Many adolescents experience worry from time to time, shifts in their moods, or times of dysphoria, including sadness or anger. Mood and anxiety disorders differ from normative concerns in that they can cause marked impairment, can produce changes in global functioning, and are pervasive. This chapter will provide an understanding of the epidemiology, clinical manifestations, diagnosis, treatment, and prevention of depression, anxiety, and other mental health disorders of children and adolescents.
The importance of recognizing and addressing mental health concerns not only is important for the individual patient, but also has a profound impact on public health. Suicide was the third leading cause of death for 10- to 24-year-olds in 2014. It followed only unintentional injury and homicide, and accounted for 5504 deaths in the United States. Significant risk factors for suicide include major depressive episodes and manic episodes.
Multiple factors play a role in mental health problems in youth. Risk factors for developing mental health problems, such as anxiety and depression, include family conflict, poverty, and school violence. Youth of color are more likely to experience greater barriers to care and higher prevalence of mental health concerns than their white peers. Heredity can be a risk factor for mood and anxiety disorders. In the case of major depression, youth with first-degree family members who are also depressed are 2 to 4 times more likely to have major depression.
Adolescence is a complicated period when individuals reach maturity in physical and sexual development, with a lag of maturity in other areas such as cognitive and emotional development. Biological changes, such as hormonal changes, may play a role in adolescents’ vulnerability toward emotional and behavioral issues. Regions of the adolescent brain, such as the prefrontal cortex, which controls executive function, are still in the process of developing until the mid-20s. There is discussion that the changes that occur during adolescence are possibly linked to the vulnerability during adolescence of mood disorders, schizophrenia, and other conditions.
Initial screening for mood, anxiety, and other disorders may be done through the clinical screening during a medical visit (eg, HEADSS exam) and screening questionnaires. However, an extensive diagnostic interview to include self-report, caregiver report, history of symptoms, and other formal assessments are the ideal standard for the diagnosis of a mental health disorder.
MAJOR DEPRESSIVE DISORDER AND PERSISTENT DEPRESSIVE DISORDER
Major depression and other depressive disorders are further discussed in Chapter 94. This discussion focuses on these disorders in the adolescent patient.
The clinical presentation of depression varies with age. Unlike school-aged children, adolescents are less likely to present with primarily somatic complaints, and unlike adults, adolescents are less likely to appear melancholic or sullen. More often, adolescents present with symptoms of irritable mood; anhedonia; boredom; hopelessness; sleep changes such as insomnia, hypersomnia, or day/night reversal; weight changes; and psychomotor retardation. Excessive feelings of guilt, shame, hopelessness, and helplessness are indicators of severity of depression and should prompt further screening for suicidal ideation, self-harm, and bullying. Adolescents with depression are more likely to engage in substance use and risky behaviors such as unsafe sex. Adolescents are more likely than children to experience suicidal ideation, act on suicidal feelings, and utilize more lethal means for suicide.
According to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), persistent depressive disorder (dysthymia) is characterized by depressed mood lasting at least 1 year in adolescents (compared to 2 years in adults). At least 2 of the following symptoms are present: changes in appetite, sleep difficulties, low energy, low self-esteem, poor concentration, and hopelessness. The adolescent may report having always felt this way, as symptoms are never absent for more than 2 months.
EPIDEMIOLOGY AND ETIOLOGY
Lifetime prevalence of depressive disorders is approximately 12%. According to the Youth Risk Behavior Surveillance System, in 2015, 29.9% of youth reported feeling sad or hopeless, daily, for 2 or more weeks, in the past 12 months. According to the National Survey on Drug Use and Health, 11.4% (approximately 2.8 million) adolescents (ages 12–17 years) reported experiencing a major depressive episode in the past 12 months. Prevalence of major depression is higher for youth/young adults (18–29 years) than the rest of the adult population. Beginning in early adolescence, females are twice as likely as males to develop major depression, a trend that continues throughout adulthood. The DSM-5 indicates that the 12-month prevalence for persistent depressive disorder in the United States is approximately 0.5%. In addition, early onset, before age 21, is associated with a higher risk of personality disorders or substance use disorders.
