How far have we come: in understanding obsessive-compulsive disorder in children and adolescents? Suffering from OCD often means feeling like a prisoner in you own mind and body, not being able to enjoy life to the fullest and having to live a life that is all consumed by anxiety & fear.
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|Publication:||Name: Annals of the American Psychotherapy Association Publisher: American Psychotherapy Association Audience: Academic; Professional Format: Magazine/Journal Subject: Psychology and mental health Copyright: COPYRIGHT 2011 American Psychotherapy Association ISSN: 1535-4075|
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The purpose of this paper is to review the current empirical literature on obsessive-compulsive disorder in children and adolescents. The results are discussed from a developmental perspective, thus emphasizing different factors responsible for the development and maintenance of OCD in children and adolescents. The main contributing factors include genetic transmission in families as well as the effect of the environment (family, society, culture). The study concludes that a comprehensive theoretical model is needed to take all empirical results into consideration in order to present a developmental explanation of the predisposition, onset, development, and maintenance of OCD in children and adolescents.
KEYWORDS: obsessive-compulsive disorder; childhood psychopathology; epidemiology
UNDERSTANDING OCD IN CHILDREN AND ADOLESCENTS
Obsessive-compulsive disorder (OCD) is an anxiety disorder, characterized by obsessive thoughts which cause anxiety and distress and compulsions which aim at neutralizing this anxiety. OCD can take different forms and can cause a high degree of impairment in everyday life. In particular, rituals and other compulsive behavior can be extremely time-consuming. Suffering from OCD often means feeling like a prisoner in your own mind and body, not being able to enjoy life to the fullest and having to live a life that is all consumed be anxiety and fear. Every day life can become unbearable, and even minor tasks might take an eternity to be completed until the never-ending compulsions and rituals are obediently carried out. The more habits to avoid the anxieties that are developed, the harder it will become to face the fear.
In the following section, different clinical aspects of OCD in children and adolescents are presented and contrasted with OCD in adults. The different causes of OCD are then briefly summarized. The main body of the paper reviews empirical results of genetic influences and environmental effects on OCD in children and adolescents.
OCD IN CHILDREN AND ADOLESCENTS: EPIDEMIOLOGY AND CLINICAL FEATURES
The essential features of OCD are recurrent obsessions and compulsions that are extremely time-consuming and cause a severe distress and impairment. Obsessions are defined as recurrent thoughts and images, compulsions are defined as recurrent behaviors (American Psychiatric Association, 2000). Obsessions can be about contamination, religion, superstitions and perfectionism. Compulsions can take many different forms, such as decontamination, hoarding, checking, counting, touching, etc. The most important aspect from the developmental perspective is whether OCD in children and adolescents is different from OCD in adults. The classification of OCD in children and adolescents according to the latest edition of DSMIV-TR is similar to that in adults. The exception is that children are not expected to recognize that their obsessions or compulsions are excessive or unreasonable (American Psychiatric Association, 2000).
Although the symptoms are distressing somehow to these children, they cannot recognize or express a direct relation between their obsessive symptoms and compromised daily life activities. Moreover, the cognitive development of children may not facilitate the observation and description of his/her own thoughts. Often children may be frightened or confused by their thoughts, making them more likely to hide their symptoms from parents and clinicians. Consequently, children are less likely to report their obsessions and can be underdiagnosed and undertreated.
OCD usually emerges during childhood or adolescence. It has been estimated that around 80% of adults with OCD identify their onset of symptoms before age 18 (Pauls et al., 1995). Lifetime prevalence of OCD in adults and adolescents is between 1-3%; however, there are no estimates of prevalence of OCD in children (Riddle, 1998). Estimates of the mean age at onset for children and adolescents range between 10 and 11.44 for boys and between 10.2 and 13.5 for girls (Hanna, 1995; Toro et al., 1992). Geller et al. (2001) find in their sample of 101 subjects that mean age of onset is 6 in children, 10 in adolescents and 21 in adults, where all these numbers refer to males.
In adults, OCD is equally common in males and females. In contrast, it has been observed that boys have a higher rate of OCD than girls during childhood and adolescence. Hanna (1995) estimates the male-female ratio to be 3:2, Geller et al. (2001) estimates it at 2:1 and observe that boys have both an earlier age of onset and more severe symptoms than girls.
