OCD An Indian Perspective

Obsessive Compulsive Disorder
– An Indian Perspective
Sumant Khanna, MD, PhD, MAMS, Y.C. Janardhan Reddy,

MRCPsych Associate Professor,
Consultant Psychiatrist, New Delhi Department of Psychiatry, NIMHANS,
Former Additional Professor of Bangalore 560029.
Psychiatry, NIMHANS, Bangalore
Abbott
About the Authors
Dr. Sumant Khanna
Dr. Sumant Khanna is currently a Consultant Psychiatrist in Delhi. Till last

year he was working as an Additional Professor in the Department of Psychiatry,
National Institute of Medical Sciences, Bangalore. His PhD work was on
understanding the neurobiology of Obsessive Compulsive Disorder. He has received
various national and international awards in recognition of his research
presentations and work. His areas of interest include clinical psychopharmacology,
obsessive compulsive disorder, personality disorders and serotonin. He ran an
OCD Clinic in the Institute. He is Convenor of the Clinical Psychopharmacology
Research Group in India. He has had projects funded by the Ministry of Science
and Technology in the area of serotonin in psychiatric disorders. He has also
conducted many clinical trials. He currently teaches research methodology to
psychiatrists involved in clinical trials across Asia and Europe. He has over
a 140 publications in Indian and foreign journals and 220 presentations in
national and internanational conferences.
He is currently involved in organizing research and conducting training

programs for prospective researchers. He also trains people internationally in
the usage of research instruments in psychiatry, and also develops interviews
for conducting such excercises. He has been the lead country principal investigator
for 2 protocols for multi-national companies which has also involved preparing
and signing off reports for international regulatory agencies. He is also involved
in designing research programs and is in the process of setting up facilities
to obtain grants and fund such programs in India. He continues to be involved
as a co-Investigator in many International Phase III studies, inspite of having
left Bangalore.
Dr.Y.C.Janardhan Reddy
Dr. Janardhan Reddy is currently working at NIMHANS, Bangalore as an

Additional Professor of Psychiatry. Dr. Reddy completed his post-graduation
in psychiatry from NIMHANS in 1991. Dr. Reddy's areas of interest include
OCD, Bipolar disorder and clinical drug trials.
He was a commonwealth research fellow at the Oxford University, Department
of Psychiatry, Warneford Hospital, Oxford, UK. During the period of fellowship,
He underwent training in cognitive behavior therapy in OCD. He has many
publications in international peer-reviewed journals on subjects pertaining
to his area of interest.
CONTENTS
1. Clinical Features of Obsessive Compulsive Disorder 1
2. Juvenile Obsessive Compulsive Disorder 11
3. Comorbidity in OCD 23
4. Biology of Obsessive Compulsive Disorder 33
5. Pharmacotherapy of Obsessive Compulsive Disorder 39
6. Behavior Therapy in OCD 43

Contributors
Shoba Srinath, YC Janardhan Reddy, M.D.D.P.M
Professor and Head, Child and Associate Professor,

Adolescent Psychiatry Services. Department of Psychiatry, NIMHANS,
Department of Psychiatry, NIMHANS, Bangalore 560029.
Bangalore 560029 E-mail: jreddy@nimhans.kar.nic.in
Y.P. Mukesh, D. Pravin,

Senior Resident, Child and Adolescent Senior Resident, Child and Adolescent
Psychiatry Services. Psychiatry Services
Department of Psychiatry, NIMHANS, Department of Psychiatry,
Bangalore 560029 NIMHANS, Bangalore 560029
Sumant Khanna, MD, PhD, MAMS, MRC Dr BM Suresh, MD, DNB, PGDMLE
PsychConsultant Psychiatrist, Senior Resident
New Delhi Former Additional Department of Psychiatry, NIMHANS,
Professor of Psychiatry, NIMHANS, Bangalore 560029
Bangalore E-mail: sbm@nimhans.kar.nic.in
Dr T. Jaideep,
Senior Resident
Department of Psychiatry, NIMHANS,
Bangalore 560029
PREFACE
O bsessive-compulsive disorder is the fourth commonest mental disorder with

disability in severe cases often comparable to the disability associated
with mental illnesses such as schizophrenia and bipolar disorder. However, till
recently it was considered to be a rare disorder with a prevalence rate of less
than 5 per 1000 adults. Epidemiological studies have shown that roughly about
2% of adults suffer from this intriguing disorder. It is now evident that the
prevalence of OCD in adolescents is comparable to that in adults although
the exact prevalence of OCD in children is not known. Despite such a high
prevalence only a minority of sufferers seek treatment and that too after several
years of suffering. This is because of the secretive nature of the condition.
Substantial progress has been made in the last two decades in understanding
the various aspects of the disorder that include its prevalence, clinical
presentation, comorbidity, etiology, and treatment. Significant research on OCD
has been conducted in an Indian population also. A number of studies have
shown that the clinical picture is similar across cultures. Several double-blind
controlled studies have clearly demonstrated the efficacy of serotonin reuptake
inhibitors in the treatment of OCD. Similarly, several studies have demonstrated
the efficacy of behavior therapy and cognitive behavior therapy in OCD.
Significant progress has been made in understanding the pathophysiology
of OCD although the exact cause of the disorder is still unknown. Most notable
are the neuroimaging studies that have implicated the frontal-basal ganglia-
thalamo-cortical circuit in the pathogenesis of the disorder. Efficacy of the
serotonin reuptake inhibitors have contributed to the popular serotonergic
hypothesis of OCD. In recent years there has been an interest in the immunologic
hypothesis of OCD particularly in children. In the last decade, there has been
considerable interest in a group of disorders called obsessive-compulsive spectrum
disorders that are believed to share some of the features of OCD.
i
Despite the progress made in the understanding and treatment of OCD,
the disorder continues to run a chronic course in a majority of patients with
waxing and waning of symptoms. Because of its high comorbidity with depression
and other anxiety disorders, and the secretive nature of the patients, the disorder
often gets misdiagnosed as depression and anxiety. Therefore, it is important
to correctly diagnose and treat OCD.
This book on OCD provides a comprehensive account of all aspects of OCD.
The book includes chapters on clinical features, comorbidity, biology, behavior
therapy, pharmacotherapy, and childhood OCD. The book tries to provide a
comprehensive summary of all aspects of OCD without attempting to give
exhaustive factual information and extensive references. Only important references
are provided. The book is primarily aimed at busy practicing psychiatrists,
and general physicians who need a ready and handy reference on OCD. Therefore,
the emphasis is on the clinical aspects of the disorder. Abbott India Ltd. (Lenbrook
Division) has to be thanked for having come forward to publish a book on
OCD, which will hopefully serve the needs of the intended users of the book.
Sumant Khanna
YC Janardhan Reddy
All rights reserved

Published in 2004
This book has been pubilshed by
Abbott India Ltd
Lenbrook Division
17, R Kamani Marg, Mumbai 400001
ii
CLINICAL FEATURES OF OBSESSIVE COMPULSIVE DISORDER 1
CLINICAL FEATURES OF OBSESSIVE

COMPULSIVE DISORDER
Dr YC Janardhan Reddy
Additional Professor, Department of Psychiatry, NIMHANS, Bangalore 560029.
O bsessive-compulsive disorder (OCD) is an intriguing and disabling illness

characterized by the presence of obsessions (unwanted thoughts, images
or impulses) and/or compulsions (repetitive behaviors) (Khanna et al., 1990).
As recently as in the 1980s, OCD was considered to be a rare disorder that
was hardly responsive to treatment. Much of the progress in understanding
the OCD has occurred following the finding of the National Epidemiological
Catchment Area (ECA) survey (Karno et al., 1988) that OCD is the fourth
most common psychiatric disorder. An important additional impetus to the
increased interest in diagnosing OCD is the availability of effective treatments.
However, despite the high prevalence only a minority of the sufferers seek
professional help because of the secretive nature of the illness. Those who suffer
from OCD often find it embarrassing to talk about their unwanted thoughts
resulting in considerable delay in seeking treatment. By the time medical help
is sought, many years of illness would have elapsed.
PREVALENCE
In the large epidemiological study, the ECA survey, conducted in the United
States in 1984, OCD was the fourth most common psychiatric disorder with
a lifetime prevalence of 2.5%. Another study examined the prevalence of OCD
in diverse cultures (Cross-National Collaborative Study) and reported lifetime
prevalence of 1.9% to 2.5% with the exception of Taiwan where for unknown
reasons the prevalence of OCD was low (Weissman et al., 1994). In contrast
2 CLINICAL FEATURES OF OBSESSIVE COMPULSIVE DISORDER
to the findings of these two studies, in the National Survey of Psychiatric

Morbidity conducted in Britain (Jenkins et al., 1997), prevalence of OCD was
about 1%. To summarize, it would appear that the prevalence of OCD in the
community may be about 2%. This means that the OCD is highly prevalent
and more prevalent than the schizophrenia and bipolar disorder.
In clinical samples of adult OCD, there is roughly equal ratio of men to
women. However in epidemiological samples, there is some what higher
representation of OCD in women (1.5%) compared to men (1%). In childhood
onset OCD, about 60% of patients are male possibly due to the earlier age
at onset in males (Reddy et al., 2000).
CLINICAL FEATURES
Obsessions and compulsions constitute the core clinical features of OCD.

Obsessions are characterized by recurrent and persistent thoughts, images or
impulses that are perceived as intrusive and inappropriate. The obsessions cause
marked distress and/or anxiety. Most patients who suffer from obsessions readily
admit that their thoughts/images/impulses are irrational, excessive and unwanted.
They also admit that they are a product of their own mind and not imposed
from without. The recognition by the OCD sufferer that the obsessions are
a product of his or her own mind differentiates them from the delusional thoughts
characteristic of schizophrenia. Because the obsessions are intrusive, unwanted
and distressing, attempts are made to ignore, suppress or neutralize them with
some other action or thought (compulsions). It should be borne in mind that
the obsessions are not simply excessive worries about real problems. This is
important to remember because excessive worrying about real-life problems is
often present in generalized anxiety disorder and depression and should not
get misdiagnosed as OCD.
Compulsions are repetitive behaviors (e.g., hand washing, checking) or
mental acts (e.g., praying, counting) that the person feels driven to perform
in response to an obsession, or according to certain rules that must be applied
rigidly. The compulsions are aimed at preventing or reducing distress (e.g.,washing
hands repeatedly to get over the feeling of being contaminated, repeated praying
to overcome an unwanted sexual thought about a family member) or preventing
some dreaded event from occurring (e.g., counting to prevent family members
from meeting with a fatal accident). These behaviors are either not connected
in a realistic way with what they are designed to prevent, or are clearly excessive.
For example, counting numbers in a particular fashion does not in a realistic
way prevent an accident from occurring. Similarly, hand-washing may remove
the dirt but one may not have to wash for hours to remove the dirt. This
is clearly excessive.
The diagnostic guidelines according to the International Classification of
Mental and Behavioral Disorders (ICD-10) are given below.
For a definite diagnosis, obsessional symptoms or compulsive acts, or both,
must be present on most days for at least 2 successive weeks and be a source
of distress or interference with activities. The obsessional symptoms should have
the following characteristics:
(a) They must be recognized as the individual’s own thoughts or impulses;
(b) There must be at least one thought or act that is still resisted unsuccessfully,
even though others may be present which the sufferer no longer resists;
(c) The thought of carrying out the act must not in itself be pleasurable (simple
relief of tension or anxiety is not recognized as pleasure in this sense);
(d) The thoughts, images, or impulses must be unpleasantly repetitive
Traditionally, awareness of the senselessness or unreasonableness of obsessions
and the accompanying resistance against the obsessions has been considered
to be the hallmark of the disorder. However, it is increasingly being recognized
that a substantial proportion of patients consider their obsessions to be somewhat
reasonable with varying degree of insight. For example, in an Indian study,
25% of the patients had poor insight (Ravikishore et al, in press). It is to
be noted here that although poor insight was not infrequent, lack of insight
amounting to delusional belief was rarely seen.
The following are the common obsessive-compulsive symptoms
Obsessions % Compulsions %
Fear of contamination 61 Cleaning & washing 50

Aggressive thoughts, images & impulses 43 Ordering 41
Need for symmetry 35 Repeating 38
Sexual 31 Checking 18
Religion 30 Hoarding 7
Pathological doubt 21 Miscellaneous 41
Miscellaneous 40
Jaisoorya TS, Reddy YCJ & Srinath S (2003)
Most patients have multiple obsessions and compulsions over time although
a particular obsession may dominate the clinical picture at any one time. The
presence of only obsessions without compulsions is unusual. Similarly, only
compulsions without obsessions are unusual particularly in adults. However,
pure compulsions do occur in children. The following description of some common

obsessions and compulsions illustrates the clinical presentation of OCD.
Contamination
Contamination obsessions are the most common type of obsessions in OCD.
They are typically characterized by a fear of dirt or germs. Patients frequently
fear that they may contract a disease or spread a disease because of exposure
to contaminants. However, the fear is occasionally not based on disease but
based on a subjective feeling of not being clean enough. Contamination obsessions
may also involve environmental contaminants (asbestos, radiation, pesticides),
household items (cleansers, solvents), bodily waste or secretions (urine, feces,
saliva), sticky substances (adhesives, grease, oil), and animal waste (feces, urine).
Most patients with contamination fears extensively avoid feared contaminants.
For example, they may not touch door knobs or light switches touched by others,
pick up fallen objects, or use money handled by others. They may even use
rubber gloves, don’t shake hands, not go anywhere near people whom they
consider dirty or sick, and won’t use articles used by others. There are also
patients who do not take bath for days to weeks because of the fear of
contamination associated with using the bathroom used by others. Exposure
to any of the feared contaminants causes intense anxiety and distress which
in turn results in excessive cleaning and washing. The cleaning compulsions
include excessive or ritualized hand washing, showering, bathing, tooth brushing,
and elaborate toilet routines. Patients may wash hands like surgeons scrubbing
before an operation, and use harsh detergents. It is also well known that many
patients indulge in elaborate cleaning rituals like repeated cleaning of the floors,
and household items particularly utensils used in kitchen. These washing and
cleaning rituals usually take long hours and exhaust the patient. It is not unusual
to find patients who brush their teeth for an hour and take bath for several
hours often emptying the water tank.
Sexual and aggressive obsessions