The average length of a major depressive episode in children and adolescents ranges from 3 to 6 months for community samples and 5 to 8 months for referred samples. Length of episode is correlated positively with comorbidity of anxiety, dysthymic disorder, and substance abuse. The probability of recurrence is 40% in 2 years and 70% in 5 years. Between 20% and 40% of children and adolescents who experience an episode of major depression will go on to develop bipolar I disorder within 5 years. Depression has a high probability of recurrence that increases with each subsequent episode. Increase in time between episodes is correlated positively with recovery.
The diagnosis of a depressive disorder requires consideration of severity, pervasiveness, and level of impairment in addition to gathering information on the presence of symptoms such as depressed mood, guilt, worthlessness, suicidal thoughts, irritability, decline in school performance, and withdrawal from social and other pleasurable activities. Diagnosis is best made by a thorough combined interview of the adolescent and caregivers. It is paramount to interview the adolescent separately, as it may be difficult for him/her to share certain thoughts, behaviors, or concerns in front of caregivers. In addition to clinical interviews, certain instruments such as the Children’s Depression Inventory (CDI) for 8- to 13-year-olds and the Beck Depression Inventory for older adolescents may be useful in assessing symptoms. The Patient Health Questionnaire-9 (PHQ-9) can also be used to screen for depressive symptoms and additionally screens for difficulty of symptoms in daily life (eg, to do work at home). Clinicians should assess the extent to which symptoms are interfering with school, social, and family functioning, and assess for safety.
Early intervention for the treatment of adolescent depression is correlated with increased effectiveness. Given that depressive episodes may spontaneously resolve in adolescents, mild depressive episodes are typically treated with psychotherapy alone. Studies such as the Treatment for Adolescents with Depression Study (TADS) suggest that for moderate to severe depression, combination treatment with psychotherapy and medication are most effective, and if cognitive behavioral therapy (CBT) is added to psychotropic medication, recovery is accelerated.
There are 2 empirically supported psychotherapy approaches for depression in adolescents: CBT and interpersonal therapy (IPT). CBT focuses on improving mood by challenging, reframing, and restructuring negative self-beliefs. It can be administered in individual or group formats. Family involvement may also be helpful. IPT is a three-stage treatment that aims to improve the quality of the adolescent’s interpersonal relationships, which is, in turn, thought to improve mood symptoms. Similar to CBT, family involvement may be helpful for adolescents involved in IPT.
The selective serotonin reuptake inhibitors (SSRIs) are the first line of treatment for depression. SSRIs with US Food and Drug Administration (FDA) approval for adolescents include fluoxetine and escitalopram and are typically recommended first-line treatments. Others, such as sertraline, fluvoxamine, and citalopram, have an evidence base in adults or for other disorders (such as anxiety disorders) in children and adolescents and may be used off-label for depression in adolescents. Typical side effects include gastrointestinal issues, headache, dry mouth, sedation, or insomnia. Medications that block both serotonin and norepinephrine—such as venlafaxine, mirtazapine, and duloxetine—may also be used off-label. Bupropion, a medication that targets norepinephrine and dopamine, is used often for depression as well as attention problems, but carries a risk of reducing the threshold for seizures.
In 2004, the FDA issued a black box warning regarding the use of antidepressants in children and adolescents, which was later expanded to include individuals under the age of 24 years. This was based on a meta-analysis reporting higher rates of suicidal ideation and attempts by those on antidepressants versus placebo (4% on antidepressants vs. 2% on placebo). There were relatively few suicide attempts, and no completed suicides. Studies subsequently have failed to demonstrate a consistent increased risk of suicidal ideation or attempts in youth or young adults taking antidepressants. Given this warning, the recommendation for physicians is continued use of antidepressants for patients who warrant treatment, with discussion of the warning with patients and families, and close follow-up (such as weekly visits or telephone check-in) for the first few months of treatment.
BIPOLAR DISORDERS AND CYCLOTHYMIC DISORDER
Bipolar disorder manifests as depressive and manic or hypomanic episodes. There is controversy about how broadly or narrowly to apply criteria, leading to questions of whether bipolar disorder is overdiagnosed in childhood. Some of these concerns were addressed in the DSM-5 with the addition of disruptive mood dysregulation disorder (DMDD), characterized by persistent irritability and frequent episodes of behavior dysregulation. Although this pattern of symptoms may seem congruent with bipolar disorder due to the presence of outbursts, it has been found that as children mature, this symptom pattern usually manifests as a depressive or anxiety disorder.
