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The Social Security Administration (SSA) Listing of Impairments for mood disorders includes within the
same diagnostic category criteria for the following diagnoses: major depressive syndrome, manic syndrome,
and bipolar or cyclothymic syndrome. However, according to the Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition (DSM-5) (APA, 2013), the mood disorders that may have a childhood onset
are (1) major depression, (2) persistent depressive disorder (PDD), and (3) disruptive mood dysregulation
disorder (DMDD). In a departure from DSM-IV, DSM-5 treats bipolar disorders as a separate category.
Pediatric bipolar disorder (PBD) will be addressed separately following a discussion of depression.
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DEPRESSION
Age
The age of onset for depression among children and youth is variable because the expression of depressive
symptoms may differ by development stage. Irritability, for example, may be more prominent among
younger depressed children (Birmaher et al., 2009). Preschool children with depressive syndrome may
manifest subthreshold diagnostic criteria for depression of shorter duration (Luby et al., 2014). These early
depressive symptoms are significant because in clinical samples they are predictive of major depressive
disorder in later childhood even after controlling for a maternal history of depression and other risk factors
(Luby et al., 2014). Furthermore, this relationship may persist because subthreshold depressive symptoms
have also been found to be predictive of major depressive disorder (MDD) onset in young adulthood (Klein
et al., 2013). Some of the best established risk factors for MDD include childhood anxiety and parental
depression (Thapar et al., 2012).
Sex
The risk for early-onset depression among children (i.e., 12 years or younger) does not vary by gender;
however, during adolescence the risk among girls substantially increases. Findings from most studies on
children suggest that there are no differences in the rates of depression between boys and girls or only a
slight elevation in boys compared to girls (Brooks-Gunn and Petersen, 1991; Costello et al., 1996; Garrison
et al., 1989; Lewinsohn et al., 1998b; Nolen-Hoeksema et al., 1991; Petersen et al., 1991; Rutter et al.,
1986; Wesselhoeft et al., 2014). In contrast, during adolescence the rate of depression among girls almost
always exceeds that of boys (Avenevoli et al., 2015; Costello et al., 2003; Ferrari et al., 2013; Lewinsohn et
al., 1998b; Offord et al., 1989), and this trend persists into early adulthood (Costello et al., 2003; Ferrari et
al., 2013; Rao et al., 1999; Rohde et al., 2013). There is evidence that hormonal, rather than psychological
or sociological, reasons account for the appearance of this adolescent gender difference, which persists until
menopause (Angold et al., 1998).
Race/Ethnicity
The findings regarding differences in rates of depression among youth by race or ethnicity are mixed, and
the variation is likely due to differences in study design, target populations, and how depression was
identified. Among a nationally representative sample of adolescents, major depression based upon youth-
reported symptoms did not vary by race or ethnicity (Avenevoli et al., 2015). Using data from the National
Health and Nutrition Examination Survey (NHANES) for children ages 8 to 15 years, a study found no
differences in the prevalence of mood disorders by race or ethnicity, possibly because of the small sample
size (Merikangas et al., 2010). In contrast, an analysis of data from the National Comorbidity Study-
Adolescent Supplement (NCS-A) found higher rates of mood disorders among Hispanic adolescents than
among non-Hispanic whites (Merikangas et al., 2010). Furthermore, findings from the National
Longitudinal Study of Adolescent Health indicated that youth from racial or ethnic minority backgrounds
were more likely to report depressive symptoms than non-minority youth (Rushton et al., 2002). This
finding is consistent with that of a study that examined the variation in prevalence rates of depression
among children and youth enrolled in Medicaid (Richardson et al., 2003).
Socioeconomic Status
Although studies of adults suggest that depression is associated with lower social class (Kessler et al.,
2003), results from studies of children and adolescents are inconsistent (Merikangas et al., 2009). Some
studies report a lack of association between depressive and anxiety disorders and social class (Costello et al.,
2003), whereas others report a significant association, at least for the most impoverished groups (Costello et
al., 1996; Gilman et al., 2003; Reinherz et al., 2003). There are also data on lifetime risk of depression that
indicate that a low socioeconomic status (SES) in childhood is related to a higher risk of depression later in
life (Gilman et al., 2002). Consequently the precise nature of the relationship between mood disorders in
children or adolescents and poverty is unknown.
