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3. Crowley TJ, Riggs PD: Adolescent substance use disorder with conduct disorder, and comorbid conditions. In Adolescent Drug Abuse: Clinical Assessment and Therapeutic Interventions. NIDA, Research Monograph Series, 1995. 4. Kazdin AE: Psychosocial treatments for conduct disorder in children. J Child Psycho1 Psychiatry 38: 161-178, 1997. 5. Lewis DO: Conduct disorder. In Lewis M (ed): Child and Adolescent Psychiatry: A Comprehensive Textbook. Baltimore, Williams & Wilkins, 1991, 6. Moftitt TE: The neuropsychology of conduct disorder. Dev Psychopathol 5:135-15 I , 1993. 7. Moffitt TE: Adolescence-limited and life-course-persistent antisocial behavior: A developmental taxonomy. Psycho1 Rev 100:67&701, 1993. 8. Offord DR, Bennett KJ: Conduct disorder: Long-term outcomes and intervention effectiveness. J Am Acad Child Adolesc Psychiatry 33:1994. 9. Raine A, Lenez T, Bihrle S, LaCass L, Colletti P: Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. Arch Gen Psychiatry 57: 1 19-127, 2000. 10. Riggs PD, Whitmore EA: Substance use disorders and disruptive behavior disorders. In Henderson R (ed): Disruptive Behavior Disorders in Children and Adolescents. Washington, DC, American Psychiatric Association Press, 1999. 1 1. Robins LN, Regier DA (eds): Psychiatric Disorders in America. The Epidemiologic Catchment Area Study. New York. Macmillan, 1991. 12. Rutter M, Giller H, Hagell A: Antisocial Behavior in Young People. Cambridge, UK, Cambridge University Press, 1998. 13. Steiner H: Practice parameters for the assessment of children and adolescents with conduct disorder. J Am Acad Child Adolesc Psychiatry 36(10 Suppl): 122S-I39S, 1997. 14. Zubieta JK, Alessi NE: Is there a role of serotonin in the disruptive behavior disorders? A literature review. J Child Adolesc Psychopharm 3: 1993.

58. OBSESSIVE-COMPULSIVE DISORDER IN CHILDREN A N D ADOLESCENTS

Frederick B. Hebert, M D
1. Define obsessive-compulsivedisorder. Obsessive-compulsive disorder (OCD) was formerly thought to be rare and to have a poor prognosis. It is now known to be one of the most treatable of psychiatric disorders. OCD is a lifelong condition that waxes and wanes and often is complicated by depression and anxiety. Defined as a type of anxiety disorder, the symptoms of OCD consist of obsessions or compulsions, and sometimes both. 2. What are obsessions? Obsessions are demonstrated by recurrent and persistent ideas, thoughts, impulses, or images that are felt as intrusive and recognized as senseless. The person attempts to ignore, suppress, or neutralize the obsessions with some other thought or action. The obsessions are recognized as the product of the persons own mind rather than imposed from without (except perhaps in children). If another disorder is present, the content is not related (i.e., the obsession is not about guilt or depression). Typical themes are aggression, fear of contamination, doubting, or ordering of objects.

3. What kinds of behavior demonstrate compulsions? Compulsions consist of repetitive behaviors that appear purposeful and intentional, performed in response to an obsession or according to certain rules in a stereotyped fashion. The behavior is designed to neutralize or prevent discomfort or some dreaded event; however, the activity is not connected in a realistic way or is clearly excessive. The person recognizes that the behavior is excessive or unreasonable (children may not). Common compulsions are hand-washing, checking, counting, hoarding, or touching performed in a rigid manner.

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4. Since almost everyone has a few obsessions or compulsions, does everyone have OCD? No. The obsessions or compulsions must cause marked distress and take more than 1 h o d d a y or
significantly interfere with occupational or social functioning to meet DSM IV criteria for diagnosis.

