Depression, Anxiety, and Other Disorders
Kim Peter Norman
Mood disorders differ from the normal ups and downs of childhood and the moodiness of adolescence; they persist over time and seriously interfere with school performance and social and family functioning. Adolescents suffering from mood disorders are at least 3 times more likely than those without mood disorders to abuse drugs, fight or carry weapons, and engage in risky behaviors such as unprotected sex. More than half of all adolescent suicide attempts are associated with mood disorders. Mood disorders in childhood and adolescence have often been misdiagnosed or underdiagnosed. In fact, childhood depression was not officially recognized in the United States until 1975 when participants of a National Institute of Mental Health Conference modified adult depression diagnostic criteria to allow for childhood stages of language and cognitive development.1
Bipolar disorder in childhood and adolescence is now recognized as a distinct illness that occurs independent of highly comorbid disorders, such as attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder, and conduct disorder. Without the duration criterion for diagnosis, the diagnosis of bipolar disorder became possible. Standardized testing may be helpful, but the initial diagnosis of a mood disorder in childhood or adolescence must be based on careful interviews with patients and their parents, and the diagnosis must be confirmed by careful follow-up over time, sometimes months to years.
Standardized psychological tests may be helpful but should not be relied upon to establish a diagnosis. Few pediatricians ask adolescents about their mental health; they are more likely to ask girls than boys, but rates of mental health symptoms are equivalent or greater in boys.3 Because 28% of high school students report having experienced a period of depressed mood lasting more than 2 weeks (major depression), 14.5% report having had serious thoughts of suicide, and 6.9% report having made a suicide attempt, all in the past 12 months,4 every physician who sees young people should know the signs and symptoms of mood disorders in children and adolescents and routinely incorporate mental health questions into their clinical histories during their annual health maintenance visit. Mental health screening should include, at the minimum, questions about suicide ideation, plans, and intentions. See Chapter 93 for more information on this topic, including Table 93-1, which provides the American Psychiatric Association’s definitions of the 3 broad categories for diagnosing a mood disorder.
MOOD DISORDERS
MAJOR DEPRESSION AND DYSTHYMIC DISORDER
Major depression and dysthymic disorders are further discussed in Chapter 93. This discussion is focused upon the adolescent patient.
EPIDEMIOLOGY
Depressive disorders affect approximately 8.3% of adolescents, 2.8% of children and about 0.5% of preschool children at any given time.4-6 Among younger adolescents, the reported rates range from 1% to 9%. By the end of adolescence, 25% to 30% will have experienced at least one episode of depression,7-9 which is comparable to the lifetime rate of major depression in adults. In adolescence, females are twice as likely as males to develop major depression, a trend that continues throughout adulthood.
ETIOLOGY
Adolescents may be especially vulnerable to depression because their brains are still developing and are more susceptible to stress. Studies of neurobiological responses to stress in specific mood-sensitive regions of the brain, including the prefrontal cortex, hippocampus, amygdala, and ventral striatum, support this hypothesis and may explain the dramatic gender difference in depression susceptibility that emerges in adolescence.14
CLINICAL FEATURES
The most common mood symptoms in adolescents are associated with adjustment reactions to specific stressors, family discord, school failure, or difficulty with peers. This presentation often responds to a few sessions of supportive counseling, with the pediatrician and adolescent working together to focus on problem identification and strategies to manage specific problems. If family discord appears to be prominent, problem-solving interventions should involve the entire family. The clinical presentation of depression varies with age.
