Pediatric Depression

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Pediatric depression is a relatively common psychiatric condition that generally continues episodically into adulthood. Whether damaging experiences or biologic processes trigger depressive episodes remains subject to debate; however, the final common pathways to depression involve biochemical changes in the brain.

A major depressive episode in children and adolescents typically includes at least 5 of the following symptoms (including at least 1 of the first 2) during the same 2-week period: [1]

Depressed (or irritable) mood

Diminished interest or loss of pleasure in almost all activities

Sleep disturbance

Weight change, appetite disturbance, or 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

Symptoms must cause significant distress or impairment of important functioning and must not be attributable to the direct action of a substance or to a medical or other psychiatric condition.

Depression may occur with or without the following:

Psychotic symptoms

Chronicity

Melancholic features

Catatonic features

Seasonality

Depression may also have atypical features, including mood reactivity and at least 2 of the following for 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

Medical evaluation is always indicated to rule out organic etiologies that may imitate a depressive disorder, such as the following:

Infection

Medication

Endocrine disorder

Tumor

Neurologic disorder

Miscellaneous disorders

See Presentation for more detail.

No specific laboratory evaluations that identify depression, but other potential etiologies must be ruled out. Workup may include the following:

Complete blood count (CBC) with differential

Serum electrolytes

Blood urea nitrogen (BUN)

Creatinine clearance and concentration

Urine osmolality

Drug monitoring (if relevant)

Other tests that may be indicated or helpful include the following:

Electroencephalography (EEG)

Electrocardiography (ECG)

Liver and thyroid function tests

Children’s Depression Inventory

See Workup for more detail.

Interventions to be considered include the following:

Cognitive-behavioral therapy (CBT)

Psychodynamic psychotherapy

Interpersonal therapy

Behavior therapy

Family therapy

Supportive psychotherapy

Group psychotherapy

Pharmacotherapy

Overall, the choice of the initial acute therapy depends on the following factors:

Severity

Number of prior episodes

Chronicity

Subtype

Age of the patient

Contextual issues

Adherence to treatment

Previous response to treatment

Motivation of the patient and family for treatment

In mild-to-moderate cases, psychosocial interventions are often recommended as first-line treatments; in more severe cases, the addition of pharmacotherapy is often recommended. Pharmacotherapy is insufficient as the only treatment.

Factors that appear to be related to the response to psychotherapy include the following:

Age at onset of depression

Severity of depression

Presence of comorbid psychiatric disorders

Presence or absence of social support

Parental psychopathology

Family conflict

Exposure to stressful life events

Socioeconomic status

Quality of treatment

Therapist’s expertise

Motivation of the patient and therapist

Studies on pharmacotherapy for youths with major depressive disorder are few. Agents that have been used or proposed for use include the following:

Tricyclic antidepressants (TCAs)

Selective serotonin reuptake inhibitors (SSRIs)

Other antidepressants – Heterocyclics (eg, amoxapine and maprotiline), monoamine oxidase inhibitors (MAOIs), bupropion, venlafaxine, and nefazodone (found useful in adults)

See Treatment and Medication for more detail.

Pediatric depression in the form of childhood and adolescent major depressive disorder (MDD) is a relatively common psychiatric 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. (See Etiology.)

Whether damaging experiences or biologic processes trigger depressive episodes remains the topic of some debate. However, the final common pathways to depression involve biochemical changes in the brain. (See Pathophysiology and Etiology.)

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM5), uses the same basic criteria to diagnose depression in adults and children. (See Presentation.)

The choice of initial acute therapy depends on the following factors:

Severity

Number of prior episodes

Chronicity

Subtype

Patient age

Contextual issues – Eg, family conflict, academic problems, exposure to negative life events

Ability to adhere to treatment recommendations

Previous response to treatment

Patient’s and family’s motivation for treatment

In mild cases, psychosocial interventions and psychotherapies are often recommended as first-line treatments, whereas, in the most severe cases, medication in addition to psychotherapeutic intervention is often recommended. (See Treatment.)

Cognitive-behavioral therapy (CBT) has been shown in multiple randomized, clinical trials to be effective in the treatment of mild MDDs in children and adolescents. For moderate-to-severe depression, psychotherapies and psychopharmacologic treatment are recommended. Hospitalization should be considered for severely depressed patients for whom an effective safety plan and supervision cannot be provided at home and for those patients and families unable or unlikely to adhere to treatment recommendations. [2, 3] (See Treatment and Medication.)

Go to Depression for complete information on this topic.

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 may contribute to depression.

