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Attention-deficit hyperactivity disorder
Attention-Deficit Hyperactivity Disorder (ADHD), or Hyperkinetic Disorder as officially known in the UK (though ADHD is more commonly used), is a contentious diagnosis considered by critics to be a fictional complaint . The disorder is believed by its proponents to present itself during childhood, and is believed by them to be characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility. ADHD is currently considered by its proponents to be a persistent and chronic condition for which no medical cure is available. ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults. About 60% of children diagnosed with ADHD are believed by proponents of the complaint to retain the disorder as adults. The disorder is believed by its supporters to be highly heritable, with contributions on occasion from trauma or toxic exposure. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counseling. Certain social critics are highly skeptical that the diagnosis denotes a genuine impairment and question virtually all that is known about ADHD. The symptoms of ADHD are not as profoundly different from normal behavior as are those of other chronic mental disorders. Still, by definition those said to be suffering from ADHD must display impaired functioning and many adverse life outcomes are also associated with ADHD.
ADHD is believed by its proponents to be a developmental neurological disorder. The term "developmental" means that certain traits such as impulse control significantly lag in development when compared to the general population. This developmental lag has been estimated to range between 30-40 percent in ADHD sufferers in comparison to their peers; consequently these delayed attributes are considered an impairment. ADHD has also been classified as a behavior disorder and a neurological disorder or combinations of these classifications such as neurobehavioural or neurodevelopmental disorders. These compounded terms are now more frequently used in the field to describe the disorder. Those with Predominately Inattentive ADHD often display few or no overt behaviors.
During the elementary years astudent considered by ADHD proponents to suffer from the complaint will have more difficulties with work completion, productivity, planning, remembering things needed for school, and meeting deadlines. Oppositional and socially aggressive behaviour is seen in 40-70 percent of children at this age. Even children thought by ADHD proponents to suffer from ADHD, with average to above average intelligence, show "chronic and severe under achievement". Fully 46% of those with ADHD have been suspended and 11% expelled. Thirty seven percent of those with ADHD do not get a high school diploma even though many of them will receive special education services. The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish highschool. Only five percent of those with ADHD will get a college degree compared to twenty seven percent of the general population. (US Census, 2003)
Formal diagnosis is based on a number of strict criteria, laid down in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV ), 4th edition. These criteria have been created for research purposes. Based on the DSM-IV criteria listed below, three types of ADHD are classified. Critics of the diagnosis argue that these criteria are subjective and vague, and cannot be tested against any objective diagnosis:
The terminology of ADD expired with the revision of the most current version of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which 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).
DSM-IV Criteria for ADHD
I. Either A or B:
A. Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:
B. Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:
II. Some symptoms that cause impairment were present before age 7 years.
III. Some impairment from the symptoms is present in two or more settings (e.g. at school/work and at home).
IV. There must be clear evidence of significant impairment in social, school, or work functioning.
V. The symptoms do not happen only during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder. The symptoms are not better accounted for by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).
In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the symptoms of ADD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10) 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".
The first criterion can be satisfied by using an ADHD-specific instrument such as the Conners' Rating Scale. The second criterion is best fulfilled by examining the individual's history. This history can be obtained from parents and teachers, or a patient's memory. The requirement that symptoms be present in more than one setting is very important because the problem may not be with the child, but instead with teachers or parents who are too demanding. The use of intelligence testing, psychological testing, and neuropsychological testing (to satisfy the third criterion) is essential in order to find or rule out other factors that might be causing or complicating the problems experienced by the patient.
The Centers for Disease Control and Prevention (CDC) state that a diagnosis of ADD should only be made by trained health care providers, as many of the symptoms may also be part of other conditions, such as bodily illness or other physiological disorders, such as hyperthyroidism. It is not uncommon that physically and mentally nonpathological individuals exhibit at least some of the symptoms from time to time. Severity and pervasiveness of the symptoms leading to prominent functional impairment across different settings (school, work, social relationships) are major factors in a positive diagnosis.