Adolescents are less likely than school-aged children to present with somatic complaints or look depressed but are more likely to present with symptoms of anhedonia, boredom, hopelessness, diurnal variation, insomnia, hypersomnia, weight change, psychomotor retardation, and delusions. Delusions, when present, center on themes of guilt, excessive shame, deserved punishment, physical disease, death, and occasionally persecution. Adolescents with depression are more likely than their peers to smoke cigarettes, drink alcohol, abuse drugs, and engage in risky behaviors such as unsafe sex. The severity of suicide ideation in children and adolescents is similar, but adolescents are likely to choose more lethal methods in their suicide attempts. There may be gender differences in presentation among depressed adolescents because males are more likely to manifest hostility, anger, and aggressiveness while not revealing feelings of depression, whereas females are more likely to appear sad, tearful, and ruminative and to express depressive feelings.15-17
The average length of a major depressive episode in children and adolescence is 9 months. 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. Children and adolescents who present with psychomotor retardation and/or psychotic symptoms are especially at risk. Childhood-onset dysthymic disorder typically lasts for 4 years, with 76% later developing major depression and 13% developing bipolar disorder.18
ASSESSMENT
Thorough interviewing of both the adolescent and parents is necessary in the diagnosis of depression. The adolescent is the more accurate reporter of subjective symptoms, including depressed mood, guilt, worthlessness, and suicidal thoughts; the parents more accurately note subjective signs such as irritability, decline in school performance, withdrawal from social and other pleasurable activities, and accident proneness. In assessing depression, clinicians should ask not only about sadness but also about other negative moods, including grouchy (irritable), mad (angry), bored, lonely (isolated), empty, and alienated (“I don’t fit in” or “nothing matters”). Useful assessment screens include the Children’s Depression Inventory (CDI) for 8- to 13-year-olds and the Beck Depression Inventory for older adolescents. A newer, 6-item scale for adolescents, the Kutcher Adolescent Depression Scale,20 appears both sensitive and specific for depression. In addition to making a diagnosis, it is essential that clinicians assess the extent to which symptoms are interfering with school, social’ and family functioning, and it is imperative to always assess for safety. Guidelines for the assessment and treatment of adolescent depression in primary care settings have recently been published.21,22
TREATMENT
A substantial body of evidence supports the use of antidepressants and/or psychotherapy in the treatment of adolescent depression, with multiple studies supporting the view that both approaches together are more effective than either alone. The selective serotonin reuptake inhibitors fluoxetine, sertraline, paroxetine, citalopram, and escitalopram are generally the first line of pharmacologic treatment. Medications that block both serotonin and norepinephrine reuptake—venlafaxine, mirtazapine, and duloxetine—are also used because of their generally low side-effect profile. Buproprion, a dopamine agonist frequently prescribed for attention deficit disorder, is also commonly prescribed despite presenting an increased risk for seizures. 
In September 2004, the FDA issued a black box warning regarding the use of antidepressants in children and adolescents based on its review of randomized clinical trials studying 9 different antidepressants. These studies showed that children on antidepressants had a higher rate of suicide ideation and suicide behavior than those taking placebo. Subsequent studies have failed to demonstrate a significant increase in the risk of completed suicides or serious suicide attempts when antidepressants are used and rather demonstrate that antidepressants prevent suicides. Standard of care thus endorses the use of antidepressants for children and adolescents providing that there is close follow-up (weekly visits or telephone check-ins) for the first few months of treatment and that children and their families are warned about and told to be alert for increased suicide ideation or behavior.
Cognitive behavior therapy, which focuses on improving mood by challenging negative self-beliefs, and interpersonal psychotherapy for adolescents, which focuses on interpersonal conflicts emanating from unresolved grief, relationship disputes or life transitions, such as leaving home for college, are evidence-based psychotherapies for the treatment of depression in children and adolescents. Family therapy is part of interpersonal psychotherapy for adolescents and is always recommended when family discord is apparent. Group therapy for depression, based on principles of cognitive behavior therapy, is successful in the treatment of adult depression but is not well studied in children and adolescents. Regular exercise reduces symptoms of anxiety, stress, and depressed mood and thus is recommended for children and adolescents with depressive symptoms, but it is considered adjunctive, because exercise alone will not likely reverse moderate or severe major depression.
