Attention Deficit Disorder

Attention-deficit hyperactivity disorder (ADHD) (sometimes also referred to as ADD) is a psychiatric diagnosis that identifies hyperactivity, forgetfulness, mood shifts, poor impulse control, and distractibility as symptoms of a neurological disorder.

ADHD is commonly diagnosed among children. When diagnosed in adults, it is regarded as adult attention-deficit disorder (AADD). It is believed that approximately 30 to 70% of children diagnosed with ADHD retain the disorder as adults.

Contents
1 Formal definitions
2 Symptoms
3 Diagnosis
4 Comparative behavior
5 Incidence
6 Testing for ADHD
6.1 Psychological testing
6.2 Other forms of testing
7 Possible causes
7.1 Genetic vulnerabilities
7.2 Neuro-chemical imbalance
7.3 Smoking during pregnancy
7.4 Nutrition
7.5 Sleep apnea
7.6 Head injuries
8 Treatment
8.1 Mainstream treatments
8.2 Alternative treatments 
 

Formal definitions
According to the U.S. Surgeon General, and ICD-10-CM (International Classification of Disease Revised Edition 2005), ADHD is a metabolic form of encephalopathy, impairing the release and homeostasis of neurological chemicals, and reducing the function of the limbic system. Research, however, indicates that the frontal lobes, their connections to the basal ganglia, and the central aspects of the cerebellum (vermis) are most likely to be involved in this disorder, as may be a region in the middle or medial aspect of the frontal lobe, known as the anterior cingulate.

According to the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders-IV (Text Revision) (DSM-IV-TR), ADHD is a developmental disorder that arises in childhood, in most cases before the age of 7 years, is characterized by developmentally inappropriate levels of inattention and/or hyperactive-impulsive behavior, and results in impairment in one or more major life activities, such as family, peer, educational, occupational, social, or adaptive functioning. There are three subtypes of ADHD: Predominantly Inattentive, Predominantly Hyperactive-Impulsive, and Combined Type.

Symptoms
In children the disorder is characterized by inattentiveness, destructiveness, impulsive behavior, and restlessness. The inattentiveness often appears as a difficulty with sustaining attention or persisting toward activities, particularly those that are not especially interesting or rewarding. This is often combined with problems inhibiting responding to distracting events that often draw the person off-task. Those with ADHD also have difficulties re-engaging the previous task once they have been distracted. The hyperactivity is typically most evident in early to middle childhood and declines significantly with age. By adulthood, it is most evident in a feeling of restlessness or inner or subjective hyperactivity as well as a need to be busy or engaged in physical activities. The impulsiveness or poor inhibition persists throughout childhood into adulthood and may be manifest verbally (excessive talking, interrupting others, blurting out answers before question are finished, saying what's on your mind without regard to its consequences, etc.) or physically, as in doing things on impulse or a dare. Those with ADHD are often more involved in risk-taking activities and, as a consquence, suffer 2-4 times the rate of accidental injuries as do normal children or adults. A newly identified subset of children now classified as having ADHD are called the Predominantly Inattentive Type and may often appear to be daydreamy, spacey, confused, in a fog, staring frequently, slow moving, sluggish and hypo-active. Researchers call these children Sluggish Cognitive Tempo but this is not a commonly used diagnostic label.

In adults the problem is often seen as a difficulty with time management, organization, risk-taking, careless behavior, and distractible and impulsive behavior. They often show an inability to structure their lives and plan complex daily tasks. Their greatest difficulties are in self-control or executive functioning, which refers to inhibit off-task behavior, the ability to direct behavior toward future goals and tasks and to keep those tasks in mind until completed (typically called working memory), to self-motivate such behavior in the absence of rewards, to innovate or re-organize goal-directed behavior as obstacles arise, and to evaluate one's own performance.

Recommended reading: How To Conquer Add.