A legitimate question stemming from all these differences between children and adults regarding the epidemiology of OCD is how similar juvenile and adult forms of OCD are. Geller et al. (2001) demonstrates that there is a clear discontinuity between the OCD in adults and the OCD in children and adolescents. This result suggests that juvenile OCD is a unique developmental subtype of adult OCD.
The preceding discussion of clinical features makes clear that OCD in children and adolescents has many different aspects which demonstrate the importance of a developmental perspective on OCD.
CAUSES AND CONTRIBUTING FACTORS FOR OCD IN CHILDHOOD AND ADOLESCENCE
Several theories have been proposed to explain the development and maintenance of OCD, and the fact that the overwhelming majority of OCD patients have an onset of the disorder in childhood or adolescence. Generally, these theories can be divided into biological and genetic models emphasizing the role of genetic factors, neurological processes and brain malfunctions, and psychological models focusing on the influences of cognitive processes, learning of behavior, and environmental factors (family, culture, and religion). The review of the literature in the following sections will focus exclusively on the genetic and the environmental factors which contribute to the pathogenesis of OCD in children and adolescents.
Over the years, many studies have indicated that OCD is likely to have genetic origins. Therefore, there may be an underlying predisposition for OCD to occur in certain children and adolescents stemming from heritable factors. Evidence for genetic influences in the onset of OCD during childhood has come primarily from family and twin studies.
Family studies provide one of the common means of analysis of genetic factors since all family members share common genes. There are two techniques used to determine prevalence of OCD in relatives: the family-history method and the family-study method. Early studies applying the family-history method assessed relatives and determined diagnoses based solely on the information provided by the proband. In contrast, more recent studies have used the family-study method, in which all available first-degree relatives are interviewed directly (Billett et al., 1998; Alsobrook et al., 1998).
Especially in the case of children and adolescents, the family-study method appears to be the more suitable alternative since children have more difficulties explaining in detail the obsessive-compulsive behavior of their relatives than adults. Although not as many family studies with children were conducted as with adults, there is nevertheless enough evidence that early onset of OCD in childhood is affected by heritable factors. Riddle et al. (1990) interviewed the parents of 21 children and adolescents between the ages of 7-17 with OCD. Fifteen of them (71%) had a parent with either OCD or obsessive-compulsive symptoms. In other words, 15 of the 42 parents (35.7%) were diagnosed with clinical or subclinical OCD. Unfortunately, this study gives no information concerning siblings or rates of diagnosis in siblings. Moreover, no control group was included which makes conclusions more difficult to make.
Lenane et al. (1990) interviewed not only parents but also siblings of 45 children and adolescents with severe OCD. A total of 145 first-degree relatives were interviewed. Twenty-five percent of fathers and 9% of mothers had OCD. When obsessive-compulsive behavior is included, the risk for all first-degree relatives was 35%. As in the previous study, there was again no control group. Lenane et al. (1990) also looked for any relationship between the children's primary OCD symptoms and those of their respective relatives. They found no consistent pattern between parents and children, or between older and younger siblings. Hence, it cannot be simply stated that obsessive-compulsive symptoms are observed and learned by younger relatives.
Furthermore, in another family study Last et al. (1991) interviewed first and second-degree relatives of 152 children with different anxiety disorders. In contrast to previous studies, a control group of 87 children was also included. The results indicate that a trend for OCD is more prevalent among relatives of children with OCD than among relatives of children with other anxiety disorders. This in turn suggests that the risk was specific for OCD, and further supports the genetic model of early onset of OCD.
Toro et al. (1992) explored parents and siblings of 72 children and adolescents aged 5-18 with a diagnosis of OCD. The majority of the probands (57%) had some first-degree relative with a psychiatric diagnosis, however only 11 probands (15.3%) had a first-degree relative diagnosed with OCD. This result is much lower than the previous studies, but it is mainly due to the procedure used for diagnosing the relatives. No interviews were conducted, only the diagnoses stated in the clinical records of the children were used.