Adults often continue to be impaired by ADD. Adults with ADD are diagnosed under the same criteria, including the stipulation that their symptoms must have been present prior to the age of seven. Adults face some of their greatest challenges in the areas of self-control and self-motivation, as well as executive functioning, usually having more symptoms of inattention and fewer of hyperactivity or impulsiveness than children do.
Common comorbid conditions are Oppositional Defiance Disorder (ODD). About 20% to 25% of children with ADD meet criteria for a learning disorder. Learning disorders are more common when there are inattention symptoms.
Studies show that there may be a familial transmission of the disorder which does not occur through adoptive relationships. Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population. While the majority of ADHD is believed to be genetic in nature, roughly 1/5 of all ADHD cases are thought to be acquired after conception due to brain injury caused by either toxins or physical trauma prenatally or postnatally. According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded as a chronic disorder for which there are some effective treatments, but no true cure. Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counseling. The symptoms of ADHD are not as profoundly different from normal behavior as are those of other chronic mental disorders. Still, ADHD has been shown to often impair functioning, and many adverse life outcomes are associated with ADHD.
The exact cause of ADHD remains unknown and its proponents believe that in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology. Still, there is a wide body of evidence which indicates that the overriding cause of ADD is genetics. Research suggests that a large majority of ADHD arises from a combination of various genes, many of which affect dopamine transporters. Suspect genes include the 10-repeat allele of the DAT1 gene, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI). Additionally, SPECT scans found people with ADHD to have reduced blood circulation, and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead.
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 ADD, but the brain's ability to produce dopamine itself. The study was done by injecting 20 ADD 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 across the board. They speculated that since ADD 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.
An early PET scan study found that global cerebral glucose metabolism was 8.1% lower in medication-naive adults who had been diagnosed as ADHD while children. The image on the left illustrates glucose metabolism in the brain of a 'normal' adult while doing an assigned auditory attention task; the image on the right illustrates the areas of activity in the brain of an adult who had been diagnosed with ADHD as a child when given that same task; these are not pictures of individual brains, which would contain substantial overlap, these are images constructed to illustrate group-level differences. Additionally, the regions with the greatest deficit of activity in the ADHD patients (relative to the controls) included the premotor cortex and the superior prefrontal cortex. A second study in adolescents failed to find statistically significant differences in global glucose metabolism between ADD patients and controls, but did find statistically significant deficits in 6 specific regions of the brains of the ADD patients (relative to the controls). Most notably, lower metabolic activity in one specific region of the left anterior frontal lobe was significantly inversely correlated with symptom severity. These findings strongly imply that lowered activity in specific regions of the brain, rather than a broad global deficit, is involved in ADHD symptoms. However, these readings are of subjects doing an assigned task. They could be found in ADHD diagnosed patients because they simply were not attending to the task. Hence the parts of the brain used by others doing the task would not show equal activity in the ADHD patients.
The estimated contribution of non genetic factors to the contribution of all cases of ADHD is 20 percent. The environmental factors implicated are common exposures and include alcohol, in utero tobacco smoke and lead exposure. Lead concentration below the Center for Disease Control's action level account for slightly more cases of ADHD than tobacco smoke (290 000 versus 270 000, in the USA, ages 4 to 15). Complications during pregnancy and birth—including premature birth—might also play a role. It has been observed that women who smoke while pregnant are more likely to have children with ADHD. This could be related to the fact that nicotine is known to cause hypoxia (lack of oxygen) in utero, but it could also be that ADD women have more probabilities to smoke both in general and during pregnancy, being more likely to have children with ADHD due to genetic factors.
Head injuries can cause a person to present ADD-like symptoms, possibly because of damage done to the patient's frontal lobes. Because these types of symptoms can be attributable to brain damage, the earliest designation for ADHD was "Minimal Brain Damage".
There is no compelling evidence that social factors alone can create ADD. Many researchers believe that attachments and relationships with caregivers and other features of a child's environment have profound effects on attentional and self-regulatory capacities. It is noteworthy that a study of foster children found that an inordinate number of them had symptoms closely resembling ADHD. An editorial in a special edition of Clinical Psychology in 2004 stated that "our impression from spending time with young people, their families and indeed colleagues from other disciplines is that a medical diagnosis and medication is not enough. In our clinical experience, without exception, we are finding that the same conduct typically labelled ADHD is shown by children in the context of violence and abuse, impaired parental attachments and other experiences of emotional trauma." Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.
