Gender dysphoria in children (GD), also known as gender incongruence of childhood, is a formal diagnosis for children who experience significant discontent (gender dysphoria) due to a mismatch between their assigned sex and gender identity. The diagnostic label gender identity disorder in children (GIDC) was used by the Diagnostic and Statistical Manual of Mental Disorders (DSM) until it was renamed gender dysphoria in children in 2013 with the release of the DSM-5. The diagnosis was renamed to remove the stigma associated with the term disorder.
Gender dysphoria in children is more heavily linked to adult homosexuality than to an adult transgender identity, especially with regard to boys. According to prospective studies, the majority of children diagnosed with gender dysphoria cease to desire to be the other sex by puberty, with most growing up to identify as gay, lesbian, or bisexual, with or without therapeutic intervention. If the dysphoria persists during puberty, it is very likely permanent.
Controversy surrounding the pathologization and treatment of a transgender identity and associated behaviors, particularly in children, has been evident in the literature since the 1980s. Proponents of the GD diagnoses argue that therapeutic intervention helps children be more comfortable in their bodies, have better peer relations and therefore better self-esteem, that research indicates there exists forms of distress associated directly with children’s gender variance, and that treatment can prevent adult GD. Opponents have compared therapeutic interventions that aim to alter a child’s gender identity to conversion (or reparative) therapy for gay men and lesbians. The World Professional Association for Transgender Health (WPATH) states that treatment aimed at trying to change a person’s gender identity and gender expression to become more congruent with sex assigned at birth “is no longer considered ethical.”
Critics also argue that therapeutic interventions that aim to alter a child’s gender identity rely on the assumption that an adult transgender identity is undesirable, challenging this assumption along with the lack of clinical data to support outcomes and efficacy. Other therapeutic interventions do not seek to change a child’s gender identity, but are instead focused on creating a supportive and safe environment for the child to explore their gender identity and gender expression.
In the DSM of mental disorders used by psychologists in the United States, gender identity disorder is given two sets of criteria. Criterion A indicates that a child identifies as a member of the opposite sex. The child needs to demonstrate a number of the following symptoms: dressing as a member of the opposite sex, primarily befriending members of the opposite sex, demonstrating a desire to engage in play activities characteristic of the opposite sex, and actively stating that they wish to be the opposite sex. Criterion B, on the other hand, indicates that the child does not identify with the sex they were born. This could manifest itself as a dislike of styles of dress characteristic of the sex they were born, avoidance of association with members of their born sex, and distress towards the aspects of their physiology which indicate their born gender.
In May 2013, the American Psychiatric Association published the DSM-5 in which the GIDC diagnosis was removed and replaced with gender dysphoria, for the first time in its own distinct chapter. Subtyping by sexual orientation was deleted. The diagnosis for children was separated from that for adults. The creation of a specific diagnosis for children reflects the lesser ability of children to have insight into what they are experiencing, or ability to express it in the event that they have insight.
The International Statistical Classification of Diseases and Related Health Problems (ICD-10) lists several disorders related to gender identity, including gender identity disorder of childhood (F64.2): Persistent and intense distress about one’s assigned gender, manifested prior to puberty. The current edition has five different diagnoses for gender identity disorder, including one for when it manifests during childhood. The diagnoses of gender identity disorder is not given to intersex individuals (those born with “ambiguous” genitalia). Additionally, as with all psychological disorders, these symptoms must cause direct distress and an impairment of functioning of the individual exhibiting the symptoms.
F64.2 Gender identity disorder of childhood: A disorder, usually first manifest during early childhood (and always well before puberty), characterized by a persistent and intense distress about assigned sex, together with a desire to be (or insistence that one is) of the other sex. There is a persistent preoccupation with the dress and activities of the opposite sex and repudiation of the individual’s own sex. The diagnosis requires a profound disturbance of the normal gender identity; mere tomboyishness in girls or girlish behavior in boys is not sufficient. Gender identity disorders in individuals who have reached or are entering puberty should not be classified here but in F66.0.
The ICD-11, which will come into effect on 1 January 2022, significantly revises classification of gender identity-related conditions. Under “conditions related to sexual health”, the ICD-11 lists “gender incongruence”, which is coded into three conditions:
Children with persistent gender dysphoria are characterized by more extreme gender dysphoria in childhood than children with desisting gender dysphoria. Some (but not all) gender variant youth will want or need to transition, which may involve social transition (changing dress, name, pronoun), and, for older youth and adolescents, medical transition (hormone therapy or surgery).
Signs and symptoms, as outlined by the DSM-5, include a marked incongruence between experienced/expressed gender and assigned gender, of at least six months duration, as manifested by at least six of the following (one of which must be criterion A1):
B. The condition is associated with clinically significant distress or impairment in social, school, or other important areas of functioning.
Therapeutic approaches for GD differ from those used on adults and have included behavior therapy, psychodynamic therapy, group therapy, and parent counseling. This includes aiming to reduce gender dysphoria, making children more comfortable with their bodies, lessening ostracism, and reducing the child’s psychiatric comorbidity.
Traditional therapeutic intervention seeks to identify and resolve underlying factors (including familial factors), encourage the child to identify with their assigned sex, and encourage same-sex friendships. Parent counseling involves setting limits on the child’s cross-gender behavior, encouraging gender-neutral or sex-typical activities, examining familial factors, and examining parental factors such as psychopathology. Researchers Kenneth Zucker and Susan Bradley state that it has been found that boys with GD often have mothers who, to an extent, reinforced behavior more stereotypical of young girls. They also state that children with GD tend to come from families where cross-gender role behavior was not explicitly discouraged. However, they also acknowledge that one could view these findings as merely indicative of the fact that parents who were more accepting of their child’s cross-gender role behavior are also more likely to bring their children to a clinical psychiatrist as opposed to parents who are less accepting of cross-gender role behavior in their children.
In 2002, Zucker acknowledged limited data on gender dysphoria in children, stating that “apart from a series of intrasubject behaviour therapy case reports from the 1970s, one will find not a single randomized controlled treatment trial in the literature”. He has stated that “the therapist must rely on the ‘clinical wisdom’ that has accumulated and to utilize largely untested case formulation conceptual models to inform treatment approaches and decisions.”
The consensus of the World Professional Association for Transgender Health is that treatment aimed at trying to change a person’s gender identity and expression to become more congruent with sex assigned at birth “is no longer considered ethical.” Edgardo Menvielle, a child-adolescent psychiatrist at the Children’s National Medical Center in Washington states, “Therapists who advocate changing gender variant behaviours should be avoided.” Developmental and clinical psychologist Diane Ehrensaft told the Psychiatric Times, “The mental health profession has been consistently doing harm to children who are not ‘gender normal,’ and they need to retrain.”
Other therapeutic interventions do not seek to change a child’s gender identity. Instead, clinicians advise children and their parents to avoid goals based on gender identity and to instead cope with the child’s distress by embracing psychoeducation and to be supportive of their gender variant identity and behavior as it develops. A clinician may suggest that the parent be attentive, listen, and encourage an environment for the child to explore and express their identified gender identity, which may be termed the true gender. This can remove the stigma associated with their dysphoria, as well as the pressure to conform to a gender identity or role they do not identify with, which may be termed the false gender self.
Treatment may also take the form of puberty blockers (such as leuprorelin), cross-sex hormones (i.e., administering estrogen to a child assigned male at birth or testosterone to a child assigned female at birth), or sex reassignment surgery with the aim of bringing one’s physical body in line with their identified gender. Delaying puberty allows for the child to mentally mature while preventing them from developing a body they may not want, so that they may hopefully make a more informed decision about their gender identity once they are an adolescent. It can also help reduce anxiety and depression.
The Endocrine Society does not recommend endocrine treatment of prepubertal children because clinical experience suggests that GD can be reliably assessed only after the first signs of puberty. It recommends treating transgender adolescents by suppressing puberty with puberty blockers until age 16 years old, after which cross-sex hormones may be given. In its 2017 updated version of its guideline on treating those with gender dysphoria, it states, “We recognize that there may be compelling reasons to initiate sex hormone treatment prior to the age of 16 years in some adolescents with GD/gender incongruence, even though there are minimal published studies of gender-affirming hormone treatments administered before age 13.5 to 14 years.” The organization states, “As with the care of adolescents ≥16 years of age, we recommend that an expert multidisciplinary team of medical and MHPs manage this treatment.”
Some medical professions disagree that adolescents are cognitively mature enough to make a decision with regard to hormone therapy or surgery, and advise that irreversible genital procedures should not be performed on individuals under the age of legal consent in their respective country.
Gender dysphoria in children is more heavily linked to adult homosexuality than to an adult transgender identity, especially with regard to boys. The majority of children diagnosed with gender dysphoria cease to desire to be the other sex by puberty, with most growing up to identify as gay, lesbian, or bisexual, with or without therapeutic intervention. Prospective studies indicate that this is the case for 60 to 80% of those who have entered adolescence; puberty alleviates their gender dysphoria. Bonifacio et al. state, “There is research to suggest, however, that [some desistance of GD] may be caused, in part, by an internalizing pressure to conform rather than a natural progression to non–gender variance.”
If gender dysphoria persists during puberty, it is very likely permanent. For those with persisting or remitting gender dysphoria, the period between 10 to 13 years is crucial with regard to long-term gender identity.
Gregor et al. state that “children who are not brought to the attention of specialised clinics do not feature in these studies and thus there may be a far greater prevalence of children with gender identity issues (who may or may not experience distress as a result) than these studies suggest.”
Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by difficulty paying attention, excessive activity, and acting without regards to consequences, which are otherwise not appropriate for a person’s age. Some individuals with ADHD also display difficulty regulating emotions or problems with executive function. For a diagnosis, the symptoms should appear before a person is twelve years old, be present for more than six months, and cause problems in at least two settings (such as school, home, or recreational activities). In children, problems paying attention may result in poor school performance. Additionally there is an association with other mental disorders and substance misuse. Although it causes impairment, particularly in modern society, many people with ADHD can have sustained attention for tasks they find interesting or rewarding (known as hyperfocus).
Despite being the most commonly studied and diagnosed mental disorder in children and adolescents, the exact cause is unknown in the majority of cases. Genetic factors are estimated to make up about 75% of the risk. Nicotine exposure during pregnancy may be an environmental risk. It does not appear to be related to the style of parenting or discipline. It affects about 5–7% of children when diagnosed via the DSM-IV criteria and 1–2% when diagnosed via the ICD-10 criteria. As of 2015, it was estimated to affect about 51.1 million people globally. Rates are similar between countries and depend mostly on how it is diagnosed. ADHD is diagnosed approximately two times more often in boys than in girls, although the disorder is often overlooked in girls because their symptoms differ from those of boys. About 30–50% of people diagnosed in childhood continue to have symptoms into adulthood and between 2–5% of adults have the condition. In adults inner restlessness rather than hyperactivity may occur. They often develop coping skills which make up for some or all of their impairments. The condition can be difficult to tell apart from other conditions, as well as to distinguish from high levels of activity that are still within the range of normal behaviors.
ADHD management recommendations vary by country and usually involve some combination of counseling, lifestyle changes, and medications. The British guideline only recommends medications as a first-line treatment in children who have severe symptoms and for medication to be considered in those with moderate symptoms who either refuse or fail to improve with counseling, though for adults medications are a first-line treatment. Canadian and American guidelines recommend behavioral management first line in preschool-aged children while medications and behavioral therapy together is recommended after that. Treatment with stimulants is effective for at least 14 months; however, their long-term effectiveness is unclear and there are potentially serious side effects.
The medical literature has described symptoms similar to those of ADHD since the 18th century. ADHD, its diagnosis, and its treatment have been considered controversial since the 1970s. The controversies have involved clinicians, teachers, policymakers, parents, and the media. Topics include ADHD’s causes and the use of stimulant medications in its treatment. Most healthcare providers accept ADHD as a genuine disorder in children and adults, and the debate in the scientific community mainly centers on how it is diagnosed and treated. The condition was officially known as attention deficit disorder (ADD) from 1980 to 1987, while before this it was known as hyperkinetic reaction of childhood.
