For more information on attention deficit (hyperactivity) disorder (ADD or ADHD), visit Britannica.com.
A common psychiatric disorder of childhood characterized by attentional difficulties, impulsivity, and hyperactivity; known earlier as attention deficit disorder. Other older names for this disorder include minimal brain dysfunction, minimal brain damage, hyperactivity, hyperkinesis, and hyperactive child syndrome. Over time, these names were modified due to their implications about etiology and core symptoms: minimal brain dysfunction seemed to imply that children with this disorder were brain-damaged, while hyperactivity and its synonyms named a feature seen in many but not all of these children.
The three defining symptoms of attention deficit disorder are as follows:
(1) Attentional deficits. The child is described as having a short attention span. The child often fails to finish things he or she starts, does not seem to listen, and is easily distracted or disorganized. In more severe instances the child is unable to focus attention on anything, while in less severe cases attention can be focused on things of interest to the child.
(2) Impulsivity. The child is often described as acting before thinking, shifting excessively and rapidly from one activity to another, or having difficulty waiting for a turn in games or group activities.
(3) Hyperactivity. Many children with this disorder are hyperactive—and indeed, may have been noted to be so prior to birth. They may fidget, wiggle, move excessively, and have difficulty keeping still. This excessive activity is not noticeable when the children are playing; however, in the classroom or other quiet settings, the child cannot decrease his or her activity appropriately. Some affected children are active at a normal level or even sluggish. On the basis of the predominating symptoms, children with attention deficit hyperactivity disorder are subcategorized as having hyperactive symptoms (hyperactive type), lacking hyperactivity (inattentive type), and having both inattention and hyperactivity or impulsivity (combined type).
Many children with attention deficit hyperactivity disorder frequently show an altered response to socialization. They are often described by their parents as obstinate, impervious, stubborn, or negativistic. With peers, many affected children are domineering or bullying, and thus may prefer to play with younger children. Another characteristic often seen in children with the disorder is emotional lability. Their moods change frequently and easily, sometimes spontaneously, and sometimes reactively. Because of their behavioral difficulties, children with the disorder often have conflicts with parents, teachers, and peers. Commonly, difficulties in discipline and inadequacies in schoolwork lead to reproof and criticism. As a consequence, children with the disorder usually also have low self-esteem. Attention deficit hyperactivity disorder is frequently associated with other disorders, including disruptive behavior disorders, internalizing (mood and anxiety) disorders, and developmental disorders. See also Affective disorders.
Formerly believed to be largely caused by brain damage, and more recently believed by some to be caused by food allergy, attention deficit hyperactivity disorder is now considered to be mainly hereditary. It is estimated that 3–10% of children of elementary school age (roughly 6–19 years) manifest significant symptoms of attention deficit hyperactivity disorder. About twice as many boys as girls are affected with the disorder. The girls are much less likely than the boys to be aggressive and have serious behavioral difficulties, making the girls vulnerable to underidentification and undertreatment. It was formerly believed that attention deficit hyperactivity disorder was out-grown during adolescence. Although some signs of the disorder such as excessive activity may diminish or disappear in some affected children, other signs such as attentional difficulties, impulsivity, and interpersonal problems may persist. Despite the fact that this disorder is not uncommon in adults, the lower rates of hyperactivity in adults may result in the condition being frequently overlooked.
The treatment of the child or adult with this disorder involves three steps: evaluation, explanation of the problem to parents and child, and therapeutic intervention. Evaluation requires a detailed history of the child's psychological development and current functioning. Next, because the disorder is frequently associated with learning problems in school, it is desirable to obtain an individual intelligence test as well as a test of academic achievement. Since attention deficit hyperactivity disorder is often associated with other psychiatric disorders, it is important to carefully evaluate the presence of these other conditions. If a diagnosis of attention deficit hyperactivity disorder is confirmed, the parents or family should be educated regarding the nature of the condition and other associated conditions. Medication and guidance are the mainstays of the treatment. Approximately 70–80% of the children manifest a therapeutic response to one of the major stimulant drugs, such as amphetamines and methylphenidate. When effective, these medications increase attention, decrease impulsivity, and usually make the child more receptive to parental and educational requests and demands. Hyperactivity, when present, is usually diminished as well. Although usually less effective, other medications can be helpful to individuals who cannot tolerate or do not respond to stimulants. The common mechanism of action for such medications is their impact upon the neurotransmitters dopamine and norepinephrine.
Definition
Attention-deficit/hyperactivity disorder (AD/HD) is a neurobiological disorder characterized by hyperactivity, impulsive behavior, and the inability to remain focused on tasks or activities.
Description
AD/HD, also known as hyperkinetic disorder (HKD) outside of the United States, is estimated to affect 3–7 percent of school-aged children, and seems to afflict boys more often than girls. However, the prevalence in boys may be cited because often girls are not diagnosed until later in age. Although difficult to assess in infancy and toddlerhood, signs of AD/HD may begin to appear as early as age two or three, but visible symptoms change as adolescence approaches. Many symptoms, particularly hyperactivity, diminish in early adulthood, while impulsivity and inattention problems often continue.
First documented in 1902, AD/HD has been called minimal brain dysfunction, hyperkinetic reaction, and attention-deficit disorder (ADD). The name AD/HD reflects the various behaviors of inattention, hyperactivity, and impulsiveness that characterize the disorder. Its more precise classification is a result of the Diagnostic and Statistical Manual, fourth edition (DSM-IV) system for characterizing and diagnosing mental and behavioral disorders.
Children with AD/HD have difficulties with inattention that can be manifest as a lack of concentration, an easily distracted focus, and an inability to know when and how long to focus. The characteristics of inattention vary with each AD/HD child; however, all most often translate into poor grades and difficulties in school and other social arenas. AD/HD children act impulsively, taking action first and thinking later. They are constantly moving, running, climbing, squirming, and fidgeting. Yet, they often have trouble with gross and fine motor skills and, as a result, they may be physically clumsy and awkward. Their clumsiness may also extend to their social skills. They are sometimes shunned by peers due to their impulsive and intrusive behavior.
Demographics
Of the 3–7 percent of school-aged children with AD/HD, some will have a reduction of symptoms as they reach adulthood. However, 65 percent of AD/HD children will continue to display characteristics of AD/HD through adulthood. Until recently, it was believed that boys were three times more likely to have AD/HD; however, that gap has been narrowed. It is more likely that the presence of AD/HD is distributed equally between boys and girls. The reason for the discrepancy was, in part, because young boys tend to more readily and overtly manifest the characteristics of AD/HD, making diagnosis easier. In addition, the inattentive form affects girls more than the hyperactive form; as a result, girls may be less likely to be diagnosed.
Causes and Symptoms
The causes of AD/HD are not specifically known. However, it is a neurologically based disease that may be genetic. Children with an AD/HD parent or sibling are more likely to develop the disorder themselves. Although the exact cause of AD/HD is not known, an imbalance or deficiency of certain neurotransmitters—the chemicals in the brain that transmit messages between nerve cells—is believed to be the mechanism behind AD/HD symptoms.
A widely publicized study conducted by Dr. Ben Feingold in the early 1970s suggested that allergies to certain foods and food additives caused the characteristic hyperactivity of AD/HD children. By eliminating the food allergen, the premise was that AD/HD characteristics would disappear. Although some children may have adverse reactions to certain foods and food additives that can affect their behavior, carefully controlled follow-up studies have uncovered no link between food allergies and AD/HD. Another popularly held misconception about food and AD/HD is that the consumption of sugar causes the hyperactive behavior in an AD/HD child. Again, studies have shown no link between sugar intake and AD/HD. (In a recent study conducted by the National Institute of Mental Health, the level of glucose use in the brain was actually lower in individuals with AD/HD. Since glucose is the main source of fuel for the brain, this is a significant finding.) Finally, parenting style is not a cause for AD/HD. While certain parenting skills and/or deficiencies can affect the environment of an AD/HD child and, as a result, exasperate or help manage the characteristics of AD/HD, it appears that neurological issues are the primary causal agents at play.
In order to diagnose AD/HD, psychologists and other mental health professionals typically use the criteria listed in the DSM-IV. DSM-IV requires the presence of at least six of the following symptoms of inattention, or six or more symptoms of hyperactivity and impulsivity combined.