Duration
Childhood-onset depression is a chronic disorder, with an estimated average duration of 6 months. Among a
longitudinal cohort of 816 high school students (ages 14 to 18) with depression, the mean age of onset was
15 years, and the mean duration of a major depressive episode was 26 weeks, but the duration varied widely,
from 2 to 520 weeks (Rohde et al., 2013). The risk factors related to longer depressive episodes were earlier
onset (age 15 years and younger), suicidal ideation, and seeking mental health treatment (Rohde et al.,
2013). These findings are consistent with the NCS-A, which found the mean duration of a major depressive
episode to be 27 weeks among a nationally representative sample of U.S. youth (Avenevoli et al., 2015).
The median duration of major depressive episodes among clinically referred samples has been found to be
considerably longer, most likely reflecting the greater clinical severity among children who access and
receive continuous mental health care. In such samples, the median duration of depression ranged from 7 to
9 months, which was more than three times longer than that found in a community-based sample (Kovacs,
1996).
Adolescent depression also tends to recur. A recent review of outcomes of childhood depression reached the
following conclusions (Costello and Maughan, 2015): (1) One in two children with a diagnosis of
depression had one or more further episodes as an adult; (2) depression alone has a much better prognosis
than depression accompanied by any of the following: anxiety disorders, oppositional defiant disorder, or
substance use disorder; and (3) family conflict predicts continuity of depression into adulthood. Among
adolescents in the community who recovered from a depressive episode, 5 percent experienced another
major depression within 6 months, 12 percent within 1 year, and approximately 33 percent within 4 years
(Rohde et al., 2013). Within clinically referred samples, an estimated 70 percent of depressed young patients
had at least one recurrence within 5 or more years (Kovacs, 1996). These findings are consistent with
international studies that suggest that children and adolescents with depression are more likely to suffer
major depression and to manifest suicidal tendencies as adults (Fergusson et al., 2005; Harrington et al.,
1990).
Comorbidities
Comorbid disorders are common among children and youth with depressive disorders, and childhood onset
may increase the risk for comorbidity (Fernando et al., 2011). Children and youth with depression are more
likely to suffer from anxiety disorders, conduct disorder, oppositional defiant disorder, and attention deficit
hyperactivity disorder (ADHD) as well as alcohol and drug abuse (Costello et al., 2003; Fleming and
Offord, 1990; Hipwell et al., 2011; Meinzer et al., 2013). Among a community-based cohort of adolescents
with major depressive disorder, 43 percent also had a lifetime occurrence of another mental disorder. Of
those teens with major depression, for example, 20 percent had an anxiety disorder, 13 percent abused
alcohol, 18 percent abused drugs, 4 percent had conduct disorder, 3 percent had oppositional defiant
disorder, 3 percent had ADHD, 8 percent had core symptoms of bipolar disorder, and 30 percent reported
smoking cigarettes daily (Lewinsohn et al., 1998b). In a study following older teens into adulthood, the rates
of comorbid major depression and of alcohol abuse or dependence were both only 2 percent during
adolescence, but they increased in early adulthood to 11 and 7 percent, respectively (Briere et al., 2014).
Compared to major depression only (i.e., without other diagnoses), the prognosis for youth with combined
depression and substance use disorders is poorer. Youth with both disorders are at higher risk for alcohol
dependence, suicide attempt, impaired role functioning, academic problems, life dissatisfaction, and less
treatment utilization (Briere et al., 2014; Lewinsohn et al., 1998b).
