Brief Pithy Description Obsessive Compulsive Disorder OCD is an by MikeJenny


									Brief Pithy Description

       Obsessive Compulsive Disorder (OCD) is an anxiety disorder that involves “recurrent

obsessions or compulsions severe enough to be time consuming or cause marked distress or

significant impairment” in a person’s life.     This person may or may not realize that their

obsessions or compulsions are “excessive or unreasonable.” (APA, 1994)

DSM-IV Diagnostic Criteria For Obsessive Compulsive Disorder

(American Psychiatric Association, 1994, p. 418-23)

       To be diagnosed with OCD, a person must have either obsessions or compulsions.

Obsessions are “recurrent and persistent thoughts, impulses, or images that are experienced, at

some time during the disturbance, as intrusive and inappropriate and that cause marked anxiety

or distress.” They are not “simply excessive worries about real-life problems.” The person

“attempts to ignore or suppress such thoughts, impulses, or images, or to neutralize them with

some other thought or action,” while recognizing that they are “a product of his or her own

mind.” Some examples are “repeated thoughts about contamination, repeated doubts, a need to

have things in a particular order, aggressive or horrific impulses, and sexual imagery.”

       Compulsions are “repetitive behaviors or mental acts that the person feels driven to

perform in response to an obsession, or according to rules that must be applied rigidly.” These

compulsions are “aimed at preventing or reducing distress or preventing some dreaded event or

situation” yet are not realistic.   Examples are “hand washing, ordering, checking, praying,

counting, and repeating words silently.”

       “At some point during the course of the disorder, the person has recognized that the

obsessions or compulsions are excessive or unreasonable.” If the person has OCD with poor

insight, this does not occur. Also, this does not apply to childhood OCD.

       “The obsessions or compulsions cause marked distress, are time consuming (take more

than 1 hour a day), or significantly interfere with the person’s normal routine, occupational (or

academic) functioning, or usual social activities or relationships.”

       “If another Axis I disorder is present, the content of the obsessions or compulsions is not

restricted to it” and OCD “is not due to the direct physiological effects of a substance or a

general medical condition.”

Background and History

       Jenike (2001) writes that “centuries ago, individuals with obsessive, blasphemous, or

sexual thoughts were considered to be possessed, and exorcism was the treatment of choice, with

the person subjected to torture in an effort to drive out the intruding entity.” Montgomery and

Zohar (1999) quote 17th century bishop John Moore describing obsessive thoughts as “naughty,

sometimes blasphemous thoughts [which] start in their minds, while they are exercised in the

Worship of God [despite] all their endeavors to stifle and suppress them the more they struggle

with them, the more they increase.” (2) Shakespeare described the repetitive hand-washing

behavior of Lady Macbeth: “it is an accustomed action with her, to seen thus washing her hands.

I have known her continue with this a quarter of an hour.” (Macbeth, V.i.28)

       As years passed, the religious view of obsessions and compulsions was replaced by a

medical view of the condition. Esquirol first described OCD in 1838, and by the end of the

century it was thought of as part of melancholy or depression. (Jenike, 2001) In the beginning of

the 20th century, psychological explanations were surfacing, and Janet “reported successful

treatment of rituals with behavioral techniques.” (6) With Freud’s writings, OCD was recognized

as resulting from internal and subconscious conflicts that were isolated from one’s emotions and

treatment was shifted towards resolving such conflicts. Recent OCD research has focused on the

biology, genetics, and pharmacological treatments of the disorder.

Rubric One: Quantity (see summary chart)

       There have been several studies measuring the incidence and prevalence of OCD in

various populations throughout the world. Karno et al (1988) studied the prevalence of OCD in

five US communities as part of the Epidemiologic Catchment Area (ECA) study. They sampled

over 18,000 people in households and about 2,500 in institutions using the Diagnostic Interview

Schedule, which consists of questions “designed to elicit the presence or absence of symptoms

sufficient to establish the diagnosis of approximately 40 mental disorders.” (1094) The study

found a total lifetime prevalence of 2.5% with a range of 1.9% to 3.3%. Nestadt et al (1998)

traced the Baltimore cohort of the ECA study and re-interviewed the subjects from 1993 to 1996

to measure the incidence rate of OCD in the population. The study utilized the Diagnostic

Interview Schedule, which was modified to reflect the DSM-III-R changes made. Nestadt et al

found that the annual incidence rate for OCD in this population to be .55 per 1,000 person years,

and 13 new cases of OCD in the sample of 1920 people.

       Weismann et al (1994) conducted a study measuring the prevalence of OCD in the USA,

Canada, Puerto Rico, Germany, Taiwan, Korea, and New Zealand. The Diagnostic Interview

Schedule was used by investigators to determine cases and non-cases of OCD. Prevalence of

OCD ranged from 0.7% in Korea to 2.5% in Puerto Rico, but most ranged from 1.9%-2.5%. The

annual prevalence of OCD ranged from 1.1% in Korea to 1.8% in Puerto Rico with Korea at

0.4%. Korea also has very low rates for other psychiatric disorders, so these findings are

consistent. This study standardized the prevalence rates to the age and sex distribution of the

ECA study from which the USA data was derived, but could not make “accurate comparisons of

sex ratios, age at onset, and demographic and clinical characteristics of OCD because of

differences in sampling, methods of analyses, and weighting procedures.” Some have criticized

the DIS assessment because it was designed for lay interviewers, who tend to over-diagnose, and

not psychiatrists. Hollander and Stein (1997) report that studies done by psychiatrists tend to

yield lower rates of OCD, so the prevalence data in the study could be a bit inflated.