Diagnosis
A diagnosis of ADHD is based on a checklist of symptoms from DSM-IV-TR. DSM-IV-TR Criteria for ADHD

The Centers for Disease Control and Prevention (CDC) emphasizes that a diagnosis of ADHD should only be made by trained health care providers. This is important, as many of the criteria are shared between other disorders. Different psychiatric disorders may present with the symtoms of inattentiveness (depressive and anxiety disorders) or hyperactivity and distractability (manic phase of bipolar illness).It is also important to note that ADHD symtoms to a certain degree are present in many individuals, what makes it a disorder is a significant severity and pervasiveness of the symtoms leading to prominent functional impairement across different settings ( school, work, social relationships).

Comparative behavior
It is thought that ADHD adults are less noticeable than children because they may have found certain occupational specialties or niches in which their symptoms are not as problematic, apparent, or impairing. Or, they may have learned better coping skills and other forms of adaptive behavior, such as relying on more organized partners, spouses, or co-workers and friends to help keep them focused on important goals.

While some advocates for ADHD believe that those with ADD/ADHD are very creative, scientific studies have not found this to be the case, finding that they are no more or less creative than other individuals. They may, however, be less productive in their daily lives and often under-achieve in their occupations because of the interference created by their disorder. While a number of famous actors, writers, artists and inventors have been diagnosed with the disorder, the disorder can be found in nearly all occupational specialties.

ADHD is associated with poorer school performance, especially low productivity, with higher occurrences of grade retention (25-50%), suspensions and expulsions (10-20%), and school drop-out rates(30-40%). It is also highly associated with increased difficulties with driving, including greater speeding citations, traffic accidents(2-4 times the risk), and worse accidents leading to a 2-3 fold increase in license suspensions. Those with ADHD are also more likely to be involved in a teen-age pregnancy (30-35%) and carry a greater risk for sexually transmitted disease due to a reduced use of contraception. At work, they may experience not only their usual problems with attention, time management, organization, and poor impulse control, but also have greater risks for on-the-job injuries (more than double the risk). They change jobs more often out of boredom and/or may be fired more often due to poor work performance or difficulties controlling their emotions in the workplace. ADHD is associated with a greater risk for financial difficulties, including over-use of credit, poor saving habits, and even bankruptcies. A conjectured positive aspect of medication is that the person with the disorder can then put into action their individual intelligence and interests.

On the other hand, symptoms are often identified in school or business settings, where individual interests are regarded as distractions and originality is discouraged. In this context, medication serves the purpose of normalizing the school or business atmosphere.

Incidence
ADHD has been found to exist in every country and culture studied to date. While it is most commonly diagnosed in the United States of America, rates of diagnosis are rising in most industrialized countries as they become more aware of the disorder, its diagnosis, and its management.

According to the 2000 edition of DSM-IV-TR, ADHD affects three to seven percent of all children in the U.S. According to 2002 data from the Centers for Disease Control and Prevention annual National Health Interview Survey, released in 2004, nearly 4 million children younger than 18 in the United States had been diagnosed with attention deficit hyperactivity disorder (ADHD). In general, 5-8% of children likely have ADHD while 4-5% of adults do so. The 2002 data indicated that twice as many boys were diagnosed with ADHD as girls (10% vs. 4%). Some experts theorize that ADHD is under-diagnosed in girls, since their symptoms tend to be less dramatic than those in boys and thus draw less attention from parents and teachers. This may be due to a lower likelihood of aggressive and antisocial behavior in girls and possibly a higher incidence of the inattentive-type of ADHD among girls. Even girls with hyperactivity, however, are under-detected because their hyperactivity might manifest in non-physical ways, such as excessive talking.

Speculation exists to explain the higher diagnostical quota in the U.S. One theory suggests that due to the high-risk traits of ADHD-affected people, it can be suggested that there was a higher prevalence for ADHD in the immigrants heading for America in former centuries than in the general population. No evidence exists at the moment to support such a popular idea. And it is becoming increasingly evident that ADHD can be found in equally high rates of countries with far less migratory patterns, such as in Japan and China.