BIPOLAR DISORDERS AND CYCLOTHYMIC DISORDER
EPIDEMIOLOGY
Bipolar disorders are equally common in males and females across the life cycle. A 2007 study found that the diagnosis of bipolar disorder in children from birth to 19 years old increased 40-fold between 1994 and 2003, from 25 per 100,000 to 1003 per 100,000.25 Among adolescent, 5.7% meet criteria for manic symptoms that fall short of bipolar I diagnosis but meet criteria for bipolar II or cyclothymic disorder. Full-blown bipolar disorder does not often begin before the ages of 15 to 19 years27 but can begin at any age. There is extremely high comorbidity in childhood bipolar disorder, including up to a 90% association with ADHD, oppositional defiant disorder, conduct disorder, and/or panic disorder. Bipolar disorder can be differentiated from ADHD by the presence of elation, grandiosity, mania, and ultrarapid cycling.28
ETIOLOGY
Genetic factors play a major role in the development of bipolar disorder: A child who has 1 parent with bipolar disorder has a 25% chance of developing the illness, and a child with 2 bipolar parents has a 50% to 75% chance of acquiring the illness. Neuroimaging studies of children and adolescents with bipolar disorder show changes in the mesiotemporal, amygdala, and hippocampal regions in the brain similar to changes found in adults.29 Manic symptoms can also be triggered by medications such as antidepressants and steroids and by drugs of abuse such as amphetamines, cocaine, and marijuana.
CLINICAL FEATURES 
Typically, adolescents during manic episodes show periods of prolonged excitation, euphoria, racing thoughts, rapid speech, grandiosity, sensation seeking including substance abuse, and promiscuous sexual behavior. When children and adolescents with bipolar disorder are depressed, they often present as anergic (ie, low energy and slow), hypersomnic, and psychotic. Bipolar disorders in children and adolescents are much more likely to be highly rapidly cycling (moods may shift during the course of a day) than in adults, and children and adolescents are more likely than adults to present with a mixed state (both manic and depressed symptoms occurring simultaneously). Cyclothymic disorder is characterized by repeated mood swings for at least 1 year that are not severe enough to warrant the diagnosis of bipolar disorder or major depression. Untreated, manic and depressive episodes can last for months. Bipolar disorder and cyclothymic disorder are considered chronic illnesses present for life.
ASSESSMENT
There are no biologic markers, laboratory tests, or screening questionnaires diagnostic for bipolar disorder. Diagnosis is based on careful history and mental status examination showing elevated mood (euphoria), pressured speech, flight of ideas, delusions of grandeur and possibly paranoid ideation during manic states, depressed mood, psychomotor retardation, anhedonia, hopelessness, and hypersomnia during depressed states. A family history of bipolar disorder is supportive of a diagnosis.
TREATMENT
Mood stabilization is the goal of treatment in bipolar disorder and cyclothymic disorder. Lithium is effective in the treatment of acute manic states as well as bipolar depression and is the gold standard for prophylaxis against mood swings. Lamotrigine, an anticonvulsant, also is FDA approved for bipolar prophylaxis and is especially effective in the treatment of bipolar depression. There is also evidence that the anti-convulsants carbamazepine and oxcarbazepine are effective pharmacologic treatments for bipolar disorders. The anticonvulsant valproic acid is very effective for treating acute manic states, as are the atypical antipsychotics olanzepine, risperdone, quetiapine, ziprasidone, and aripiprazole. Aripiprazole also has FDA approval for bipolar maintenance. Antidepressants can trigger manic episodes and should be avoided in the treatment of bipolar disorder unless necessary, when mood stabilizers successfully control mania but bipolar depression persists. In cases of bipolar disorder where anti-depressants are necessary, antimanic agents and/or mood stabilizers should also be given.
SUICIDE AND SUICIDAL BEHAVIOR
One of the most serious consequences of an adolescent mood disorder can be suicide. For a complete discussion of this issue see Chapter 93.
ANXIETY DISORDERS
According to the Surgeon General of the United States, at least 13% of adolescents suffer from anxiety disorders,30 and among adolescents who are dependent on or abuse alcohol and other drugs, which includes 1% to 2% of 12 year olds and increases with age to afflict up to 25% of 21 year olds, a significant proportion are self-medicating for anxiety.31 Approximately half of all anxiety disorders are present by early adolescence, and about half of all adolescents with anxiety disorders suffer from another psychiatric disorder, most commonly depression.32 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.33 Anxiety disorders and their treatment are disscussed further in Chapter 88.