       In a study done by Stein et al (1997) in Canada, lay interviewers “administered a

modified version of the OCD section of the Comprehensive International Diagnostic Interview

(CIDI)” and found a “weighted 1-month prevalence of OCD in the entire sample (n=2261)” of

3.1%. (1120) Those with suspected cases and subclinical cases were blindly re-interviewed by

“research personnel experienced in the assessment of OCD, using the Structured Clinical

Interview for DSM-IV and the Yale Brown Obsessive Compulsive Scale” and the 1 month

prevalence rate was found to be 0.6% with clinical OCD and 0.6% with subclinical OCD. (1120)

The authors suspect that their rate could be low because the instrument they used (CIDI) was

modified and there are new versions available that may be more precise, though the CIDI has

been shown possess an “excellent interrater reliability for OCD in comparison with a clinician

interview.” (1124)

        Valleni-Basile et al (1996) investigated the incidence of OCD in a sample of adolescents

by conducting a two-stage epidemiological study. Subjects completed the CES-D self-rating

scale used to assess depressive symptoms, as the study was originally intended to investigate

major depression in adolescents.     The authors state that CES-D has performed as well in

screening for other psychiatric disorders as it does for major depression in adolescents. Subjects

were invited with their mothers for diagnostic interviews based on their scores on the CES-D and

by random and these interviews were repeated once or twice. Subjects present at least two

consecutive years were included in the statistical analysis, which yielded a one year incidence

rate of 0.7% for clinical OCD and 8.4% for subclinical OCD.

       In another study of adolescents performed by Maggini et al (2001) in Parma, Italy,

subjects were assessed using the Leyton Obsessional Inventory-Child Version (LOI-CV), which

consists of a 20 item questionnaire “asking for the presence or absence of a number of obsessive

preoccupations and behaviors, as well as, for each positive response, a rating of interference in

personal functioning.” (442) The authors claim this instrument has been proven valid and they

are able to compare their data to other studies. This study however, does not classify subjects by

a DSM diagnosis, but uses the terms “high interference” for those with the most OCD

symptomatolgy and “supernormal” for those with lesser symptoms based on the LOI-CV score.

Maggini et al found that 4.1% were classified as high interference and 3.0% make up the

supernormal group. This study did not utilize interviews, which is a main downfall, but the

authors suggest that the use of questionnaires allows those who are secretive about their OCD

symptoms to express themselves anonymously. The authors also state that the LOI-CV tends to

yield more false positives- their result of a prevalence of 4.1% is higher than the other studies

discussed here.

       In general, the findings of many prevalence studies spanning many nations suggest the

lifetime prevalence to be around 2-3%, which suggests that OCD is a significant problem

worldwide. However, since many of these studies involved using lay interviewers, this rate

could be exaggerated. It is possible that many of those classified as having OCD have a

subclinical form of the disorder, which was reported as being common in the Valleni-Basile

(1996) study. OCD should be recognized by all health professionals as being a common mental

disorder that causes significant impairment in those it affects.

Rubric 2: Location

Age-   OCD affects children, adolescents, and adults. Hollander and Stein (1997) report that

65% of patients develop OCD before age 25, with males having an earlier age of onset than

females. It is rare for someone to develop OCD after the age of 45. (DeSilva and Rachman,

1998) Weissman et al. (1994) report an average age of onset in the range of 21.9-35.5 years of

age in their study of OCD in seven countries. Montgomery and Zohar (1999) report that in

retrospective studies of adults with OCD, 30-50% report that their symptoms began in childhood

or adolescence. DeSilva and Rachman (1998) write that in a case series of patients in a London

hospital, 92% of patients with OCD developed the condition between the ages of 10 and 40.

       Geller et al. (2001) compared the OCD symptoms of children, adolescents, and adults to

investigate the differences between childhood and adult onset OCD. The mean age of onset for

children was 6 years of age, for adolescents 10 years of age, and for adults 21 years of age. The

study found that “children and adolescents had much higher rates of aggressive obsessions

(including fears of catastrophic events, such as death or illness in self or loved ones) than

adults…religious obsessions were over represented in adolescents compared with children and

adults, and sexual obsessions were underrepresented in children compared with adolescents and

adults.” (473) In the British nationwide survey of child mental health, Heyman et al (2001) found

that prevalence rates of OCD increased as age increased, with children aged 5-7 had a .026%

prevalence and children age 13-15 had a .63% prevalence. The authors hypothesize that most

cases in adolescents and young adults occur between the ages of 16-18, as the study’s overall

prevalence of .25% was less that that of other studies’ findings.

Sex-    There has not been completely consistent evidence about a significant difference in

prevalence between males and females. In the Weismann et al (1994) cross-national study, the

lifetime prevalence was higher for females than males in 6 of the 7 locations. In the USA,

females had a lifetime prevalence of 2.8% while males had a 1.7% prevalence rate. The ECA

study found that gender was not associated with prevalence of OCD in adults.

       However, when considering OCD in children, boys present for treatment more than girls

do. Diler and Avci (2002) studied the demographics of OCD in Turkish children and found that

almost twice as many boys than girls were diagnosed. They also report that the onset of OCD

has been found to be1.5 to 2.5 years later in girls than boys. Geller et al (2001) found that “both

child and adolescent groups showed clear male preponderance (67% and 64%) that differed

significantly from the adult sample (46%).” (473) Overall, studies show that though there may be

slight gender differences in various age groups, both genders are at risk of developing OCD.

Geography-      The table presenting the incidence and prevalence rates of OCD shows that the

lifetime prevalence of the disorder is about 2-3% for all countries sampled, except for Taiwan

where it was only 0.7%. Taiwan has a lower rate of all psychiatric disorders, and Juang and Liu

(2001) show that the clinical characteristics of OCD in their patient sample were similar to those

reported in studies from other countries.

Religiosity-   It has been hypothesized that individuals with high degrees of religiosity may

have higher rates of OCD. Sica et al (2002) researched the association among Catholics in Italy

who were of high, medium, and low degrees of religiosity by using the Obsessive Beliefs

Questionnaire, Interpretation of Intrusions Inventory, Padua Inventory, Beck Anxiety Inventory,

and Beck Depression Inventory. The study found that “individuals with a high or medium

degree of religiosity showed higher levels of obsessionality and OC cognitions than individuals

with a low degree of religiosity of the same age, education, and gender.” (820) Abramowitz et al.

(2002) studied the differences between high and low religiosity in Catholics, Protestants, and

Jews. They found that highly religious people experienced a greater fear of God, but Jews had

much less of this fear than Catholics and Protestants. This was also true for the fear of sin. This

study, however, was done in a population of college students, which may not be representative of

the general population.