Not all studies report such high rates of OCD in families. In particular, phenotype definition and age at onset appear to influence the family aggregation of OCD. For instance, Black et al. (1992) interviewed 120 first-degree relatives of 32 probands with OCD and 33 psychiatrically normal controls. The OCD probands had a mean onset age of 11.04 years. The first-degree relatives of probands with OCD were significantly more likely to experience anxiety disorders than were relatives of controls. However, the prevalence of OCD itself was very low among both groups' relatives. Only 3% of the relatives of OCD patients were diagnosed with OCD. When obsessive-compulsive behavior was included, this number climbed to 21%. These results indicate that an anxiety disorder may be transmitted in families in which a member has OCD, but its expression within these families is variable.
Similarly, Pauls et al. (1995) gathered interview data from 466 first-degree relatives of 100 probands with OCD. The mean onset age here was 10.2 years. In addition, 113 first-degree relatives of 33 psychiatrically unaffected probands were studied with the same interviews. The results show that 10.3% of the relatives were diagnosed with OCD as compared to only 1.9% in the control group. Eight percent of relatives were diagnosed with obsessive-compulsive behavior. These results, paired with those from the study by Black et al. (1992) indicate that OCD is a heterogeneous condition. Some cases were familial, but in other cases there appeared to be no family history of OCD. However, there was a two-fold increased risk for OCD and a four-fold increased risfor obsessive-compulsive behavior in relatives of probands with childhood-onset OCD as compared to a later onset (after the age of 18). This is a sign that an early onset of OCD can be interpreted as a more severe form of the disorder with a greater genetic loading. This certainly distinguishes OCD in children and adolescents from OCD in adults.
In a more recent family study, similar results were achieved. Nestadt et al. (2000) interviewed 80 probands with OCD and 343 of their relatives: A control group of similar dimensions was included. The first-degree relatives of probands diagnosed with OCD had a nearly 5-fold higher lifetime prevalence of OCD when compared to the controls. The median age at onset of symptoms was about 11 years; more than 75% of the probands had onset by age 14 years, and 90% by age 17 years. The prevalence of OCD in the relatives of probands with an onset age below 17 was 38 (13.8%) of 276, whereas the prevalence in relatives of probands with later onset was 0 (0%) of 49. Thus, no cases of OCD were found in the case of relatives of probands with late onset of OCD. In other words, the younger the age at onset, the higher the familiality of OCD. This suggests that cases of OCD with early age at onset are more likely to yield information about the genetic origins of this disorder--a further sign that developmental aspects and genetics are intertwined in the case of OCD.
Black et al. (1992) and Pauls et al. (1995) have observed that OCD in children and adolescents can be a heterogeneous condition, with some cases being familial and others not. Albert et al. (2002) conducts the most recent family study with 74 probands with OCD onset in childhood and adolescence (mean onset age is 12.1 years). First-degree relatives were diagnosed either using the family-history or the family-study method. Eleven percent of the probands had at least one family member with OCD, which is again in the range of previous estimates. The interesting result of this study however is the finding that there is no significant difference between the phenomenological characteristics of OCD probands with OCD family members and OCD probands with normal family members.
In summary, family studies suggest that genetic factors lead to a certain vulnerability of children and adolescents to develop OCD. The estimates of the rate of OCD in first-degree relatives from the studies discussed above range from 3% to 15%. However, if the obsessive-compulsive behavior of first-degree relatives is included, then the range increases to 17-35%, which is overwhelmingly higher than the normal prevalence rate of 1-2%. The big differences in the estimates appear to be mainly due to different methodologies used. As already mentioned, some include control groups, other did not. Some base their diagnoses of the relatives from direct structured interviews, other used data from existing data on relatives in the folders of child probands. Despite all those differences, the results of the family studies are in favor of a heritable factor in OCD. Moreover, symptom patterns have generally been observed to differ between probands and relatives, making an environmental explanation less likely.
