eMedicine Specialties > Pediatrics: Developmental and Behavioral > Medical Topics

Mood Disorder: Depression

Author: Tami D Benton, MD, Director of Clinical Services, Program Director, Department of Psychiatry, Children's Hospital of Philadelphia; Assistant Professor, University of Pennsylvania
Contributor Information and Disclosures

Updated: Mar 3, 2008

Introduction

Background

Childhood and adolescent major depressive disorder (MDD) is a prevalent, familial, and recurrent condition that generally continues episodically into adulthood. Childhood depression seems to be evident at earlier ages in successive cohorts and often occurs with comorbid psychiatric disorders, increased risk for suicide, substance abuse, and behavior problems. Children and adolescents with depression frequently have poor psychosocial, academic, and family functioning.

Pathophysiology

Several areas of the brain are involved in mood functions. Sleep, appetite, and memory are commonly disturbed in persons with depression. Except for the pituitary, all cerebral components responsible for these functions are broadly considered to be a part of the limbic system; all components normally receive signals from neurons that secrete serotonin or norepinephrine or from neurons of both types. Reductions in the activity of circuits that use serotonin and norepinephrine are thought to contribute to depression.

Frequency

United States

Reported prevalence rates for depression in children and adolescents vary. Differences may be due to different populations sampled and variable criteria used.

In 1988, Kashani and Sherman conducted epidemiologic studies in the United States that revealed the incidence of depression to be 0.9% in preschool-aged children, 1.9% in school-aged children, and 4.7% in adolescents.¹ A study of a randomly selected sample of high school students revealed that 22.3% of females and 11.4% of male high school students reported one current or lifetime episode of unipolar depression. The percentage of male and female students with 2 or more episodes was 4.9% and 1.6%, respectively. In 1997, Garrison et al conducted a study of adolescents aged 11-16 years in the southeastern United States and found that the 1-year incidence of major depression was 3.3%.²

As these studies demonstrate, the occurrence of depression is not rare and is encountered regularly in pediatric and psychiatric practice.

International

Available data on the international incidence of major depression in children and adolescents are sparse. Reported adult prevalence rates generally mirror those of the United States.

Helgason examined the entire Icelandic birth cohort of 1895-97 with periodic follow-up until cohort individuals reached age 74-76 years. The lifetime estimates of risk for any affective disorder were 14.8% for females and 9.8% for males.

The Stirling County Study, which began shortly after World War II, offers a 40-year perspective of the prevalence and incidence of psychiatric disorders among an adult population in Atlantic, Canada. In 2000, Murphy et al found the overall prevalence of depression remained stable at 5% across 3 separate samples in 1952, 1970, and 1992.³ They reported a redistribution in the most recent sample that indicated prevalence had shifted from older to younger persons and that the female-to-male ratio had increased.

In 1999, a European study by Copeland et al sought to assess the prevalence of depression in 9 European nations in order to design intervention for elderly persons who were depressed.⁴ They found widely ranging prevalences in their study centers. Prevalence for females was higher than for males. They found no constant association between prevalence and age. Meta-analysis revealed an overall prevalence of 12.3% and sex frequencies of 14.1% for females and 8.6% for males.

According to Jablensky in 1981, the World Health Organization (WHO) collaborative study on the assessment of depressive disorders examined depressive patients in Canada, Iran, Japan, and Switzerland and found considerable similarity in depressive symptomatology across cultures.⁵

Mortality/Morbidity

As many as 15% of those with depression or bipolar disorder commit suicide each year. In 1996, the Centers for Disease Control and Prevention (CDC) listed suicide as the ninth leading cause of death in the United States, accounting for 30,862 deaths. Many believe this number is a gross underestimate. For example, children's deaths are often ruled as accidental when the intent of the deceased is not apparent. The feasibility of suicide among children is frequently unthinkable, even to health professionals. Because mood disorders, such as depression, substantially increase the risk of suicide, suicidal behavior is a matter of serious concern for clinicians who deal with the mental health problems of children and adolescents. The incidence of suicide attempts reaches a peak during the mid adolescent years; the mortality rate from suicide increases steadily through the teenage years; suicide is the third leading cause of death in that age group.

Risk factors for completed suicide include the presence of a major mood disorder, occurrence of command auditory hallucinations, use of substances, and evidence of specific plans and an attempt to prevent discovery. Major depression with psychotic features, such as hallucinations, places an individual at increased risk of harm to themselves or others. Psychosis and risk of harm to self or others are indications for hospitalization.

Race

Cultural norms associated with differing racial and ethnic groups can affect the experience and reporting of symptoms of depression. For example, in some cultures, depression may be experienced largely in somatic terms, in place of sadness or guilt. Several studies point toward the role of culture in childhood and adolescent depression. For example, the stress of acculturation was found to have a role in the increased incidence of depressive symptoms and suicidal ideation among Hispanic youths.

In an epidemiologic study of youths aged 12-17 years in Los Angeles County in 1998, Siegel et al found that Hispanic youths reported more symptoms of depression, independent of socioeconomic status, when compared with white, African American, or Asian American adolescents, using the Children's Depression Inventory (CDI).⁶ This study also found significant effects of social class on depression. As income decreased, the average level of depression increased.

