| 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 psychiatric[1] and a neurobehavioral disorder.[2] It is characterized by either significant difficulties of inattention or hyperactivity and impulsiveness or a combination of the two. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), symptoms emerge before seven years of age.[3] There are three subtypes of the disorder which consist of it being predominantly inattentive (ADHD-PI or ADHD-I), predominately hyperactive-impulsive (ADHD-HI or ADHD-H), or the two combined (ADHD-C). Oftentimes people refer to ADHD-PI as "Attention deficit disorder" (ADD), however, the term was revised in the 1994 version of the DSM.
ADHD impacts school-aged children and results in restlessness, acting impulsively, and lack of focus which impairs their ability to learn properly. It is the most commonly studied and diagnosed psychiatric disorder in children, affecting about 3 to 5 percent of children globally[4][5] and diagnosed in about 2 to 16 percent of school-aged children.[6] It is a chronic disorder[7] with 30 to 50 percent of those individuals diagnosed in childhood continuing to have symptoms into adulthood.[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, applied behavior analysis (ABA, previously known as behavior modification), 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] 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.[19][20][21] The National Institute for Clinical Excellence in 2004, while acknowledging controversies and criticisms, stated that the current therapeutic treatment interventions and methods of diagnosis for ADHD are based on the dominant view of the academic literature.[22]:p.133 NICE further concluded that despite such criticism, ADHD represented a valid clinical condition,[22]:p.138 with genetic, environmental, neurobiological, and demographic factors.[22]:p.139 According to NICE, only children with severe ADHD symptoms should be considered for medication as a first-line treatment option. Medication therapy can also be considered for those with moderate ADHD symptoms who either refuse psychotherapeutic options or else fail to respond to psychotherapeutic input.[22]:p.317
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Contents
- 1 Classification
- 2 Signs and symptoms
- 2.1 Comorbid disorders
- 2.2 In children who have a high IQ
- 2.3 In adults
- 3 Cause
- 3.1 Genetics
- 3.2 Evolution
- 3.3 Environmental
- 3.4 Social
- 3.4.1 Social construct theory of ADHD
- 3.4.2 Low arousal theory
- 4 Pathophysiology
- 5 Diagnosis
- 5.1 DSM-IV
- 5.2 ICD-10
- 5.3 Other guidelines
- 5.4 Differential
- 6 Management
- 6.1 Psychosocial
- 6.2 Medication
- 7 Prognosis
- 8 Epidemiology
- 9 History
- 10 Society and culture
- 10.1 Legal status of medications
- 10.2 Controversies
- 11 References
- 12 Further reading
- 13 External links
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Classification
ADHD may be seen as one or more continuous traits found normally throughout the general population.[22] 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.[23] However, the definition of ADHD is based on behaviour and it does not imply a neurological disease.[22] ADHD is classified as a disruptive behavior disorder along with oppositional defiant disorder, conduct disorder and antisocial personality disorder.[24]
The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) classifies ADHD according to the predominance of symptoms of:
- Inattention;
- Hyperactivity–impulsivity;
- or a combination of both (Combined type).[25]
This subdivision is based on presence of at least six out of nine long-term maladaptive symptoms (lasting at least 6 months) of either inattention, hyperactivity–impulsivity, or both. Thus, a child who is diagnosed with the inattention subtype may also show signs of hyperactivity–impulsivity, and vice-versa. To be considered, the symptoms must have appeared before the age of 6, manifest in more than one environment (eg at home and at school or work), and not be better explained by another mental disorder.[25]
Most children with ADHD have the combined type. Children with the inattention subtype are less likely to act out or have difficulties getting along with other children. They may sit quietly, but without paying attention to what they are doing. Therefore, the child may be overlooked, and parents and teachers may not notice symptoms of ADHD.[25]
Signs and symptoms
Children with ADHD tend to get distracted from schoolwork rather easily, and they often behave disruptively.
[26][27]
Inattention, hyperactivity, disruptive behavior and impulsivity are common in ADHD.[27] Academic difficulties are also frequent.[27] 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 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]
- Be easily distracted, miss details, forget things, and frequently switch from one activity to another
- Have difficulty maintaining focus on one task
- Become bored with a task after only a few minutes, unless doing something enjoyable
- Have difficulty focusing attention on organizing and completing a task or learning something new or trouble completing or turning in homework assignments, often losing things (e.g., pencils, toys, assignments) needed to complete tasks or activities
- Not seem to listen when spoken to
- Daydream, become easily confused, and move slowly
- Have difficulty processing information as quickly and accurately as others
- Struggle to follow instructions.