Patients with these obsessions are plagued by thoughts, images or urges that
are sexual or aggressive in nature. For example, sexual obsessions could be
in the form of intrusive sexual thoughts/images about family members. Patients
often fear that they may commit a sexually unacceptable act such as touching
the private parts of immediate family members. Occasionally, patients may also
harbor doubts as to whether they are gay even though there is every reason
to believe that they are heterosexual. Aggressive obsessions include fears that
one might harm self or others on an impulse (fear of stabbing with a knife,
jumping in front of a car, leaping out of an open window) or because not careful
enough (fear of hitting a pedestrian because of not being careful), and fear
of blurting out obscenities or insults. Patients may also have violent or horrific
images such as images of family members involved in gruesome accidents. The
obsessions of sexual or aggressive nature cause intense guilt, shame and anxiety
because of the abhorrent nature of the thoughts. Patients often suffer for years
without revealing their thoughts to anyone because of the embarrassing nature
of the thoughts. Their constant fear is also that they may act out on their
obsessions. As a result of this fear, they tend to avoid anything that triggers
their obsessions. For example, a person harboring sexual thoughts about family
members may never look in to their eyes. Similarly, a mother who harbors
an urge to harm her child may remove all the sharp objects from the house
and may even not take care of the child. Patients with these obsessions also
seek repeated reassurance from others that they are actually not capable of
doing what they are worried about. The reassurance seeking behavior can be
a great annoyance to others, particularly family members, because the patients
are not happy if reassured once, they need to be reassured all the time.
Pathological doubt and checking

Patients with doubts typically worry that something terrible may happen because
they have not completed an act thoroughly or completely. As a result they check
frequently. Sometimes they insist that others observe their act so that they
can be reassured later. Such patients can spend hours checking before leaving
their home. They don’t trust their memory and senses. The doubts usually
involve daily routine activities. For example, the doubt that the gas knob is
not turned off properly and as a result gas may leak and cause a fire accident.
Other examples include repeatedly checking door locks, electrical appliances
and faucets.
Religion
Patients with religious obsessions typically experience intrusive unacceptable
thoughts or images about God or religion. For example, intrusive thoughts of
abusive nature towards God whenever one try to pray or on seeing the photographs
or when one visits places of worship. Similarly some experience intrusive images
of stepping on photographs of deities, and images of smearing feces. These
thoughts cause intense guilt and distress because it is considered blasphemous
to harbor such thoughts.
Need for symmetry, order and exactness

This includes a drive to order or arrange things in a symmetrical manner,
or perfectly, or in an exact sequence. Patients typically describe an urge to
repeat acts until they feel “just right” that the act has been completed perfectly.
They describe feeling uneasy or unsettled rather than anxious or fearful when
things are not done perfectly or according to an order. However, there are some
who do things in a particular order to prevent harm occurring to loved ones.
These patients may experience anxiety if things are not arranged in a particular
order. Examples of need for symmetry include being bothered that shoe laces
are not tied with same tension, that hair is not parted exactly straight or
that hair is not precisely of same length on either side of the head. In orderliness,
there is a need to arrange things in a particular order, for example, arranging
books according to their sizes. Some patients are very exacting in their needs.
For example, excessive botheration that the wall hangings are not straight or
that their clothing should not have any wrinkles.
Repeating rituals
Patients with repeating rituals repeat routine activities either due to doubt
or due to fear that some thing terrible may happen to self or others if not
repeated. Typical examples include taking clothes on/off, turning scooter on/
off, in/out of chair, going through doorway repeatedly and re-reading and re-
writing.
Hoarding
Hoarders have an urge to hoard or save things because they are worried that
they may discard things that is valuable or may be of some use in future.
They may pile up old newspapers, collect useless objects or may have problems
in discarding things that have no actual utility. Sometimes living rooms and
houses of hoarders can be cluttered with piles of trash making living difficult.
However, hoarding should be distinguished from hobbies and the practice of
preserving things for monitory or sentimental reasons.
ASSESSMENT
Rater-administered scales
The most widely used instrument is the Yale-Brown Obsessive Compulsive Scale
(Y-BOCS), the best scale available to assess severity of OCD (Goodman et al.,
1989). It is a clinician administered instrument. It has an exhaustive checklist
of OC symptoms in addition to the severity scale. The severity scale has 10

items, five each for obsessions and compulsions. Obsessions and compulsions
are separately assessed for severity on five dimensions: time spent interference,
distress, resistance and control. Each is rated on a 0-4 scale. The maximum
total score is 40. Total score above 15 is indicative of clinical OCD.
The Comprehensive Psychopathological Rating Scale (CPRS) consists of several
subscales for psychiatric symptoms; the OCD subscale contains eight items:
rituals, inner tension, compulsive thoughts, concentration difficulties, worry over
trifles, sadness, lassitude and indecision (Asberg et al., 1978). It is evident
that the scale is non-specific and measures depression and related symptoms
also. It is not as good as Y-BOCS in measuring OCD symptom severity.
The National Institute of Mental Health (NIMH)-Global Obsessive-Compulsive
Scale (GOCS), is a rater administered point scale (1-15 points) (Rachman and
Hodgson, 1980). It contains five severity categories (1-3, normal; 4-6 subclinical;
7-9, clinical OCD, 10-12, severe OCD; 13-15, very severe OCD).
The Brown Assessment of Beliefs Scale (BABS) (Eisen et al) and Overvalued
Ideas Scale (OVIS) measure insight (Neziroglu et al., 1999).
Self-rated scales
The most widely used self-rating scales are the Muadsley Obsessive Compulsive
Inventory (MOCI) (Rachman and Hodgson, 1980), and the Leyton Obsessional
Inventory (LOI) (Cooper, 1970). The LOI has 69 yes/no questions. The scale
measures both symptoms and traits. The LOI is a useful screening instrument,
but it does not cover all obsessional symptoms. It may not be as good as Y-
BOCS to measure severity. The MOCI consists of 30 questions designed to yield
a total score and four subscale scores. A score of 18 out of 30 is indicative
of clinical OCD. The main disadvantage of MOCI is that it relies on specific
symptom sets and sometimes the chief obsessions of an individual are not listed.
COURSE
The OCD usually begins in adolescence or early adulthood although it can begin
in childhood. Nearly 65% of the patients have their onset before age 25 whereas
fewer than 15% have onset after age 35 (Rasmussen and Eisen 1998). In our
clinic samples a majority of patients had onset before 18 years (Jaisoorya
et al., 2003).
Although prognosis of OCD has traditionally been considered to be poor,
availability of effective treatments has considerably improved the prognosis.
In a recent study of course of OCD in adults (Eisen et al., 1999) 47% of the
patients had remitted by the end of 2years (full remission in 12% and partial
remission in 31%). In a 40-year follow up, nearly 80% of individuals improved
with nearly full recovery in almost 50% of the patients (Skoog and Skoog 1999).
However, a synthesis of findings of various studies seems to suggest that about
25% of the patients recover completely and about 15% continue to suffer with
deteriorating course. Most follow a course marked by chronicity with some
symptom fluctuation over time, but without clear-cut remissions or deterioration.
It should be noted here that there is no follow-up data on adult OCD subjects
from India.
HOW TO IDENTIFY AN OCD SUFFERER?
Following simple questions are suggested encourage OCD patients to talk about
their symptoms:
Do you wash or clean a lot more than others?
Do you check things a lot?
Are there any thoughts that keep bothering you and you would like to get
rid of but cannot? For example:
■ personally unacceptable religious or sexual thoughts
■ urges to harm self or others
■ thoughts of something terrible happening to self or loved ones (e.g.,
accidents)
■ worried that you may get some illness such as AIDS
Do your daily activities take a very long time to finish?
Are you concerned about orderliness and symmetry?
Do you repeat routine activities such as in/out of chair, walking through
doorway?
Do you collect useless objects and have difficulty in discarding them?
CONCLUSIONS
The OCD is a common psychiatric disorder that is often undiagnosed. Only

a small proportion of OCD sufferers seek treatment because of the associated
embarrassment, shame and guilt. It is important to correctly diagnose the disorder
early because effective treatments are now available to treat OCD. The OCD
tends to run a chronic course with fluctuations in symptom severity. Complete
recovery occurs in only a quarter of patients.
REFERENCES
1. Asberg M, Montgomery S, Perris C, Schalling D, Sedvall G. A comprehensive
psychopathological rating scale. Acta Psychiatr Scand 1978; 271 (suppl.):5.
2. Cooper J. The Leyton Obsessional Inventory. Psychiatr Med 1970; 1: 48-54.
3. Eisen JL, Goodman WK, Keller MB et al. Patterns of remission and relapse in obsessive-
compulsive disorder: a 2-year prospective study. J Clin Psychiatry 1999; 60:346-351.
4. Eisen JL, Phillips KA, Rasmussen SA et al. The Brown Assessment of Beliefs Scale
(BABS): reliability and validity. Am J Psychiatry 1998; 155:102-108.
5. Goodman W, Price L, Rasmussen SA et al. The Yale-Brown Obsessive-Compulsive Scale.
I. Development, use, and reliability. Arch Gen Psychiatry 1989; 46:1006-1011.
6. Jaisoorya TS, Janardhan Reddy YC, Srinath S. The relationship of obsessive-compulsive
disorder to putative spectrum disorders: results from an Indian study. Comprehensive
Psychiatry 2003; 44:317-323.
7. Janardhan Reddy YC, Srinivas Reddy P, Shobha S, Khanna S, Sheshadri SP, Girimaji
SC. Comorbidity in juvenile obsessive-compulsive disorder : a report from India. Canadian
Journal of Psychiatry 2000; 45:274-278.
8. Jenkins R, Bebbington PE, Brugha T et al. The National Psychiatric Morbidity Surveys
of Great Britain: I. Strategy and methods. Psychological Medicine 1997; 27:765-774.
9. Karno M, Golding JM, Sorenson SB, Burnam MA. The epidemiology of obsessive-
compulsive disorder in five US communities. Arch Gen Psychiatry 1988; 45:1094-1099
10. Khanna S, Kaliaperumal VG, Channabasavanna SM. Clusters of obsessive-compulsive
phenomena in obsessive-compulsive disorder. Br J Psychiatry 1990; 156: 51-4.
11. Neziroglu F, McKay D, Yariura-Tobias JA, Stevens KP, Todaro J. The Overvalued Ideas
Scale: development, reliability and validity in obsessive compulsive disorder. Behav Res
Ther 1999; 37: 881-902.
12. Rachman SJ, Hodgson RJ. Obsessions and Compulsions. Prentice-Hall, Englewood Clifs,
1980.
13. Ravikishore V, Samar R, Janardhan Reddy YC, Chandrasekahr CR, Thennarasu K. Clinical
characteristics and treatment response in poor and good insight obsessive-compulsive
disorder. European Psychiatry (in press).
14. Rasmussen SA, Eisen JL. Phenomenology and clinical features of obsessive-compulsive
disorder. In: Obsessive Compulsive Disorders: Practical Mangement, 3rd Edition. Edited
by Jenike MA, Baer L, Minichiello WE. St.Louis, MO, CV Mosby, 1998, pp 12-43.
15. Skoog G, Skoog I. A 40-year follow-up of patients with obsessive-compulsive disorder.
Arch Gen Psychiatry 1999; 56:121-132.
16. Weissman MM, Bland RC, Canino GJ et al. The cross-national epidemiology of obsessive-
compulsive disorder. J Clin Psychiatry 1994; 55 (Suppl. 3):5-10
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Clinical Descriptions and Diagnostic Guidelines, World Health Organization, Geneva.
JUVENILE OBSESSIVE COMPULSIVE DISORDER 11
JUVENILE OBSESSIVE COMPULSIVE

DISORDER
Dr Shoba Srinath, Professor and Head, Child and Adolescent Psychiatry Services
Dr D. Pravin, Senior Resident, Child and Adolescent Psychiatry Services
Dr Y. P. Mukesh, Senior Resident, Child and Adolescent Psychiatry Service
Department of Psychiatry, National Institute of Mental Health and Neurosciences
(NIMHANS), Bangalore 560029
INTRODUCTION
O bsessive compulsive disorder (OCD) is a common childhood psychiatric

condition which largely remains undiagnosed and untreated for a long
time. Till recently, it was believed to be a very rare disorder in young people.
Epidemiological and clinical studies have now revealed that OCD is far more
prevalent among children and adolescents than previously thought.
EPIDEMIOLOGY
Systematic studies have shown that from one third to one half of adult cases
with OCD have their onsets in childhood and adolescence (Flament & Cohen,
2002; Jaisoorya et al., 2003). Epidemiological studies on adolescent OCD have
shown varying rates ranging from 1% to 4%, possibly because of varying
methodologies and sample sizes but the rates are similar to those in adults
(Flament & Cohen, 2002). There is no community data on prevalence of OCD
in children, but the frequency in clinical samples is about 2%.
A study done in a school population in India showed a point prevalence
rate of 1.45%, which is comparable to the rates described in the Western literature
(Kirthi Kumar, Personal communication, 1998). Clinic based prevalence rate
12 JUVENILE OBSESSIVE COMPULSIVE DISORDER
at the Child and Adolescent Psychiatric Services of the National Institute of