Twin studies have shown ADHD to be highly inheritable, almost as much as height. Other research shows that certain versions of genes, known as polymorphisms, may be linked to the disorder. A commonly identified one is the 7-repeat allele of the Dopamine receptor type 4 gene (DRD4). This gene has inconsistently been associated with novelty seeking aspects of personality and may be more frequent in populations that were more migratory in early human history -- the so-called "Out of Africa" theory. However, because at least 4-7 genes thus far are thought to be associated with ADHD, this is conjecture at this point. Individuals without ADHD also have the 7-repeat allele, though in smaller numbers. Some researchers refer to this allele as the "response ready" allele. Other genes found to date that may be candidates for association with ADHD are the dopamine transporter gene (DAT1), the dopamine beta hydroxylase gene (DBH TaqI), and the dopamine receptor type 5 gene (DRD5).

A study by Olfson (2003) reports that the ADHD treatment rate amongst Caucasian children is significantly higher than among African Americans (4.4% versus 1.7% in 1997). On the other hand, it is also possible that social and other factors may prevail here. At the University of Florida Regina Bussing has conducted research showing that the obstacles to ADHD treatment are higher in the African-American and female populations. Cultural factors also inhibit treatment being sought.

A different, often related theory, links the statistical difference mainly to a higher problem awareness and competence in the U.S. due to the longer research and public acquaintance with ADHD. Although all of these theories have some support, many are debated.

Testing for ADHD

Psychological testing
Psychological or psychiatric evaluation for ADHD generally consists of obtaining multiple types of information from multiple sources along with a careful history that is then used in the process of differential diagnosis (differentiation from other mental disorders). These usually include a clinical interview reviewing the DSM-IV criteria for ADHD diagnosis. The interview also needs to rule out as much as possible other types of syndromes which can cause attention problems, such as depression, anxiety, allergies and psychosis. Rating scales can be administered which provide measurement of the person's own view of their symptoms, as well as the views of parents, teachers, and significant others. A review of prior records from school is also critical to establishing the presence of impairment in the educational setting. Psychological testing of intelligence is essential to rule out subnormal intelligence as a contributor to school problems or those in adaptive functioning. Achievement testing of reading, math, spelling, etc. is often necessary to determine if a comorbid learning disability is present, as it often is in 25-50% of clinical cases.

Computerized tests of attention are not especially helpful in providing a further independent assessment because they have a high rate of false negatives (real cases of ADHD can pass the tests in 35% or more of cases), they do not correlate well with actual behavioral problems at home or school, and are not especially helpful in determining treatments. Both the American Academy of Pediatrics and American Academy of Child and Adolescent Psychiatry have recommended against the use of such computerized tests for now in view of their lack of appropriate scientific validation as diagnostic tools. In the USA, the process of obtaining referrals for such assessments is being promoted vigorously by the President's New Freedom Commission on Mental Health.

Other forms of testing
Neurometrics, PET scans, or SPECT scans have been used for a more objective diagnosis. However, these are not usually suitable for very young children, may result in unacceptable exposure to radiation with no increase in benefit from the scan, and do not have acceptable data on their predictive power to detect ADHD to be used in clinical practice. Currently, the American Academy of Pediatrics and the American Academy of Child and Adolescent Psychiatry recommend against using these neuro-imaging methods for clinical diagnosis of individuals who may have ADHD. They remain useful research tools, however, when studying groups of patients with ADHD. A recent review of all of the scientific literature on scanning in ADHD by Alan Zametkin, M.D., an expert in neuro-imaging at the NIMH (see The ADHD Report, October 2005, www.guilford.com), concluded as well that these methods should not be used for clinical diagnosis as they lack adequate scientific information on their accuracy in doing so.

Possible causes
ADHD is broadly defined and pervasive, and it is likely that the symptoms attributed to ADHD have a variety of different causes. The initial triggers could include genetic vulnerabilities, viral or bacterial infections, brain injury, or nutritional deficits. A 1990 study at the U.S. National Institute of Mental Health correlated ADHD with a series of metabolic abnormalities in the brain, providing further evidence that ADHD is a neurological disorder. While heredity is often indicated, some cases may arise from problems in prenatal development, birth complications, or later neurological damage may contribute to ADHD. The most compelling evidence at the moment suggests some role for maternal smoking and alcohol use to contribute to risk for the disorder (2.5 times increased risk for each). the total number of pregnancy complications may also increase risk for disorder. Prematurity has been repeatedly established as being associated with markedly elevated risk for disorder (30-50%), apparently due to the traumatic effects of birth on the premature brain resulting in minor bleeding and brain immaturity itself. The burgeoning field of epigenetics -- the study of what causes genes to express or not express -- is examining the questions concerning the interaction of these and other risk factors with genes that also contribute to risk for the disorder. There has been a surge in alternative approaches to causation ADHD, such as excess sugar, TV-viewing, video-game use, etc. but these have little research in support of them and have been vigorously disputed.