Oppositional defiant disorder (ODD) is listed in the DSM-5 under Disruptive, impulse-control, and conduct disorders and defined as “a pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness” in children and adolescents. Unlike children with conduct disorder (CD), children with oppositional defiant disorder are not aggressive towards people or animals, do not destroy property, and do not show a pattern of theft or deceit.
Oppositional defiant disorder was first defined in the DSM-III (1980). Since the introduction of ODD as an independent disorder, the field trials to inform the definition of this disorder have included predominantly male subjects. Some clinicians have debated whether the diagnostic criteria presented above would be clinically relevant for use with females. Furthermore, some have questioned whether gender-specific criteria and thresholds should be included. Additionally, some clinicians have questioned the preclusion of ODD when conduct disorder is present. According to Dickstein, the DSM-5 attempts to:
Oppositional defiant disorder has a prevalence of 1% to 11%. The average prevalence is approximately 3.3%. Gender and age play an important role in the rate of the disorder. In fact, ODD gradually develops and becomes apparent in preschool years; often before the age of eight years old. However, it is very unlikely to emerge following early adolescence. There is difference in prevalence between boys and girls. The ratio of this prevalence is 1.4 to 1 in favor of boys being more prevalent than girls before adolescence. On the other hand, girls’ prevalence tends to increase after puberty. When researchers observed the general prevalence of oppositional defiant disorder throughout cultures, they noticed that it remained constant. However, the sex difference in ODD prevalence is only significant in Western cultures. There are two possible explanations for this difference which are that in non-Western cultures there is a decrease prevalence of ODD in boys or an increase prevalence of ODD in girls. Other factors can influence the prevalence of the disorder. One of these factors is the socioeconomic status. Youths living in families of low socioeconomic status have a higher prevalence. Another factor is based on the criteria used to diagnose an individual. When the disorder was first included in the DSM-III, the prevalence was 25% higher than when the DSM-IV revised the criteria of diagnosis. The DSM-V made more changes to the criteria grouping certain characteristics together in order to demonstrate that ODD display both emotional and behavioral symptomatology. In addition, criteria were added to help guide clinicians in diagnosis because of the difficulty found in identifying whether the behaviors or symptoms are directly related to the disorder or simply a phase in a child’s life. Consequently, future studies may obtain results indicating a decline in prevalence between the DSM-IV and the DSM-V due to these changes.
The fourth revision of the Diagnostic and Statistical Manual (DSM-IV-TR) (now replaced by DSM-5) stated that the child must exhibit four out of the eight signs and symptoms to meet the diagnostic threshold for oppositional defiant disorder. These symptoms include:
These behaviors are mostly directed towards an authority figure such as a teacher or a parent. Although these behaviors can be typical among siblings they must be observed with individuals other than siblings for an ODD diagnosis. Children with ODD can be verbally aggressive. However, they do not display physical aggressiveness, a behavior observed in conduct disorder. Furthermore, they must be perpetuated for longer than six months and must be considered beyond a normal child’s age, gender and culture to fit the diagnosis. For children under 5 years of age, they occur on most days over a period of 6 months. For children over 5 years of age they occur at least once a week for at least 6 months. It is possible to observe these symptoms in only 1 setting, most commonly home. Thus the severity would be mild. If it is observed in two settings then it would be characterized as moderate and if the symptoms are observed in 3 or more settings then it would be considered severe.
These patterns of behavior result in impairment at school and/or other social venues.
There is no specific element that has yet been identified as directly causing ODD. Researchers looking precisely at the etiological factors linked with ODD are limited. The literature often examines common risk factors linked with all disruptive behaviors, rather than specifically about ODD. Symptoms of ODD are also often believed to be the same as CD even though the disorders have their own respective set of symptoms. When looking at disruptive behaviors such as ODD, research has shown that the causes of behaviors are multi factorial. However, disruptive behaviors have been identified as being mostly due either to biological or environmental factors.
Research indicates that parents pass on a tendency for externalizing disorders to their children that may be displayed in multiple ways, such as inattention, hyperactivity, or oppositional and conduct problems. Research has also shown that there is a genetic overlap between ODD and other externalizing disorders. Heritability can vary by age, age of onset, and other factors. Adoption and twin studies indicate that 50% or more of the variance causing antisocial behavior is attributable to heredity for both males and females. ODD also tends to occur in families with a history of ADHD, substance use disorders, or mood disorders, suggesting that a vulnerability to develop ODD may be inherited. A difficult temperament, impulsivity, and a tendency to seek rewards can also increase the risk of developing ODD. New studies into gene variants have also identified possible gene-environment (G x E) interactions, specifically in the development of conduct problems. A variant of the gene that encodes the neurotransmitter metabolizing enzyme mono amine oxidase-A (MAOA), which relates to neural systems involved in aggression, plays a key role in regulating behavior following threatening events. Brain imaging studies show patterns of arousal in areas of the brain that are associated with aggression in response to emotion-provoking stimuli.
Many pregnancy and birth problems are related to the development of conduct problems. Malnutrition, specifically protein deficiency, lead poisoning or exposure to lead, and mother’s use of alcohol or other substances during pregnancy may increase the risk of developing ODD. In numerous research, substance abuse prior to birth has also been associated with developing disruptive behaviors such as ODD. Although pregnancy and birth factors are correlated with ODD, strong evidence of direct biological causation is lacking.
Deficits and injuries to certain areas of the brain can lead to serious behavioral problems in children. Brain imaging studies have suggested that children with ODD may have subtle differences in the part of the brain responsible for reasoning, judgment and impulse control.[medical citation needed] Children with ODD are thought to have an overactive behavioral activation system (BAS), and under active behavioral inhibition system (BIS).
The BAS stimulates behavior in response to signals of reward or non punishment. The BIS produces anxiety and inhibits ongoing behavior in the presence of novel events, innate fear stimuli, and signals of non reward or punishment. Neuroimaging studies have also identified structural and functional brain abnormalities in several brain regions in youths with conduct disorders. These brain regions are the amygdala, prefrontal cortex, anterior cingulate, and insula, as well as interconnected regions.
As many as 40 percent of boys and 25 percent of girls with persistent conduct problems display significant social-cognitive impairments. Some of these deficits include immature forms of thinking (such as ego centrism), failure to use verbal mediators to regulate his or her behavior, and cognitive distortions, such as interpreting a neutral event as an intentional hostile act. Children with ODD have difficulty controlling their emotions or behaviors. In fact, students with ODD have limited social knowledge that is based only on individual experiences, which shapes how they process information and solve problems cognitively. This information can be linked with the social information processing model (SIP) that describes how children process information in order to respond appropriately or inappropriately in social settings. This model explains that children will go through five stages before displaying behaviors: encoding, mental representations, response accessing, evaluation and enactment. However, children with ODD have cognitive distortions and impaired cognitive processes. This will therefore directly impact their interactions and relationship negatively. It has been shown that social and cognitive impairments result in negative peer relationships, loss of friendship and an interruption in socially engaging in activities. Children learn through observational learning and social learning. Therefore, observations of models have a direct impact and greatly influence children’s behaviors and decision-making processes. Children often learn through modeling behavior. Modeling can act as a powerful tool to modify children’s cognition and behaviors.
Negative parenting practices and parent–child conflict may lead to antisocial behavior, but they may also be a reaction to the oppositional and aggressive behaviors of children. Factors such as a family history of mental illnesses and/or substance abuse as well as a dysfunctional family and inconsistent discipline by a parent or guardian can lead to the development of behavior disorders. Parenting practices not providing adequate or appropriate adjustment to situations as well as high ratio of conflicting events within a family have been shown to be causal factors of risk for developing ODD.
Insecure parent–child attachments can also contribute to ODD. Often little internalization of parent and societal standards exists in children with conduct problems. These weak bonds with their parents may lead children to associate with delinquency and substance abuse. Family instability and stress can also contribute to the development of ODD. Although the association between family factors and conduct problems is well established, the nature of this association and the possible causal role of family factors continues to be debated.
In a number of studies, low socioeconomic status has also been associated with disruptive behaviors such as ODD.
Other social factors such as neglect, abuse, parents that are not involved, and lack of supervision can also contribute to ODD.
Externalizing problems are reported to be more frequent among minority-status youth, a finding that is likely related to economic hardship, limited employment opportunities, and living in high-risk urban neighborhoods. Studies have also found that the state of being exposed to violence was also a contribution factor for externalizing behaviors to occur.
Conduct disorder (CD) is a mental disorder diagnosed in childhood or adolescence that presents itself through a repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate norms are violated. These behaviors are often referred to as “antisocial behaviors.” It is often seen as the precursor to antisocial personality disorder, which is per definition not diagnosed until the individual is 18 years old. Conduct disorder is estimated to affect 51.1 million people globally as of 2013.
One of the symptoms of conduct disorder is a lower level of fear. Research performed on the impact of toddlers exposed to fear and distress shows that negative emotionality (fear) predicts toddlers’ empathy-related response to distress. The findings support that if a caregiver is able to respond to infant cues, the toddler has a better ability to respond to fear and distress. If a child does not learn how to handle fear or distress the child will be more likely to lash out at other children. If the caregiver is able to provide therapeutic intervention teaching children at risk better empathy skills, the child will have a lower incident level of conduct disorder.
Increased instances of violent and antisocial behaviour are also associated with the condition; examples may range from pushing, hitting and biting when the child is young, progressing towards beating and inflicted cruelty as the child becomes older.
Currently, two possible developmental courses are thought to lead to conduct disorder. The first is known as the “childhood-onset type” and occurs when conduct disorder symptoms are present before the age of 10 years. This course is often linked to a more persistent life course and more pervasive behaviors. Specifically, children in this group have greater levels of ADHD symptoms, neuropsychological deficits, more academic problems, increased family dysfunction, and higher likelihood of aggression and violence.
There is debate among professionals regarding the validity and appropriateness of diagnosing young children with conduct disorder. The characteristics of the diagnosis are commonly seen in young children who are referred to mental health professionals. A premature diagnosis made in young children, and thus labeling and stigmatizing an individual, may be inappropriate. It is also argued that some children may not in fact have conduct disorder, but are engaging in developmentally appropriate disruptive behavior.
The second developmental course is known as the “adolescent-onset type” and occurs when conduct disorder symptoms are present after the age of 10 years. Individuals with adolescent-onset conduct disorder exhibit less impairment than those with the childhood-onset type and are not characterized by similar psychopathology. At times, these individuals will remit in their deviant patterns before adulthood. Research has shown that there is a greater number of children with adolescent-onset conduct disorder than those with childhood-onset, suggesting that adolescent-onset conduct disorder is an exaggeration of developmental behaviors that are typically seen in adolescence, such as rebellion against authority figures and rejection of conventional values. However, this argument is not established and empirical research suggests that these subgroups are not as valid as once thought.
In addition to these two courses that are recognized by the DSM-IV-TR, there appears to be a relationship among oppositional defiant disorder, conduct disorder and antisocial personality disorder. Specifically, research has demonstrated continuity in the disorders such that conduct disorder is often diagnosed in children who have been previously diagnosed with oppositional defiant disorder, and most adults with antisocial personality disorder were previously diagnosed with conduct disorder. For example, some research has shown that 90% of children diagnosed with conduct disorder had a previous diagnosis of oppositional defiant disorder. Moreover, both disorders share relevant risk factors and disruptive behaviors, suggesting that oppositional defiant disorder is a developmental precursor and milder variant of conduct disorder. However, this is not to say that this trajectory occurs in all individuals. In fact, only about 25% of children with oppositional defiant disorder will receive a later diagnosis of conduct disorder. Correspondingly, there is an established link between conduct disorder and the diagnosis of antisocial personality disorder as an adult. In fact, the current diagnostic criteria for antisocial personality disorder require a conduct disorder diagnosis before the age of 15. However, again, only 25-40% of youths with conduct disorder will develop antisocial personality disorder. Nonetheless, many of the individuals who do not meet full criteria for antisocial personality disorder still exhibit a pattern of social and personal impairments or antisocial behaviors. These developmental trajectories suggest the existence of antisocial pathways in certain individuals, which have important implications for both research and treatment.
