Etiology

Childhood depression is likely to be caused by both genetic and environmental factors, and by their interactions. It is estimated that up to 40% of variance can be explained by genetic factors, and the remaining variances can be explained by environmental factors and by the interactions between genetic factors and the environment.[13][14] Life stress has been strongly associated with risk of depression, especially in girls.[15]

Pathophysiology

Exactly how genetic and environmental factors lead to the clinical manifestation of a depressive disorder is not fully understood. It is suspected that the process is complex and multifactorial. The pathophysiology of childhood depression is less well understood than that of adult depression. Fewer studies have been conducted in the pediatric population, and some of the adult findings have not been demonstrated in childhood depression. Although in adults with depression cortisol hypersecretion is a consistent finding, the relationship between cortisol levels in childhood depression is less clear and in places contradictory.[16] Increased morning cortisol in youth at risk for depression predicts onset of depression.[17] There is some evidence to suggest that young people who develop depression in adolescence have higher than typical levels of cortisol, but that those who develop symptoms earlier may have unusually low levels, suggesting the possibility of hypothalamic-pituitary-adrenal axis blunting over time in response to ongoing depression.[18] There is also evidence indicating the dysregulation of the central serotonergic systems in childhood depression. Prepubertal depressed children were found to have attenuated cortisol, but increased prolactin secretion responding to L-5-hydroxytryptophan challenge.[19] It is suggested that dysregulation of the central serotonergic system could lead to an impaired stress and emotional response, decreased impulse control, and emotional dysregulation.[20][21]

Studies in adults with depression have indicated several sleep abnormalities through polysomnographic studies, including reduced sleep continuity, reduced slow-wave sleep, shortened rapid eye movement (REM) latency, and increased REM density. However, sleep studies in children and adolescents with depression have been inconsistent. Some studies indicate that depressed children and adolescent inpatients have sleep continuity disturbances, and an increase in REM pressure (shortened REM latency and increased REM sleep %), but not disturbances in slow-wave sleep.[22][23][24][25][26] The results in outpatients have been mixed.[27][28][29]

The disruption in the motivation-and-reward neurologic pathway has also been indicated in pediatric depression.[30] There is evidence of the involvement of the glutamatergic system in the pathophysiology of depressive disorders.[31] Imaging studies have found volumetric and functional disruptions in multiple brain regions and pathways (e.g., in the amygdala, anterior cingulate, prefrontal cortex) that are important in emotional regulation, stress response, motivation, behavioral inhibition, and in the manifestation of depressive symptoms.[32][33][34][35]

Classification

Diagnostic and statistical manual of mental disorders, fifth edition, text revision (DSM-5-TR): classification of depressive disorders[1]

Categorizes depressive disorders into the following categories: major depressive disorder (MDD), persistent depressive disorder, disruptive mood dysregulation disorder (DMDD), premenstrual dysphoric disorder, substance/medication-induced depressive disorder, depressive disorder due to another medical condition, other specified depressive disorder, and unspecified depressive disorder. This topic focuses on MDD and persistent depressive disorder.

MDD

  • Similar to adults, characterized by at least 5 depressive symptoms, occurring over the same 2-week period.

  • Depressive symptoms include: depressed mood, diminished interest or pleasure, significant weight loss or gain, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue or loss of energy, feelings of worthlessness, diminished concentration and recurrent thoughts of death, suicidal ideation or suicide attempt.

  • Children and adolescents may have irritability instead of depression as 1 of the primary mood symptoms.

  • A child needs to have at least one of the key symptoms (sad or irritable mood, anhedonia), associated with a significant impairment in functioning in multiple areas, such as school or socially.

Persistent depressive disorder

  • Represents a consolidation of the diagnoses of chronic MDD and dysthymic disorder.

  • A more chronic form of depressive disorder than MDD.

  • Characterized by a chronic sad or irritable mood that lasts for at least 1 year (must be 2 years in adults).

  • Must also have at least 2 of the following symptoms: disturbed appetite, insomnia or hypersomnia, decreased energy level, low self-esteem, poor concentration, and feelings of hopelessness.

  • During the 1-year period, a child never has been without the minimum 3 symptoms for more than 2 consecutive months.

International classification of diseases, 11th revision (ICD-11)[2]

The ICD-11 is overall consistent with the DSM-5-TR criteria. The ICD-11 threshold for "depressive episode" is the same, with at least five of the characteristic symptoms: depressed mood (or irritability in children), diminished interest or pleasure in activities, poor concentration, low self-worth, recurrent thoughts of death, disrupted sleep, change in appetite, psychomotor agitation, or retardation and fatigue; in addition, ICD-11 includes an extra symptom of hopelessness that is not included in the DSM-5-TR.

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