Genetic vulnerabilities
It has been demonstrated that children who have at least one parent diagnosed with ADHD are more likely to be diagnosed with ADHD. Scientific evidence suggests most strongly that, in many cases, the disorder is genetically transmitted. If a parent has ADHD, their child is 8 times more likely to have ADHD, and a sibling is 5-7 times more likely to also have the same disorder. The concordance between identical twins if one has the disorder is 78-92%. Candidate genes have been identified as having some association with the disorder, as noted above. These genes imply that ADHD may result from an imbalance or deficiency in certain chemicals that regulate the efficiency with which the brain controls behavior. Current research is examining which genes may be involved. A team at the University of California suggest that genes contributing to (ADHD) overlap an area of chromosome 16p13, a marker that has repeatedly come up in genome-wide scans for autism genes. The two conditions appear related, with both (ADHD) and autism frequently involving inattentiveness and/or hyperactivity. Other studies have associated ADHD with the 10-repeat allele of the DAT1 gene and the 7-repeat allele of the DRD4 gene, both dopamine genes [1]. Several studies have now documented an association with the dopamine beta hydrozylase gene (DBH TaqI). Such research suggests that ADHD likely arises from a combination of these various risk genes rather than from a single gene. In the future it is likely that ADHD will be subtyped according to which risk genes individuals possess as these subtypes are likely to have different risks, life courses, and responses to treatment, particularly to medications.

There is no compelling evidence that social factors, alone, can create ADHD. What environmental factors have been identified to date fall in the realm of bio-hazards such as alcohol, tobacco smoke, lead poisoning, premature birth, excessively complicated pregnancy, etc.

Neuro-chemical imbalance
There is increasing evidence that variants in the gene for the dopamine transporter are related to the development of ADHD (Roman et al., 2004, American Journal of Pharmacogenomics 4:83-92). This evidence is consonant with the theory of inefficacy of dopamine in people with ADD/ADHD; according to other recent studies, some people with ADHD usually have relatively high dopamine transporter levels, which clears dopamine from between neurons before the full effect is gained from dopamine. Stimulant medications used to treat ADHD are all capable of either inhibiting the action of dopamine transporter (as methylphenidate does) or promoting the release of dopamine itself (as the amphetamine-class medications do). Therefore, it is theorized that stimulant medication allows the brain to enhance the effect of dopamine by blocking dopamine transporters or increasing the release of dopamine. Currently this is the most widely accepted model of ADD/ADHD etiology in the scientific and medical community.

New studies consider the possibility that norepinephrine also plays a role. (see Krause, Dresel, Krause in Psycho 26/2000 p.199ff). Drugs that manipulate norepinephrine levels in certain brain regions, such as atomoxetine, have shown effectiveness for managing the disorder.

Smoking during pregnancy
The finding of another possible cause stemmed from the observation that children of women who smoked during pregnancy are more likely to be diagnosed with ADHD (Kotimaa et al., 2003, J Am Acad Child Adol Psychiatry 42, 826-833). Given that nicotine is known to cause hypoxia (too little oxygen) in the uterus, and that hypoxia causes brain damage, smoking during pregnancy could be an important contributing factor leading to ADHD (or a phenocopy). It may even help explain in part the increase in ADHD diagnoses, as the number of women smokers has increased. However, there are not nearly enough women smoking during pregnancy to account for all the ADHD diagnoses, and the mothers of many of those diagnosed with ADHD did not smoke during or before pregnacy. It is also possible that cause and effect could be confounded in this study, since many mothers who smoke during pregnancy may be ADHD suffers themselves; therefore the cause may simply be the shared genetic material of mother and child, rather than the mother's smoking.