Inattention:
Hyperactivity:
Impulsivity:
Of those symptoms, AD/HD can be categorized further by three subtypes. Each subtype exhibits particular behaviors that make up the general symptoms of a child with AD/HD. They are:
AD/HD predominantly inattentive type (AD/HD-I)
AD/HD predominantly hyperactive-impulsive type (AD/HD-HI)
AD/HD combined type (AD/HD-C) is a combination of the symptoms exhibited by the other two subtypes (inattentive type and hyperactive-impulsive type). Also, for a complete diagnosis, DSM-IV requires that some symptoms develop before age seven, and that they significantly impair functioning in two or more settings (e.g., home and school) for a period of at least six months.
Diagnosis
AD/HD cannot be diagnosed with a laboratory test. Diagnosis is difficult and it takes into consideration many aspects of the child's behavior. Often the child's teacher is the one to bring the first signs to the attention of the parents. However, the first step in determining if a child has AD/HD is to consult with a pediatrician. The pediatrician can make an initial evaluation of the child's developmental maturity compared to other children in his or her age group. The physician should also perform a comprehensive physical examination to rule out any organic causes of AD/HD symptoms, such as an overactive thyroid or vision or hearing problems.
If no organic problem can be found, a psychologist, psychiatrist, neurologist, neuropsychologist, or learning specialist is typically consulted to perform a comprehensive AD/HD assessment. A complete medical, family, social, psychiatric, and educational history is compiled from existing medical and school records and from interviews with parents and teachers. Interviews may also be conducted with the child, depending on his or her age. Along with these interviews, several clinical inventories may also be used, such as the Conners' Rating Scales (Teacher's Questionnaire and Parent's Questionnaire), Child Behavior Checklist (CBCL), and the Achenbach Child Behavior Rating Scales. These inventories provide valuable information on the child's behavior in different settings and situations.
Other disorders such as depression, anxiety disorder, and learning disorders can cause symptoms similar to AD/HD. A complete and comprehensive psychiatric assessment is critical to differentiate AD/HD from other possible mood and behavioral disorders. Bipolar disorder, for example, may be misdiagnosed as AD/HD.
Public schools are required by federal law to offer free AD/HD testing upon request. A pediatrician can also provide a referral to a psychologist or pediatric specialist for AD/HD assessment. Parents should check with their insurance plans to see if these services are covered.
Treatment
Despite similar behavioral characteristics, AD/HD must be treated individually by developing an approach combining various types of treatment. The use of medication in combination with behavioral interventions, classroom accommodations, and proactive parents provide the best treatment option.
Psychostimulants and their effects have been studied in approximately 6,000 children and the positive results of their use have been documented. Such psychostimulants as dextroamphetamine (Dexedrine, Dextrostat), pemoline (Cylert), methylphenidate (Ritalin, Concerta, Metadate, Focalin), and mixed salts of a single-entity amphetamine product (Adderall, Adderall XR) are commonly prescribed to control hyperactive and impulsive behavior as well as to increase attention. They work by stimulating the production of certain neurotransmitters in the brain. Generally, short-acting medication lasts for four hours, while long-lasting preparations will last for six to eight hours. Some medication is effective for 10–12 hours. Specific dosages depend upon the patient and that is determined by trial and error in conjunction with close monitoring by a physician in order to find the most beneficial strength. Possible side effects of stimulants include nervous tics, irregular heartbeat, loss of appetite, and insomnia. However, the medications are usually tolerated and safe in most cases. In fact, 70–80 percent of AD/HD children respond well to psychostimulants.
In children who do not respond well to stimulant therapy, nonstimulant medications are prescribed. In 2002, the Food and Drug Administration (FDA)approved atomoxetine (Strattera) for the treatment of AD/HD. Unlike the stimulant medications, atomoxetine is not a controlled substance and can be prescribed with refills. (With the use of stimulant medication, the physician must write prescriptions each month of treatment.) Atomoxetine usually takes three to four weeks of use until its effect is evident. In January 2005 the FDA warned that evidence of atleast two cases of liver problems in an adult and teenage patient taking atomoxetine were reported. In both cases, the individuals fully recovered. The manufacturer of atomoxetine (Strattera) planned to notify users of the new FDA warning; however, the company, Eli Lilly & Co., believed that the risk-benefit analysis during trials of the drug was still positive. Such tricyclic antidepressants as desipramine (Norpramin, Pertofane) and amitriptyline (Elavil) are frequently recommended as well. Reported side effects of these drugs include persistent dry mouth, sedation, disorientation, and cardiac arrhythmia (particularly with desipramine).
Other medications prescribed for AD/HD therapy include buproprion (Wellbutrin), an antidepressant; fluoxetine (Prozac), an SSRI antidepressant; and carbamazepine (Tegretol, Atretol), an anticonvulsant drug. Clonidine (Catapres), an antihypertensive medication, has also been used to control aggression and hyperactivity in some AD/HD children, although it should not be used in combination with Ritalin.
A child's response to medication will change with age and maturation, so AD/HD symptoms should be monitored closely and prescriptions adjusted accordingly.
Behavior interventions are also crucial to AD/HD treatment. In a Nation Institute of Mental Health (NIMH) study conducted on 579 children over the course of 14 months it was observed that the children receiving AD/HD medication or both medication and behavioral interventions were more likely to see the most relief from their symptoms than those children that only received community aid. The use of a reward system to reinforce good behavior and task completion can be implemented both in the classroom and at home. A chart system may be used to visually illustrate the child's progress and encourage continued success with the use of larger rewards after a certain number of daily rewards are achieved. The reward system stays in place until the appropriate behavior becomes second nature to the child.
A variation of this technique, cognitive-behavioral therapy, works to decrease impulsive behavior by getting the child to recognize the connection between thoughts and behavior, and to change behavior by changing negative thinking patterns.
Individual psychotherapy can help an AD/HD child build self-esteem, give them a place to discuss their worries and anxieties, and help them gain insight into their behavior and feelings. Family therapy may also be beneficial in helping family members develop coping skills and in working through feelings of guilt or anger parents may be experiencing.
AD/HD children perform better within a familiar, consistent, and structured routine with an emphasis on positive reinforcements for good behavior and minimal use of punishments. When a negative behavior must be acknowledged and corrected, "time outs" give the child with AD/HD an opportunity to regroup without negative reinforcement. Family, friends, and caretakers should all be educated on the special needs and behaviors of the AD/HD child.
Alternative Treatment
A number of alternative treatments exist for AD/HD; however, there are very few studies to prove their efficacy. When choosing a treatment option, it is important to investigate authoritative sources that provide a basis through documented studies for the validity of the treatment. AD/HD is not a disorder that can be cured but rather it is one that is managed by a variety of treatment options. Some of the more popular alternative treatments include:
There are many advertised alternative and complementary treatment options for AD/HD. Only a few are listed here; however, it is always necessary to consult a physician to develop a fine-tuned treatment plan specific to each child's needs.
Nutritional Concerns
As mentioned, links between nutrition and AD/HD have not been confirmed through medical studies. However, it is important to note that a nutritionally balanced diet is important for normal development in all children.
Prognosis
Untreated, AD/HD negatively affects a child's social and educational performance and can seriously damage his or her self-esteem. Children with AD/HD have impaired relationships with their peers, and may be looked upon as social outcasts. They may be perceived as slow learners or troublemakers in the classroom. Siblings and even parents may develop resentful feelings towards the AD/HD child.
Some AD/HD children also develop a conduct disorder. For those adolescents who have both AD/HD and a conduct disorder, up to 25 percent go on to develop antisocial personality disorder and the criminal behavior, substance abuse, and high rate of suicide attempts that are symptomatic of it. Children diagnosed with AD/HD are also more likely to have a learning disorder, a mood disorder such as depression, or an anxiety disorder.
Approximately 70–80 percent of AD/HD patients treated with stimulant medication experience significant relief from symptoms, at least in the short-term. Approximately half of AD/HD children seem to "outgrow" the disorder in adolescence or early adulthood; the other half will retain some or all symptoms of AD/HD as adults. With early identification and intervention, careful compliance with a treatment program, and a supportive and nurturing home and school environment, children with AD/HD can flourish socially and academically.