DIAGNOSTIC CRITERIA
The American Psychiatric Association’s Diagnostic and Statistical Manual IV Test Revision (DSM-IV TR) provides diagnostic criteria for anxiety disorders. The criteria for diagnosing social anxiety disorder (social phobia), specific phobia, general anxiety disorder, obsessive-compulsive disorder (OCD), panic disorder, and posttraumatic stress disorder (PTSD) are summarized in Table 88-2. Anxiety disorders that often present in adolescence are discussed in further detail below, and in Chapter 88. Common to all of these disorders is that they include excessive worries, fears, or anxieties that are extreme or out of context, and they have 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 and significantly interfere with school and/or social functioning. Both genetic34 and environmental factors are involved. Anxiety disorders fit well within the existing psychiatric paradigm of the biopsychosocial model, although they vary in emphasis. OCD is viewed primarily as a brain disorder and PTSD as fundamentally an adaptation to external events.
Anxiety disorders tend to run in families, and neuroimaging studies support a link among temperament, brain activity, and the development of anxiety disorders.35,36 Hardship and adversity, including poverty, witnessing or being a victim of trauma, living with chronic illness, and family disruption, including illness, death, and divorce, all place children at increased risk of developing an anxiety disorder. Poor self-esteem is both a cause and a consequence of anxiety disorders.
SOCIAL PHOBIA
Although more than half of all adolescents and adults identify themselves as shy, people with social phobia, or social anxiety disorder, experience persistent, overwhelming anxiety and extreme self-consciousness in everyday social situations. They suffer from intense fears of being judged, embarrassed, or rejected. They may be anxious for weeks prior to a dreaded event like a school dance. Social phobia 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. There is a high degree of comorbidity between social phobia and other psychiatric disorders, especially depression, other anxiety disorders, and alcoholism. People with social phobia are more likely to have poor social skills, low self-esteem and distorted body image.37 In addition to emotional distress, people with social phobia experience a number of physical symptoms, including blushing, sweating, trembling, palpitations, nausea, lightheadedness or fainting, and possibly stammering.
EPIDEMIOLOGY AND ETIOLOGY
Social phobia occurs more frequently in females than in males, with studies showing generally a 2 to 1 difference. Males, however, may be more likely than females to seek treatment. The 12-month prevalence of social phobia among 18 to 29 year olds is 6.8%; the lifetime prevalence is 13.6%.38 The onset is typically between the ages of 11 and 19 and rarely emerges after 25.
Genetic vulnerability in social phobia is supported by studies of identical twins reared apart and by a 2 to 3 times greater risk of developing social phobia 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 social phobia.39 However, biologic vulnerability is not the whole story: Parents with any kind of anxiety disorder or depression are more likely to raise anxious or socially phobic children. For example, shyness in adoptive parents is associated with shyness in their adoptive children.
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 bring out or worsen social phobia.
Diagnosis and Treatment
The diagnosis of social phobia is based on history. There are no standardized psychological tests, nor are there any diagnostic laboratory tests, except to rule out medical conditions such as hyperthyroidism or substance abuse.
Treatment studies consistently emphasize the importance of early diagnosis and treatment.40 Social anxiety begins in late childhood or early adolescence but usually is not treated for years or until the development of another psychiatric disorder such as depression or substance abuse. Pharmacotherapy plus cognitive behavior therapy are the treatments of choice.