The 4 most reported symptoms of bipolar disorder are increased energy, distractibility, pressured speech, and irritability. According to the DSM-5, a manic episode is defined as a discrete episode in which mood is abnormally elevated, expansive, or irritable. Adolescents with mania may also exhibit rapid speech, racing thoughts, highly goal-directed behaviors (eg, working on multiple projects or goals), grandiose self-esteem, and distractibility. Hypomanic episodes are characterized by elated or irritable mood and usually do not cause significant distress or impairment. Of note, in younger adolescents and children, mania may present as extreme silliness or happiness beyond what would be considered developmentally appropriate. Adolescents with bipolar disorders are more likely to experience rapid mood shifts between manic and depressive episodes (ie, rapid cycling). However, depressive episodes may last minutes, hours, or in some cases days.
According to the DSM-5, cyclothymic disorder is characterized by repeated periods of subsyndromal hypomanic and depressive symptoms that last for at least 1 year. Adolescents with cyclothymic disorder experience chronic changes or fluctuations in mood most days. The mood changes are not as severe as those seen in depressive or manic episodes, and symptoms would not meet criteria for full depressive episodes. However, symptoms still cause significant distress or impairment in the adolescent’s ability to function in social or academic settings.
EPIDEMIOLOGY AND ETIOLOGY
Bipolar and related disorders occur approximately twice as often in females as in males. The 12-month prevalence of all ages ranges from 0.0% to 0.6% globally, versus 0.6% prevalence in the United States. The lifetime prevalence is about 3% in adolescents, with females reporting slightly higher frequency of bipolar I and II disorder than males (3.3% in females versus 2.6% in males). The mean age of onset is 18 years for bipolar I disorder and the mid-20s for bipolar II disorder; however, both may be diagnosed earlier by a trained professional. Cyclothymic disorder usually develops in adolescence or early adulthood.
According to the DSM-5, family history of bipolar disorder is considered the strongest, most consistent risk factor for the diagnosis, with risk increasing according to degree of kinship. The prevalence of bipolar disorder in first-degree relatives of adults is increased eightfold to tenfold over what is expected of bipolar in community samples. In addition to genetic factors, environmental factors, including higher socioeconomic status, are also thought to increase risk.
The diagnosis of a bipolar disorder or cyclothymic disorder is a clinical one, done through careful history, behavioral observation, and mental status examination showing characteristic mood changes, pressured speech, flight of ideas, and grandiosity. Collateral information from caregivers is critical in assessing bipolar disorders in children and adolescents. Scales may be helpful in assessment, such as the parent version of the Young Mania Rating Scale (YMRS) or the Child Mania Rating Scale for parents. Family history of bipolar disorder is supportive of the diagnosis.
One of the main challenges in the diagnosis of bipolar disease is that many symptoms of bipolar disease also overlap with other disorders. For example, both bipolar disorder and attention-deficit/hyperactivity disorder (ADHD) can show symptoms of irritability, accelerated speech, distractibility, and unusual energy. Thus, it is imperative that the evaluation is done thoughtfully and comprehensively with the patient’s age and development in mind. For example, adolescents are developmentally prone to take risks, which may fit in the spectrum of normal adolescent behavior or may fit within the context of bipolar. When a diagnosis of bipolar disorder is entertained, it is helpful to develop a broad differential through careful and contextual reflection of the patient’s presentation, and to utilize the consultation or referrals to child and adolescent psychiatrists to help with clarification of the diagnosis and management of the disorder.
Mood stabilization is the goal of treatment in bipolar disorder and cyclothymic disorder. Medications that have been utilized for mood stabilization in manic or mixed episodes include lithium, divalproex, carbamazepine, and atypical antipsychotic medications such as olanzapine, risperidone, quetiapine, ziprasidone, or aripiprazole. First-line treatment with monotherapy typically starts with lithium, an atypical antipsychotic, or divalproex, although a recent study called the Treatment of Early-Age Mania (TEAM) noted that risperidone was more effective than lithium or valproate for children or adolescents diagnosed with a manic or mixed bipolar disorder. Concerning side effects of lithium include tremor, nephrogenic diabetes insipidus, teratogenicity, and hypothyroidism. Notable side effects of divalproex include weight gain, sedation, teratogenicity, and hepatotoxicity. Both lithium and divalproex require monitoring of blood levels. Atypical antipsychotics, on the other hand, do not require blood monitoring, but are more commonly associated with metabolic syndrome, including weight gain and elevations in lipids and blood glucose.