Parental Concerns
Because AD/HD is often indicated when the AD/HD child is in school, parents are extremely concerned about their child's academic progress. Communication between parents and teachers is especially critical to ensure an AD/HD child has an appropriate learning environment. Educational interventions under Individuals with Disabilities Education Act (IDEA) and Section 504 of the Rehabilitation Act of 1973 mandate that AD/HD children will be served within the public school system. This means that upon request the public school is required to test the child for AD/HD as well as other learning disabilities if they are suspected. In addition, special education services are mandated for those children with AD/HD that need extra help and accommodation. It is important that parents assume a positive relationship with their child's educator and school in order to develop the best possible teaching strategies and learning environment for their AD/HD child.
Development of self-esteem is another particular concern for parents of AD/HD children. Because they often have difficulty in school and in social relationships, low self-esteem can be a factor that leads the school aged children toward dangerous or destructive behaviors as they reach adolescence. Finding one activity that the child excels at is essential in fostering a positive self-image. Often parents look to sports as an appropriate outlet. Individual sports such as karate, swimming, tennis, etc. are less socially demanding than team sports; yet they provide an opportunity for the child to thrive in a competitive activity.
AD/HD is a chronic condition. Parents can feel overwhelmed when they have to deal with AD/HD characteristics on a daily basis. Parent should face the issues honestly and directly while fostering a positive relationship with their AD/HD child. The best advocate the AD/HD child has is a parent so it is important that parents be proactive and keep up to date on the latest research. Learning about AD/HD and the various treatment options helps parents cope with their own concerns at the same time they are helping their child.
Resources
Books
Alexander-Roberts, Colleen. The ADHD Parenting Handbook: Practical Advice for Parents from Parents. Dallas: Taylor Publishing Co., 1994.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Press, Inc., 1994.
Barkley, Russell A. Taking Charge of ADHD. Revised Edition. New York: Guilford Press, 2000.
Hallowell, Edward M., and John J. Ratey. Driven to Distraction: Recognizing and Coping with Attention Deficit Disorder from Childhood Through Adulthood. New York: Touchstone, 1995.
Osman, Betty B. Learning Disabilities and ADHD: A Family Guide to Living and Learning Together. New York: John Wiley & Sons, 1997.
Periodicals
Foley, Kevin. "Experiencing Nature May Quell ADHD in Kids." Pediatric News 38 (Nov. 2004).
Franklin, Deeanna. "FDA Issues Warning for ADHD Drug." Pediatric News 39 (Jan. 2005):42.
Glicken, Anita D. "Attention Deficit Disorder and the Pediatric Patient: A Review." Physician Assistant 21, no. 4 (Apr. 1997):101-11.
Hallowell, Edward M. "What I've Learned from A.D.D." Psychology Today 30, no. 3 (May/June 1997): 40-6.
Swanson, J. M., et al. "Attention-deficit Hyperactivity Disorder and Hyperkinetic Disorder." The Lancet 351 (7 Feb. 1997): 429-33.
Organizations
American Academy of Child and Adolescent Psychiatry. (AACAP). 3615 Wisconsin Ave. NW, Washington, DC 20016. (202) 966-7300. Web site:
Children and Adults with Attention Deficit Disorder (CH.A.D.D.). 8181 Professional Place, Ste. 150, Landover, MD 20785. (800) 233-4050. (305) 306-7070.
National Attention Deficit Disorder Association. (ADDA). 9930 Johnnycake Ridge Road, Suite 3E, Mentor, OH 44060. (800) 487-2282. Web site:
Web Sites
Schwablearning.org: A Parent's Guide to Helping Kids with Learning Difficulties. (cited March 8, 2005). Available online at: www.schwablearning.org.
[Article by: Jacqueline L. Longe Paula A. Ford-Martin]
Attention deficit/hyperactivity disorder (ADHD) is a condition characterized by inattention and/or impulsivity and hyperactivity that begins in children prior to the age of seven. Their inattention leads to daydreaming, distractibility, and difficulties sustaining effort on a single task for a prolonged period of time. Their impulsivity disrupts classrooms and creates problems with peers, as they blurt out answers, interrupt others, or shift from schoolwork to inappropriate activities. Their hyperactivity is frustrating to those around them and poorly tolerated at school. Children with ADHD show academic underachievement and conduct problems. As they grow older, they are at risk for low self-esteem, poor peer relationships, conflict with parents, delinquency, smoking, and substance abuse.
Course, Prevalence, and Treatment
Although the longitudinal course of this condition and its prevalence in adulthood have been sources of controversy, a growing literature has documented the persistence of ADHD into adulthood, with about two-thirds of ADHD children continuing to experience impairing symptoms of the disorder though adulthood. Over time, symptoms of hyperactivity and impulsivity are more likely to diminish compared with symptoms of inattention.
Prevalence studies from North America, Europe, and Asia show that ADHD affects about 5 percent of the population. The impact of the disorder on society, in terms of financial cost, stress to families, and disruption in schools and workplaces, is enormous. Although current treatments for the disorder are not 100 percent effective, clinical trials have shown that stimulant medications, such as methylphenidate and amphetamine, relieve symptoms and lessen adverse outcomes, while showing few adverse side effects. Because these medicines increase the availability of the neurotransmitter dopamine in the brain, dysregulation of dopamine systems has been a primary candidate for the pathophysiology of ADHD. But drugs like desipramine and alomoxeline, which have their effects on other brain systems, also exert strong anti-ADHD effects. This suggests that dysregulation of dopamine systems cannot completely explain the pathophysiology of ADHD.
Neuropsychological and neuroimaging studies provide converging evidence for the hypothesis that brain dysfunction causes the symptoms of ADHD. Neuropsychological tests show many ADHD patients to have deficits in the executive functions needed for organizing, planning, sequencing, and inhibiting behaviors. These performance deficits are similar to, albeit milder than, the deficits seen among patients with frontal lobe disorders. Several structural and functional neuroimaging studies implicate networks of regions throughout the brain, not just in the frontal lobes.
The Genetic Epidemiology of Adhd
Family, twin, and adoption studies provide strong support for the idea that genes influence the etiology of ADHD. Family studies find the parents and siblings of ADHD children to have a five-fold increase in the risk for ADHD. Children of ADHD adults have a ten-fold increase in risk, which has led to the idea that persistent cases of ADHD may have a stronger genetic component. Consistent with a genetic theory of ADHD, second-degree relatives (such as cousins) are at increased risk for the disorder but their risk is lower than that seen in first-degree relatives.
Family studies have provided evidence for the genetic heterogeneity of ADHD. Studies that systematically assess other psychiatric disorders suggest that ADHD and major depression often occur together in families; that ADHD children with conduct and/or bipolar disorders might be a distinct familial subtype of ADHD; and that ADHD is familially independent from anxiety disorders and learning disabilities. It may therefore be appropriate to divide ADH children into those with and those without conduct and bipolar disorders, thus forming more familially homogeneous subgroups. In contrast, major depression may be a nonspecific manifestation of different ADHD subforms.
Several twin studies have provided evidence of genetic influence on hyperactive and inattentive symptoms. An early study found the heritability of hyperactivity to be 64 percent. A study of ADHD in twins who also had reading disabilities reported the heritability of attention-related behaviors to be 98 percent. All twin studies considered together suggest that the heritability of ADHD is about 70 percent, which makes it one of the most heritable of psychiatric disorders.
Adoption studies also implicate genes in the etiology of ADHD. Two early studies found that the adoptive relatives of hyperactive children were less likely to be hyperactive or have associated conditions than the biological relatives. Biological relatives of hyperactive children also performed more poorly on standardized measures of attention than did adoptive relatives. A study using the contemporary definition of ADHD found that biological, not adoptive, relationships account for the transmission of ADHD.
The Molecular Genetics of Adhd
Molecular genetic studies have already implicated several genes as mediating the susceptibility to ADHD. Researchers have examined candidate genes in dopamine pathways because animal models, theoretical considerations, and the effectiveness of stimulant treatment implicate dopaminergic dysfunction in the pathophysiology of this disorder. Dopamine is a neural trans-Dopamine mitter in the brain used in both movement control and pleasure/reward systems. In its simplest form, the dopamine hypothesis holds that excess clearance of dopamine between neurons may contribute to ADHD.