Besides the traditional family studies on OCD, more recent studies on family transmission have focused on comorbidity between OCD and other disorders. Bellodi et al. (2001) proposed for instance that eating disorders should be considered a specific type of OCD. They found that the morbidity risk for obsessive-compulsive spectrum disorders was significantly higher among the first-degree relatives of the eating disorder probands (adolescent females) than among the relatives of the controls. Grados (2001) examined whether tic disorders are part of the familial phenotype of OCD. Their results show that OCD probands and their first-degree relatives had a greater lifetime prevalence of tic disorders compared to controls. Younger age-at-onset of OCD symptoms and male gender in the OCD probands were associated with increased tic disorders in relatives. Such studies are limited by being unable to neutralize the environmental effect contrary to adoption studies and particularly the subtype of cross fostering design to exclude environmental effects, although no research articles are available with this methodology as the case for adults.
Twin studies have provided some additional evidence for the heritability of OCD. These studies provide some indication of the relative rates for concordant and discordant Monozygotic and Dizygotic twin pairs. The method used consists of comparing the number of MZ twins in which both members have OCD with the number of corresponding DZ twin pairs. If the concordance of MZ twins is higher than in DZ twins, genetic factors are certainly contributing to the development of OCD. Unfortunately, no recent twin studies exist. But in general studies from 1980s and early 1990s find a concordant MZ:DZ ratio of 2:1 for OCD, which further supports the effect of genes on the onset of OCD in children and adolescents (Billett et al., 1998).
Family aggregation of OCD is necessary, but not sufficient, for the interference of genetic transmission, because parents and relatives transmit not only genes to their children, but also sociocultural factors that can lead to different phenotypes. In other words, common environmental factors can also contribute to the development of OCD in children with different genes. The best way to analyze environmental factors is to conduct adoption and separation studies. Unfortunately, such studies are nonexistent in the context of OCD due to the fact that extremely few children or twins with OCD are taken apart and adopted by different families. Studies on twins (concordance rate among monozygotic twins sharing 100% of the nuclear DNA versus dizygotic twins sharing only 50% of nuclear DNA) and adoption studies are lacking in the literature for this specific age group.
Once genetic factors were found to play a role in the early onset of OCD during childhood and adolescence, the main focus of research shifted away from family and twin studies, and concentrated on the application of DNA technology to the study of OCD. Therefore, most recent literature on the genetics of OCD is found in the area of molecular genetics where researchers try to isolate the specific genes (the common genes implicated in the etiology of OCD like those of MAO-B enzyme on the X chromosome, 5-HT reuptake proteins, 5-HT 2a and 2c receptors) which seem to be responsible for the early onset and development of OCD (Pato et al, 2002).
While OCD is widely recognized to have a strong genetic component, psychosocial factors are also acknowledged to be important. The primary focus of this section is on familial and cultural/religious context as possible risk factors in the development and maintenance of the disorder in children and adolescents.
Freeman et al. (2000) presents the case of 10-year old boy and a 7-year-old girl diagnosed with OCD. The boy had been repeatedly sexually abused by an older peer, and the obsession concerning contamination by germs and sexual images started immediately after the abuse stopped. No family history of OCD was found in the family, thus environmental factors (abuse by peers) seem to be the trigger of OCD. The case of the girl involves an incident of unwanted "sex play" with a peer. After this incident compulsive hand washing rituals developed. This shows the important role of guilt feelings of being the victim to sexual abuse provoked by the conscience in OCD psychopathology. When subjected to traumatic events children and adolescents often blame themselves. A common example of that is that many children see themselves as the reason their parents marriage ended in divorce and moreover interpret the events leading up to it as if they were among causes of such divorce. Children with their immature cognitive structures may have their own way of attributing cause-event relation, and are more liable for self-blaming. The mother of the girl had OCD, which is a possible factor for the predisposition of her daughter, but the trigger was clearly an environmental factor (the "sex play"). These two cases suggest that OCD is a heterogeneous condition. Genetics can play a role, but environmental factors can be not only a trigger but the main reason for developing OCD in children.
A more recent study by Lochner et al. (2002) explores the link between a traumatic event in childhood and the development of OCD in children and adolescents. 74 female probands and 31 controls were included in the study. The age of the probands was as low as 12, but there were no exact numbers on the percentage of children or adolescents. The OCD probands exhibit much higher rates of severe childhood trauma (sexual and physical abuse as well as emotional neglect) than the controls, thus indicating that traumatic events in the childhood may be the reason for the early onset of OCD. This finding is further supported by Mangold et al. (2000) who found that boys with a family history of alcoholism reported more obsessive-compulsive behavior than females and controls.
