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Help children and teens stop impulsive hair pulling
Trichotillomania (TTM) is distressing to pediatric patients who pull their hair and to their parents who feel helpless to stop the destructive behavior. Hair-pulling with psychiatric comorbidity requires comprehensive assessment and treatment, but we have found that cognitive-behavioral therapy (CBT) alone can help children and adolescents with uncomplicated TTM.
This article describes a typical patient with adolescent-onset mild-to-moderate TTM and the three-step CBT approach—awareness training, stimulus control, and habit reversal—that we find effective in reducing pediatric hair pulling.
Jane, age 12, was referred to our clinic by her primary doctor after an 8-week trial of fluoxetine, 80 mg/d, failed to stop her hair pulling. Jane, who is right-handed, has been pulling her hair for 2 years, mostly in the right front scalp. Her shame over the hair loss makes her reluctant to participate in social activities. A dermatologist found no medical cause for her behavior, such as alopecia or folliculitis.
Jane’s parents say she has no history of a major mood disorder or anxiety. Her hair pulling causes significant “tension and stress” for all family members.
WHY DO PATIENTS PULL HAIR?
Cognitive-behavioral theory suggests that chronic TTM originates as a normal response to stress that often escapes personal and social awareness but gradually increases in frequency and severity (Box).1-8 Thus, hair pulling becomes associated with internal and external cues through conditioning and is maintained primarily by positive reinforcement. Hair-pulling urges that are reinforced by pulling intensify the need to pull, perpetuating the behavioral cycle.
A genetic link? Familial research has associated TTM with increased rates of obsessive-compulsive disorder (OCD) or other excessive habits—such as nail biting or skin picking—among first-degree relatives.6,9,10 Neuroimaging of persons with TTM has shown hyperactivity in the left cerebellum and right superior parietal lobe11 as well as possible structural abnormalities in the left putamen,12 left inferior frontal gyrus, and right cluneal cortex.13
These findings do not necessarily indicate pre-existing brain pathology, however. Perhaps TTM leads to changes in brain structure or function, or both TTM and the brain abnormalities may be caused by another as-yet-unknown variable.
Decreased pain sensitivity. Patients with TTM often report that hair pulling is not painful,2 though we suspect that persons without TTM would disagree and derive no pleasure from it. Changes in pain sensitivity may influence the reinforcing quality of pulling behavior. One possible mechanism for such alterations is upregulation of the endogenous opioid system; some intriguing evidence suggests that opioid receptor antagonists such as naltrexone may reduce pulling.14
Trichotillomania (TTM) is an impulse control disorder characterized by repetitive hair pulling,1 which typically emerges during adolescence. In a large clinical sample of adult hair pullers, mean age of onset was 13.2 Very-early onset (before age 5) may be a more benign form of TTM that tends to abate spontaneously and requires little or no therapeutic intervention.3
Despite the absence of body hair in prepubertal children, their pulling patterns are consistent with those of adults. The scalp is the most common pulling site, followed by eyelashes and eyebrows.4
Psychiatric comorbidity. In two studies evaluating psychiatric comorbidity in pediatric clinical samples, 60% to 70% of children and teens with TTM had at least one comorbid axis I disorder.5,6 Disruptive behavior disorders were most common in one study,6 whereas overanxious disorder was most common in the other.5 In a large clinical sample of adults with TTM, 51% met criteria for comorbid depression.2
Early identification and treatment of TTM are recommended because of the disorder’s distressing nature and social stigma. Early interventions also may help prevent later adult psychiatric comorbidity and functional impairment, although no studies have been done to demonstrate this benefit.7,8
Pain tolerance at the preferred pulling site has not been studied, however. For patients who feel pain from hair pulling, the pain itself may reinforce the behavior by distracting the individual from negative emotional or physiologic states.15
CASE CONTINUED: COUNTING THE WAYS
Jane and her parents agree that she pulls her hair 5 to 8 times daily, one hair at a time with her right index finger and thumb while doing homework or watching TV. The trigger, she says, is “an itch” on her scalp; “sometimes pulling relieves the itch.” She fails to resist pulling her hair 9 out of 10 times.
Table 1
Defining hair pulling: What to ask the pediatric patient
| Response description | How many times do you pull your hair each day? |
| How many hairs do you pull each time? | |
| From what body areas do you pull hair? | |
| What are all the steps involved in pulling (Touching the head before pulling? Pulling one hair at a time with the thumb and index finger)? | |
| Response detection | Under what circumstances do you sense the urge to pull? |
| How strong is the urge on a scale of 1 to 10, with 10 being the greatest intensity you ever felt? | |
| How do you try to resist and overcome the urge to pull? | |
| Precursors | External cues (Do you pull when you look at yourself in a mirror?) |
| Internal cues (Do you pull when you are nervous?) | |
| High-risk situations | What are you usually doing when you get the urge to pull? (reading, talking on the telephone, watching TV, using a computer, etc.) |
| Consequences that reinforce the behavior | Do you pull to reduce physical sensations (such as itching) at the site of pulling? |
| Does pulling relieve sadness or worry about problems at home or in school? | |
| Do you pull to create a more even hairline? |
Psychiatric comorbidity is common—if not the norm—in adults with TTM. Although axis I comorbidity is also seen in children and adolescents, their hair pulling is frequently uncomplicated. Jane meets criteria for TTM, as determined by the Trichotillomania Diagnostic Interview,16 but her history does not support a comorbid disorder. After discussing the diagnosis with Jane and her parents, the psychiatrist begins treatment with CBT alone.
MEDICATION OR CBT?
SSRIs. Literature on TTM pharmacotherapy is very limited and equivocal. Medications that have helped adults with TTM have been described,17 but the lack of a single, randomized, controlled trial in pediatric TTM severely limits treatment recommendations for children.
Selective serotonin reuptake inhibitors (SSRIs) have shown efficacy for treating anger and other impulse control problems but not for TTM. Some practitioners use SSRIs for TTM because of the belief that TTM is a variant of OCD. However, TTM may be maintained by positive reinforcement rather than compulsive tendencies and thus may not respond to SSRIs.
CBT. Evidence on CBT justifies cautious recommendations for pediatric TTM. In randomized trials, CBT reduced hair pulling in adults and was more effective than SSRIs or placebo.18,19
REDUCING THE URGE
Obtain detailed information about a child or adolescent’s hair-pulling episodes (Table 1), as recognizing triggers and reactions is vital to effective CBT. Explain to the patient that:
- the pleasure or satisfaction she derives from pulling reinforces the urge to pull
- she can reduce the urge by learning and using awareness training, stimulus control, and habit reversal (Table 2).
Awareness training involves patient self-monitoring to gain awareness of urges to pull and of pulling behavior. The child must become alert to every hair pulled and to response precursors, such as placing her hand on her head. For a patient such as Jane, a useful technique is to post reminders on the TV and school notebook and in the bedroom and bathroom—wherever pulling typically occurs.
A “PULLING CALENDAR”
Jane begins a daily “pulling calendar” in which she records each time she pulls a hair while watching TV or doing homework. She is asked to include the total number of hairs pulled and the intensity of the “itch to pull” on a scale of 1 to 10.
Stimulus control. Most patients can identify high-risk situations, such as time in the bathroom, talking on the phone, watching TV, driving, reading, or while falling asleep. Boredom, frustration, anxiety, and sadness may serve as pulling cues.
With stimulus control, the patient tries to reduce her ability to freely engage in pulling behavior in high-risk situations. For instance, you might encourage a child who pulls hairs while doing homework to stick Band-Aid®-type adhesive strips on her thumb and index finger tips before she starts studying as an impediment to gripping hairs. Such “speed bumps” may allow her to delay pulling and reach for tools that assist in habit reversal.
TREATMENT THAT APPEALS
Jane agrees to apply adhesive strips to her fingers and understands why. Because she is a fan of Peter Pan, we place Peter Pan stickers on her books and notebooks and on the TV remote control as reminders not to pull.
Table 2
CBT strategies to reduce the hair-pulling urge
| Awareness training | Increases patient’s awareness of pulling |
| Stimulus control | Establishes an environment less conducive to pulling |
| Habit reversal/ response | Patient develops alternate activities that provide competing positive reinforcement comparable to that gained from pulling |
Habit reversal and competing response procedures provide pleasurable physical stimulation as an alternative to pulling. The most effective methods engage the same motions as used in hair pulling. Examples include sculpting with clay, hulling sunflower seeds, and playing with Koosh® balls—small rubbery balls filled with a jellylike plasma and covered with hundreds of soft “tentacles.”
‘CALMER, HAPPIER’
We explain habit reversal to Jane and instruct her to use the Koosh ball a few times a day. She enjoys pulling its rubber strands, an action that uses the same muscles as hair pulling. Because she will need Koosh balls during all identified high-risk situations, we instruct her to buy one for her book bag and to leave one near the couch where she watches TV.
Over time, Jane reports a gradual decrease of hair pulling with the use of awareness training and stimulus control techniques. Using the Koosh ball (habit reversal) helps her improve. By the 10th week, Jane and her parents report a 70% decrease in hair pulling, based on the pulling calendar entries and other objective evidence of treatment response. All report feeling “calmer and happier.”
CONCLUSION
Cognitive and behavioral strategies are useful and safe for treating pediatric TTM. Enlisting the parents and patient in identifying problem situations and applying creative solutions may increase the chances of success.
Follow-up is important for maintaining new cognitive and behavioral patterns. We recommend that you see patients monthly for at least 3 months, depending on how the patient feels about additional sessions. We encourage families to call and report on progress or relapses. Booster CBT sessions can help deal with setbacks.
Related resources
- Trichotillomania Learning Center, Inc.; devoted to improving TTM understanding and providing access to treatments and support groups. www.trich.org. Accessed Sept. 17, 2004.
- Golomb RG, Vavrichek SM. The hair pulling “habit” and you: how to solve the trichotillomania puzzle (rev ed). Silver Spring, MD: Writer’s Cooperative of Greater Washington; 2000. Book for children and teenagers.
Drug brand names
- Fluoxetine • Prozac
- Naltrexone • Depade, ReVia
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
Preparation of this article was supported in part by a grant from the National Institute of Mental Health (MH61457).
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed., text rev. Washington, DC: American Psychiatric Association Press; 2000;674-7.
2. Christenson GA, Mackenzie TB, Mitchell JE. Characteristics of 60 adult chronic hairpullers. Am J Psychiatry 1991;148:365-70.
3. Swedo SE, Leonard HL. Trichotillomania: an obsessive compulsive spectrum disorder? Psychiatr Clin North Am 1992;15:777-90.
4. Reeve E. Hair pulling in children and adolescents. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Association Press, 1999;201-24.
5. Reeve EA, Bernstein GA, Christenson GA. Clinical characteristics and psychiatric comorbidity in children with trichotillomania. J Am Acad Child Adolesc Psychiatry 1992;31:132-8.
6. King RA, Scahill L, Vitulano LA, et al. Childhood trichotillomania: clinical phenomenology, comorbidity, and family genetics. J Am Acad Child Adolesc Psychiatry 1995;34:1451-9.
7. Franklin ME, Bux DA, Foa EB. Pediatric trichotillomania: conceptualization and treatment implications. In: Orvashel H, Faust J, Hersen M, eds. Handbook of conceptualization and treatment of child psychopathology. Oxford, UK: Elsevier Science; 2001;379-98.
8. Keuthen NJ, Franklin ME. Trichotillomania: psychopathology and treatment development [presentation]. Reno, NV: Association for the Advancement of Behavior Therapy annual meeting, 2002.
9. Bienvenu OJ, Samuels JF, Riddle MA, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: results from a family study. Biol Psychiatry 2000;48:287-93.
10. Lenane MC, Swedo SE, Rapoport JL, et al. Rates of obsessive compulsive disorder in first degree relatives of patients with trichotillomania: a research note. J Child Psychol Psychiatry 1992;33:925-33.
11. Swedo SE, Rapoport JL, Leonard HL, et al. Regional cerebral glucose metabolism of women in trichotillomania. Arch Gen Psychiatry 1991;48:828-33.
12. O’Sullivan RL, Rauch SL, Breiter HC, et al. Reduced basal ganglia volumes in trichotillomania measured via morphometric magnetic resonance imaging. Biol Psychiatry 1997;42:39-45.