Socioeconomic Status-         Karno et al (1988), in their study of five US communities, found a

moderate association between lower SES and OCD, and also found an association between being

unemployed and having OCD. Millet et al (2001) compared French and Turkish OCD patients

and found that education level was significantly higher in the French patients than the Turkish

group. The ECA study did not report any association with OCD and level of educational

attainment. In the British nationwide survey of child mental health, children with OCD were

more likely to be of lower SES that healthy children. (Heyman, 2001) Diler and Avci (2002)

report that most of the Turkish children and adolescents with OCD were of middle or upper SES.

Obviously, the role of SES in OCD is not consistent, and more studies need to be done before a

solid association is made.

Race- Many studies have found no association between race and OCD, but there have not been

many studies done in very diverse populations. The ECA study showed that black respondents

had significantly lower rates of OCD than non-Hispanic whites. (Karno et al, 1988) Valleni-

Basile (1996) found that black adolescents had a significantly higher risk of OCD than their

white counterparts, although the authors state that their findings are not consistent with those of

other studies which report mostly white patients presenting for treatment. However, white

patients may seek treatment more or have more resources to do so than black patients.

Comorbidity-          Many studies investigate the presence of other psychiatric disorders in

those with OCD. Tukel et al (2002) studied the presence of Axis I disorders in OCD patients and

found a presence of 68.7%, the most common being major depression (39.5%). In a study of the

phenomenology of OCD in Taiwan, Juang and Liu (2001) found that 41.5% of the OCD patients

had a comorbid depressive disorder. Brown et al. (2001) studied the comorbidity of DSM-IV

anxiety and mood disorders and discovered that patients with OCD had a significantly higher

risk of major depressive disorder. Fireman et al (2001) report that 75% of OCD patients had a

comorbid psychiatric diagnosis, the most common being major depression (56%) and other

anxiety disorders (26%). Weismann et al (1994) found that patients with OCD in all seven

countries studied had a higher risk of major depression and another anxiety disorder than those

without OCD (odds ratios range from 3.8-13.5 for major depression and 5.8-14.3 for another

anxiety disorder).

       Heyman et al. (2001) also found that two thirds of children diagnosed with OCD had at

least one other psychiatric diagnosis. Geller et al (2001) report that children with OCD had a

lower rate of major depression (39%) than did adolescents (62%) and adults (78%). Children

also had a higher rate of Tourette’s disorder (25%) than adolescents (9%) and adults (6%).

Speranza et al (2001) report that current and lifetime prevalence of OCD in those with eating

disorders is significantly higher than in the general population. Milos et al (2002) found a

prevalence rate for OCD of 29.5% in eating disorder patients with no difference between

anorexics and bulimics.

Genetics-     Many studies have investigated the possibility of a genetic component in the

development of OCD by performing family studies and genetic analyses. A review study of the

genetic epidemiology of anxiety disorders found that OCD, among other anxiety disorders, had

significant familial aggregation. There was significant association between OCD in the probands

and in first degree relatives. In the Johns Hopkins OCD family study, OCD was significantly

more common in the first degree relatives on OCD probands than in the first degree relatives of

controls. (Nestadt et al, 2000) Nestadt et al (2001) found that generalized anxiety disorder and

agoraphobia share a common familial etiology with OCD. Cavallini et al (1999) performed

complex segregation analysis among Italian families with probands with OCD and found a

dominant model of transmission with a higher penetrence for females. Similarly, Nestadt et al

(2000) found a Mendelian-dominant model with significant sex effects and with residual familial


Immunocompetence-            Dinn et al (2001) write that “a postinfectious, autoimmune

response my be associated with the development of pediatric OCD.” (311) Their study found an

increased rate of immune-related symptoms and syndromes among adult OCD patients compared

to other anxiety and mood disorder patients. Asbahr et al (1998) studied children and adolescents

who had been recently diagnosed with rheumatic fever with or without Sydenham’s chorea.

They found that OCD symptoms appeared 2 months after the disease onset in 70% of patients

with chorea and were absent in all patients without chorea.

Neurobiology-         Researchers have been investigating the role of serotonin and other

neurotransmitters in those with OCD. Pharmacological treatment studies suggest that OCD in

related to a 5-HT deficit and that SSRIs improve this and reduce OCD symptoms. (Micallef and

Blin, 2001)     Animal studies have shown that high doses of dopaminergic agents cause

movements and behaviors in animals that resemble those seen in OCD. Billett et al (1998)

conducted a genetic association study of dopamine system genes in OCD and found “significant

differences in allele frequencies between patients and controls for the D4 receptor gene.” (163)

Rubric 3: Causes

       There is no one established cause for OCD, although there are many hypotheses being

tested and researched. This section will discuss the sub-headings under the previous “Location”

rubric which have compelling evidence for causal significance. For some of the sub-headings

there are only a few studies that are somewhat convincing, but for others there is a larger body of

evidence that links the risk factor to OCD more conclusively, namely the genetic,

immunocompetence, and neurobiology categories.

       As previously mentioned, there have been many family studies and genetic analyses to

investigate the possible genetic cause of OCD. Nestadt et al (2000) sought to determine whether

OCD was familial and to investigate possible familial subtypes. Case probands met DSM-IV

criteria for OCD and both cases and controls were excluded if they were diagnosed with

schizophrenia, mental retardation, dementia, or Tourette's disorder, or if OCD occurred only

during a major depressive episode. Interviewers were blind to whether the subject was a case or

control relative or case or control proband. The study found that the prevalence of definite OCD

was significantly higher in case relatives (11.7%) than control relatives (2.7%), as was the

prevalence of definite and probable OCD (16.3% case relatives vs. 5.7% control relatives). The

odds ratio for definite OCD in relatives was 5.5, indicating a strong and specific association.

Additionally, significant odds ratios were found for “all definitions of the affected phenotype,

indicating that first degree relatives of cases met criteria for OCD-related phenotypes

significantly more often than first degree relatives of controls.” (360)

       Grados et al (2001) studied whether tic disorders were part of the familial phenotype of

OCD and excluded Tourette’s syndrome in probands.             Case (OCD diagnosis) and control

probands and their first degree relatives were interviewed by psychiatrists and psychologists who

were blinded to case/control/proband/relative status. The study found that case probands and

case relatives had a greater lifetime prevalence of tic disorders compared with control subjects.