Mental Health and Neurosciences (NIMHANS), Bangalore in the year 2003
was 2.8% (27 cases out of 935).
The mean age at onset of OCD in children and adolescents ranges from
6 to 11 years of age, with a bimodal distribution with peaks in early childhood
and early adolescence. Children with early onset OCD (<7years) are predominantly
male and are more likely to have a family history of OCD than those
with onset at a later age. Overall, in juvenile OCD, boys outnumber girls
2:1 or 3:1.
ETIOLOGY
OCD is essentially a neuropsychiatric disorder. Evidence from neuroimaging

studies implicates the involvement of frontal-subcortical circuit involving
orbitofrontal cortex, cingulated cortex and the basal ganglia-most particularly
the caudate nuclei (reviewed in an earlier chapter). Studies have shown that
after psychological or pharmacological treatment, there is demonstrable reduction
of the hypermetabolism of the frontal lobes.
Efficacy of serotonin reuptake inhibitors (SRIs) in treating OCD has inspired
a “serotonergic hypothesis” of OCD although there is no evidence for primary
serotonergic abnormality in OCD. This topic has been dealt with in detail in
the chapter on neurobiology of OCD.
Family genetic studies have shown that OCD is more common in relatives
of individuals with OCD than in the general population. It is well known that
the risk is greater in the relatives of juvenile onset OCD subjects than in the
relatives of adult onset OCD subjects (20% vs. 11%) (Pauls et al., 1995). It
has also been suggested that at least some forms of OCD, particularly juvenile
onset OCD, could be genetically related to Tourette’s syndrome (TS). However,
in an Indian study, morbid risk of OCD in first-degree relatives of juvenile
OCD subjects was only 5% and none of the relatives had TS suggesting most
juvenile OCD subjects were nonfamilial and unrelated to TS (Reddy et al.,
2001).
A subgroup of children with OCD seems to have their symptoms triggered
or exacerbated by Group A beta haemolytic streptococcal infection (GABHS).
The symptoms seem to be caused from the caudate swelling that is caused
in these children because of an auto-immune reaction between caudate tissue
and antineuronal antibodies formed against GABHS similar to as in Sydenham’s
chorea. This subtype of OCD, called Paediatric Auto-immune Neuropsychiatric
Disorders Associated with Streptococcal infection (PANDAS), is characterized

by sudden and dramatic onset or exacerbation of OCD or tic symptoms, associated
with neurologic findings, and a recent streptococcal infection (Swedo et al.,
1998). However these findings have not been replicated in other studies and
the proportion of these ‘immunologic’ OCD cases remains unknown.
CLINICAL FEATURES
The diagnostic criteria for OCD in children and adolescents are not different
from the criteria in adults. The only difference in criteria between children
and adults is with regard to criterion B in the DSM-IV that specifies that
the person should at some point during the course of the disorder recognize
the obsessions and compulsions are excessive or unreasonable. However, this
does not apply to children where insight may be poor. The clinical presentation
of OCD in children and adolescents has been documented in various cultures
including India (Khanna & Srinath, 1989; Reddy et al., 2003; Jaisoorya et al.,
2003).The most common obsessions are related to contamination fears, often
accompanied by protracted or ritualized compulsive washing and avoidance of
“contaminated objects”, leading to increasing constriction of functioning. An
obsessive worry about safety, usually of parents or themselves, is common along
with obsessions related to morality or religiosity. A common feature of many
obsessive worries is an exaggerated perception of risk on the part of the child
that is decreased by the compulsive ritual.
Common compulsions are checking, washing, repeating, touching, counting,
and ordering. Similar to adults, children have compulsions with obsessions,
but compulsions in the absence of obsessions are often found in young children
or children with tic disorders who often describe their rituals as being performed
in response to an irresistible urge, an “empty” feeling, or an otherwise vague
sensation (the “just right” phenomenon).
Mental rituals may consist of silent praying, repetition, counting, or having
to think about or look at something in a particular way until it feels “just
right”. Unlike many adults children may be unable to specify the dreaded
consequences their compulsive rituals are intended to avert, beyond a vague
premonition of something bad happening. Simple compulsions such as touching
or ordering may lack a discernable ideational component and may be
indistinguishable from complex tics. The performance of the ritual transiently
reduces the obsessional worry, albeit at the potential cost of increasing impairment
and constriction of functioning.
Children like adults can have pure obsessions without compulsions. The
common themes include sex, aggression, and harm to self or others. Childhood
OCD is reactive to stress as in adults; many children experience worsening
of symptoms during times of stress (e.g., start of a school year, moving to
a new home, death of or separation from a family member) or illness.
CO-MORBIDITY
Comorbid psychiatric disorders are common in juvenile OCD. Though the rate
of comorbidity varies across studies, as many as 80% of children with OCD
meet diagnostic criteria for an additional Axis I disorder, and as many as 50%
experience multiple comorbid conditions. In an Indian study 69% of the subjects
had a comorbid disorder (Reddy et al., 2000)
Nearly one third to one half of the children with OCD seems to have a
current or past history of another anxiety disorder. In children, overanxious
and separation anxiety disorders are the commonest whereas in adolescents,
generalized anxiety and panic disorders are the commonest. Prevalence of
depression is in the range of 13% to 70%, adding to the dysfunction already
caused by OCD. Depression and anxiety can predate OCD or develop later.
Of particular interest is the high comorbidity between OCD and tic disorders
including TS. Tic disorders have been reported in 17% to 60% of juvenile subjects
(Reddy et al., 2000). At least 50% of children with TS develop OC symptoms
or OCD by adulthood. This and a biredirectional familial comorbidity between
TS and OCD suggest that some forms of OCD are genetically related to TS.
The relationship between putative obsessive-compulsive spectrum disorders
and OCD has been dealt with in a previous chapter on OCD. Children with
pervasive developmental disorders (PDD) (autism, Asperger’s and related
disorders) often manifest stereotypic behaviors and routines, as well as unusual
preoccupations and fixed interests that many describe as “obsessive-compulsive”.
The cognitive and language difficulties characteristic of PDD frequently makes
it difficult to assess the extent of personal distress, irrationality, intrusiveness
and excessive nature of the symptom characteristic of true obsessions. However,
the OC symptoms in PDD share certain common features with uncomplicated
OCD, in being highly prevalent in relatives of children with PDD and a good
response to SSRIs.
Rarely schizophrenia can co-occur with OCD. There are also reports suggesting
increased prevalence of bipolar disorder in children with OCD. It is important
to identify bipolar disorder since drugs used in the treatment of OCD can
precipitate mania.
A high prevalence of attention deficit hyperactivity disorder (ADHD), conduct

disorder and oppositional defiant disorder have been reported in children with
OCD (Geller et al., 1996). In Indian studies rates of ADHD have ranged from
9% to 18% (Reddy et al., 2000; Jaisoorya et al., 2003), whereas in other studies
rates range from 33% to 57% (Geller et al., 1996, 2001).
DIFFERENTIAL DIAGNOSIS
Symptoms of OCD should be differentiated from normal childhood rituals such

as bedtime rituals, not stepping on cracks, counting, having lucky and unlucky
numbers, and wanting things in their right place. These developmentally normal
rituals are common in younger children and mostly disappear by 8 years. Unlike
rituals in OCD, these rituals are not time consuming and are not considered
unwanted; do not cause anxiety; and does not interfere in functioning. There
is no evidence that children with normal rituals develop OCD later. Other anxiety
disorders have to be differentiated from OCD.
Tics occurring in TS may sometimes resemble compulsions but they are
generally avolitional and occur in the absence of a triggering obsessional thought,
although complex motor tics may be difficult to differentiate from OCD
compulsions.
Stereotypic behaviors seen in children with PDD can be differentiated from
compulsions by the fact that the former behaviors are often enjoyable and are
not performed in response to a distressing thought or sensation. Also children
with OCD generally do not lack the social or language deficits.
Children with OCD can act in bizarre ways sometimes almost appearing
to be delusional in their potential unrealistic dangers or the necessity of
performing rituals, and have a dramatic deterioration in adaptive functioning
similar to that in psychosis. However, the absence of thought disorder or
hallucinations and preservation of reality testing outside the area of obsessional
concern help distinguish the symptoms from those in psychosis.
ASSESSMENT
The successful diagnosis and treatment of OCD requires careful and systematic
evaluation. Initially, a thorough diagnostic evaluation is necessary to accurately
establish a diagnosis of OCD, to rule out phenomenologically similar conditions,
and to identify comorbid conditions that may influence treatment planning.
Baseline symptom severity and profile assessment is very essential for systematic
and serial evaluation of treatment response. These are also essential for developing
exposure and response prevention exercises for CBT.

The children’s Yale Brown Obsessive-Compulsive Scale (C-YBOCS) is a reliable
and valid clinician administered measure adapted from the adult version of
the YBOCS and is currently the scale of choice to assess the severity and response
to treatment in children with OCD (Scahill et al., 1997). The initial section
consists of a symptom checklist covering a comprehensive array of obsessions
and compulsions. The C-YBOCS severity score is derived from the second section
of the measure, in which the global ratings of time spent, interference, distress,
resistance, and control are measured for obsessions and compulsions separately
and a total score is derived. Separate scores, ranging from 0 to 20, are obtained
for obsessions and compulsions, which, when combined yield a total severity
score of 0 to 40. A C-YBOCS score of greater than or equal to 16 indicates
clinically significant OCD. Scores repeated at intervals give an idea of the
treatment response.
The Child Version of the Leyton Obsessional Inventory (LOI-CV) is a useful
self-rated symptom and severity inventory for children older than 10 years (Berg
et al., 1998). It is available in paper and pencil and card sorting forms. The
instrument has 44 items and generates scores on symptoms, interference and
resistance.
Data regarding global functioning which can be assessed using measures
such as Clinical Global Impairment (CGI)-severity and improvement subscales
are useful since patients may become symptom free but do not achieve functional
improvement, thus helping in making important treatment decisions.
TREATMENT
Established treatments for OCD include clomipramine, the serotonin reuptake

inhibitor (SRI), and specific serotonin reuptake inhibitors (SSRIs) and cognitive
behavior therapy (CBT).
Pharmacotherapy
The clomiprmaine is a SRI. The SSRIs include fluoxetine, sertraline, fluvoxamine,
paroxetine and citalopram. Of these, clomipramine, fluvoxamine, sertaline, and
fluoxetine are approved by the FDA for use in OCD although others are also
effective in treating OCD.
In the absence of direct head-to-head trials comparing the relative efficacy
of various SRI/SSRIs, it is not known whether one is more effective than others
in treating OCD in juvenile population although in metaanalytical studies of
adults, clomipramine is found to have slightly more anti obsessional activity

than the SSRIs. In practice therefore, the clinicians’ agent of choice is guided
side effect profile and drug interactions. Clomipramine has most anticholinergic
side effects and sedation. In higher doses, it is also associated with increased
risk for seizures. Overdose with clomipramine can be fatal. The SSRIs are
associated with headaches, nausea, insomnia and agitation. In view of the
unfavorable side effect profile associated with clomipramine, most clinicians
would prefer to start with a SSRI.
According to expert consensus guidelines (King & March, 1998), the decision
to use pharmacotherapy in children and adolescents depends upon the severity
of illness. In mild OCD without significant comorbidity, CBT is preferred over
medications. However, in India, because of the manpower constraints CBT cannot
be readily offered to all patients, instead pharmacotherapy as the first choice
is the most practical approach.
An adequate trial with medication is required to determine whether a child
is a responder to a given medication or not (10 to 12 weeks of treatment with
adequate dose). In OCD trials, the SRI/SSRIs have been used in high doses
(Table 1) and it is believed that OCD patients require much higher doses than
those with depression. However, side effects are dose dependent. Therefore,
SRI/SSRIs have to be started at low doses and progressively increased in case
of poor response with lower doses.
Although it is not known whether one medication works better than the
other, failure to respond to one compound does not necessarily predict poor
response to other SRI/SSRIs. Thus, if there is no response after 10-12 weeks
of adequate trial with one drug, switching to another is reasonable. Most clinicians
TABLE 1
Pharmacological Treatment of OCD in children
Drug Dosage in Children /Day Duration
First Line Agents