Multiple studies support the use of selective serotonin reuptake inhibitors. More than 50% of patients treated with fluoxetine or paroxetine show significant improvement.41 Other classes of antidepressants, including the selective norepinepherine reuptake inhibitors venlafaxine, mirtazapine, and duloxetine, are also efficacious. Tricyclics and monoamine oxidase inhibitors are effective but rarely prescribed because of their side-effect profile. Although a black box warning was issued in 2004 regarding an increase in suicide ideation in children and adolescents prescribed antidepressants for depression but not specifically when prescribed for social phobia, it is generally accepted that patients and families should be warned about this phenomenon, and patients should be monitored closely whenever antidepressants are prescribed. The use of benzodiazepines is not evidence based and should be avoided because of their dependency and abuse potential. A novel pharmacologic approach using the tuberculosis antibiotic D-cycloserine, a partial glycine agonist acting at the N-methyl-D-aspartate receptor complex in the brain, prior to exposure to a social situation like public speaking, is promising in the treatment of adults with social anxiety but has not been studied in children and adolescents.42
Cognitive behavior therapy that addresses the relation among thoughts, emotions, and beliefs about oneself, combined with exposure to anxious situations, is as effective as pharmacotherapy in the treatment of social anxiety. Unlike in the treatment of depression, it is unclear whether psychotherapy plus pharmacotherapy is better than either alone. Family therapy interventions may be helpful, especially in situations in which parental overinvolvement or excessive criticism contributes the development of social phobia.
SPECIFIC PHOBIA
These are discussed in Chapter 88.
GENERALIZED ANXIETY DISORDER
Generalized anxiety disorder (GAD) is characterized by excessive, irrational, and uncontrollable worry about everyday things and is associated with a number of physical symptoms. The most commonly associated symptoms are feelings of tension (100%), apprehension (94%), negative self-image (90%), need for reassurance (86%), irritability (77%), physical complaints (75%), difficulty concentrating (69%), brooding (67%), and fatigue (65%).43
EPIDEMIOLOGY AND ETIOLOGY
GAD begins in childhood and early adolescence. Studies of prevalence rates among 9 to 13 year olds vary but range from 0.9% to 9% for females and 0.6% to 3.8% for males.44 The incidence tends to increase with age, and females outnumber males 2–3 to 1. The etiology of GAD is multifactorial, with temperament, parental anxiety and parenting styles, and life experiences, including exposure to the evening news,45 all 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 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 AND TREATMENT
Diagnosis is established by careful history that includes questions about emotions (fear, worries), physical symptoms (tachycardia, sweating, dizziness, lightheadedness, etc), and behaviors (procrastination, avoidance, poor concentration), and by ruling out other medical conditions (hyperthyroidism, hypoglycemia, migraines, seizure disorders, lead intoxication), substance abuse (including excessive caffeine intake), and medication side effects. Primary doctors should be aware that patients with GAD often present with somatic complaints such as stomachaches, headaches, or insomnia.
Cognitive behavior therapy is the treatment of choice for generalized anxiety disorder. Treatment includes education to distinguish healthy from unhealthy worry; monitoring to increase awareness of triggers; cognitive control to challenge negative, catastrophic, or magical thoughts; and exposure to anxiety-inducing situations or events. Mindfulness-based cognitive behavior therapy approaches46 add strategies for controlling the physical effects of anxiety by teaching deep breathing and progressive relaxation exercises.
A number of pharmacologic agents have demonstrated efficacy in the treatment of anxiety, including generalized anxiety disorder (see Table 88-5).47 Buspirone, which acts as a serotonin agonist and dopamine-mixed agonist/antagonist, is commonly prescribed. It is nonsedating and nonaddictive but may take several weeks to be effective. Benzodiazepines, such as diazepam, lorazepam, clonazepam, and alprozolam, are effective in quickly reducing anxiety symptoms but are sedating, cause cognitive impairment, and are highly addicting. The antidepressants, including selective serotonin reuptake inhibitors, serotonin and norepinephrine inhibitors, monoamine oxide inhibitors, and tricyclics, are effective in treating generalized anxiety but may take up to 6 weeks to work and can cause an increase in anxiety at the onset of treatment. The anticonvulsants gabapentin, pregabalin, and tiagabine are also effective in reducing anxiety without the dependency or abuse concerns of the benzodiazepines. The antihistamine hydroxyzine reduces anxiety independent of its sedative effects. Beta-blockers reduce anxiety but are most helpful in specific and/or social phobias, such as performance anxiety. The atypical antipsychotics such as olanzepine and risperdal are effective in reducing severe anxiety, but risks of weight gain and type II diabetes limit their use.