13. Grachev ID. MRI-based morphometric topographic parcellation of human neocortex in trichotillomania. Psychiatry Clin Neurosci 1997;51:315-21.
14. Carrion VG. Naltrexone for the treatment of trichotillomania: a case report. J Clin Psychopharmacol 1995;15:444-5.
15. Christenson GA, Mansueto CS. Trichotillomania: descriptive characteristics and phenomenology. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Press, 1999;1-41.
16. Rothbaum BO, Ninan PT. The assessment of trichotillomania. Behav Res Ther 1994;32(6):651-62.
17. Lundt LP. Trichotillomania: a heads-up on severe cases. Current Psychiatry 2004;3(5):89-105.
18. Ninan PT, Rothbaum BO, Marsteller FA, et al. A placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillomania. J Clin Psychiatry. 2000;61:47-50.
19. Azrin NH, Nunn RG, Frantz SE. Treatment of hairpulling (trichotillomania): a comparative study of habit reversal and negative practice training. J Behav Ther Exp Psychiatry 1980;11:13-20.
Trichotillomania (TTM) is distressing to pediatric patients who pull their hair and to their parents who feel helpless to stop the destructive behavior. Hair-pulling with psychiatric comorbidity requires comprehensive assessment and treatment, but we have found that cognitive-behavioral therapy (CBT) alone can help children and adolescents with uncomplicated TTM.
This article describes a typical patient with adolescent-onset mild-to-moderate TTM and the three-step CBT approach—awareness training, stimulus control, and habit reversal—that we find effective in reducing pediatric hair pulling.
Jane, age 12, was referred to our clinic by her primary doctor after an 8-week trial of fluoxetine, 80 mg/d, failed to stop her hair pulling. Jane, who is right-handed, has been pulling her hair for 2 years, mostly in the right front scalp. Her shame over the hair loss makes her reluctant to participate in social activities. A dermatologist found no medical cause for her behavior, such as alopecia or folliculitis.
Jane’s parents say she has no history of a major mood disorder or anxiety. Her hair pulling causes significant “tension and stress” for all family members.
WHY DO PATIENTS PULL HAIR?
Cognitive-behavioral theory suggests that chronic TTM originates as a normal response to stress that often escapes personal and social awareness but gradually increases in frequency and severity (Box).1-8 Thus, hair pulling becomes associated with internal and external cues through conditioning and is maintained primarily by positive reinforcement. Hair-pulling urges that are reinforced by pulling intensify the need to pull, perpetuating the behavioral cycle.
A genetic link? Familial research has associated TTM with increased rates of obsessive-compulsive disorder (OCD) or other excessive habits—such as nail biting or skin picking—among first-degree relatives.6,9,10 Neuroimaging of persons with TTM has shown hyperactivity in the left cerebellum and right superior parietal lobe11 as well as possible structural abnormalities in the left putamen,12 left inferior frontal gyrus, and right cluneal cortex.13
These findings do not necessarily indicate pre-existing brain pathology, however. Perhaps TTM leads to changes in brain structure or function, or both TTM and the brain abnormalities may be caused by another as-yet-unknown variable.
Decreased pain sensitivity. Patients with TTM often report that hair pulling is not painful,2 though we suspect that persons without TTM would disagree and derive no pleasure from it. Changes in pain sensitivity may influence the reinforcing quality of pulling behavior. One possible mechanism for such alterations is upregulation of the endogenous opioid system; some intriguing evidence suggests that opioid receptor antagonists such as naltrexone may reduce pulling.14
Trichotillomania (TTM) is an impulse control disorder characterized by repetitive hair pulling,1 which typically emerges during adolescence. In a large clinical sample of adult hair pullers, mean age of onset was 13.2 Very-early onset (before age 5) may be a more benign form of TTM that tends to abate spontaneously and requires little or no therapeutic intervention.3
Despite the absence of body hair in prepubertal children, their pulling patterns are consistent with those of adults. The scalp is the most common pulling site, followed by eyelashes and eyebrows.4
Psychiatric comorbidity. In two studies evaluating psychiatric comorbidity in pediatric clinical samples, 60% to 70% of children and teens with TTM had at least one comorbid axis I disorder.5,6 Disruptive behavior disorders were most common in one study,6 whereas overanxious disorder was most common in the other.5 In a large clinical sample of adults with TTM, 51% met criteria for comorbid depression.2
Early identification and treatment of TTM are recommended because of the disorder’s distressing nature and social stigma. Early interventions also may help prevent later adult psychiatric comorbidity and functional impairment, although no studies have been done to demonstrate this benefit.7,8
Pain tolerance at the preferred pulling site has not been studied, however. For patients who feel pain from hair pulling, the pain itself may reinforce the behavior by distracting the individual from negative emotional or physiologic states.15
CASE CONTINUED: COUNTING THE WAYS
Jane and her parents agree that she pulls her hair 5 to 8 times daily, one hair at a time with her right index finger and thumb while doing homework or watching TV. The trigger, she says, is “an itch” on her scalp; “sometimes pulling relieves the itch.” She fails to resist pulling her hair 9 out of 10 times.
Table 1
Defining hair pulling: What to ask the pediatric patient
| Response description | How many times do you pull your hair each day? |
| How many hairs do you pull each time? | |
| From what body areas do you pull hair? | |
| What are all the steps involved in pulling (Touching the head before pulling? Pulling one hair at a time with the thumb and index finger)? | |
| Response detection | Under what circumstances do you sense the urge to pull? |
| How strong is the urge on a scale of 1 to 10, with 10 being the greatest intensity you ever felt? | |
| How do you try to resist and overcome the urge to pull? | |
| Precursors | External cues (Do you pull when you look at yourself in a mirror?) |
| Internal cues (Do you pull when you are nervous?) | |
| High-risk situations | What are you usually doing when you get the urge to pull? (reading, talking on the telephone, watching TV, using a computer, etc.) |
| Consequences that reinforce the behavior | Do you pull to reduce physical sensations (such as itching) at the site of pulling? |
| Does pulling relieve sadness or worry about problems at home or in school? | |
| Do you pull to create a more even hairline? |
Psychiatric comorbidity is common—if not the norm—in adults with TTM. Although axis I comorbidity is also seen in children and adolescents, their hair pulling is frequently uncomplicated. Jane meets criteria for TTM, as determined by the Trichotillomania Diagnostic Interview,16 but her history does not support a comorbid disorder. After discussing the diagnosis with Jane and her parents, the psychiatrist begins treatment with CBT alone.
MEDICATION OR CBT?
SSRIs. Literature on TTM pharmacotherapy is very limited and equivocal. Medications that have helped adults with TTM have been described,17 but the lack of a single, randomized, controlled trial in pediatric TTM severely limits treatment recommendations for children.
Selective serotonin reuptake inhibitors (SSRIs) have shown efficacy for treating anger and other impulse control problems but not for TTM. Some practitioners use SSRIs for TTM because of the belief that TTM is a variant of OCD. However, TTM may be maintained by positive reinforcement rather than compulsive tendencies and thus may not respond to SSRIs.
CBT. Evidence on CBT justifies cautious recommendations for pediatric TTM. In randomized trials, CBT reduced hair pulling in adults and was more effective than SSRIs or placebo.18,19
REDUCING THE URGE
Obtain detailed information about a child or adolescent’s hair-pulling episodes (Table 1), as recognizing triggers and reactions is vital to effective CBT. Explain to the patient that:
- the pleasure or satisfaction she derives from pulling reinforces the urge to pull
- she can reduce the urge by learning and using awareness training, stimulus control, and habit reversal (Table 2).
Awareness training involves patient self-monitoring to gain awareness of urges to pull and of pulling behavior. The child must become alert to every hair pulled and to response precursors, such as placing her hand on her head. For a patient such as Jane, a useful technique is to post reminders on the TV and school notebook and in the bedroom and bathroom—wherever pulling typically occurs.
A “PULLING CALENDAR”
Jane begins a daily “pulling calendar” in which she records each time she pulls a hair while watching TV or doing homework. She is asked to include the total number of hairs pulled and the intensity of the “itch to pull” on a scale of 1 to 10.
Stimulus control. Most patients can identify high-risk situations, such as time in the bathroom, talking on the phone, watching TV, driving, reading, or while falling asleep. Boredom, frustration, anxiety, and sadness may serve as pulling cues.
With stimulus control, the patient tries to reduce her ability to freely engage in pulling behavior in high-risk situations. For instance, you might encourage a child who pulls hairs while doing homework to stick Band-Aid®-type adhesive strips on her thumb and index finger tips before she starts studying as an impediment to gripping hairs. Such “speed bumps” may allow her to delay pulling and reach for tools that assist in habit reversal.
TREATMENT THAT APPEALS
Jane agrees to apply adhesive strips to her fingers and understands why. Because she is a fan of Peter Pan, we place Peter Pan stickers on her books and notebooks and on the TV remote control as reminders not to pull.
Table 2
CBT strategies to reduce the hair-pulling urge
| Awareness training | Increases patient’s awareness of pulling |
| Stimulus control | Establishes an environment less conducive to pulling |
| Habit reversal/ response | Patient develops alternate activities that provide competing positive reinforcement comparable to that gained from pulling |
Habit reversal and competing response procedures provide pleasurable physical stimulation as an alternative to pulling. The most effective methods engage the same motions as used in hair pulling. Examples include sculpting with clay, hulling sunflower seeds, and playing with Koosh® balls—small rubbery balls filled with a jellylike plasma and covered with hundreds of soft “tentacles.”
‘CALMER, HAPPIER’
We explain habit reversal to Jane and instruct her to use the Koosh ball a few times a day. She enjoys pulling its rubber strands, an action that uses the same muscles as hair pulling. Because she will need Koosh balls during all identified high-risk situations, we instruct her to buy one for her book bag and to leave one near the couch where she watches TV.
Over time, Jane reports a gradual decrease of hair pulling with the use of awareness training and stimulus control techniques. Using the Koosh ball (habit reversal) helps her improve. By the 10th week, Jane and her parents report a 70% decrease in hair pulling, based on the pulling calendar entries and other objective evidence of treatment response. All report feeling “calmer and happier.”
CONCLUSION
Cognitive and behavioral strategies are useful and safe for treating pediatric TTM. Enlisting the parents and patient in identifying problem situations and applying creative solutions may increase the chances of success.
Follow-up is important for maintaining new cognitive and behavioral patterns. We recommend that you see patients monthly for at least 3 months, depending on how the patient feels about additional sessions. We encourage families to call and report on progress or relapses. Booster CBT sessions can help deal with setbacks.
Related resources
- Trichotillomania Learning Center, Inc.; devoted to improving TTM understanding and providing access to treatments and support groups. www.trich.org. Accessed Sept. 17, 2004.
- Golomb RG, Vavrichek SM. The hair pulling “habit” and you: how to solve the trichotillomania puzzle (rev ed). Silver Spring, MD: Writer’s Cooperative of Greater Washington; 2000. Book for children and teenagers.
Drug brand names
- Fluoxetine • Prozac
- Naltrexone • Depade, ReVia
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
Preparation of this article was supported in part by a grant from the National Institute of Mental Health (MH61457).
Trichotillomania (TTM) is distressing to pediatric patients who pull their hair and to their parents who feel helpless to stop the destructive behavior. Hair-pulling with psychiatric comorbidity requires comprehensive assessment and treatment, but we have found that cognitive-behavioral therapy (CBT) alone can help children and adolescents with uncomplicated TTM.
This article describes a typical patient with adolescent-onset mild-to-moderate TTM and the three-step CBT approach—awareness training, stimulus control, and habit reversal—that we find effective in reducing pediatric hair pulling.
Jane, age 12, was referred to our clinic by her primary doctor after an 8-week trial of fluoxetine, 80 mg/d, failed to stop her hair pulling. Jane, who is right-handed, has been pulling her hair for 2 years, mostly in the right front scalp. Her shame over the hair loss makes her reluctant to participate in social activities. A dermatologist found no medical cause for her behavior, such as alopecia or folliculitis.
Jane’s parents say she has no history of a major mood disorder or anxiety. Her hair pulling causes significant “tension and stress” for all family members.
WHY DO PATIENTS PULL HAIR?
Cognitive-behavioral theory suggests that chronic TTM originates as a normal response to stress that often escapes personal and social awareness but gradually increases in frequency and severity (Box).1-8 Thus, hair pulling becomes associated with internal and external cues through conditioning and is maintained primarily by positive reinforcement. Hair-pulling urges that are reinforced by pulling intensify the need to pull, perpetuating the behavioral cycle.