6.2% of case relatives had a tic disorder compared with 1.7% of control relatives. An earlier age

of onset of OCD symptoms is associated with lifetime tic disorder as well.          The authors

concluded that tic disorders are part of the familial OCD phenotype based on their results and

those of previous studies.

       Hettema et al (2001) conducted meta-analysis of data from family and twin studies of

OCD to investigate the role of genetic and environmental components in the disease.        They

reviewed five studies and found that there was a significant association between OCD in

probands and in their first-degree relatives. The authors calculated a Mantel-Haenszel summary

odds ratio of 4.0, and found an unadjusted aggregate risk for OCD-proband relatives to be 8.2%

compared to 2.0% in control proband relatives.         This study adds to the growing body of

consistent research that supports the familial and heritable component of OCD.

       Nestadt et al (2000) wanted to explore the mode of inheritance of OCD in the US

population, and they used case and control probands and their first-degree relatives to do so.

Controls were matched to cases on sex, race, and age, and probands were excluded if they were

diagnosed with schizophrenia, mental retardation, dementia, or Tourette's disorder, or if OCD

occurred exclusively during a major depressive episode. Interviewers were blinded to the status

of the subjects. The authors conducted complex segregation analysis using a program with

regressive logistic models to test for the “presence of a major susceptibility locus, residual

correlations in risk among related individuals, and the effect of measured risk factors.” (1612) A

sporadic model, Mendelian models (dominant, recessive, and codominant), and an environmental

model were tested. The authors found evidence of heterogeneity between families regarding

male and female probands and then performed separate segregation analyses on each family.

Among the female probands, neither the dominant nor codominant Mendelian models were

rejected, and the dominant model fit the best. The baseline risk for high-risk genotypes for

females was found to be 24.5 and for males 3.7. The authors concluded that “the results from the

total sample and the stratified subgroups were consistent with Mendelian inheritance of a

dominant allele leading to a high risk of having OCD.” (1614) This study and the others show

that the genetic cause of OCD satisfies the causal criteria of strength of association, consistency,

specificity, plausibility, and coherence.

       There has been increasing evidence for a neurobiological cause of OCD which centers

around a serotonin abnormality. Montgomery and Zohar (1999) state that serotonin is thought to

be involved in OCD because of the positive response of OCD patients to clomipramine, a drug

that inhibits the reuptake of serotonin. The decrease in OCD symptomology is consistent with

the 5-HT receptor indices such as changes in 5-HIAA, a serotonin metabolite, in the

cerebrospinal fluid. Studies have given OCD patients the serotonin agonist mCPP and these

patients experienced significant anxiety and depression following mCPP compared with the

placebo group. This finding has been replicated in some studies but not others. Researchers are

trying to identify a 5-HT subtype that may be responsible for OCD. Several 5-HT 1-a receptors

have been ruled out but the 5-HT2C and 5-HT1D receptors are more likely candidates based on

the mCPP, MK-212, and ipsapirone challenge studies that show exacerbation of symptoms with

the 5-HT1D agonist sumatriptan. (Montgomery and Zohar, 1999) The evidence for involvement

of the serotonergic system in the cause of OCD is strong, but not always consistent in terms of

subtypes and details. Researchers agree that the cause of OCD is so complex it cannot be

attributed to a single neurotransmitter, so other possible neurobiologic causes are being studied.

       Dopamine is also thought to be involved as a cause for OCD. Animal studies have

shown that high doses of dopaminergic agents caused stereotyped movements in animals that

resemble compulsive behaviors in human OCD patients. (Micallef and Blin, 2001) Swerdlow

(1995) demonstrated that adjunctive neuroleptic therapy, which blocks dopamine receptors,

added to SSRIs to reduce OCD in patients resistant to SSRIs alone reduces the severity of OCD

symptoms. Stahl et al (1988) hypothesize that a decrease in serotonin inhibitory influences on

dopamine neurons could lead to increased dopaminergic function as a result of the functional

connections between dopamine and 5-HT neurons in the basal ganglia. Micallef and Blin (2001)

report that “functional brain imaging studies in OCD are strongly suggestive of an abnormality in

basal ganglia-thalamic-orbitofrontal-cortical circuitry in OCD, which may normalize to some

extent during treatment.” (199) Overall, there are many more studies to be done to test the role of

neurotransmitters in the role of OCD.       There is definite biological plausibility and some

consistency for the serotonin hypothesis especially, but the mechanism seems so complex

already that new theories will continue to emerge.

       Studies are also investigating autoimmune diseases such as Sydenham’s chorea and

streptococcal infections as causes of OCD in children. A subtype of OCD called PANDAS

(pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) has

been proposed. Arnold and Richter (2001) describe Sydenham’s chorea as developing after a

group A B-hemolytic streptococcal infections and as one type of rheumatic fever. A “molecular

mimicry” process occurs when “antistreptococcal antibodies cross-react with basal ganglia

proteins, triggering an inflammatory response and producing the symptoms of Sydenham’s

chorea.” (1354) Psychiatric symptoms include OCD behavior, emotional lability, and ADHD

symptoms. D8/17 has been identified as a risk marker for PANDAS, as elevated levels of D8/17

have been found in children with PANDAS, and in subjects with early onset OCD and tic

disorders. Increased basal ganglia volumes have been found on volumetric MRI in those with

PANDAS, and “higher antistreptococcal antibodies that correlated with increased basal ganglia

volumes in subjects with either attention deficit hyperactivity disorder or OCD.” (1355) There is

consistency with other studies, a strong strength of association, and some degree of specificity

for OCD among children with autoimmune disorders.

       A study done by Asbahr et al (1998) evaluated new cases of rheumatic fever with and

without chorea for six months after diagnosis. The children did not have OCD symptoms or any

other psychiatric disorder at the beginning of the study. The study found that OCD symptoms

peaked at two months after the onset of rheumatic fever in 70.0% of patients with chorea but

were absent in all patients without chorea. OCD was diagnosed in 16.7% of those with chorea.

These results are consistent in supporting the role of Sydenham’s chorea in the development of

childhood onset OCD and also fulfill the causal criteria of temporality, with the chorea occurring

before the OCD.