Many studies have focused on the D4 dopamine receptor gene (DRD4) which encodes a protein receptor that mediates the post-synaptic action of dopamine. A meta-analysis of these studies showed a small but statistically significant association, which could not be accounted for by any single study or by publication biases. Although the nature of the mutations in DRD4 have not been conclusively described, a version of the gene known as the 7repeat allele has generated much interest because this allele causes a blunted response to dopamine and has been implicated in novelty seeking, a personality trait of many ADHD patients.
Several authors have reported an association between ADHD and a particular allele of the dopamine transporter (DAT) gene. This finding has been replicated by some, but not all studies. The link between the DAT gene and ADHD is further supported by a study that relates this gene to poor methylphenidate response in humans, a "knockout" mouse study showing that its elimination leads to hyperactivity in mice, and two molecular neuroimaging studies that found elevated DAT density in the striatum of ADHD adults.
Molecular genetics studies of ADHD have also targeted other genes that are related to the dopamine system. Four studies have examined the Catechol-O-Methyltransferase (COMT) gene, whose protein product breaks down dopamine and norepinephrine. Although one study found ADHD was associated with the high-activity form of COMT, three others could not replicate the finding. Other candidate genes that show promising results for ADHD are the D5 dopamine receptor gene and the serotonin 1B receptor. This latter finding is intriguing because, although serotonergic medicines do not help ADHD symptoms, these systems have been implicated in animal models of the disorder.
Bibliography
Faraone, S. V., D. Tsuang, and M. T. Tsuang. Genetics of Mental Disorders: A Guide for Students, Clinicians, and Researchers. New York: Guilford, 1999.
Faraone, S. V., and A. Doyle. "The Nature and Heritability of Attention Deficit Hyperactivity Disorder." Child and Adolescent Psychiatric Clinics of North America 10 (2001): 299-316.
Faraone, S. V., and J. Biederman. "Neurobiology of Attention Deficit Hyperactivity Disorder." Biological Psychiatry 44 (1998): 951-958.
—Stephen V. Faraone
The cause of ADHD is unknown, although there appears to be a genetic component in some cases. Intake of sugars is no longer considered to be a factor. Some studies suggest that although food additives, such as colorings, do not cause symptoms in the general population, they may aggravate hyperactivity in some susceptible individuals. It has been shown that people with ADHD have less activity in areas of the brain that control attention. Treatment usually includes behavioral therapy and emotional counseling combined with medications such as methylphenidate hydrochloride (Ritalin) or dextroamphetamine (Dexedrine) that correct neurochemical imbalances in the brain; over the long term, however, such medications do not appear to offer any benefits. Symptoms may decrease after adolescence, although they often persist into adulthood.
The most common reason that children are referred to child-guidance clinics is for attention deficit hyperactivity disorder (ADHD). ADHD is a behavioral disorder with a strong hereditary component, which likely results from neurological dysfunction. According to the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Text Revision (DSM-IV-TR), there are three diagnostic categories of ADHD: (1) ADHD, Predominantly Inattentive Type; (2) ADHD, Predominantly Hyperactive-Impulsive Type; and (3) ADHD, Combined Type. ADHD often occurs simultaneously with other behavioral and learning problems, such as learning disabilities, emotional or behavioral disabilities, or Tourette's syndrome.
A 1998 study by Russell A. Barkley stated that ADHD is a deficit in behavior inhibition, which sets the stage for problems in regulating behavior. Students with ADHD may experience problems in working memory (remembering things while performing other cognitive operations), delayed inner speech (self-talk that allows people to solve problems), problems controlling emotions and arousal, and difficulty analyzing problems and communicating solutions to others. Hence, students with ADHD may find it difficult to stay focused on tasks such as schoolwork - tasks that require sustained attention and concentration, yet are not intrinsically interesting. In addition, the majority of individuals with ADHD experience significant problems in peer relations and demonstrate a higher incidence of substance abuse than that of the general population.
Although professionals did not recognize ADHD as a diagnostic category until the 1980s, evidence of the disorder dates from the beginning of the twentieth century. The physician George F. Still is credited with being one of the first authors to bring those with "defective moral control" to the attention of the medical profession in 1902. In the 1930s and 1940s Heinz Werner and Alfred Strauss were able to identify children who were hyperactive and distractible - children who exhibited the Strauss syndrome. Later, in the middle of the twentieth century, the term minimal brain injury was used to refer to children of normal intelligence who were inattentive, impulsive, and/or hyperactive. This term fell out of favor and was replaced by hyperactive child syndrome. Professionals eventually rejected this term, as inattention, not hyperactivity, was recognized as the major behavior problem associated with the disorder.
Students with ADHD are eligible for special education services under the category "other health impaired (OHI)." This category has dramatically increased in size; however, the number of students served in this category remains well below the estimated prevalence rate of 3 to 5 percent of the school-age population. From discrepancies such as this, researchers have estimated that fewer than half of all students with ADHD are receiving special education services.
As Barkley noted in his 1998 study, the effective diagnosis of ADHD requires a medical exam, a clinical interview, and teacher and parent rating scales. During the medical exam the physician must rule out other possible causes of the behavior problem, and through the clinical interview, the clinician obtains information from both parents and child about the child's physical and psychological characteristics. Finally, parents, teachers, and in some cases children themselves, complete behavioral rating scales, such as the Connors scales and the ADHD Rating Scale - IV in order to quantify observed behavior patterns.
Frequently students with ADHD are treated with psychostimulants, such as methylphenidate (Ritalin), which stimulate areas of the brain responsible for inhibition. Despite some negative publicity in the media, most authorities in the area of ADHD are in favor of Ritalin's use. In addition to medication, students with ADHD also benefit from carefully designed educational programming. In the early 1960s William Cruickshank was one of the first to establish an educational program for students who would meet what has become the criteria for ADHD. This program, proposing a degree of classroom structure rarely seen in the early twenty-first century, advocated: (1) a reduction of stimuli irrelevant to learning and enhancement of material important for learning and (2) a structured program with a strong emphasis on teacher direction. In addition to educational programs that emphasize and provide structure, a 1997 study by Robert H. Horner and Edward G. Carr indicated that students with ADHD benefited from instructional approaches examining the consequences, antecedents, and setting events that maintain inappropriate behaviors. Other researchers' findings indicated that they also profited from behavior management systems in which the student with ADHD learns to monitor his or her own behavior. These strategies, although effective, are not generally powerful enough to completely remedy the symptoms of children with ADHD. The majority of children diagnosed with ADHD continue to demonstrate symptoms in adulthood.
Bibliography
American Psychiatric Association. 1994. Diagnostic and Statistical Manual of Mental Disorders, Text Revision, 4th edition. Washington, DC: American Psychiatric Association.
Barkley, Russell. A. 1998. Attention-Deficit Hyperactive Disorder: A Handbook for Diagnosis and Treatment. New York: Guilford Press.
Connors, C. Keith. 1989. Connors Teacher Rating Scale-28. Tonawanda, NY: Multi-Health Systems.
Dupaul, George J.; Power, Thomas J.; Anastopolous, Arthur D.; and Reid, Robert. 1998. ADHD Rating Scale - IV: Checklists, Norms, and Clinical Interpretations. New York: Guilford Press.
Hallahan, Daniel P., and Cottone, E. A. 1997. "Attention Deficit Hyperactivity Disorder." In Advances in Learning and Behavioral Disabilities, Vol. 11, ed. Thomas E. Scruggs and Margo A. Mastropieri. Greenwich, CT: JAI Press.
Horner, Robert H., and Carr, Edward G. 1997. "Behavioral Support for Students with Severe Disabilities: Functional Assessment and Comprehensive Intervention." Journal of Special Education 31:1 - 11.
Shapiro, Edward S.; Dupaul, George J.; and Bradley-Klug, Kathy L. 1998. "Self-Management as a Strategy to Improve the Classroom Behavior of Adolescents with ADHD." Journal of Learning Disabilities 31:545 - 555.
