Pediatric Persistent Depressive Disorder (Dysthymia)

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Persistent depressive disorder, or PDD, represents the DSM-5 consolidation of previously defined DSM-IV-TR diagnoses (persistent depressive disorder and chronic major depressive disorder). [1]  PDD may be diagnosed in pediatric patients, either children or adolescents, when a pervasive depressed or irritable mood is present for at least 1 year. Two additional symptoms of depression must also be present for most of the day at least half of the time during that year to make the diagnosis. Depressive symptoms typical in persisten depressive disorder include the following [1] (see Prognosis, Presentation, and Workup):

Diminished or increased appetite

Insomnia or hypersomnia

Low energy or fatigue

Poor self-esteem

Difficulties with concentration or decision making

Feelings of hopelessness

To qualify for a diagnosis of PDD, a child may have never had a manic or hypomanic episode. A child may not have had symptom-free intervals lasting longer than two months.

Education about the long-term risks of dysthymic disorder and the role of behavioral and cognitive-behavioral interventions, as well as instruction in social and interpersonal skills, can be helpful adjuncts to treatment. (See Treatment.)

For patient education information, see the Depression Center, as well as Depression.

Depressive disorders are etiologically heterogeneous. Genetic, biologic, psychological, and environmental factors contribute to depression. Much of the following discussion applies to many depressive disorders, including persistent depressive disorder. Persistent depressive disorder and depression likely arise from a complex relationship among elements such as genetic predisposition, disrupted attachments, internal psychological representations and attributions, dysfunctional social interactions, risk and protective factors, and melancholic endocrine changes.

Genetic factors are considered to account for approximately 50% of the variance in the transmission of depressive disorders. Children of parents who are depressed are 3 times more likely to experience a depressive episode than are children of parents who are not depressed; 20-45% of parents of depressed children have depressive disorders.

However, the specificity of these findings is clouded by the fact that psychopathology generally is more common in parents of depressed children and depressed parents generally produce children with other psychopathology as well.

Transmission of depression in families may also occur by means of nongenetic pathways; environmental stressors increase in families with depressed members. Temperament modulates the expression of genetic variance. Temperament is defined as a long-standing behavioral style, mostly inherited, evident early in life, stable during time, and observable in various settings. Some temperamental patterns are likely to make individual children more vulnerable to depression and other disorders.

The biologic substrate for mood disorders is the basis of pharmacologic treatment. Several neurotransmitter systems have been hypothesized to be involved in the emergence of depressive disorders, including the noradrenergic, serotonergic, cholinergic, and dopaminergic systems.

The biogenic amines, norepinephrine and serotonin, regulate mood, sleep, appetite, and activity; they are implicated in persistent depressive disorder and are modified by the current antidepressant drugs.

Studies of adults with depression have shown blunted responses of cortisol secretion in response to serotonergic challenges. One study’s results suggested that depressed children may also show a blunted cortisol secretion response when challenged with serotonergic agents.

In addition, studies in adults have shown that there are lower levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF) of persons who attempt suicide and those who complete it. Studies have indicated that children with depressive disorders may have blunted growth hormone responses when challenged with adrenergic agents, such as clonidine (Catapres).

Among adults with depression, evidence of sleep abnormalities have been reported, including reduced slow wave (delta) sleep, diminished latency to rapid eye movement (REM) sleep, increased REM density, and increased awakening during the night. Sleep disturbance studies in children and adolescents experiencing depression widely vary. Some evidence suggests that children and adolescents with recurrent depression may have shorter REM latency during the period of depression, as well as during periods of remission.

Biologic measures cannot be used to rule in or out particular mood disorders. It is hypothesized that maturational differences in neurotransmitter systems account for psychobiologic differences observed in pediatric and adult depressive disorders.

Three main theories have been studied in the etiology of depressive disorders. Psychoanalytic theory relates the origin of depression to loss of love objects. Behavioral theories focus on the concept of learned helplessness. Cognitive behavioral theories suggest that depressive disorders are related to negative appraisals of the self and of one’s competence and abilities. All of the above models suggest that a person vulnerable to depression responds to adversity by withdrawal and inaction.