Clomipramine 75-250mg (Max 5 mg/kg) 10-12 weeks
Fluoxetine 20mg-60mg 10-12 weeks
Fluvoxamine 200-250 mg 10-12 weeks
Sertraline 100-200 mg 10-12 weeks
Paroxetine 20-60mg 10-12 weeks
Citalopram 20-60mg 10-12 weeks
Augmenting Agents
Clonazepam 5 mg 4-6 weeks
Haloperidol 3 mg 4-6 weeks
Risperidone 0.5-2 mg 4-6weeks
prefer to use SSRIs for the first 2 trials and use clomipramine if the SSRIs
fail. If the response to SRI/SSRIs is inadequate augmentation with clonazepam,
risperidone, haloperidol or buspirone may be considered. In children with comorbid
tic disorder or schizotypal disorder, augmentation with low dose risperidone
or haloperidol is recommended since response to SRI/SSRIs alone is poor in
this subgroup of children.
The optimal duration of maintenance treatment is unclear. It is recommended
that medications be continued for 12 to 18 months after satisfactory improvement
is obtained. Once the decision to withdraw the medication is made, tapering
should be gradual, preferably overall several months since relapse following
discontinuation is frequent. In some children maintenance medication for longer
periods may be warranted in view of potential relapses. In such situations,
a potential alternative such as CBT has to be considered since CBT is associated
with lesser chances of relapse. However, it should be mentioned here that not
all children comply with CBT; therefore, medications may be the only option
in such children. The optimal maintenance dose is also unclear; however, after
prolonged remission, an attempt may be made to use the minimum effective
dose to prevent relapse.
Cognitive-Behavioral Therapy
The theoretical rationale and practice is similar to that in adults. March and
Mulle (1987) have developed a manualised approach to CBT in OCD children
with the aims of facilitating compliance. Treatment takes place over 4 steps
distributed across 16 weekly sessions. Each session would include a statement
of goals for that session, review of preceding week, introduction of new
information, “nuts and bolts practice”, and homework for the coming week,
and monitoring procedure.
Step 1 involves psychoeducation emphasizing to the child that it is the OCD,
and not the child, that is the problem. For young children, the OCD may
even be given a nasty nickname and the “good guys” (child, parents, and therapist)
work on getting rid of the “bad guys” (the OCD). This type of alliance helps
engage the child in treatment. Step 1 also explores the risks and benefits of
the behavior therapy programme and introduces story metaphors by placing
OCD in a narrative context. The use of story methodology facilitates the therapy
process. Step 2 and 3 map the child’s experience with OCD including avoidance
behaviors within a narrative context. They also include trial ERP tasks to gauge
the child’s level of understanding and willingness to comply with ERP. Step
4 implements both ERP and anxiety management. Anxiety management involves
relaxation, constructive self talk, breathing techniques and positive coping

strategies providing the child with tools to use during ERP.
ERP for OCD involves (1) daily exposure to cues avoided because of their
inducing discomfort and rituals, and (2) maintaining exposure and not ritualizing
for at least an hour or until the discomfort slowly subsides. A minimal trial
consists of 10 to 20 hours of treatment with both exposure and response
prevention.
At the end of Step 1, the family is given information booklets about OCD.
Family psychopathology is neither necessary nor sufficient for the onset of OCD.
Nonetheless families influence the treatment and course of the disorder and
are often severely affected by the disorder in child. Some families become over
involved in the child’s rituals or reassurance seeking behavior; others become
hostile to child’s behavior. Parents need guidance about how to handle their
child’s behaviors (which may be severely disruptive to family life) and how
to avoid punitive responses or get involved in their rituals. The family’s
involvement is essential for implementation of both CBT and pharmacotherapy
in children. A parent as “co-therapist” generally works best for the child.
CBT must be tailored to specific symptoms, for example, ERP alone is not
generally appropriate for scrupulousity and moral guilt or pathological doubts
where CT may be helpful. Contamination fears, symmetry rituals, counting/
repeating, hoarding, and aggressive urges are more amenable to ERP. Obsessional
slowness appears not to respond well to either behavioral or medication treatment;
techniques such as modeling (implicitly or explicitly demonstrating adaptive
behaviors) and shaping (positively reinforcing successive approximations to a
target behavior) may be considered. Obviously, children who acknowledge the
senselessness of their obsessions and rituals are more likely to have better
outcomes, as they are more likely to be treatment compliant.
Investigative treatments
Tramadol, Transcranial Magnetic Stimulation, Neurosurgery and ECT have been
reported to be useful for adults in OCD. However, data for children is lacking.
COURSE AND OUTCOME OF OCD
What happens to juvenile OCD in the long term? Several studies have attempted
to document the course and outcome of in OCD in children. Most well known
study is the prospective longitudinal follow-up of 54 children 2 to 7 years later.
All the subjects in this study were intensively treated with clomipramine and
other SSRIs and some of them also underwent behavior therapy, individual
psychotherapy and family therapy. At follow-up, 43% still had clinical OCD;
the remaining had shown varying degrees of improvement. Twenty eight percent
had obsessive-compulsive symptoms, 18% has subclinical OCD and 11% had
recovered. However, only 6% were in true remission (recovered and not on
treatment). A German study reported remission in 29% of the subjects (Wewetzer
et al., 2001). In contrast to the findings of these studies, a 2 to 9 year (mean
5 years) follow-up of largely self-referred, drug-naïve juvenile OCD subjects
reported from NIMHANS, Bangalore, India (Reddy et al., 2003), found clinical
OCD in only 21% of the subjects. In this study, after initial consultation, about
75% of the children were adequately treated with SRI/SSRIs. A majority did
not have OCD (62%) and 17% had subclinical OCD. The most interesting finding
of this study was that 48% of the subjects were in true remission (no OCD
and not on treatment) suggesting an overall favorable outcome. It is possible
that the poor outcome reported in previous studies could be because of some
kind of sampling bias. Another interesting observation of some studies is that
episodic OCD is common in children (Wewetzer et al., 2001).
A poor response to initial treatment, parental Axis I diagnosis, and lifetime
history of a tic disorder (Leonard et al, 1993; Wewetzer et al, 2001) have been
associated with a worse OCD outcome. In the Indian study (Reddy et al.,
2003), none of the earlier known potential predictors were significantly associated
with OCD outcome. Instead, earlier age-at-onset of OCD and longer follow-
up was associated with better outcome.
REFERENCES
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of the Leyton Obsessional Inventory-Child Version: norms from an epidemiological study.
Journal of American Acdemy of Child and Adolescent Psychiatry 27:759-763.
2. Flament MF, Cohen D. Child and adolescent obsessive-compulsive disorder: a review.
In: Obsessive-Compulsive Disorder 2nd edition Editors. Maj M, sartorius N, Okasha A,
Zohar J. WPA Series Evidence and Experience in Psychaitry, John Wiley & Sons, West
Sussex, 2002, pp 147-183.
3. Geller DA, Biederman J, Griffin S et al (1996). Comorbidity of juvenile obsessive-compulsive
disorder with disruptive behavior disorders. Journal of American Acdemy of Child and
Adolescent Psychiatry 35: 1637-1646.
4. Geller DA, Biederman J, Faraone S et al (2001). Developmental aspects of obsessive-
compulsive disorder: findings in children, adolescents, and adults. Journal of Nervous
and Mental Diseases, 189:471-477.
5. Jaisoorya TS, Janardhan Reddy YC, Srinath S (2003). Is juvenile obsessive-compulsive
disorder a developmental subtype of the disorder? Findings from an Indian study. European
Child and Adolescent Psychiatry 12: 290-297.

6. Janardhan Reddy YC, Srinivas Reddy P, Srinath S, Khanna S, Sheshadri SP, Girimaji
SC (2000). Comorbidity in juvenile obsessive-compulsive disorder: a report from India.
Canadian Journal of Psychiatry 45: 274-278.
7. Janardhan Reddy YC, Srinath S, Prakash HM et al (2003). A follow up study of juvenile
obsessive-compulsive disorder in India. Acta Psychiatrica Scandinavica: 107:457-464.
8. Khanna S, Srinath S (1989). Childhood obsessive-compulsive disorder. I. Psychopathology.
Psychopathology 32: 47-54.
9. King RA, March J.S., Leonard H.L (1998) Practice parameters for the Assessment and
Treatment of Children and Adolescents with Obsessive-Compulsive Disorder. Journal
of the American Academy child and adolescent Psychiatry, 37:(suppl. 10), 27S-45S
10. Leonard HL, Swedo SE, Lenane MC et al (1993). A 2- to 7-year follow-up of 54 obsessive-
compulsive children and adolescents. Archives of General Psychiatry 50: 429-439.
11. March JS, and Mulle K (1987) How I ran OCD off my land. Durham. Duke university
medical centre.
12. Pauls D, Alsobrook J, Goodman W, Rasmussen S, Leckman J (1995). A family study
of obsessive-compulsive disorder. American Journal of Psychiatry 152: 76-84.
13. Scahill L, Riddle MA, McSwiggan-Hardin MT et al (1997). The Children’s Yale-Brown
Obsessive-Compulsive Scale: Preliminary report of reliability and validity. Journal of
American Academy of Child and Adolescent Psychiatry 36:844-853.
14. Srinivas Reddy P, Janardhan Reddy YC, Srinath S, Khanna S, Sheshadri SP, Girimaji
SR (2001). A family study of juvenile obsessive-compulsive disorder. Canadian Journal
of Psychiatry 46: 346-351.
15. Swedo SE, Leonard HL, Garvey M et al (1998)Pediatric autoimmune neuropsychiatric
disorders associated with streptococcal infections: clinical descriptions of first 50 cases.
American Journal of Psychiatry 155: 264-271
16. Thomsen PH., Mikkelson HU. (1995) Obsessive-compulsive disorder in children and
adolescents: a prospective follow up study of 23 Danish cases. Journal of the American
Academy child and adolescent Psychiatry, 34:1432-1440.
17. Wewetzer C, Jans T, Muller B et al (2001). Long term course outcome and prognosis
in Obsessive-compulsive disorder with onset in childhood and adolescence. European
child and adolescent Psychiatry, 10: 37-46.
COMORBIDITY IN OCD 23
COMORBIDITY IN OCD
Dr BM Suresh, Senior Resident
Dr YC Janardhan Reddy, Associate Professor of Psychiatry
Department of Psychiatry, NIMHANS, Bangalore 560029
O CD is a common mental disorder, and is often disabling. In addition, a

majority of patients with OCD are at high risk of having one or more
comorbid (co-existing) psychiatric illness. Anxiety disorders and depression are
the common comorbid conditions reported in most studies of OCD. In the
Epidemiological Catchment Area (ECA) study, two thirds of those with OCD
had a comorbid psychiatric illness (Karno et al., 1988). The most common
concurrent psychiatric disorders were major depression (30-55%), social phobia
(11-23%), generalized anxiety disorder (GAD) (18-20%), simple phobia (7-21%),
panic disorder (6-12%), eating disorder (8-15%), tic disorders (5-8%) and Tourette’s
syndrome (5%). The Cross-National Epidemiological Study (Weissman et al.,
1994) also found high rates of anxiety disorders (24-70%), and depression (12-
60%).
In addition to anxiety and depressive disorders, a fascinating group of
conditions called obsessive-compulsive spectrum disorders are also found to be
highly comorbid with OCD. These include Tourette’s syndrome and other tic
disorders, Hypochondriasis, body dysmorphic disorder, trichotillomania, and eating
disorders (Jaisoorya et al., 203). These disorders are considered to be related
to OCD because of similarity in clinical picture (morbid preoccupations and
compulsive behavior), high rate of comorbidity, and somewhat similar treatment
response.
It is extremely important to identify and treat coexisting psychiatric conditions
because untreated comorbid conditions could contribute to poor treatment response
and prognosis. Studying comorbidity also helps in understanding the possible
etiological relationship between the disorders.
24 COMORBIDITY IN OCD
MOOD DISORDERS
Major depressive disorder

Depression is the most common comorbid disorder in OCD. With the available
studies it can be concluded that out of every four OCD patients one will be
suffering from depression at any given point of time. It is characterized by
depressed mood, loss of interest or pleasure in daily activities, and fatigue
or loss of energy. Other typical symptoms of major depression include decreased
psychomotor activity, decreased sleep, decreased libido, decreased appetite, ideas
of guilt/sin, feelings of helplessness/hopelessness/worthlessness and death wishes/
suicidal ideas or attempts. Most patients with OCD view their depression as
secondary to the hopelessness associated with their obsessive-compulsive
symptoms. It is of great clinical relevance to identify and treat depression because
untreated depression interferes significantly with treatment particularly with
behavior therapy.
Bipolar disorder
It is a disorder characterized by episodes of mania and depression. A manic
episode is characterized by euphoria/elation, expansive or irritable mood, inflated
self-esteem or grandiosity, increased activity, decreased need for sleep,
overtalkativity, subjective experience that thoughts are racing, distractibility,
increased libido, and excessive involvement in pleasurable activities that have
a high potential for painful consequences (unrestrained buying sprees, sexual
indiscretions, or unrealistic business investments).
There is limited data on the comorbidity of OCD and bipolar disorder but
the available data suggests that nearly 15% of OCD patients have bipolar disorder,
mainly hypomania that is often precipitated by use of antidepressants (Freeman
et al., 2002). It has also been found that 21% of the bipolar patients in the
ECA sample had OCD (Chen et al., 1995). A comorbid diagnosis of bipolar
disorder in OCD has important clinical implication in that the mood stabilization
may have to be achieved before prescribing antidepressant medications to treat
OCD. Antidepressant medications are known to precipitate mania.
ANXIETY DISORDERS
Comorbidity of OCD with anxiety disorders is quite high, ranging from 25¯60%.
Conversely, studies in primary anxiety disorders have showed comorbid OCD
in 11-14% of the patients.
Generalized Anxiety Disorder (GAD)