— DEVERY R. MOCK, DANIEL P. HALLAHAN
A childhood neurologic disorder that manifests itself as excessive movement, irritability, immaturity, and an inability to concentrate or control impulses. It affects learning and skill acquisition.
| Attention-deficit/hyperactivity disorder | |
|---|---|
| Classification and external resources | |
Children with ADHD find it more difficult to focus and to complete their schoolwork. |
|
| ICD-10 | F90 |
| ICD-9 | 314.00, 314.01 |
| OMIM | 143465 |
| DiseasesDB | 6158 |
| MedlinePlus | 001551 |
| eMedicine | med/3103 ped/177 |
| MeSH | D001289 |
Attention deficit hyperactivity disorder (ADHD) is a developmental disorder.[1] It is characterized primarily by "the co-existence of attentional problems and hyperactivity, with each behavior occurring infrequently alone" and symptoms starting before seven years of age.[2]
ADHD is the most commonly studied and diagnosed psychiatric disorder in children, affecting about 3 to 5 percent of children globally[3][4] and diagnosed in about 2 to 16 percent of school-aged children.[5] It is a chronic disorder[6] with 30 to 50 percent of those individuals diagnosed in childhood continuing to have symptoms into adulthood.[7][8] Adolescents and adults with ADHD tend to develop coping mechanisms to compensate for some or all of their impairments.[9] It is estimated that 4.7 percent of American adults live with ADHD.[10] Standardized rating scales such as the World Health Organization's Adult ADHD Self-Report Scale can be used for ADHD screening and assessment of the disorder's symptoms' severity.[11]
ADHD is diagnosed two to four times more frequently in boys than in girls,[12][13] though studies suggest this discrepancy may be partially due to subjective bias of referring teachers.[14] ADHD management usually involves some combination of medications, behavior modifications, lifestyle changes, and counseling. Its symptoms can be difficult to differentiate from other disorders, increasing the likelihood that the diagnosis of ADHD will be missed.[15] In addition, most clinicians have not received formal training in the assessment and treatment of ADHD, in particular in adult patients.[15]
ADHD and its diagnosis and treatment have been considered controversial since the 1970s.[16] 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.[17][18][19] Most healthcare providers accept that ADHD is a genuine disorder with debate in the scientific community centering mainly around how it is diagnosed and treated.[20][21][22] The American Medical Association concluded in 1998 that the diagnostic criteria for ADHD are based on extensive research and, if applied appropriately, lead to the diagnosis with high reliability.[23]
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Contents
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ADHD may be seen as one or more continuous traits found normally throughout the general population.[24] It is a developmental disorder in which certain traits such as impulse control lag in development. Using magnetic resonance imaging of the prefrontal cortex, this developmental lag has been estimated to range from 3 to 5 years.[25] However, the definition of ADHD is based on behaviour and it does not imply a neurological disease.[24] ADHD is classified as a disruptive behavior disorder along with oppositional defiant disorder, conduct disorder and antisocial personality disorder.[26]
ADHD has three subtypes:[27]
Inattention, hyperactivity, and impulsivity are the key behaviors of ADHD. The symptoms of ADHD are especially difficult to define because it is hard to draw the line at where normal levels of inattention, hyperactivity, and impulsivity end and clinically significant levels requiring intervention begin.[15] To be diagnosed with ADHD, symptoms must be observed in two different settings for six months or more and to a degree that is greater than other children of the same age.[28]
The symptom categories of ADHD in children yield three potential classifications of ADHD—predominantly inattentive type, predominantly hyperactive-impulsive type, or combined type if criteria for both subtypes are met:[15]:p.4
Predominantly inattentive type symptoms may include:[29]
Predominantly hyperactive-impulsive type symptoms may include:[29]
and also these manifestations primarily of impulsivity:[29]
Most people exhibit some of these behaviors, but not to the degree where such behaviors significantly interfere with a person's work, relationships, or studies—and in the absence of significant interference or impairment, a diagnosis of ADHD is normally not appropriate. The core impairments are consistent even in different cultural contexts.[30]
Symptoms may persist into adulthood for up to half of children diagnosed with ADHD. This rate is difficult to estimate, as there are no official diagnostic criteria for ADHD in adults.[15] ADHD in adults remains a clinical diagnosis. The signs and symptoms may differ from those during childhood and adolescence due to the adaptive processes and avoidance mechanisms learned during the process of socialisation.[31]
A 2009 study found that children with ADHD move around a lot because it helps them stay alert enough to complete challenging tasks.[32][33]
Inattention and "hyperactive" behavior are not necessarily the only problems in children with ADHD. ADHD exists alone in only about 1/3 of the children diagnosed with it. The combination of ADHD with other conditions can greatly complicate diagnosis and treatment. Many co-existing conditions require other courses of treatment and should be diagnosed separately instead of being grouped in the ADHD diagnosis.
There is a strong association between persistent bed wetting and ADHD[34] Multiple research studies have also found a significant association between ADHD and language delay.[35] Anxiety and depression are some of the disorders that can accompany ADHD. Academic studies, and research in private practice suggest that depression in ADHD appears to be increasingly prevalent in children as they get older, with a higher rate of increase in girls than in boys, and to vary in prevalence with the subtype of ADHD. Where a mood disorder complicates ADHD, it would be prudent to treat the mood disorder first, but parents of children with ADHD often wish to have the ADHD treated first, because the response to treatment is quicker.[36]
Some of the associated conditions are:
Researchers found that 60 percent of the children diagnosed with ADHD continue having symptoms well into adulthood.[42][43] Many adults, however, remain untreated.[42] Untreated adults with ADHD often have chaotic lifestyles, may appear to be disorganized and may rely on non-prescribed drugs and alcohol to get by.[44] They often have such associated psychiatric comorbidities as depression, anxiety disorder, substance abuse, or a learning disability.[44] A diagnosis of ADHD may offer adults insight into their behaviors and allow patients to become more aware and seek help with coping and treatment strategies.[43] There is controversy amongst some experts on whether ADHD persists into adulthood. Recognized as occurring in adults in 1978, it is currently not addressed separately from ADHD in childhood. Obstacles that clinicians face when assessing adults who may have ADHD include developmentally inappropriate diagnostic criteria, age-related changes, comorbidities and the possibility that high intelligence or situational factors can mask ADHD.
The specific causes of ADHD are not known.[45] There are, however, a number of factors that may contribute to, or exacerbate ADHD. They include genetics, diet and the social and physical environments.