A genetic link? Familial research has associated TTM with increased rates of obsessive-compulsive disorder (OCD) or other excessive habits—such as nail biting or skin picking—among first-degree relatives.6,9,10 Neuroimaging of persons with TTM has shown hyperactivity in the left cerebellum and right superior parietal lobe11 as well as possible structural abnormalities in the left putamen,12 left inferior frontal gyrus, and right cluneal cortex.13
These findings do not necessarily indicate pre-existing brain pathology, however. Perhaps TTM leads to changes in brain structure or function, or both TTM and the brain abnormalities may be caused by another as-yet-unknown variable.
Decreased pain sensitivity. Patients with TTM often report that hair pulling is not painful,2 though we suspect that persons without TTM would disagree and derive no pleasure from it. Changes in pain sensitivity may influence the reinforcing quality of pulling behavior. One possible mechanism for such alterations is upregulation of the endogenous opioid system; some intriguing evidence suggests that opioid receptor antagonists such as naltrexone may reduce pulling.14
Trichotillomania (TTM) is an impulse control disorder characterized by repetitive hair pulling,1 which typically emerges during adolescence. In a large clinical sample of adult hair pullers, mean age of onset was 13.2 Very-early onset (before age 5) may be a more benign form of TTM that tends to abate spontaneously and requires little or no therapeutic intervention.3
Despite the absence of body hair in prepubertal children, their pulling patterns are consistent with those of adults. The scalp is the most common pulling site, followed by eyelashes and eyebrows.4
Psychiatric comorbidity. In two studies evaluating psychiatric comorbidity in pediatric clinical samples, 60% to 70% of children and teens with TTM had at least one comorbid axis I disorder.5,6 Disruptive behavior disorders were most common in one study,6 whereas overanxious disorder was most common in the other.5 In a large clinical sample of adults with TTM, 51% met criteria for comorbid depression.2
Early identification and treatment of TTM are recommended because of the disorder’s distressing nature and social stigma. Early interventions also may help prevent later adult psychiatric comorbidity and functional impairment, although no studies have been done to demonstrate this benefit.7,8
Pain tolerance at the preferred pulling site has not been studied, however. For patients who feel pain from hair pulling, the pain itself may reinforce the behavior by distracting the individual from negative emotional or physiologic states.15
CASE CONTINUED: COUNTING THE WAYS
Jane and her parents agree that she pulls her hair 5 to 8 times daily, one hair at a time with her right index finger and thumb while doing homework or watching TV. The trigger, she says, is “an itch” on her scalp; “sometimes pulling relieves the itch.” She fails to resist pulling her hair 9 out of 10 times.
Table 1
Defining hair pulling: What to ask the pediatric patient
| Response description | How many times do you pull your hair each day? |
| How many hairs do you pull each time? | |
| From what body areas do you pull hair? | |
| What are all the steps involved in pulling (Touching the head before pulling? Pulling one hair at a time with the thumb and index finger)? | |
| Response detection | Under what circumstances do you sense the urge to pull? |
| How strong is the urge on a scale of 1 to 10, with 10 being the greatest intensity you ever felt? | |
| How do you try to resist and overcome the urge to pull? | |
| Precursors | External cues (Do you pull when you look at yourself in a mirror?) |
| Internal cues (Do you pull when you are nervous?) | |
| High-risk situations | What are you usually doing when you get the urge to pull? (reading, talking on the telephone, watching TV, using a computer, etc.) |
| Consequences that reinforce the behavior | Do you pull to reduce physical sensations (such as itching) at the site of pulling? |
| Does pulling relieve sadness or worry about problems at home or in school? | |
| Do you pull to create a more even hairline? |
Psychiatric comorbidity is common—if not the norm—in adults with TTM. Although axis I comorbidity is also seen in children and adolescents, their hair pulling is frequently uncomplicated. Jane meets criteria for TTM, as determined by the Trichotillomania Diagnostic Interview,16 but her history does not support a comorbid disorder. After discussing the diagnosis with Jane and her parents, the psychiatrist begins treatment with CBT alone.
MEDICATION OR CBT?
SSRIs. Literature on TTM pharmacotherapy is very limited and equivocal. Medications that have helped adults with TTM have been described,17 but the lack of a single, randomized, controlled trial in pediatric TTM severely limits treatment recommendations for children.
Selective serotonin reuptake inhibitors (SSRIs) have shown efficacy for treating anger and other impulse control problems but not for TTM. Some practitioners use SSRIs for TTM because of the belief that TTM is a variant of OCD. However, TTM may be maintained by positive reinforcement rather than compulsive tendencies and thus may not respond to SSRIs.
CBT. Evidence on CBT justifies cautious recommendations for pediatric TTM. In randomized trials, CBT reduced hair pulling in adults and was more effective than SSRIs or placebo.18,19
REDUCING THE URGE
Obtain detailed information about a child or adolescent’s hair-pulling episodes (Table 1), as recognizing triggers and reactions is vital to effective CBT. Explain to the patient that:
- the pleasure or satisfaction she derives from pulling reinforces the urge to pull
- she can reduce the urge by learning and using awareness training, stimulus control, and habit reversal (Table 2).
Awareness training involves patient self-monitoring to gain awareness of urges to pull and of pulling behavior. The child must become alert to every hair pulled and to response precursors, such as placing her hand on her head. For a patient such as Jane, a useful technique is to post reminders on the TV and school notebook and in the bedroom and bathroom—wherever pulling typically occurs.
A “PULLING CALENDAR”
Jane begins a daily “pulling calendar” in which she records each time she pulls a hair while watching TV or doing homework. She is asked to include the total number of hairs pulled and the intensity of the “itch to pull” on a scale of 1 to 10.
Stimulus control. Most patients can identify high-risk situations, such as time in the bathroom, talking on the phone, watching TV, driving, reading, or while falling asleep. Boredom, frustration, anxiety, and sadness may serve as pulling cues.
With stimulus control, the patient tries to reduce her ability to freely engage in pulling behavior in high-risk situations. For instance, you might encourage a child who pulls hairs while doing homework to stick Band-Aid®-type adhesive strips on her thumb and index finger tips before she starts studying as an impediment to gripping hairs. Such “speed bumps” may allow her to delay pulling and reach for tools that assist in habit reversal.
TREATMENT THAT APPEALS
Jane agrees to apply adhesive strips to her fingers and understands why. Because she is a fan of Peter Pan, we place Peter Pan stickers on her books and notebooks and on the TV remote control as reminders not to pull.
Table 2
CBT strategies to reduce the hair-pulling urge
| Awareness training | Increases patient’s awareness of pulling |
| Stimulus control | Establishes an environment less conducive to pulling |
| Habit reversal/ response | Patient develops alternate activities that provide competing positive reinforcement comparable to that gained from pulling |
Habit reversal and competing response procedures provide pleasurable physical stimulation as an alternative to pulling. The most effective methods engage the same motions as used in hair pulling. Examples include sculpting with clay, hulling sunflower seeds, and playing with Koosh® balls—small rubbery balls filled with a jellylike plasma and covered with hundreds of soft “tentacles.”
‘CALMER, HAPPIER’
We explain habit reversal to Jane and instruct her to use the Koosh ball a few times a day. She enjoys pulling its rubber strands, an action that uses the same muscles as hair pulling. Because she will need Koosh balls during all identified high-risk situations, we instruct her to buy one for her book bag and to leave one near the couch where she watches TV.
Over time, Jane reports a gradual decrease of hair pulling with the use of awareness training and stimulus control techniques. Using the Koosh ball (habit reversal) helps her improve. By the 10th week, Jane and her parents report a 70% decrease in hair pulling, based on the pulling calendar entries and other objective evidence of treatment response. All report feeling “calmer and happier.”
CONCLUSION
Cognitive and behavioral strategies are useful and safe for treating pediatric TTM. Enlisting the parents and patient in identifying problem situations and applying creative solutions may increase the chances of success.
Follow-up is important for maintaining new cognitive and behavioral patterns. We recommend that you see patients monthly for at least 3 months, depending on how the patient feels about additional sessions. We encourage families to call and report on progress or relapses. Booster CBT sessions can help deal with setbacks.
Related resources
- Trichotillomania Learning Center, Inc.; devoted to improving TTM understanding and providing access to treatments and support groups. www.trich.org. Accessed Sept. 17, 2004.
- Golomb RG, Vavrichek SM. The hair pulling “habit” and you: how to solve the trichotillomania puzzle (rev ed). Silver Spring, MD: Writer’s Cooperative of Greater Washington; 2000. Book for children and teenagers.
Drug brand names
- Fluoxetine • Prozac
- Naltrexone • Depade, ReVia
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
Preparation of this article was supported in part by a grant from the National Institute of Mental Health (MH61457).
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed., text rev. Washington, DC: American Psychiatric Association Press; 2000;674-7.
2. Christenson GA, Mackenzie TB, Mitchell JE. Characteristics of 60 adult chronic hairpullers. Am J Psychiatry 1991;148:365-70.
3. Swedo SE, Leonard HL. Trichotillomania: an obsessive compulsive spectrum disorder? Psychiatr Clin North Am 1992;15:777-90.
4. Reeve E. Hair pulling in children and adolescents. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Association Press, 1999;201-24.
5. Reeve EA, Bernstein GA, Christenson GA. Clinical characteristics and psychiatric comorbidity in children with trichotillomania. J Am Acad Child Adolesc Psychiatry 1992;31:132-8.
6. King RA, Scahill L, Vitulano LA, et al. Childhood trichotillomania: clinical phenomenology, comorbidity, and family genetics. J Am Acad Child Adolesc Psychiatry 1995;34:1451-9.
7. Franklin ME, Bux DA, Foa EB. Pediatric trichotillomania: conceptualization and treatment implications. In: Orvashel H, Faust J, Hersen M, eds. Handbook of conceptualization and treatment of child psychopathology. Oxford, UK: Elsevier Science; 2001;379-98.
8. Keuthen NJ, Franklin ME. Trichotillomania: psychopathology and treatment development [presentation]. Reno, NV: Association for the Advancement of Behavior Therapy annual meeting, 2002.
9. Bienvenu OJ, Samuels JF, Riddle MA, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: results from a family study. Biol Psychiatry 2000;48:287-93.
10. Lenane MC, Swedo SE, Rapoport JL, et al. Rates of obsessive compulsive disorder in first degree relatives of patients with trichotillomania: a research note. J Child Psychol Psychiatry 1992;33:925-33.
11. Swedo SE, Rapoport JL, Leonard HL, et al. Regional cerebral glucose metabolism of women in trichotillomania. Arch Gen Psychiatry 1991;48:828-33.
12. O’Sullivan RL, Rauch SL, Breiter HC, et al. Reduced basal ganglia volumes in trichotillomania measured via morphometric magnetic resonance imaging. Biol Psychiatry 1997;42:39-45.
13. Grachev ID. MRI-based morphometric topographic parcellation of human neocortex in trichotillomania. Psychiatry Clin Neurosci 1997;51:315-21.
14. Carrion VG. Naltrexone for the treatment of trichotillomania: a case report. J Clin Psychopharmacol 1995;15:444-5.
15. Christenson GA, Mansueto CS. Trichotillomania: descriptive characteristics and phenomenology. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Press, 1999;1-41.
16. Rothbaum BO, Ninan PT. The assessment of trichotillomania. Behav Res Ther 1994;32(6):651-62.
17. Lundt LP. Trichotillomania: a heads-up on severe cases. Current Psychiatry 2004;3(5):89-105.
18. Ninan PT, Rothbaum BO, Marsteller FA, et al. A placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillomania. J Clin Psychiatry. 2000;61:47-50.
19. Azrin NH, Nunn RG, Frantz SE. Treatment of hairpulling (trichotillomania): a comparative study of habit reversal and negative practice training. J Behav Ther Exp Psychiatry 1980;11:13-20.
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed., text rev. Washington, DC: American Psychiatric Association Press; 2000;674-7.
2. Christenson GA, Mackenzie TB, Mitchell JE. Characteristics of 60 adult chronic hairpullers. Am J Psychiatry 1991;148:365-70.
3. Swedo SE, Leonard HL. Trichotillomania: an obsessive compulsive spectrum disorder? Psychiatr Clin North Am 1992;15:777-90.