Children with conduct disorder have a high risk of developing other adjustment problems. Specifically, risk factors associated with conduct disorder and the effects of conduct disorder symptomatology on a child’s psychosocial context have been linked to overlap with other psychological disorders. In this way, there seems to be reciprocal effects of comorbidity with certain disorders, leading to increased overall risk for these youth.
ADHD is the condition most commonly associated with conduct disorders, with approximately 25-30% of boys and 50-55% of girls with conduct disorder having a comorbid ADHD diagnosis. While it is unlikely that ADHD alone is a risk factor for developing conduct disorder, children who exhibit hyperactivity and impulsivity along with aggression is associated with the early onset of conduct problems. Moreover, children with comorbid conduct disorder and ADHD show more severe aggression.
Conduct disorder is also highly associated with both substance use and abuse. Children with conduct disorder have an earlier onset of substance use, as compared to their peers, and also is tend to use multiple substances. However, substance use disorders themselves can directly or indirectly cause conduct disorder like traits in about half of adolescents who have a substance use disorder. As mentioned above, it seems that there is a transactional relationship between substance use and conduct problems, such that aggressive behaviors increase substance use, which leads to increased aggressive behavior.
Substance use in conduct disorder can lead to antisocial behavior in adulthood.
While the cause of conduct disorder is complicated by an intricate interplay of biological and environmental factors, identifying underlying mechanisms is crucial for obtaining accurate assessment and implementing effective treatment. These mechanisms serve as the fundamental building blocks on which evidence-based treatments are developed. Despite the complexities, several domains have been implicated in the development of conduct disorder including cognitive variables, neurological factors, intraindividual factors, familial and peer influences, and wider contextual factors. These factors may also vary based on the age of onset, with different variables related to early (e.g., neurodevelopmental basis) and adolescent (e.g., social/peer relationships) onset.
The development of conduct disorder is not immutable or predetermined. A number of interactive risk and protective factors exist that can influence and change outcomes, and in most cases conduct disorder develops due to an interaction and gradual accumulation of risk factors. In addition to the risk factors identified under cause, several other variables place youth at increased risk for developing the disorder, including child physical abuse, prenatal alcohol abuse and maternal smoking during pregnancy. Protective factors have also been identified, and most notably include high IQ, being female, positive social orientations, good coping skills, and supportive family and community relationships.
However, a correlation between a particular risk factor and a later developmental outcome (such as conduct disorder) cannot be taken as definitive evidence for a causal link. Co-variation between two variables can arise, for instance, if they represent age-specific expressions of similar underlying genetic factors. For example, the tendency to smoke during pregnancy (SDP) is subject to substantial genetic influence (D’Onofrio et al., 2007), as is conduct disorder. Thus, the genes that dispose the mother to SDP may also dispose the child to CD following mitotic transmission. Indeed, Rice et al. (2009) found that in mother-fetus pairs that were not genetically related (by virtue of in-vitro fertilisation), no link between SDP and later conduct problems arose. Thus, the distinction between causality and correlation is an important consideration.
While language impairments are most common, approximately 20-25% of youth with conduct disorder have some type of learning disability. Although the relationship between the disorders is complex, it seems as if learning disabilities result from a combination of ADHD, a history of academic difficulty and failure, and long-standing socialization difficulties with family and peers. However, confounding variables, such as language deficits, SES disadvantage, or neurodevelopmental delay also need to be considered in this relationship, as they could help explain some of the association between conduct disorder and learning problems.
In terms of cognitive function, intelligence and cognitive deficits are common amongst youths with conduct disorder, particularly those with early-onset and have intelligence quotients (IQ) one standard deviation below the mean and severe deficits in verbal reasoning and executive function. Executive function difficulties may manifest in terms of one’s ability to shift between tasks, plan as well as organize, and also inhibit a prepotent response. These findings hold true even after taking into account other variables such as socioeconomic status (SES), and education. However, IQ and executive function deficits are only one piece of the puzzle, and the magnitude of their influence is increased during transactional processes with environmental factors.
Beyond difficulties in executive function, neurological research on youth with conduct disorder also demonstrate differences in brain anatomy and function that reflect the behaviors and mental anomalies associated in conduct disorder. Compared to normal controls, youths with early and adolescent onset of conduct disorder displayed reduced responses in brain regions associated with social behavior (i.e., amygdala, ventromedial prefrontal cortex, insula, and orbitofrontal cortex). In addition, youths with conduct disorder also demonstrated less responsiveness in the orbitofrontal regions of the brain during a stimulus-reinforcement and reward task. This provides a neural explanation for why youths with conduct disorder may be more likely to repeat poor decision making patterns. Lastly, youths with conduct disorder display a reduction in grey matter volume in the amygdala, which may account for the fear conditioning deficits. This reduction has been linked to difficulty processing social emotional stimuli, regardless of the age of onset. Aside from the differences in neuroanatomy and activation patterns between youth with conduct disorder and controls, neurochemical profiles also vary between groups. Individuals with conduct disorder are characterized as having reduced serotonin and cortisol levels (e.g., reduced hypothalamic-pituitary-adrenal (HPA) axis), as well as reduced autonomic nervous system (ANS) functioning. These reductions are associated with the inability to regulate mood and impulsive behaviors, weakened signals of anxiety and fear, and decreased self-esteem. Taken together, these findings may account for some of the variance in the psychological and behavioral patterns of youth with conduct disorder.
Aside from findings related to neurological and neurochemical profiles of youth with conduct disorder, intraindividual factors such as genetics may also be relevant. Having a sibling or parent with conduct disorder increases the likelihood of having the disorder, with a heritability rate of .53. There also tends to be a stronger genetic link for individuals with childhood-onset compared to adolescent onset. In addition, youth with conduct disorder also exhibit polymorphism in the monoamine oxidase A gene, low resting heart rates, and increased testosterone.
Elements of the family and social environment may also play a role in the development and maintenance of conduct disorder. For instance, antisocial behavior suggestive of conduct disorder is associated with single parent status, parental divorce, large family size, and young age of mothers. However, these factors are difficult to tease apart from other demographic variables that are known to be linked with conduct disorder, including poverty and low socioeconomic status. Family functioning and parent-child interactions also play a substantial role in childhood aggression and conduct disorder, with low levels of parental involvement, inadequate supervision, and unpredictable discipline practices reinforcing youth’s defiant behaviors. Peer influences have also been related to the development of antisocial behavior in youth, particularly peer rejection in childhood and association with deviant peers. Peer rejection is not only a marker of a number of externalizing disorders, but also a contributing factor for the continuity of the disorders over time. Hinshaw and Lee (2003) also explain that association with deviant peers has been thought to influence the development of conduct disorder in two ways: 1) a “selection” process whereby youth with aggressive characteristics choose deviant friends, and 2) a “facilitation” process whereby deviant peer networks bolster patterns of antisocial behavior. In a separate study by Bonin and colleagues, parenting programs were shown to positively affect child behavior and reduce costs to the public sector.
In addition to the individual and social factors associated with conduct disorder, research has highlighted the importance of environment and context in youth with antisocial behavior. However, it is important to note that these are not static factors, but rather transactional in nature (e.g., individuals are influenced by and also influence their environment). For instance, neighborhood safety and exposure to violence has been studied in conjunction with conduct disorder, but it is not simply the case that youth with aggressive tendencies reside in violent neighborhoods. Transactional models propose that youth may resort to violence more often as a result of exposure to community violence, but their predisposition towards violence also contributes to neighborhood climate.
Childhood schizophrenia (also known as childhood-onset schizophrenia, and very early-onset schizophrenia) is schizophrenia – characterized by hallucinations, disorganized speech, delusions, and negative symptoms, such as blunted affect and avolition, with onset before 13 years of age. It is rarely found.
The disorder presents symptoms such as auditory and visual hallucinations, strange thoughts or feelings, and abnormal behavior, profoundly impacting the child’s ability to function and sustain normal interpersonal relationships. Delusions are often not systematized and vague. Among the psychotic symptoms seen in childhood schizophrenia non-verbal auditory hallucinations are the most common, and include noises such as shots, knocks, bangs. Other symptoms can include irritability, searching for imaginary objects, or low performance. It typically presents after the age of seven. About 50% of young children diagnosed with schizophrenia experience severe neuropsychiatric symptoms. Studies have demonstrated that diagnostic criteria are similar to those of adult schizophrenia. Diagnosis is based on behavior observed by caretakers and, in some cases depending on age, self reports.
Schizophrenia has no definite cause; however, certain risk factors such as family history seem to correlate. There is no known cure, but childhood schizophrenia is controllable with the help of behavioral therapies and medications.
Childhood schizophrenia was not directly added to the DSM until 1968, when it was added to the DSM-II, which set forth diagnostic criteria similar to that of adult schizophrenia. “Schizophrenia, childhood type” was a DSM-II diagnosis with diagnostic code 295.8. It’s equivalent to “schizophrenic reaction, childhood type” (code 000-x28) in DSM-I (1952). “Schizophrenia, childhood type” was successfully removed from the DSM-III (1980), and in the Appendix C they wrote: “there is currently no way of predicting which children will develop Schizophrenia as adults”. Instead of childhood schizophrenia they proposed to use of “infantile autism” (299.0x) and “childhood onset pervasive developmental disorder” (299.9x).
In the DSM-III-R (1987), DSM-IV (1994), DSM-IV-TR (2000), DSM-5 (2013) there are no “childhood schizophrenia”. The rationale for this approach was that since the clinical picture of adult schizophrenia and childhood schizophrenia is identical, childhood schizophrenia should not be a separate disorder. However, the section in schizophrenia’s Development and Course in DSM-5, includes references to childhood-onset schizophrenia.
The diagnosis of schizophrenia was[when?] often given to children who by today’s standards would be diagnosed as having of autism or pervasive developmental disorder. This may be because the onset of schizophrenia is gradual, with symptoms relating developmental difficulties or abnormalities appearing before psychotic symptoms.
In the International Classification of Diseases 8th revision (ICD-8, 1967) there was a category (295.8) “Other” in the schizophrenia section (295). “Other” includes: atypical forms of schizophrenia, infantile autism, schizophrenia, childhood type, NOS (Not Otherwise Specified), schizophrenia of specified type not classifiable under 295.0–295.7, schizophreniform attack or psychosis.
Unspecified psychoses with origin specific to childhood (code 299.9) in the International Classification of Diseases 9th revision (ICD-9) includes “child psychosis NOS”, “schizophrenia, childhood type NOS” and “schizophrenic syndrome of childhood NOS”.
“Childhood type schizophrenia” available in the Soviet adapted version of the ICD-9 (code 299.91) and the Russian adapted version of the 10th revision ICD-10 (code F20.8xx3). This diagnosis is widely used by Russian psychiatrists.
Schizophrenia is a mental disorder that is expressed in abnormal mental functions and disturbed behavior.
The signs and symptoms of childhood schizophrenia are nearly the same as adult-onset schizophrenia. Some of the earliest signs that a young child may develop schizophrenia are lags in language and motor development. Some children engage in activities such as flapping the arms or rocking, and may appear anxious, confused, or disruptive on a regular basis. Children may experience hallucinations, but these are often difficult to differentiate from just normal imagination or child play. Visual hallucinations are more commonly found in children than in adults. It is often difficult for children to describe their hallucinations or delusions, making very early-onset schizophrenia especially difficult to diagnose in the earliest stages. The cognitive abilities of children with schizophrenia may also often be lacking, with 20% of patients showing borderline or full intellectual disability.
Very early-onset schizophrenia refers to onset before the age of thirteen. The prodromal phase, which precedes psychotic symptoms, is characterized by deterioration in school performance, social withdrawal, disorganized or unusual behavior, a decreased ability to perform daily activities, a deterioration in self-care skills, bizarre hygiene and eating behaviors, changes in affect, a lack of impulse control, hostility and aggression, and lethargy.
