Review of Child and Adolescent Psychiatry

The prevalence of ADHD is a matter of controversy, in part because of differences in the definitions used. The prevalence of ADHD as defined by DSM-IV-TR is in the range of 5%–10%, with a male-to-female ratio of about 3:1. Boys present more frequently with disruptive behavior, and girls are more likely to exhibit the inattentive subtype.

Comorbidity is common. Approximately 45% of youths with ADHD also have conduct disorder or oppositional defiant disorder, 25% have a comorbid anxiety disorder, and up to 20% have a substance use disorder (6, 7).

Research has shown clearly that ADHD has a biological basis. Patients with ADHD appear to have a neuroanatomical deficit in the frontal and basal ganglia areas of the brain that is related to impairment in the dopamine and/or norepinephrine pathways. A relative deficit in frontal lobe volume and asymmetry of the caudate nucleus have been postulated as etiological factors associated with disturbed executive function. ADHD is thought to have a genetic basis. Estimates of the heritability of ADHD run up to 0.9, and twin studies suggest even higher rates. Research findings support the involvement of the dopamine transporter gene chromosome 5p15.3 and the dopamine receptor gene on chromosome 11p15.5. Important external etiological factors include head injury, prenatal insults such as maternal smoking and substance abuse during pregnancy, perinatal complications, and lead poisoning. In addition, specific genetic disorders, such as fragile X syndrome and neurofibromatosis, are associated with ADHD (6–8).

The DSM-IV-TR diagnosis of ADHD is based on clinical evaluation and the presence of six or more of nine symptoms of hyperactivity and six or more of nine symptoms of inattention or impulsiveness. Some of the symptoms must have been present before age 7 years, and some must be present in two or more settings. In boys, the majority of diagnoses are made by 4 years of age because of externalizing symptoms. In girls, because of a preponderance of inattentive symptoms, diagnosis tends to come later. Generally, clinical vigilance is needed to make the correct diagnosis in girls. Corroboration from teachers and other sources aside from the parents is required. The use of standard scales, such as the Conners Parent Rating Scale and the Conners Teacher Rating Scale, can assist not only in diagnosis but also in objectively monitoring the course of treatment (9).

Two main approaches are used in the treatment of ADHD: pharmacological, primarily with stimulant medications, and behavioral, primarily with cognitive behavior therapy and psychosocial interventions. Recent data from the National Institute of Mental Health’s Multimodal Treatment of ADHD (MTA) trials indicate that use of stimulants (typically methylphenidate) works best in treating pure ADHD and that behavioral interventions with or without stimulants work best in treating ADHD accompanied by comorbid disorders.

Psychostimulants have remained the main arm of pharmacological treatment over the past five decades. These agents include methylphenidate, which has been approved by the Food and Drug Administration (FDA) for use in patients aged 6 years and up, and amphetamine salts, which have FDA approval for use in patients aged 3 years and up. Both agents are available in various forms, including in rapid-release and extended-release formulations.

The use of stimulants is backed by evidence from more than 170 randomized controlled trials with nearly 6,000 patients, in which an efficacious response was seen in 65%–70% of patients, compared with 5%–30% in the placebo groups. Although the evidence thus far covers only short-term benefits, ongoing large randomized controlled trials, such as the MTA trials, are expected to shed light on the long-term utility of stimulant treatment. The extended-release forms of methylphenidate and mixed amphetamine salts have been favored in recent years. Pemoline, another stimulant, is used sparingly because of the risk of hepatotoxic effects.

Atomoxetine, a selective norepinephrine reuptake inhibitor, is a nonstimulant agent that has been shown in a variety of placebo-controlled studies to be efficacious in treating ADHD. It received FDA approval for use in children aged 6 years and up, and it is now considered, along with stimulants, a first-line agent for ADHD. Its effect size is around 0.5, compared with 0.7 for stimulants. Careful monitoring of weight, height, emergence of aggression, sleep loss, appetite loss, and possible abuse of the drug is essential.

Antidepressants (notably tricyclics and bupropion) and alpha-adrenergic agonists (such as clonidine and guanfacine) are considered clinically useful alternatives when treatment with stimulants fails or is accompanied by unacceptable side effects.

Two psychosocial interventions have an evidence base for efficacy in the treatment of ADHD: behavioral parent training and behavioral interventions in the classroom setting. Both are based on positive reinforcement, stimulus control, extinction, and appropriate consequences for deviant behavior.