Patients who do not tolerate 1 medication may need to switch to another medication. Patients who do not respond to monotherapy, particularly those with psychosis, may respond to a combination of a mood stabilizer and an atypical antipsychotic. Adjunctive use of benzodiazepines may be utilized to help with acute agitation or insomnia. For severe illness in adolescents resistant to treatment with pharmacotherapy, electroconvulsive therapy (ECT) may be utilized depending on whether it is legal in the state. For bipolar depressive episodes, the adult literature suggests the use of monotherapy with lithium, valproate, or atypical antipsychotics, or a combination of an SSRI with a mood stabilizer. Caution should be exercised with the use of SSRIs in patients with bipolar disorder, particularly without concurrent mood stabilization, as they may trigger episodes of mania, hypomania, mixed episodes, or rapid cycling. In cases of bipolar depression where SSRIs are used, mood stabilizing agents should be given.
Supportive psychotherapy may be included in treatment as an adjunct to psychopharmacological treatment approaches. Family psychoeducation with skill building currently has the most empirical support. Parents may also benefit from attending parent support groups.
SUICIDE AND SUICIDAL BEHAVIOR
The most serious consequence of an adolescent mood disorder is suicide. Risk factors associated with suicide include nonsuicidal self-injury, a previous attempt or attempts, alcohol or substance abuse, the diagnosis of clinical depression, feelings of hopelessness, and isolation from others. Risk increases by gender (male), age (adolescents, older adults), isolation, and feelings of hopelessness. Protective factors include effective clinical care, family and community support, and support from mental and medical health workers. While some of the risk factors are unalterable (eg, family history of suicide), many protective factors can be initiated and employed through clinical treatment modalities (ie, access to care). The risk of suicide is highest during a major depressive episode. Therefore, targeted, proactive, preventive evidence-based treatments and support should be employed to reduce the risk of suicide for adolescents. For a complete discussion of this issue, see Chapter 94.
Anxiety disorders are the most commonly encountered mental health condition in adolescents, with lifetime prevalence estimated at 30%. Approximately half of all anxiety disorders in adults are present by early adolescence, and about half of all adolescents with anxiety disorders have another psychiatric disorder, most commonly depression. Fifty-eight percent of patients diagnosed with major depression have comorbid anxiety disorders, including 22.4% with a social phobia, 17.2% with generalized anxiety, and 9.9% with panic disorder. Anxiety disorders and their treatment are discussed further in Chapter 93.
Unifying features of anxiety disorders include excessive worries, fears, or anxieties that are extreme or out of context, and psychological (eg, fear of failure, fear of rejection), physiological (eg, dry mouth, sweating, accelerated heart rate), and behavioral (eg, procrastination, avoidance, rituals, impaired concentration) manifestations that persist over several months. All diagnosable anxiety disorders significantly interfere with school and/or social functioning. Both genetic and environmental factors are involved.
Anxiety disorders tend to run in families, and neuroimaging studies support a link among temperament, brain activity, and the development of anxiety disorders. Hardship and adversity, including poverty, witnessing or being a victim of trauma, living with chronic illness, and family disruption, including illness, death, and divorce, are risk factors for developing an anxiety disorder.
SOCIAL ANXIETY DISORDER (SOCIAL PHOBIA)
Although more than half of all adolescents and adults identify themselves as shy, people with social anxiety disorder (SAD) experience persistent, overwhelming anxiety and extreme self-consciousness in everyday social situations. In adolescents, the fear of social situations is fairly broad. According to the DSM-5, patients with social anxiety have fears of being judged, embarrassed, or rejected because of perceived embarrassing behavior or displays of anxiety. They may be anxious for weeks prior to a dreaded event like a school dance. SAD may be specific, such as a fear of eating in public or of public speaking, or general, in which any or all social situations are painful. In addition to emotional distress, people with SAD can experience physical symptoms, including blushing, sweating, trembling, palpitations, nausea, lightheadedness or fainting, and stammering. People with SAD are more likely to have poor social skills, low self-esteem, and distorted body image. To receive a diagnosis of SAD, adolescents must experience an extended period of symptoms (about 6 months) and the symptoms must interfere significantly with their routine and/or cause significant distress.