GAD is characterized by chronic, uncontrollable excessive anxiety and worry
(apprehensive expectation) about a number of events or activities such as work,
finances, job responsibilities, safety of family members or even minor matters
such as household chores, car repairs, or being late to office. The person finds
it difficult to control the worry and also report of associated symptoms like
restlessness or feeling keyed up or on edge, being easily fatigued, difficulty
in concentrating, irritability, muscle tension and sleep disturbance. There may
be associated symptoms of anxiety such as trembling, twitching, cold and clammy
hands, dry mouth, sweating, palpitations, nausea, increased frequency of
micturition and defecation, and an exaggerated startle response. The excessive
worry along with physical symptoms causes clinically significant distress or
impairment in social, occupational, or other important areas of functioning.
The comorbidity of OCD with GAD is of interest because of the seeming similarity
between obsessions in OCD and worries in GAD. Obsessions are not simply
excessive worries about everyday or real life problems, but rather are unwanted,
irrational and unreasonable intrusions. In addition, most obsessions are
accompanied by compulsions that reduce the anxiety.
Panic Disorder
In order to fully describe panic disorder, it is first necessary to define panic
attacks. A panic attack is “a discrete period of intense fear or discomfort”,
associated with prominent somatic or cognitive symptoms such as sweating,
trembling or shaking, shortness of breath, a sensation of choking, chest pain,
palpitations, nausea or abdominal discomfort, dizziness or feeling faint, fear
of losing control or going crazy, fear of dying, numbness/tingling sensation, feelings
of being detached from reality, and feelings of being detached from oneself.
The primary feature of panic disorder is a history of panic attacks, as defined
above, followed by persistent anticipatory anxiety about having further panic
attacks, excessive concern about the implications and/or consequences of the
panic attacks (e.g., losing control, having a heart attack, “going crazy”) and
substantial modification of daily activities in an effort to avoid further panic
attacks. They may develop agoraphobia. Basically, they avoid any situation they
fear would make them feel helpless if a panic attack occurs. These include
fears of being outside the home alone, being in a crowd or standing in a line,
being on a bridge and traveling in a bus, train or automobile. Some patients
become house bound because of fear of traveling alone or going out alone.
Phobias
Phobias are characterized by recurrent, excessive, irrational fear of a specific
object or situation. Exposure to the feared object or situation results in an
immediate and intense anxiety, sometimes to the extent of having a panic attack.
Despite recognizing that the anxiety is excessive, individuals with a phobia
will go to great lengths to avoid exposure to the feared object or situation
in order to prevent the emotional distress it causes. The anxiety and associated
avoidance behaviors can cause significant emotional distress and may considerably
interfere with daily functioning. Some examples of phobias include fears of
flying, heights, water, elevators, insects, blood, darkness, tunnels, bridges, enclosed
spaces, and dental procedures.
Social Anxiety Disorder

Social anxiety disorder also known as social phobia is an intense, recurrent
fear of social or performance situations. Individuals with social anxiety are
afraid that they may behave in an embarrassing manner in front of others
and that they may be ridiculed or negatively evaluated. Because of the fear
of criticism and negative evaluation, individuals with social phobia avoid social
interactions or endure with significant anxiety. Exposure to the feared social
situation sometimes results in a panic attack. The anxiety and avoidance behaviors
cause significant emotional distress, and may considerably interfere with daily
functioning particularly in the area of interpersonal relationships. Some examples
of feared social situations include public speaking, interacting with superiors
and with people who are not very well known to them, attending personal
interviews, speaking to opposite sex, eating and writing in public, using public
restrooms/toilets, and participation in social events such as parties and wedding
ceremonies.
THE OBSESSIVE - COMPULSIVE SPECTRUM DISORDERS
There are various conditions that have shared features with OCD. These disorders
are frequently described as obsessive-compulsive spectrum disorders (OCSD)
(Allen & Hollander, 2000; Jaisoorya et al., 2003). They include hypochondriasis,
body dysmorphic disorder (BDD), anorexia nervosa, Tourette syndrome (TS),
trichotillomania, binge eating, compulsive buying, kleptomania, pathological
gambling, and sexual compulsions. The shared features include similarities in
symptom profile and treatment response and possibly somewhat similar
pathophysiology. The OCSDs are characterized by pathological preoccupations
that are similar to obsessions and either compulsive or impulsive behaviors.

For example, in hypochondriasis, BDD and anorexia nervosa there is morbid
preoccupation with fear of having a disease, imagined ugliness or defects in
appearance, and with thinness respectively. Individuals with OCD may repeatedly
wash their hands in an attempt to reduce the anxiety associated with fear
of contamination. In hypochondriasis, there is compulsive doctor shopping to
investigate a disease and in BDD, they check themselves compulsively in front
of mirror exploring their imagined ugliness or defects in appearance. In addition
to similarities in clinical picture, both OCD and OCSDs respond well to a class
of antidepressants called serotonin reuptake inhibitors.
Body Dysmorphic Disorder

BDD is an obsessive preoccupation with a perceived defect in one’s physical
appearance. The BDD obsessions may manifest as excessive, disproportionate
concerns about a minor flaw, or as recurrent, anxiety-provoking thoughts about
an entirely imagined defect. The obsessions are most frequently focused on
the head and face (misshapen nose, protruding jaw), but may involve any body
part (genitals, breasts). BDD goes beyond normal concern with one’s appearance,
and may significantly impair academic and professional functioning, as well
as interpersonal relationships. The individuals often fear they will be rejected
or ridiculed by others because of their ugliness or defects in appearance and
have a tendency to avoid social situations. In extreme cases, an individual may
completely shun any contact with people in an effort to avoid having the defect
being observed by others. In order to alleviate their anxiety, patients may partake
in compulsive behaviors such as repetitive mirror-checking, excessive grooming,
touching and/or measuring of a minor or imagined defect/flaw in front of mirror.
A relatively high comorbidity exists between BDD and OCD. Nearly 12–24%
of the patients with OCD have comorbid BDD. Similarly about on third of
BDD patients have OCD. The symptoms of the two disorders are similar; they
are characterized by obsessive preoccupations and checking. However, if the
focus of the obsession is only about appearance, a diagnosis of BDD is preferred
over OCD. The characteristic difference between these disor-ders is insight.
Insight of patients with BDD seems to be significantly more impaired than
that of patients with OCD. This lack of insight can lead to a delay in seeking
psychiatric treatment. Instead, because they consider their perceived defects
to be real, many people with BDD present to specialists such as plastic surgeons,
dermatologists, or dentists.
Hypochondriasis
The fear or belief that one has a severe illness characterizes hypochondriasis.
This fear is based on an individual’s misinterpretation of signs and symptoms,
and results in multiple doctor visits and medical tests. Patients tend to indulge
in repetitive checking of the body for symptoms of an alleged medical condition,
and Internet searching for information about illnesses and their symptoms
(“cyberchondria”). This behavior persists despite medical reassurance that the
individual does not have a disease or illness. Recent studies have shown that
hypochondriasis and OCD are common comorbid conditions. Both the conditions
have similar clinical picture. OCD patients with somatic or illness obsessions
are often indistinguishable from patients with hypochondriasis. As in OCD,
hypochondriac fears are intrusive, distressing and not easily responsive to
reassurance. Patients with hypochondriasis also indulge in compulsive checking
of one’s body or with others. However, there are some differences, which
help in differentiating OCD from hypochondriasis. In OCD there is a fear of
getting an illness whereas in hypochondriasis there is a fear of having an illness.
Insight is fairly well preserved in OCD and patients often admit their fears
are unrealistic but in hypochondriasis there is a high degree of conviction that
they have a disease. An exception to this difference is the OCD patients with
poor insight. Lastly, hypochondriac fears are usually secondary to somatic
sensations.
Trichotillomania
Trichotillomania is the recurrent, compulsive pulling out of one’s own hair,

resulting in observable hair loss. The most common hair pulling sites are the
scalp, eyebrows, and eyelashes. An individual may use his or her fingernails,
as well as tweezers, pins or other mechanical devices. Usually, but not always,
hair pulling is preceded by a high level of tension and a strong “urge”. Likewise,
hair pulling is usually, but not always, followed by a sensation of relief or
pleasure. Hair pulling is usually done alone, often while watching TV, reading,
talking on the phone, driving or while grooming in the bathroom. Sometimes
hair pulling is done as a conscious behavior, but it is frequently done as an
unconscious habit. Trichotillomania often coexists with depression, OCD, skin
picking, BDD and tic disorders.
Tic disorders
In the recent past, there has considerable interest in the relationship between
tic disorders, particularly the Gilles de la Tourette syndrome (GDLT) and OCD.
The group of tic disorders includes transient and chronic tic disorders and the
GDLT. In the transient tic disorder, tics usually do not persist for more than
12 months whereas in chronic tic disorders either motor or vocal tics persist
for longer periods. The GDLT is a classic syndrome consisting of multiple chronic
motor tics, and one or more vocal tics and coprolalia with onset during childhood
or adolescence.
Tics are defined as rapid, repetitive muscle contractions or sounds that usually
are experienced as outside volitional control and which often resemble aspects
of normal movement or behavior. Tics can be elicited by stimuli or preceded
by an urge or sensation. They are usually beyond attempts at suppression.
Examples of motor tics include eye blinking, head jerks, shoulder jerks, finger
and hand movements and stomach jerks. Vocal tics include throat clearing,
coughing, grunting sounds, repeating certain words and sentences, repeating
others’ speech, and coprolalia (repeating obscene or socially unacceptable words).
Some complex tics include facial gestures, grooming behaviors, jumping, touching,
stamping and hopping.
Patients with GDLT have a high rate (30-40%) of comorbid OCD and obsessive-
compulsive symptoms. Conversely nearly one fifth of OCD patients have a lifetime
history of multiple tics and 5% to 10 % have GDLT. Family studies of GDLT
and OCD clearly show a relationship between the two disorders. Relatives of
GDLT patients report a high rate of OCD and relatives of OCD patients report
a high rate of tic disorders and GDLT. In an Indian study, tic disorders were
present in 18% of OCD patients but the rate of GDLT was only 3% (Jaisoorya
et al., 2003). The subgroup of OCD plus tic disorder patients have an earlier
age-at-onset of OCD with high family loading for GDLT and OCD (Pauls et
al., 1995). In a study of children and adolescents with OCD, 56% had tics
and 14% has GDLT (Leonard et al., 1992). However, in an Indian study of
children and adolescents with OCD, tic disorders were present in 17% of the
subjects and GDLT in only 7% (Reddy et al., 2003). It appears that tic disorders
are not uncommon in Indian OCD patients but for some unknown reasons,
GDLT is a rare comorbid diagnosis.
Eating disorders
In anorexia nervosa, patients restrict their food intake to the point of being
underweight and experience distressing concerns about their shape and weight,
particularly intense fear of weight gain or being “fat” even though grossly
underweight for their age and height. They deny the seriousness of low body
weight and further feel driven to exercise for hours a day and use other extreme
measures such as laxatives, diuretics, or self-induced vomiting in their attempts

to lose weight or maintain low body weight. In essence, they have an obsessive
fear of being fat and are characterized by a relentless pursuit of being thin.
In bulimia nervosa, patients have episodes of “binge eating” in which they
consume a large amount of food in a discrete period of time, often with the
feeling of being “out of control.” In addition, they feel driven to use extreme
measures to prevent weight gain, such as self-induced vomiting, laxatives,
diuretics, fasting, or excessive exercise. Differentiating point from anorexia nervosa
is repeated episodes of bingeing and purging.
Resistance to maintaining body weight at or above a minimally normal weight,
purging, vomiting, and restricting certain diets results in serious medical
consequences. Health consequences can include electrolyte imbalance, nutritional
cardiomyopathy, osteoporosis, loss of menstrual periods in female gender and
in some cases death is inevitable if not recognized earlier and treated.
Western studies have reported high rates of comorbid OCD and eating
disorders. However, in Indian clinic populations, eating disorders are extremely
rare in OCD patients (Jaisoorya et al., 2003).
PERSONALITY DISORDERS
Nearly a half of patients with OCD also have at least one diagnosable personality
disorder. The most frequently diagnosed personality disorders among patients
with OCD are avoidant, dependent, histrionic, passive-aggressive and obsessive-
compulsive personality disorders. Some researchers report no specific association
between obsessive-compulsive personality disorder (OCPD) and OCD but few
recent studies have reported high rates of OCPD in OCD. Less frequently
diagnosed were paranoid, borderline and schizotypal personality disorders, which
are found to be associated with poor outcome.
The issue of whether PD is the primary or secondary disorder is debatable.
Early onset OCD imparts its signature as traits on the development of personality
of an OCD patient. Recent literature shows that the number of personality
disorder diagnoses, and scores on personality disorder measures, declined in
half of the OCD patients following successful treatment. Now it becomes all
the more important to recognize it and treat it before it becomes enduring
personality trait.
PSYCHOSIS
Studies on schizophrenia and OCD suggest that a significant number of patients

with schizophrenia (8%–40%) have co-existing obsessive-compulsive symptoms.
Comorbid OCD in schizophrenia is associated with poor outcome. Conversely,

subjects with OCD appear to be at no greater risk of developing schizophrenia
than the general population although some studies have reported up to 4%
rate of schizophrenia in those with primary OCD. However, patients with poor
insight OCD should be differentiated from psychosis and schizophrenia.
CONCLUSION
Comorbid psychiatric disorders are common in OCD. Depressive and anxiety

disorders are the most common comorbid conditions in OCD. Recently, there
has been considerable interest in comorbid OCSDs. The putative OCSDs that
are strongly related to OCD include tic disorders, hypochondriasis, BDD, eating
disorders and trichotillomania. Relationship between schizophrenia, bipolar
disorders and OCD requires further exploration.
REFERENCES
1. Allen A, Hollander E. Obsessive Compulsive Spectrum Disorders. Psychiatric Clinics