Limited data are available to support the use of alternative regimens, such as dietary restrictions, biofeedback, sensory integrative training, vision training, chiropractic manipulations, music therapy, and herbal regimens (4, 9–11).

There is evidence that ADHD persists into adulthood, and current studies indicate that some 50% of patients continue to have troublesome symptoms after the age of 18 years. In these patients, hyperactive symptoms often diminish while inattentive/impulsive symptoms remain. Use of stimulants is associated with less polysubstance and alcohol use and may act as a protective factor against substance abuse (1–3).

The prevalence of depression in children is in the range of 1%–2% during the preadolescent years and 5%–6% during adolescence. At any given time, 1 in 20 youths suffer from depression. The ratio of girls to boys is 1:1 during childhood, and then it increases to 2:1 in adolescence (17). When the family history includes a past depression in one or both parents, a child has a significantly higher risk of developing depression.

An episode of depression in a child lasts 8 to 13 months on average, and the recovery rate is 90% (5). In adolescents, episodes last 3 to 9 months on average, with recovery rates ranging from 50% to 90%. Relapse rates in children range from 30% to 70%, depending on length of follow-up. Among adolescents, 40% relapse in 2 years and 70% in 5 years (18, 19). First-episode preadolescent depression can be a harbinger of bipolar illness, with about 20% developing bipolar disorder (20).

Suicide is an important risk factor associated with depression. Boys attempt suicide less often than girls but are more likely to complete suicide (21). Risk factors for suicide and depression include substance abuse, impulsivity, aggression, a history of suicide attempts, a family history of suicide, firearms in the home or access to firearms, physical or sexual abuse, homosexuality, and being sexually active. In a recent study of 100,000 high school students, about 20% acknowledged having suicidal ideation during the previous year (22). Another study reported that 2.9 per 100,000 girls and 14.6 per 100,000 boys attempted suicide requiring medical treatment (23). Assessment of suicidality is an important part of the workup for depression in a child or adolescent. It is encouraging that there was a significant decline in suicide rates, from 6.2 to 4.6 per 100,000 population, in the 10- to 19-year-old age group between 1992 and 2001 (24).

It is important to exclude some common medical conditions that can mimic depression, such as thyroid disorders, anemia, and infectious mononucleosis. A detailed and thorough family history should be taken, especially in preadolescent depressed youths, to explore the possibility of a family history of mania. Any history of suicide in the family should be thoroughly explored in the evaluation process as well. Screening and evaluation of comorbid symptoms of anxiety, ADHD, learning disability, and substance use disorders in adolescents is important. In gathering information, the clinician should bear in mind that the youth will relate internal states better and the parents will give a better description of external or behavioral symptoms. The use of clinician-based diagnostic rating scales and self-reported, parent-reported, and clinician-based clinical scales during treatment is helpful in overall management (25).

Several key steps should be taken early in the management of depression in children and adolescents. Providing psychoeducation about depression, to both the youth and the parents, is essential. Gauging the youth’s sense of helplessness and hopelessness is also important, with a view to preventing self-harm and acting-out behaviors. When appropriate, a no-suicide pact can be made with the youth, with clear direction about whom to contact when the patient is in need. Any firearms in the home should be removed (22).

Two main approaches are used in the treatment of depression: psychotherapy and pharmacotherapy with antidepressants. Both are supported by evidence from clinical trials, and ongoing research continues to clarify their utility and efficacy. Cognitive behavior therapy, family therapy, and interpersonal psychotherapy have been shown to be efficacious. Cognitive behavior therapy in adolescents, lasting 3–4 months with up to 16 sessions, has been shown to be more beneficial than other forms of therapy in treating adolescent depression. Its benefit in very young children has not been established. Cognitive behavior therapy is focused on problem solving, amelioration of self-defeating and dysfunctional thought processes, and management of interpersonal skills. Individual and group-based cognitive behavior therapy have both been proven beneficial, and trials are under way to evaluate the efficacy of interpersonal psychotherapy in adolescents. In some cases psychotherapy must be continued at length to prevent early relapse.

Selective serotonin reuptake inhibitors (SSRIs)—fluoxetine, sertraline, and citalopram—have proven efficacy in the treatment of pediatric depression in randomized controlled trials (26–29), with an overall response rate of 60%–65% and a favorable side effect profile. Currently fluoxetine is the only medication that has FDA approval for treatment of depression in children aged 7–18 years. The starting dose of an SSRI is approximately 5 mg fluoxetine-equivalents for 5–7 days, although a lower dosage may be used to alleviate any initial side effects. The dosage is then titrated to 10–20 mg fluoxetine-equivalents over 2–4 weeks. It generally takes about 6 weeks for any benefit to become apparent, and in some patients it can take up to 10 weeks. Children and adolescents generally require higher dosages and longer courses of initial treatment than adults before any benefit shows. Tricyclic antidepressants have not been shown to be superior to placebo in any of the clinical trials conducted thus far, and hence they have no role in the treatment of pediatric depression (30).