Life events and family functioning are considered to be potential risk factors or protective factors in the development of dysthymia and other depressive disorders. Families with poor coping abilities, low levels of communication within the family, high levels of intrafamilial conflict, and inconsistent emotional response teach children maladaptive affective regulation. If traumatic life events occur, children reared in chaotic environments have increased vulnerability to depressive outcomes.

Studies have shown that negative life events are more likely to be associated with the onset of emotional disorders if maternal distress and a poor mother-child relationship are present. Alternatively, good parent-child and good familial relationships can mitigate the effects of traumatic life events. Recent studies support multiple-level models of resilience indicating effects of both biological and psychosocial factors. [2]

Point prevalence rates of 0.6-1.7% in children and 1.6-8% in adolescents have been reported.

Rates in Europe generally correspond with US rates. Developing countries have a higher prevalence of minor psychiatric illnesses in general. A study of children and adolescents in an urban environment in Turkey concluded that persistent depressive disorder was the most common depressive disorder. Low maternal education, low socioeconomic status, dysfunctional interaction with the father, anxiety, and low self-esteem, which were all associated with depression, may be the target of interventions for prevention and treatment of depression. [3]

Limited data suggest that the prevalence of dysthymia among ethnic minority pediatric populations is similar to or lower than the prevalence in white pediatric populations in the United States.

Major depressive disorder has a male-to-female prevalence ratio of 1:1 in prepubertal children and 1:2 in adolescents. In children, persistent depressive disorder appears to occur equally in both sexes. Authors have speculated as to why rates of depression go up in adolescence, especially in girls. Biologic, psychosocial, and cognitive factors probably contribute.

One hypothesis is that girls are more likely to deal with stressors in a ruminative and openly expressive way, in addition to entering puberty earlier than boys (with the concomitant psychosocial and biologic consequences). As adolescents, females are more likely to be exposed to sexual abuse, worry about their body image, and feel pressure to conform to restrictive social images than are males.

Studies of depression in the pediatric population show a rise in frequency with age. Rates and gender ratios approach adult levels with older adolescents, although these data are subject to interpretation based on changing diagnostic criteria for depression over time.

Years ago, depression was not diagnosed in childhood. According to the Freudian concept that depression is based on the individual’s response to loss, children were thought to be incapable of depression because their psychosexual development was believed to be too immature to produce it.

In the 1960s, it was suggested that children suffer “masked depression”; that is, that typical depressive symptoms are expressed as equivalents such as hyperactivity, learning disabilities, and encopresis. However, scrutiny of clinical reports over the last 100 years had led to the conclusion that the same core symptoms of depression observed in adolescents and adults also occur in children.

Children are now widely believed to express depressive symptoms in a manner consistent with their developmental level, including their ability to articulate their feelings and reflect on their mood. Thus, the frequency of various depressive symptoms in children is developmentally linked; depressed prepubertal children may manifest more somatic complaints, self-esteem difficulties, and sad facial expression than do adolescents and adults.

The core depressive symptoms in affective disorders can be shown to be present in children as well as in adults if the assessment tool used is developmentally sensitive.

Children who experience persistent depressive disorder (PDD) have a mean episode length of 3–4 years (1-year duration is required for the diagnosis). The presence of a comorbid externalizing disorder appears to add almost 2.5 years to the episode length, which suggests that the comorbidity should be addressed first.

The spontaneous remission rate for all patients with PDD disorder (adult and child) may be as low as 10% per year, but the outcome is significantly better with active treatment.

Children whose parents have depressive disorders are as much as 3 times more likely to develop a mood disorder.

Anhedonia, or markedly diminished interest or pleasure, is a severity marker that should always alert the diagnosing clinician. It is always associated with the development of a more severe prognostic course. [4]

PDD causes severe and prolonged social, interpersonal, and academic dysfunction. If a child has a parent with a depressive disorder—children whose parents have depressive disorders are as much as 3 times likely to develop a mood disorder—the youngster may be exposed to an unstable home and stressful life events, increasing the risk for dysfunction even further.