5. How often does OCD occur? What is the prognosis? OCD occurs frequently in most ethnic groups, with a 2.5% prevalence rate. The onset is in childhood in 33-50% of the cases, with an average onset at age 15. Onset over age 40 is rare. Typically, onset is gradual and follows some trivial precipitant. The family may have a scrupulous religious background; the disorder is recognized among all major religions and is known as scrupulosity. Girls are afflicted more frequently, but boys have an earlier onset. In families with one affected member, 20% of relatives meet OCD criteria, and another 20% meet criteria for compulsive personality disorder. A patients prognosis worsens with concurrent cluster A personality traits (schizoid, schizotypal, paranoid), but a patients prognosis is not worsened with compulsive personality or passive traits. As an example, an 1 1-year-old boy became depressed. When he gradually became obsessed with the idea that his mother would be harmed and simultaneously had suicidal thoughts, he was hospitalized. On the ward, he would pace around the perimeter of the day room. At each comer, he would stop for a ritual of hand wringing. This ritual decreased when it was interrupted by staff, and an antidepressant was started. While one of his siblings also suffered from obsessive thoughts, the mother was quite organized in her work and suffered no disabling rituals.

6. Whats the cause of OCD?

The underlying mechanism causing OCD is unknown. Recent biologic, clinical, radiologic, and physiologic evidence of problems in the caudate nucleus or connections from the caudate to prefrontal area of the brain point to an ultimate organic or biologic cause. Self-grooming problems in dogs, particularly canine acral lick disorder (ALD), suggest overstirnulation of parallel CNS pathways from a disturbed serotonin balance. Canine ALD is helped by use of selective serotonin reuptake inhibitors (e.g., fluoxetine).
7. What other disorders frequently are associated with OCD? Depression frequently is associated with OCD; a significant number of children with OCD have major depression. As many as one-half suffered from some other anxiety disorder; 20% have tics, and 5% have Tourettes disorder, which is otherwise rare among the general population.

8. How does OCD present to other health care practitioners? OCD often is initially seen by family practitioners, pediatricians, and dermatologists. Pediatricians see parents exhausted by the stress of the cleaning or-checking rituals of their children. Sometimes a child will use an entire roll of toilet paper for a single bowel movement. If the child cannot attend school or is repeatedly late to school, truancy officials may make the first intervention. Family practitioners or dermatologists may see OCD presenting as nonspecific dermatitis. In children and adolescents, OCD often takes the form of multiple daily showers, an otherwise uncommon behavior in this age group. Children are sometimes noticed when they erase and reerase until they have worn holes in their school papers. Pediatric neurologists may see OCD when consulting for children with repetitive movements after a streptococcal infection. Sydenhams chorea may thus present as a compulsion in the form of repetitive leg movements. Such patients often have radiologic abnormalities. Surgeons frequently are asked by patients with OCD to perform cosmetic surgery for minimal disfigurement (more specifically defined as body dysmorphic disorder). This obsessive demand for bodily perfection is especially seen in adolescent performing artists. Dentists may be the first to see children with OCD, when they present with bleeding gums secondary to repetitive brushing.

9. What is the differential diagnosis of OCD?

In generalized anxiety disorder, the patient has anxiety most of the time, but it is not focused on one idea or behavior. In specific phobias, the patient is symptom-free except from a particular stirnulus that causes anxiety. In OCD, the patient is focused on the symptom, yet the patient is also upset

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by it. Adolescents with OCD know their symptoms come from their own mind. Children with OCD may not know that their symptoms are the product of their own thinking, making the diagnosis more difficult. It is necessary to rely instead on a history of time-consuming rituals from the parents. Patients with OCD generally are not considered psychotic. Major depressive episodes may present with concurrent obsessional thinking; however, the mood disturbance dominates the clinical picture, with obsessing occumng later and remitting with successful treatment of depression.