Religion as a part of the cultural and familial environment can also play a key role in the genesis of OCD in children and adolescents. Although the epidemiology of OCD appears to be stable across cultures (Weissman et al., 1994), patients with religious obsessions may be over-represented in clinical populations of Muslim and Jewish cultures, as compared with clinical populations from the West and the Far East. The frequency of religious obsessions in clinical populations diagnosed with OCD is reported to be between 5-10% in USA and Western Europe, as compared to 40-60% in Saudi Arabia, Israel and Egypt (Tek et al., 2001).
Tek et al. (2001) conducted a study with 45 patients diagnosed with OCD in Turkey. Religious obsessions were the main symptom of OCD in nineteen of the patients. Patients with religious obsessions, many of them adolescents, were significantly younger than patients without them. A family history of OCD characterized 40% of the patients without religious obsessions and 45% of those with religious obsessions. Although the study does not mentioned whether the OCD of the relatives was religious in nature, it can be concluded that such a high percentage of genetic loading is improbable when compared with the results of the family studies in the section on genetic factors above. It is more likely that religious obsessions and rituals performed by parents were observed by children and adolescents and contributed strongly to the development of OCD, without neglecting the fact that genetics play a role in the vulnerability and predisposition of such children.
Moreover, religious rituals often involve decontamination and purification practices. In many religions the blasphemous thoughts are brushed off through repeated prayers or alleviating the guilt about committing a sin through confession in certain cultures. All these factors certainly increase the development of obsessive thoughts and compulsive behaviors based on religious teachings and practices. In some societies, religion plays a more dominant role than in others. Under pressure by society, family, and peers, or through education in religious schools, children and adolescents are more likely to develop OCD with religious obsessions.
Rituals are more common in Muslim and Jewish cultures, as both have many rituals as part of their religious practice representing a medium to carry those obsessive symptoms. For example it is common in religions like Islam to pray several times a day at specific scheduled times during the day and night. Washing rituals and other practices may be included in the daily activities of a person's life. Blasphemous thoughts as a medium for obsessive thoughts are quite common in communities where religious practices are widely present. The most recent study in the area takes religious education into account. Sica et al. (2002) examined 165 probands which were classified in three groups according to the degree of their religiosity. All probands were from Italy, a country where the Catholic religion plays a central role in the society. One central question in determining the religiosity was regarding attending a religious (Catholic) school. Individuals with a high or medium degree of religiosity showed higher levels of OCD than individuals with a low degree of religiosity of the same age, education and gender. Furthermore, perfectionism was one of the dominant symptoms, which the authors link to the teaching of the Catholic religious thought at religious schools.
Okasha et al. (2001) studied the prevalence of obsessive-compulsive symptoms (OCS) in a large sample of Egyptian adolescents. The risk and cultural factors associated with obsessive compulsive behavior include female gender, and first born, with aggressive, contamination, religious obsessions, and cleaning compulsions being most common.
In summary, recent evidence indicates that besides genetic factors, environmental factors can play an important role in explaining the early onset of OCD in children and adolescents. Traumatic events or familial relations can be the main trigger for OCD in children without any family history of OCD. At the same time, environmental factors can be the decisive event that unleashes an underlying genetic vulnerability to OCD in children with family history of OCD.
One of the main features of OCD is its onset which begins for the overwhelming majority of patients in childhood or adolescence. Many different developmental theories have been suggested in order to explain the early onset of OCD and its contributing factors. Genetic models emphasize the genetic transmission of OCD from one generation to the next, neurological models suggest different malfunctions in the brain which in turn influence behavior, psychological studies have focused on cognitive distortions and psychosocial factors as the main contributors to the pathogenesis of OCD, and learning theories use conditioning to explain the onset of obsessions and compulsions. Although each of these theories has a certain degree of empirical support, there is no comprehensive model that can evaluate and order the different developmental pathways involved in the pathogenesis of OCD. Bolton (1996) proposes a neurodevelopmental pathway and a cognitive developmental pathway, but disregards genetics and environmental factors such as cultural and familial aspects.
