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Obsessive Compulsive Disorder - An Indian Perspective: Sumant Khanna, Y.C. Janardhan Reddy
Obsessive Compulsive Disorder - An Indian Perspective: Sumant Khanna, Y.C. Janardhan Reddy
An Indian Perspective
Sumant Khanna,
MRCPsych
Abbott
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.
2.
11
3.
Comorbidity in OCD
23
4.
33
5.
39
6.
43
Contributors
Shoba Srinath,
YC Janardhan Reddy,
Associate Professor,
Bangalore 560029.
Bangalore 560029
E-mail: jreddy@nimhans.kar.nic.in
Y.P. Mukesh,
D. Pravin,
Psychiatry Services.
Psychiatry Services
Department of Psychiatry,
Bangalore 560029
M.D.D.P.M
PsychConsultant Psychiatrist,
Bangalore 560029
Bangalore
E-mail: sbm@nimhans.kar.nic.in
Sumant Khanna,
Dr T. Jaideep,
Senior Resident
Department of Psychiatry, NIMHANS,
Bangalore 560029
PREFACE
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 gangliathalamo-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.
Sumant Khanna
YC Janardhan Reddy
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
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 individuals 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
50
43
Ordering
41
35
Repeating
38
Sexual
31
Checking
18
Religion
30
Hoarding
Pathological doubt
21
Miscellaneous
41
Miscellaneous
40
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,
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, dont shake hands, not go anywhere near people whom they
consider dirty or sick, and wont 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.
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.
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.
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 rewriting.
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
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 YBOCS 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.
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 obsessivecompulsive 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 obsessivecompulsive 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 obsessivecompulsive disorder. J Clin Psychiatry 1994; 55 (Suppl. 3):5-10
17. World Health Organization. The ICD-10 Classification of Mental and Behavioral Disorders.
Clinical Descriptions and Diagnostic Guidelines, World Health Organization, Geneva.
11
INTRODUCTION
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
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 Tourettes 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 Sydenhams
chorea. This subtype of OCD, called Paediatric Auto-immune Neuropsychiatric
13
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.
14
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, Aspergers 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.
15
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
16
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
17
Duration
10-12
10-12
10-12
10-12
10-12
10-12
Augmenting Agents
Clonazepam
Haloperidol
Risperidone
5 mg
3 mg
0.5-2 mg
4-6 weeks
4-6 weeks
4-6weeks
weeks
weeks
weeks
weeks
weeks
weeks
18
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.
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 childs experience with OCD including avoidance
behaviors within a narrative context. They also include trial ERP tasks to gauge
the childs level of understanding and willingness to comply with ERP. Step
4 implements both ERP and anxiety management. Anxiety management involves
19
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.
20
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-nave 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.
2003), none of the earlier known potential predictors were significantly associated
with OCD outcome. Instead, earlier age-at-onset of OCD and longer followup was associated with better outcome.
REFERENCES
1. Berg CZ, Whitaker A, Davies M, Flament MF, Rapoport JL (1989). The survey from
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 obsessivecompulsive 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
21
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
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
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 2560%.
Conversely, studies in primary anxiety disorders have showed comorbid OCD
in 11-14% of the patients.
COMORBIDITY IN OCD
25
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.
26
COMORBIDITY IN OCD
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.
COMORBIDITY IN OCD
27
28
COMORBIDITY IN OCD
Hypochondriasis
The fear or belief that one has a severe illness characterizes hypochondriasis.
This fear is based on an individuals 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 ones body or with others.
sensations.
Trichotillomania
Trichotillomania is the recurrent, compulsive pulling out of ones 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
COMORBIDITY IN OCD
29
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 obsessivecompulsive 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
30
COMORBIDITY IN OCD
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 obsessivecompulsive 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.
COMORBIDITY IN OCD
31
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.
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 Tourettes 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 obsessivecompulsive disorder. The Cross National Collaborative Group. Journal of Clinical Psychiatry
1994; Suppl 55: 5-10.
33
SEROTONIN:
34
in
OCD patients. However the volume of the right head of caudate was increased
in these patients when compared with normal controls.
left frontal hemisphere and caudate is observed during image flooding, with
the positive correlation between the OCD severity and rCBF.
These findings
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 MRIs 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
35
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
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
36
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
37
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.
39
PHARMACOTHERAPY OF OBSESSIVE
COMPULSIVE DISORDER
Sumant Khanna, MD, PhD, MAMS, MRCPsych
Consultant Psychiatrist, New Delhi
Former Additional Professor of Psychiatry, NIMHANS, Bangalore
40
which showed a
41
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, Tourettes 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
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.
43
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 anxietyprovoking 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.
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
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.
45
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 ones 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
46
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.
47
100
Anxiety
(Watching TV at Home)
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
30
40
50
60
65
70
80
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.
48
49
Possibly less effective in patients with poor insight and in pure obsessionals.
50
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, thoughtaction fusion, perfectionism and need to control thoughts and beliefs about religion,
morality and superstitions. Cognitivebehavior therapy lays the groundwork
for greater acceptance of ERP. ERP is an essential component of CBT.
REFERENCES
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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
51
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 49129.
4. Foa EB, Kozak MJ. Psychological treatment for obsessive-compulsive disorder. In Longterm 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
Psychiatry 1992; 53 (Suppl. 4): 38-41.
6. Kobak KA, Greist JH, Jefferson JW, Katzlenick DJ, Henk HJ. Behavioral versus
pharmacological treatments of obsessive-compulsive disorder. Psychopharmacology. 1998;
136: 205-216.
7. Salkovskis PM, Forrester E, Richards C. Cognitive-behavioral approach to understanding
obsessional thinking. British Journal of Psychiatry 1998; 173: 53-63.
8. Schwartz JM. Neuroanatomical aspects of cognitive-behavioral therapy response in
obsessive-compulsive disorder. An evolving perspective on brain and behavior. British
Journal of Psychiatry 1998; 173: 38-44
9. Schwartz JM, Beyette B. Brain Lock: Free Yourself from Obsessive-Compulsive Behavior.
Harper Collins, New York, 1997.