Functional Impairment
A large proportion of children and adolescents with mood disorders have significant levels of functional
impairment, defined as a reduced capacity to meet normal expectations in their roles at home, at school, and
with peers and adults. Based on the NCS-A, 63 percent of youth with past-year major depression reported
significant disability in at least one domain of functioning (Avenevoli et al., 2015). These findings are
consistent with the 2001–2004 NHANES, which found that about half of children with a depressive
diagnosis also showed significant functional impairment (Merikangas et al., 2010). Further, among a large
epidemiologic sample, The Great Smoky Mountains Study of youth aged 9 to 13 found that 73 percent of a
community sample with depression had significant functional impairment (Costello et al., 1996).
In addition, children with depression run a high risk of impaired functioning that continues into adulthood
(Costello and Maughan, 2015). In the Great Smoky Mountains Study, four areas of functioning were defined
as contributing to functional impairment in adulthood: (1) health, (2) education and income (SES), (3) social
relationships, and (4) criminality or self-injurious behavior (Copeland et al., 2015). In all four areas,
participants with early depression were significantly worse off than those with no psychiatric history, and
they were the most likely of any diagnostic group to perform poorly as adults. Results from international
studies are also consistent with these findings. In a Swedish sample (Jonsson et al., 2011) depressed
adolescent females grew into adults who were more likely than other adults to be divorced, to be single
parents, to have miscarried, to have experienced intimate partner violence, or to have had a sexually
transmitted disease. In the Brisbane birth cohort study (Keenan-Miller et al., 2007), even after controlling
for adult depression, early adolescent depression continued to be associated with poorer interviewer-rated
health, poorer self-perceived general health, higher health care utilization, and increased work impairment
due to physical health.
TABLE 11-1
Commonly Prescribed Antidepressant Medications for Depressive Disorders Among Adolescents.
Overall, the phases of treatment for depressive disorders are conceptualized as acute, continuation, and
maintenance and are defined by the goal to be achieved. The goal of the acute phase is to achieve response
(i.e., the patient having no symptoms or a significant reduction in symptoms for at least 2 weeks) and,
ideally, full symptomatic remission (i.e., a period of at least 2 weeks and less than 2 months with no or few
depressive symptoms) (AACAP, 2007). Continuation treatment is required for all depressed youths in order
for them to avoid relapses (AACAP, 2007). This phase typically lasts 6 to 12 months. The goal of the
maintenance phase is to avoid recurrences, especially among youth with depression of greater clinical
severity. This phase may last 1 year or longer, and little research is available to guide national
recommendations for when treatment during the maintenance phase should end (AACAP, 2007).
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Comorbidities
Comorbid disorders among teens with bipolar disorder are common and include ADHD, anxiety disorders,
oppositional defiant disorder, and substance use disorders (Bernardi et al., 2010; Birmaher et al., 2009; Jolin
et al., 2008; Masi et al., 2006; Pini et al., 2006; Sala et al., 2014; Stephens et al., 2014). In a national
household sample, rates of ADHD and alcohol use were three times higher among adolescents with bipolar
disorder who received treatment than among those who received no treatment; those who received treatment
often had much more severe bipolar disorder (Khazanov et al., 2015). Among youth hospitalized for their
first manic episode, the rate of comorbid substance abuse is high. In one study, almost one-half (48 percent)
of youth hospitalized for bipolar disorder had a substance use disorder either at baseline or within the
following year (Stephens et al., 2014). Furthermore, early onset of mania may increase a youth's risk for
substance abuse (Gao et al., 2010), and combined bipolar and substance use disorders is associated with
legal and academic difficulties, pregnancy, and suicidality (Goldstein and Bukstein, 2010).
Functional Impairment
The extent of functional impairment among children with pediatric bipolar disease is influenced by the
severity of the child's illness and by the complexity of the disorder. Because PBD is a chronic and serious
disorder, severe impairments in functioning are very common. Youth with PBD have documented
impairments in academic functioning and achievement due to executive functioning deficits (Biederman et
al., 2011; Perlman et al., 2013). Research also shows that children and adolescents with PBD have
difficulties reading facial expressions (Schenkel et al., 2012; Whitney et al., 2013), which is key to effective
social functioning. Current longitudinal studies underway (see Findling et al., 2010 will elucidate the extent
of functional impairments associated with this diagnosis.