       In a case series performed by Dinn et al (2001), medical records of adult OCD patients

were reviewed to see if they, compared to patients of other psychiatric diagnoses, had “a higher

incidence of recurrent infections and other conditions suggestive of compromised immune

function.” (311) The study found that OCD patients had an increased rate of immune-related

symptoms and syndromes in comparison to those with other anxiety and mood disorders. The

groups did not differ in the incidence of non-immune symptoms and syndromes. The authors

believe that their findings support the theory that an autoimmune reaction disrupts a basal

ganglia-thalamocortical circuit which produces OCD symptoms.               The possibility that

autoimmune diseases could cause OCD is supported by consistent evidence that warrants further


Rubric 4: Causal Mechanisms (Clinical Course and Natural History)

       As stated earlier, OCD usually begins in young adulthood, and rarely cases develop after

the age of 45. However, many children are affected by this disorder, which may develop as early

as five years of age. (Heyman et al, 2001). Geller et al (2001) investigated the differences in

childhood, adolescent, and adult onset OCD to test a hypothesis of developmental discontinuity

between juvenile and adult OCD.        The authors point out that “research efforts aimed at

identifying OCD-associated genes are likely to be more successful if developmentally

homogenous samples are studied instead of combining data from children, adolescents, and

adults.” (471) The study found evidence of developmental heterogeneity where specific

correlates were associated with OCD in different age groups. Childhood and adolescent OCD

was male preponderant and patients experienced more aggression/catastrophe obsessions,

hoarding and saving compulsions, multiple obsessions and compulsions, and poor insight

compared to adult OCD. Rates for Tourette’s syndrome were inversely proportional with age, as

were those for ADHD, suggesting differences in juveniles and adults. This study provides an

interesting idea for future research into the clinical differences between adult and child onset

OCD, as the natural histories of the two groups may be different for OCD.

       There are not many studies that evaluate the clinical course of OCD over a long period of

time. Probably the best study done on the natural history of OCD was a 40 year follow up of

patient with OCD done by Skoog and Skoog (1999). Patients admitted to a hospital with the

diagnosis of OCD from 1947-1953 were examined by one of the authors (a psychiatrist) between

1954 and 1956 and were reexamined by the same author between 1989 and 1993. The average

follow up time from onset of OCD to the second exam was 47.2 years. The authors found that

“In 1989 to 1993, 83% of all patients had improved and 48% showed clinical recovery, but only

20% showed complete recovery. In those who had recovered, the improvement was slow and

gradual in 65%, fast in 9%, and difficult to evaluate in 26%. Among those who were recovered

at the second examination, 38% had already recovered at the first examination.” (122) Symptoms

of OCD changed in 58% of the patients.        Patients with a combination of obsessions and

compulsions at first examination, 59% still had symptoms at the second exam, compared with

only 41% of those with obsessions only. Age of onset was earlier in men than in women, with

44% of men having onset before age 20 and 22% of the women having onset before age 20.

Those who had onset before age 20 were less likely to be in recovery at second examination than

those with a later onset, and more likely to have an unchanged or deteriorated condition than

those with a later onset.

       In terms of clinical course, “an intermittent course was most common from onset to the

first examination (56%), while a chronic course was most common in the time up to the second

examination (44%).” (125) Social functioning was also measured in the patients using the Global

Assessment of Functioning (GAF) scale, and a significant relationship was found between

change in social functioning and change in clinical severity of OCD symptoms from exam 1 to

exam 2.      Change in social functioning was consistent in direction with change in clinical

severity in 49% of the patients. Overall, this study demonstrates that OCD is generally a chronic

that can last for decades. Of those followed up 50 years after onset, 37% still had OCD.

Complete recovery occurred in only about 20% of patients, though most showed some

improvement in symptoms. The authors state that their findings were consistent with other

studies with shorter follow up periods. This area should be studied more to learn about the

clinical course of OCD in children and adults to further investigate a heterogeneity.

       One study done by Wewetzer et al (2001) looked at the clinical course of childhood OCD

by following a sample of inpatients and outpatients who were diagnosed with OCD and received

treatment between 1980 and 1991. The average age of onset was 12.5 years and the patients’

mean age of follow up was 25.7 years. The study found that 36.4% of the patients still had OCD

at follow up, and 70.9% had at least one psychiatric disorder at follow up. 29.1% no longer

demonstrated OCD symptoms after treatment, 27.3% still had subclinical OCD, 30% had an

episodic case of OCD, and in 12.7% a chronic course of OCD was found. More men suffered

from chronic OCD than women and those with OCD at follow up were more likely to have

another clinical disorder. Inpatient treatment, terminating treatment against advice of therapist,

and experiencing tics in childhood or adolescence were significantly associated with more severe

OCD symptoms at follow up. This study lends insight into the course of childhood onset OCD,

but was limited due to the large number of non-participants and that fact that none of the patients

received any therapy or medication during the follow up period. The natural history of this

disorder could become more clear if similar studies with high participation rates were performed.

Rubric 5: Prevention and Control

       Medication is often used to treat OCD, and Jenike (2001) states that “there is

overwhelming evidence from multiple randomized, double blind, placebo-controlled studies

supporting the efficacy of serotonin reuptake inhibitors in the treatment of OCD.” (10) Such

drugs include fluvoxamine, fluoxetine, paroxetine, sertraline, and citalopram and all have been

shown to be more effective than non-SRI tricyclic antidepressants in placebo and non placebo-

controlled trials. These drugs act to correct the serotonin dysfunction discussed earlier in the

“causes” section by blocking the pre-synaptic uptake of serotonin. The average response to

SSRIs in OCD patients is a 35% reduction in symptoms after 12 weeks of treatment. SSRIs can

be augmented with drugs such as buspirone, fenfluramine, and trazodone/nefazodone.

Sometimes SSRIs do not work because the 5-HT is depleted, and one possibility is to use

buspirone to slow neuronal impulse flow so serotonin can build up and 5-HT can be produced.