Predominantly hyperactive-impulsive type symptoms may include:[29]
- Fidget and squirm in their seats
- Talk nonstop
- Dash around, touching or playing with anything and everything in sight
- Have trouble sitting still during dinner, school, and story time
- Be constantly in motion
- Have difficulty doing quiet tasks or activities
and also these manifestations primarily of impulsivity:[29]
- Be very impatient
- Blurt out inappropriate comments, show their emotions without restraint, and act without regard for consequences
- Have difficulty waiting for things they want or waiting their turns in games
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]
Some children, adolescents, and adults with ADHD have an increased risk of experiencing difficulties with social skills, such as social interaction and forming and maintaining friendships. About half of children and adolescents with ADHD experience rejection by their peers compared to 10-15 percent of non-ADHD children and adolescents. Training in social skills, behavioural modification and medication may have some limited beneficial effects. The most important factor in reducing emergence of later psychopathology, such as major depression, criminality, school failure, and substance use disorders is formation of friendships with people who are not involved in delinquent activities.[31] Adolescents with ADHD are more likely to have difficulty making and keeping friends due to impairments in processing verbal and nonverbal language.[32]
Handwriting difficulties seem to be common in children with ADHD.[33] Delays in speech and language as well as motor development occur more commonly in the ADHD population.[34][35][33] A 2009 study found that children with ADHD move around a lot because it helps them stay alert enough to complete challenging tasks.[36][37]
Comorbid disorders
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.
Some of the associated conditions are:
- Oppositional defiant disorder and conduct disorder, which occur with ADHD at a rate of 50 percent and 20 percent respectively,[38] are characterized by antisocial behaviors such as stubbornness, aggression, frequent temper tantrums, deceitfulness, lying, or stealing,[39] inevitably linking these comorbid disorders with antisocial personality disorder (ASPD); about half of those with hyperactivity and ODD or CD develop ASPD in adulthood.[40] However, modern brain imaging technology indicates that conduct disorder and ADHD are two distinct conditions.[41]
- Borderline personality disorder, which was according to a study on 120 female psychiatric patients diagnosed and treated for BPD associated with ADHD in 70 percent of those cases.[42]
- Primary disorder of vigilance, which is characterized by poor attention and concentration, as well as difficulties staying awake. These children tend to fidget, yawn and stretch and appear to be hyperactive in order to remain alert and active.[39]
- Mood disorders. Boys diagnosed with the combined subtype have been shown likely to suffer from a mood disorder.[43]
- Bipolar disorder. Adults with ADHD sometimes have co-morbid bipolar disorder, which requires careful assessment in order to accurately diagnose and treat both conditions.[44]
- Anxiety disorder, which has been found to be common in girls diagnosed with the inattentive subtype of ADHD.[45]
- Obsessive-compulsive disorder. OCD can co-occur with ADHD and shares many of its characteristics.[39]
- Substance use disorders. Adolescents and adults with ADHD are at a significantly increased risk of developing a substance abuse problem which can interfere with the evaluation and treatment of ADHD. The most commonly misused substances by the ADHD population are alcohol and cannabis; serious substance misuse problems should be treated first due to the serious risks and impairments that occur,[46][22]:p.38 with long-term alcohol misuse and long-term cannabis misuse and other drug misuse.
There is a strong association between persistent bed wetting and ADHD[47] as well as dyspraxia with up to 50 percent of dyspraxics having ADHD.[48] Multiple research studies have also found a significant association between ADHD and language delay.[49] 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.[50]
In children who have a high IQ
There has been some controversy as to whether ADHD children with a high IQ have significant impairments. Research has shown that high IQ children with ADHD are more likely to repeat grades and have more social and functional impairments; more than half require additional academic support compared to children without ADHD. Additionally, more than half of high IQ ADHD people experience major depressive disorder or oppositional defiant disorder at some point in their lives. Generalised anxiety disorder, separation anxiety disorder and social phobia is also more common in high IQ ADHD individuals. There is some evidence that high IQ ADHD individuals are not at an increased risk of substance abuse and conduct disorder compared to low and average IQ ADHD young people. High IQ children and adolescents with ADHD can have their high intelligence level missed when standard testing is performed; high IQ ADHD people tend to require more comprehensive testing to detect their true intelligence level.[51] High IQ ADHD children have a unique neuropsychological profile which typically shows a gap of 20 points or more between the verbal IQ and the performance IQ when tested on the Wechsler Intelligence Scale for Children; high IQ children without ADHD do not usually present with this sizable gap.[52]
In adults
Main article: Adult attention deficit hyperactivity disorder
Between 2 and 5 percent of adults have ADHD.[53] Between one-third,[54] and up to 80 percent of the children diagnosed with ADHD continue having symptoms well into adulthood.[55] Many adults, however, remain untreated.[56] 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.[57] They often have such associated psychiatric comorbidities as depression, anxiety disorder, substance abuse, or a learning disability.[57] 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.