Brain development in the uterus and during the first year of life may be compromised by drug use during pregnancy or environmental toxins.

Nutrition
It has also been suggested that ADHD may be the result of a poor diet and other external factors, rather than from any physiological source. Recent studies have begun to find metabolic differences in these children, indicating that it is not so much a poor diet, as it may be an inability to handle certain elements of the diet. For example, in 1990 the English chemist N.I. Ward showed that children with ADHD lose zinc when exposed to a food dye. Waring, McFadden, and others have shown that children with autism or ADHD are low in sulfation metabolism, in particular the enzyme Phenol Sulfotransferase-P.

Some children with ADHD seem to be addicted to milk. It has been proposed by Norwegian and British scientists that this is due to the casomorphins, peptides formed by incomplete digestion of the casein protein. While interesting, there is no compelling evidence that this in fact contributes to risk for the disorder.

It has, however, been established conclusively that some children are sensitive to dyes and other food additives, while a few may be sensitive to sugar, caffeine, etc. (Jacobson and Schardt, 1999, Diet, ADHD & Behavior, Center for Science in the Public Interest, Washington, DC). More studies supporting the connection between diet and behavior, including more than 30 double-blind studies, can be found at diet-studies.com.

Critics of dietary intervention for ADHD continue to claim that fewer than 5% of ADHD children appear to be diet sensitive. They say that the available evidence is insufficient to either prove or disprove a dietary connection.

Nutritional data has been well summarized in a review article (Burgess et al., 2000, Am J Clin Nutr 71:327-330). A few studies suggest that children with ADHD may have lower levels of key fatty acids but this remains to be replicated convincingly. In fact, one study found that the lower the levels, the worse the symptoms. The possibility that fatty acid deficiency is a trigger for ADHD may be plausible as nutrition scientists have recently demonstrated that the American diet is extremely deficient in omega-3 fatty acids. At the same time, ADHD diagnoses are rapidly increasing. More support for this idea comes from findings that breast-fed children have much lower levels of ADHD, and that until quite recently, infant formula contained NO omega-3 fatty acids. These remain purely correlational findings, however, that cannot be used to infer cause or the exact direction of the effects between these agents and ADHD symptoms. At present, experts do not accept the involvement of fatty acids as significant to the disorder or to its treatment.

A recent randomized double-blind experiment compared a fatty acid supplement with placebo in children with developmental coordination disorder (which exhibits a high degree of overlap with ADHD diagnoses). Fatty acid supplements improved spelling, reading, and behaviour after three months (Richardson and Montgomery, Pediatrics, 2005, 115:1360-1366). Numerous studies have shown an improvement in cognitive function, in mood, and in vision when omega 3 fatty acid supplements are given. While not directly showing a causal link between ADHD and fatty acids, increased levels of fatty acids has a beneficial effect on related behaviour.

Furthermore, creating a deficiency of omega-3 fatty acids in pregnant rats produces pups that are hyperactive and that have altered brain levels of dopamine in the same brain regions as seen in humans and other rat models of hyperactivity. More research, however, is clearly needed before dietary supplements, such as those involving fatty acids can be recommended for clinical use.

Sleep apnea
There is also new evidence that brief pauses in breathing (apnea) during infancy may be a cause of ADHD. Dr. Glenda Keating of Emory University presented data at the Society for Neuroscience annual meeting in October 2004, showing that repetitive drops in blood oxygen levels in newborn rats similar to that caused by apnea in some human infants is followed by a long-lasting reduction in dopamine levels, associated with ADHD. Apnea occurs in up to 85% of prematurely born human infants. [2] Though intriguing, these findings with rats must be replicated in humans.

Head injuries
It has been known for some decades that head injuries can cause a person to experience and display ADHD-like symptoms.

