how these groups have responded to conventional tricyclic antidepressants
less robustly than depressed adults. Emerging research suggests that juvenile
depression may respond better to serotonergic and atypical pharmacologic
agents, so guidelines for selection and administration of these agents
are provided.
Ray-Sanchez, and Gutierrez-Casares (1997)
provide an open trial of paroxetine in children with major depressive disorder.
This study included 45 participants under the age of 14. Each was
assessed with the Clinical Global Severity (CGS) scale and a semi-structured
interview by an experienced child psychiatrist. Assessments were
done at the beginning of the protocol, at 1 month, at 3 months, and when
the protocol terminated. It should be noted that all children were
treated until their depressive episode was resolved, the longest of which
was 6 months.
Each participant was given paroxetine, a selective
serotonin reuptake inhibitor (SSRI), in specified and progressive doses.
Any side effects were mild and disappeared with dosage adjustment.
The researchers concluded that the drug was well tolerated within this
population. In addition, it was noted that paroxetine may serve as
an alternative to tricyclic antidepressants for children and adolescents.
However, more research was suggested, particularly incorporating a double-blinded
design that would include a placebo group comparison.
Rao, Lutchmansingh, and Poland (1999) assessed
REM sleep responses to scopolamine in 5 normal 14-18 year olds and 7 normal
adults in order to assess the influence of development on the regulation
of REM sleep by cholinergic systems. Subjects were studied on two separate
occasions for 3 consecutive nights. They received placebo or scopolamine
(1.5 mug/kg) on night 2. As expected scopolamine delayed REM latency and
suppressed REM sleep on night 2 in both age groups. Subtle differences
were seen, with scopolamine having a tendency to suppress REM sleep less
effectively in younger Subjects. On night 3 (recovery), REM latency was
shortened and REM sleep was increased to comparable extent in both the
adolescents and adults. The comparable REM sleep responses to scopolamine
between normal adolescents and adults, particularly on night 3, are discussed
in relation to the age-related expression of REM sleep abnormalities in
depression.
James (1999) describes 4 cases where children
and adolescents with major depressive disorder fail to respond to 1st-line
psychological therapies. The author suggests potential treatments
and a protocol for more resistant depression. The treatment of depression
requires a multimodal approach, starting with a comprehensive assessment
and psychological treatments such as cognitive-behavioural therapy, family
therapy and interpersonal therapy. Physical treatments are necessary for
severe depression and can be prescribed in a logical manner starting with
serotonin reuptake inhibitor antidepressants and should include the possibility
of augmentation of antidepressant action with either lithium or T3, followed
by, or alternatively, a combined serotonin-noradrenergic blocking antidepressant,
such as venlafaxine or mirtazapine. ECT should be reserved for the very
few resistant cases of endogenous, psychotic depression and those with
a risk of suicide.
Birmaher, Waterman, Ryan, Perel, and
others (1998) describe a randomized, controlled trial of amitriptyline
versus placebo for adolescents with “treatment-resistant” major depression.
27 participants in this study were referred to an in-patient hospital for
long-term care and were aged 12- to 18-years-old. Each was diagnosed
with major depressive disorder by a trained nurse using the Schedule for
Affective Disorders and Schizophrenia-Present Episode (K-SADS-P) and the
Hamilton Depression Rating Scale (HDRS). Any potential participant
was excluded if there was an accompanying diagnosis of bipolar disorder,
psychosis, substance abuse, pregnancy, or medical or neurological problems.
It was determined that all participants were taking some form of medication,
therefore within four weeks of admission, all medications were progressively
limited until no longer necessary. A multimodal approach to depression
was recommended by the researchers, with further study deemed necessary
for children and adolescents with major depressive disorder.
Psychosocial Interventions
Gladstone and Beardslee (2000) outline their
preventative intervention approach for child and adolescent depression.
Their intervention strategy focuses on increasing children’s resilience
to depression, especially with children who may be at high risk for developing
the disorder (i.e., children of depressed parents). Four main principles
guided Gladstone and Beardslee in the design of their intervention.
First, the fact that the intervention follows a developmental perspective
necessitates that age-appropriate children be identified. Due to
the cognitive component of the intervention strategies, the authors targeted
children between the ages of 8 and 15. Second, since research shows
that the majority of individuals suffering from depression will be treated
by their general practitioner, the intervention was designed to be compatible
with all types of health care practitioners. Third, since depression
often has a strong impact on family functioning, the family was the level
of intervention and the focus was on strengthening the role of the parent
in supporting their children. Finally, the focus of the approach
was on prevention, thus, children not meeting DSM-IV criteria for depression
were targeted. The preventive intervention project consisted of two
components, clinician-facilitated intervention (i.e., 6-10 sessions in
which the clinician meets with both parents and children individually and
as a group) and lecture (group format meetings without children present).
A total of 100 families participated in the present longitudinal study.
Results indicate that both intervention approaches helped to improve family
communication, reduce levels of parent guilt regarding depression, and
increase children’s understanding of their parent’s illness. According
to the authors, “Children whose parents reported a positive response to
intervention correspondingly reported better outcomes, in terms of depressive
symptoms and current global functioning. The reported findings indicate
that providing parents with factual information regarding risk and resiliency
in children can result in changes in illness-related behaviors and attitudes.”