More extensive studies of ethnic subpopulations of adolescents who are depressed are needed. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) states that a symptom should not be dismissed because it is part of a cultural norm.⁷ Likewise, culturally distinctive experiences (eg, fear of being hexed or bewitched; experience of visitations from the dead) should be distinguished from actual hallucinations or delusions that may be part of a major depressive episode with psychotic features.

Sex

Sex issues and depression in youths has been the subject of much research. In 1998, Hankin et al conducted a prospective, 10-year, longitudinal study of preadolescents through young adulthood and found that the most critical time for sex differences to emerge is the period when adolescents are aged 15-18 years.⁸ During this period, the increase of the overall rates of depression and onset of new cases of depression peak. The rates of depression increase dramatically for both sexes, and the rate of depression in females grows to twice the prevalence rate for males. No sex differences are noted for depression symptom severity or recurrence.

Age

Evidence suggests that the presentation of some symptoms may change with age. Symptoms, such as somatic complaints, irritability, and social withdrawal, are more common in children, whereas psychomotor retardation, hypersomnia, and delusions are less common prior to puberty than in adolescence and adulthood.

Clinical

History

The Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III); the Diagnostic and Statistical Manual of Mental Disorders, Third Edition Revised (DSM-III-R); and the DSM-IV use the same basic criteria to diagnose depression in adults and children. A few small adjustments were made to the diagnostic criteria to account for the differences in age and stage of development in adults and children.

The DSM-IV diagnostic criteria for depressive disorders are the same for children and adolescents as they are for adults, with small exceptions stated as notations to the criteria.

• The DSM-IV defines a major depressive episode as a syndrome in which at least 5 of the following symptoms have been present during the same 2-week period:
  • Depressed mood (for children and adolescents, this also can be an irritable mood)
  • Diminished interest or loss of pleasure in almost all activities
  • Sleep disturbance
  • Weight change or appetite disturbance (for children this can be failure to achieve expected weight gain)
  • Decreased concentration or indecisiveness
  • Suicidal ideation or thoughts of death
  • Psychomotor agitation or retardation
  • Fatigue or loss of energy
  • Feelings of worthlessness or inappropriate guilt
• At least one of the symptoms must be diminished interest/pleasure or depressed mood. The symptoms must cause significant distress or impairment of functioning in social, occupational, or other important areas. Depression should not have been precipitated by the direct action of a substance or the result of a medical condition and should not be better explained by bereavement or schizoaffective disorder. Additionally, a major depressive episode should not be superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or a psychotic disorder not otherwise specified.
• Depressive disorders can be rated as mild, moderate, or severe. The disorder can also occur with or without psychotic symptoms, which can be mood congruent or incongruent. Depressive disorders can be determined to be in full or partial remission. When an episode lasts more than 2 consecutive years, the depression should be diagnosed as chronic. Depression may also have melancholic features. Either a loss of pleasure in almost all activities or a lack of reactivity to usually pleasurable stimuli are present. Additionally, at least 3 of the following are required:
  • A depressed mood that is distinctly different from the kind felt when a loved one is deceased
  • Depression that is worse in the morning
  • Waking up 2 hours earlier than usual
  • Observable psychomotor retardation or agitation
  • Significant weight loss or anorexia
  • Excessive or inappropriate guilt
• Depressive episodes can also be present with catatonic features that require at least 2 of the following, as illustrated in the DSM-IV:
  • Motoric immobility in the form of catalepsy or stupor
  • Motor overactivity that seems purposeless and not in response to external stimuli
  • Extreme negativism or mutism
  • Voluntary movement peculiarities such a posturing, grimacing, stereotypy, and mannerisms
  • Echolalia or echopraxia
• The seasonality of a depressive disorder can also be specified. To diagnose a seasonal mood disorder, a regular temporal relationship should exist between the depression and a particular time of year. An individual should demonstrate at least 2 episodes of depressive disturbance in the prior 2 years, and seasonal episodes should substantially outnumber nonseasonal episodes. Diagnosing seasonal affective disorder in children is difficult because they experience the recurrent universal stressor of beginning school every autumn. Also, a young child might present with an apparent seasonal depressive disorder but not yet have had prior episodes.
• A depression may also be identified as having atypical features. Characteristics of this subtype are mood reactivity and exclusion of melancholic and catatonic subtypes in addition to 2 or more of the following for the a period of at least 2 weeks:
  • Increase in appetite or significant weight gain
  • Increased sleep
  • Feelings of heaviness in arms or legs
  • A pattern of long-standing interpersonal rejection sensitivity that extends far beyond the mood disturbance episodes and results in significant impairment in social or occupational functioning
• The DSM-IV also includes a category for depressive disorders not otherwise specified. This category includes disorders with features of depression that do not meet criteria for a specific mood disorder or adjustment disorder with depressed mood. Examples include a depressive episode superimposed on residual schizophrenia, a recurrent mild depressive disturbance that does not meet criteria for dysthymia, or non–stress-related episodes that do not meet the criteria for a major depressive episode. Consult the DSM-IV for further details as to the diagnostic criteria for depressive disorders not otherwise specified.