Fenfluramine is a serotonin releaser and causes the neurons to release 5-HT, which would allow

the SSRI to block its reuptake. Trazodone and nefazodone act by blocking 5-HT2 receptors,

which causes 5-HT2 downregulation. (Micallef and Blin, 2001)

       Clomipramine has also been recognized as successful in treating OCD since the 1980s,

though it was first recognized as a treatment for depression. Clomipramine is not selective like

the aforementioned drugs, and it has “pharmacologically significant affinity for cholinergic and

adrenergic receptors,” which produces more side effects. (Dougherty and Rauch, 1997, 147) It is

thought that the drug works by blocking 5-HT reuptake and preventing serotonin reuptake. The

effectiveness of clomipramine has been found in several double blind trials, and one trial

concluded that patients given the drug decreased their OCD symptoms by 35-42% compared

with 2-5% in the placebo group. (Micallef and Blin, 2001)

       Behavioral therapy is often effective in patients being treated with medication. It consists

of exposure and response prevention (ERP), where a patient, by himself or with a therapist, is

confronted with his feared object or circumstance. The patient must then resist performing

rituals and compulsions in response to the exposure. Studies show that behavior therapy is

effective for 70-80% of OCD patients, especially those with cleaning or hand-washing

compulsions. (Silvestre and Aronowitz, 1997) Therapy that allows some rituals to continue is

less effective that use total response prevention, a more strict method. Also, therapist controlled

exposures are more effective than self-controlled exposures patients do on their own. (Neziroglu

et al, 2000) Silvestre and Aronowitz (1997, 236) list the “necessary ingredients of behavioral

therapy as :

       1. Psychoeducation with patient and /or significant others about OCD.

       2. Rationale for and description of the components of ERP in behavioral therapy and the

           setting of realistic treatment expectations.

       3. A behavioral contact between patient and therapist.

       4. ERP with enlistment of family members, when available or clinically indicated, to

           serve as behavioral therapy cotherapists; individualized behavioral therapy sessions

           for sufficient habituation to occur.

       5. Design of daily homework.

       6. Termination.

       7. Relapse-prevention strategies.

       8. Booster sessions.

       Cognitive therapy is also used in treating OCD, though not always in conjunction with

behavior therapy. Cognitive therapy was found to be just as effective as behavior therapy in

patients with obsessions only, and was associated with a decrease in discomfort and an increase

in social and work functioning after six sessions of therapy. (Neziroglu et al, 2000) Family

involvement in therapy was also shown to be effective. Patients whose families were enrolled in

group therapy with them showed a significant decrease in symptoms compared to patients

without family involvement. For very serious cases of OCD that do not respond to any of the

treatment for the disease, neurosurgery can be performed by cutting the neuronal loop connecting

the cortex with the basal ganglia. There is no evidence for the long term outcome, but early

studies have shown that neurosurgery is effective for those with severe, refractory OCD.

(Micallef and Blin, 2001)

       There is a dearth of information about the prevention of OCD, and it is difficult to

imagine how the symptoms could actually be prevented from occurring. However, people at

high risk for the disorder can be identified by their physicians or therapists based on some of the

causes discussed earlier. Children diagnosed with Sydenham’s chorea or similar autoimmune

disease should be monitored by their physicians and parents for OCD symptoms, which usually

come on suddenly. Children with Tourette’s or tic disorder, who may be under the care of a

psychiatrist already, would be at high risk for development of OCD. Those with close family

member who have OCD or OCD spectrum disorders should be monitored by their physicians.

Since many with OCD wait many years before seeking treatment, identification of early

symptoms before clinical OCD is present would possibly improve the prognosis of the patient.

Directions for Future Research

       After reviewing many articles and books about OCD, I believe there are three main areas

in which future research should center. The first would be to characterize juvenile OCD as its

own subtype of the disorder or as a definite part of adult OCD. The literature has already

identified several differences between child-onset and adult-onset OCD, and if such a subtype

exists in children, the causes for the disorder would be more easily seen and the treatment could

be tailored to the specific type of OCD the patient is suffering from.          Research should

concentrate on the replication of the study done by Geller et al (2001) on the differences between

child, adolescent, and adult onset OCD in clinical and community samples. Also, studies should

focus on the differences in etiology by performing brain imaging studies and looking for

biological differences between children and adults with OCD. Studies researching the genetics

and familial aggregation of OCD should be specific to child and adult onset OCD in order to

determine if a subtype does exist. Doing so could result in a more accurate diagnosis and more

successful and specific treatment for OCD in various sub-populations.

       The second area in which future research should focus is on the clinical course and long

term outcome of patients with OCD who are receiving different treatments. There is not much

information on this topic, but the study done by Skoog and Skoog (1999) is an excellent

example, especially since the same psychiatrist assessed the patients at baseline and 40 years

later, which gives the study good internal validity. Research needs to identify what factors are

associated with more positive outcomes from OCD and why certain people recover fully and

others do not. Age of onset, gender, type of obsessions/compulsions, familial aggregation, and

comorbidity with other psychiatric disorders are some factors that could affect a patient’s

outcome. It would also be helpful to establish an association between certain drugs, types of

therapy, and combinations of these treatments and long term outcome of OCD.                When

performing these studies, it would be useful to estimate the burden of having OCD by calculating

DALYs or other measures of lost functioning and productivity. The estimate would definitely

show the negative impact of OCD on patients’ and their families’ lives. Such studies will help

guide clinicians in providing the appropriate treatment to patients with different types of OCD,

as no two cases are exactly alike and some may respond differently than others to the same form

of treatment.

       The third area in which OCD research should concentrate is the relationship between

autoimmune function and OCD. There is already significant evidence that children may develop

OCD as a result of a streptococcal infection and Sydenham’s chorea, and the OCD symptoms

appear rapidly in a large proportion of these children. One of the previously noted studies noted

an increased amount of immune-related diseases in adult OCD patients, and this topic deserves

more investigation, as the cause of OCD is not known. A study was recently published that

hypothesized a link between eating disorders and autoimmune function, and eating disorders

have a strong comorbidity with OCD with some psychiatrists considering anorexia and bulimia

types of OCD. If OCD could be linked to a specific infection and a causal pathway established,

prevention measures could be developed and treatment could center around the autoimmune

disease as well as the OCD. Studies should look at the processes in the brain that are associated

with autoimmune disease and OCD, particularly the activity in the basal ganglia. The morbidity

rates of OCD could be decreased significantly if research could establish a connection and move

on from there to find a treatment that targets the neurobiologic functioning affecting the OCD

patient. Hopefully researchers will be diligent in these areas and others so that more positive

outcomes    can   be   achieved   for   those    at   risk   for   and   suffering   from   OCD.