Despite the lack of evidence that nutrition causes ADD, studies have found that malnutrition is correlated with attention deficits.
According to an advanced high-precision imaging study by researchers at the United States National Institutes of Health's National Institute of Mental Health, an actual delay in physical development in some brain structures, with a median value of three years, was observed in the brains of 223 ADHD patients beginning in elementary school, during the period when cortical thickening during childhood begins to change to thinning following puberty. The delay was most prominent in the frontal cortex and temporal cortex, which are believed responsible for the ability to control and focus thinking, attention and planning, suppress inappropriate actions and thoughts, remember things from moment to moment, and work for reward, all functions whose disturbance is associated with a diagnosis of ADHD; the region with the greatest average delay, the middle of the prefrontal cortex, lagged a full five years in development in the ADHD patients. 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 both be required for the restlessness and fidgetiness that characterise an ADHD diagnosis. Aside from the delay, both groups showed a similar back-to-front development of brain maturation with different areas peaking in thickness at different times. This contrasts with the pattern of development seen in other disorders such as autism, where the peak of cortical thickening occurs much earlier than normal.
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.
There are several clinically proven effective options available to treat people diagnosed with ADHD. It has been believed that ADHD is treated most effectively, and cost efficiently, with medication. However, recent long term studies now cast serious doubt to this assertion. "[D]rugs such as Ritalin and Concerta work no better than therapy after three years of treatment. The findings by an influential US study also suggested long-term use of the drugs could stunt children's growth. It said that the benefits of drugs had previously been exaggerated." Psychotherapy is another option, with or without medication Omega-3 fatty acids, zinc and magnesium may have benefits with regards to ADHD symptoms.
Comorbid disorders or substance abuse can make finding the proper diagnosis and the right overall treatment more costly and time-consuming.
Social impairment for those with ADHD is seen at both school and work. They often have more troubled relationships with peers or family members. At the workplace, they change jobs more often and are more likely to get fired. Their income level does not rise as quickly as their peers, even when education level, IQ, and their neighborhood is accounted for. Thirty five percent of all those with ADHD will be self employed in their mid-thirties. Those with ADHD are at greater risk of: injury, abnormal risk taking, smoking, having learning disabilities, other mental disorders, teen pregnancy, substance abuse, involvement with the criminal justice system, and having a poorer driving record.
ADHD's prevalence worldwide is estimated to be a bit over 5%, with most of the reported variability being due to methodological characteristics of studies. 10% of males, and (only) 4% of females have been diagnosed in the U.S. This apparent sex difference may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.
Some sources claim to have identified historical and literary references to ADHD before 1900. However, the condition we refer to as "ADHD" dates to the mid-twentieth century, when physicians developed a diagnosis for a set of conditions variously referred to as "minimal brain damage", "learning/behavioural disabilities" or "hyperactivity". In 493 BC, physician-scientist Hippocrates described a condition that seems to be compatible with what we now know as ADHD. He described patients who had "quickened responses to sensory experience, but also less tenaciousness because the soul moves on quickly to the next impression". Hippocrates attributed this condition to an "overbalance of fire over water”. His remedy for this "overbalance" was "barley rather than wheat bread, fish rather than meat, water drinks, and many natural and diverse physical activities." Shakespeare made reference to a "malady of attention", in King Henry VIII. In 1845, Dr. Heinrich Hoffmann (a German physician and poet who wrote books on medicine and psychiatry) became interested in writing for children when he couldn't find suitable materials to read to his 3-year-old son. The result was a book of poems, complete with illustrations, about children and their undesirable behaviours. "Die Geschichte vom Zappel-Philipp" (The Story of Fidgety Philip) in Der Struwwelpeter was a description of a little boy who could be interpreted as having attention deficit hyperactivity disorder, or as merely a moral fable to amuse young children and encourage them to behave properly.