TABLE 11-2
Commonly Prescribed Medications for Bipolar Disorder in Adolescents.
Although the short-term efficacy of recommended first-line mood stabilizers and antipsychotic medication
treatment has been established, there are few, if any, studies examining the long-term efficacy of medication
treatment. Among a cohort of 263 children and adolescents with bipolar spectrum disorders, approximately
70 percent recovered from their index episode, but 50 percent had at least one syndromal recurrence,
particularly depressive episodes (Birmaher et al., 2006). Clinically, the extent of improvement is likely
influenced by clinical severity and complexity (i.e., comorbid substance abuse), timely access to care,
treatment adherence, and environmental factors such as social support, family functioning, and schooling.
The duration of treatment for this chronic disorder also varies from individual to individual. Common short-
term goals for treatment usually include a reduction in target symptoms. Longer-term goals include
improvement in social and academic functioning, which may include a reduction in high-risk behaviors such
as substance abuse.
FINDINGS
Diagnosis requires a comprehensive psychiatric diagnostic evaluation. Screening tools are available
to detect symptoms of depression, particularly in adolescents. There are no well-established
laboratory tests for mood disorders.
Mood disorders of childhood may occur in children of all ages. However, the risk of mood disorders
increases during adolescence, especially among girls. A younger age of onset is a risk factor for
increased severity and duration.
While symptoms may wax and wane, mood disorders cause significant functional impairment that
often persist or recur through childhood and into adulthood.
Mood disorders frequently co-occur with other mental disorders.
There is evidence for the effectiveness of medication treatment and psychotherapies for mood
disorders. Improvements in functional impairments are enhanced with a combination of evidence-
based psychotherapy and medication.
Bipolar disorder in children and youth is classified by the DSM-5 as a diagnosis distinct from
depression. Severe impairments in functioning are very common and frequently persist, even with
treatment.
Psychologists
Theories
Studies
Research Methods
1. Atypical Psychology
2. Depression
Psychological Theories of
Depression
By Saul McLeod, published 2015
Depression is a mood disorder which prevents individuals from leading a normal life, at
work socially or within their family. Seligman (1973) referred to depression as the
‘common cold’ of psychiatry because of its frequency of diagnosis.
Depending on how data are gathered and how diagnoses are made, as many as 27% of
some population groups may be suffering from depression at any one time (NIMH, 2001;
data for older adults).
Behaviorist Theory
Behaviorism emphasizes the importance of the environment in shaping behavior. The
focus is on observable behavior and the conditions through which individuals' learn
behavior, namely classical conditioning, operant conditioning and social learning theory.
Therefore depression is the result of a person's interaction with their environment.
For example, classical conditioning proposes depression is learned through associating
certain stimuli with negative emotional states.Social learning theory states behavior is
learned through observation, imitation and reinforcement.
Operant Conditioning
Operant conditioning states that depression is caused by the removal of positive
reinforcement from the environment (Lewinsohn, 1974). Certain events, such as losing
your job, induce depression because they reduce positive reinforcement from others (e.g.
being around people who like you).
Depressed people usually become much less socially active. In addition depression can also
be caused through inadvertent reinforcement of depressed behavior by others.
For example, when a loved one is lost, an important source of positive reinforcement has
lost as well. This leads to inactivity. The main source of reinforcement is now the sympathy
and attention of friends and relatives.
However this tends to reinforce maladaptive behavior i.e. weeping, complaining, talking of
suicide. This eventually alienates even close friends leading to even less reinforcement,
increasing social isolation and unhappiness. In other words depression is a vicious cycle in
which the person is driven further and further down.
Also if the person lacks social skills or has a very rigid personality structure they may find
it difficult to make the adjustments needed to look for new and alternative sources of
reinforcement (Lewinsohn, 1974). So they get locked into a negative downward spiral.
Critical Evaluation
Behavioral/learning theories makes sense in terms of reactive depression, where there is a
clearly identifiable cause of depression. However, one of the biggest problems for the
theory is that of endogenous depression. This is depression that has no apparent cause (i.e.
nothing bad has happened to the person).