Childhood PDD is associated with an increased risk for subsequent major depressive disorder and bipolar disorder, as well as a less likely, but still significant, increase in the risk for substance use disorders and anxiety disorders.

Approximately 70% of pediatric patients with PDD develop a superimposed major depressive disorder within 5 years. Fifty percent of pediatric patients with PDD have other psychiatric disorders as well, including anxiety disorders (40%), conduct disorder (30%), attention deficit hyperactivity disorder (ADHD; 24%), and elimination disorders (ie, enuresis, encopresis; 15%). Approximately 15% of pediatric patients with dysthymic disorder have 2 or more comorbid disorders.

Early onset PDD is associated with an increased risk of subsequent major depressive disorder and substance abuse. Indeed, depressed children are more likely to use tobacco, alcohol, and other substances in adolescence and adulthood. Increased mortality and morbidity are of course associated with these behaviors.

Comorbid conditions in patients with PDD need treatment, because they may influence the maintenance and recurrence of depression, lengthen the duration of depressive episodes, increase the risk of suicide, and increase the rate of mental health service use. Individuals with additional psychiatric disorders have poorer outcomes, poorer response to treatment, and more severe social impairment.

PDD increases the risk for development of major depressive disorder, with its concomitant possibility for suicidal thoughts and suicide attempts. Children who have PDD along with an exacerbation of depressive symptoms, including recurrent suicidal ideation, may be diagnosed with major depression in conjunction with PDD.

Suicidal thoughts are not uncommon in preadolescent children with depression, although attempts are less common than in adolescents or adults and are less likely to be lethal. Community studies have shown 8.9% of preadolescent depressed children express suicidal ideas and 3% make threats or mild attempts. [5]

Among US adolescents, suicide is the third-ranking cause of death (rate of 7.4 cases per 100,000 population for the age range 15-19 years, rate of 1.2 cases per 100,000 population for the age range 10-14 years, rate of 4.3 cases per 100,000 for the age range 10-19 years), after accidents and homicide. Nearly one fourth of high school students in the United States report having considered suicide, approximately 18% acknowledged more serious intent by making a specific suicide plan, and nearly 8% have attempted suicide, with almost 3% requiring medical attention for associated injuries. [5]

Suicide rates vary according to sex and ethnicity, with American Indians/Alaska natives having roughly twice the rate of death by suicide than do whites, who have a rate roughly twice that of blacks and Asians/Pacific Islanders (8 cases per 100,000 population compared with 4.7 cases per 100,000 population and 2.5 cases per 100,000 population, respectively).

Males outnumber females in terms of death from suicide in all ethnic groups, with ratios ranging from 3:1 in Asian/Pacific Islanders to 4:1 in Native Americans to 5:1 in whites to almost 6:1 in blacks. The gender differences parallel those in adults; men are more likely than women to die from suicide attempts, due to use of more lethal means.

Although suicidality is not a predominant symptom in dysthymia, mood disorders are considered a spectrum disorder, and suicidal tendencies should be carefully assessed in all patients with depressive symptoms.

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Jeffrey S Forrest, MD 

Disclosure: Nothing to disclose.

Colleen A Kraft, MD, FAAP Medical Director, Health Network by Cincinnati Children’s, Cincinnati Children’s Hospital

Colleen A Kraft, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, Academic Pediatric Association, American Academy of Pediatrics, American Association for Physician Leadership, American Medical Association, Medical Society of Virginia

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.

Edwin S Rogers, PhD, ABPP Clinical Psychologist, Director of Behavioral Medicine Fellowship, Professor, Department of Family Medicine, University of Tennessee Graduate School of Medicine

Edwin S Rogers, PhD, ABPP is a member of the following medical societies: Association for Behavioral Science and Medical Education, North American Primary Care Research Group, and Society of Teachers of Family Medicine

Disclosure: Nothing to disclose. Steven L Spalding, MD Staff Physician, Family Medicine, Norton Community Medical Associates

Steven L Spalding, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Family Physicians, American Medical Association, and American Psychiatric Association

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 Persistent Depressive Disorder (Dysthymia)

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