One abnormality that was discovered in an area of the brain that helps to control emotional reactions has contributed to a new understanding of why some people develop depression and other affective disturbances. Using positron emission tomographic (PET) scanning, researchers found an area of the prefrontal cortex with abnormally diminished activity in patients with unipolar depression and bipolar depression. [4] This region is related to emotional response and has widespread connections with other areas of the brain.

These other areas of the brain 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 radiation.

Magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and magnetoencephalography (MEG) are best suited to study the structural, physiologic, 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 using these modalities. [5]

Steingard et al, in a study using MRI, compared 65 latency-aged children and adolescents who were hospitalized with depression with 18 hospitalized psychiatric controls who did not have a depressive disorder. The authors found that 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, [6] suggesting these alterations in cerebral volumes may signal a role for the frontal lobes in the development of early-onset depression.

Tutus et al used single-photon emission computed tomography (SPECT) to examine associations between perfusion indices and clinical variables. Significant differences between perfusion index values were found when comparing 14 adolescent outpatients (aged 11-15 y) with MDD and 11 age-matched controls. [7]

These differences in perfusion index values were indicative of relatively reduced perfusion in the left anterofrontal and left temporal cortical areas. The investigators suggested that adolescents with MDD may have regional blood flow deficits in left anterofrontal and left temporal cortical regions, with greater right-left perfusion asymmetry than healthy controls have.

Neurotransmitter system abnormalities are being investigated to understand the biology of depression. Nobile et al found that human platelet 5-hydroxytryptamine (5-HT; serotonin) uptake is differentially influenced in nondepressed and depressed children by a common genetic variant of the promoter region of 5-HTT. [8]

Birmaher et al found that before the onset of affective illness, high-risk children had the same pattern of neuroendocrine response to 5-hydroxy-L-tryptophan (L-5-HTP) challenge as did children with MDD. [9] These findings could lead to identification of a trait marker for pediatric depression.

De Bellis et al, in a study examining nocturnal secretion of adrenocorticotropin (ACTH), cortisol, growth hormone (GH), and prolactin in a group of prepubertal children who were depressed and a control group, reported that prepubertal children who were depressed had lower cortisol secretion during the first 4 hours of sleep than did children in the control group. [10] ACTH, GH, and prolactin secretion did not differ between the 2 groups.

Psychosocial stressors are posited to be mediators for the development of depression. The final common pathways to depression involve biochemical changes in the brain. (See Pathophysiology.)

Several studies of adults who are depressed, such as those reported by Akiskal and Weller [11] and Weissman et al [12] suggest a genetic component in the etiology of depressive disorders.

The parent-child relation model conceptualizes pediatric 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. [13] A child who is affectively ill often has a parent who is affectively ill. It is not uncommon for children to report abuse and/or neglect by the parent or parents who are affectively ill.

Hammen et al reported a significant temporal association between maternal and child stress and depression. [14] They found that children with substantial stress exposure who also had a symptomatic mother were significantly more depressed than children who were exposed to comparable levels of stress only.

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. [15]

Increased time spent using electronic devices (e.g., cell phones, tablets, computers, etc.) may have played a role in the increased rates of depression and suicide observed between 2010 and 2015, especially among girls, according to one study. Researchers found that adolescents who spent more time on new media (including social media) were more likely to report mental health issues, and adolescents who spent more time on nonscreen activities (in-person social interaction, sports/exercise, homework, print media, and attending religious services) were less likely. Although the study demonstrates a correlation between long hours of daily screen time and symptoms of alienation, it does not prove that one causes the other. [16]

 

Reported US prevalence rates for depression in children and adolescents vary. Differences may be due to different populations sampled and variable criteria used. Studies have demonstrated that the occurrence of depression is not rare and is encountered regularly in pediatric and psychiatric practice.

Birmaher et al found the incidence of depression to be approximately 2% in children and 4-8% in adolescents. [3]

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%. [17]

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. [18]

In 2000, Murphy et al, using data from the Stirling County Study of adults in Atlantic Canada, found that the overall prevalence of depression remained stable at 5% across 3 separate samples in 1952, 1970, and 1992. [19] The investigators also reported a redistribution in the most recent sample, indicating that prevalence had shifted from older to younger persons and that the female-to-male ratio had increased. The Stirling County Study, which began shortly after World War II, offered a 40-year perspective of the prevalence and incidence of psychiatric disorders among an adult population in Atlantic Canada.