Pharmacotherapy for depression in children and adolescents is currently the subject of a highly controversial debate (31, 32). Concerns have been expressed around the world about the use of SSRIs, and warnings have been issued by regulatory agencies about the potential risk of suicidality. In a comparison study of first-time exposure to one of two SSRIs (fluoxetine and paroxetine) and two tricyclics (amitriptyline and dothiepin) in patients undergoing a first episode of depression accompanied by nonfatal suicidal behavior or ideation, an increased risk of suicidality was noted during the first month after initiation of antidepressant therapy, and particularly during the first 10 days (33).

In the United Kingdom, the Medicines and Healthcare Products Regulatory Agency has placed restrictions on the use of all SSRIs except fluoxetine in the pediatric population. Similar warnings have been issued in the United States, initially with an emphasis on the risks associated with paroxetine and venlafaxine, and in September 2004 an FDA advisory panel recommended that a “black box” warning about pediatric suicidality be included with all antidepressant medications.

Clearly, increased vigilance and close follow-up monitoring are required in the initial phase of pharmacotherapy for children and adolescents with depression. In our pediatric psychopharmacology clinic, among the measures we use are a weekly objective assessment of depressive symptoms via telephone and faxed weekly feedback from the parents or caregivers. In selected cases a quick follow-up appointment is made within the first 15 days of initiating treatment with an SSRI.

The diagnostic criteria for anorexia nervosa are a body weight maintained at a level less than 85% of normal weight for age and height, an intense fear of becoming fat, a disturbed experience of one’s body weight or shape, and amenorrhea for at least three consecutive menstrual cycles (46–48). A pathological reduction in body weight accompanied by a lack of insight into the weight loss is the cardinal sign of this disorder. DSM-IV-TR specifies two types of anorexia nervosa. The restricting type is characterized by strict dieting, fasting, or excessive exercise, and in postmenarcheal females it presents with cessation of menstruation. In the binge-eating/purging type, enormous intake of food is followed by vomiting or use of laxatives or others means of purging (46, 47).

Anorexia nervosa is mostly seen in women, with female-to-male ratio of 9:1. The incidence is about 3% among women in adolescence and young adulthood; young women aged 16–24 years are a high-risk group. There is some indication of a rise in incidence among males (46–49).

The etiology of anorexia nervosa is not known and is considered multifactorial, with psychological and genetic components. Family conflict and the level and appropriateness of communication are important. Also, among first-degree relatives of patients with anorexia nervosa, elevated rates of eating disorders are seen. Although anorexia nervosa is mostly seen in industrialized societies, its incidence is on the rise in the metropolitan populations of developing countries.

Anorexia nervosa presents important challenges in medical management, among them dehydration, hypocalcemia, leukopenia, hypothermia, abnormal liver function tests, abnormal thyroid function, and hyponatremia. Thus, a team approach is required that includes monitoring and treatment of medical issues. The elements of treatment are stabilization of the patient’s weight, identification and resolution of psychosocial stressors, and development of healthy eating habits along with weight maintenance. Anorexia nervosa frequently requires hospitalization and treatment of bradycardia, hypertension, syncope, and cardiac arrhythmias; prolongation in the QT interval is the main indication for hospital treatment and management (1–3, 46, 48, 50, 51). The disorder has a relatively high mortality rate at 0.56% per year (49).

In outpatient management, the treatment target is a weight gain of about 1 pound per week. Family therapy and psychoeducation for family members facilitates treatment, especially when the patient’s symptoms began before the age of 18 years. The cornerstone of treatment is behavior modification therapy to have the patient focus on achieving a healthy weight, decrease medical risk factors, and address emotional issues. Mood and anxiety symptoms are managed with SSRIs and benzodiazepines. Pharmacological agents have limited efficacy in the treatment of anorexia nervosa itself, however (46–51).

Bulimia nervosa is characterized by repeated episodes of uncontrollable eating of huge amounts of food in a short time, usually followed by an attempt to compensate for the excessive caloric intake. Compensatory behavior includes mechanically or chemically induced vomiting, strict fasting, and use of laxatives, enemas, diuretics, and even thyroid medications. For a diagnosis, DSM-IV-TR criteria require that the binge eating and compensatory behavior occur twice a week for at least 3 months.