Brain scan technology has revealed differences in the size, symmetry, metabolism, and chemistry of the brain in those who have ADHD. However, it should be noted that there is yet no clear determination of the source of these differences. Some recent studies, such as that by Loo and colleagues at UCLA Medical School (Journal of the American Academy of Child and Adolescent Psychiatry, 2005) suggest that they are likely to be associated with the differences in genes discussed above. For instances, differences in the length of the DAT1 gene have been found to be linked to both differences in EEG patterns and to likelihood of responding to methylphenidate.

Treatment
There are many options available to treat people diagnosed with ADHD. The options with the greatest scientific support include a variety of medications, behavior-changing therapies, and educational interventions.

Mainstream treatments
The first-line medication used to treat ADHD are mostly stimulants, which work by stimulating the areas of the brain responsible for focus, attention, and impulse control. The use of stimulants to treat a syndrome often characterized by hyperactivity is sometimes referred to as a paradoxical effect. But there is no real paradox in that stimulants activitate brain inhibitory and self-organizing mechanisms permitting the individual to have greater self-regulation. The stimulants used include:

Methylphenidate -- Available in:
Regular formulation, sold as Ritalin, Metadate, Focalin,or Methylin. Duration: 4-6 hours per dose. Usually taken morning, lunchtime, and in some cases, afternoon.
Long acting formulation, sold as Ritalin SR, Metadate ER. Duration: 6-8 hours per dose. Usually taken twice daily.
All-day formulation, sold as Ritalin LA, Metadate CD, Concerta, Focalin XR. Duration: 10-12 hours per dose. Usually taken once a day.
Amphetamines --
Dextroamphetamine -- Available in:
Regular formulation, sold as Dexedrine. Duration: 4-6 hours per dose. Usually taken 2-3 times daily.
Long-acting formulation, sold as Dexedrine Spansules. Duration: 8-12 hours per dose. Taken once a day. Also known as dexamphetamine in Australia.
Adderall, a trade name for a mixture of dextroamphetamine and laevoamphetamine salts. -- Available in:
Regular formulation, Adderall. Duration: 4-6 hours a dose.
Long-acting formulation, Adderall XR. Duration: 12 hours. Taken once a day.
Methamphetamine -- Available in:
Regular formulation, sold as Desoxyn by Ovation Pharmaceutical Company. Usually taken twice daily.
Wellbutrin
Atomoxetine. A Selective Norepinephrine Reuptake Inhibitor (SNRI) introduced in 2003, it is the newest class of drug used to treat ADHD, and the first non-stimulant medication to be used as a first-line treatment for ADHD. Available in:
Once daily formulation, sold by Eli Lilly and Company as Strattera. Duration: 24 hours per dose. Taken once or twice a day.
Second-line medications include:

Benzphetamine -- a less powerful stimulant. Research on the effectiveness of this drug is not yet complete.
Provigil/Alertec/modafinil -- Research on this drug is not yet complete.
Cylert/Pemoline -- a stimulant used with great success until the late 1980s when it was discovered that this medication could cause liver damage. Although some physicians do continue to prescribe Cylert, it can no longer be considered a first-line medicine. In March 2005 the makers of Cylert announced that it would discontinue the medication's production.
Clonidine -- Initially developed as a treatment for high blood pressure, low doses in evenings and/or afternoons are sometimes used in conjunction with stimulants to help with sleep and because Clonidine sometimes helps moderate impulsive and oppositional behavior and may reduce tics.article
Because most of the medications used to treat ADHD are Schedule II under the U.S. DEA schedule system, and are considered powerful stimulants with a potential for diversion and abuse, there is controversy surrounding prescribing these drugs for children and adolescents. However, research studying ADHD sufferers who either receive treatment with stimulants or go untreated has indicated that those treated with stimulants are in fact much less likely to abuse any substance than ADHD sufferers who are not treated with stimulants.[3]

Alternative treatments
There are many alternative treatments for ADHD, most of them heavily disputed or relegated to adjunct status with medication treatment. This section attempts to deal with the most prominent of the alternative treatments. Bear in mind that the term "alternative" often means unscientific because there simply are little or no credible scientific studies to support these suggested interventions. If there were, they would be called scientifically based interventions, not alternative ones.