10. What are the so-called OCD spectrum disorders? Several disorders that may be related to OCD are called spectrum disorders. Compulsive hair pulling or trichotillomania, urinary and bowel obsessions, and body dysniorphias (obsessive concern that one part of the body is misshapen) are most likely variants of OCD, and are referred to as spectrum disorders. Ritualistic vomiting associated with bulimia is under active debate as a variant, because the vomiting often continues without significant weight loss or obvious personal gain. All of these disorders may have their onset in childhood or adolescence. 11. Are there different types of OCD? Yes. Most patients (up to 85%) are cleaners at some time in their illness. Some are checkers, endlessly testing whether they have shut doors or turned off a switch. Other children classify baseball cards in endless ways or count ceiling tiles over and over. Some patients must have a special symmetry, such as lining up pencils, colored crayons, or shoes; others balance everything that they do or say, such as reading until the number of pages is divisible by two. Far less commonly, the child cannot enter a doorway without a ritual behavior or taps out a rhythm on a fence while repeatedly walking a certain route. A common presentation in many children is to ask questions over and over. Adolescents who need to have the last word may have an obsessive fear that things will not be evened out if they do not. 12. What are the nonmedication treatments? OCD is particularly interesting among psychiatric disorders, because research indicates an overall low response to both placebo and psychotherapy. In behavior therapy, successes and failures have been noted. Systematic desensitization techniques (gradual increase in the presentation of a feared stimulus) were tried first, but failed. Other behavioral techniques also have been demonstrated to reduce anxiety, but not obsessions. Exposure in vivo (stimulus exposure) has been known to be effective for some time. This technique requires the patient to come in contact with the obsessive stimulus, such as door handles or toilet seats. Response prevention (interrupting or interfering with the patients response after the obsessive stimulus) keeps the patient from performing the usual cleaning ritual. Several studies, both controlled and uncontrolled, have demonstrated 7 0 4 0 % rates of effectiveness. Individuals who receive both imagined and actual exposure tend to maintain their gains more successfully over time. Patients with prolonged stimulus exposure do better than those with less exposure. In response prevention, there were no differences between patients who received 24-hour supervision and patients with minimal supervision. A cotherapist, including a family member, who works with the practitioner has improved results. One author found that about 60% of patients could be treated overall as outpatients with assigned homework, which stressed an opportunity to learn new strategies. He also found that most of the treatment needed to be carried out in the patients immediate environment where the rituals take place. However, up to 25% of patients drop out of behavior therapy, and many refuse to follow through with the treatment. The 75% success rate is obtained in the 75% of patients who complete treatment (for an overall response rate of 50%). Persistent reductions in compulsive rituals over time have been seen most often with behavior therapy, but it is less effective with obsessions, because it is impossible to deal with them in vivo. For such patients, particularly those with severe obsessions, medications are indicated.
13. What medications should be used? Most antidepressant medications with serotonergic mechanisms of action have been shown to be beneficial in treating OCD. Clomipramine, a tricyclic antidepressant with prominent serotonergic effects, was first noted to reduce obsessions in 1968 in a European study. Several double-blind

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comparisons with other medications have substantiated these results. In one early study combining clomipramine and behavior therapy, medication improved depression, anxiety, social adjustment, and rituals as well as compliance with behavior therapy. In other studies, clomipramine in lower doses reduced obsessive thoughts, but lower doses had no effect on rituals. Clomipramine has a typical tricyclic antidepressant side-effect profile: dry mouth, constipation, and tremor are frequent. Less often, dizziness, sedation headache, and fatigue occur. Sometimes sweating, weight increase, and ejaculation failure are seen. All side effects are reported less frequently by children and adolescents. Clomipramine remains the drug most often used in studies. Onset of action is in 2-4 weeks, with final improvement over 8-10 weeks. The dose of clomipramine is up to 200 mg/day or 3 mg/kg for children or adolescents. Selective serotonin reuptake inhibitors (SSRIs) are effective in the treatment of OCD. Of the SSRIs, only sertraline and fluvoxamine have been approved for the treatment of childhood OCD. Doses often are double that used for the treatment of depression. A dose of 100 mg of sertraline per day or 100-300 mg/day of fluvoxamine often is necessary. Fluvoxamine usually is given in divided doses because of its shorter half-life, and because it is more sedating. Whatever drug is used, starting at a low dose and moving slowly upward works best. Monoamine oxidase inhibitors have been noted to reduce OCD behavior in patients who also had panic attacks. Overall, symptoms are reduced by 70%. Less than 10% of children can be expected to drop out of treatment, but children and adolescents include a greater number of placebo responders; thus, children actually may not respond as well as adults. Patients with OCD and an avoidant style or sexual themes in their obsessions have poorer response

14. All of the medications are antidepressants.Does the patient have to be depressed? No. The antiobsessive effect is independent of antidepressant effect and is usually maintained with treatment.

15. What if the patient does not respond in 8-10 weeks? If behavior therapy and clomipramine are not effective, augmentation of the medication with lithium or buspirone may be effective. If side effects limit use of clomipramine, fluoxetine may be administered after tapering clomipramine over 1 week. Fluoxetine is long-acting and frequently competes with other plasma-bound medications for receptor sites; thus care must be taken if other drugs are given. Fluoxetine alone often works well; only 16% of patients report insomnia or anxiety. Stomachaches are frequent if the drug is taken without food. It is best not to start with fluoxetine, because treatment failure may require a drug-free period of up to 5 weeks. Sertraline has a shorter duration of action and may interact less with other drugs than fluoxetine because of less interference with cytochrome P-450 metabolic pathways. Patients with tics and OCD often need an additional neuroleptic or clonidine for sustained response. Neuroleptics may increase the blood levels of clomipramine significantly.
16. Do patients with OCD need hospitalization? Very few. Treatment of OCD usually can be accomplished on an outpatient basis, with a combination of behavior therapy and medication.