EPIDEMIOLOGY AND ETIOLOGY
SAD occurs approximately twice as frequently in females as in males. The 12-month prevalence of SAD in adolescents is about 7%, comparable to the prevalence in adults. Lifetime prevalence is approximately 9% in adolescents, with females reporting higher levels than males. The median age of onset is 13 years, with 75% of individuals having an onset between the ages of 8 and 15 years. Onset may be acute or gradual.
A genetic basis for developing SAD is supported by twin studies demonstrating a risk of developing SAD that is 2 to 3 times greater in adolescents who have at least 1 first-degree relative with this disorder. Single-photon emission tomography has shown that altered serotonin and dopamine activity may play a role in the development of SAD. However, parents with any kind of anxiety disorder or depression are more likely to raise anxious or socially phobic children, suggesting an epigenetic mechanism. Similarly, traumatic social experiences, such as being humiliated in the classroom, can trigger the onset or worsen the course of social phobia. Repetitive trauma, such as being bullied or excluded from social cliques, can also precipitate SAD.
The diagnosis of SAD is based on history, usually collected through a psychodiagnostic interview, behavioral observation, parent-report measures, and child-report measures. The Social Phobia and Anxiety Inventory for Children (SPAI-C) is an example of a psychometrically sound instrument that includes both parent-report and child-report versions that can help quickly screen for symptoms and aid in the treatment planning for SAD.
Treatment studies consistently emphasize the importance of early diagnosis and treatment, with CBT and pharmacotherapy being the treatments of choice.
Two CBT approaches are supported by the American Psychological Association in the treatment of SAD in children and adolescents: 1) Social Effectiveness Training for Children and Adolescents (SET-C), and 2) the C.A.T. Project. SET-C incorporates group skills training and individualized behavioral exposure to treat SAD in 7- to 17-year-olds. This program has demonstrated superiority to pharmacological treatment. The C.A.T. Project, a cognitive-behavioral program designed specifically for adolescents with SAD, includes setting goals to overcome social fears through a “FEAR plan” and use of a workbook.
Please refer to Chapter 93 for a discussion on specific phobias.
GENERALIZED ANXIETY DISORDER
Generalized anxiety disorder (GAD) is characterized by inappropriate, excessive anxiety and worry about multiple events or activities. The worry is wide-ranging and difficult to control and results in clinically significant distress and/or impairment. Children and adolescents may tend to worry more about things such as competence or quality of performance on tasks.
EPIDEMIOLOGY AND ETIOLOGY
GAD likely begins in childhood and early adolescence; however, median age of diagnosis is 30 years. Many individuals with GAD recall being anxious most of their lives, suggesting that onset may be younger but is considered as temperamental anxiety. The 12-month prevalence rates among adolescents is estimated at 0.9%, with 2.2% of adolescents reporting lifetime prevalence. The incidence increases with age, and females outnumber males 2–3 to 1. The etiology of GAD is multifactorial, with temperament and environment playing roles.
GAD is a classic example supporting the biopsychosocial model of understanding psychiatric illness. GAD runs in families, and thus genetic susceptibility and being raised by anxious, worried parents are risk factors. Childhood adversity, including poverty, witnessing trauma, and living with chronic illnesses such as asthma and diabetes, are also risk factors. Family disruptions, including parental illness, death, or divorce, may also contribute to the development of GAD. Children whose psychological needs are unmet and who are emotionally and/or physically neglected or abused are also at increased risk for developing GAD.
Diagnosis is established by careful history that includes questions about emotions (eg, fear, worries), physical symptoms (eg, tachycardia, sweating, dizziness, lightheadedness), and behaviors (eg, procrastination, avoidance, poor concentration), and by ruling out other medical conditions (eg, hyperthyroidism, hypoglycemia, migraines, seizure disorders, lead intoxication), substance abuse (including excessive caffeine intake), and medication side effects. Primary care providers are aware that patients with GAD can present with somatic complaints such as stomachaches, headaches, or insomnia.
CBT is the treatment of choice for GAD. Treatment includes education to distinguish healthy from unhealthy worry; monitoring to increase awareness of triggers; cognitive restructuring to challenge negative, catastrophic, or magical thoughts; and exposure to anxiety-inducing situations or events. Mindfulness-based CBT approaches add strategies for controlling the physical effects of anxiety by teaching deep breathing and progressive relaxation exercises.