Like anorexia nervosa, bulimia nervosa occurs predominantly in females, and 50% of patients develop the disorder before the age of 18 years. Treatment includes elimination of the binge eating cycle, establishment of healthy eating habits, and skill training in emotional problem solving. Cognitive behavior therapy to address the sense of despair that is linked to binge eating is a cornerstone of treatment. Use of tricyclic antidepressants (desipramine, up to 300 mg per day, and imipramine, up to 300 mg per day) is supported by clinical data, although SSRIs have become the mainstay of pharmacotherapy in recent years. Fluoxetine (up to 60 mg per day) is the only drug that has FDA approval for treating adults with bulimia nervosa. Unlike in anorexia nervosa, which is not amenable to pharmacotherapy, treatment of bulimia nervosa with SSRIs is associated with a response rate of about 40% (46, 47, 50).

The incidence of mental retardation is about 1% in the general population. Mental retardation is frequently seen in adult psychiatric practices and is usually associated with psychiatric comorbidity, which is frequently missed. For a diagnosis of mental retardation, the patient must have an IQ of approximately 70 or below before the age of 18 years. Table 1 lists the clinical features of mental retardation.

Mental retardation is best managed by applying a comprehensive biopsychosocial model. If comorbid psychiatric conditions, such as ADHD, anxiety disorders, and mood disorders, are present, they should be treated according to established guidelines. There is some evidence suggesting that methylphenidate is effective in ameliorating ADHD symptoms and SSRIs in ameliorating anxiety and depressive symptoms in this population. Treatment should also include a variety of nonpharmacological interventions, such as special education, speech and language instruction, and vocational training (52, 53).

Autistic spectrum disorders are characterized by impairment in social communication and social interactions and a restricted range of interests, along with repetitive stereotypic movements, repetitive behavior, and deviant mannerisms. Patients with these disorders frequently present with sensory problems and hypersensitivity to sensory stimuli. The incidence of autistic spectrum disorders is on the rise, a trend that has been attributed to increased case finding, greater awareness of autism, and rediagnosis for the purpose of obtaining services. The incidence is thought to be between 6 and 10 per 1,000 children, and higher figures have been reported for pervasive developmental disorder not otherwise specified.

The average age at the time a diagnosis of an autistic spectrum disorder is made is around 3 to 4 years. About 30% of children diagnosed show normal development at first, followed by regression at some time between 15 and 21 months of age. Several organic causes of autism have been identified, namely, prenatal rubella infection, postnatal encephalitis, and other infections; genetic and metabolic disorders, such as phenylketonuria, tuberous sclerosis, and fragile X syndrome; and in utero exposure to certain medications, such as anticonvulsants. However, these etiological factors account for a small proportion of autistic individuals (about 10%); for the majority of patients with autism, the cause is not known.

Autism is considered a genetic disorder; the incidence among identical monozygotic twins is 65%–70%. A higher concordance has been noted for autism among monozygotic twins than among dizygotic twins. The incidence in siblings is between 4% and 6%. Suspect genes have been identified on chromosomes 15, 2q, 7q, 16p, and 19p. The incidence of neurological disorders (such as seizures [25%] and macrocephaly [30%]) is also higher throughout life among patients with autism.

The majority of cases of autism are characterized by acquisition and then loss of language. Most autistic children show signs and symptoms early. With an emphasis in recent years on early diagnosis and intervention, screening instruments have been developed, such as the Checklist of Autism in Toddlers (54), which has high sensitivity but low specificity. High-functioning autistic phenotypes, such as Asperger’s disorder, may present later, after the child enters school. Asperger’s disorder, which overlaps with high-functioning autism, is characterized by preservation of language, continued social deficits, and occasional stereotypic abnormal interests (54–63).

Fragile X syndrome is the most common form of genetically inherited mental retardation, with an incidence of 1 in 1,250 males and 1 in 2,500 females. It is characterized by prognathism, macrocephaly, and, in boys, macroorchidism. Other physical signs include flat feet, smooth skin, a high, arched palate, and hyperextensible joints. Children with fragile X syndrome commonly have sleep abnormalities, seizures, infections, hernia, strabismus, and scoliosis. They frequently exhibit hand flapping and gaze aversion. Boys usually have a low IQ, but girls, because they have two X chromosomes, may have normal intelligence with learning disorders. ADHD symptoms are common in both sexes. Anxiety disorders may be present, especially in girls, and are manifested as social anxiety, isolation, shyness, poor eye contact, social oddness, and specific speech and language deficits. Approximately 20% of patients with fragile X syndrome meet the criteria for autistic spectrum disorder. Other psychiatric disorders have an elevated incidence in patients with this syndrome. Treatment is based on alleviating the presenting deviant and abnormal symptoms (64, 65).