Physical

• A complete mental health evaluation should always include a medical evaluation.
• Organic etiologies that might imitate a depressive disorder must be ruled out.
• Conditions believed to mimic depressive disorders fall into the major general categories, including the following:
  • Infection
  • Medication
  • Endocrine disorder
  • Tumor
  • Neurologic disorder
  • Miscellaneous disorder

Causes

Whether ego-damaging experiences or biological processes cause depression remains the topic of some debate. The final common pathways to depression involve biochemical changes in the brain.

• Neuroimaging
  • A recently discovered abnormality in an area of the brain that helps to control emotional reactions contributes to a new understanding of why persons develop depression and other affective disturbances. By using positron emission tomographic (PET) images, researchers found an area of the prefrontal cortex with an abnormally diminished activity in patients with unipolar depression and bipolar depression. This region is related to emotional response and has widespread connections with other areas of the brain. These other areas are responsible for the regulation of dopamine, noradrenaline, and serotonin, which have important roles in the regulation of mood. PET imaging provides the means for the study of receptor volume and the effect a compound may have on receptors; however, PET is problematic for use with children and adolescents because it requires complex equipment and uses radiation.
  • MRI, magnetic resonance spectroscopy (MRS), and magnetoencephalography (MEG) are best suited to study the structural, physiological, and developmental brain abnormalities in youths because they do not involve ionizing radiation or radioactive isotopes. To date, few neuroimaging studies have been performed in depressed youths. In 1996, Steingard et al observed 65 latency-aged children and adolescents who were hospitalized with depression.⁹ MRI was used to compare depressed patients with 18 hospitalized psychiatric controls who did not have a depressive disorder. Depressed youths had a significantly smaller ratio of frontal lobe volume to total cerebral volume and a significantly larger ratio of lateral ventricular volume to total cerebral volume than controls. The researchers in this study suggest that these alterations in cerebral volumes may suggest a role for the frontal lobes in the development of early-onset depression.
  • In 1998, Tutus et al observed adolescents with MDD using single-photon emission tomography (SPET) in order to examine cerebral perfusion and any association between perfusion indices and clinical variables.¹⁰ Fourteen adolescent outpatients (aged 11-15 y) with MDD and 11 age-matched controls were studied. Significant differences were found between the perfusion index values of untreated depressed patients and those of the controls. The findings were indicative of relatively reduced perfusion in the left anterofrontal and left temporal cortical areas. They suggest that adolescents with MDD may have regional blood flow deficits in left anterofrontal and left temporal cortical regions with greater right-left perfusion asymmetry compared with healthy controls.
• Neuroendocrine abnormalities
  • In 1996, De Bellis et al studied neuroendocrine changes in prepubertal children who were depressed.¹¹ They examined nocturnal secretion of adrenocorticotropin (ACTH), cortisol, growth hormone (GH), and prolactin in the depressed groups and control groups, respectively. Prepubertal children who were depressed had lower cortisol secretion during the first 4 hours of sleep than did children in the control group. ACTH, GH, and prolactin secretion did not differ between the 2 groups.
  • Possible abnormalities of the neurotransmitter systems remain under investigation. In 1999, Nobile et al found that human platelet 5-HT (serotonin) uptake is differentially influenced in nondepressed and depressed children by a common genetic variant of the promotor region of 5-HTT.¹² In 1997, Birmaher et al found that, prior to onset of affective illness, children who were at high risk had the same pattern of neuroendocrine response to 5-hydroxy-L-tryptophan (L-5-HTP) challenge as did children with major depression.¹³ These findings could constitute the identification of a trait marker for depression in children.
• Genetic studies: Several studies of adults who are depressed, such as those reported by Akiskal and Weller in 1989¹⁴ and Weissman et al in 1984,¹⁵ suggest a genetic component in the etiology of depressive disorders.
• Parent-child relation model
  • This model conceptualizes depression as the result of poor parent-child interaction. Adults with depression report low paternal involvement and high maternal overprotection during early childhood. Troubled relationships with parents, siblings, and peers are common in children and adolescents with affective illness. A child who is affectively ill often has a parent who is affectively ill. For children to report abuse and/or neglect by their parent(s) who is affectively ill is not uncommon.
  • In 1991, Hammen et al reported a significant temporal association between mother and child.¹⁶ They found that children with substantial stress exposure who also had symptomatic mothers were significantly more depressed than children who were exposed to comparable levels of stress only.
• Cohort effect: In 1987, Klerman and Gershon reported a progressive increase in the lifetime cases of major depression over the last 70 years. They found high rates of affective disorders among relatives, with a younger age of onset in successive cohorts.

• Search for CME/CE on This Topic »

• Dysthymic Disorder (Psychiatry)

• Depression Overview
• Depression Causes
• Depression Symptoms
• Depression Treatment
• Depression Center
• Antidepressants Center
• Understanding Antidepressant Medications
• Substance Abuse Center
• Substance Abuse Overview

• Mood Disorders Common in Women With Polycystic Ovary Syndrome