Twin studies indicate that the disorder is highly heritable and that genetics are a factor in about 75 percent of all cases.[24] Hyperactivity also seems to be primarily a genetic condition; however, other causes have been identified.[46]
Researchers believe that a large majority of ADHD cases arise from a combination of various genes, many of which affect dopamine transporters. Candidate genes include α2A adrenergic receptor, dopamine transporter, dopamine receptors D2/D3,[47] dopamine beta-hydroxylase monoamine oxidase A, catecholamine-methyl transferase, serotonin transporter promoter (SLC6A4), 5HT2A receptor, 5HT1B receptor,[48] the 10-repeat allele of the DAT1 gene,[49] the 7-repeat allele of the DRD4 gene,[49] and the dopamine beta hydroxylase gene (DBH TaqI).[50] A common variant of a gene called LPHN3 is estimated to be responsible for about 9% of the incidence of ADHD, and ADHD cases where this gene is present are particularly responsive to stimulant medication.[51]
The hunter vs. farmer theory is a hypothesis proposed by author Thom Hartmann about the origins of ADHD. The theory proposes that hyperactivity may be an adaptive behavior in pre-modern humans[52] and that those with ADHD retain some of the older "hunter" characteristics associated with early pre-agricultural human society. According to this theory, individuals with ADHD may be more adept at searching and seeking and less adept at staying put and managing complex tasks over time.[53] Further evidence showing hyperactivity may be evolutionarily beneficial was put forth in 2006 in a study that found it may carry specific benefits for certain forms of society. In these societies, those with ADHD are hypothesized to have been more proficient in tasks involving risk or competition (i.e., hunting, mating rituals, etc.).[54] A genetic variant associated with ADHD (DRD4 48bp VNTR 7R allele) has been found to be at higher frequency in more nomadic populations and those with more of a history of migration.[55] Consistent with this, another group of researchers observed that the health status of nomadic Ariaal men was higher if they had the ADHD associated genetic variant (7R alleles). However in recently sedentary (non-nomadic) Ariaal those with 7R alleles seemed to have slightly worse health.[56]
Twin studies to date have suggested that approximately 9 to 20 percent of the variance in hyperactive-impulsive-inattentive behavior or ADHD symptoms can be attributed to nonshared environmental (nongenetic) factors.[57][58][59][60] Environmental factors implicated include alcohol and tobacco smoke exposure during pregnancy and environmental exposure to lead in very early life.[61] The relation of smoking to ADHD could be due to nicotine causing hypoxia (lack of oxygen) to the fetus in utero.[62] It could also be that women with ADHD are more likely to smoke[63] and therefore, due to the strong genetic component of ADHD, are more likely to have children with ADHD.[64] Complications during pregnancy and birth—including premature birth—might also play a role.[65] ADHD patients have been observed to have higher than average rates of head injuries;[66] however, current evidence does not indicate that head injuries are the cause of ADHD in the patients observed.[67] Infections during pregnancy, at birth, and in early childhood are linked to an increased risk of developing ADHD. These include various viruses (measles, varicella, rubella, enterovirus 71) and streptococcal bacterial infection.[68][69]
A 2007 study linked the organophosphate insecticide chlorpyrifos, which is used on some fruits and vegetables, with delays in learning rates, reduced physical coordination, and behavioral problems in children, especially ADHD.[70]
A 2010 study found that pesticide exposure is strongly associated with an increased risk of ADHD in children. Researchers analyzed the levels of organophosphate residues in the urine of more than 1,100 children aged 8 to 15 years old, and found that those with the highest levels of dialkyl phosphates, which are the breakdown products of organophosphate pesticides, also had the highest incidence of ADHD. Overall, they found a 35 percent increase in the odds of developing ADHD with every 10-fold increase in urinary concentration of the pesticide residues. The effect was seen even at the low end of exposure: children who had any detectable, above-average level of pesticide metabolite in their urine were twice as likely as those with undetectable levels to record symptoms of ADHD.[71][72]
Three government-funded longitudinal studies from 2010 and 2011 examined environmental exposure to organophosphate pesticides between pregnancy and grade school. Although the studies varied in techniques to measure pesticide exposure, they reached similar conclusions. Children exposed to higher levels of organophosphates during pregnancy were more likely to have lower IQs and problems focusing or solving problems. One study suggested that genetics play a strong role in whether exposure to organophosphates causes damage. Two studies found higher rates of ADHD diagnosis among children exposed to higher levels of organophosphate pesticides.[73]
A study[74] published in The Lancet in 2007 found a link between children’s ingestion of many commonly used artificial food colors, the preservative sodium benzoate and hyperactivity. In response to these findings, the British government took prompt action. According to the Food Standards Agency, the food regulatory agency in the UK, food manufacturers are being encouraged to voluntarily phase out the use of most artificial food colors by the end of 2009. Following the FSA’s actions, the European Commission ruled that any food products containing the “Southampton Six” (The contentious colourings are: sunset yellow FCF (E110), quinoline yellow (E104), carmoisine (E122), allura red (E129), tartrazine (E102) and ponceau 4R (E124)) must display warning labels on their packaging by 2010.[75] In the US, little has been done[clarification needed] to curb food manufacturer’s use of specific food colors, despite the new evidence presented by the Southampton study. However, the existing US Food Drug and Cosmetic Act[76] had already required that artificial food colors be approved for use, that they must be given FD&C numbers by the FDA, and the use of these colors must be indicated on the package.[77] This is why food packaging in the USA may state something like: "Contains FD&C Red #40." As of March 2011, the FDA was evaluating the scientific evidence of a link between dyes and ADHD; a preliminary analysis found there was no link.[78]
The World Health Organization states that the diagnosis of ADHD can represent family dysfunction or inadequacies in the educational system rather than individual psychopathology.[79] Other researchers believe that relationships with caregivers have a profound effect on attentional and self-regulatory abilities. A study of foster children found that a high number of them had symptoms closely resembling ADHD.[80] Researchers have found behavior typical of ADHD in children who have suffered violence and emotional abuse.[24][81] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD.[82] ADHD is also considered to be related to sensory integration dysfunction.[83]
A 2010 article by CNN suggests that there is an increased risk for internationally adopted children to develop mental health disorders, such as ADHD and ODD.[84] The risk may be related to the length of time the children spent in an orphanage, especially if they were neglected or abused. Many of these families who adopted the affected children feel overwhelmed and frustrated, since managing their children may entail more responsibilities than originally anticipated. The adoption agencies may be aware of the child's behavioral history, but decide to withhold the information prior to the adoption. This in turn has resulted in some parents suing adoption agencies, in the abuse of children, and even in the relinquishment of the child.
Proponents of the neurodiversity theory assert that atypical (neurodivergent) neurological development is a normal human difference that is to be tolerated and respected just like any other human difference. Social critics argue that while biological factors may play a large role in difficulties with sitting still in class and/or concentrating on schoolwork in some children, these children could have failed to integrate others' social expectations of their behavior for a variety of other reasons.[85] As genetic research into ADHD proceeds, it may become possible to integrate this information with the neurobiology in order to distinguish disability from varieties of normal or even exceptional functioning in people along the same spectrum of attention differences.[86]
Social construction theory states that it is societies that determine where the line between normal and abnormal behavior is drawn. Thus society members including physicians, parents, teachers, and others are the ones who determine which diagnostic criteria are applied and, thus, determine the number of people affected.[87] This is exemplified in the fact that the DSM IV arrives at levels of ADHD three to four times higher than those obtained with use of the ICD 10.[13] Thomas Szasz, a proponent of this theory, has argued that ADHD was "invented and not discovered."[88][89]
According to the low arousal theory, people with ADHD need excessive activity as self-stimulation because of their state of abnormally low arousal.[90] The theory states that those with ADHD cannot self-moderate, and their attention can be gained only by means of environmental stimuli, which in turn results in disruption of attentional capacity and an increase in hyperactive behaviour.[91]
Without enough stimulation coming from the environment, an ADHD child will create it him or herself by walking around, fidgeting, talking, etc. This theory also explains why stimulant medications have high success rates and can induce a calming effect at therapeutic dosages among children with ADHD. It establishes a strong link with scientific data that ADHD is connected to abnormalities with the neurochemical dopamine and a powerful link with low-stimulation PET scan results in ADHD subjects.