Epidemiological and clinical data from a variety of cultural and geographic settings on obsessive-compulsive disorder, and many of the obsessive-compulsive spectrum disorders, suggest that this is a group of disorders with a good degree of transcultural homogeneity (Matsunaga & Seedat, 2007). However, the content and themes that predominate in patients with these disorders and the course of the illness can be shaped by cultural, ethnic, and religious experiences. Across cultures, OCD is commonly comorbid with mood, anxiety and impulse-control disorders.
Future research in different areas such as molecular genetics, neurobiology, cognitive psychology, etc. should not emphasize so much the specific perspective, but should try to integrate different approaches and empirical finding in order to better explain the development and maintenance of OCD in children and adolescents.
This article is approved by the following for 1 continuing education credit:
The American College of Forensic Examiners International is approved by the American Psychological Association to sponsor continuing education for psychologists. The American College of Forensic Examiners International maintains responsibility for this program and its content.
The American Psychotherapy Association[R] provides this continuing education credit(s) for Diplomates and certified members, who we recommend obtain 15 credits per year to maintain their status.
Measurable and observable learning objectives:
Explain the main differences of OCD in children and adolescents versus adults.
Discuss epidemiology and clinical features of OCD in children and adolescents.
Identify causes and contributing factors of OCD in children and adolescents.
TARGET AUDIENCE: Psychotherapy researchers, psychologists, psychotherapists
PROGRAM LEVEL: Intermediate
DISCLOSURES: The author has nothing to disclose.
POST CE TEST QUESTIONS
(Answer the following questions after reading the article)
1. Kelly is a musician and she loves the fact that she constantly hears new melodies in her head. In fact, she cannot remember a time when she did not hear music. Why is this NOT an example of an obsession?
a. Obsessions must be accompanied by ritualistic actions.
b. Obsessions must come on suddenly in response to a stressful life event.
c. Obsessions must be voluntary thoughts that a person knows are irrational.
d. Obsessions must be intrusive thoughts the person finds disturbing.
2. Which of the following is characteristic of the obsessions seen in OCD?
a. The obsessions serve to alleviate the anxiety created by the compulsions.
b. The obsessions are clearly related to a traumatic event.
c. The obsessions are rarely related to the compulsions exhibited.
d. The individual with OCD knows that their obsessions are irrational.
3. Historically, why has little attention been paid to OCD in children?
a. Mental illness was not recognized in children.
b. OCD in children was viewed as a childhood version of adult disorders.
c. All signs of OCD in children were assumed to reflect some developmental stage that would be outgrown.
d. Society viewed children as inherently good and accepted all behavior unconditionally.
4. One of the main features of OCD is its onset which begins for the overwhelming majority of patients in:
a. Childhood or adolescence.
c. Early adulthood.
d. Middle or late adulthood.
5. What is the link between genetic factors and OCD?
a. There is no link.
b. Genetic predisposition can cause OCD.
c. Genetics factors play a role fort the development of OCD in female children only.
d. Genetic factors play a role for the development of OCD in male children only.
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DR. KARIN TOCHKOV is an Assistant Professor and Director of the Master's Program in Clinical Psychology at Texas A&M University--Commerce. A native of Germany, she completed her undergraduate work in Psychology at the Ruprecht Karls University in Heidelberg, Germany. She received her Ph.D. in Clinical Psychology from the State University of New York at Albany in 2007. As head of the Addictive Behaviors Research Laboratory, Dr. Tochkov's research focuses on the role of emotions and cognitive distortions in the development and maintenance of addictive behaviors. The results of her research have been presented at several national and international conferences, including the Annual Convention of the Association for the Advancement of Behavior Therapy, the British Psychological Society Annual Meeting, and the World Congress of Psychology. Her publications have appeared, among others, in Judgment and Decision Making and international Gambling Studies. At Texas A&M University--Commerce, Dr. Tochkov regularly teaches graduate classes in Psychopatholgy, Assessment, and Group Psychotherapy. On the undergraduate level Dr. Tochkov teaches classes in Abnormal Psychology and Theories of Personality. She is also chairing the dissertation and thesis committees of students in the Educational Psychology Ph.D. program and the Master program in Clinical Psychology at Texas A&M University--Commerce. In 2010 Dr. Tochkov received the Provost Award for Research & Creative Activity at Texas A&M University--Commerce and in Spring 2011 the Student Recognition Award for Teaching Excellence from the Texas A&M University System.