The authors end by discussing related prevention projects and make recommendations
for future directions of research in the area of preventive intervention.
Kendall (2000) provides a brief review of
empirically supported treatments for various childhood disorders including
child and adolescent depression. Of the seven treatment outcome studies
of children with depressive symptomatology, “…only the self-control behavioral
treatment program developed by Stark and colleagues approached the criteria
for probably efficacious status, as defined by the 1995 task force.
No treatments met the criteria for well-established.
Lewinsohn and Clarke (1999) provided an overview
of psychosocial treatments of adolescent depression. Meta-analysis
of CBT therapies that have been utilized in the treatment of adolescent
depression revealed that 63% of individuals receiving some form of cognitive-behavioral
therapy showed significant improvements. Thus, while CBT methods
vary drastically from one clinician to the next, it appears that the overall
efficacy of CBT methods is well documented. The authors provide an
overview of the commonalities found across CB therapies as well as examples
of the various formats within which CBT can be administered (i.e., group
therapy, individual therapy, educational settings, intensity and duration
considerations, etc.). The authors conclude by calling attention
to the absence of research examining cognitive-behavioral treatments in
working with African American, Native American, Hispanic, and other ethnic
groups.
Bandura, Pastorelli, Barbaranelli, and Caprara,
(1999) provide a longitudinal study of self-efficacy and childhood depression.
Their research analyzed how different facets of perceived self-efficacy
operate in concert within a network of sociocognitive influences in childhood
depression. Perceived social and academic inefficacy contributed to concurrent
and subsequent depression both directly and through their impact on academic
achievement, prosocialness, and problem behaviors. In the shorter
run, children were depressed over beliefs in their academic inefficacy
rather than over their actual academic performances. In the longer
run, the impact of a low sense of academic efficacy on depression was mediated
through academic achievement, problem behavior, and prior depression. Perceived
social inefficacy had a heavier impact on depression in girls than in boys
in the longer term. Depression was also more strongly linked over time
for girls than for boys.
Stark, Laurent, Livingston, Boswell, and Swearer
(1999) provide a conceptualization that integrates components of cognitive
theory with those of attachment theory in an attempt to better understand
and treat childhood and adolescent depression. The authors posit
that depressive schemas (i.e., negative self-schema) proposed by cognitive
theory may be understood in children via their attachment relationships.
For example, a child with an overly critical parent who consistently demeans
and rejects him/her may fail to develop a positive self-schema that is
common of other children his/her age. In the authors words, “the
diathesis of depressive disorder a lack of a positive sense of self which
is formed through early interactions within the family and maintained by
interactions within the family and with peers as well as through other
day-to-day experiences.” Furthermore, it is hypothesized that the
lack of a positive sense of self will, over time, result in the formation
of negative sense of self and in negative self-schemas that are associated
with depression in adults. This critical interplay between a child’s
attachment with his/her primary caregiver and the subsequent development
of negative self-schemas is the crux of the integrative theory of attachment
theory and cognitive theory. Although the article is theoretical
in nature, not treatment focused, the empirical evidence the authors do
provide within each theory individually yields important treatment recommendations.
Specifically, the authors argue that prevention and intervention of childhood
depression needs to incorporate both cognitive (negative self-schemas,
negative cognitions) and interpersonal (i.e., parent-child interaction
patterns) domains.
Harrington, Whittaker, Shoebridge, and Campbell,
(1998) approach depression treatment with a systematic review of efficacy
of cognitive behavioral therapies in childhood and adolescent depressive
disorder. Their article reviewed six studies that utilized cognitive
behavior therapy with children and adolescents. The age of the participants
varied within each study, with an overall range of 8- to 18-years-old,
with all participants diagnosed with mild or moderate depressive disorder.
The cognitive behavioral therapies used included a depression coping course,
structured learning therapy, and specific depression treatment programs.
The therapy consisted of eight to 12 weekly sessions. A comparison
condition was part of each research design, with some control groups consisting
of participants on waiting lists or involved in placebo conditions.
Five out of the six studies assessed
outcomes using the Schedule for Affective Disorders and Schizophrenia Child
(K-SADS). The remaining study utilized a global rating of improvement
using the Child Depression Inventory (CDI) and other assessments not noted.
It was found that the rate of remission was significantly higher in the
cognitive behavior therapy group (62%) versus the comparison groups (36%).
It was concluded that cognitive behavioral therapy was effective in treating
mild to moderate depressive disorder. However, further research is
necessary due to the limited number of studies within this report, as well
as the need for the study of children and adolescents with severe depression.
Within a more specific population, McArt,
E.W., Shulman, D.A., Gajary, E. (1999) describe the development of an educational
workshop on teen depression and suicide. Community outreach activities
showed that adolescents and parents in Monroe County, New York, had difficulty
identifying and accessing mental health crisis services for youths. The
need to address this deficit led to the development of an educational workshop
on teen depression and suicide. Local, national, and international trends
in teen suicide led the authors to suggest a proa