The pathophysiology of ADHD is unclear and there are a number of competing theories.[92] Research on children with ADHD has shown a general reduction of brain volume, but with a proportionally greater reduction in the volume of the left-sided prefrontal cortex. These findings suggest that the core ADHD features of inattention, hyperactivity, and impulsivity may reflect frontal lobe dysfunction, but other brain regions in particular the cerebellum have also been implicated.[93] Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are used only for research and not diagnostic purposes.[94] A 2005 review of published studies involving neuroimaging, neuropsychological genetics, and neurochemistry found converging lines of evidence to suggest that four connected frontostriatal regions play a role in the pathophysiology of ADHD: The lateral prefrontal cortex, dorsal anterior cingulate cortex, caudate, and putamen.[95]
In one study a delay in development of certain brain structures by an average of three years occurred in ADHD elementary school-aged patients. The delay was most prominent in the frontal cortex and temporal lobe, which are believed to be responsible for the ability to control and focus thinking. In contrast, the motor cortex in the ADHD patients was seen to mature faster than normal, suggesting that both slower development of behavioral control and advanced motor development might be required for the fidgetiness that characterizes ADHD.[96] It should be noted that stimulant medication itself may affect growth factors of the central nervous system.[97]
The same laboratory had previously found involvement of the "7-repeat" variant of the dopamine D4 receptor gene, which accounts for about 30 percent of the genetic risk for ADHD, in unusual thinness of the cortex of the right side of the brain; however, in contrast to other variants of the gene found in ADHD patients, the region normalized in thickness during the teen years in these children, coinciding with clinical improvement.[98]
In addition, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity),[99] and a significantly higher concentration of dopamine transporters in the striatum, which is in charge of planning ahead.[100][101] A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain's ability to produce neurotransmitters like dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine (hypodopaminergia) across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients but to "childhood learning problems" in healthy subjects as well.[102] One interpretation of dopamine pathway tracers is that the biochemical "reward" mechanism works for those with ADHD only when the task performed is inherently motivating; low levels of dopamine raise the threshold at which someone can maintain focus on a task that is otherwise boring.[103] Neuroimaging studies also found that neurotransmitters level (e.g. dopamine and serotonin) in the synaptic cleft goes down during depression.[104][105]
A 1990 PET scan study by Alan J. Zametkin et al. found that global cerebral glucose metabolism was 8 percent lower in medication-naive adults who had been hyperactive since childhood.[106] Further studies found that chronic stimulant treatment had little effect on global glucose metabolism,[107] a 1993 study in girls failed to find a decreased global glucose metabolism, but found significant differences in glucose metabolism in 6 specific regions of the brains of ADHD girls as compared to control subjects. The study also found that differences in one specific region of the frontal lobe were statistically correlated with symptom severity.[108] A further study in 1997 also failed to find global differences in glucose metabolism, but, likewise, found differences in glucose normalization in specific regions of the brain. The 1997 study also noted that their findings were somewhat different than those in the 1993 study, and concluded that sexual maturation may have played a role in this discrepancy.[109] The significance of the research by Zametkin has not been determined and neither his group nor any other has been able to replicate the 1990 results.[110][111][112]
Critics, such as Jonathan Leo and David Cohen, who reject the characterization of ADHD as a disorder, contend that the controls for stimulant medication usage were inadequate in some lobar volumetric studies, which makes it impossible to determine whether ADHD itself or psychotropic medication used to treat ADHD is responsible for the decreased thickness observed[113] in certain brain regions. While the main study in question used age-matched controls, it did not provide information on height and weight of the subjects. These variables it has been argued could account for the regional brain size differences rather than ADHD itself.[114][115] They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology.[114][116]
ADHD is diagnosed via a psychiatric assessment; to rule out other potential causes or comorbidities, physical examination, radiological imaging, and laboratory tests may be used.[117]
In North America, the DSM-IV criteria are often the basis for a diagnosis, while European countries usually use the ICD-10. If the DSM-IV criteria are used, rather than the ICD-10, a diagnosis of ADHD is 3–4 times more likely.[13] Factors other than those within the DSM or ICD however have been found to affect the diagnosis in clinical practice. A child's social and school environment as well as academic pressures at school are likely to be of influence.[118]
Many of the symptoms of ADHD occur from time to time in everyone; in patients with ADHD, the frequency of these symptoms is greater and patients' lives are significantly impaired. Impairment must occur in multiple settings to be classified as ADHD.[28] As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA these criteria are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:
The previously used term ADD expired with the most recent revision of the DSM. As a consequence, ADHD is the current nomenclature used to describe the disorder as one distinct disorder that can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD, predominately inattentive type) or both (ADHD combined type).
The diagnostic criteria outlined in DSM-IV assume that attention deficits (1) are a distinct, differentiated condition; (2) can be reliably measured using objective, behavioral measures; and (3)are abnormalities resulting from organic/biological origins.[120]
IA. Six or more of the following signs of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:
IB. Six or more of the following signs of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:
II. Some signs that cause impairment were present before age 7 years.
III. Some impairment from the signs is present in two or more settings (such as at school/work and at home).
IV. There must be clear evidence of significant impairment in social, school, or work functioning.
V. The signs do not happen only during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder. The signs are not better accounted for by another mental disorder (such as Mood Disorder, Anxiety Disorder, Dissociative Identity Disorder, or a Personality Disorder).[121]
In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the signs of ADHD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10[122]) is present, the condition is referred to as "Hyperkinetic conduct disorder". Otherwise the disorder is classified as "Disturbance of Activity and Attention", "Other Hyperkinetic Disorders" or "Hyperkinetic Disorders, Unspecified". The latter is sometimes referred to as, "Hyperkinetic Syndrome".[122]
The American Academy of Pediatrics Clinical Practice Guideline for children with ADHD emphasizes that a reliable diagnosis is dependent upon the fulfillment of three criteria:[123]
All three criteria are determined using the patient's history given by the parents, teachers and/or the patient.
Adults often continue to be impaired by ADHD. Adults with ADHD are diagnosed under the same criteria, including the stipulation that their signs must have been present prior to the age of seven.[124] Adults face some of their greatest challenges in the areas of self-control and self-motivation, as well as executive functioning, usually having more signs of inattention and fewer of hyperactivity or impulsiveness than children do.[125]
The American Academy of Child Adolescent Psychiatry (AACAP) considers it necessary that the following be present before attaching the label of ADHD to a child:
If a child seems too active on the playground but not elsewhere, the problem might not be ADHD. It might also not be ADHD if the behaviors occur in the classroom but nowhere else. A child who shows some symptoms would not be diagnosed with ADHD if his or her schoolwork or friendships are not impaired by the behaviors.[126]
To make the diagnosis of ADHD, a number of other possible medical and psychological conditions must be excluded.
Medical conditions
Medical conditions that must be excluded include: hypothyroidism, anemia, lead poisoning, chronic illness, hearing or vision impairment, substance abuse, medication side-effects, sleep impairment and child abuse,[127] and cluttering (tachyphemia) among others.
Sleep conditions
As with other psychological and neurological issues, the relationship between ADHD and sleep is complex. In addition to clinical observations, there is substantial empirical evidence from a neuroanatomic standpoint to suggest that there is considerable overlap in the central nervous system centers that regulate sleep and those that regulate attention/arousal.[128] Primary sleep disorders play a role in the clinical presentation of symptoms of inattention and behavioral dysregulation. There are multilevel and bidirectional relationships among sleep, neurobehavioral functioning and the clinical syndrome of ADHD.[129]
Behavioral manifestations of sleepiness in children range from the classic ones (yawning, rubbing eyes), to externalizing behaviors (impulsivity, hyperactivity, aggressiveness), to mood lability and inattentiveness.[128][130][131] Many sleep disorders are important causes of symptoms that may overlap with the cardinal symptoms of ADHD; children with ADHD should be regularly and systematically assessed for sleep problems.[128][132]
From a clinical standpoint, mechanisms that account for the phenomenon of excessive daytime sleepiness include:
Methods of treatment often involve some combination of behavior modification, life-style changes, counseling, and medication. A 2005 study found that medical management and behavioral treatment is the most effective ADHD management strategy, followed by medication alone, and then behavioral treatment.[134] While medication has been shown to improve behavior when taken over the short term, they have not been shown to alter long-term outcomes.[135] Medications have at least some effect in about 80% of people.[136]
The evidence is strong for the effectiveness of behavioral treatments in ADHD.[137] It is recommended first line in those who have mild symptoms and in preschool-aged children.[138] Psychological therapies used include psychoeducational input, behavior therapy, cognitive behavioral therapy (CBT), interpersonal psychotherapy (IPT), family therapy, school-based interventions, social skills training, parent management training,[24] neurofeedback,[139] and nature exposure.[140][141] Parent training and education have been found to have short-term benefits.[142] There is a deficiency of good research on the effectiveness of family therapy for ADHD, but the evidence that exists shows that it is comparable in effectiveness to treatment as usual in the community and is superior to medication placebo.[143] Several ADHD specific support groups exist as informational sources and to help families cope with challenges associated with dealing with ADHD.