4. Reeve E. Hair pulling in children and adolescents. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Association Press, 1999;201-24.
5. Reeve EA, Bernstein GA, Christenson GA. Clinical characteristics and psychiatric comorbidity in children with trichotillomania. J Am Acad Child Adolesc Psychiatry 1992;31:132-8.
6. King RA, Scahill L, Vitulano LA, et al. Childhood trichotillomania: clinical phenomenology, comorbidity, and family genetics. J Am Acad Child Adolesc Psychiatry 1995;34:1451-9.
7. Franklin ME, Bux DA, Foa EB. Pediatric trichotillomania: conceptualization and treatment implications. In: Orvashel H, Faust J, Hersen M, eds. Handbook of conceptualization and treatment of child psychopathology. Oxford, UK: Elsevier Science; 2001;379-98.
8. Keuthen NJ, Franklin ME. Trichotillomania: psychopathology and treatment development [presentation]. Reno, NV: Association for the Advancement of Behavior Therapy annual meeting, 2002.
9. Bienvenu OJ, Samuels JF, Riddle MA, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: results from a family study. Biol Psychiatry 2000;48:287-93.
10. Lenane MC, Swedo SE, Rapoport JL, et al. Rates of obsessive compulsive disorder in first degree relatives of patients with trichotillomania: a research note. J Child Psychol Psychiatry 1992;33:925-33.
11. Swedo SE, Rapoport JL, Leonard HL, et al. Regional cerebral glucose metabolism of women in trichotillomania. Arch Gen Psychiatry 1991;48:828-33.
12. O’Sullivan RL, Rauch SL, Breiter HC, et al. Reduced basal ganglia volumes in trichotillomania measured via morphometric magnetic resonance imaging. Biol Psychiatry 1997;42:39-45.
13. Grachev ID. MRI-based morphometric topographic parcellation of human neocortex in trichotillomania. Psychiatry Clin Neurosci 1997;51:315-21.
14. Carrion VG. Naltrexone for the treatment of trichotillomania: a case report. J Clin Psychopharmacol 1995;15:444-5.
15. Christenson GA, Mansueto CS. Trichotillomania: descriptive characteristics and phenomenology. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Press, 1999;1-41.
16. Rothbaum BO, Ninan PT. The assessment of trichotillomania. Behav Res Ther 1994;32(6):651-62.
17. Lundt LP. Trichotillomania: a heads-up on severe cases. Current Psychiatry 2004;3(5):89-105.
18. Ninan PT, Rothbaum BO, Marsteller FA, et al. A placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillomania. J Clin Psychiatry. 2000;61:47-50.
19. Azrin NH, Nunn RG, Frantz SE. Treatment of hairpulling (trichotillomania): a comparative study of habit reversal and negative practice training. J Behav Ther Exp Psychiatry 1980;11:13-20.
Germ warfare: Arm young patients to fight obsessive-compulsive disorder
Adam, age 10, is extremely distressed at school. Because of obsessional contamination fears, he avoids contact with other children and refuses to eat in the cafeteria. He washes his hands 20 times per day and changes his clothes at least three times daily.
His primary obsessions involve contact with bodily fluids—such as saliva or feces—and excessive concerns that this contamination would cause him serious illness.
Adam’s parents say their son’s worries about dirt and germs began when he entered kindergarten. They sought treatment for him 2 years ago, and he has been receiving outpatient psychotherapy since then. They have brought him to an anxiety disorders specialty clinic for evaluation because his obsessive-compulsive symptoms are worsening,
When treating patients such as Adam, our approach is to use cognitive-behavioral therapy (CBT) and adjunctive drug therapies to relieve their symptoms and help them reclaim their lives. Diagnosis of pediatric OCD is often delayed, and few children receive state-of-the-art treatment.1 The good news, however, is that skillful CBT combined, as needed, with medication is highly effective.
Although family dysfunction does not cause OCD, families affect and are affected by OCD. Control struggles over the child’s rituals are common, as are differences of opinion about how to cope with OCD symptoms. It is important to address these issues early in treatment, as helping the family combat the disorder—rather than each other—is crucial to effective treatment.
Parents need to know that neither they nor the child are to blame. OCD is a neurobehavioral illness, and treatment is most effective when the patient, therapist, and family are aligned to combat it. Families are often entangled in the child’s OCD symptoms, and disentangling them by eliminating their role in ritualizing (such as giving excessive reassurance) is important to address in therapy.
Scaling family involvement is part of the “art” of CBT, and it will remain so until empiric studies determine the family’s role in the treatment plan.2
‘Contaminated’ mother.
Adam becomes distressed when he comes in contact with objects that have been touched by others (such as doorknobs). He is especially anxious when these items are associated with public bathrooms or sick people.
Adam’s mother is a family physician who has daily patient contact. In the last 6 months, Adam has insisted that his mother change her work clothes before she enters his room, touches him, prepares his food, or handles his possessions.
As in Adam’s case, the family often gets caught up in a child or adolescent’s obsessive rituals (Box 1).2 After a detailed discussion with Adam and his parents and because his symptoms were severe, we recommended combined treatment with sertraline and CBT. Adam was willing to consider CBT and medication because he recognized that he was having increasing difficulty doing the things he wanted to do in school and at home.
SNAPSHOT OF PEDIATRIC OCD
Approximately 1 in 200 children and adolescents suffer from clinically significant OCD.3 They experience intrusive thoughts, urges, or images to which they respond with dysphoria-reducing behaviors or rituals.
Common obsessions include:
- fear of dirt or germs
- fear of harm to oneself or someone else
- or a persistent need to complete something “just so.”
Corresponding compulsions include hand washing, checking, and repeating or arranging.
OCD appears more common in boys than in girls. Onset occurs in two modes: first at age 9 for boys and age 12 for girls, followed by a second mode in late adolescence or early adulthood.
Two practice guidelines address OCD in youth: an independent expert consensus guideline4 and the American Academy of Child and Adolescent Psychiatry’s practice parameters for OCD.5
For uncomplicated OCD, these guidelines recommend CBT as first-line treatment. If symptoms do not respond after six to eight sessions, a selective serotonin reuptake inhibitor (SSRI) is added to CBT.
For complicated OCD, medication is considered an appropriate initial treatment. Complicated OCD includes patients who:
- display severe symptoms—such as with scores >30 on the Children’s Yale-Brown Obsessive Compulsive Scale (CY-BOCS)
- or have comorbidity such as depression or panic disorder that is likely to complicate treatment.
KEYS TO SUCCESSFUL TREATMENT
OCD is remarkably resistant to insight-oriented psychotherapy and other nondirective therapies. The benefits of CBT, however, are well-established, with reported response rates of >80% in pilot studies.6,7 Although confirming studies have yet to be conducted, successful CBT for pediatric OCD appears to include four elements (Table 1).
Exposure and response prevention (EX/RP) is central to psychosocial treatment of OCD.7,8 In specialized centers, exposure can be applied intensively (three to five times per week for 3 to 4 weeks).9 In most practices, however, exposure is more gradual (weekly for 12 to 20 weeks). With repeated exposure, the child’s anxiety decreases until he or she no longer fears contact with the targeted stimuli.8,10
Not ‘misbehavior.’ Children—and less commonly adolescents—with this disorder may not view their obsessions as senseless or their compulsions as excessive. Even when insight is clearly present, young OCD patients often hide their symptoms because of embarrassment or fear of being punished for their behavior.
Response predictors. A key to CBT in children or adolescents is that they come to see obsessions and compulsions as symptoms of an illness. The symptoms, therefore, require a skillfully applied “antidote,” as taught by the clinician and implemented by the child, family, and others on the child’s behalf. Besides overt rituals, three response predictors include the patient’s:
- desire to eliminate symptoms
- ability to monitor and report symptoms
- willingness to cooperate with treatment.
Table 1
Pediatric OCD: 4 keys to successful cognitive therapy
| Treat OCD as a neurobehavioral disorder, not a misbehavior |
| Help the child develop a “tool kit” to manage dysphoria and faulty thinking |
| Expose the patient to anxiety-producing stimuli until he or she becomes desensitized and can refrain from the usual compulsive responses (exposure and response prevention) |
| Educate family members and school personnel |
CBT may be difficult with patients younger than age 6 and will invariably involve training the parents to serve as “coaches;” a CBT protocol for patients ages 4 to 6 is under investigation (H. Leonard, personal communication). CBT also can be adapted for patients with intellectual deficits.11
A ‘tool kit.’ Successful exposure therapy for OCD relies on equipping children and adolescents with the knowledge and skills to battle the illness. They often have tried unsuccessfully to resist OCD’s compulsions and must be convinced that EX/RP techniques will work. Using a “tool kit” concept reminds young patients that they have the implements they need to combat OCD (Table 2).
A ‘germ ladder’ and ‘fear thermometer.’
Adam’s tools include a stimulus hierarchy called a “germ ladder,” which the therapist and Adam create collaboratively. It ranks stimuli from low (his own doorknob) to very high (public toilets, sinks, and door handles).
As part of his treatment, Adam begins to touch objects in his room and house while voluntarily refraining from ritualizing. He uses another tool—a fear thermometer—to record his distress level on a scale of 1 to 10 during and after these exposures.
Adam discovers that when he comes into contact with less-threatening items his fear ratings typically return to baseline within 20 to 30 minutes. This insight helps him modify his assessment of the risk they pose.
Table 2
OCD ‘tool box’ can help patients build new behaviors
| Tool | Function |
|---|---|
| Training in exposure response prevention (EX/RP) therapy | Helps patients learn to confront rather than avoid feared stimuli |
| ‘Fear thermometer’ | Enables patients to express the intensity of their distress on a scale of 1 (lowest) to 10 (highest) |
| Positive self-statements | Teaches patients to use statements such as “I can do this” and “I’m the boss of OCD now” to build confidence that they can control their response to feared stimuli |
During office visits, he confronts similar items around the clinic, with the therapist providing encouragement and instruction for additional exposure homework. Eventually Adam works on the clinic’s public bathroom, which he perceived to be relatively clean but less so than his own bathroom. After fear in response to this bathroom is reduced, the therapist and Adam graduate to more-public facilities, such as the bathrooms at Adam’s pool and the local train station.
Exposure therapy. EX/RP is most successful when the child—rather than the therapist—chooses exposure targets from a hierarchy of fears,2 particularly when the list includes behaviors the child is resisting. In a collaborative spirit, the child takes the lead in placing items on the hierarchy and deciding when to confront them.
The therapist and child revise the hierarchy periodically, which demonstrates progress and allows them to add items as the child overcomes fears that cause less distress.
Reducing need for reassurance.
Adam has a habit of repeatedly asking his mother whether contact with particular objects in public is risky. By the third treatment session, he and the therapist agree that he will try to refrain from asking such questions.
His mother, in turn, is asked to reiterate the rationale for response prevention whenever Adam slips. She will offer encouragement and support without answering “OCD’s questions.”
ADJUNCTIVE DRUG THERAPY
While Adam is working with the behavioral therapist to reduce his anxieties and need for reassurance, he is also receiving gradually increasing dosages of sertraline. As discussed, he is considered a candidate for CBT plus medication because of his symptoms are severe. Drug treatment can benefit most pediatric OCD patients.
SSRIs. Two SSRIs are approved for pediatric OCD—fluvoxamine for ages 8 to 18 and sertraline for ages 6 to 18. Most SSRIs are likely effective for OCD in youth (Table 3),12-14 although reports have suggested a link between paroxetine and suicidality in pediatric patients. Other options may be more suitable choices unless further evidence supports the use of paroxetine as a first- or second-line agent for pediatric OCD.
