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Recent Advancesin Pediatrics 23 Hot Topics CH 17
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17 Obsessive Compulsive
Disorder
Rachana Pole, GK Vankar
INTRODUCTION
Obsessions are defined as persistent thoughts, images, or impulses that are
ego-dystonic, intrusive, and, for the most part, senseless. ‘‘Compulsions
are repetitive, purposeful, and intentional behaviors that are performed
in response to an obsession, according to certain rules, or in a stereotyped
fashion.’’
Obsessions generate intense fear whereas compulsions are the mental or
physical acts performed in order to relieve the distress caused by obsessions.
Whilst adolescents and adults often realize irrationality of their thoughts,
children often fail to do that and thus differ from adult obsessive-compulsive
disorder (OCD).
EPIDEMIOLOGY
Childhood OCD tends to be more common in females than in males.
However by adolescence the ratio equalizes. in adults the disorder is slightly
more common in females than males.1 The Isle of Wight study,2 reported
‘‘mixed obsessional/anxiety disorders’’ in 7 of 2199 (0.3%) in a survey of 10-
and 11-year-old children. In a whole-population adolescent epidemiologic
study of OCD, Flament and colleagues in1988 reported a prevalence rate of
0.8% and a lifetime prevalence of 1.9%.3 These figures suggest that OCD is a
relatively common psychiatric disorder in adolescents.
ETIOLOGY
Biological Factors
Serotonin-dysregulation of serotonin has been hypothesized to have a role
in etiopathogenesis of OCD. The positive therapeutic response to SSRI is a
evidence in favor of this hypothesis. Researchers have measured the levels
of 5HIAA in CSF and have found variable levels of the same in CSF in OCD
patients.
Norepinephrine-dysregulation of norepinephrine has been proposed to
play a role in etiological role.
The response to pharmacotherapeutic agent clonidine is in favor of this
hypothesis.
Neuroimmunological Theory
Poststreptococcal autoimmunity is hypothesized to be an additional etiologic
pathway in a subset of children with OCD and tic disorders.4 This subset of
children experiences a sudden onset of OCD and/or motor tics in association
with group A streptococcal (GAS) infections (e.g. ‘‘strep throat’’), a disorder
classified as pediatric autoimmune neuropsychiatric disorders associated
with streptococcal infections (PANDAS). Box 17.1 presents its characteristic
features.
Positive streptococcal titers and cultures are very frequent in children
during regional streptococcal outbreaks, triggering the requirement for two
infection-associated exacerbations.
The cause of OCD and tics in the PANDAS subgroup is unknown but
is theorized to occur as a result of post-streptococcal autoimmunity in a
manner similar to that of Sydenham’s chorea. The working hypothesis for the
Neuroimaging
Neuroimaging in patients with OCD has indicated altered function in
the neurocircuitry between orbitofrontal cortex, caudate, and thalamus.
Positron emission tomography (PET) studies have shown increased activity
in the frontal lobes, the basal ganglia and the cingulum of patients with
OCD. Pharmacological and behavioral treatments reportedly reverse these
abnormalities. Computed tomographic (CT) and magnetic resonance imaging
(MRI) studies have found bilaterally smaller caudates in patients with OCD.5
Genetics
First-degree relatives of individuals with OCD were approximately four-fold
risk to develop OCD than relatives of unaffected controls. Family studies
suggest that early-onset OCD may be particularly heritable form of the
disorder, with relatives of early-onset OCD cases being ten-fold more likely
than control relatives to develop the disorder. Similarly, within adulthood
OCD cohorts, earlier age of onset has been associated with increased
heritability of symptoms.
First-degree relatives of OCD patients also appear to be at higher risk of
developing tic symptoms.6
Pauls and colleagues7 to hypothesized initially that some forms of OCD
may represent alternative expressions of the genes responsible for TS. Despite
large ongoing genetic studies, the gene for OCD or TS has not been identified.
Behavioral Factors5
According to learning theorists, obsessions are conditioned stimuli. A
relatively neutral stimulus becomes associated with fear or anxiety through
a process of respondent conditioning by being paired with events that are
noxious or anxiety-producing. Thus, previously neutral objects and thoughts
become conditioned stimuli capable of provoking anxiety or discomfort.
Psychosocial Factors
Personality Disorder
Obsessive-compulsive personality disorder is characterized by an obsessive
concern for details, perfectionism, and other similar personality traits. Only
about 15–35% of patients with OCD have had premorbid obsessional traits
(Box 17.2).
Psychodynamic Factors8
In classic psychoanalytic theory, OCD was termed obsessive-compulsive
neurosis and was considered a regression from the oedipal phase to the anal
psychosexual phase of development. When patients with OCD feel threatened
by anxiety about retaliation for unconscious impulses or by the loss of a
significant object’s love, they retreat from the oedipal position and regress to
an intensely ambivalent emotional stage associated with the anal phase.