17. What is a PANDA? PANDA is a pediatric autoimmune neuropsychiatric disorder associated with streptococcal (group A beta-hemolytic streptococcal) infections. Swedo and her group first reported on these children in 1998. All the children had the five working diagnostic criteria: presence of OCD or a tic disorder, prepubertal onset, episodic course of symptom severity, association with group A beta hemolytic infections, and association with neurological abnormalities. The presence of abnormal movements in children following streptococcal infection has been known for years as Saint Vitus dance. It was thought to be a rare complication. Swedos group was the first to make the connection that this is a form of OCD caused by an autoimmune response.

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BIBLIOGRAPHY

I . Flament MF, et al: Obsessive compulsive in adolescents: An epidemiological study. J Am Acad Child Adolescent Psychiatry 27:764-771, 1988. 2. Geller DA, et al: Similarities in response to fluoxetine in the treatment of children and adolescents with obsessive-compulsivedisorder. J Am Acad Adolescent Psychiatry 34:3644, 1995. 3. Insel TR, Akiskal HS: Obsessive-compulsivedisorder with psychotic features: A phenomenologic analysis. Am J Psychiatry 143:1527-1533, 1986. 4. Jenike MA, et al: Obsessive-compulsivedisorder: A double-blind, placebo-controlled trial of clomipramine in 27 patients. Am J Psychiatry 146:1328-1 330, 1989. 5 . Kirk JW: Behavioral treatment of obsessive-compulsivepatients in routine clinical practice. Behav Res Ther 21:57-62, 1983. 6 . Marks I, OSullivan J: Drugs and psychological treatment for agoraphobidpanic and obsessive-compulsive disorders: A review. Br J Psychiatry 153:650-658, 1988. 7. March JF, et al: Sertraline in children and adolescents with obsessive-compulsive disorder. JAMA 280:1752-1756, 1998. 8. Perse T: OCD: A treatment review. J Clin Psychiatry 49:48-55, 1988. 9. Reynynghe deVoxrie G: Anafranil in obsession. Acta Neurol Belg 68:787-792, 1968. 10. Rapoport JL: The Boy Who Couldnt Stop Washing. New York, Plume, 1989. 1 1. Rasmussen SA: Obsessive-compulsivedisorder in dermatologic practice. J Am Acad Dermatol 13:965-967, 1985. 12. Swedo SE, et al: Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection: Clinical descriptions of the first 50 cases. Am J Psychiatry 155:26&27 1, 1998. 13. Zak JP, et al: The potential role of serotonin reuptake inhibitors in the treatment of obsessive-compulsivedisorder. J Clin Psychiatry 49(Suppl):23-29, 1988.

59. ENCOPRESIS A N D ENURESIS

Bevzjanzivz P. Greevz, M.D.

ENCOPRESIS
1. Define encopresis. How common is it?
As defined by the Diagnostic and Statistic Manual-IV (DSM-IV), encopresis is the repeated involuntary or intentional passage of feces into inappropriate places, such as into clothing or onto the floor, at a frequency of at least monthly for a duration of 3 or more months. To qualify for this diagnosis the patient must be at least 4 years old (corrected for mental and developmental age), and the condition must not be due to a medication (e.g.. laxative) or caused by a general medical (somatic) condition other than constipation. Although encopresis may occur at any age-especially among individuals with severe organic brain disease-it is primarily an affliction of childhood. Approximately 15% of 8 year olds and 0.8% of 1 1 year olds suffer from this disorder; the ma1e:female ratio is 3: 1 .

2. Are there clinically significant subtypes?

Although historically much has made of the distinction between primary encopresis (in which bowel continence has never been achieved) and secondary encopresis (in which incontinence has been established but then lost), the most useful clinical subtyping is organized around the presence or absence of constipation with overflow incontinence. Constipated or retentive encopresis is usually associated with small, soft, poorly formed stools that leak out both day and night. When constipation is absent, the stools tend to be large, well formed and intermittently deposited, often in particularly offensive places. The nonretentive type is more likely associated with oppositional and defiant behavior.