of North America Volume 23, 2000
2. Chen YW, Dilsaver C. Comorbidity for obsessive compulsive disorder in bipolar and unipolar
disorders. Psychiatry Research 1995; 59:57-64.
3. Freeman MP, Freeman SA, McElroy SL. The comorbidity of bipolar and anxiety disorders:
prevalence, psychobiology, and treatment issues. Journal of Affective Disorders 2002;
68: 1-23
4. Jaisoorya TS, Janardhan Reddy YC, Srinath S. The relationship of obsessive-compulsive
disorder to putative spectrum disorders: results from an Indian study. Comprehensive
Psychiatry 2003; 44:317-323.
5. Janardhan Reddy YC, Srinath S, Prakash HM, Girimaji SC, Sheshadri SP, Khanna S,
Subakrishna DK. A follow-up study of juvenile obsessive-compulsive disorder from India.
Acta Psychiatrica Scandinavica 2003; 107:457-464.
6. Karno M, Golding JM, Sorenson SB et al. The epidemiology of obsessive compulsive
disorder in five US communities. Archives of General Psychiatry 1988; 45:1094-1099.
7. Leckman J F, Peterson B S, Pauls D etal: Tic Disorders, The Psychiatric Clinics Of
North America 20:839-863,1998.
8. Leonard HL, Lenane MC, Swedo SE et al. Tics and Tourette’s disorder: A 2- to 7-year
follo-up study of 54 obsessive-compulsive disorder children. American Journal of Psychiatry
1992; 1244-1251
9. Pauls DL, Alsobrook MP, Goodman W et al. A family study of obsessive compulsive disorder.
American Journal of Psychiatry 1995; 152:76-84
10. Weissman MM, Bland RC, Canino GJ et al. The cross-national epidemiology of obsessive-
compulsive disorder. The Cross National Collaborative Group. Journal of Clinical Psychiatry
1994; Suppl 55: 5-10.
BIOLOGY OF OBSESSIVE COMPULSIVE DISORDER 33
BIOLOGY OF OBSESSIVE COMPULSIVE

DISORDER
Sumant Khanna, MD, PhD, MAMS, MRCPsych
Consultant Psychiatrist, New Delhi
Former Additional Professor of Psychiatry, NIMHANS, Bangalore
SEROTONIN: There are essentially three kinds of studies in this field. The
first approach is to study serotonin in peripheral tissues such as blood elements.
Platelets which are a major reservoir of serotonin in blood ,show normal uptake
or content of serotonin. One study found a decreased number of platelet sites
in OCD patients, this has not been replicated. In the second approach CSF
5-HIAA has been studied with largely normal results. Lastly serotonin challege
tests have shown blunted hormonal response. No changes have been noted with
L-tryptophan, fenfluramine, ipsapirone. mCPP produces behavioural exacerbation
associated with a blunted neuro-endocrine response in unmedicated OCD. The
strongest evidence to implicate serotonin continues to come from the fact that
serotonin uptake inhibitors are effective in its treatment, while drugs acting
at other receptor sites alone are not.
Other neurotransmittors nor-adrenaline and dopamine have been implicated
in the etiology of OCD.
BRAIN IMAGING AND OCD
One of the most common physiological findings in OCD patients is a variety

of alterations in the functioning and neuroanatomy of the basal ganglia and
areas of the frontal cerebral cortex associated with limbic function. Magnetic
Resonance Imaging, CT, PET exploring neuroanatomical structures and measuring
regional cerebral blood flow (rCBF) have been used to document differences
34 BIOLOGY OF OBSESSIVE COMPULSIVE DISORDER
between normal controls and OCD patients, as well as to uncover unilateral

hemispheric abnormalities in OCD patients.
(i) Unilateral Abnormalities: One MRI study found a proportionately higher
signal intensity in the left caudate nucleus, compared with the right side in
OCD patients. However the volume of the right head of caudate was increased
in these patients when compared with normal controls. Baxter has noted
increased activity in the left or right orbitofrontal regions during measures
of glucose metabolic rates. Other studies found that increased rCBF in the
left frontal hemisphere and caudate is observed during image flooding, with
the positive correlation between the OCD severity and rCBF. These findings
provide evidence that OCD may be linked to a unilateral dysfunction in the
basal ganglia or brain areas of the cerebral cortex closely associated with limbic
sites.
Studies documenting PET scan changes during OCD treatment has shown
unilateral changes in basal ganglia and cerebral limbic cortical functions. Baxter
has shown that the metabolic activity of glucose in the right caudate nucleus
following a ten week course treatment with fluoxetine or behavioural therapy
was decreased compared with baseline measurement and clinical global
improvement was correlated positively with decreases in the activity of the
right caudate nucleus. One study found a correlation between the degree of
decreased activity in the right orbitofrontal cortical area and favourable treatment
response.
(ii) Bilateral Abnormalities : Some studies have shown bilateral
abnormalities in OCD patients. In one study PET scan indicated an increased
metabolic rate in the head of the caudate compared with age and sex matched
controls. Bilateral caudate atrophy and increased ventrical : brain ratios was
observed on CT in another study. CT and MRI’s of OCD patients with a probable
history of encephalopathy have shown lentiform nulceus lesions especially in
the pallidum, an important component of the limbic loop of the basal ganglia.
NEUROANATOMIC CIRCUITS
Post-synaptic receptor dysfunction or abnormalities in direct projections of the

Dorsal rahe nucleus (DRN) to the caudate and lenticular nuclei, the thalamus
or frontal cortical regions has been postulated to mediate OCD symptoms through
overstimulation of strial-thalamic-cortical-strial circuits. The descrete
neuroanatomy of these strial-thalamic-cortical-strial circuits is linked to specific
input nuclei and mediates different functions as shown in the table.
Hyperexcitability of each of these extrapyrammidal loops may produce symptoms
observed in OCD.
In an attempt to unite the diverse biological findings in OCD mentioned
above, like altered activity and morphological changes in the basal ganglia,
increased metabolic activity in cortial regions controlling limbic and behavioural
functions, altered serotonergic dopaminergic markers, blunted or increased
neuroendecrine response to pharmacological probes and altered response illness
in serotogenergic, dopaminergic, nor adrenergic and endogenous opiate systems,
a model has been proposed to explain pathogenesis of SSRI reponsive OCD.
At the crux of this model lies the assumption that a single, midline regulatory
structure the dorsal raphe nucleus,which ramifies bilaterally to components
of the basal ganglia and frontal cortex,may not receive appropriate feedback
inhibition from components of the basal ganglia and cortex to simultaneously
regulate both a diseased hemisphere and a normal contralateral component.
Resultant dysregulation of the DRN may occur owing to decreased unilateral
inhibitory input from a damaged SNpc nucleus (substantia nigra pars compacta)
resulting in DRN disinhibition. Chronic dysregulation due to decreased SNpc
inhibition may produce increased activity in the DRN,followed chronically by
alterations in the receptor sub type population or increased inhibition from
the contralateral SNpc. Increased contralateral SNpc activity (as an effort
to regulate the basal ganglia by decreasing DRN trasmission) or resultant receptor
abnormalties may be the ultimate events that trigger over excitation of strial-
thalamic cortical-strial circuits. These changes could account for the over
stimulation of the basal ganglia and resultant obsessive compulsive symptoms.
GENETICS
Twin studies have been a valuable paradigm to help asses the genetic contributions
to a disorder. Rasmussen and Eisen summarised the literature on twin studies
relavent to OCD. They noted that 32 pairs of monozygotic twins concordant
for OCD and 19 pairs discordant for OCD have been reported and that there
is a general agreement about the diagnosis and monozygosity of 13 pairs of
concordant twins and seven pairs of discordant twins. The much higher proportion
of concordant compared with discordant pairs may be taken as evidence supporting
the genetic trasmission of OCD. Unfortunately there have been no adoption
studies on OCD and molecular genetics are just getting under way. Richter
et al recently reported that the dopamine D3 receptor gene polymorphism is
not involved in the susceptibility to OCD. A rare variant of the serotonin
transporter gene has recently been associated with OCD.
36 BIOLOGY OF OBSESSIVE COMPULSIVE DISORDER
Clinical investigations over the past few decades have repeatedly indicated
that OCD is familial. A consistent finding seems to be a multitude of other
psychopathologies also occur more frequently in families of OCD probands than
would be expected by chance. The genetic association with tics appear to be
very strong. Comings proposes that many individuals with Tourette may be
homozygous for a Tourette syndrome gene. They suggest the inheritance in
Tourette syndrome may be best described as semi dominent,semi recessive. The
absence of a large enough clinical population of Tourette syndrome in India
prevents a systematic study, but there is evidence to suggest that this genetic
pool of Tourette and OCD may be absent in India.
NEUROPSYCHOLOGICAL STUDIES
Studies can be divided into two groups: those which look for a regional dysfunction
and those which explored a neuropsychological paradigm. Majority of the studies
have demonstrated frontal deficits, although non-dominent tempro-parietal deficits
have also been seen. Functions tested include impaired associate learning,impaired
ability to change sets and attention failure during stress. These can be viewed
as frontal tasks. Laplane has shown that primary basilar gangliar diseases
may have frontal deficits. Refinement in neuropsychological testing will help
in further exploring the neurobiology of OCD. Most electrophysiological paradigms
implicate dysfunction of frontal lobes in OCD, but issues regarding laterality
have not been adequately addressed.
INFECTIOUS ETIOLOGY
Various case reports have been there about the co-morbidity with infectious
diseases, although no clear cut pattern had earlier emerged. One large study
from India suggested the association of herpes simplex viral infection with OCD.
Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal
infections (PANDAS) is a condition occurring after streptococcal infection in
childhood associated with obsessive compulsive symptoms, but again there are
no case reports from India.
CONCLUSIONS
In general the neurobiological evidence for OCD exists at two planes. At the
first level OCD seems to be a disease of serotonergic dysfunction. At the second
level it seems to affect only some parts of the brain, such as the caudate prefrontal
cortex and cingulate regions, suggesting that there may be a circuit involved
linking these different regions which is dysfunction in OCD. Linking the first
hypothesis, it appears that these circuits are serotonergic. These specific pathways
seem amiable to remediation both by pharmacotherapy and cognitive behaviour
therapy.
REFERENCES
1. Khanna S (1999) Obsessive Compulsive Disorder. In Textbook of Postgraduate Psychiatry

vol. 1 ed Vyas JN, Ahuja N. New Delhi: Jaypee Publishers, pp 262-274.
2. Khanna S, Venkatsubramaniam G (2003) Obsessive Compulsive Disorders. In Postgraduate
Psychiatry by Ten Teachers ed Vyas JN, Nathawat SS. New Delhi, Aditya Medical
Publishers, pp 51-74.
3. Rauch SL, Cora-Locatelli G, Greenberg BD (2002) Pathogenesis of Obsessive Compulsive
Disorder. In Textbook of Anxiety Disorders ed Stein DJ, Hollander E. Washington: American
Psychiatric Publishing, pp 191-206.
PHARMACOTHERAPY OF OBSESSIVE COMPULSIVE DISORDER 39
PHARMACOTHERAPY OF OBSESSIVE
COMPULSIVE DISORDER
Sumant Khanna, MD, PhD, MAMS, MRCPsych
Consultant Psychiatrist, New Delhi
Former Additional Professor of Psychiatry, NIMHANS, Bangalore
O CD patients tend to respond to medications with only a 30% to 60% symptom

reduction and patients tend to remain clinically symptomatic to some degree
despite the best of pharmacologic interventions. Nonetheless, patients usually
experience this degree of improvement as quite significant.
In general OCD patients worry a great deal about the side effects of the
treatment. Since long term pharmacotherapy will be needed for most patients,
side effects which are likely to affect compliance and hence drug exposure,
play a major role in the level of success achieved in many cases. Due to the
above fact Serotonin Reuptake Inhibitors ( SSRI ) are considered to be the
first line of treatment.
Clomipramine (CMI) is a tricyclic compound very similar in structure to
imipramine. It is serotonergic uptake inhibitor as well as a noradrenergic uptake
inhibitor.
Although Reynghe de Voxrie reported a reduction in obsessional symproms
with CMI way back in 1968, it was not until 1980 that double blind, placebo
controlled trials confirmed the efficacy of CMI in OCD.
The usual starting dose is as low as 25-75 mgs in divided doses, because
of side effects and the onset of nausea and vomiting in some subjects, requiring
discontinuation. The dose can be increased every 1-3 days by 25 mgs to a maximum
daily dose of 250-300 mgs. or till when the side effects become intolerable or
side effect profile outweighs therapeutic profile. Traditionally, doses lower than
150 mgs are believed to be subtherapeutic, though some studies report minimum
effective dose to be 75 mgs. Patients responding to this therapy will experience
40 PHARMACOTHERAPY OF OBSESSIVE COMPULSIVE DISORDER
a linear, incremental response which gradually builds up over several weeks.