SAMPLE SIZE / AUTHORS MEAN AGE METHODOLOGY BELLODI ET AL. Probands Utilized family study and (2001) family history methods. n =136 (M = 22.12; SD = 4.93) Studied the prevalence of obsessive-compulsive Controls spectrum disorders in first-degree relatives n = 72 (M = 39; SD of probands with eating = 12.84) disorders. Case Relatives Proband inclusion was determined by clinical n = 436 diagnosis Father: M = 53.54; SD = First-degree relatives of 7.60 probands were interviewed directly or were Mother: M = 49.80; SD = evaluated by family 8.90 history methods to determine symptoms. Brothers: M = 23.30; SD = 9.21 Sisters: M = 22.97; SD = 8.71 Control Relatives n = 358 Father: M = 64.63; SD = 12.22 Mother: M = 61.87; SD= 11.73 Brothers: M = 36.97; SD =14.97 Sisters: M = 43.20; SD= 14.57 BLACK ET AL. Probands Utilized family study and (1992) family history methods. n = 32 (M = 38.3; SD = 10.9) Included OCD and subsyndromal OCD symptoms Controls Probands met DSM-III n = 33 (M = 38.1; criteria for OCD. SD = 10.0) Relatives were evaluated Case Relatives with structured and unstructured interview n = 120 (Interviewed) methods as well as several scales and M = 41.8; SD = 15.7 inventories Control Relatives n = 129 (Interviewed) M = 41.1;SD = 15.7 NESTADT ET AL. Probands Utilized family study and (2000) family history methods. n = 80 (M = 36.6; SD = 11.6) Probands met DSM-IV criteria for OCD. Controls Collected data on OCD as n = 73 (M = 38.5; SD = well as obsessions and 11.8) compulsions Case Relatives Relatives were evaluated with direct interviews n = 343 (M = 48.1; SD = using structured and 18.9) semi-structured instruments; family Control Relatives history information was collected through n = 300 (M = 44.5; informant; various SD = 18.8) inventories were used CRADOS ET AL. Probands Utilized family study and (2001) family history methods. n = 77 Probands met DSM-IV Controls criteria for OCD. n = 66 Probable and definite diagnoses of tic Case Relatives disorders and OCD were considered in the n = 323 analysis. Control Relatives The prevalence and severity of tic disorders n = 289 and age-at-onset of OCD symptoms and were analyzed in relatives Symptoms and severity were assessed by direct interviews, collateral informants, as well as several scales LAST ET AL. Anxiety Probands Utilized family study and (1991) n = 94 family history methods. AND Probands First and second-degree n = 58 relatives of children with anxiety disorders NPI Probands were compared with relatives of children n = 87 with ADHD and children who have never had a Anxiety Case Relatives psychiatric condition. First Degree - n = 274 Probands met DSM-III-R criteria for their OCD Second Degree - n = 812 or ADHD AND Case Relatives Utilized direct structured interviews and First Degree - n =152 diagnostic scales, as well as the family Second Degree - n = 484 history method with first-degree relatives. NPI Case Relatives Second-degree relatives First Degree - n = 240 were assessed using the family history method. Second Degree - n = 718 Probands n = 46 LENANE ET AL. Case relatives Utilized family study and (1990) family history methods. n = 145 Structured interviews, family histories and several inventories were used to assess DSM-III OCD criteria, subclinical OCD and related symptoms, and other psychiatric disorders PAULS ET AL. Probands with OCD Utilized family study and (1995) family history methods. n = 100 Probands met criteria for Probands without OCD DSM-III-R OCD. n = 33 Definite and probable (sub-threshold) diagnoses OCD Case Relatives were used in analysis Available first-degree n = 466 relatives were interviewed directly with Non-OCD Case Relatives structured interviews, and family histories were n =113 taken from each informant using a semi-structured interview. Several scales were also used to assess symptoms. Utilized family study and family history methods. Probands met DSM-IV criteria for OCD Utilized structured and ALBERT ET AL. Probands semi-structured clinical (2002) interviews as well as n = 74 (M = 34.3; rating scales with SD = 11.8) available relatives. Case Relatives Information about unavailable relatives was n = 251 (Total) collected through structured family history n = 231 (Directly interviews with the interviewed; M = 42.5; SD proband and other family = 21.3) members