Clomipramine—a nonselective tricyclic—was the first medication studied in treating OCD in children and adolescents. It is now usually considered only after two or three failed SSRI trials because of its potential for cardiac toxicity.15-17
Table 3
Suggested dosages (mg/d) for drug therapy of pediatric OCD
| Drug | Usual starting dosage | Approximate mean dosage* | Typical range | Usual maximum dosage |
|---|---|---|---|---|
| Citalopram | 20 | 40 | 20 to 60 | 80 |
| Clomipramine | 50 | 150 | 200 | 300 |
| Escitalopram | 5 | 10 | 10 to 20 | 30 |
| Fluoxetine | 20 | 40 | 40 to 60 | 80 |
| Fluvoxamine | 50 | 175 | 150 to 250 | 300 |
| Sertraline | 50 | 125 | 150 | 225 |
| *Mean dosage derived from registration trials, expert recommendation, and the authors’ clinical experience | ||||
Dosing. Fixed-dose studies suggest that dosing schedules for OCD are similar to those used for depression. For example, sertraline, 50 mg/d, or fluoxetine, 20 mg/d, are as effective as higher dosages.18
The common misconception that OCD requires higher dosages likely results from:
- increasing the dosage too early in the time-response window for a drug effect to emerge
- giving medication without concomitant exposure therapy.19
Delayed response. Although many patients respond early to an SSRI, others do not respond until 8 or even 12 weeks of treatment at therapeutic dosages. It often takes 3 to 4 weeks for evidence of benefit to emerge, so wait at least 3 weeks between dosage increases. Maintain therapeutic dosages at least 6 to 8 weeks before changing agents or beginning augmentation therapy.
Two-barrel approach.
In treating Adam, we began with sertraline, using a flexible titration schedule keyed to whether he experienced OCD symptom remission.
The starting dosage of 50 mg was titrated to 150 mg over 8 weeks while he was receiving behavioral therapy. We made adjustments with a time-response window of 2 to 3 weeks, allowing us to observe a response to each dosage escalation.
Adam’s OCD symptoms responded well to CBT plus sertraline. The maximum drug effect helped him confront the most difficult EX/RP tasks at the top of his stimulus hierarchy, which he attacked near the end of treatment.
Lessons learned. Multicenter trials have taught important lessons about drug therapy for OCD:
- OCD patients experience little or no placebo effect, unlike patients with depression.
- Clinical effects may appear as early as 2 to 3 weeks after medications are started and plateau at 10 to 12 weeks.
- Partial response is the rule; SSRIs reduce OCD symptoms by about 30%—which correlates with “moderately” to “markedly” improved ratings on patient satisfaction measures.
- Side effects and magnitude of improvement are comparable in pediatric and adult medication trials.
In some children, OCD or tic symptoms arise from or are exacerbated by group A beta hemolytic streptococcal infection (GABHS), which has been labeled pediatric autoimmune neuropsychiatric disorders associated with Streptococcus (PANDAS).21 Obsessive-compulsive symptoms are not uncommon in pediatric patients with Sydenham’s chorea, a neurologic variant of rheumatic fever. OCD is far more common in patients with rheumatic fever when chorea is present.
Acute-onset or dramatic exacerbation of OCD or tic symptoms should prompt investigation of GABHS infection. Immunomodulatory treatments—including antibiotics, plasmapheresis, or IV immunoglobulin G—may benefit some patients.22
MANAGING RESISTANT OCD
Adequate SSRI monotherapy trials fail to relieve OCD symptoms in one-third of patients. Some patients benefit from combination therapy—such as an SSRI plus risperidone—especially when comorbid schizotypal personality disorder or a tic-spectrum disorder is present.
Drug switching or augmentation trials often produce only partial response and cause unnecessary suffering. A more effective strategy for many patients is to augment drug treatment with CBT until symptoms normalize.
On the other hand, augmentation is appropriate when nonresponse or partial response to SSRI monotherapy leaves a patient clinically symptomatic and functionally impaired. Clonazepam, clomipramine, and the amino acid L-tryptophan have been used successfully. Lithium and buspirone also have been tried but seem not to be effective in controlled studies in adults and anecdotal experience in youth.
When augmenting an SSRI, adding clomipramine, 25 to 50 mg/d, is a reasonable choice. However, fluoxetine or paroxetine can inhibit clomipramine metabolism by cytochrome P-450 (CYP) 2D6, with potential for cardiac arrhythmias or seizures. Sertraline or fluvoxamine are less likely to elevate clomipramine levels.20 Fluvoxamine may be the most compatible SSRI with clomipramine because it inhibits CYP 1A2—the enzyme that demethylates clomipramine to its inactive desmethyl metabolite—thereby preserving more of the active parent compound.
Clinical evidence suggests that augmentation’s success may depend in part on a patient’s comorbidities. For example, clonazepam may be particularly helpful for children with comorbid panic symptoms.
MAINTENANCE THERAPY
We typically provide 14 weekly CBT sessions, followed by monthly contacts for a few months to ensure than a patient’s gains are maintained. Standard procedure with drug therapy is to continue maintenance treatment for up to 1 year, although some have suggested continuing maintenance treatment indefinitely.
Related resources
- Chansky TE. Freeing your child from obsessive compulsive disorder: A powerful, practical program for parents of children and adolescents. New York: Crown Publishing Group, 2001.
- March JS, Mulle K. OCD in children and adolescents: A cognitive behavioral treatment manual. New York: Guilford Press, 1998.
- Moritz EK, Jablonsky J. Blink, blink, clop, clop: Why do we do things we can’t stop? An OCD storybook. Newton, MA: Professional Books, Inc, 1998.
- Wagner AP. Up and down the worry hill: A children’s book about obsessive compulsive disorder and its treatment. Rochester, NY: Lighthouse Press, Inc. 2000.
Drug brand names
- Buspirone • BuSpar
- Citalopram • Celexa
- Clomipramine • Anafranil
- Clonazepam • Klonopin
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Paroxetine • Paxil
- Risperidone • Risperdal
- Sertaline • Zoloft
Disclosure
Dr. March receives research support from Pfizer Inc., Eli Lilly and Co., and Wyeth Pharmaceuticals and is a speaker for and/or consultant to Solvay Pharmaceuticals, Pfizer Inc., GlaxoSmithKline, Wyeth Pharmaceuticals, Novartis Pharmaceuticals Corp., and Shire Pharmaceuticals Group.
Dr. Franklin and Dr. Foa report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
Preparation of this manuscript was supported in part by National Institute of Mental Health grants 1 K24 MHO1557 and 1 R10 MH55121 to Dr. March and by contributions from the Robert and Sarah Gorrell family and the Lupin Family Foundation.
1. Kendall PC, Southam-Gerow MA. Issues in the transportability of treatment: the case of anxiety disorders in youths. J Consult Clin Psychol 1995;63(5):702-8.
2. March J, Mulle K. OCD in children and adolescents: A cognitive-behavioral treatment manual. New York: Guilford Press, 1998.
3. Flament MF, Whitaker A, Rapoport JL, et al. Obsessive compulsive disorder in adolescence: an epidemiological study. J Am Acad Child Adolesc Psychiatry 1988;27(6):764-71.
4. March J, Frances A, Kahn D, Carpenter D. Expert consensus guidelines: treatment of obsessive-compulsive disorder. J Clin Psychiatry 1997;58(suppl 4):1-72.
5. King R, Leonard H, March J. Practice parameters for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 1998;37(10, suppl):27-45.
6. March JS. Cognitive-behavioral psychotherapy for children and adolescents with OCD: a review and recommendations for treatment. J Am Acad Child Adolesc Psychiatry 1995;34(1):7-18.
7. Franklin ME, Kozak MJ, Cashman LA, et al. Cognitive-behavioral treatment of pediatric obsessive-compulsive disorder: an open clinical trial. J Am Acad Child Adolesc Psychiatry 1998;37(4):412-19.
8. March JS, Mulle K, Herbel B. Behavioral psychotherapy for children and adolescents with obsessive-compulsive disorder: an open trial of a new protocol-driven treatment package. J Am Acad Child Adolesc Psychiatry 1994;33(3):333-41.
9. Franklin ME, Tolin DF, March JS, Foa EB. Treatment of pediatric obsessive-compulsive disorder: A case example of intensive cognitive-behavioral therapy involving exposure and ritual prevention. Cognit Behav Pract 2001;8(4):297-304.
10. March J, Mulle K. Manualized cognitive-behavioral psychotherapy for obsessive-compulsive disorder in childhood: a preliminary single case study. J Anxiety Disord 1995;9(2):175-84.
11. Franklin ME, Rynn M, March JS, Foa EB. Obsessive-compulsive disorder. In: Hersen M (ed). Clinical behavior therapy: adults and children. New York: John Wiley & Sons, 2002;276-303.
12. March JS, Biederman J, Wolkow R, et al. Sertraline in children and adolescents with obsessive-compulsive disorder: a multicenter randomized controlled trial. JAMA 1998;280(20):1752-6.
13. Riddle MA, Reeve EA, Yaryura-Tobias JA, et al. Fluvoxamine for children and adolescents with obsessive-compulsive disorder: a randomized, controlled, multicenter trial. J Am Acad Child Adolesc Psychiatry 2001;40(2):222-9.
14. Geller DA, Hoog SL, Heiligenstein JH, et al. Fluoxetine treatment for obsessive-compulsive disorder in children and adolescents: a placebo-controlled clinical trial. J Am Acad Child Adolesc Psychiatry 2001;40(7):773-9.
15. Leonard H, March J, Rickler K, Allen A. Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6):725-36.
16. DeVeaugh-Geiss J, Moroz G, Biederman J, et al. Clomipramine hydrochloride in childhood and adolescent obsessive-compulsive disorder—a multicenter trial. J Am Acad Child Adolesc Psychiatry 1992;31(1):45-9.
17. Wilens TE, Biederman J, March JS, et al. Absence of cardiovascular adverse effects of sertraline in children and adolescents. J Am Acad Child Adolesc Psychiatry 1999;38(5):573-7.
18. Greist JH, Jefferson JW, Kobak KA, et al. A 1-year double-blind placebo-controlled fixed dose study of sertraline in the treatment of obsessive-compulsive disorder. Int Clin Psychopharmacol 1995;10(2):57-65.
19. Marks IM. Drug versus behavioral treatment of obsessive-compulsive disorder. Biolog Psychiatry 1990;28(12):1072-3.
20. Leonard HL, March J, Rickler KC, Allen AJ. Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6):725-36.
21. Leonard HL, Swedo SE. Paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). Int J Neuropsychopharmacol 2001;4(2):191-8.
22. Perlmutter SJ, Leitman SF, Garvey MA, et al. Therapeutic plasma exchange and intravenous immunoglobulin for obsessive-compulsive disorder and tic disorders in childhood. Lancet 1999;354 (9185):1153-8.
Adam, age 10, is extremely distressed at school. Because of obsessional contamination fears, he avoids contact with other children and refuses to eat in the cafeteria. He washes his hands 20 times per day and changes his clothes at least three times daily.
His primary obsessions involve contact with bodily fluids—such as saliva or feces—and excessive concerns that this contamination would cause him serious illness.
Adam’s parents say their son’s worries about dirt and germs began when he entered kindergarten. They sought treatment for him 2 years ago, and he has been receiving outpatient psychotherapy since then. They have brought him to an anxiety disorders specialty clinic for evaluation because his obsessive-compulsive symptoms are worsening,
When treating patients such as Adam, our approach is to use cognitive-behavioral therapy (CBT) and adjunctive drug therapies to relieve their symptoms and help them reclaim their lives. Diagnosis of pediatric OCD is often delayed, and few children receive state-of-the-art treatment.1 The good news, however, is that skillful CBT combined, as needed, with medication is highly effective.
Although family dysfunction does not cause OCD, families affect and are affected by OCD. Control struggles over the child’s rituals are common, as are differences of opinion about how to cope with OCD symptoms. It is important to address these issues early in treatment, as helping the family combat the disorder—rather than each other—is crucial to effective treatment.
Parents need to know that neither they nor the child are to blame. OCD is a neurobehavioral illness, and treatment is most effective when the patient, therapist, and family are aligned to combat it. Families are often entangled in the child’s OCD symptoms, and disentangling them by eliminating their role in ritualizing (such as giving excessive reassurance) is important to address in therapy.
Scaling family involvement is part of the “art” of CBT, and it will remain so until empiric studies determine the family’s role in the treatment plan.2
‘Contaminated’ mother.
Adam becomes distressed when he comes in contact with objects that have been touched by others (such as doorknobs). He is especially anxious when these items are associated with public bathrooms or sick people.
Adam’s mother is a family physician who has daily patient contact. In the last 6 months, Adam has insisted that his mother change her work clothes before she enters his room, touches him, prepares his food, or handles his possessions.
As in Adam’s case, the family often gets caught up in a child or adolescent’s obsessive rituals (Box 1).2 After a detailed discussion with Adam and his parents and because his symptoms were severe, we recommended combined treatment with sertraline and CBT. Adam was willing to consider CBT and medication because he recognized that he was having increasing difficulty doing the things he wanted to do in school and at home.