Panic disorder is characterized by recurrent, unexpected panic attacks that consist of an acute sense of fear or distress that lasts for a few minutes. Attacks may be accompanied by a sense of dread or impending doom. Patients may believe they are about to die or are going crazy. Physical symptoms of hyperventilation, tachycardia, shortness of breath, dizziness, sweating, and trembling can be present. Patients with panic disorder are very worried about having future attacks and will change their behavior to avoid having attacks. As such, panic attacks are terrifying and can be disabling. They are frequently diagnosed in emergency departments where patients present believing they are dying of a heart attack or are going crazy. Patients are often afraid of having an attack in public, and agoraphobia is present in more than a third of cases.
EPIDEMIOLOGY AND ETIOLOGY
The 12-month prevalence rate of panic disorder is 2% to 3% in adults and adolescents, with rates being about 2 times higher in females. Lifetime prevalence estimates are around 2.3%. Prevalence increases during adolescence. The symptoms of juvenile panic disorder are similar to those of adults and include heart palpitations, sweating, shortness of breath, trembling, faintness, nausea, and abdominal distress. Childhood panic disorder is associated with other anxiety disorders, including GAD and specific phobia, somatization disorder, major depression, dysthymic disorder, and bipolar disorder.
Anxiety disorders in parents place children at risk for the development of panic disorder, and separation anxiety in young children may be a precursor to the development of panic disorder in adolescents. Panic disorder may be viewed as a dysregulation of the fight-or-flight response wherein the response is turned on by a trigger, but the capacity to modulate and turn it off is diminished or lost. In addition to stimulants, panic attacks can be triggered by lactic acid, carbon dioxide, carbon monoxide (cigarette smoke), and cholecystokinin.
Panic disorder is diagnosed through clinical interview with the patient and his/her parents. A psychometrically sound screening tool, such as the Revised Children’s Anxiety and Depression Scale, may also be useful in gathering the appropriate data.
Panic disorder is treated with CBT and medication. CBT, particularly exposure-based intervention, has been shown to be an effective way to treat panic disorder. Exposure-based intervention is designed to inhibit a patient’s avoidance response to induced panic symptoms while utilizing behavioral coping strategies (eg, deep breathing) to reduce the symptoms.
PHARMACOLOGICAL TREATMENT OF ANXIETY DISORDERS
SSRIs and serotonin-norepinephrine reuptake inhibitors (SNRIs) are the first line of treatment for anxiety disorders, despite most of these medications not having an indication for the above anxiety disorders in the pediatric population. Duloxetine is the exception, as it has received an FDA indication for the treatment of GAD in adolescents, and can be titrated to a maximum dosage of 120 mg/day. Regardless of the lack of indication, SSRIs and SNRIs are readily utilized for anxiety disorders in pediatric patients, and have a solid evidence base that supports their efficacy and tolerability. A recent meta-analysis of all randomized, double-blind, placebo-controlled trials of SSRIs and SNRIs in pediatric patients with fear-based anxiety disorders showed modest effect size and did not show a statistically significant risk of suicidality.
While tricyclic antidepressants have been used for anxiety disorders and show efficacy, they have been greatly limited by severity of side effects. In addition to the antidepressants, other medications studied in anxiety disorders include benzodiazepines, buspirone, and atomoxetine. Benzodiazepines bind to the gamma-aminobutyric acid A (GABAA) receptor and potentiate the inhibitory effects of gamma-aminobutyric acid (GABA). In randomized clinical trials of benzodiazepines versus placebo, there were no statistically significant differences in anxiety or clinical global improvement in patients treated with benzodiazepines, but notable side effects were drowsiness, irritability, and oppositional behavior. Additionally, benzodiazepines are highly addictive and may be abusable. Therefore, they are not the first-line medications for anxiety disorders. Buspirone, a 5-HT1A agonist, was studied in a large, unpublished study, where it did not demonstrate statistically significant improvement over placebo. Atomoxetine was studied in a multicenter, double-blind, placebo-controlled trial for youth with ADHD and a comorbid anxiety disorder, and reductions in both anxiety and ADHD symptomatology were noticed, with limited side effects. Other medications that may be considered include gabapentin, pregabalin, tiagabine, hydroxyzine, beta blockers, and atypical antipsychotics. The recommendation for anxiety disorders is to start with an SSRI or SNRI, and to utilize other agents for switching or augmentation with failure of first-line treatments.