Auditory hallucinations are the most common of the positive symptoms in children. Auditory hallucinations may include voices that are conversing with each other or voices that are speaking directly to the children themselves. Many children with auditory hallucinations believe that if they do not listen to the voices, the voices will harm them or someone else. Tactile and visual hallucinations seem relatively rare. Children often attribute the hallucinatory voices to a variety of beings, including family members or other people, evil forces (“the Devil“, “a witch“, “a spirit“), animals, characters from horror movies (Bloody Mary, Freddy Krueger) and less clearly recognizable sources (“bad things,” “the whispers”). Command auditory hallucinations (also known as imperative hallucinations) were common and experienced by more than ½ of the group in a research at the Bellevue Hospital Center’s Children’s Psychiatric Inpatient Unit. And voices repeat and repeat: “Kill somebody!”, “Kill her, kill her!”. Delusions are reported in more than half of children with schizophrenia, but they are usually less complex than those of adults. Delusions are often connected with hallucinatory experiences. In a research delusions were characterized as persecutory for the most part, but some children reported delusions of control. Many said they were being tortured by the beings causing their visual and auditory hallucinations, some thought disobeying their voices would cause them harm.
Some degree of thought disorder was observed in a test group of children in Bellevue Hospital. They displayed illogicality, tangentialiry (a serious disturbance in the associative thought process), and loosening of associations.
There is no known single cause or causes of schizophrenia, however, it is a heritable disorder.
Several environmental factors, including perinatal complications and prenatal maternal infections could cause schizophrenia. These factors in a greater severity or frequency could result in an earlier onset of schizophrenia. Maybe a genetic predisposition is an important factor too, familial illness reported for childhood-onset schizophrenic patients.
There is “considerable overlap” in the genetics of childhood-onset and adult-onset schizophrenia, but in childhood-onset schizophrenia there is a higher number of “rare allelic variants”. An important gene for adolescent-onset schizophrenia is the catechol-O-methyltransferase gene, a gene that regulates dopamine. Children with schizophrenia have an increase in genetic deletions or duplication mutations and some have a specific mutation called 22q11 deletion syndrome, which accounts for up to 2% of cases.
Neuroimaging studies have found differences between the medicated brains of individuals with schizophrenia and neurotypical brains, though research does not know the cause of the difference. In childhood-onset schizophrenia, there appears to be a faster loss of cerebral grey matter during adolescence.
The ICD-10 criteria are typically used in most of the world, while the DSM-5 criteria are used in USA.
In 2013, the American Psychiatric Association released the fifth edition of the DSM (DSM-5). According to the manual, to be diagnosed with schizophrenia, two diagnostic criteria have to be met over much of the time of a period of at least one month, with a significant impact on social or occupational functioning for at least six months. The DSM diagnostic criteria outlines that the person has to be experiencing either delusions, hallucinations, or disorganized speech. In other words, an individual does not have to be experiencing delusions or hallucinations to receive a diagnosis of schizophrenia. A second symptom could be negative symptoms, or severely disorganized or catatonic behavior. Only two symptoms are required for a diagnosis of Schizophrenia, resulting in different presentations for the same disorder.
In practice, agreement between the two systems is high. The DSM-5 criteria puts more emphasis on social or occupational dysfunction than the ICD-10. The ICD-10, on the other hand, puts more emphasis on first-rank symptoms. The current proposal for the ICD-11 criteria for schizophrenia recommends adding self-disorder as a symptom.
First-rank symptoms are psychotic symptoms that are particularly characteristic of schizophrenia, which were put forward by Kurt Schneider in 1959. Their reliability for the diagnosis of schizophrenia has been questioned since then. A 2015 systematic review investigated the diagnostic accuracy of first rank symptoms:
Depression is a state of low mood and aversion to activity. It can affect a person’s thoughts, behavior, motivation, feelings, and sense of well-being. It may feature sadness, difficulty in thinking and concentration and a significant increase or decrease in appetite and time spent sleeping. People experiencing depression may have feelings of dejection, hopelessness and, sometimes, suicidal thoughts. It can either be short term or long term. The core symptom of depression is said to be anhedonia, which refers to loss of interest or a loss of feeling of pleasure in certain activities that usually bring joy to people. Depressed mood is a symptom of some mood disorders such as major depressive disorder or dysthymia; it is a normal temporary reaction to life events, such as the loss of a loved one; and it is also a symptom of some physical diseases and a side effect of some drugs and medical treatments.
Adversity in childhood, such as bereavement, neglect, mental abuse, physical abuse, sexual abuse, or unequal parental treatment of siblings can contribute to depression in adulthood. Childhood physical or sexual abuse in particular significantly correlates with the likelihood of experiencing depression over the victim’s lifetime.
Life events and changes that may influence depressed moods include (but are not limited to): childbirth, menopause, financial difficulties, unemployment, stress (such as from work, education, family, living conditions etc.), a medical diagnosis (cancer, HIV, etc.), bullying, loss of a loved one, natural disasters, social isolation, rape, relationship troubles, jealousy, separation, or catastrophic injury. Adolescents may be especially prone to experiencing a depressed mood following social rejection, peer pressure, or bullying.
Changes in personality or in one’s social environment can affect levels of depression. High scores on the personality domain neuroticism make the development of depressive symptoms as well as all kinds of depression diagnoses more likely, and depression is associated with low extraversion. Other personality indicators could be: temporary but rapid mood changes, short term hopelessness, loss of interest in activities that used to be of a part of one’s life, sleep disruption, withdrawal from previous social life, appetite changes, and difficulty concentrating.
Depression may also be the result of healthcare, such as with medication induced depression. Therapies associated with depression include interferon therapy, beta-blockers, isotretinoin, contraceptives, cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist.
Several drugs of abuse can cause or exacerbate depression, whether in intoxication, withdrawal, and from chronic use. These include alcohol, sedatives (including prescription benzodiazepines), opioids (including prescription pain killers and illicit drugs such as heroin), stimulants (such as cocaine and amphetamines), hallucinogens, and inhalants.
Depressed mood can be the result of a number of infectious diseases, nutritional deficiencies, neurological conditions, and physiological problems, including hypoandrogenism (in men), Addison’s disease, Cushing’s syndrome, hypothyroidism, hyperparathyroidism, Lyme disease, multiple sclerosis, Parkinson’s disease, chronic pain, stroke, diabetes, and cancer.
Measures of depression as an emotional disorder include, but are not limited to: Beck Depression Inventory-11 and the 9-item depression scale in the Patient Health Questionnaire. Both of these measures are psychological tests that ask personal questions of the participant, and have mostly been used to measure the severity of depression. The Beck Depression Inventory (BDI) is a self-report scale that helps a therapist identify the patterns of depression symptoms and monitor recovery. The responses on this scale can be discussed in therapy to devise interventions for the most distressing symptoms of depression. Several studies, however, have used these measures to also determine healthy individuals who are not suffering from depression as a mental disorder, but as an occasional mood disorder. This is substantiated by the fact that depression as an emotional disorder displays similar symptoms to minimal depression and low levels of mental disorders such as major depressive disorder; therefore, researchers were able to use the same measure interchangeably. In terms of the scale, participants scoring between 0-13 and 0-4 respectively were considered healthy individuals.
Another measure of depressed mood would be the IWP Multi-affect Indicator. It is a psychological test that indicates various emotions, such as enthusiasm and depression, and asks for the degree of the emotions that the participants have felt in the past week. There are studies that have used lesser items from the IWP Multi-affect Indicator which was then scaled down to daily levels to measure the daily levels of depression as an emotional disorder.
Alcohol can be a depressant which slows down some regions of the brain, like the prefrontal and temporal cortex, negatively affecting our rationality and memory. It also lowers the level of serotonin in our brain, which could potentially lead to higher chances of a depressive mood.
The connection between the amount of alcohol intake, level of depressed mood, and how it affects the risks of experiencing consequences from alcoholism, were studied in a research done on college students. The study used 4 latent, distinct profiles of different alcohol intake and level of depression; Mild or Moderate Depression, and Heavy or Severe Drinkers. Other indicators consisting of social factors and individual behaviors were also taken into consideration in the research. Results showed that the level of depression as an emotion negatively affected the amount of risky behavior and consequence from drinking, while having an inverse relationship with protective behavioral strategies, which are behavioral actions taken by oneself for protection from the relative harm of alcohol intake. Having an elevated level of depressed mood does therefore lead to greater consequences from drinking.
Social abuse, such as bullying, are defined as actions of singling out and causing harm on vulnerable individuals. In order to capture a day-to-day observation of the relationship between the damaging effects of social abuse, the victim’s mental health and depressive mood, a study was conducted on whether individuals would have a higher level of depressed mood when exposed to daily acts of negative behavior. The result concluded that being exposed daily to abusive behaviors such as bullying has a positive relationship to depressed mood on the same day.
The study has also gone beyond to compare the level of depressive mood between the victims and non-victims of the daily bullying. Although victims were predicted to have a higher level of depressive mood, the results have shown otherwise that exposure to negative acts has led to similar levels of depressive mood, regardless of the victim status. The results therefore have concluded that bystanders and non-victims feel as equally depressed as the victim when being exposed to acts such as social abuse.
Divergent thinking is defined as a thought process that generates creativity in ideas by exploring many possible solutions. Having a depressed mood will significantly reduce the possibility of divergent thinking, as it reduces the fluency, variety and the extent of originality of the possible ideas generated.
However, some depressive mood disorders might have an positive effect for creativity. Upon identifying several studies and analyzing data involving individuals with high levels of creativity, Christa Taylor was able to conclude that there is a clear positive relationship between creativity and depressive mood. A possible reason is that having a low mood could lead to new ways of perceiving and learning from the world, but it is unable to account for certain depressive disorders. The direct relationship between creativity and depression remains unclear, but the research conducted on this correlation has shed light that individuals who are struggling with a depressive disorder may be having even higher levels of creativity than a control group, and would be a close topic to monitor depending on the future trends of how creativity will be perceived and demanded.
There are empirical evidences of a connection between the type of stress management techniques and the level of daily depressive mood.
Problem-focused coping leads to lower level of depression. Focusing on the problem allows for the subjects to view the situation in an objective way, evaluating the severity of the threat in an unbiased way, thus it lowers the probability of having depressive responses. On the other hand, emotion-focused coping promotes a depressed mood in stressful situations. The person has been contaminated with too much irrelevant information and loses focus on the options for resolving the problem. They fail to consider the potential consequences and choose the option that minimizes stress and maximizes well-being.
Bipolar disorder in children, or pediatric bipolar disorder (PBD), is a mental disorder in children and adolescents that, like bipolar disorder (BD) in adults, is characterized by extreme changes in mood and behavior accompanying periods of depressed or irritable moods and periods of elevated moods called manic or hypomanic episodes. These shifts are sometimes quick, but usually are gradual. The average age of onset of PBD is unclear, but the risk increases with the onset of puberty. PBD is typically more severe and has a poorer prognosis than BD with onset in late-adolescence or adulthood.
The DSM has specified that the criteria for BD can be applied to children since 1980. However, the exact criteria for diagnosing PBD remains controversial and heavily debated. There are big differences in how commonly it is diagnosed across clinics and in different countries. There has been a rapid increase in research on the topic, but training and clinical practice lag behind.
Identifying BD in youth is challenging. While adults with BD often have distinct periods of depression and mania that last for weeks, months, or longer, youth diagnosed with BD frequently have depressive and manic symptoms that occur daily, and sometimes simultaneously either as rapid shifts or periods of high energy negative mood. Comorbid disorders are common, which makes determining what symptoms are signs of BD and which are due to other disorders (e.g., depression, ADHD, disruptive behavior problems) crucial both for accurate diagnosis and effective treatment.
Diagnosis is made based on a clinical interview by a psychiatrist or other licensed mental health practitioner. There are no blood tests or brain scans to diagnose BD. Obtaining information on family history and the use of questionnaires and checklists are helpful in making an accurate diagnosis. Commonly used assessment tools include the K-SADS (Kiddie Schedule for Affective Disorders and Schizophrenia), the Diagnostic Interview Schedule for Children (DISC), and the Child Mania Rating Scale (CMRS).