Cause
The specific causes of ADHD are not known.[58] There are, however, a number of factors that may contribute to, or exacerbate ADHD. They include genetics, diet and the social and physical environments.
Genetics
Twin studies indicate that the disorder is highly heritable and that genetics are a factor in about 75 percent of all cases.[22] Hyperactivity also seems to be primarily a genetic condition; however, other causes have been identified.[59]
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,[60] dopamine beta-hydroxylase monoamine oxidase A, catecholamine-methyl transferase, serotonin transporter promoter (SLC6A4), 5HT2A receptor, 5HT1B receptor,[61] the 10-repeat allele of the DAT1 gene,[62] the 7-repeat allele of the DRD4 gene,[62] and the dopamine beta hydroxylase gene (DBH TaqI).[63] 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.[64]
Evolution
See also: Hunter vs. farmer hypothesis
As ADHD is more common than 1 percent of the population, researchers have proposed that due to the high prevalence of ADHD that natural selection has favoured ADHD possibly because the individual traits may be beneficial on their own, and only become dysfunctional when these traits combine to form ADHD.[65] The high prevalence of ADHD may in part be because women in general are more attracted to males who are risk takers, thereby promoting ADHD in the gene pool.[66]
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, competition, and/or unpredictable behavior (i.e. exploring new areas, finding new food sources, etc.), where these societies may have benefited from confining impulsive or unpredictable behavior to a small subgroup. In these situations, ADHD would have been beneficial to society as a whole even while severely detrimental to the individual.[66] More recent research suggests that because ADHD is more common in mothers who are anxious or stressed that ADHD is a mechanism of priming the child with the necessary traits for a stressful or dangerous environment, such as increased impulsivity and explorative behaviour etc.[67] 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.[68] 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.[69]
Environmental
ADHD is predominantly a genetic disorder with environmental factors contributing a small role to the etiology of ADHD. Twin studies have shown that ADHD is largely genetic with 76 percent of the phenotypic variance being explained by inherited genetic factors.[70][71] Environmental factors implicated include alcohol and tobacco smoke exposure during pregnancy and environmental exposure to lead in very early life.[72] The relation of smoking to ADHD could be due to nicotine causing hypoxia (lack of oxygen) to the fetus in utero.[73] It could also be that women with ADHD are more likely to smoke[74] and therefore, due to the strong genetic component of ADHD, are more likely to have children with ADHD.[75] Complications during pregnancy and birth—including premature birth—might also play a role.[76] ADHD patients have been observed to have higher than average rates of head injuries;[77] however, current evidence does not indicate that head injuries are the cause of ADHD in the patients observed.[78] 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.[79][80]
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.[81]
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.[82][83]
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.[84]
Diet
Main article: Diet and attention deficit hyperactivity disorder
A study[85] 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.[86] 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.[87]
Social
The World Health Organization states that the diagnosis of ADHD can represent family dysfunction or inadequacies in the educational system rather than individual psychopathology.[88] 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.[89] Researchers have found behavior typical of ADHD in children who have suffered violence and emotional abuse.[22][90] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD.[91] ADHD is also considered to be related to sensory integration dysfunction.[92] 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.[93]
Social construct theory of ADHD
Main article: Social construct theory of ADHD
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.[94] 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."[95][96]
Low arousal theory
Main article: Low arousal theory
According to the low arousal theory, people with ADHD need excessive activity as self-stimulation because of their state of abnormally low arousal.[97] 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.[98]
Pathophysiology
Diagram of the human brain
The pathophysiology of ADHD is unclear and there are a number of competing theories.[99] 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.[100] Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are used only for research and not diagnostic purposes.[101] 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.[102]
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.[103] It should be noted that stimulant medication itself may affect growth factors of the central nervous system.[104]
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.[105]