Obsessive thoughts and tendencies can be normal and adaptive. In obsessive-compulsive disorder (OCD), obsessions are intrusive and distressing, and persistent thoughts, images, or impulses may seem senseless and inconsistent with one’s personal beliefs. Obsessions may involve fears of contamination, and intrusive thoughts may be aggressive, blasphemous, or sexual in content. Although the thoughts are rarely acted out, the fears are debilitating. Compulsions are repetitive, ritualistic mental acts or behaviors that the individual feels driven to perform in order to neutralize the obsessions and their associated fears. Examples of compulsions include hoarding, checking behavior, and hand washing. Obsessions and compulsions may change over time.
EPIDEMIOLOGY AND ETIOLOGY
The median age of onset of OCD is 19.5 years, with a quarter of cases having their onset by the age of 14 years. The onset of OCD is bimodal with the first peak onset being around age 11 and the second occurring in early adulthood. Males have an earlier onset than females; however, by adolescence, rates of OCD are reported equally. Onset is usually gradual with a waxing and waning course. Twelve-month prevalence rates are estimated to be 1.2%.
A genetic basis for OCD is supported by twin studies and by the discovery of an OCD gene, a mutation in the human serotonin transporter gene hSERT. Animal models created by deleting certain genes in mice have produced offspring that obsessively groom until their fur falls off. Neuroimaging studies show abnormalities in brain activity, particularly in the anterior cingulate gyrus, and may differentiate hoarding from nonhoarding OCD. High-resolution magnetic resonance images show differences in the brain structures of individuals with OCD. Other risk factors include family history and stressful life events.
The diagnosis of OCD requires a history taken with the parent and with the child. Behavioral observation and rating scales may also be useful in supporting a clinical interview. The Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), a brief screening checklist, is widely used and has strong psychometric properties.
CBT and pharmacotherapy are the treatments of choice. The CBT technique used to treat OCD is exposure and response prevention (ERP). This technique inhibits the patient from engaging in his or her dysfunctional compulsion in response to anxiety, which allows the patient to learn more adaptive responses to cope with the anxiety. For example, a patient who has to wash his or her hands immediately after touching a doorknob may not be allowed to do so for a period of time and instead is coached in breathing practices or other behavioral strategies for coping with the anxiety. ERP should only be performed by a trained clinician.
Treatment of OCD in adolescents typically consists of combination therapy with psychotherapy and psychopharmacology. Agents that block serotonin reuptake have resulted in improvement in symptoms. These medications must be titrated to sufficiently high doses for sufficient periods of time to constitute adequate trials. Blinded, placebo-controlled trials have studied clomipramine, fluoxetine, fluvoxamine, sertraline, and paroxetine. In adolescents, clomipramine has been studied most rigorously but is limited by problematic side effects such as dizziness, vision changes, tachycardia, and sedation. Given its impact on the heart and the liver, it is recommended that providers obtain electrocardiograms and liver function studies periodically throughout treatment. Fewer side effects are reported for SSRIs. Fluoxetine was superior to placebo in double-blind, placebo-controlled trials with a maximum dosage of 60 mg/day, and is now indicated by the FDA for the treatment of OCD in the pediatric population. Sertraline was found to be superior to placebo in a multisite, double-blind, placebo-controlled trial where the maximum dosage used was 200 mg/day, and also has earned an indication for the treatment of OCD in the pediatric population. Fluvoxamine also showed response in reducing symptoms in a double-blind, placebo-controlled trial with doses up to 200 mg/day, making it an indicated treatment for OCD in the pediatric population. In a head-to-head trial of clomipramine versus different SSRIs, clomipramine was significantly more effective than the SSRIs and the SSRIs performed similarly to each other and outperformed placebo. However, given the significant side effect profile of clomipramine, SSRIs are the first line for treatment of OCD.
POST-TRAUMATIC STRESS DISORDER
Post-traumatic stress disorder (PTSD) is a cluster of symptoms that develop following exposure to 1 or more traumatic events. Examples of traumatic events that might result in PTSD include serious accidents (eg, car, train, and plane crashes); natural disasters (eg, floods, hurricanes, earthquakes); manmade atrocities (eg, terrorist attacks, random shootings, arson, war); violent personal attacks (eg, sexual assault, kidnapping, mugging, torture); physical, sexual, or emotional abuse; abandonment; and neglect. Chronic illnesses such as asthma, with suffocation as a near-death experience, and multiple surgeries in young children with congenital abnormalities can also lead to PTSD.