In both the American Psychiatric Association’s DSM-5 and the World Health Organization’s ICD-10, the same criteria used to diagnose BD in adults are used to make the diagnosis in children with some adjustments to account for differences in age and developmental stage. For example, the DSM-5 specifies that in children, depressive episodes can manifest as persistently irritable moods.
In diagnosing manic episodes, it is important to compare the changes in mood and behavior to the child’s normal mood and behaviors at baseline instead of to other children or adults. For example, grandiosity (i.e., unrealistic overestimation of one’s intelligence, talent, or abilities) is normal at varying degrees during childhood and adolescence. Therefore, grandiosity is only considered symptomatic of mania in children when the beliefs are held despite being presented with concrete evidence otherwise or when they lead to a child attempting activities that are clearly dangerous, and most importantly, when the grandiose beliefs are an obvious change from that particular child’s normal self-view in between episodes.
The diagnosis of childhood BD is controversial. although it is recognized that BD typical symptoms are dysfunctional and have negative consequences for minors suffering them. Main discussion is centered on whether what is called BD in children refers to the same disorder than when diagnosing adults, and the related question on whether adults’ criteria for diagnosis are useful and accurate when applied to children. More specifically, main discussion over diagnosis in children circles around mania symptomatology and its differences between children and adults.
Diagnostic criteria may not correctly separate children with BD from other problems such as ADHD, and emphasize fast mood cycles.
Medications can produce important side effects, so interventions have been recommended to be closely monitored and families of patients to be informed of the different possible problems that can arise. Atypical antipsychotics are more effective than mood stabilizers, but have more side effects Typical antipsychotics may produce weight gains as well as other metabolic problems, including diabetes mellitus type 2 and hyperlipidemia. Extrapyramidal secondary effects may appear with these medications. These include tardive dyskinesia, a difficult-to-treat movement disorder (dyskinesia) that can appear after long-term use of anti-psychotics. Liver and kidney damage are a possibility with mood stabilizers.
Psychological treatment usually includes some combination of education on the disease, group therapy and cognitive behavioral therapy. Children with BD and their families are informed, in ways accordingly to their age and family role, about the different aspects of BD and its management including causes, signs and symptoms and treatments. Group therapy aims to improve social skills and manage group conflicts, with role-playing as a critical tool. Finally, cognitive-behavioral training is directed towards the participants having a better understanding and control over their emotions and behaviors.
Chronic medication is often needed, with relapses of individuals reaching rates over 90% in those not following medication indications and almost to 40% in those complying with medication regimens in some studies. Compared to adults, a juvenile onset has in general a similar or worse course, although age of onset predicts the duration of the episodes more than the prognosis. A risk factor for a worse outcome is the existence of additional (comorbid) pathologies.
Children with BD are more likely to commit suicide than other children.
The prevalence of bipolar in youth is estimated at 2%.
Descriptions of children with symptoms similar to contemporary concepts of mania date back to the 18th century. In 1898, a detailed psychiatric case history was published about a 13-year-old that met Jean-Pierre Falret and Jules Baillarger‘s criteria for folie circulaire, which is congruent to the modern conception of bipolar I disorder. In Emil Kraepelin‘s descriptions of BD in the 1920s, which he called “manic depressive insanity”, he noted the rare possibility that it could occur in children. In addition to Kraepelin, Adolf Meyer, Karl Abraham, and Melanie Klein were some of the first to document BD symptoms in children in the first half of the 20th century. In general though, it was considered exceedingly rare and was not mentioned much in the literature until the 1970s when interest in researching the subject increased. It became more accepted as a diagnosis in children in the 1980s after the DSM-III (1980) specified that the same criteria for diagnosing BD in adults could also be applied to children.
Recognition came twenty years after, with epidemiological studies showing that approximately 20% of adults with BD already had symptoms in childhood or adolescence. Nevertheless, onset before age 10 was thought to be rare, below 0.5% of the cases. During the second half of the century misdiagnosis with schizophrenia was not rare in the non-adult population due to common co-occurrence of psychosis and mania, this issue diminishing with an increased following of the DSM criteria in the last part of the 20th century
Panic disorder is an anxiety disorder characterized by reoccurring unexpected panic attacks. Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something terrible is going to happen. The maximum degree of symptoms occurs within minutes. There may be ongoing worries about having further attacks and avoidance of places where attacks have occurred in the past.
The cause of panic disorder is unknown. Panic disorder often runs in families. Risk factors include smoking, psychological stress, and a history of child abuse. Diagnosis involves ruling out other potential causes of anxiety including other mental disorders, medical conditions such as heart disease or hyperthyroidism, and drug use. Screening for the condition may be done using a questionnaire.
Panic disorder is usually treated with counselling and medications. The type of counselling used is typically cognitive behavioral therapy (CBT) which is effective in more than half of people. Medications used include antidepressants and occasionally benzodiazepines or beta blockers. Following stopping treatment up to 30% of people have a recurrence.
Panic disorder affects about 2.5% of people at some point in their life. It usually begins during adolescence or early adulthood but any age can be affected. It is less common in children and older people. Women are more often affected than men.
Panic disorder sufferers usually have a series of intense episodes of extreme anxiety during panic attacks. These attacks typically last about ten minutes, and can be as short-lived as 1–5 minutes, but can last twenty minutes to more than an hour, or until helpful intervention is made. Panic attacks can wax and wane for a period of hours (panic attacks rolling into one another), and the intensity and specific symptoms of panic may vary over the duration.
In some cases, the attack may continue at unabated high intensity or seem to be increasing in severity. Common symptoms of an attack include rapid heartbeat, perspiration, dizziness, dyspnea, trembling, uncontrollable fear such as: the fear of losing control and going crazy, the fear of dying and hyperventilation. Other symptoms are a sensation of choking, paralysis, chest pain, nausea, numbness or tingling, chills or hot flashes, faintness, crying and some sense of altered reality. In addition, the person usually has thoughts of impending doom. Individuals suffering from an episode have often a strong wish of escaping from the situation that provoked the attack. The anxiety of panic disorder is particularly severe and noticeably episodic compared to that from generalized anxiety disorder. Panic attacks may be provoked by exposure to certain stimuli (e.g., seeing a mouse) or settings (e.g., the dentist’s office). Other attacks may appear unprovoked. Some individuals deal with these events on a regular basis, sometimes daily or weekly. The outward symptoms of a panic attack often cause negative social experiences (e.g., embarrassment, social stigma, social isolation, etc.).
Limited symptom attacks are similar to panic attacks but have fewer symptoms. Most people with PD experience both panic attacks and limited symptom attacks.
Studies investigating the relationship between interoception and panic disorder have shown that people with panic disorder feel heartbeat sensations more intensely when stimulated by pharmacological agents, suggesting that they experience heightened interoceptive awareness compared to healthy subjects.
While there is not just one explanation for the cause of panic disorder, there are certain perspectives researchers use to explain the disorder. The first one is the biological perspective. Past research concluded that there is irregular norepinephrine activity in people who have panic attacks. Current research also supports this perspective as it has been found that those with panic disorder also have a brain circuit that performs improperly. This circuit consists of the amygdala, central gray matter, ventromedial nucleus of the hypothalamus, and the locus ceruleus.
There is also the cognitive perspective. Theorists believe that people with panic disorder may experience panic reactions because they mistake their bodily sensations for life-threatening situations. These bodily sensations cause some people to feel as though are out of control which may lead to feelings of panic. This misconception of bodily sensations is referred to as anxiety sensitivity, and studies suggest that people who score higher on anxiety sensitivity surveys are fives times more likely to be diagnosed with panic disorder.
Panic disorder has been found to run in families, which suggests that inheritance plays a strong role in determining who will get it.
Psychological factors, stressful life events, life transitions, and environment as well as often thinking in a way that exaggerates relatively normal bodily reactions are also believed to play a role in the onset of panic disorder. Often the first attacks are triggered by physical illnesses, major stress, or certain medications. People who tend to take on excessive responsibilities may develop a tendency to suffer panic attacks. Post-traumatic stress disorder (PTSD) patients also show a much higher rate of panic disorder than the general population.
Prepulse inhibition has been found to be reduced in patients with panic disorder.
Substance abuse is often correlated with panic attacks. In a study 39% of people with panic disorder had abused substances. Of those who used alcohol 63% reported that the alcohol use began prior to the onset of panic, and 59% of those abusing illicit drugs reported that drug use began first. The study that was conducted documented the panic-substance abuse relationship. Substance abuse began prior to onset of panic and substances were used to self-medicate for panic attacks by only a few subjects.
In another study, 100 methamphetamine-dependent individuals were analyzed for co-morbid psychiatric disorders; of the 100 individuals, 36% were categorized as having co-morbid psychiatric disorders. Mood and Psychotic disorders were more prevalent than anxiety disorders, which accounted for 7% of the 100 sampled individuals.
Tobacco smoking increases the risk of developing panic disorder with or without agoraphobia and panic attacks; smoking started in adolescence or early adulthood particularly increases this risk of developing panic disorder. While the mechanism of how smoking increases panic attacks is not fully understood, a few hypotheses have been derived. Smoking cigarettes may lead to panic attacks by causing changes in respiratory function (e.g. feeling short of breath). These respiratory changes in turn can lead to the formation of panic attacks, as respiratory symptoms are a prominent feature of panic. Respiratory abnormalities have been found in children with high levels of anxiety, which suggests that a person with these difficulties may be susceptible to panic attacks, and thus more likely to subsequently develop panic disorder. Nicotine, a stimulant, could contribute to panic attacks. However, nicotine withdrawal may also cause significant anxiety which could contribute to panic attacks.
It is also possible that panic disorder patients smoke cigarettes as a form of self-medication to lessen anxiety. Nicotine and other psychoactive compounds with antidepressant properties in tobacco smoke which act as monoamine oxidase inhibitors in the brain can alter mood and have a calming effect, depending on dose.
A number of clinical studies have shown a positive association between caffeine ingestion and panic disorder and/or anxiogenic effects. People who have panic disorder are more sensitive to the anxiety-provoking effects of caffeine. One of the major anxiety-provoking effects of caffeine is an increase in heart rate.
Certain cold and flu medications containing decongestants may also contain pseudoephedrine, ephedrine, phenylephrine, naphazoline and oxymetazoline. These may be avoided by the use of decongestants formulated to prevent causing high blood pressure.
About 30% of people with panic disorder use alcohol and 17% use other psychoactive drugs. This is in comparison with 61% (alcohol) and 7.9% (other psychoactive drugs) of the general population who use alcohol and psychoactive drugs, respectively. Utilization of recreational drugs or alcohol generally make symptoms worse. Most stimulant drugs (caffeine, nicotine, cocaine) would be expected to worsen the condition, since they directly increase the symptoms of panic, such as heart rate.
Deacon and Valentiner (2000) conducted a study that examined co-morbid panic attacks and substance use in a non-clinical sample of young adults who experienced regular panic attacks. The authors found that compared to healthy controls, sedative use was greater for non-clinical participants who experienced panic attacks. These findings are consistent with the suggestion made by Cox, Norton, Dorward, and Fergusson (1989) that panic disorder patients self-medicate if they believe that certain substances will be successful in alleviating their symptoms. If panic disorder patients are indeed self-medicating, there may be a portion of the population with undiagnosed panic disorder who will not seek professional help as a result of their own self-medication. In fact, for some patients panic disorder is only diagnosed after they seek treatment for their self-medication habit.
While alcohol initially helps ease panic disorder symptoms, medium- or long-term alcohol abuse can cause panic disorder to develop or worsen during alcohol intoxication, especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long-term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquilizers to people with alcohol problems. The reason chronic alcohol misuse worsens panic disorder is due to distortion of the brain chemistry and function.