An additional problem of the behaviorist approach is that it fails to take into account
cognitions (thoughts) influence on mood.
Psychodynamic Theory
During the 1960's psychodynamic theories dominated psychology and psychiatry.
Depression was understood in terms of:
1. inwardly directed anger (Freud, 1917),
2. introjection of love object loss,
3. severe super-ego demands (Freud, 1917),
4. excessive narcissistic, oral and/or anal personality need (Chodoff, 1972),
5. loss of self-esteem (Bibring, 1953; Fenichel, 1968), and
6. deprivation in the mother child relationship during the first year (Kleine, 1934).
Cognitive Approach
This approach focuses on people’s beliefs rather than their behavior. Depression results
from systematic negative bias in thinking processes.
Emotional, behavioral (and possibly physical) symptoms result from cognitive
abnormality. This means that depressed patients think differently to clinically normal
people. The cognitive approach also assumes changes in thinking precede (i.e. come
before) the onset of depressed mood.
As these three components interact, they interfere with normal cognitive processing,
leading to impairments in perception, memory and problem solving with the person
becoming obsessed with negative thoughts.
Beck believed that depression prone individuals develop a negative self-schema. They
possess a set of beliefs and expectations about themselves that are essentially negative and
pessimistic. Beck claimed that negative schemas may be acquired in childhood as a result
of a traumatic event. Experiences that might contribute to negative schemas include:
Death of a parent or sibling.
Parental rejection, criticism, overprotection, neglect or abuse.
Bullying at school or exclusion from peer group.
Such thoughts exacerbate, and are exacerbated by the cognitive triad. Beck believed these
thoughts or this way of thinking become automatic. When a person’s stream of automatic
thoughts is very negative you would expect a person to become depressed. Quite often
these negative thoughts will persist even in the face of contrary evidence.
Critical Evaluation
Alloy et al. (1999) followed the thinking styles of young Americans in their early 20’s for 6
years. Their thinking style was tested and they were placed in either the ‘positive thinking
group’ or ‘negative thinking group’. After 6 years the researchers found that only 1% of the
positive group developed depression compared to 17% of the ‘negative’ group. These
results indicate there may be a link between cognitive style and development of depression.
However such a study may suffer from demand characteristics. The results are also
correlational. It is important to remember that the precise role of cognitive processes is yet
to be determined. The maladaptive cognitions seen in depressed people may be a
consequence rather than a cause of depression.
Learned Helplessness
Martin Seligman (1974) proposed a cognitive explanation of depression called learned
helplessness. According to Seligman’s learned helplessness theory, depression occurs when
a person learns that their attempts to escape negative situations make no difference.
As a consequence they become passive and will endure aversive stimuli or environments
even when escape is possible.
Seligman based his theory on research using dogs.
A dog put into a partitioned cage learns to escape when the floor is electrified. If the dog is
restrained whilst being shocked it eventually stops trying to escape.
Dogs subjected to inescapable electric shocks later failed to escape from shocks even when
it was possible to do so. Moreover, they exhibited some of the symptoms of depression
found in humans (lethargy, sluggishness, passive in the face of stress and appetite loss).
This led Seligman (1974) to explain depression in humans in terms of learned helplessness,
whereby the individual gives up trying to influence their environment because they have
learned that they are helpless as a consequence of having no control over what happens to
them.
Although Seligman’s account may explain depression to a certain extent, it fails to take into
account cognitions (thoughts). Abramson, Seligman, and Teasdale (1978) consequently
introduced a cognitive version of the theory by reformulating learned helplessness in term
of attributional processes (i.e. how people explain the cause of an event).
The depression attributional style is based on three dimensions, namely locus (whether the
cause is internal - to do with a person themselves, or external - to do with some aspect of
the situation), stability (whether the cause is stable and permanent or unstable and
transient) and globalor specific (whether the cause relates to the 'whole' person or just
some particular feature characteristic).