A European study by Copeland et al, which sought to assess the prevalence of depression in 9 European nations in order to design intervention for elderly persons who were depressed, found widely ranging prevalences in the study centers. [20] Prevalence for females was higher than for males. There was 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, 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. [21]

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 they are in adolescence and adulthood. [22, 23, 24, 25]

A report recently released by the Substance Abuse and Mental Health Services Administration (SAMHSA) indicates that sex differences in depression rates emerge at 12-17 years. The report states that girls aged 12-17 years are 3 times more likely than boys aged 12-17 years to have had a major depressive episode in the last year. [26]

During this period, the increase of the overall rates of depression and the 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 3 times the prevalence rate for males. No sex differences are noted for depression symptom severity or recurrence.

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 1 current or lifetime episode of unipolar depression. [27] The percentage of male and female students with 2 or more episodes was 4.9% and 1.6%, respectively. [17]

Cultural norms associated with differing racial and ethnic groups can affect the experience and reporting of symptoms of depression. In some cultures, for example, 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. [28]

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). [29] 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, Fifth Edition (DSM5), states that a symptom should not be dismissed because it is part of a cultural norm. [1] 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.

A 2014 World Health Organization (WHO) report, “Health for the World’s Adolescents: A Second Chance in the Second Decade,” states that depression is the most frequent cause worldwide of illness and disability in persons aged 10-19 years, with the rate being highest in females. [30, 31] The report also states that as many as half of all mental disorders arise by age 14 years but are usually not recognized. Suicide is listed as the third leading cause of death among adolescents, behind road injuries and HIV/AIDS.

According to the American Academy of Child and Adolescent Psychiatry, practice parameters for depressive disorders in childhood and adolescence, a history of a previous depressive episode, subsyndromal symptoms of depression, dysthymia, and anxiety disorders increase the risk for future depression. [32]

In a study of an epidemiologic sample of 776 adolescents, Pine and associates found that symptoms of major depression in adolescence strongly predicted adult episodes of major depression.

There were 41,149 deaths from suicide in 2013. In 2015, the CDC reported suicide as the third leading cause of death among persons aged 10-14 years and the second among persons aged 15-34 years. [33]

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 midadolescent years, and the mortality rate from suicide increases steadily through the teenage years, with suicide being the third leading cause of death in that age group.

Risk factors for completed suicide include the presence of a major mood disorder, recent life stressor, occurrence of command auditory hallucinations, use of substances, and evidence of specific plans and an attempt to prevent discovery, as well as patient perception of failure of the issues that precipitated suicidal thinking to change. This lack of action tends to escalate the patients’ sense of hopelessness.

The Clinical Trial Registration Information–Treatment of SSRI-Resistant Depression in Adolescents (TORDIA) study noted that a history of nonsuicidal self injury (NSSI) can be predictive of future NSSI and suicide attempts in adolescents with treatment-resistant depression. [34]

Another study noted a significant NSSI rate (3,000 in 10,000) among Native American youths aged 10-14 years, specifically the White Mountain Apache tribe. Females reported a higher rate of NSSI than males; severe substance abuse was also noted among both boys and girls. While NSSI is largely unaddressed among the White Mountain Apache Tribe and likely other reservation communities, it is important to recognize that this mental health issue could serve as a precursor to suicide in this population. [35]

Educating parents about children’s emotional problems is very important. Education is known to result in better compliance with treatment and to improve parents’ understanding toward their children. Patients should be educated in a manner congruent with individual development, level of impairment, and clinician judgment.

The clinician should instruct parents and others in the homes of depressed youths to remove firearms or other lethal weapons from their homes to decrease the risk of suicide. Household medications also should not be accessible to depressed youths.

For patient education resources, see the Depression Center, as well as Depression, Substance Abuse, and Antidepressant Medications.

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Angelo P Giardino, MD, MPH, PhD Professor and Section Head, Academic General Pediatrics, Baylor College of Medicine; Senior Vice President and Chief Quality Officer, Texas Children’s Hospital

Angelo P Giardino, MD, MPH, PhD is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American Professional Society on the Abuse of Children, Harris County Medical Society, International Society for the Prevention of Child Abuse and Neglect, Ray E Helfer Society

Disclosure: Nothing to disclose.

Tami D Benton, MD Clinical Director, Child and Adolescent Psychiatry, Psychiatrist-in-Chief, Executive Director, Department of Child and Adolescent Psychiatry and Behavioral Science, Children’s Hospital of Philadelphia

Tami D Benton, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Caroly Pataki, MD Health Sciences Clinical Professor of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, David Geffen School of Medicine

Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Jacqueline Lynch, MSW, Research Assistant, Department of Child and Adolescent Psychiatry, Children’s Hospital of Philadelphia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Pediatric Depression

Research & References of Pediatric Depression|A&C Accounting And Tax Services
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