Stimulant medications are the medical treatment of choice.[144] There are a number of non-stimulant medications, such as atomoxetine, that may be used as alternatives.[144] There are no good studies of comparative effectiveness between various medications, and there is a lack of evidence on their effects on academic performance and social behaviors.[145] While stimulants and atomoxetine are generally safe, there are side-effects and contraindications to their use.[144] Medications are not recommended for preschool children, as their long-term effects in such young people are unknown.[24][146] There is very little data on the long-term benefits or adverse effects of stimulants for ADHD.[147] Any drug used for ADHD may have adverse drug reactions such as psychosis and mania,[148] though methylphenidate-induced psychosis is uncommon.[149] People with ADHD have an increased risk of substance abuse, and stimulant medications reduce this risk.[150][151] Stimulant medications in and of themselves however have the potential for abuse and dependence.[152] Guidelines on when to use medications vary internationally, with the UK's National Institute of Clinical Excellence, for example, recommending use only in severe cases, while most United States guidelines recommend medications in nearly all cases.[153]
Children diagnosed with ADHD have significant difficulties in adolescence, regardless of treatment.[154][155] In the United States, 37 percent of those with ADHD do not get a high school diploma even though many of them will receive special education services.[156] A 1995 briefing citing a 1994 book review says the combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish high school.[157] Also in the US, less than 5 percent of individuals with ADHD get a college degree[158] compared to 28 percent of the general population.[159] The proportion of children meeting the diagnostic criteria for ADHD drops by about 50 percent over three years after the diagnosis. This occurs regardless of the treatments used and also occurs in untreated children with ADHD.[127][160][161] ADHD persists into adulthood in about 30 to 50 percent of cases.[7] Those affected are likely to develop coping mechanisms as they mature, thus compensating for their previous ADHD.[9]
ADHD's global prevalence is estimated at 3 to 5 percent in people under the age of 19. There is, however, both geographical and local variability among studies. Children in North America appear to have a higher rate of ADHD than children in Africa and the Middle East.[163] Published studies have found rates of ADHD as low as 2 percent and as high as 14 percent among school-aged children.[164] The rates of diagnosis and treatment of ADHD are also much higher on the East Coast of the USA than on the West Coast.[165] The frequency of the diagnosis differs between male children (10%) and female children (4%) in the United States.[166] This difference between genders may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.[167]
Rates of ADHD diagnosis and treatment have increased in both the UK and the USA since the 1970s. In the UK an estimated 0.5 per 1,000 children had ADHD in the 1970s, while 3 per 1,000 received ADHD medications in the late 1990s. In the USA in the 1970s 12 per 1,000 children had the diagnosis, while in the late 1990s 34 per 1,000 had the diagnosis and the numbers continue to increase.[24]
In the UK in 2003 a prevalence of 3.6 percent is reported in male children and less than 1 percent is reported in female children.[168]
Hyperactivity has long been part of the human condition. Sir Alexander Crichton describes "mental restlessness" in his book An Inquiry Into the Nature and Origin of Mental Derangement written in 1798.[169][170] The terminology used to describe the symptoms of ADHD has gone through many changes over history including: "minimal brain damage", "minimal brain dysfunction" (or disorder),[171] "learning/behavioral disabilities" and "hyperactivity". In the DSM-II (1968) it was the "Hyperkinetic Reaction of Childhood". In the DSM-III "ADD (Attention-Deficit Disorder) with or without hyperactivity" was introduced. In 1987 this was changed to ADHD in the DSM-III-R and subsequent editions.[172] The use of stimulants to treat ADHD was first described in 1937.[173]
The media have reported on many issues related to ADHD. In 2001 PBS's Frontline aired a one-hour program about the effects of the diagnosis and treatment of ADHD in minors, entitled "Medicating Kids."[174] The program included a selection of interviews with representatives of various points of view. In one segment, entitled Backlash, retired neurologist Fred Baughman and Peter Breggin whom PBS described as "outspoken critics who insist [ADHD is] a fraud perpetrated by the psychiatric and pharmaceutical industries on families anxious to understand their children's behavior"[175] were interviewed on the legitimacy of the disorder. Russell Barkley and Xavier Castellanos, then head of ADHD research at the National Institute of Mental Health (NIMH), defended the viability of the disorder. In the interview with Castellanos, he stated that little is scientifically understood.[176] Lawrence Diller was interviewed on the business of ADHD along with a representative from Shire Plc (then known as Shire-Richwood).[citation needed]
A number of notable individuals have given controversial opinions on ADHD. Scientologist Tom Cruise's interview with Matt Lauer was widely watched by the public in 2005. In this interview he spoke about postpartum depression and also referred to Ritalin and Adderall as being "street drugs" rather than as ADHD medication.[177] In England Baroness Susan Greenfield, a leading neuroscientist, spoke out publicly in 2007 in the House of Lords about the need for a wide-ranging inquiry into the dramatic increase in the diagnosis of ADHD in the UK and possible causes following a BBC Panorama programme that highlighted US research (The Multimodal Treatment Study of Children with ADHD by the University of Buffalo) suggesting drugs are no better than other forms of therapy for ADHD in the long term.[178] However, in 2010 the BBC Trust criticized the 2007 BBC Panorama programme for summarizing the US research as showing "no demonstrable improvement in children's behaviour after staying on ADHD medication for three years" when in actuality "the study found that medication did offer a significant improvement over time."[179]
As of 2009[update], eight percent of all Major League Baseball players have been diagnosed with ADHD, making the disorder epidemic among this population. The increase coincided with the League's 2006 ban on stimulants (q.v. Major League Baseball drug policy).[180]
Stimulants legal status was recently reviewed by several international organizations:
ADHD and its diagnosis and treatment have been considered controversial since the 1970s.[16][18][183] The controversies have involved clinicians, teachers, policymakers, parents and the media. Opinions regarding ADHD range from not believing it exists at all[17] to believing there are genetic and physiological bases for the condition as well as disagreement about the use of stimulant medications in treatment.[17][18][19] Some sociologists consider ADHD to be a "classic example of the medicalization of deviant behavior, defining a previously nonmedical problem as a medical one".[16] Most healthcare providers in U.S. accept that ADHD is a genuine disorder with debate in centering mainly around how it is diagnosed and treated.[20][21][22] However, The British Psychological Society said in a 1997 report that physicians and psychiatrists should not follow the American example of applying medical labels to such a wide variety of attention-related disorders: "The idea that children who don’t attend or who don’t sit still in school have a mental disorder is not entertained by most British clinicians."[184][185] In 2009, the British Psychological Society, in collaboration with the Royal College of Psychiatrists, released a set of guidelines for the diagnosis and treatment of ADHD.[186] In its guideline, it state that available evidence indicate that ADHD is a valid diagnosis. However, it states that the diagnosis lack any biological basis and that "[c]ontroversial issues surround changing thresholds applied to the definition of illness as new knowledge and treatments are developed and the extent to which it is acknowledged that clinical thresholds are socially and culturally influenced and determine how an individual's level of functioning within the 'normal cultural environment' is assessed". It further states that "the acceptable thresholds for impairment are partly driven by the contemporary societal view of what is an acceptable level of deviation from the norm."
Others have included that it may stem from a misunderstanding of the diagnostic criteria and how they are utilized by clinicians,[15]:p.3 teachers, policymakers, parents and the media.[17] Debates center around key controversial issues; whether ADHD is a disability or merely a neurological description, the cause of the disorder, the changing of the diagnostic criteria, the rapid increase in diagnosis of ADHD, and the use of stimulants to treat the disorder.[187] Possible long-term side-effects of stimulants and their usefulness are largely unknown because of a lack of long-term studies.[188] Some research raises questions about the long-term effectiveness and side-effects of medications used to treat ADHD.[189]
In 1998, the US National Institutes of Health (NIH) released a consensus statement on the diagnosis and treatment of ADHD. The statement, while recognizing that stimulant treatment is controversial, supports the validity of the ADHD diagnosis and the efficacy of stimulant treatment. It found controversy only in the lack of sufficient data on long-term use of medications, and in the need for more research in many areas.[190]
With a "wide variation in diagnosis across states, races, and ethnicities"[191] some investigators[who?] suspect that factors other than neurological conditions play a role when the diagnosis of ADHD is made.[191][192] Two studies published in 2010 suggest that the diagnosis is more likely to be made in the younger children within a grade; the authors propose that such a misdiagnosis of ADHD within a grade may be due to different states of maturity and may lead to potentially inappropriate treatment.[191][192] A further study involving a million children in British Columbia (Canada) published in 2012 using data from 1997 to 2008 unambiguously confirmed the phenomenon, finding children born in December (the youngest) 39% more likely to be diagnosed with ADHD than those born in January (the oldest).[193]
| Look up ADHD, ADHD-PI, ADHD-C, or ADHD-PH/I in Wiktionary, the free dictionary. |
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