OBSESSIVE-COMPULSIVE DISORDER
Obsessive thoughts and tendencies can be normal and adaptive, such as a mother’s preoccupation with a newborn that she checks incessantly or an on-call doctor’s vigilant concerns about a patient’s vital signs and blood indices. In obsessive-compulsive disorder (OCD), obsessions are intrusive, distressing, and persistent thoughts, images, or impulses that seem senseless and inconsistent with one’s personal beliefs. 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. As with adults, some children with OCD are hoarders, irrationally clinging to objects such as nail clippings; used Band-aids; or tattered, worn-out clothing, or are compelled to collect and store large quantities of the same items, including junk. 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. Specific symptoms do not differentiate subtypes, but age of onset and etiology might. Age of onset before 10 has a male preponderance, family history of OCD, high comorbidity with ADHD, and is likely to have related tic disorders.48 Another subgroup of children develops OCD and/or tic disorders as autoimmune neuropsychiatric sequelae following exposure to group A β-hemolytic streptococcal infection (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections, or PANDAS).
EPIDEMIOLOGY AND ETIOLOGY
At least 1 in 200 children and adolescents suffer from OCD. Lifetime prevalence for 18 to 29 year olds is 2%,38 and up to one half of adults with OCD report onset during childhood or adolescence. Lower rates of OCD in clinic populations suggest that the disorder may be underdiag-nosed.49 A genetic basis for familial OCD is supported by twin studies and by the discovery of an “OCD gene,” a mutation in the human serotonin transporter gene hSERT.50 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 gyrus51 and may differentiate hoarding from nonhoarding OCD.52 High-resolution magnetic resonance images show differences in the brain structures of individuals with OCD.53 Psychological factors may exacerbate OCD, but little evidence supports a psychological theory of etiology. Traumatic events can result in intrusive images (flashbacks) and lead to repetitions of the trauma (repetition compulsion), but these PTSD phenomena are specific to the trauma suffered and are not experienced as irrational or at odds with one’s beliefs or personality.
DIAGNOSIS AND TREATMENT
The diagnosis of obsessive-compulsive disorder is established by clinical history. The Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), a brief screening checklist available online, may assist in the diagnosis. Cognitive behavior therapy and pharmacotherapy are the treatments of choice. Although usually done in combination, studies have not clearly demonstrated that combined therapies is better than either approach alone.
The cognitive behavior therapy technique used in obsessive-compulsive disorder (OCD) is called exposure and response prevention, which involves learning to tolerate the anxiety associated with not performing a ritual by being prevented from doing so. For example, a patient who has to wash his hands immediately after touching a doorknob may not be allowed to do so for a period of time. Antidepressants that increase serotonin activities, the selective serotonin reuptake inhibitors and the tricyclic anafranil, are effective in treating OCD. The higher dose range of these medications is usually required. Benzodiazepines are often prescribed to patients who are titrating upwards on selective serotonin reuptake inhibitors, but they are not evidence based as effective in OCD by themselves, and they have a high risk for abuse and dependency. Atypical antipsychotic medications such as quetiapine may be helpful in low doses but may make symptoms worse at high doses because of their dose-dependent effect as dopamine receptor antagonists at low doses and 5-HT2A receptor blockers at high doses. The anticonvulsants gabapentin and lamotrigine may be useful as adjunctive treatments.
Novel treatment approaches under investigation include the use of the antituberculosis agent D-cycloserine, use of the naturally occurring sugar inositol (which appears to modulate serotonin activity), and transcranial magnetic stimulation. Opiates may reduce OCD symptoms, but their use is off label and not standard because of concerns about abuse and dependency.
PANIC DISORDER
Panic disorder is characterized by episodes of intense anxiety lasting from 1 to 20 minutes but typically lasting for about 10 minutes. There is overwhelming fear with a sense of dread or impending doom. Patients typically believe they are about to die or lose their minds. In addition, physical symptoms of hyperventilation, tachycardia, shortness of breath, dizziness, sweating, and trembling are usually present. Patients are often afraid of having an attack in public, and agoraphobia is present in more than a third of cases. Panic attacks can occur during sleep and can be distinguished from night terrors in that the patient usually becomes fully awake.
