Depressive Disorders



Depressive Disorders


David A. Brent

V. Robin Weersing



In this chapter, we describe the nosology and epidemiology of unipolar depressive disorders in youth, risk factors for depression onset and recurrence, and the evidence base for psychosocial and pharmacological treatments. We conclude with suggested areas for future inquiry.


Clinical Picture

Depressive disorders in childhood and adolescence are characterized by core persistent and pervasive sadness, anhedonia, boredom or irritability that is functionally impairing, and relatively unresponsive to usual experiences that might usually bring relief, such as pleasurable activities and interactions and attention from other people. The single most important distinction between depression as an illness and the “normal ups and downs” of childhood and adolescence is that depression is associated with functional impairment, mediated through the intensity, duration, and lack of responsiveness of depressed mood and associated symptoms.

Depressive disorders exist on a continuum, and are classified on the basis of severity, pervasiveness, and presence or absence of mania (1). At the mildest end of the spectrum are adjustment disorders with depressed mood, which are mild, self-limited, and occur in response to a clear stressor. Depression not otherwise specified (NOS), also referred to as “minor” or subsyndromal depression, is diagnosed in the presence of depressed mood, anhedonia, or irritability, and up to three symptoms of major depression (2). Dysthymic disorder is a chronic condition with fewer symptoms than major depression, but lasts a minimum of one year. Major depression is the most severe condition, with either sad or irritable mood, or anhedonia, along with at least five other symptoms, such as social withdrawal, worthlessness, guilt, suicidal thoughts or behavior, sleep increase or decrease, decreased motivation and/or concentration, and increased or decreased appetite. Minor depression and dysthymic disorder are functionally impairing and are often precursors to major depression (2,3). Furthermore, dysthymia and major depression can coexist in a state referred to as “double depression,” which is associated with a particularly chronic course (3). Rarely, young patients with major depression also have psychotic symptoms such as auditory hallucinations or delusions, usually with self-derogatory, paranoid, or depressive content.

Comorbidity is the rule rather than the exception in depressed children and adolescents, especially in clinical samples (4). Anxiety is frequently a precursor of mood disorder and may also occur simultaneously with depression. ADHD and depression are also often comorbid and the two disorders may be cotransmitted in families (5). Alcohol, drug, and tobacco abuse are associated with depression, and longitudinal studies suggest a bidirectional causality, with substance abuse both leading to, and occurring as a consequence of, depression (6,7,8). Conduct disorder is frequently comorbid with depression, particularly in prepubertal samples (9). Comorbidity with depression may arise because sharing of risk factors that are common to both conditions. For example, the comorbidity of mood disorders and behavioral disorders and substance abuse may be due to common factors, such as parental substance abuse and criminality, exposure to family violence, and family discord (10). Comorbidity may also arise because a condition is either a precursor or a consequence to depression, in the cases of anxiety and tobacco use, respectively.


Descriptive Epidemiology


Estimates of Population Prevalence

The point prevalence of depressive disorders is 1–2% of prepubertal children and 3–8% of adolescents, with a lifetime prevalence by the end of adolescence of around 20% (11,12,13).


Gender Distribution and the Onset of Puberty

The 3:1 female predominance in mood disorders first emerges in adolescence (13). The higher female than male rate of depression after the onset of puberty may be due to: 1) increases in estradiol and testosterone associated with the onset of puberty in females, 2) higher rates of anxiety disorder and a tendency to rumination in females, which in turn predispose to depressive disorders, and 3) adolescent increases in interpersonal conflict that seem to be driven by genetic self-selection into risky environments and maladaptive responses to stress (14,15,16).



Age and Developmental Factors

Most typically, prepubertal depression has a set of risk factors and course similar to conduct disorder, with comorbid behavioral problems; family adversity such as family discord, parental criminality and parental substance abuse; and increased risk of antisocial disorder, but not depression in adult life (17,18,19). Less commonly, prepubertal depression is highly familial, with multigenerational loading for depression, with high rates of anxiety and bipolar disorder, and recurrences of mood disorder in adolescence and adulthood (18,20). Adolescent-onset depression is more likely to result in recurrent episodes in adult life (18,21). Recent work with structured diagnostic assessments has demonstrated the existence of depression even in preschool children, with the most prominent symptoms being sad or irritable mood, anhedonia, low energy, and change in level of activity (22).

Early-onset of puberty increases the risk of depression in girls (23). Other developmental factors that may contribute to an increased risk of depression after puberty include experimentation with tobacco, drugs and alcohol, decreased adult supervision and contact, and a greater physiological need for sleep, along with a tendency to actually obtain less sleep (6,7,8,24,25).


Risk Factors For Depression Onset and Recurrence


Genetic

Twin studies demonstrate that depressive symptoms have a greater concordance among monozygotic than among dizygotic twins, and a heritability of around 40–65%, with higher estimates of heritability in adolescent vs. prepubertal children (26,27,28,29,30). Both “bottom-up” and “top-down” family studies have shown a 2–4-fold increased risk of depression in first-degree relatives (31,32). Twin studies suggest a greater genetic component in adolescent vs. pre-pubertal onset depression, supportive of the view that very early onset depression may often be a response to a chaotic environment (30).

There is evidence that liability to depression is cotransmitted along with anxiety symptoms, with a heritability of 61–65% (32,33,34. Genes that influence the risk of anxiety may in turn lead to a higher rate of postpubertal depression by increasing sensitivity to life events, and also by increasing the likelihood of exposure to depressogenic life events (35,36). This formulation is consistent with the results of longitudinal studies (37,38

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Jun 8, 2016 | Posted by in PSYCHIATRY | Comments Off on Depressive Disorders

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