Approximately 10% of patients will experience notable protracted withdrawal symptoms, which can include panic disorder, after discontinuation of benzodiazepines. Protracted withdrawal symptoms tend to resemble those seen during the first couple of months of withdrawal but usually are of a subacute level of severity compared to the symptoms seen during the first 2 or 3 months of withdrawal. It is not known definitively whether such symptoms persisting long after withdrawal are related to true pharmacological withdrawal or whether they are due to structural neuronal damage as result of chronic use of benzodiazepines or withdrawal. Nevertheless, such symptoms do typically lessen as the months and years go by eventually disappearing altogether.
A significant proportion of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia have developed these conditions as a result of alcohol or sedative abuse. Anxiety may pre-exist alcohol or sedative dependence, which then acts to perpetuate or worsen the underlying anxiety disorder. Someone suffering the toxic effects of alcohol abuse or chronic sedative use or abuse will not benefit from other therapies or medications for underlying psychiatric conditions as they do not address the root cause of the symptoms. Recovery from sedative symptoms may temporarily worsen during alcohol withdrawal or benzodiazepine withdrawal.
Obsessive–compulsive disorder (OCD, F42 in ICD-10) is a mental disorder in which a person feels the need to perform certain routines repeatedly (called “compulsions”), or has certain thoughts repeatedly (called “obsessions”). The person is unable to control either the thoughts or activities for more than a short period of time. Common compulsions include hand washing, counting of things, and checking to see if a door is locked. Some may have difficulty throwing things out. These activities occur to such a degree that the person’s daily life is negatively affected, often taking up more than an hour a day. Most adults realize that the behaviors do not make sense. The condition is associated with tics, anxiety disorder, and an increased risk of suicide.
The cause is unknown. There appear to be some genetic components, with both identical twins more often affected than both non-identical twins. Risk factors include a history of child abuse or other stress-inducing event. Some cases have been documented to occur following infections. The diagnosis is based on the symptoms and requires ruling out other drug-related or medical causes. Rating scales such as the Yale–Brown Obsessive Compulsive Scale (Y-BOCS) can be used to assess the severity. Other disorders with similar symptoms include anxiety disorder, major depressive disorder, eating disorders, tic disorders, and obsessive–compulsive personality disorder.
Treatment involves psychotherapy, such as cognitive behavioral therapy (CBT), and sometimes antidepressants, such as selective serotonin reuptake inhibitors (SSRIs) or clomipramine. CBT for OCD involves increasing exposure to what causes the problems while not allowing the repetitive behavior to occur. Contrary to this, Metacognitive therapy encourages the ritual behaviors as to alter the relationship to ones thoughts about them. While clomipramine appears to work as well as SSRIs, it has greater side effects and thus is typically reserved as a second-line treatment. Atypical antipsychotics may be useful when used in addition to an SSRI in treatment-resistant cases but are also associated with an increased risk of side effects. Without treatment, the condition often lasts decades.
Obsessive–compulsive disorder affects about 2.3% of people at some point in their lives. Rates during a given year are about 1.2%, and it occurs worldwide It is unusual for symptoms to begin after the age of 35, and half of people develop problems before 20. Males and females are affected about equally. The phrase obsessive–compulsive is sometimes used in an informal manner unrelated to OCD to describe someone as being excessively meticulous, perfectionistic, absorbed, or otherwise fixated.
OCD can present with a wide variety of symptoms. Certain groups of symptoms usually occur together. These groups are sometimes viewed as dimensions or clusters that may reflect an underlying process. The standard assessment tool for OCD, the Yale–Brown Obsessive Compulsive Scale (Y-BOCS), has 13 predefined categories of symptoms. These symptoms fit into three to five groupings. A meta-analytic review of symptom structures found a four-factor structure (grouping) to be most reliable. The observed groups included a “symmetry factor”, a “forbidden thoughts factor”, a “cleaning factor”, and a “hoarding factor”. The “symmetry factor” correlated highly with obsessions related to ordering, counting, and symmetry, as well as repeating compulsions. The “forbidden thoughts factor” correlated highly with intrusive and distressing thoughts of a violent, religious, or sexual nature. The “cleaning factor” correlated highly with obsessions about contamination and compulsions related to cleaning. The “hoarding factor” only involved hoarding-related obsessions and compulsions and was identified as being distinct from other symptom groupings.
While OCD has been considered a homogeneous disorder from a neuropsychological perspective, many of the putative neuropsychological deficits may be due to comorbid disorders. Furthermore, some subtypes have been associated with improvement in performance on certain tasks such as pattern recognition (washing subtype) and spatial working memory (obsessive thought subtype). Subgroups have also been distinguished by neuroimaging findings and treatment response. Neuroimaging studies on this have been too few, and the subtypes examined have differed too much to draw any conclusions. On the other hand, subtype-dependent treatment response has been studied, and the hoarding subtype has consistently responded least to treatment.
Obsessions are thoughts that recur and persist despite efforts to ignore or confront them. People with OCD frequently perform tasks, or compulsions, to seek relief from obsession-related anxiety. Within and among individuals, the initial obsessions, or intrusive thoughts, vary in their clarity and vividness. A relatively vague obsession could involve a general sense of disarray or tension accompanied by a belief that life cannot proceed as normal while the imbalance remains. A more intense obsession could be a preoccupation with the thought or image of someone close to them dying or intrusions related to “relationship rightness“. Other obsessions concern the possibility that someone or something other than oneself—such as God, the devil, or disease—will harm either the person with OCD or the people or things that the person cares about. Other individuals with OCD may experience the sensation of invisible protrusions emanating from their bodies or have the feeling that inanimate objects are ensouled.
Some people with OCD experience sexual obsessions that may involve intrusive thoughts or images of “kissing, touching, fondling, oral sex, anal sex, intercourse, incest, and rape” with “strangers, acquaintances, parents, children, family members, friends, coworkers, animals, and religious figures”, and can include “heterosexual or homosexual content” with persons of any age. As with other intrusive, unpleasant thoughts or images, some disquieting sexual thoughts at times are normal, but people with OCD may attach extraordinary significance to the thoughts. For example, obsessive fears about sexual orientation can appear to the person with OCD, and even to those around them, as a crisis of sexual identity. Furthermore, the doubt that accompanies OCD leads to uncertainty regarding whether one might act on the troubling thoughts, resulting in self-criticism or self-loathing.
Most people with OCD understand that their notions do not correspond with reality; however, they feel that they must act as though their notions are correct. For example, an individual who engages in compulsive hoarding might be inclined to treat inorganic matter as if it had the sentience or rights of living organisms, while accepting that such behavior is irrational on a more intellectual level. There is a debate as to whether or not hoarding should be considered with other OCD symptoms.
OCD sometimes manifests without overt compulsions, referred to as Primarily Obsessional OCD. OCD without overt compulsions could, by one estimate, characterize as many as 50 percent to 60 percent of OCD cases.
Some people with OCD perform compulsive rituals because they inexplicably feel they have to, while others act compulsively so as to mitigate the anxiety that stems from particular obsessive thoughts. The person might feel that these actions somehow either will prevent a dreaded event from occurring or will push the event from their thoughts. In any case, the individual’s reasoning is so idiosyncratic or distorted that it results in significant distress for the individual with OCD or for those around them. Excessive skin picking, hair-pulling, nail biting, and other body-focused repetitive behavior disorders are all on the obsessive–compulsive spectrum. Some individuals with OCD are aware that their behaviors are not rational, but feel compelled to follow through with them to fend off feelings of panic or dread.
Some common compulsions include hand washing, cleaning, checking things (e.g., locks on doors), repeating actions (e.g., turning on and off switches), ordering items in a certain way, and requesting reassurance. Compulsions are different from tics (such as touching, tapping, rubbing, or blinking) and stereotyped movements (such as head banging, body rocking, or self-biting), which usually are not as complex and are not precipitated by obsessions. It can sometimes be difficult to tell the difference between compulsions and complex tics. About 10% to 40% of individuals with OCD also have a lifetime tic disorder.
People rely on compulsions as an escape from their obsessive thoughts; however, they are aware that the relief is only temporary, that the intrusive thoughts will soon return. Some people use compulsions to avoid situations that may trigger their obsessions. Although some people do certain things over and over again, they do not necessarily perform these actions compulsively. For example, bedtime routines, learning a new skill, and religious practices are not compulsions. Whether or not behaviors are compulsions or mere habit depends on the context in which the behaviors are performed. For example, arranging and ordering DVDs for eight hours a day would be expected of one who works in a video store, but would seem abnormal in other situations. In other words, habits tend to bring efficiency to one’s life, while compulsions tend to disrupt it.
In addition to the anxiety and fear that typically accompanies OCD, sufferers may spend hours performing such compulsions every day. In such situations, it can be hard for the person to fulfill their work, family, or social roles. In some cases, these behaviors can also cause adverse physical symptoms. For example, people who obsessively wash their hands with antibacterial soap and hot water can make their skin red and raw with dermatitis.
People with OCD can use rationalizations to explain their behavior; however, these rationalizations do not apply to the overall behavior but to each instance individually. For example, a person compulsively checking the front door may argue that the time taken and stress caused by one more check of the front door is much less than the time and stress associated with being robbed, and thus checking is the better option. In practice, after that check, the person is still not sure and deems it is still better to perform one more check, and this reasoning can continue for as long as necessary.
The DSM-V contains three specifiers for the level of insight in OCD. Good or fair insight is characterized by the acknowledgment that obsessive-compulsive beliefs are or may not be true. Poor insight is characterized by the belief that obsessive-compulsive beliefs are probably true. Absence of insight makes obsessive-compulsive beliefs delusional thoughts, and occurs in about 4% of people with OCD.
Some people with OCD exhibit what is known as overvalued ideas. In such cases, the person with OCD will truly be uncertain whether the fears that cause them to perform their compulsions are irrational or not. After some discussion, it is possible to convince the individual that their fears may be unfounded. It may be more difficult to do ERP therapy on such people because they may be unwilling to cooperate, at least initially. There are severe cases in which the person has an unshakable belief in the context of OCD that is difficult to differentiate from psychotic disorders.
Though it was once believed to be associated with above-average intelligence, this does not appear to be the case. A 2013 review reported that people with OCD have mild but wide-ranging cognitive deficits; significantly regarding spatial memory, to a lesser extent with verbal memory, fluency, executive function, and processing speed, while auditory attention was not significantly affected. People with OCD show impairment in formulating an organizational strategy for coding information, set-shifting, and motor and cognitive inhibition.
Specific subtypes of symptom dimensions in OCD have been associated with specific cognitive deficits. For example, the results of one meta-analysis comparing washing and checking symptoms reported that washers outperformed checkers on eight out of ten cognitive tests. The symptom dimension of contamination and cleaning may be associated with higher scores on tests of inhibition and verbal memory.
Approximately 1–2% of children are affected by OCD. Obsessive–compulsive disorder symptoms tend to develop more frequently in children that are 10–14 years of age, with males displaying symptoms at an earlier age and a more severe level than the females. In children, symptoms can be grouped into at least four types.
People with OCD may be diagnosed with other conditions, as well as or instead of OCD, such as the aforementioned obsessive–compulsive personality disorder, major depressive disorder, bipolar disorder, generalized anxiety disorder, anorexia nervosa, social anxiety disorder, bulimia nervosa, Tourette syndrome, transformation obsession, autism spectrum disorder, attention deficit hyperactivity disorder, dermatillomania (compulsive skin picking), body dysmorphic disorder and trichotillomania (hair pulling). More than 50 percent of people experience suicidal tendencies, and 15 percent have attempted suicide. Depression, anxiety and prior suicide attempts increase the risk of future suicide attempts.
Individuals with OCD have also been found to be affected by delayed sleep phase syndrome at a substantially higher rate than the general public. Moreover, severe OCD symptoms are consistently associated with greater sleep disturbance. Reduced total sleep time and sleep efficiency have been observed in people with OCD, with delayed sleep onset and offset and an increased prevalence of delayed sleep phase disorder.
Behaviorally, there is some research demonstrating a link between drug addiction and the disorder as well. For example, there is a higher risk of drug addiction among those with any anxiety disorder (possibly as a way of coping with the heightened levels of anxiety), but drug addiction among people with OCD may serve as a type of compulsive behavior and not just as a coping mechanism. Depression is also extremely prevalent among people with OCD. One explanation for the high depression rate among OCD populations was posited by Mineka, Watson and Clark (1998), who explained that people with OCD (or any other anxiety disorder) may feel depressed because of an “out of control” type of feeling.