Panic disorder is not currently classified in the DSM-IV TR as a childhood disorder. This is surprising because 40% of all adults with panic disorder report their onset before age 20, with peak onset between 15 and 20 years old. Case reports of panic disorder in younger children abound, although the exact incidence is not known. The symptoms of juvenile panic disorder are very similar to those of adults and include heart palpitations, sweating, shortness of breath, trembling, faintness, nausea, and abdominal distress.54 Childhood panic disorder is highly associated with other anxiety disorders, including generalized anxiety disorder and specific phobia, somatization disorder, major depression, dysthymic disorder, and bipolar disorder. The lifetime prevalence in 18 to 29 year olds is 4.4%, with women twice as likely as men to develop the condition.
Anxiety disorders in parents place children at risk for the development of panic disorder,55 and separation anxiety in young children may be a precursor for the development of panic disorder in adolescents. There is a strong association between substance abuse and panic disorder both as triggers in the case of stimulants (caffeine, nicotine, amphetamine, and cocaine) and as self-medication in the case of alcohol and sedatives. 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 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 going crazy.
Panic disorder is treated with cognitive behavior therapy and medication. Cognitive behavior therapy educates patients about possible triggers and teaches strategies for self-soothing, including cognitive reassurance to diminish fear and deep breathing or progressive relaxation to control physical symptoms. Antidepressant medications, including selective serotonin reuptake inhibitors, serotonin and norepinephrine inhibitors, tricyclics, and monoamine oxide inhibitors, are effective prophylaxes against panic disorders. Benzodiazepines will immediately relieve a panic episode, and regular use will prevent their onset, but benzodiazepines must be monitored carefully due to their potential for dependency and abuse.
POSTTRAUMATIC STRESS DISORDER
Posttraumatic stress disorder (PTSD) is an emotionally painful and often debilitating syndrome that arises from experiencing or witnessing a terrifying physical or emotional event in which life is lost, injured, or threatened. Examples of catastrophic events that might result in PTSD include serious accidents (eg, car, train, plane crashes); natural disasters (eg, floods, hurricanes, earthquakes); manmade atrocities (eg, terrorist attacks, random shootings, arson, war); violent personal attacks (eg, rape, 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 the development of PTSD.
People with PTSD are plagued by frequent and persistent intrusive, frightening thoughts, memories, nightmares, and flashbacks (intensely vivid mental imagery that is experienced more as a reliving than a memory of a traumatic event.) People with PTSD are hypervigilant, hyperaroused, and easily startled. They often report feeling emotionally numb; are prone to dissociation, including derealization (things seem strange or unreal, or “Alice in Wonderland-like”) and depersonalization (estrangement from one’s body, including numbness and “out-of-body” experiences); and are avoidant of triggers (eg, may refuse to return to the city where an assault occurred). The complete avoidance of triggering is impossible because triggers can involve any of the 5 senses. Words, symbols, and emotions themselves can be triggers. PTSD victims are likely to suffer from comorbid anxiety disorders and depression, and they often self-medicate with alcohol and drugs of abuse. 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.
Traumatic reenactment is a key feature of PTSD. Young children tell their stories in repetitive play (eg, cops and robbers following a home invasion robbery), and adolescents who have been sexually abused may place themselves in harm’s way by becoming promiscuous. Adults who were abused as children tend to lack normal self-protectiveness. Women who were sexually abused as children are 3 times more likely to be raped than are women who were not abused as children.
Adolescents with PTSD resemble adults with PTSD. Like younger children, they are likely to incorporate aspects of the trauma into their daily lives. Adolescents are more likely than younger children and adults to act impulsively and aggressively.