Following exposure to a traumatic event, individuals with PTSD experience intrusive symptoms such as recurrent dreams, distressing memories and/or flashbacks, and extreme distress when faced with reminders of the event. Individuals with PTSD will actively avoid anything associated with the trauma, including memories and external cues such as people, places, or objects that bring up memories of the event. Those who experience PTSD will also exhibit changes in their cognitive functioning and mood as associated with the trauma. For example, they may have difficulty remembering parts of the trauma, feel detached from others, experience exaggerated negative beliefs about themselves or others, or struggle to feel positive emotions. Lastly, individuals with PTSD will exhibit marked arousal symptoms such as hypervigilance, exaggerated startle response, and irritability.
PTSD patients may suffer from comorbid anxiety disorders and depression, and they may self-medicate with alcohol and drugs. A universal response to trauma is the experience of guilt and shame. Trauma victims, in an effort to feel control, will sacrifice self-image and self-esteem.
EPIDEMIOLOGY AND ETIOLOGY
The lifetime prevalence rate of PTSD is estimated to be 9%. The National Comorbidity Survey Replication Adolescent Supplement states that the 12-month prevalence rate of PTSD among adolescents is approximately 5% with females reporting higher rates than males. More than two-thirds of Americans experience a significant trauma in their lives, and up to 20% experience such an event in any given year. Exposure to trauma is even higher in parts of the world ravaged by warfare, poverty, and famine. The likelihood of developing PTSD varies with the severity, duration, and proximity of the traumatic experience. Over half of all boys and girls in the general population are exposed to some form of trauma during their childhood and adolescence, including physical assault (47%), maltreatment (10%), sexual victimization (6%), and witnessing violence (25%).
Risk factors for the development of PTSD include female gender, previous exposure to trauma, previous psychiatric conditions, parental psychopathology, and low levels of social support. Neurobiological studies implicate deficiencies in the hypothalamic–pituitary–adrenal axis with lower-than-expected cortisol levels in PTSD patients. This may combine with higher-than-expected release of fight-or-flight response catecholamines that exacerbate the experience of trauma and intensify the creation of traumatic memories. Neuroimaging studies show differences between PTSD study participants with a preponderance of hyperarousal and those with more dissociative symptoms.
Adolescents with PTSD resemble adults with PTSD. However, it is important to consider the critical developmental time period of adolescence, including identity development and possible consequences of experiencing trauma during this time; treatment of PTSD is critical.
The diagnosis of PTSD is established through a thorough, structured or semistructured clinical interview such as the Anxiety Disorders Interview Schedule (ADIS) for children and parents. Clinicians must be sensitive to the fact that children and adolescents may be unable to verbalize traumatic experiences or may be too afraid to disclose trauma. The clinical interview may be traumatizing, so clinicians must allow patients to disclose at their own pace. A brief screen for self-report symptoms with strong psychometric properties is the Child PTSD Symptom Scale (CPSS), which takes approximately 10 minutes to administer.
Trauma-focused CBT (TF-CBT) is the most comprehensively studied psychotherapeutic intervention and has the strongest evidence base to support its use in PTSD. TF-CBT incorporates exposure techniques (ie, encourages the patient to talk about the traumatic event), behavioral relaxation techniques, and cognitive restructuring to challenge false beliefs and distorted thoughts about the trauma. Caregiver psychoeducation and involvement are usually incorporated into TF-CBT.
There are limited studies looking at pharmacological intervention in PTSD. Most studies are done in adults, and conclusions are extrapolated for children and adolescents. Some studies have suggested that in the child and adolescent population the use of beta blockers immediately after trauma can prevent the development of PTSD, a finding that has been contradicted in the adult literature. However, the adult literature recommends the use of SSRIs as first-line treatment for PTSD. In addition, some studies show support for prazosin, an alpha1 agonist, in overall symptom improvement and a decrease in nightmares and sleep disturbances. Preliminary studies suggest that venlafaxine may be efficacious in the treatment of adult PTSD, and that bupropion is not effective in reducing symptoms. Atypical antipsychotics have been useful in children and adolescents with PTSD, as well as alpha1 agonists such as clonidine and guanfacine. Further research would be useful in guiding the diagnosis and treatment of PTSD in children and adolescents.
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