Psychodynamic theory also provides explanations about maintenance
of OCD symptoms through secondary gain, family attitudes and avoidance
from personal stressors as well.
Cognitive Factors8
According to cognitive view, OCD results from the interpretation of intrusive
thoughts rather than the frequency or content of these cognitions. Intrusive
thoughts lead to a perception that he or she is responsible for causing or
failing to prevent harm, hence obsessions result. In attempts to neutralize
intrusive thoughts (or obsessions) by motor or cognitive rituals, avoidance,
and reassurance-seeking behavior the patient’s tries to get rid of anxiety. The
most common cognitive error include thought-action fusion or the tendency
to equate thought with action (e.g. ‘I have thought something bad, that
means I have done it’), and exaggerated responsibility for potential untoward
consequences of inaction (e.g. “if I do not wash my hands and my children
will be sick, that would be my fault”).
Cognitive errors maintain and expand OCD symptoms in individuals
with biological vulnerability for OCD development.7 CTP).
CLINICAL FEATURES
Case Vignette
K is a 7-year-old girl whose mother has brought her to the psychiatrist for
she is concerned that her behavior has for last 3 months has become odd.
She washes her hands often and used soap whole day so much so that her
skin of palm peels off. K vehemently denies that there is anything wrong
with her. She does not touch door knob, handles, for fear of getting dirty. If
someone touches her pen she scrupulously washes the pen with detergent.
She worries that if she does not wash, she may contract some disease or
germs may jeopardize her own as well as her family members’ health. She
also refuses to play with other children. Though she attends school she
takes two hours before she is ready for the school van. She uses so much
water that her sibs have hardly any water to take bath. Recently rather than
entering from classroom door, she sneaked through the window to avoid
touching ‘dirty’ door knob. The teacher punished her for being naughty
and called her parents to school.
Obsessions are repetitive thoughts, images, or impulses that are distressing
to the patient and compulsions are mental or physical acts done in order to
relieve the anxiety.
Most common obsessions in children and adolescents include excessive
concerns about contamination (dirt, germs, and illness), harm coming to
the self or others (e.g. parents might be kidnapped), doing the right thing
(i.e. scrupulosity), reassurance, or intrusive sexual thoughts. Sometimes
the need (urge) for evenness, order, or exactness may be described, with an
accompanying feeling of ‘‘incompleteness.’’ The most common compulsive
rituals are washing, repeating, checking, counting, touching, arranging, and
hoarding 2. Obsessions and compulsions seen in adults are similar to those
seen in children, but the obsessions are more age appropriate (e.g. children
worry that they may be kidnapped or that their parents may be killed). It is
not unusual for the OCD symptoms to change over time, and most children
will have had most of the symptoms at some time in the course of their.8
Although childhood onset OCD is similar to adult OCD in many aspects
childhood-onset OCD is more likely to be associated with tic disorders
and disruptive behavior disorders such as attention-deficit/hyperactivity
disorder. Individuals who have childhood-onset OCD are more likely to
have first-degree relatives who have OCD. Although there is a male:female
predominance in childhood-onset OCD, the opposite is true for adult-onset
OCD. Finally, patients who have childhood-onset OCD appear to have a more
favorable outcome.9
Table 17.1 gives the incidence of obsessions and compulsions in child-
adolescent OCVD.
The phenomenology of OCD in these studies is similar to that reported in
a group of 70 young patients in USA.11,12
Common symptoms of pediatric OCD obsession are listed in Table 17.2.
A SOCS score of 6 or more differentiated OCD cases with a sensitivity of 0.97 AND The specificity
was 0.88. Thus the screener identifies almost all true cases of OCD.
TREATMENT
Treatment of OCD can be broadly divided into psychotherapeutic
interventions and pharmacotherapy (Tables 17.5 and 17.6).
Although cognitive behavioral therapy (CBT) alone, combined CBT plus
SSRI medication, and SSRI medication alone all are considered acceptable
initial treatments for children who have OCD,17 CBT alone is an appropriate
initial treatment for children who have conditions of mild-to-moderate
severity.18 In comparison with medication, CBT is notable for having a
more robust and longer-lasting symptom reduction effect. For children who
have more severe symptoms, less insight, and resistance to psychotherapy,
combined treatment with medication and CBT may be most effective.
Table 17.6: Medications and dose ranges for pediatric obsessive compulsive disorder
Medication Dosage (mg/day)
Fluoxetine 20–60
Sertraline 50–200
Fluvoxamine 50–200
Paroxetine 20–60
Escitalopram 5–20
Citalopram 20–60
Clomipramine 50–200
PHARMACOTHERAPY
Fluoxetine
Fluoxetine showed superiority over placebo for treatment of childhood
OCD.20 A crossover study21 used fixed doses of 20 mg, but proposed that
clinical treatment be started at a lower dose because behavioral activation
occurred as an adverse effect in a few children, prompting one to leave the
study early because of suicidal ideation. The maximum dose was extended
to 80 mg with no withdrawals because of adverse effects, suggesting that
fluoxetine is effective across the full dose range in children with OCD.