                           Table 1: Prevalence and Incidence of Obsessive Compulsive Disorder
                                (Portions of this chart from Montgomery and Zohar, 1999, 8)

STUDY                   LOCATION        SAMPLE           LIFETIME               ANNUAL             INCIDENCE
                                        AGE             PREVALENCE            PREVALENCE
Robins et al 1984         USA           Adult               2.5%                   ---                   ---
Bland et al 1988          Canada        Adult               3.0%                   ---                   ---
Karno et al 1988          USA           Adult               2.5%                   ---                   ---
Zohar et al 1992a         Israel        Adolescent          3.6%                   ---                   ---
Reinherz et al 1993       USA           Adolescent          2.1%                   ---                   ---
Chen et al 1993           Hong Kong     Adult               2.1%                   ---                   ---
Weismann et al 1994       USA           Adult               2.3%                  1.3%                   ---
                          Canada        Adult               2.3%                  1.4%                   ---
                          Puerto Rico   Adult               2.5%                  1.8%                   ---
                          Germany       Adult               2.1%                  1.6%                   ---
                          Taiwan        Adult               0.7%                  0.4%                   ---
                          Korea         Adult               1.9%                  1.1%                   ---
                          New Zealand   Adult               2.2%                  1.1%                   ---
Valleni-Basile et al 1994 USA           Adult               3.0%                   ---                   ---
Valleni Basile et al 1996 USA           Adolescent           ---                   ---                  0.7%
Nestadt et al 1998        USA           Adult                ---                   ---          .55/ 1000 person yrs.
Maggini et al 2001        Italy         Adolescent          4.1%                   ---                   ---
Heyman et al 2001         England       Children           0.25%                   ---                   ---
Fireman et al 2001        USA           All ages             ---                 .084%                   ---


Abramowitz, J, Huppert, J, Cohen, A, Tolin, D, and Cahill, S 2002. Religious obsessions
     and compulsions in a non-clinical sample: the Penn Inventory of Scrupulosity.
     Behaviour Research and Therapy 40: 825-38.

American Psychiatric Association. Diagnostic and statistical manual of mental disorders.
      4th ed. Washington: The Association; 1994

Asbahr, F, Negrao, A, Gentil, V, Zanetta, D, da Paz, J, Marques-Diaz, M, and Kiss, M
      1998. Obsessive Compulsive Disorder and Related Symptoms in Children and
      Adolescents With Rheumatic Fever With and Without Chorea: A prospective 6
      month study. American Journal of Psychiatry 155: 1122-24.

Barrett, P and Healy, L 2001. An examination of the cognitive process involved in
        childhood obsessive compulsive disorder. Behavior Research and Therapy: In

Billet, E, Richter, M, Sam, F, Swinson, R, Dai, X, King, N, Badri, F, Sasaki, T,
        Buchanan, J, and Kennedy, J 1998. Investigation of dopamine system genes in
        obsessive compulsive disorder. Psychiatric Genetics 8: 163-9.

Brown, T, Campbell, L, Lehman, C, Grisham, J, and Mancill, R 2001. Current and
      Lifetime Comorbidity of the DSM-IV Anxiety and Mood Disorders in a Large
      Clinical Sample. Journal of Abnormal Psychology 110 (4): 585-99.

Cavallini, M, Pasquale, L, Bellodi, L, and Smeraldi, E 1999. Complex Segregation
       Analysis for Obsessive Compulsive Disorder and Related Disorders. American
       Journal of Medical Genetics (Neuropsychiatric Genetics) 88: 38-43.

DeSilva, P and Rachman, S.       Obsessive Compulsive Disorder: the Facts.       Oxford
      University Press, 1998.

Diler, R, and Avci, A 2002. Sociodemographic and Clinical Characteristics of Turkish
        Children and Adolescents with Obsessive Compulsive Disorder. Croation
        Medical Journal 43 (3): 324-9.

Dinn, W, Harris, C, McGonical, K, and Raynard, R 2001. Obsessive compulsive
       disorder and immunocompetence. International Journal of Psychiatry Med 31 (3):

Dougherty, D, and Rauch, S. Serotonin Reuptake Inhibitors in the Treatment of OCD. In
      Hollander and Stein: Obsessive Compulsive Disorders, Diagnosis, Etiology,
      Treatment. Marcel Dekker, Inc 1997.

Fireman, B, Koran, L, Leventhal,J, and Jacobson, A 2001. The Prevalence of Clinically

       Recognized Obsessive Compulsive Disorder in a Large Health Maintenance
       Organization. American Journal of Psychiatry 158: 11, November 2001.

Geller, D, Biederman, J, Faraone, S, Agranat, A, Cradock, K, Hagermoser, L, Kim, G,
        Frazier, J, and Coffey, B. Developmental Aspects of Obsessive Compulsive
        Disorder: Findings in Children, Adolescents, and Adults. The Journal of Nervous
        and Mental Disease 189: 471-7.

Grados, M, Riddle, M, Samuels, J, Liang, K, Saric, R, Bienvenu, J, Walkup, J, Song, D,
      and Nestadt, G 2001. The Familial Phenotype of Obsessive Compulsive Disorder
      in Relation to Tic Disorders: The Hopkins OCD Family Study. Biological
      Psychiatry 50: 559-65.

Hettema, J, Neale, M, Kendler, K 2001. A Review and Meta-Analysis of the Genetic
      Epidemiology of Anxiety Disorders. American Journal of Psychiatry 158: 1568-

Heyman, I, Fomobonne, E, Simmons, H, Ford, T, Meltzer, H, and Goodman, R 2001.
     Prevalence of obsessive compulsive disorder in the British nationwide survey of
     child mental health. British Journal of Psychiatry 179: 324-29.