In this new version of the theory, the mere presence of a negative event was not considered
sufficient to produce a helpless or depressive state. Instead, Abramson et al. argued that
people who attribute failure to internal, stable, and global causes are more likely to become
depressed than those who attribute failure to external, unstable and specific causes. This is
because the former attributional style leads people to the conclusion that they are unable
to change things for the better.
Critical Evaluation
Gotlib and Colby (1987) found that people who were formerly depressed are actually no
different from people who have never been depressed in terms of their tendencies to view
negative events with an attitude of helpless resignation.
This suggests that helplessness could be a symptom rather than a cause of depression.
Moreover, it may be that negative thinking generally is also an effect rather than a cause of
depression.
Humanist Approach
Humanists believe that there are needs that are unique to the human species. According
to Maslow (1962) the most important of these is the need for self-actualization (achieving
out potential). The self actualizing human being has a meaningful life. Anything that blocks
our striving to fulfil this need can be a cause of depression. What could cause this?
1. Parents imposing conditions of worth on their children. I.e. rather than accepting
the child for who s/he is and giving unconditional love, parents make love conditional
on good behavior. E.g. a child may be blamed for not doing well at school, develop a
negative self-image and feel depressed because of a failure to live up to parentally
imposed standards.
2. Some children may seek to avoid this by denying their true self and projecting an
image of the kind of person they want to be. This façade or false self is an effort to
please others. However the splitting off of the real self from the person you are
pretending to be causes hatred of the self. The person then comes to despise
themselves for living a lie.
3. As adults self actualization can be undermined by unhappy relationships and
unfulfilling jobs. An empty shell marriage means the person is unable to give and
receive love from their partner. An alienating job means the person is denied the
opportunity to be creative at work.
References
Abramson, L. Y., Seligman, M. E., & Teasdale, J. D. (1978). Learned helplessness in
humans: critique and reformulation. Journal of abnormal psychology, 87(1), 49.
Alloy, L. B., Abramson, L. Y., Whitehouse, W. G., Hogan, M. E., Tashman, N. A., Steinberg,
D. L., ... & Donovan, P. (1999). Depressogenic cognitive styles: Predictive validity,
information processing and personality characteristics, and developmental
origins. behavior research and therapy, 37(6), 503-531.
Beck, A. T. (1967). Depression: Causes and treatment. Philadelphia: University of
Pennsylvania Press.
Beck, A. T., Epstein, N., & Harrison, R. (1983). Cognitions, attitudes and personality
dimensions in depression. British Journal of Cognitive Psychotherapy.
Bibring, E. (1953). The mechanism of depression.
Brown, G. W., & Harris, T. (1978). Social origins of depression: a reply. Psychological
Medicine, 8(04), 577-588.
Chodoff, P. (1972). The depressive personality: A critical review. Archives of General
Psychiatry, 27(5), 666-673.
Fenichel, O. (1968). Depression and mania. The Meaning of Despair. New York: Science
House.
Freud, S. (1917). Mourning and melancholia. Standard edition, 14(19), 17.
Gotlib, I. H., & Colby, C. A. (1987). Treatment of depression: An interpersonal systems
approach. Pergamon Press.
Klein, M. (1934). Psychogenesis of manic-depressive states: contributions to
psychoanalysis. London: Hogarth.
Lewinsohn, P. M. (1974). A behavioral approach to depression.
Maslow, A. H. (1962). Towards a psychology of being. Princeton: D. Van Nostrand
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National Institute of Mental Health. (2001). Depression research at the National Institute
of Mental Health. Retrieved
from http://www.nimh.nih.gov/health/publications/depression/complete-index.shtml.
Seligman, M. E. (1973). Fall into helplessness. Psychology today, 7(1), 43-48.
Seligman, M. E. (1974). Depression and learned helplessness. John Wiley & Sons.
Further Information
Abnormal Psychology CBTA-level Psychology Psychopathology Revision
NotesPsychoanalysisMedical Model of AbnormalityBehavioral TherapyCognitive
TherapyList of Support GroupsCampaign against Living MiserablyMen do cry: one man’s
experience of depressionNHS Self Help Guides
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