Fluvoxamine
A placebo-controlled multicenter study reported fluvoxamine’s efficacy in
children aged 8–17 years, as measured by the CY-BOCS.22 It noted significant
improvement as early as week 1, which continued to the trial end-point at
week 10 the trial suggested that fluvoxamine has satisfactory efficacy and
tolerability in childhood OCD.
Sertraline
A large RCT has examined sertraline alone, CBT alone, sertraline combined
with CBT, or pill placebo in children and adolescents.23 The active treatments
were well tolerated but the lack of a matched control treatment for CBT limited
conclusions about relative efficacy. Sertraline alone and in combination with
CBT was efficacious compared with pill placebo. An analysis of the pooled
data from the childhood OCD studies compared ‘numbers needed to treat’
Paroxetine
Paroxetine was well tolerated in a multicenter RCT by Geller et al (2004),25
who reported efficacy for the drug (10–50 mg) in children and adolescents
7 years of age and older. However, response rates decreased with increasing
psychiatric comorbidity.
A comparison of SRI treatment trials in child and adult OCD found it
impossible to discriminate between the efficacy and tolerability of SRIs in the
two groups, implying a similar treatment response in both.26
Clomipramine
In a multicenter study involving children and adolescents with OCD, a
37% improvement in Children’s Yale–Brown Obsessive–Compulsive Scale
(CY-BOCS) score was recorded with clomipramine, compared with an 8%
improvement with placebo.27
A 10-week double-blind crossover trial showed clomipramine to be
superior to desipramine at reducing OCD symptoms.28 Response to treatment
with clomipramine was not predicted by age at onset, duration and severity
of illness, type of symptom, or plasma drug concentrations. In this study, 64%
of the participants who received clomipramine as the first active treatment
showed signs of relapse during desipramine treatment.
Psychotherapy
The most studied and effective treatment for Child and adolescent OCD is
cognitive behavior therapy. CBT uses the principle of exposure and response
prevention (ERP).29
Figure 17.1 shows how ERP works in OCD. Obsessive thoughts generate
anxiety and distress which in turn causes compulsions. The compulsive
symptoms, supported by irrational beliefs, are intended to neutralize this
anxiety and distress. The compulsions provide immediate relief and thereby
Family Therapy
An assessment of the family usually is a necessary component of an
evaluation of an adolescent with OCD. By dealing with the specific family
dynamic issues and their resulting obstacles to engage in treatment, the
family can participate in the OCD treatment plan of the identified patient in
constructive and positive ways.33 Although there are no systematic studies of
family therapy, it may be useful to address issues of family discord, marital
difficulties, and inappropriate roles or boundaries, which interfere with the
adolescent’s ability to participate in treatment for his or her OCD.
OUTCOME
The OCD can be a chronic condition that persists into adulthood. Early
recognition and treatment might prevent chronicity. Pediatric OCD may
follow a waxing and waning course, a chronic stable course, or may be
characterized by dramatic exacerbations and remissions. Follow-up studies
of OCD in children and adolescents have reported low rates of remission.34-36
Similarly, studies of adult OCD have reported worse course in those with early
onset of illness.37-38 Reddy et al. in their Indian follow-up study of 58 children
and adolescents with DSM-III-R OCD for two to nine year.39 The subjects were
largely ‘self-referred’ and ‘drug-naïve’ at the time of consultation. 48% were
in true remission (full remission and not on any treatment) and were not
receiving treatment for a mean period of 58 months. Duration of follow-up
and age-at-onset emerged as significant predictors of full remission. The
high rate of ‘true remitters’ is in sharp contrast to the 6% rate in the study by
Leonard and others.40 Better prognosis in this study could be due to moderate
severity, relatively low rate of comorbidity.
REFERENCES
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders, 5th edn. Arlington VA: APA 2013.
2. Rutter M. Isle of Wight studies, 1964–1974. Psychol Med 1976;6:313-332.
3. Flament MF, Whitaker A, Rapoport JL, et al. Obsessive compulsive disorder in
adolescence: An epidemiological study. J Am Acad Child Adolesc Psychiatry
1988;27:764-771.
4. Swedo SE, Leonard HL, Garvey M, et al. Pediatric autoimmune neuropsychiatric
disorders associated with streptococcal infections: clinical description of the first 50
cases. Am J Psychiatry 1998;155:264-271.
5. Lewin Adam B, John P. Obsessive-compulsive disorder of infancy, childhood,
and adolescence. In: Sadock BJ, Sadock VA, Ruiz P (Eds): Kaplan and Sadock’s
Comprehensive Textbook of Psychiatry, 9th edn. Philadelphia: Lippincott Williams &
Wilkins 2009:3671-3678.