Generalized anxiety disorder is manifested mainly as excessive worry that is prolonged, intense, and uncontrollable, combined with a general sense of perfectionism. A DSM-IV-TR diagnosis requires that the worries last at least 6 months and occur both at home and at school. Children with generalized anxiety disorder have a pessimistic demeanor, are avoidant and shy, and have frequent self-doubts and worries. They have been described as being in a constant state of fright, fight, or flight reactions. Thumb sucking that is age-inappropriate, nail biting, and scab picking or hair pulling are frequently seen. Children sometimes report their anxiety symptoms much more accurately than their parents, other caregivers, or teachers do. The Screen for Child Anxiety Related Emotional Disorders, the Multidimensional Anxiety Scale for Children, and the Pediatric Anxiety Rating Scale are frequently used in clinical practice for objective assessment and treatment (66).

The incidence of generalized anxiety disorder has been reported in various studies to be in the range of 3%–14%. The disorder is predominant in females in adolescence. It is frequently comorbid with mood disorders and with ADHD (66, 67). Generalized anxiety disorder appears to have a strong genetic component, and frequently there is a parental history of the disorder.

The treatment of choice, with strong support from clinical trials, is cognitive behavior therapy. Therapy has four major components: recognizing anxious feelings and physical reactions to anxiety; identifying and modifying negative self statements; generating strategies to cope with anxiety-provoking situations; and providing rewards for successful attempts to cope (66). Relaxation training, with or without imagery, has also been used successfully.

Pharmacological management of generalized anxiety disorder is based on the use of benzodiazepines, tricyclics, SSRIs, and monoamine oxidase inhibitors. Open trials with fluoxetine and buspirone (66, 68–70) have shown efficacy in the pediatric population with the drugs administered at half the adult dosages. The SSRI sertraline, in lower dosages, has FDA approval for use in the treatment of generalized anxiety disorder in children, and there is clinical evidence that fluvoxamine is efficacious. Paroxetine and venlafaxine are being used less with children and adolescents now, after cautions were issued by the FDA in response to concerns about the potential for thoughts of self-harm (67, 68, 71, 72).

The DSM-IV-TR criteria for a diagnosis of social anxiety disorder in children are the same as for adults. The disorder is characterized by specific fears of social encounters and public performances. The fears are persistent and irrational, they are not normal for the child’s age, and they cause functional impairment; for diagnosis, they must have been present for at least 6 months. The rate of social anxiety disorder is about 1%, although the lifetime rate is about 13% in adolescent samples. Rates for specific phobias are around 5%.

The etiology of phobias is multifactorial, with components in genetics, inheritance, temperament, family dynamics, and modeling. The onset of specific phobias can sometimes occur during growth and development, and their severity can wax and wane over time. Most phobias remit, but a small proportion persist, requiring treatment.

Evaluation and diagnosis require a thorough history and close observation with an emphasis on the expression of anxiety symptoms. In younger children, play or art work can be used for this purpose. In very young children, symptoms are expressed by freezing, crying, temper tantrums, and clinging, whereas older children and adolescents are able to verbalize the inner state of fear connected with a situation.

Treatment of phobias requires a tailored approach. The evidence is strongest for the efficacy of cognitive behavior therapy. The cornerstone of treatment is systemic desensitization through exposure and response prevention, along with the provision of coping skills and problem-solving skills in a variety of situations. Real-time imagery is occasionally employed. The SSRIs fluoxetine and sertraline have been found to be efficacious in treating social anxiety disorder, and fluvoxamine has supportive data in the treatment of social phobia, especially. However, it is important to bear in mind that the primary arm of treatment is cognitive behavior therapy focusing on relaxation, desensitization, gradual exposure, modeling, coping skills, and reinforcement. The therapy can be provided in individual or group format, and it is frequently focused on addressing distorted beliefs (72, 73).

The diagnostic criteria for PTSD in children differ somewhat from those for adults. Children present with more distractibility, more perceptual distortions, more avoidance (generally auditory and tactile), and greater separation issues. Children’s reexperiencing of traumatic events often differs from that of adults. They may have nightmares with content about the events or related thematically to the events, and they may reenact traumatic events in play, as opposed to experiencing flashbacks. Prevalences of PTSD have been reported in the range of 0.5% to 14% in a variety of clinical settings.