SNAPSHOT OF PEDIATRIC OCD
Approximately 1 in 200 children and adolescents suffer from clinically significant OCD.3 They experience intrusive thoughts, urges, or images to which they respond with dysphoria-reducing behaviors or rituals.
Common obsessions include:
- fear of dirt or germs
- fear of harm to oneself or someone else
- or a persistent need to complete something “just so.”
Corresponding compulsions include hand washing, checking, and repeating or arranging.
OCD appears more common in boys than in girls. Onset occurs in two modes: first at age 9 for boys and age 12 for girls, followed by a second mode in late adolescence or early adulthood.
Two practice guidelines address OCD in youth: an independent expert consensus guideline4 and the American Academy of Child and Adolescent Psychiatry’s practice parameters for OCD.5
For uncomplicated OCD, these guidelines recommend CBT as first-line treatment. If symptoms do not respond after six to eight sessions, a selective serotonin reuptake inhibitor (SSRI) is added to CBT.
For complicated OCD, medication is considered an appropriate initial treatment. Complicated OCD includes patients who:
- display severe symptoms—such as with scores >30 on the Children’s Yale-Brown Obsessive Compulsive Scale (CY-BOCS)
- or have comorbidity such as depression or panic disorder that is likely to complicate treatment.
KEYS TO SUCCESSFUL TREATMENT
OCD is remarkably resistant to insight-oriented psychotherapy and other nondirective therapies. The benefits of CBT, however, are well-established, with reported response rates of >80% in pilot studies.6,7 Although confirming studies have yet to be conducted, successful CBT for pediatric OCD appears to include four elements (Table 1).
Exposure and response prevention (EX/RP) is central to psychosocial treatment of OCD.7,8 In specialized centers, exposure can be applied intensively (three to five times per week for 3 to 4 weeks).9 In most practices, however, exposure is more gradual (weekly for 12 to 20 weeks). With repeated exposure, the child’s anxiety decreases until he or she no longer fears contact with the targeted stimuli.8,10
Not ‘misbehavior.’ Children—and less commonly adolescents—with this disorder may not view their obsessions as senseless or their compulsions as excessive. Even when insight is clearly present, young OCD patients often hide their symptoms because of embarrassment or fear of being punished for their behavior.
Response predictors. A key to CBT in children or adolescents is that they come to see obsessions and compulsions as symptoms of an illness. The symptoms, therefore, require a skillfully applied “antidote,” as taught by the clinician and implemented by the child, family, and others on the child’s behalf. Besides overt rituals, three response predictors include the patient’s:
- desire to eliminate symptoms
- ability to monitor and report symptoms
- willingness to cooperate with treatment.
Table 1
Pediatric OCD: 4 keys to successful cognitive therapy
| Treat OCD as a neurobehavioral disorder, not a misbehavior |
| Help the child develop a “tool kit” to manage dysphoria and faulty thinking |
| Expose the patient to anxiety-producing stimuli until he or she becomes desensitized and can refrain from the usual compulsive responses (exposure and response prevention) |
| Educate family members and school personnel |
CBT may be difficult with patients younger than age 6 and will invariably involve training the parents to serve as “coaches;” a CBT protocol for patients ages 4 to 6 is under investigation (H. Leonard, personal communication). CBT also can be adapted for patients with intellectual deficits.11
A ‘tool kit.’ Successful exposure therapy for OCD relies on equipping children and adolescents with the knowledge and skills to battle the illness. They often have tried unsuccessfully to resist OCD’s compulsions and must be convinced that EX/RP techniques will work. Using a “tool kit” concept reminds young patients that they have the implements they need to combat OCD (Table 2).
A ‘germ ladder’ and ‘fear thermometer.’
Adam’s tools include a stimulus hierarchy called a “germ ladder,” which the therapist and Adam create collaboratively. It ranks stimuli from low (his own doorknob) to very high (public toilets, sinks, and door handles).
As part of his treatment, Adam begins to touch objects in his room and house while voluntarily refraining from ritualizing. He uses another tool—a fear thermometer—to record his distress level on a scale of 1 to 10 during and after these exposures.
Adam discovers that when he comes into contact with less-threatening items his fear ratings typically return to baseline within 20 to 30 minutes. This insight helps him modify his assessment of the risk they pose.
Table 2
OCD ‘tool box’ can help patients build new behaviors
| Tool | Function |
|---|---|
| Training in exposure response prevention (EX/RP) therapy | Helps patients learn to confront rather than avoid feared stimuli |
| ‘Fear thermometer’ | Enables patients to express the intensity of their distress on a scale of 1 (lowest) to 10 (highest) |
| Positive self-statements | Teaches patients to use statements such as “I can do this” and “I’m the boss of OCD now” to build confidence that they can control their response to feared stimuli |
During office visits, he confronts similar items around the clinic, with the therapist providing encouragement and instruction for additional exposure homework. Eventually Adam works on the clinic’s public bathroom, which he perceived to be relatively clean but less so than his own bathroom. After fear in response to this bathroom is reduced, the therapist and Adam graduate to more-public facilities, such as the bathrooms at Adam’s pool and the local train station.
Exposure therapy. EX/RP is most successful when the child—rather than the therapist—chooses exposure targets from a hierarchy of fears,2 particularly when the list includes behaviors the child is resisting. In a collaborative spirit, the child takes the lead in placing items on the hierarchy and deciding when to confront them.
The therapist and child revise the hierarchy periodically, which demonstrates progress and allows them to add items as the child overcomes fears that cause less distress.
Reducing need for reassurance.
Adam has a habit of repeatedly asking his mother whether contact with particular objects in public is risky. By the third treatment session, he and the therapist agree that he will try to refrain from asking such questions.
His mother, in turn, is asked to reiterate the rationale for response prevention whenever Adam slips. She will offer encouragement and support without answering “OCD’s questions.”
ADJUNCTIVE DRUG THERAPY
While Adam is working with the behavioral therapist to reduce his anxieties and need for reassurance, he is also receiving gradually increasing dosages of sertraline. As discussed, he is considered a candidate for CBT plus medication because of his symptoms are severe. Drug treatment can benefit most pediatric OCD patients.
SSRIs. Two SSRIs are approved for pediatric OCD—fluvoxamine for ages 8 to 18 and sertraline for ages 6 to 18. Most SSRIs are likely effective for OCD in youth (Table 3),12-14 although reports have suggested a link between paroxetine and suicidality in pediatric patients. Other options may be more suitable choices unless further evidence supports the use of paroxetine as a first- or second-line agent for pediatric OCD.
Clomipramine—a nonselective tricyclic—was the first medication studied in treating OCD in children and adolescents. It is now usually considered only after two or three failed SSRI trials because of its potential for cardiac toxicity.15-17
Table 3
Suggested dosages (mg/d) for drug therapy of pediatric OCD
| Drug | Usual starting dosage | Approximate mean dosage* | Typical range | Usual maximum dosage |
|---|---|---|---|---|
| Citalopram | 20 | 40 | 20 to 60 | 80 |
| Clomipramine | 50 | 150 | 200 | 300 |
| Escitalopram | 5 | 10 | 10 to 20 | 30 |
| Fluoxetine | 20 | 40 | 40 to 60 | 80 |
| Fluvoxamine | 50 | 175 | 150 to 250 | 300 |
| Sertraline | 50 | 125 | 150 | 225 |
| *Mean dosage derived from registration trials, expert recommendation, and the authors’ clinical experience | ||||
Dosing. Fixed-dose studies suggest that dosing schedules for OCD are similar to those used for depression. For example, sertraline, 50 mg/d, or fluoxetine, 20 mg/d, are as effective as higher dosages.18
The common misconception that OCD requires higher dosages likely results from:
- increasing the dosage too early in the time-response window for a drug effect to emerge
- giving medication without concomitant exposure therapy.19
Delayed response. Although many patients respond early to an SSRI, others do not respond until 8 or even 12 weeks of treatment at therapeutic dosages. It often takes 3 to 4 weeks for evidence of benefit to emerge, so wait at least 3 weeks between dosage increases. Maintain therapeutic dosages at least 6 to 8 weeks before changing agents or beginning augmentation therapy.
Two-barrel approach.
In treating Adam, we began with sertraline, using a flexible titration schedule keyed to whether he experienced OCD symptom remission.
The starting dosage of 50 mg was titrated to 150 mg over 8 weeks while he was receiving behavioral therapy. We made adjustments with a time-response window of 2 to 3 weeks, allowing us to observe a response to each dosage escalation.
Adam’s OCD symptoms responded well to CBT plus sertraline. The maximum drug effect helped him confront the most difficult EX/RP tasks at the top of his stimulus hierarchy, which he attacked near the end of treatment.
Lessons learned. Multicenter trials have taught important lessons about drug therapy for OCD:
- OCD patients experience little or no placebo effect, unlike patients with depression.
- Clinical effects may appear as early as 2 to 3 weeks after medications are started and plateau at 10 to 12 weeks.
- Partial response is the rule; SSRIs reduce OCD symptoms by about 30%—which correlates with “moderately” to “markedly” improved ratings on patient satisfaction measures.
- Side effects and magnitude of improvement are comparable in pediatric and adult medication trials.
In some children, OCD or tic symptoms arise from or are exacerbated by group A beta hemolytic streptococcal infection (GABHS), which has been labeled pediatric autoimmune neuropsychiatric disorders associated with Streptococcus (PANDAS).21 Obsessive-compulsive symptoms are not uncommon in pediatric patients with Sydenham’s chorea, a neurologic variant of rheumatic fever. OCD is far more common in patients with rheumatic fever when chorea is present.
Acute-onset or dramatic exacerbation of OCD or tic symptoms should prompt investigation of GABHS infection. Immunomodulatory treatments—including antibiotics, plasmapheresis, or IV immunoglobulin G—may benefit some patients.22
MANAGING RESISTANT OCD
Adequate SSRI monotherapy trials fail to relieve OCD symptoms in one-third of patients. Some patients benefit from combination therapy—such as an SSRI plus risperidone—especially when comorbid schizotypal personality disorder or a tic-spectrum disorder is present.
Drug switching or augmentation trials often produce only partial response and cause unnecessary suffering. A more effective strategy for many patients is to augment drug treatment with CBT until symptoms normalize.
On the other hand, augmentation is appropriate when nonresponse or partial response to SSRI monotherapy leaves a patient clinically symptomatic and functionally impaired. Clonazepam, clomipramine, and the amino acid L-tryptophan have been used successfully. Lithium and buspirone also have been tried but seem not to be effective in controlled studies in adults and anecdotal experience in youth.
When augmenting an SSRI, adding clomipramine, 25 to 50 mg/d, is a reasonable choice. However, fluoxetine or paroxetine can inhibit clomipramine metabolism by cytochrome P-450 (CYP) 2D6, with potential for cardiac arrhythmias or seizures. Sertraline or fluvoxamine are less likely to elevate clomipramine levels.20 Fluvoxamine may be the most compatible SSRI with clomipramine because it inhibits CYP 1A2—the enzyme that demethylates clomipramine to its inactive desmethyl metabolite—thereby preserving more of the active parent compound.
Clinical evidence suggests that augmentation’s success may depend in part on a patient’s comorbidities. For example, clonazepam may be particularly helpful for children with comorbid panic symptoms.
MAINTENANCE THERAPY
We typically provide 14 weekly CBT sessions, followed by monthly contacts for a few months to ensure than a patient’s gains are maintained. Standard procedure with drug therapy is to continue maintenance treatment for up to 1 year, although some have suggested continuing maintenance treatment indefinitely.
Related resources
- Chansky TE. Freeing your child from obsessive compulsive disorder: A powerful, practical program for parents of children and adolescents. New York: Crown Publishing Group, 2001.
- March JS, Mulle K. OCD in children and adolescents: A cognitive behavioral treatment manual. New York: Guilford Press, 1998.
- Moritz EK, Jablonsky J. Blink, blink, clop, clop: Why do we do things we can’t stop? An OCD storybook. Newton, MA: Professional Books, Inc, 1998.
- Wagner AP. Up and down the worry hill: A children’s book about obsessive compulsive disorder and its treatment. Rochester, NY: Lighthouse Press, Inc. 2000.