Patience is often required whilst waiting for the full therapeutic effect to develop.
Side effects of CMI are anticholinergic effects like constipation, dry mouth
and urinary retention. Other side effects include anorgasmia, drowsiness,
orthostatic hypotension, lowering of seizure threshold and weight gain.
Many studies have been conducted which compare the efficacy of CMI and
other tricyclic antidepressants in OCD.
Since its introduction in the market Fluoxetine has extensively been used
in OCD. A number of open trials suggest that it has anti obsessional effect.
It acts by enhancing serotonergic neurotransmission through potent and selective
inhibition of neuronal reuptake of serotonin.. Half life of fluoxetine is 7-9 days.
Many study have shown fluoxetine to be effective in the dose range of 40-
80 mg/day. Treatment is initially started with 40-60 mgs/day and hiked further
if the patient does not show adequate response in 4 weeks. To consider a patient
nonresponder 80 mgs of fluoxetine for a period of 8 weeks is considered is
necessary.
OCD patients are relatively resistant to side effects of fluoxetine. Some of
the common CNS side effects are headache, nervousness, insomnia, drowsiness,
anxiety, tremor and dizziness. Gastrointestinal side effects are nausea, diarrhoea,
dry mouth and anorexia. Other side effects are excessive sweating, weight loss
and very rarely suicidal ideation and violent behaviour.
Fluvoxamine was the first SSRI to be extensively studied in OCD. A number
of placebo controlled studies have been performed (Goodman et al 1989.
Montgomery et al 1990, Perse et al 1987, Cottraux et al 1990.) which demonstrated
efficacy for fluvoxamine. Fluvoxamine treatment was associated with significant
improvement on measure of obsessive compulsive symptoms, anxiety and
depression.
Jenike et al in a study of efficacy of fluvoxamine in patients with OCD
reported the mean maximum dose as 294 mgs/day. Side effects were mild and
consisted mainly of insomnia, nausea, fatigue and headache. Overall fluvoxamine
had no serious side effects. Fluvoxamine was an effective antiobsessional agent
when compared with placebo. The comorbidity of panic attacks with OCD has
been found to predict good therapeutic response to fluvoxamine.
Sertraline has been studied in a variety of trials including two flexible dose
studies (Chownard et al 1990, Kronig et al 1994) both of which showed a
significant improvement in OCD symptoms. A fixed dose study (Greist 1995)
also showed that a significant clinical response was obtained at the minimum
50mgs daily dosage and the two higher dosage groups. Onset of therapeutic
action was seen to be 2-4 weeks in a study by Kronig et al 1994. Side effect
PHARMACOTHERAPY OF OBSESSIVE COMPULSIVE DISORDER 41
includes insomnia, gastritis, headache and anorexia. Sertraline has recently

been available in India. Early reports suggest that it is effective in OCD.
Paroxetine has also been seen to be effective in OCD, as has been citalopram
and escitalopram, although the number of studies with these molecules are
small. The SNRI venlafaxine has not been found effective in OCD.
Head on trials between the different members of this class have generally
failed to reveal significant differences. One meta-analysis however did reveal
a greater effect size for clomipramine as compared to the SSRIs. However
clomipramine was less well tolerated.
AUGMENTING STRATEGIES
Since a large percentage of OCD patients do not respond adequately to the

first trial of an SRI (failiure rates are around 40-60 %), various alternative
pharmacological strategies need to be kept in mind based on the existing
literature. It needs to be stressed at this stage itself that Cognitive Behaviour
Therapy has a major role to play in the treatment of OCD, and its combination
with pharmacotherapy is considered the best option in most treatment guidelines.
The first approach would be to look for other co-morbid disorders such
as social anxiety or Bipolar disorders, and direct additional pharmacological
strategies towards their control. Co-morbid borderline personality disorder has
been known to make the condition relatively refractory to treatment. Recent
studies have also demonstrated the presence of hoarding as being a poor prognostic
indicator.
The first strategy which seems to work in some patients is to switch SSRIs.
This must be done after keeping in mind that an adequate duration (8-12 weeks)
of the maximal dose, which is normally much higher than the doses used in
depression, have been tried.
In augmenting strategies, various drugs have been tried but the most
promising seem to be risperidone, clonazepam and another SSRI. Data from
a double blind placebo controlled risperidone augmentation study has shown
that the addition of this drug at low doses (1-2 mg) brings significant reduction
in obsessive-compulsive symptomatology. This is contrarian to earlier beliefs
that the presence of tic disorder, Tourette’s syndrome, schizotypal disorder or
schizophrenia, along with OCD, were the only rationale for using this augmenting
strategy. There has been a negative placebo controlled study with olanzapine.
The mechanism of action of ziprasidone on 5HT2a receptors seems to suggest
that this molecule may be of some benefit, but results of ongoing studies are
awaited.
42 PHARMACOTHERAPY OF OBSESSIVE COMPULSIVE DISORDER
Clonazepam seems to be important when anxiety is high and the patient

is getting disabled because of this dimension in OCD. Social phobia as a co-
morbid condition can also be an indication. There is a debate whether co-
prescription of benzodiazepines decreases the ability of a person to engage in
cognitive behaviour therapy; at the same time disabling levels of anxiety can
interfere in the very ability to engage in CBT. A balance needs to be drawn
in the usage of this drug, at times proactively in different phases of the disease.
Although the most common co-prescritpion with an SSRI is another SRI/
SSRI, Montgomery and others strongly frown on this practice, as having the
potential of producing a serotonergic syndrome, which could be fatal. Controlled
data supporting this practice is also missing. However due to tolerability issues
with clomipramine, often lead to low doses of this drug being co-prescribed
with SSRIs.
Other strategies such as using lithium and buspirone have not stood the
test of scientific scrutiny.
OTHER PHYSICAL METHODS
Electroconvlsive therapy has been used in OCD but without sustained benefit.
There are a few open series in the literature which suggest that co-morbid
severe depression with suicidal risk may be one of best predictors for usage
in OCD. Earlier frontal lobotmies have given way to stereotactic procedures
in alleviating the symptoms of OCD. Although the sample sizes are small, and
the facilities limited, this seems to be an area of promise for the well-evaluated
refractory patient. Transcranial magnetic stimulation is a new emerging area
of academic and therapeutic relevance in OCD and although a recent Cochrane
review failed to find evidence of its efficacy in OCD, the final verdict is awaited.
Finally deep brain stimulation, a technique whereby needles are implanted in
chosen brain areas and stimulated whenever required, seems to be emerging
as a viable option in refractory OCD.
REFERENCES
1. Goodman WK (2002) Pharmacotherapy for Obsessive Compulsive Disorder. In Textbook

of Anxiety Disorders ed Stein DJ, Hollander E. Washington: American Psychiatric
Publishing, pp 207-220
2. Khanna S (1999) Obsessive Compulsive Disorder. In Textbook of Postgraduate Psychiatry
vol. 1 ed Vyas JN, Ahuja N. New Delhi: Jaypee Publishers, pp 262-274.
3. Khanna S, Venkatsubramaniam G (2003) Obsessive Compulsive Disorders. In Postgraduate
Psychiatry by Ten Teachers ed Vyas JN, Nathawat SS. New Delhi, Aditya Medical
Publishers, pp 51-74.
BEHAVIOR THERAPY IN OCD 43
BEHAVIOR THERAPY IN OCD

Dr T. Jaideep, Senior Resident
Dr Y.C. Janardhan Reddy, Associate Professor and Consultant, OCD Clinic
Department of Psychiatry, NIMHANS, Bangalore
I n the last three decades, much progress has been made in the
psychotherapeutic treatment of OCD. Although many behavioral techniques
have been tried in the past in treating OCD, exposure and response prevention
(ERP) has proved to be the most effective psychotherapy for OCD (Abramowitz,
1998). In ERP, the patients are persuaded to expose themselves to the anxiety-
provoking stimuli and prevented from doing compulsions or rituals. Repeated
and prolonged exposure without recourse to rituals or avoidance helps to
disconfirm the mistaken fears and beliefs and promotes habituation to previously
fearful thoughts and situations.
Theoretical basis of exposure and response prevention

The acquisition of obsessions and compulsions is believed to occur in two stages.
In the first stage (classical conditioning), anxiety is linked to a neutral thought,
event or object. For example, anxiety after touching doorknobs touched by others
because of the belief that one may contract a disease by touching ‘contaminated
or dirty’ objects. Note that the act of touching the doorknobs used by others
is not realistically capable of spreading a disease but the act causes intense
anxiety. This is followed by attempts to reduce the anxiety by excessive hand
washing (compulsion or ritual). Because the hand washing reduces the anxiety
generated by touching the doorknobs, the washing behavior is reinforced (operant
conditioning). Every time an object believed to be dirty or contaminated evokes
anxiety, the patient performs the compulsive act of washing to immediately
reduce the anxiety. In addition to the compulsive act, patient begins to avoid
touching or coming in to contact with objects or situations that cause anxiety.
44 BEHAVIOR THERAPY IN OCD
For example, one may not use the toilets, bathrooms or sinks used by others.
Because of extensive avoidance and compulsive behaviors, patients do not get
an opportunity to disconfirm their fears and fail to be habituated to the stimuli
that arouse anxiety. This leads to maintenance of obsessions and compulsions.
However, most patients are not able to recall conditioning events. Therefore,
the evidence for acquisition of obsessions by classical conditioning is weak.
However, the theory accounts well for the maintenance of symptoms by operant
conditioning.
Initially the compulsions are linked to the original cues that provoke anxiety.
Later the compulsions may be evoked by other cues that are in some way
linked to the original cue. In other words stimulus generalization occurs.
Exposure and response prevention

Exposure involves making the patient confront the anxiety-provoking stimulus
and remaining in that situation until reduction in anxiety occurs through
habituation. Response prevention consists of preventing the patient from doing
compulsions or rituals that reduce the anxiety, thereby breaking the cycle of
operant conditioning.
Why ERP works

ERP is based on a well-established scientific principle that fear is overcome
by daring to face the very objects or situations that cause fear. For example,
fear of water can be overcome only by getting in to water repeatedly and getting
used to being in water. It cannot be overcome by avoidance of water. In essence,
exposure relies on two important principles of learning: habituation and extinction.
Habituation is the natural tendency of the nervous system to “numb out”
from repeated prolonged contact with an anxiety-provoking stimulus. In other
words, one gets used to the fearful stimulus after repeated and prolonged contact.
One example would be the initial fear of getting in to a lift if one has phobia
of lifts and enclosed spaces. This fear will fade gradually if one is encouraged
to use the lift on a regular basis without avoidance; however, fear will persist
if lifts are avoided. The same principle applies to obsessional thoughts and
behaviors. For example, fear of dirt and contamination will fade gradually if
one is repeatedly exposed to stimuli believed to be dirty (e.g., doorknobs, toilets,
sinks etc) but prevented from washing.
Extinction is based on the principle that our behavior is governed by the
consequences of behavior.
Evidence base for ERP

In a study (Foa et al., 1985) that pooled the results of 273 patients who received
ERP, 90% had at least 30% reduction in symptoms. Symptom reduction of 70%
and 30-69% was seen in 51% and 39%of the patients respectively. The results
of 330 patients were pooled in a later study (Foa and Kozak, 1996), which
found that after treatment with ERP, 83% were ‘much’ or ‘very much improved’.
There is also some evidence that severity of illness decreases more with ERP
than with anti-obsessional medicines (Greist and Baer 2002). Best evidence
for the efficacy of ERP comes from a recent meta-analysis that included 77
studies with 4651 patients (Kobak et al., 1998). In addition, there is evidence
that the gains made with ERP are maintained for significant length of time
after cessation of therapy, in contrast to medications (Foa & Kozak 1996).
It is evident from the available literature that the ERP is (1) effective in
treating OCD and the efficacy is comparable to that of drug treatment, and
(2) possibly associated with maintenance of gains substantially longer than with
drugs.
Technique of ERP
Case vignette:
Mrs. G, a 30-year-old married lady has been suffering from OCD for the
last 5 years. She has obsessive fears of dirt and contamination. She gets repetitive
thoughts that she will fall ill if she touches objects used by others (door knobs,
chairs, railings, public toilets etc). She knows that these thoughts are silly yet
is distressed by them. She has compulsive washing and avoidance. Every time
she touches any of the feared objects she washes hands for at least half an
hour applying soap 6 times. She takes 2 hours to shower, applying soap at
least 3 times. She avoids using public toilets and public transport. She makes
her husband and children to wash hands before touching her. She feels helpless
and guilty for troubling her family. Her husband thinks that she is “crazy”
and that she does not try to stop doing “silly acts”.
1. Psychoeducation of patient and family regarding OCD and the rationale behind
ERP is the first step in initiating ERP. It is extremely important that the
patient and family members understand that the intrusive thoughts and
compulsive behaviors are the symptoms of a disease. Patient should have
a clear understanding that OCD is a medical brain disorder and not a reflection
of one’s weakness or character. Mrs. G, and her family were informed that
OCD was a common mental illness affecting 2-3 people out of 100 i.e. she
was not the only person suffering from it. They were told that the illness
was characterized by repetitive unwanted illogical thoughts that provoked
anxiety and repetitive acts to reduce anxiety. In her case, thoughts about
falling ill by touching objects used by others –although unrealistic would
provoke anxiety. In order to reduce anxiety she would wash repeatedly. She
was reassured that she was not responsible for these thoughts and acts, which
were actually symptoms of a disorder. This allayed her guilt. Her husband
developed a better understanding of her predicament.
2. Since motivation and compliance with ERP procedures are crucial to the
success of therapy, patients should be educated about the rationale behind
ERP. Many patients often wonder why doctors make them do things that
generate anxiety. Therefore, patients should be made to understand that
avoidance and compulsions maintain their obsessions and that habituation
is crucial to the ERP procedure. In other words, they should know how
ERP works. Mrs. G was informed that during ERP she would have to
expose herself to feared objects (touching door knobs) repeatedly till it no
longer provokes anxiety (habituation). In addition, she would have to stop
washing her hands (response prevention). This would break the link between
washing and anxiety reduction (extinction). Importantly, she would have to
overcome avoidance of feared situations (public toilets).
3. Behavioral analysis: This includes identification of specific triggers of
obsessions, compulsions and avoidance behaviors. In Mrs. G’s case, touching
objects used by others such as doorknobs is the trigger for the obsessive fear
“I will fall ill”. The obsession provokes anxiety making Mrs. G to perform
the compulsion of washing hands. Avoidance is seen in the form of her not
using public toilets, public transportation etc. At this stage, it is pertinent
to analyze the role of family members. It is not unusual for the family members
to be involved in the patient’s rituals. Often they perform rituals by proxy.
Mrs. G’s husband and children used to wash themselves thoroughly before
entering the house and before touching her. Her husband would do most
of the shopping so that she would not have to go out of the house. He would
also open doors for her, including the door to the ladies’ toilet. Assess the
degree of insight – how much does the patient believe that feared consequences
will really occur if rituals are not done? Mrs. G was asked how mush she
believed that she would really fall ill if she did not wash hands. She reported
that although she knew that the chances of falling ill were extremely low,
she found it very difficult to convince herself while in the feared situation.
This would be considered as good insight. Patients with poor insight may
do better with cognitive therapy.