as informants. Data was collected on specific OCD symptoms and phenomenology RIDDLE (1998) N/A Provides and overview of pediatric OCD in terms of age of onset, classification, subtypes, prevalence, assessment, prognosis, and treatment. TORO (1992) Probands Clinical records of children with a DSM-III-R n = 72 (M =12.0; SD = diagnosis of OCD were 3.29) examined. Control The presence of psychiatric history in n = 72 first-degree relatives was examined. Only (Matched for age, sex, diagnoses formulated by and date of consultation) specialists and stated in clinical records of obsessive children were considered. AUTHORS RESULTS BELLODI ET AL. The morbidity risk for obsessive compulsive spectrum (2001) disorders was found to be higher among relatives of eating disorder probands in comparison to the control group. These findings were independent of a comorbid obsessive compulsive spectrum disorders in the eating disorder probands. BLACK ET AL. The morbidity risk for anxiety disorders was (1992) increased among the relatives of OCD participants, but the risk of OCD was not. First-degree relatives of probands with OCD are significantly more likely to experience anxiety disorders than relatives of psychiatrically normal controls. Risk for obsessive compulsive symptoms (not meeting the full criteria for OCD) was increased among parents of OCD participants but not among the parents of controls NESTADT ET AL. The lifetime prevalence of OCD was significantly (2000) higher in case relatives when compared with control relatives The prevalence of definite and probable OCD was higher in case relatives Case relatives had higher rates of both obsessions and compulsions--obsessions are more specific to familial aspect of OCD CRADOS ET AL. Case probands and case relatives had a greater (2001) lifetime prevalence of tic disorders compared to control subjects. First-degree relatives with OCD with tic disorders have an earlier age-at-onset of 00 symptoms compared to those that have OCD without tic disorder Younger aye-at-onset of OCD symptoms were associated with increased tic disorders in relatives. LAST ET AL. (1991) Increased prevalence of anxiety disorders in the first-degree relatives of children with anxiety disorders compared with relatives of children with ADHD and normal controls OCD and panic disorder were the only two anxiety disorders that showed a suggestion of a specific relationship in children and their relatives. The specificity of the familial component involved in childhood anxiety disorders varies between disorders. LENANE ET AL. 30% of case probands had at least one first-degree (1990) relative with OCD 45% of fathers and 65% of mothers received one or more other psychiatric diagnosis. Results showed a larger familial rate of OCD over what is expected in the general population The presenting obsessive-compulsive symptoms of case probands and their parents were usually dissimilar, which argues against simple social or cultural transmission. PAULS ET AL. The rates of OCD and sub-threshold OCD were (1995) significantly greater among the relatives of the case probands with OCD than among the comparison subjects. The rates of tics were also significantly greater among the relatives of the case probands than among the comparison subjects. The relatives of case probands with early onset were at a higher risk for both OCD and tics 11% of the case probands had at least one family ALBERT ET AL. member with OCD. (2002) There were no differences between the two types of OCD (familial versus non-familial) except for life events prior to the onset of OCD, which were more common and more severe. There is a familial component in the expression of some forms of OCD. Familial OCD patients are not characterized by peculiar clinical features, but appear to have a lower threshold for precipitating events. in non-familial OCD subtypes. RIDDLE (1998) Treatment components include long-term commitment, care management, and illness education-including (8T, behavior management, and medication. The most effective treatments are SSRIs and exposure/response prevention. TORO (1992) 57% of case probands had some first degree relative with a psychiatric diagnosis 15.3% of first-degree relatives were diagnosed with OCD.
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