Drug brand names
- Buspirone • BuSpar
- Citalopram • Celexa
- Clomipramine • Anafranil
- Clonazepam • Klonopin
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Paroxetine • Paxil
- Risperidone • Risperdal
- Sertaline • Zoloft
Disclosure
Dr. March receives research support from Pfizer Inc., Eli Lilly and Co., and Wyeth Pharmaceuticals and is a speaker for and/or consultant to Solvay Pharmaceuticals, Pfizer Inc., GlaxoSmithKline, Wyeth Pharmaceuticals, Novartis Pharmaceuticals Corp., and Shire Pharmaceuticals Group.
Dr. Franklin and Dr. Foa report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
Preparation of this manuscript was supported in part by National Institute of Mental Health grants 1 K24 MHO1557 and 1 R10 MH55121 to Dr. March and by contributions from the Robert and Sarah Gorrell family and the Lupin Family Foundation.
Adam, age 10, is extremely distressed at school. Because of obsessional contamination fears, he avoids contact with other children and refuses to eat in the cafeteria. He washes his hands 20 times per day and changes his clothes at least three times daily.
His primary obsessions involve contact with bodily fluids—such as saliva or feces—and excessive concerns that this contamination would cause him serious illness.
Adam’s parents say their son’s worries about dirt and germs began when he entered kindergarten. They sought treatment for him 2 years ago, and he has been receiving outpatient psychotherapy since then. They have brought him to an anxiety disorders specialty clinic for evaluation because his obsessive-compulsive symptoms are worsening,
When treating patients such as Adam, our approach is to use cognitive-behavioral therapy (CBT) and adjunctive drug therapies to relieve their symptoms and help them reclaim their lives. Diagnosis of pediatric OCD is often delayed, and few children receive state-of-the-art treatment.1 The good news, however, is that skillful CBT combined, as needed, with medication is highly effective.
Although family dysfunction does not cause OCD, families affect and are affected by OCD. Control struggles over the child’s rituals are common, as are differences of opinion about how to cope with OCD symptoms. It is important to address these issues early in treatment, as helping the family combat the disorder—rather than each other—is crucial to effective treatment.
Parents need to know that neither they nor the child are to blame. OCD is a neurobehavioral illness, and treatment is most effective when the patient, therapist, and family are aligned to combat it. Families are often entangled in the child’s OCD symptoms, and disentangling them by eliminating their role in ritualizing (such as giving excessive reassurance) is important to address in therapy.
Scaling family involvement is part of the “art” of CBT, and it will remain so until empiric studies determine the family’s role in the treatment plan.2
‘Contaminated’ mother.
Adam becomes distressed when he comes in contact with objects that have been touched by others (such as doorknobs). He is especially anxious when these items are associated with public bathrooms or sick people.
Adam’s mother is a family physician who has daily patient contact. In the last 6 months, Adam has insisted that his mother change her work clothes before she enters his room, touches him, prepares his food, or handles his possessions.
As in Adam’s case, the family often gets caught up in a child or adolescent’s obsessive rituals (Box 1).2 After a detailed discussion with Adam and his parents and because his symptoms were severe, we recommended combined treatment with sertraline and CBT. Adam was willing to consider CBT and medication because he recognized that he was having increasing difficulty doing the things he wanted to do in school and at home.
SNAPSHOT OF PEDIATRIC OCD
Approximately 1 in 200 children and adolescents suffer from clinically significant OCD.3 They experience intrusive thoughts, urges, or images to which they respond with dysphoria-reducing behaviors or rituals.
Common obsessions include:
- fear of dirt or germs
- fear of harm to oneself or someone else
- or a persistent need to complete something “just so.”
Corresponding compulsions include hand washing, checking, and repeating or arranging.
OCD appears more common in boys than in girls. Onset occurs in two modes: first at age 9 for boys and age 12 for girls, followed by a second mode in late adolescence or early adulthood.
Two practice guidelines address OCD in youth: an independent expert consensus guideline4 and the American Academy of Child and Adolescent Psychiatry’s practice parameters for OCD.5
For uncomplicated OCD, these guidelines recommend CBT as first-line treatment. If symptoms do not respond after six to eight sessions, a selective serotonin reuptake inhibitor (SSRI) is added to CBT.
For complicated OCD, medication is considered an appropriate initial treatment. Complicated OCD includes patients who:
- display severe symptoms—such as with scores >30 on the Children’s Yale-Brown Obsessive Compulsive Scale (CY-BOCS)
- or have comorbidity such as depression or panic disorder that is likely to complicate treatment.
KEYS TO SUCCESSFUL TREATMENT
OCD is remarkably resistant to insight-oriented psychotherapy and other nondirective therapies. The benefits of CBT, however, are well-established, with reported response rates of >80% in pilot studies.6,7 Although confirming studies have yet to be conducted, successful CBT for pediatric OCD appears to include four elements (Table 1).
Exposure and response prevention (EX/RP) is central to psychosocial treatment of OCD.7,8 In specialized centers, exposure can be applied intensively (three to five times per week for 3 to 4 weeks).9 In most practices, however, exposure is more gradual (weekly for 12 to 20 weeks). With repeated exposure, the child’s anxiety decreases until he or she no longer fears contact with the targeted stimuli.8,10
Not ‘misbehavior.’ Children—and less commonly adolescents—with this disorder may not view their obsessions as senseless or their compulsions as excessive. Even when insight is clearly present, young OCD patients often hide their symptoms because of embarrassment or fear of being punished for their behavior.
Response predictors. A key to CBT in children or adolescents is that they come to see obsessions and compulsions as symptoms of an illness. The symptoms, therefore, require a skillfully applied “antidote,” as taught by the clinician and implemented by the child, family, and others on the child’s behalf. Besides overt rituals, three response predictors include the patient’s:
- desire to eliminate symptoms
- ability to monitor and report symptoms
- willingness to cooperate with treatment.
Table 1
Pediatric OCD: 4 keys to successful cognitive therapy
| Treat OCD as a neurobehavioral disorder, not a misbehavior |
| Help the child develop a “tool kit” to manage dysphoria and faulty thinking |
| Expose the patient to anxiety-producing stimuli until he or she becomes desensitized and can refrain from the usual compulsive responses (exposure and response prevention) |
| Educate family members and school personnel |
CBT may be difficult with patients younger than age 6 and will invariably involve training the parents to serve as “coaches;” a CBT protocol for patients ages 4 to 6 is under investigation (H. Leonard, personal communication). CBT also can be adapted for patients with intellectual deficits.11
A ‘tool kit.’ Successful exposure therapy for OCD relies on equipping children and adolescents with the knowledge and skills to battle the illness. They often have tried unsuccessfully to resist OCD’s compulsions and must be convinced that EX/RP techniques will work. Using a “tool kit” concept reminds young patients that they have the implements they need to combat OCD (Table 2).
A ‘germ ladder’ and ‘fear thermometer.’
Adam’s tools include a stimulus hierarchy called a “germ ladder,” which the therapist and Adam create collaboratively. It ranks stimuli from low (his own doorknob) to very high (public toilets, sinks, and door handles).
As part of his treatment, Adam begins to touch objects in his room and house while voluntarily refraining from ritualizing. He uses another tool—a fear thermometer—to record his distress level on a scale of 1 to 10 during and after these exposures.
Adam discovers that when he comes into contact with less-threatening items his fear ratings typically return to baseline within 20 to 30 minutes. This insight helps him modify his assessment of the risk they pose.
Table 2
OCD ‘tool box’ can help patients build new behaviors
| Tool | Function |
|---|---|
| Training in exposure response prevention (EX/RP) therapy | Helps patients learn to confront rather than avoid feared stimuli |
| ‘Fear thermometer’ | Enables patients to express the intensity of their distress on a scale of 1 (lowest) to 10 (highest) |
| Positive self-statements | Teaches patients to use statements such as “I can do this” and “I’m the boss of OCD now” to build confidence that they can control their response to feared stimuli |
During office visits, he confronts similar items around the clinic, with the therapist providing encouragement and instruction for additional exposure homework. Eventually Adam works on the clinic’s public bathroom, which he perceived to be relatively clean but less so than his own bathroom. After fear in response to this bathroom is reduced, the therapist and Adam graduate to more-public facilities, such as the bathrooms at Adam’s pool and the local train station.
Exposure therapy. EX/RP is most successful when the child—rather than the therapist—chooses exposure targets from a hierarchy of fears,2 particularly when the list includes behaviors the child is resisting. In a collaborative spirit, the child takes the lead in placing items on the hierarchy and deciding when to confront them.
The therapist and child revise the hierarchy periodically, which demonstrates progress and allows them to add items as the child overcomes fears that cause less distress.
Reducing need for reassurance.
Adam has a habit of repeatedly asking his mother whether contact with particular objects in public is risky. By the third treatment session, he and the therapist agree that he will try to refrain from asking such questions.
His mother, in turn, is asked to reiterate the rationale for response prevention whenever Adam slips. She will offer encouragement and support without answering “OCD’s questions.”
ADJUNCTIVE DRUG THERAPY
While Adam is working with the behavioral therapist to reduce his anxieties and need for reassurance, he is also receiving gradually increasing dosages of sertraline. As discussed, he is considered a candidate for CBT plus medication because of his symptoms are severe. Drug treatment can benefit most pediatric OCD patients.
SSRIs. Two SSRIs are approved for pediatric OCD—fluvoxamine for ages 8 to 18 and sertraline for ages 6 to 18. Most SSRIs are likely effective for OCD in youth (Table 3),12-14 although reports have suggested a link between paroxetine and suicidality in pediatric patients. Other options may be more suitable choices unless further evidence supports the use of paroxetine as a first- or second-line agent for pediatric OCD.
Clomipramine—a nonselective tricyclic—was the first medication studied in treating OCD in children and adolescents. It is now usually considered only after two or three failed SSRI trials because of its potential for cardiac toxicity.15-17
Table 3
Suggested dosages (mg/d) for drug therapy of pediatric OCD
| Drug | Usual starting dosage | Approximate mean dosage* | Typical range | Usual maximum dosage |
|---|---|---|---|---|
| Citalopram | 20 | 40 | 20 to 60 | 80 |
| Clomipramine | 50 | 150 | 200 | 300 |
| Escitalopram | 5 | 10 | 10 to 20 | 30 |
| Fluoxetine | 20 | 40 | 40 to 60 | 80 |
| Fluvoxamine | 50 | 175 | 150 to 250 | 300 |
| Sertraline | 50 | 125 | 150 | 225 |
| *Mean dosage derived from registration trials, expert recommendation, and the authors’ clinical experience | ||||
Dosing. Fixed-dose studies suggest that dosing schedules for OCD are similar to those used for depression. For example, sertraline, 50 mg/d, or fluoxetine, 20 mg/d, are as effective as higher dosages.18
The common misconception that OCD requires higher dosages likely results from:
- increasing the dosage too early in the time-response window for a drug effect to emerge
- giving medication without concomitant exposure therapy.19
Delayed response. Although many patients respond early to an SSRI, others do not respond until 8 or even 12 weeks of treatment at therapeutic dosages. It often takes 3 to 4 weeks for evidence of benefit to emerge, so wait at least 3 weeks between dosage increases. Maintain therapeutic dosages at least 6 to 8 weeks before changing agents or beginning augmentation therapy.
Two-barrel approach.
In treating Adam, we began with sertraline, using a flexible titration schedule keyed to whether he experienced OCD symptom remission.
The starting dosage of 50 mg was titrated to 150 mg over 8 weeks while he was receiving behavioral therapy. We made adjustments with a time-response window of 2 to 3 weeks, allowing us to observe a response to each dosage escalation.
Adam’s OCD symptoms responded well to CBT plus sertraline. The maximum drug effect helped him confront the most difficult EX/RP tasks at the top of his stimulus hierarchy, which he attacked near the end of treatment.
Lessons learned. Multicenter trials have taught important lessons about drug therapy for OCD:
- OCD patients experience little or no placebo effect, unlike patients with depression.
- Clinical effects may appear as early as 2 to 3 weeks after medications are started and plateau at 10 to 12 weeks.
- Partial response is the rule; SSRIs reduce OCD symptoms by about 30%—which correlates with “moderately” to “markedly” improved ratings on patient satisfaction measures.
- Side effects and magnitude of improvement are comparable in pediatric and adult medication trials.