4. Use a scale to measure the degree of anxiety associated with specific triggers
and avoidance. For example a visual analogue scale from 0 to 100 where
“0” indicates no anxiety and “100” indicates intolerable anxiety. This scale
can be used to construct a hierarchy of triggers of obsessions and later
to demonstrate how the anxiety gradually decreases with repeated exposure
to triggers.
0 Anxiety 100
(Watching TV at Home) (Having to use a public toilet)
Touching door knob at shopping mall:
60
5. Make a hierarchy of triggers from the least anxiety provoking to the most
anxiety provoking. Exposure to triggers should be done in a graded manner
(graded exposure). Few patients are highly motivated to get exposed to
the most anxiety provoking triggers (flooding). Most patients prefer graded
exposure to flooding.
Mrs. G was asked to list situation and objects that provoked anxiety and
to arrange them based on the level of anxiety and avoidance. She came up
with the following list:
Activity Anxiety
1. Touching children before they have washed 30

2. Touching husband before he has washed 40
3. Touching door knob at home 50
4. Touching door knob at shopping mall 60
5. Touching door knob at hospital 65
6. Traveling by bus/ touching railing/seat 70
7. Touching toilet door knob 80
8. Using a public toilet 100
6. To begin the therapy, select a target behavior by discussing with the patient.
This is usually one of the less anxiety provoking triggers. Once patient becomes
confident, move up the hierarchy. Mrs. G agreed to start with touching
her husband or allowing him to touch her before washing
7. Make the patient expose to the object or situation (e.g. touching a

“contaminated” object). Exposure can be of two types, in vivo and imaginal.
In vivo exposure, wherein the patient is exposed to the actual anxiety-provoking
stimulus is generally more effective and preferred over the imaginal exposure.
Imaginal exposure, wherein the patient imagines exposure to the anxiety-
provoking stimulus is less effective. However, it may be the only option
when in vivo exposure is impractical, no external triggers are present, patient
has high levels of anxiety, marked avoidance and low motivation. Mrs. G
was made to touch her husband on his returning home from work.
8. Encourage the patient not to perform the compulsion or ritual (e.g. washing
hands). However, it may not be possible for many patients to stop doing
the compulsion entirely. In such cases, the compulsion is deferred as long
as possible, or the time and frequency is reduced in graded manner (graded
response prevention). For example, hand washing can be delayed, or duration
and frequency of washing can be reduced. Initially, therapist supervision
may be necessary in some severely ill patients (therapist-aided ERP). Take
the help of family members as co-therapists if they have fully understood
the rationale behind the therapy. Initially Mrs. G was asked to touch with
her fingertips, then with her palm and finally by hugging her husband. After
touching she was instructed not to wash or shower. Initially she was able
to postpone washing for 15min only. Gradually she could postpone washing
for longer periods and finally could stop washing altogether without becoming
anxious. She was encouraged to reduce the time for bathing from 2hours
to 90 minutes in the first week, one hour in the second week, 30 minutes
in the third week and to 20 minutes in the fourth week. Similarly frequency
and time taken to wash hands was gradually reduced. Mrs. G had great
difficulty in using public toilets. She was too anxious to use and even go
near them alone. Initially, her husband accompanied her; she waited outside
and husband used the toilet. However, she was expected to touch her husband
but was encouraged not to wash her hands. Subsequently, she started touching
doorknobs of the public toilets and ultimately uses them. When she started
using public toilets, she was initially allowed to shower but for a shorter
duration and ultimately stops showering.
9. Insist on daily exposure. It is essential to set specific targets for exposure
that can be easily verified. Encourage record keeping of ERP activities.
Emphasize the need for sustained effort. Patients need to continue exposure
to previous targets as they progress along the hierarchy. She was expected
to expose to specific targets for at least 2 hours a day and maintain a diary
of exposures, degree of anxiety generated, time taken for reduction of anxiety,

and progress made in response prevention and avoidance behaviors if any.
Progress made was reviewed in weekly sessions, difficulties in the
implementation of ERP were discussed and fresh targets set. Mrs. G was
able to move to her next target behavior (touching door knobs at home) after
a week but she allowed her children and husband to touch her (previous
targets).
10. Anticipate problems in the initial phase of therapy. Monitor compliance with
the help of family members. Watch for the development of new compulsions
especially mental rituals and subtle avoidance.
11. Incorporate relapse prevention into therapy. Taper the treatment sessions.
Plan periodic booster sessions. Educate the patient about anticipating relapse,
monitoring for new symptoms and subtle avoidance. Train the patient in
designing exposure and response prevention tasks to deal with new symptoms.
Mrs. G was encouraged to discuss about possible situations that may trigger
her obsessions in future. Weekly sessions were gradually reduced from once
a week to fortnightly sessions and later to monthly and once in three month
sessions. During the later sessions the focus was on difficulties in
implementation of ERP, subtle avoidance behaviors and new compulsions.
In essence, the focus was on consolidation of gains made and relapse prevention.
Advantages of behavior therapy

● 25% of patients refuse medications and ERP is an effective alternative for
them.
● Side effects of medicines are not present.
● Provides sustained response; relapse is less frequent
● Improvement generalizes to social and occupational functioning.
Limitations of behavior therapy

● 25% refuse behavior therapy because of intolerable anxiety and lack of
motivation.
● 20% dropout rate.
● Fewer clinicians are trained in behavior therapy.
● Requires considerable input in terms of time and money on the part of
the patient
● Co-existing severe depression is not conducive to behavior therapy
● Possibly less effective in patients with poor insight and in pure obsessionals.
Predictors of response to behavior therapy

Poor response is seen in those with poor compliance, severe depression, comorbid
schizotypal and borderline personality disorders, primary obsessives without
overt rituals, primary obsessive slowness, and poor insight (for a review see
Foa & Franklin, 2002).
Combination therapy
The combination of SSRIs and ERP is believed to be more effective than either
treatment alone. There is limited evidence to support this belief. However, most
expert clinicians advocate combined procedures wherever feasible (Greist, 1992).
The addition of SSRIs to ERP helps in treating the comorbid depression especially
when severe. It also improves compliance with ERP.
Cognitive-behavior therapy
Cognitive-behavior therapy was developed in the context of refusal of ERP by
nearly one-quarter of patients and high rates of dropouts in the course of ERP.
There was also a need to develop an alternative conceptualization of OCD.
There are two models of cognitive-behavior therapy in OCD. The medical
model is based on the hypothesis that OCD is a medical brain disorder with
associated neurochemical, and neuroanatomical dysfunction (Schwartz, 1998;
Schwartz & Beyette, 1997). Therapy proceeds through four steps: (1). Relabel
obsessions as symptoms of medical illness, (2). Reattribute obsessions as false
brain messages, reduce personal responsibility, encourage patient to act as an
impartial spectator, (3). Refocus on working around the illness and (4). Revalue
symptom vs. patient as a whole. The classic model deals with correction of
mistaken beliefs and cognitive distortions by cognitive restructuring (Salkovskis,
1998). Here the main focus is on belief modification. The typical cognitive
distortions include overestimation of risk, inflated personal responsibility, thought-
action fusion, perfectionism and need to control thoughts and beliefs about religion,
morality and superstitions. Cognitive–behavior therapy lays the groundwork
for greater acceptance of ERP. ERP is an essential component of CBT.
REFERENCES
1. Abramowitz JS. Does cognitive-behavioral therapy cure obsessive-compulsive disorder?

A meta-analytic evaluation of clinical significance. Behavior Therapy 1998; 29: 339-355.
2. Foa EB, Franklin ME. Psychotherapies for obsessive-compulsive disorder: a review. In
Obsessive-Compulsive Disorder, 2nd edition. Eds. Maj M, Sartorius N, Okasha A, Zohar
J. WPA Series Evidence and Experience in Psychiatry, John Wiley & Sons, 2002, pp
93-115.
3. Foa EB, Steketee GS, Ozarow BJ. Behavior therapy with obsessive-compulsives: from
theory to treatment. In Obsessive-Compulsive Disorders: Psychological and
Pharmacological Treatments. Ed. M. Mavissakalian. Plenum, New York, 1985, pp 49-
129.
4. Foa EB, Kozak MJ. Psychological treatment for obsessive-compulsive disorder. In Long-
term Treatments of Anxiety Disorders. Eds. M. R. Mavissakalian, R.F. Prien. American
Psychiatric Press, Washington, DC, 1996, pp 285-309.
5. Greist JH. An integrated approach to treatment of obsessive-compulsive disorder. J Clin
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pharmacological treatments of obsessive-compulsive disorder. Psychopharmacology. 1998;
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OCD An Indian Perspective

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Obsessive Compulsive Disorder

Sumant Khanna, MD, PhD, MAMS, Y.C. Janardhan Reddy,

Dr. Sumant Khanna is currently a Consultant Psychiatrist in Delhi. Till last

He is currently involved in organizing research and conducting training

Dr. Janardhan Reddy is currently working at NIMHANS, Bangalore as an

1. Clinical Features of Obsessive Compulsive Disorder 1

2. Juvenile Obsessive Compulsive Disorder 11

4. Biology of Obsessive Compulsive Disorder 33

5. Pharmacotherapy of Obsessive Compulsive Disorder 39

6. Behavior Therapy in OCD 43

Shoba Srinath, YC Janardhan Reddy, M.D.D.P.M

Professor and Head, Child and Associate Professor,

Y.P. Mukesh, D. Pravin,

O bsessive-compulsive disorder is the fourth commonest mental disorder with

All rights reserved

CLINICAL FEATURES OF OBSESSIVE

O bsessive-compulsive disorder (OCD) is an intriguing and disabling illness

to the findings of these two studies, in the National Survey of Psychiatric

Obsessions and compulsions constitute the core clinical features of OCD.

The following are the common obsessive-compulsive symptoms

Fear of contamination 61 Cleaning & washing 50

Jaisoorya TS, Reddy YCJ & Srinath S (2003)

pure compulsions do occur in children. The following description of some common

Sexual and aggressive obsessions

Pathological doubt and checking

Need for symmetry, order and exactness

of OC symptoms in addition to the severity scale. The severity scale has 10

HOW TO IDENTIFY AN OCD SUFFERER?

The OCD is a common psychiatric disorder that is often undiagnosed. Only

JUVENILE OBSESSIVE COMPULSIVE

O bsessive compulsive disorder (OCD) is a common childhood psychiatric

at the Child and Adolescent Psychiatric Services of the National Institute of

OCD is essentially a neuropsychiatric disorder. Evidence from neuroimaging

Disorders Associated with Streptococcal infection (PANDAS), is characterized

A high prevalence of attention deficit hyperactivity disorder (ADHD), conduct

Symptoms of OCD should be differentiated from normal childhood rituals such

exposure and response prevention exercises for CBT.

Established treatments for OCD include clomipramine, the serotonin reuptake

adults, clomipramine is found to have slightly more anti obsessional activity

Drug Dosage in Children /Day Duration

First Line Agents

relaxation, constructive self talk, breathing techniques and positive coping

COURSE AND OUTCOME OF OCD

Child and Adolescent Psychiatry 12: 290-297.

O CD is a common mental disorder, and is often disabling. In addition, a

Major depressive disorder

Generalized Anxiety Disorder (GAD)

Social Anxiety Disorder

THE OBSESSIVE - COMPULSIVE SPECTRUM DISORDERS

that are similar to obsessions and either compulsive or impulsive behaviors.

Body Dysmorphic Disorder

Trichotillomania is the recurrent, compulsive pulling out of one’s own hair,

measures such as laxatives, diuretics, or self-induced vomiting in their attempts

Studies on schizophrenia and OCD suggest that a significant number of patients

Comorbid OCD in schizophrenia is associated with poor outcome. Conversely,

Comorbid psychiatric disorders are common in OCD. Depressive and anxiety

1. Allen A, Hollander E. Obsessive Compulsive Spectrum Disorders. Psychiatric Clinics

BIOLOGY OF OBSESSIVE COMPULSIVE

BRAIN IMAGING AND OCD

One of the most common physiological findings in OCD patients is a variety

between normal controls and OCD patients, as well as to uncover unilateral

Post-synaptic receptor dysfunction or abnormalities in direct projections of the