Hollander, E, and Stein, D. Obsessive Compulsive Disorder: Diagnosis, Etiology,
       Treatment. Marcel Dekker, Inc. 1997.

Horwath, E and Weismann, M 2000. The epidemiology and cross-national presentation
      of obsessive compulsive disorder. Journal of Clinical Psychiatry 55 (suppl 3): 5-

Jenike, M 2001. An update on obsessive compulsive disorder. Bulletin of the Menninger
        Clinic 65(1) 4-25.

Juang, Y, and Liu, C 2001. Phenomenology of obsessive compulsive disorder in Taiwan.
       Psychiatry and Clinical Neurosciences 55: 623-7.

Karno, M, Golding, J, Sorenson, S, and Burnam, A 1988. The Epidemiology of
       Obsessive Compulsive Disorder in Five US Communities. Archives of General
       Psychiatry 45: 1094-9.

Maggini, C, Ampollini, P, Gariboldi, S, Cella, P, Pelizza, L, and Marchesi, C 2001. The
      Parma High School Epidemiological Survey: obsessive compulsive symptoms.
      Acta Psychiatrica Scandinavica 103: 441-6.

Micallef, J, and Blin, O 2001. Neurobiology and Clinical Pharmacology of Obsessive
       Compulsive Disorder. Clinical Neuropharmacology 24 (4): 191-207.

Millet, B, Leclair, M, Bourdel, M, Loo, H, Tezcan, E, and Kuloglu, M 2001.
        Comparison of Sociodemographic, Clinical and Phenomenological Characteristics
        of Turkish and French Patients Suffering from Obsessive Compulsive Disorder.
        The Canadian Journal of Psychiatry 45 (9) 848.

Milos, G, Spindler, A, Ruggiero, G, Klaghofer, R, and Schnyder, U 2002. Comorbidity
       of Obsessive Compulsive Disorders and Duration of Eating Disorders.
       International Journal of Eating Disorders 31: 284-9.

Montgomery, S, and Zohar, J. Obsessive Compulsive Disorder. Martin Duntz Press,

Nestadt, G, Bienvenu, O, Cai, G, Samuels, J, and Eaton, W 1998. Incidence of Obsessive
       Compulsive Disorder in Adults. Journal of Nervous and Mental Disorders 186:

Nestadt, G, Lan, T, Samuels, J, Ridde, M, Bienvenu, O, Liang, K, Hoehn-Saric, R,
       Cullen, B, Grados, M, Beaty, T, Shugart, Y 2000. Complex Segregation Analysis
       Provides Compelling Evidence for a Major Gene Underlying Obsessive
       Compulsive Disorder and for Heterogeneity by Sex. American Journal of Human
       Genetics 67: 1611-6.

Nestadt, G, Samuels, J, Riddle, M, Bienvenu, J, Liang, K, LaBuda, M, Walkup, J,
       Grados, M, Hoehn-Saric, R 2000. A Family Study of Obsessive Compulsive
       Disorder. Arch Gen Psychiatry 57: 358-63.

Nestadt, G, Samuels, J, Riddle, M, Liang, K, Bienvenu, O, Hoehn-Saric, R, Grados, M
       and Cullen, B 2001. The relationship between obsessive compulsive disorder and
       anxiety and affective disorders: results from the Johns Hopkins OCD Family
       Study. Psychological Medicine 31: 481-7.

Nestadt, G, Samuels, J, Riddle, M, Bienvenu, O, Liang, K, Grados, M, Cullen 2002, B.
       Obsessive Compulsive Disorder: Defining the Phenotype. Journal of Clinical
       Psychiatry 63 (6) 5-7.

Neziroglu, F, Hsia, C, and Yaryura-Tobias, Jose 2000. Behavioral, Cognitive, and
       Family Therapy for Obsessive Compulsive and Related Disorders. Psychiatric
       Clinics of North America 23(3) September 2000.

Sica, C, Novara, C, and Sanavio, E 2002. Religiousness and obsessive compulsive
       cognitions and symptoms in an Italian population. Behaviour Research and
       Therapy 40: 813-23.

Silvestre, J, and Aronowitz, B. Behavioral Treatment of OCD. In Hollander and Stein:
        Obsessive Compulsive Disorder: Diagnosis, Etiology, Treatment. Marcel Dekker
        Inc 1997.

Skoog, G and Skoog, I 1999. A 40 Year Follow Up of Patients with Obsessive
      Compulsive Disorder. Arch Gen Psychiatry 56:121-7.

Speranza, M, Corcos, M, Godart, N, Jeannet, P, and Flament, M 2001. Current and
      lifetime prevalence of obsessive compulsive disorder in eating disorders.
      Encephale Nov-Dec: 27 (6): 541-50.

Stein, M, Forde, D, Anderson, G, and Walker, J 1997. Obsessive Compulsive Disorder
       in the Community: An Epidemiologic Survey with Clinical Reappraisal. Am
       Journal of Psychiatry 154: 8, August 1997.

Tukel, R, Polat, A, Ozdemir, O, Aksut, D, and Turksoy, N 2002. Comorbid Conditions
       in Obsessive Compulsive Disorder. Comprehensive Psychiatry, 43 (3): 204-9.

Valleni-Basile, L, Garrison, C, Waller, J, Addy, C, McKeown, R, Jackson, K, Cuffe, S
       1996. Incidence of Obsessive Compulsive Disorder in a Community Sample of
       Adolescents. Journal of the American Academy of Child and Adolescent
       Psychiatry 35: 898-906.

Weissman, M, Bland, R, Canino, G, Greenwald, S, Hwu, H, Lee, C, Newman, S, Oakley-
      Browne, M, Rubio-Stipec, M, Wickramaratne, P, Wittchen, H, and Yeh, E 1994.
      The Cross National Epidemiology of Obsessive Compulsive Disorder. Journal of
      Clinical Psychiatry 55 (3, suppl) 5-10.

Wewetzer, C, Jans, T, Muller, B, Neudorfl, A, Bucherl, U, Remschmidt, H, Warnke, A<
     Herpetz, Dahlmann, B 2001. Long term outcome and prognosis of obsessive
     compulsive disorder with onset in childhood or adolescence. Euro Child and
     Adolescent Psychiatry 10: 37-46.


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