In some children, OCD or tic symptoms arise from or are exacerbated by group A beta hemolytic streptococcal infection (GABHS), which has been labeled pediatric autoimmune neuropsychiatric disorders associated with Streptococcus (PANDAS).21 Obsessive-compulsive symptoms are not uncommon in pediatric patients with Sydenham’s chorea, a neurologic variant of rheumatic fever. OCD is far more common in patients with rheumatic fever when chorea is present.
Acute-onset or dramatic exacerbation of OCD or tic symptoms should prompt investigation of GABHS infection. Immunomodulatory treatments—including antibiotics, plasmapheresis, or IV immunoglobulin G—may benefit some patients.22
MANAGING RESISTANT OCD
Adequate SSRI monotherapy trials fail to relieve OCD symptoms in one-third of patients. Some patients benefit from combination therapy—such as an SSRI plus risperidone—especially when comorbid schizotypal personality disorder or a tic-spectrum disorder is present.
Drug switching or augmentation trials often produce only partial response and cause unnecessary suffering. A more effective strategy for many patients is to augment drug treatment with CBT until symptoms normalize.
On the other hand, augmentation is appropriate when nonresponse or partial response to SSRI monotherapy leaves a patient clinically symptomatic and functionally impaired. Clonazepam, clomipramine, and the amino acid L-tryptophan have been used successfully. Lithium and buspirone also have been tried but seem not to be effective in controlled studies in adults and anecdotal experience in youth.
When augmenting an SSRI, adding clomipramine, 25 to 50 mg/d, is a reasonable choice. However, fluoxetine or paroxetine can inhibit clomipramine metabolism by cytochrome P-450 (CYP) 2D6, with potential for cardiac arrhythmias or seizures. Sertraline or fluvoxamine are less likely to elevate clomipramine levels.20 Fluvoxamine may be the most compatible SSRI with clomipramine because it inhibits CYP 1A2—the enzyme that demethylates clomipramine to its inactive desmethyl metabolite—thereby preserving more of the active parent compound.
Clinical evidence suggests that augmentation’s success may depend in part on a patient’s comorbidities. For example, clonazepam may be particularly helpful for children with comorbid panic symptoms.
MAINTENANCE THERAPY
We typically provide 14 weekly CBT sessions, followed by monthly contacts for a few months to ensure than a patient’s gains are maintained. Standard procedure with drug therapy is to continue maintenance treatment for up to 1 year, although some have suggested continuing maintenance treatment indefinitely.
Related resources
- Chansky TE. Freeing your child from obsessive compulsive disorder: A powerful, practical program for parents of children and adolescents. New York: Crown Publishing Group, 2001.
- March JS, Mulle K. OCD in children and adolescents: A cognitive behavioral treatment manual. New York: Guilford Press, 1998.
- Moritz EK, Jablonsky J. Blink, blink, clop, clop: Why do we do things we can’t stop? An OCD storybook. Newton, MA: Professional Books, Inc, 1998.
- Wagner AP. Up and down the worry hill: A children’s book about obsessive compulsive disorder and its treatment. Rochester, NY: Lighthouse Press, Inc. 2000.
Drug brand names
- Buspirone • BuSpar
- Citalopram • Celexa
- Clomipramine • Anafranil
- Clonazepam • Klonopin
- Escitalopram • Lexapro
- Fluoxetine • Prozac
- Fluvoxamine • Luvox
- Paroxetine • Paxil
- Risperidone • Risperdal
- Sertaline • Zoloft
Disclosure
Dr. March receives research support from Pfizer Inc., Eli Lilly and Co., and Wyeth Pharmaceuticals and is a speaker for and/or consultant to Solvay Pharmaceuticals, Pfizer Inc., GlaxoSmithKline, Wyeth Pharmaceuticals, Novartis Pharmaceuticals Corp., and Shire Pharmaceuticals Group.
Dr. Franklin and Dr. Foa report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Acknowledgment
Preparation of this manuscript was supported in part by National Institute of Mental Health grants 1 K24 MHO1557 and 1 R10 MH55121 to Dr. March and by contributions from the Robert and Sarah Gorrell family and the Lupin Family Foundation.
1. Kendall PC, Southam-Gerow MA. Issues in the transportability of treatment: the case of anxiety disorders in youths. J Consult Clin Psychol 1995;63(5):702-8.
2. March J, Mulle K. OCD in children and adolescents: A cognitive-behavioral treatment manual. New York: Guilford Press, 1998.
3. Flament MF, Whitaker A, Rapoport JL, et al. Obsessive compulsive disorder in adolescence: an epidemiological study. J Am Acad Child Adolesc Psychiatry 1988;27(6):764-71.
4. March J, Frances A, Kahn D, Carpenter D. Expert consensus guidelines: treatment of obsessive-compulsive disorder. J Clin Psychiatry 1997;58(suppl 4):1-72.
5. King R, Leonard H, March J. Practice parameters for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 1998;37(10, suppl):27-45.
6. March JS. Cognitive-behavioral psychotherapy for children and adolescents with OCD: a review and recommendations for treatment. J Am Acad Child Adolesc Psychiatry 1995;34(1):7-18.
7. Franklin ME, Kozak MJ, Cashman LA, et al. Cognitive-behavioral treatment of pediatric obsessive-compulsive disorder: an open clinical trial. J Am Acad Child Adolesc Psychiatry 1998;37(4):412-19.
8. March JS, Mulle K, Herbel B. Behavioral psychotherapy for children and adolescents with obsessive-compulsive disorder: an open trial of a new protocol-driven treatment package. J Am Acad Child Adolesc Psychiatry 1994;33(3):333-41.
9. Franklin ME, Tolin DF, March JS, Foa EB. Treatment of pediatric obsessive-compulsive disorder: A case example of intensive cognitive-behavioral therapy involving exposure and ritual prevention. Cognit Behav Pract 2001;8(4):297-304.
10. March J, Mulle K. Manualized cognitive-behavioral psychotherapy for obsessive-compulsive disorder in childhood: a preliminary single case study. J Anxiety Disord 1995;9(2):175-84.
11. Franklin ME, Rynn M, March JS, Foa EB. Obsessive-compulsive disorder. In: Hersen M (ed). Clinical behavior therapy: adults and children. New York: John Wiley & Sons, 2002;276-303.
12. March JS, Biederman J, Wolkow R, et al. Sertraline in children and adolescents with obsessive-compulsive disorder: a multicenter randomized controlled trial. JAMA 1998;280(20):1752-6.
13. Riddle MA, Reeve EA, Yaryura-Tobias JA, et al. Fluvoxamine for children and adolescents with obsessive-compulsive disorder: a randomized, controlled, multicenter trial. J Am Acad Child Adolesc Psychiatry 2001;40(2):222-9.
14. Geller DA, Hoog SL, Heiligenstein JH, et al. Fluoxetine treatment for obsessive-compulsive disorder in children and adolescents: a placebo-controlled clinical trial. J Am Acad Child Adolesc Psychiatry 2001;40(7):773-9.
15. Leonard H, March J, Rickler K, Allen A. Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6):725-36.
16. DeVeaugh-Geiss J, Moroz G, Biederman J, et al. Clomipramine hydrochloride in childhood and adolescent obsessive-compulsive disorder—a multicenter trial. J Am Acad Child Adolesc Psychiatry 1992;31(1):45-9.
17. Wilens TE, Biederman J, March JS, et al. Absence of cardiovascular adverse effects of sertraline in children and adolescents. J Am Acad Child Adolesc Psychiatry 1999;38(5):573-7.
18. Greist JH, Jefferson JW, Kobak KA, et al. A 1-year double-blind placebo-controlled fixed dose study of sertraline in the treatment of obsessive-compulsive disorder. Int Clin Psychopharmacol 1995;10(2):57-65.
19. Marks IM. Drug versus behavioral treatment of obsessive-compulsive disorder. Biolog Psychiatry 1990;28(12):1072-3.
20. Leonard HL, March J, Rickler KC, Allen AJ. Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6):725-36.
21. Leonard HL, Swedo SE. Paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). Int J Neuropsychopharmacol 2001;4(2):191-8.
22. Perlmutter SJ, Leitman SF, Garvey MA, et al. Therapeutic plasma exchange and intravenous immunoglobulin for obsessive-compulsive disorder and tic disorders in childhood. Lancet 1999;354 (9185):1153-8.
1. Kendall PC, Southam-Gerow MA. Issues in the transportability of treatment: the case of anxiety disorders in youths. J Consult Clin Psychol 1995;63(5):702-8.
2. March J, Mulle K. OCD in children and adolescents: A cognitive-behavioral treatment manual. New York: Guilford Press, 1998.
3. Flament MF, Whitaker A, Rapoport JL, et al. Obsessive compulsive disorder in adolescence: an epidemiological study. J Am Acad Child Adolesc Psychiatry 1988;27(6):764-71.
4. March J, Frances A, Kahn D, Carpenter D. Expert consensus guidelines: treatment of obsessive-compulsive disorder. J Clin Psychiatry 1997;58(suppl 4):1-72.
5. King R, Leonard H, March J. Practice parameters for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 1998;37(10, suppl):27-45.
6. March JS. Cognitive-behavioral psychotherapy for children and adolescents with OCD: a review and recommendations for treatment. J Am Acad Child Adolesc Psychiatry 1995;34(1):7-18.
7. Franklin ME, Kozak MJ, Cashman LA, et al. Cognitive-behavioral treatment of pediatric obsessive-compulsive disorder: an open clinical trial. J Am Acad Child Adolesc Psychiatry 1998;37(4):412-19.
8. March JS, Mulle K, Herbel B. Behavioral psychotherapy for children and adolescents with obsessive-compulsive disorder: an open trial of a new protocol-driven treatment package. J Am Acad Child Adolesc Psychiatry 1994;33(3):333-41.
9. Franklin ME, Tolin DF, March JS, Foa EB. Treatment of pediatric obsessive-compulsive disorder: A case example of intensive cognitive-behavioral therapy involving exposure and ritual prevention. Cognit Behav Pract 2001;8(4):297-304.
10. March J, Mulle K. Manualized cognitive-behavioral psychotherapy for obsessive-compulsive disorder in childhood: a preliminary single case study. J Anxiety Disord 1995;9(2):175-84.
11. Franklin ME, Rynn M, March JS, Foa EB. Obsessive-compulsive disorder. In: Hersen M (ed). Clinical behavior therapy: adults and children. New York: John Wiley & Sons, 2002;276-303.
12. March JS, Biederman J, Wolkow R, et al. Sertraline in children and adolescents with obsessive-compulsive disorder: a multicenter randomized controlled trial. JAMA 1998;280(20):1752-6.
13. Riddle MA, Reeve EA, Yaryura-Tobias JA, et al. Fluvoxamine for children and adolescents with obsessive-compulsive disorder: a randomized, controlled, multicenter trial. J Am Acad Child Adolesc Psychiatry 2001;40(2):222-9.
14. Geller DA, Hoog SL, Heiligenstein JH, et al. Fluoxetine treatment for obsessive-compulsive disorder in children and adolescents: a placebo-controlled clinical trial. J Am Acad Child Adolesc Psychiatry 2001;40(7):773-9.
15. Leonard H, March J, Rickler K, Allen A. Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6):725-36.
16. DeVeaugh-Geiss J, Moroz G, Biederman J, et al. Clomipramine hydrochloride in childhood and adolescent obsessive-compulsive disorder—a multicenter trial. J Am Acad Child Adolesc Psychiatry 1992;31(1):45-9.
17. Wilens TE, Biederman J, March JS, et al. Absence of cardiovascular adverse effects of sertraline in children and adolescents. J Am Acad Child Adolesc Psychiatry 1999;38(5):573-7.
18. Greist JH, Jefferson JW, Kobak KA, et al. A 1-year double-blind placebo-controlled fixed dose study of sertraline in the treatment of obsessive-compulsive disorder. Int Clin Psychopharmacol 1995;10(2):57-65.
19. Marks IM. Drug versus behavioral treatment of obsessive-compulsive disorder. Biolog Psychiatry 1990;28(12):1072-3.
20. Leonard HL, March J, Rickler KC, Allen AJ. Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36(6):725-36.
21. Leonard HL, Swedo SE. Paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). Int J Neuropsychopharmacol 2001;4(2):191-8.
22. Perlmutter SJ, Leitman SF, Garvey MA, et al. Therapeutic plasma exchange and intravenous immunoglobulin for obsessive-compulsive disorder and tic disorders in childhood. Lancet 1999;354 (9185):1153-8.