In 1902, the English pediatrician George Still gave a series of lectures to the Royal College of Physicians in England, and described a condition which some have claimed is analogous to ADHD. Still described a group of children with significant behavioral problems, caused, he believed, by an innate hereditary dysfunction and not by poor child rearing or environment.
The 1918–1919 influenza pandemic left many survivors with encephalitis, affecting their neurological functions. Some of these exhibited immediate behavioral problems which may correspond to ADHD (although no diagnosis for such a disorder existed at the time). This caused many later commentators to believe that the condition was the result of injury rather than heredity. The concept of hyperactivity not being caused by brain damage was first described by Stella Chess as, ""Hyperactive Child Syndrome" in 1960. This caused a significant rift in the understanding of the disorder. Europeans saw hyperkinesis as unusual and often associated it with retardation, brain damage, and conduct disorders, and changes to the ICD were not made until 1994. In the USA by 1966, following observations that the condition existed without any objectively observed pathological disorder or injury, researchers changed the terminology from Minimal Brain Damage to Minimal Brain Dysfunction.
In 1937 a Dr. Bradley in Providence, RI reported that a group of children with behavioral problems improved after being treated with stimulant medication. In 1957 the stimulant methylphenidate (Ritalin) became available. In its various forms (Ritalin, Focalin, Concerta, Metadate, and Methylin), it remains one of the most widely prescribed medications for ADHD. Ritalin was first produced in 1950. Initially the drug was used to treat narcolepsy, chronic fatigue, depression, and to counter the sedating effects of other medications. The drug began to be used for ADHD in the 1960s and steadily rose in use. In 1975 Pemoline (Cylert) was approved by the FDA for use in the treatment of ADHD. While an effective agent for managing the symptoms, the development of liver failure in 14 cases over the next 27 years would result in the manufacturer withdrawing this medication from the market. New delivery systems for medications were invented in 1999 that eliminated the need for multiple doses across the day or taking medication at school. These new systems include pellets of medication coated with various time-release substances to permit medications to dissolve hourly across an 8–12 hour period (Medadate CD, Adderall XR, Focalin XR) and an osmotic pump that extrudes a liquid methylphenidate sludge across an 8–12 hour period after ingestion (Concerta). In 2003 – Atomoxetine (Strattera) received the first FDA approval for a nonstimulant drug to be used specifically for ADHD. In 2007 Lisdexamfetamine becomes the first prodrug to receive FDA approval for ADHD. The landmark study of 1999 – The largest study of treatment for ADHD in history – is published in the American Journal of Psychiatry. Known as the Multimodal Treatment Study of ADHD (MTA Study), it involved more than 570 children with ADHD at 6 sites in the United States and Canada randomly assigned to 4 treatment groups. Results generally showed that medication alone was more effective than psychosocial treatments alone, but that their combination was beneficial for some subsets of ADHD children beyond the improvement achieved only by medication. More than 40 studies have subsequently been published from this massive dataset.
Psychiatry first codified a condition called “hyperkinetic reaction of childhood” in 1968, displaying the psychoanalytical influences of that time. The name Attention Deficit Disorder (ADD) was first introduced in DSM-III, the 1980 edition. By 1987 – The DSM-IIIR was released changing the diagnosis to "Undifferentiated Attention Deficit Disorder." Further revisions to the DSM were made in 1994 – DSM-IV described three groupings within ADHD, which can be simplified as: mainly inattentive; mainly hyperactive-impulsive; and both in combination. During 1996, ADHD accounted for at least 40% of child psychiatry references.
The ADHD diagnosis has been questioned on many fronts. Some critics focus upon the positive traits that people with ADHD are thought to have, such as "hyperfocusing." Others believe ADHD is a divergent or normal-variant human behavior (using the term neurodiversity to describe this idea), emphasizing that human behaviour is immensely variable and "ADHD" may simply represent one part of the spectrum. Such critics sometimes allege that ADHD is not actually a discrete condition and question why it should be treated with drugs. Others dispute the alleged genetic basis of ADHD.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Attention-deficit_hyperactivity_disorder". A list of authors is available in Wikipedia.|