PTSD can occur in a variety of circumstances. Whether PTSD symptoms develop depends on the manner, degree, and duration of exposure to trauma as well as the type of trauma. An important cause of PTSD is sexual or physical abuse during childhood, which have been clearly shown to be associated with lifetime psychopathology, especially in women. Even the death or serious illness of a loved one has been associated with PTSD in clinical samples.

In younger children the primary presentation might be reenactment of the trauma. A significant change in behavior accompanied by emotional lability, when these would not be expected for the child’s age or developmental stage, should trigger suspicion of PTSD. Detailed questioning of both parents and child should follow. Younger children may be placed in a play setting to allow the clinician to observe any reenactment of a trauma.

The evidence base for treatment of PTSD is limited. The primary treatment strategy involves cognitive behavior therapy tailored to the specific trauma that caused the symptoms, often accompanied by relaxation and desensitization techniques. Pharmacotherapy may be used in combination with cognitive behavior therapy. SSRIs are the drug class of choice. As experience with fluoxetine and sertraline accumulates, the body of data supporting their efficacy has grown. Clonidine and beta-blockers are occasionally used in acute clinical settings.

OCD involves persistent, recurrent thoughts or impulsive images and behaviors or mental acts, which usually accompany stress. Children and adolescents with OCD might have obsessions or compulsions or both. Many children do not have insight into the behavior.

OCD is not uncommon; rates of 1%–4% have been reported. Onset is generally earlier in boys than in girls, although by adolescence the prevalence is equal between the sexes. In one recent study of OCD in adults, the symptoms that had their onset in adulthood were first manifested in childhood (1–3, 66).

The etiology of OCD has to do with disturbances in serotonin equilibrium in specific areas of the brain. Abnormal circuitry in the frontal striatal and thalamic areas of the brain has been proposed. Recent studies also support genetic and infectious causes of OCD. For example, Swedo et al. have described “pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection” (PANDAS) in a small minority of children who have symptoms of OCD with and without tics (74).

OCD in children and adolescents is considered a chronic condition that waxes and wanes. The onset is usually gradual, although in cases of PANDAS it can be sudden; in these cases, patients have a positive throat culture and a high antistreptolysin O titer (74). The severity of obsessions, worries, and rituals in OCD generally varies over time. Comorbid disorders associated with OCD includes tics, trichotillomania, eating disorders, depression, ADHD, and oppositional defiant disorder.

OCD frequently presents with temper outbursts, academic difficulties, or altered eating patterns resulting from strict obsessions and rituals. Fear of contamination, fear of danger, compulsive and repetitive checking, frequent delays in doing homework, perfectionism, and excessive praying, counting, and touching are common symptoms of OCD. The Childhood Yale-Brown Obsessive Compulsive Scale is an important aid in diagnosis.

OCD is treated with cognitive behavior therapy and pharmacotherapy, frequently applied together. Cognitive behavior therapy is based on gradual exposure, response prevention, modeling, relaxation techniques, and habit-reversal and thought-stopping skills. Among pharmacological agents, SSRIs are the most commonly used. Use of sertraline, fluvoxamine, and fluoxetine in treating OCD has support from double-blind randomized controlled trials, and all three have FDA approval for treating OCD in children (1–3, 66, 67).

Panic disorder is rare in children but does occur in adolescents. DSM-IV-TR diagnostic criteria are the same as for adults. The disorder has physiological and psychological features, and the two can occur spontaneously. Symptoms include hyperventilation, palpitations, shortness of breath, chest pains, dizziness, and out-of-body experience. Panic disorder can occur with or without agoraphobia.

The prevalence of panic disorder is not precisely known. Although the disorder is thought have a lifetime prevalence of 1%–2%, rates are notably higher in clinical samples. The etiology of panic disorder includes biological and psychological factors. Familial patterns have been noted, and twin studies point toward a genetic contribution. Modeling has also been proposed.

Adolescents with panic symptoms are generally well able to describe their experience in enough detail for a diagnosis to be made. In evaluating younger children, the history may reveal some symptoms, but an observation by a parent of a panic attack in a child can provide much more focused information.

Treatment includes cognitive behavior therapy, family therapy, and individual therapy, followed by a trial of an SSRI. Sertraline has FDA approval for use in treating panic disorder in children (1–3, 66).