Someone exhibiting OCD signs does not necessarily have OCD. Behaviors that present as (or seem to be) obsessive or compulsive can also be found in a number of other conditions as well, including obsessive–compulsive personality disorder (OCPD), autism spectrum disorder, disorders where perseveration is a possible feature (ADHD, PTSD, bodily disorders or habit problems) or sub-clinically.
Some with OCD present with features typically associated with Tourette’s syndrome, such as compulsions that may appear to resemble motor tics; this has been termed “tic-related OCD” or “Tourettic OCD”.
OCD frequently co-occurs with both bipolar disorder and major depressive disorder. Between 60–80% of those with OCD experience a major depressive episode in their lifetime. Comorbidity rates have been reported at between 19–90% due to methodological differences. Between 9–35% of those with bipolar disorder also have OCD, compared to the 1–2% in the general population. Around 50% of those with OCD experience cyclothymic traits or hypomanic episodes. OCD is also associated with anxiety disorders. Lifetime comorbidity for OCD has been reported at 22% for specific phobia, 18% for social anxiety disorder, 12% for panic disorder, and 30% for generalized anxiety disorder. The comorbidity rate for OCD and ADHD has been reported as high as 51%.
There appear to be some genetic components with identical twins more often affected than non-identical twins. Further, individuals with OCD are more likely to have first-degree family members exhibiting the same disorders than do matched controls. In cases where OCD develops during childhood, there is a much stronger familial link in the disorder than cases in which OCD develops later in adulthood. In general, genetic factors account for 45–65% of the variability in OCD symptoms in children diagnosed with the disorder. A 2007 study found evidence supporting the possibility of a heritable risk for OCD.
A systematic review found that while neither allele was associated with OCD overall, in caucasians the L allele was associated with OCD. Another meta analysis observed an increased risk in those with the homozygous S allele, but found the LS genotype to be inversely associated with OCD.
A genome wide association study found OCD to be linked with SNPs near BTBD3 and two SNPs in DLGAP1 in a trio-based analysis, but no SNP reached significance when analyzed with case-control data.
One meta analysis found a small but significant association between a polymorphism in SLC1A1 and OCD.
The relationship between OCD and COMT has been inconsistent, with one meta analysis reporting a significant association, albeit only in men, and another meta analysis reporting no association.
It has been postulated by evolutionary psychologists that moderate versions of compulsive behavior may have had evolutionary advantages. Examples would be moderate constant checking of hygiene, the hearth or the environment for enemies. Similarly, hoarding may have had evolutionary advantages. In this view OCD may be the extreme statistical “tail” of such behaviors, possibly due to a high amount of predisposing genes.
A controversial hypothesis is that some cases of rapid onset of OCD in children and adolescents may be caused by a syndrome connected to Group A streptococcal infections, known as pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).
A review of studies examining anti-basal ganglia antibodies in OCD found an increased risk of having anti-basal ganglia antibodies in those with OCD versus the general population.
Anorexia nervosa, often referred to simply as anorexia, is an eating disorder, characterized by low weight, food restriction, fear of gaining weight, and a strong desire to be thin. Many people with anorexia see themselves as overweight even though they are, in fact, underweight. They often deny that they have a problem with low weight. They weigh themselves frequently, eat small amounts, and only eat certain foods. Some exercise excessively, force themselves to vomit, or use laxatives to produce weight loss. Complications may include osteoporosis, infertility, and heart damage, among others. Women will often stop having menstrual periods. In extreme cases, people with anorexia who continually refuse significant dietary intake and weight restoration interventions may be fed by force under restraint via nasogastric tube within specialist psychiatric hospitals.
The cause is currently unknown.There appear to be some genetic components with identical twins more often affected than non-identical twins. Cultural factors also appear to play a role with societies that value thinness having higher rates of disease. Additionally, it occurs more commonly among those involved in activities that value thinness such as high-level athletics, modelling, and dancing. Anorexia often begins following a major life-change or stress-inducing event. The diagnosis requires a significantly low weight. The severity of disease is based on body mass index (BMI) in adults with mild disease having a BMI of greater than 17, moderate a BMI of 16 to 17, severe a BMI of 15 to 16, and extreme a BMI less than 15. In children a BMI for age percentile of less than the 5th percentile is often used.
Treatment of anorexia involves restoring a healthy weight, treating the underlying psychological problems, and addressing behaviors that promote the problem. While medications do not help with weight gain, they may be used to help with associated anxiety or depression. A number of types of therapy may be useful, such as cognitive behavioral therapy or an approach where parents assume responsibility for feeding their child known as Maudsley family therapy. Sometimes people require admission to a hospital to restore weight. Evidence for benefit from nasogastric tube feeding, however is unclear; such an intervention may be highly distressing for both anorexia patients and healthcare staff when administered against the patient’s will under restraint. Some people with anorexia will just have a single episode and recover while others may have many episodes over years. Many complications improve or resolve with regaining of weight.
Globally, anorexia is estimated to affect 2.9 million people as of 2015. It is estimated to occur in 0.9% to 4.3% of women and 0.2% to 0.3% of men in Western countries at some point in their life. About 0.4% of young women are affected in a given year and it is estimated to occur ten times more commonly among women than men. Rates in most of the developing world are unclear. Often it begins during the teen years or young adulthood. While anorexia became more commonly diagnosed during the 20th century it is unclear if this was due to an increase in its frequency or simply better diagnosis. In 2013 it directly resulted in about 600 deaths globally, up from 400 deaths in 1990. Eating disorders also increase a person’s risk of death from a wide range of other causes, including suicide. About 5% of people with anorexia die from complications over a ten-year period, a nearly six times increased risk. The term “anorexia nervosa” was first used in 1873 by William Gull to describe this condition.
Anorexia nervosa is an eating disorder characterized by attempts to lose weight, to the point of starvation. A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may vary and may be present but not readily apparent.
Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause complications in every major organ system in the body Hypokalaemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa. A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage and paralysis.
Symptoms may include:
Interoception involves the conscious and unconscious sense of the internal state of the body, and it has an important role in homeostasis and regulation of emotions. Aside from noticeable physiological dysfunction, interoceptive deficits also prompt individuals with anorexia to concentrate on distorted perceptions of multiple elements of their body image. This exists in both people with anorexia and in healthy individuals due to impairment in interoceptive sensitivity and interoceptive awareness.
Aside from weight gain and outer appearance, people with anorexia also report abnormal bodily functions such as indistinct feelings of fullness. This provides an example of miscommunication between internal signals of the body and the brain. Due to impaired interoceptive sensitivity, powerful cues of fullness may be detected prematurely in highly sensitive individuals, which can result in decreased calorie consumption and generate anxiety surrounding food intake in anorexia patients. People with anorexia also report difficulty identifying and describing their emotional feelings and the inability to distinguish emotions from bodily sensations in general, called alexithymia.
Interoceptive awareness and emotion are deeply intertwined, and could mutually impact each other in abnormalities. Anorexia patients also exhibit emotional regulation difficulties that ignite emotionally-cued eating behaviors, such as restricting food or excessive exercising. Impaired interoceptive sensitivity and interoceptive awareness can lead anorexia patients to adapt distorted interpretations of weight gain that are cued by physical sensations related to digestion (e.g., fullness). Combined, these interoceptive and emotional elements could together trigger maladaptive and negatively reinforced behavioral responses that assist in the maintenance of anorexia. In addition to metacognition, people with anorexia also have difficulty with social cognition including interpreting others’ emotions, and demonstrating empathy. Abnormal interoceptive awareness and interoceptive sensitivity shown through all of these examples have been observed so frequently in anorexia that they have become key characteristics of the illness.
Other psychological issues may factor into anorexia nervosa; some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Some people have a previous disorder which may increase their vulnerability to developing an eating disorder and some develop them afterwards. The presence of Axis I or Axis II psychiatric comorbidity has been shown to affect the severity and type of anorexia nervosa symptoms in both adolescents and adults.
Obsessive-compulsive disorder (OCD) and obsessive-compulsive personality disorder (OCPD) are highly comorbid with AN, particularly the restrictive subtype. OCPD is linked with more severe symptomatology and worse prognosis. The causality between personality disorders and eating disorders has yet to be fully established. Other comorbid conditions include depression, alcoholism, borderline and other personality disorders, anxiety disorders, attention deficit hyperactivity disorder, and body dysmorphic disorder (BDD). Depression and anxiety are the most common comorbidities, and depression is associated with a worse outcome.
Autism spectrum disorders occur more commonly among people with eating disorders than in the general population. Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration.
Bulimia nervosa, also known as simply bulimia, is an eating disorder characterized by binge eating followed by purging. Binge eating refers to eating a large amount of food in a short amount of time. Purging refers to the attempts to get rid of the food consumed. This may be done by vomiting or taking laxatives. Other efforts to lose weight may include the use of diuretics, stimulants, water fasting, or excessive exercise. Most people with bulimia are at a normal weight. The forcing of vomiting may result in thickened skin on the knuckles and breakdown of the teeth. Bulimia is frequently associated with other mental disorders such as depression, anxiety, and problems with drugs or alcohol. There is also a higher risk of suicide and self-harm.
Bulimia is more common among those who have a close relative with the condition. The percentage risk that is estimated to be due to genetics is between 30% and 80%. Other risk factors for the disease include psychological stress, cultural pressure to attain a certain body type, poor self-esteem, and obesity. Living in a culture that promotes dieting and having parents that worry about weight are also risks. Diagnosis is based on a person’s medical history; however, this is difficult, as people are usually secretive about their binge eating and purging habits. Further, the diagnosis of anorexia nervosa takes precedence over that of bulimia. Other similar disorders include binge eating disorder, Kleine-Levin syndrome, and borderline personality disorder.
Cognitive behavioral therapy is the primary treatment for bulimia. Antidepressants of the selective serotonin reuptake inhibitor (SSRI) or tricyclic antidepressant classes may have a modest benefit. While outcomes with bulimia are typically better than in those with anorexia, the risk of death among those affected is higher than that of the general population. At 10 years after receiving treatment about 50% of people are fully recovered.
Globally, bulimia was estimated to affect 3.6 million people in 2015. About 1% of young women have bulimia at a given point in time and about 2% to 3% of women have the condition at some point in their lives. The condition is less common in the developing world. Bulimia is about nine times more likely to occur in women than men. Among women, rates are highest in young adults. Bulimia was named and first described by the British psychiatrist Gerald Russell in 1979
Bulimia typically involves rapid and out-of-control eating, which may stop when the person is interrupted by another person or the stomach hurts from over-extension, followed by self-induced vomiting or other forms of purging. This cycle may be repeated several times a week or, in more serious cases, several times a day and may directly cause:
These are some of the many signs that may indicate whether someone has bulimia nervosa
As with many psychiatric illnesses, delusions can occur, in conjunction with other signs and symptoms, leaving the person with a false belief that is not ordinarily accepted by others.
People with bulimia nervosa may also exercise to a point that excludes other activities.
People with bulimia exhibit several interoceptive deficits, in which one experiences impairment in recognizing and discriminating between internal sensations, feelings, and emotions. People with bulimia may also react negatively to somatic and affective states. In relation to interoceptive sensitivity, hyposensitive individuals may not detect feelings of fullness in a normal and timely fashion, and therefore are prone to eating more calories.
Examining from a neural basis also connects elements of interoception and emotion; notable overlaps occur in the medial prefrontal cortex, anterior and posterior cingulate, and anterior insula cortices, which are linked to both interoception and emotional eating.