EPIDEMIOLOGY AND ETIOLOGY
Traumatic experiences are common. More than two thirds of Americans experience a significant trauma at some point in life, and up to 20% experience such an event in any given year.56 Exposure to trauma is even higher in parts of the world ravaged by warfare, poverty, and famine. The likelihood of developing post-traumatic stress disorder (PTSD) varies with the severity, duration, and proximity of the traumatic experience. Thus, victims on site of the World Trade Center attacks of September 11, 2001, were more likely to develop PTSD than were rescue workers, who were more likely than the general population in New York City to develop PTSD.
The prevalence of PTSD following man-made violence (terrorist attacks, random shooting sprees) or technology failures (eg, plane crash, nuclear reactor meltdown, chemical plant gas release) ranges from 25% to 75% and is greater than the prevalence of PTSD following natural disasters (earthquakes, floods, hurricanes, tornadoes), which ranges from 5% to 60%, but is generally in the lower half of that range. The prevalence of PTSD in the United States is 8% to 9%. It is twice as common among women as men. Military combat is the most common source of PTSD among men, whereas sexual assault and molestation are the most common traumas for women with PTSD.57 Nearly half of all boys and girls in the general population are exposed to some form of trauma during their childhood and adolescence, with studies suggesting that 3% to 15% of girls and 1% to 6% of boys meet criteria for PTSD. Some traumas generate a particularly high rate of PTSD, with 100% of children witnessing a parental murder, 90% who are sexually abused, and 77% of students exposed to a school shooting developing the disorder. Once established, PTSD becomes chronic and debilitating.
Genetic factors may play a role in the development of PTSD because the condition tends to run in families. At least 1 twin study of Vietnam veterans supports this hypothesis.58 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.59 Neuroimaging studies show differences between PTSD study participants with a preponderance of hyperarousal and those with more dissociative symptoms.60
DIAGNOSIS AND TREATMENT
The diagnosis of posttraumatic stress disorder (PTSD) is established through careful and thorough clinical interview. Clinicians must be sensitive to the fact that children and adolescents may be unable to verbalize traumatic experiences or too afraid to disclose trauma, especially if the perpetrator of abuse is a close family member. The clinical interview itself may be retraumatizing, so clinicians must allow patients to pace themselves in exposing revelations while constantly reassuring them that they, the patient, are in control of the process and that they are not to blame.
Trauma-focused cognitive behavior therapy is the most comprehensively studied psychotherapeutic intervention and has the strongest evidence base to support its use in PTSD.61 This approach reduces the fears associated with the trauma, as well as relieves associated beliefs such as self-blame, by providing a safe environment in which traumas can be discussed. Exposure therapies, including eye movement desensitization and reprocessing (EMDR),62 are also effective and included in the practice guidelines of the American Psychiatric Association.
Pharmacotherapy includes the use of selective serotonin reuptake inhibitors to reduce symptoms of anxiety and depression. Beta-blockers such as propanolol and alpha-adrenergic blockers such as clonidine reduce the hyperausal symptoms of PTSD, and may block the formation or reinforcement of traumatic memories. The α-adrenergic blocker prazosin may be especially helpful in reducing the nightmares associated with PTSD.63 Mood stabilizers such as lithium, carbamazepine, oxcarbazepine, valproate, and lamotrigine may stabilize volatile mood and reduce aggression. Atypical antipsychotics such as risperdal and quetiapine may help with dissociation and extreme anxiety or aggression. Benzodiazepines may be used to relieve acute anxiety but should be prescribed cautiously due to the risks of abuse and dependency.
3,4-Methylenedioxymethamphetamine (MDMA; aka Ecstasy) is being studied in combination with psychotherapy on the theory that exposing PTSD patients to traumatic memories without the intense fear, anger, guilt, and shame associated with the trauma will dramatically improve the patient’s ability to master the memories without the associated PTSD reactions. (MDMA’s action on the amygdala reduces the intensity of painful emotions while increasing a sense of well-being and connectedness.) The studies have not been completed, and MDMA is an illegal drug of abuse that should not be recommended at the current time. The common thread in all effective treatments for PTSD is that they reduce the intensity of overwhelming emotions while allowing the sufferer to reexperience the trauma with a new sense of confidence and mastery.
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