People with bulimia are more likely than people without bulimia to have an affective disorder, such as depression or general anxiety disorder. One study found 70% had depression at some time in their lives (as opposed to 26% for adult females in the general population), rising to 88% for all affective disorders combined.Another study by the Royal Children’s Hospital in Melbourne on a cohort of 2,000 adolescents similarly found that those meeting at least two of the DSM-IV criteria for bulimia nervosa or anorexia nervosa had a sixfold increase in risk of anxiety and a doubled risk for substance dependency. Some with anorexia nervosa exhibit episodes of bulimic tendencies through purging (either through self-induced vomiting or laxatives) as a way to quickly remove food in their system. There may be an increased risk for diabetes mellitus type 2. Bulimia also has negative effects on a person’s teeth due to the acid passed through the mouth from frequent vomiting causing acid erosion, mainly on the posterior dental surface.
As with anorexia nervosa, there is evidence of genetic predispositions contributing to the onset of this eating disorder. Abnormal levels of many hormones, notably serotonin, have been shown to be responsible for some disordered eating behaviors. Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism.
There is evidence that sex hormones may influence appetite and eating in women, and the onset of bulimia nervosa. Studies have shown that women with hyperandrogenism and polycystic ovary syndrome have a dysregulation of appetite, along with carbohydrates and fats. This dysregulation of appetite is also seen in women with bulimia nervosa. In addition, gene knockout studies in mice have shown that mice that have the gene encoding estrogen receptors have decreased fertility due to ovarian dysfunction and dysregulation of androgen receptors. In humans, there is evidence that there is an association between polymorphisms in the ERβ (estrogen receptor β) and bulimia, suggesting there is a correlation between sex hormones and bulimia nervosa.
Bulimia has been compared to drug addiction, though the empirical support for this characterization is limited. However, people with bulimia nervosa may share dopamine D2 receptor-related vulnerabilities with those with substance abuse disorders.
Dieting, a common behaviour in bulimics, is associated with lower plasma tryptophan levels. Decreased tryptophan levels in the brain, and thus the synthesis of serotonin, increases bulimic urges in currently and formerly bulimic individuals within hours.
Abnormal blood levels of peptides important for the regulation of appetite and energy balance are observed in individuals with bulimia nervosa, but it remains unknown if this is a state or trait.
Media portrayals of an ‘ideal’ body shape are widely considered to be a contributing factor to bulimia. In a 1991 study by Weltzin, Hsu, Pollicle, and Kaye, it was stated that 19% of bulimics undereat, 37% of bulimics eat an average or normal amount of food, and 44% of bulimics overeat. A survey of 15- to 18-year-old high school girls in Nadroga, Fiji, found the self-reported incidence of purging rose from 0% in 1995 (a few weeks after the introduction of television in the province) to 11.3% in 1998. In addition, the suicide rate among people with bulimia nervosa is 7.5 times higher than in the general population.
When attempting to decipher the origin of bulimia nervosa in a cognitive context, Christopher Fairburn et al.‘s cognitive behavioral model is often considered the golden standard. Fairburn et al.’s model discusses the process in which an individual falls into the binge-purge cycle and thus develops bulimia. Fairburn et al. argue that extreme concern with weight and shape coupled with low self-esteem will result in strict, rigid, and inflexible dietary rules. Accordingly, this would lead to unrealistically restricted eating, which may consequently induce an eventual “slip” where the individual commits a minor infraction of the strict and inflexible dietary rules. Moreover, the cognitive distortion due to dichotomous thinking leads the individual to binge. The binge subsequently should trigger a perceived loss of control, promoting the individual to purge in hope of counteracting the binge. However, Fairburn et al. assert the cycle repeats itself, and thus consider the binge-purge cycle to be self-perpetuating.
In contrast, Byrne and Mclean’s findings differed slightly from Fairburn et al.‘s cognitive behavioral model of bulimia nervosa in that the drive for thinness was the major cause of purging as a way of controlling weight. In turn, Byrne and Mclean argued that this makes the individual vulnerable to binging, indicating that it is not a binge-purge cycle but rather a purge-binge cycle in that purging comes before bingeing. Similarly, Fairburn et al.‘s cognitive behavioral model of bulimia nervosa is not necessarily applicable to every individual and is certainly reductionist. Everyone differs from another, and taking such a complex behavior like bulimia and applying the same one theory to everyone would certainly be invalid. In addition, the cognitive behavioral model of bulimia nervosa is very cultural bound in that it may not be necessarily applicable to cultures outside of the Western society. To evaluate, Fairburn et al..’s model and more generally the cognitive explanation of bulimia nervosa is more descriptive than explanatory, as it does not necessarily explain how bulimia arises. Furthermore, it is difficult to ascertain cause and effect, because it may be that distorted eating leads to distorted cognition rather than vice versa.
A considerable amount of literature has identified a correlation between sexual abuse and the development of bulimia nervosa. The reported incident rate of unwanted sexual contact is higher among those with bulimia nervosa than anorexia nervosa.
When exploring the etiology of bulimia through a socio-cultural perspective, the “thin ideal internalization” is significantly responsible. The thin ideal internalization is the extent to which individuals adapt to the societal ideals of attractiveness. Studies have shown that young females that read fashion magazines tend to have more bulimic symptoms than those females who do not. This further demonstrates the impact of media on the likelihood of developing the disorder. Individuals first accept and “buy into” the ideals, and then attempt to transform themselves in order to reflect the societal ideals of attractiveness. J. Kevin Thompson and Eric Stice claim that family, peers, and most evidently media reinforce the thin ideal, which may lead to an individual accepting and “buying into” the thin ideal. In turn, Thompson and Stice assert that if the thin ideal is accepted, one could begin to feel uncomfortable with their body shape or size since it may not necessarily reflect the thin ideal set out by society. Thus, people feeling uncomfortable with their bodies may result in suffering from body dissatisfaction and may develop a certain drive for thinness. Consequently, body dissatisfaction coupled with a drive for thinness is thought to promote dieting and negative effects, which could eventually lead to bulimic symptoms such as purging or bingeing. Binges lead to self-disgust which causes purging to prevent weight gain.
A study dedicated to investigating the thin ideal internalization as a factor of bulimia nervosa is Thompson’s and Stice’s research. The aim of their study was to investigate how and to what degree media affects the thin ideal internalization. Thompson and Stice used randomized experiments (more specifically programs) dedicated to teaching young women how to be more critical when it comes to media, in order to reduce thin ideal internalization. The results showed that by creating more awareness of the media’s control of the societal ideal of attractiveness, the thin ideal internalization significantly dropped. In other words, less thin ideal images portrayed by the media resulted in less thin ideal internalization. Therefore, Thompson and Stice concluded that media greatly affected the thin ideal internalization. Papies showed that it is not the thin ideal itself, but rather the self-association with other persons of a certain weight that decide how someone with bulimia nervosa feels. People that associate themselves with thin models get in a positive attitude when they see thin models and people that associate with overweight get in a negative attitude when they see thin models. Moreover, it can be taught to associate with thinner people.
The onset of bulimia nervosa is often during adolescence, between 13 and 20 years of age, and many cases have previously suffered from obesity, with many sufferers relapsing in adulthood into episodic bingeing and purging even after initially successful treatment and remission. A lifetime prevalence of 0.5 percent and 0.9 percent for adult and adolescent sufferers, respectively, is estimated among the United States population. Bulimia nervosa may affect up to 1% of young women and, after 10 years of diagnosis, half will recover fully, a third will recover partially, and 10–20% will still have symptoms.
Adolescents with bulimia nervosa are more likely to have self-imposed perfectionism and compulsivity issues in eating compared to their peers. This means that the high expectations and unrealistic goals that these individuals set for themselves are internally motivated rather than by social views or expectations.
Bulimia nervosa can be difficult to detect, compared to anorexia nervosa, because bulimics tend to be of average or slightly above average weight. Many bulimics may also engage in significantly disordered eating and exercise patterns without meeting the full diagnostic criteria for bulimia nervosa. Recently, the Diagnostic and Statistical Manual of Mental Disorders was revised, which resulted in the loosening of criteria regarding the diagnoses of bulimia nervosa and anorexia nervosa. The diagnostic criteria utilized by the DSM-5 includes repetitive episodes of binge eating (a discrete episode of overeating during which the individual feels out of control of consumption) compensated for by excessive or inappropriate measures taken to avoid gaining weight. The diagnosis also requires the episodes of compensatory behaviors and binge eating to happen a minimum of once a week for a consistent time period of 3 months. The diagnosis is made only when the behavior is not a part of the symptom complex of anorexia nervosa and when the behavior reflects an overemphasis on physical mass or appearance. Purging often is a common characteristic of a more severe case of bulimia nervosa.
Autism spectrum, also known as autism spectrum disorder (ASD), is a range of neurodevelopmental disorders. It included autism and Asperger syndrome and other neurodevelopmental disorders until 2013 when all disorders under ASD were reclassified as ASD instead of as individual disorders. Individuals on the autistic spectrum experience difficulties with social communication and interaction and also exhibit restricted, repetitive patterns of behavior, interests, or activities. Symptoms are typically recognized between one and two years of age. Long-term problems may include difficulties in performing daily tasks, creating and keeping relationships, and maintaining a job.
The cause of autism spectrum is uncertain. Risk factors include having an older parent, a family history of autism, and certain genetic conditions. It is estimated that between 64% and 91% of risk is due to family history. Diagnosis is based on symptoms. In 2013, the Statistical Manual of Mental Disorders version 5 (DSM-5) replaced the previous subgroups of autistic disorder, Asperger syndrome, pervasive developmental disorder not otherwise specified (PDD-NOS), and childhood disintegrative disorder with the single term “autism spectrum disorder”.
Treatment efforts are generally individualized and can include behavioural therapy and the teaching of coping skills. Medications may be used to try to help improve symptoms. Evidence to support the use of medications, however, is not very strong.
Autism spectrum is estimated to affect about 1% of people (62.2 million globally) as of 2015. In the United States it is estimated to affect more than 2% of children (about 1.5 million) as of 2016. Males are diagnosed four times more often than females. The term “spectrum” refers to the variation in the type and severity of symptoms. Those in the mild range may function independently, while those with moderate to severe symptoms may require substantial support in their daily lives.
Learning disability, learning disorder or learning difficulty is a condition in the brain that causes difficulties comprehending or processing information and can be caused by several different factors. Given the “difficulty learning in a typical manner”, this does not exclude the ability to learn in a different manner. Therefore, some people can be more accurately described as having a “learning difference”, thus avoiding any misconception of being disabled with a lack of ability to learn and possible negative stereotyping. In the United Kingdom, the term “learning disability” generally refers to an intellectual disability, while difficulties such as dyslexia and dyspraxia are usually referred to as “learning difficulties”.
While learning disability, learning disorder and learning difficulty are often used interchangeably, they differ in many ways. Disorder refers to significant learning problems in an academic area. These problems, however, are not enough to warrant an official diagnosis. Learning disability, on the other hand, is an official clinical diagnosis, whereby the individual meets certain criteria, as determined by a professional (psychologist,speech language pathologist, pediatrician, psychiatrist etc.). The difference is in degree, frequency, and intensity of reported symptoms and problems, and thus the two should not be confused. When the term “learning disorder” is used, it describes a group of disorders characterized by inadequate development of specific academic, language, and speech skills. Types of learning disorders include reading (dyslexia), arithmetic (dyscalculia) and writing (dysgraphia).
The unknown factor is the disorder that affects the brain’s ability to receive and process information. This disorder can make it problematic for a person to learn as quickly or in the same way as someone who is not affected by a learning disability. People with a learning disability have trouble performing specific types of skills or completing tasks if left to figure things out by themselves or if taught in conventional ways.
Individuals with learning disabilities can face unique challenges that are often pervasive throughout the lifespan. Depending on the type and severity of the disability, interventions, and current technologies may be used to help the individual learn strategies that will foster future success. Some interventions can be quite simplistic, while others are intricate and complex. Current technologies may require student training to be effective classroom supports. Teachers, parents, and schools can create plans together that tailor intervention and accommodations to aid the individuals in successfully becoming independent learners. A multi-disciplinary team frequently helps to design the intervention and to coordinate the execution of the intervention with teachers and parents. This team frequently includes school psychologists, special educators, speech therapists (pathologists), occupational therapists, psychologists, ESL teachers, literacy coaches, and/or reading specialists.