Previously it was thought that the elevated number of dopamine transporters seen in ADHD patients was part of the pathophysiology of ADHD but it now appears that the reason for elevated striatal dopamine transporter density in ADHD individuals is due to neuroadaptations occurring due to the continuous exposure to stimulants such as methylphenidate or dexamphetamine as the body tries to counter-act the effects of the stimulants by developing a tolerance to the stimulant medications.[106] 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.[107] 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.[108]
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[109] 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.[110][111] They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology.[110][112]
Diagnosis
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.[113]
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.[114]
Children who display the behavioural symptoms of ADHD but who do not have any significant functional impairments compared to their age matched peers cannot be diagnosed as having the psychiatric disorder, ADHD.[115]
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).[citation needed]
DSM-IV
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:[115]
- ADHD, Combined Type is a combination of the two other ADHD subtypes.[115]
- ADHD Predominantly Inattentive Type presents with symptoms including being easily distracted, forgetful, daydreaming, disorganisation, poor concentration, and difficulty completing tasks.[115]
- ADHD, Predominantly Hyperactive-Impulsive Type presents with excessive fidgetiness and restlessness, hyperactivity, difficulty waiting and remaining seated, immature behaviour; destructive behaviors may also be present.[115]
For a diagnosis of ADHD to be mare the signs must not be due to 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).[116]
ICD-10
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[34]) 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".[34]
Other guidelines
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:[117]
- The use of explicit criteria for the diagnosis using the DSM-IV-TR.
- The importance of obtaining information about the child’s signs in more than one setting.
- The search for coexisting conditions that may make the diagnosis more difficult or complicate treatment planning.
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.[118] 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.[119]
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:
- The behaviors must appear before age 7.
- They must continue for at least six months.
- The symptoms must also create a real handicap in at least two of the following areas of the child’s life:
- in the classroom,
- on the playground,
- at home,
- in the community, or
- in social settings.[120]
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.[120]
Differential
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 as causing the ADHD symptoms include: hypothyroidism, anemia, lead poisoning, chronic illness, hearing or vision impairment, substance abuse, medication side-effects, sleep impairment and child abuse,[121] 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.[122] 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.[123]
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.[122][124][125] 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.[122][126]
From a clinical standpoint, mechanisms that account for the phenomenon of excessive daytime sleepiness include:
- Chronic sleep deprivation, that is insufficient sleep for physiologic sleep needs,
- Fragmented or disrupted sleep, caused by, for example, obstructive sleep apnea (OSA) or periodic limb movement disorder (PLMD),
- Primary clinical disorders of excessive daytime sleepiness, such as narcolepsy and
- Circadian rhythm disorders, such as delayed sleep phase syndrome (DSPS). A study in the Netherlands compared two groups of unmedicated 6-12-year-olds, all of them with "rigorously diagnosed ADHD". 87 of them had problems getting to sleep, 33 had no sleep problems. The larger group had a significantly later dim light melatonin onset (DLMO) than did the children with no sleep problems.[127]
Management
Main article: Attention-deficit hyperactivity disorder management
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.[128] While medication has been shown to improve behavior when taken over the short term, they have not been shown to alter long-term outcomes.[129] Medications have at least some effect in about 80% of people.[130] Dietary modifications many also be of benefit.[131]
Psychosocial
The evidence is strong for the effectiveness of behavioral treatments in ADHD.[132] It is recommended first line in those who have mild symptoms and in preschool-aged children.[133] 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,[22] neurofeedback,[134] and nature exposure.[135][136] Parent training and education have been found to have short-term benefits.[137] 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.[138] Several ADHD specific support groups exist as informational sources and to help families cope with challenges associated with dealing with ADHD.
Medication
methylphenidate (Ritalin) 10 mg tablets
Stimulant medications are the medical treatment of choice.[139][140] There are a number of non-stimulant medications, such as atomoxetine, that may be used as alternatives.[139] 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.[141] While stimulants and atomoxetine are generally safe, there are side-effects and contraindications to their use.[139] Medications are not recommended for preschool children, as their long-term effects in such young people are unknown.[22][142] There is very little data on the long-term benefits or adverse effects of stimulants for ADHD.[143] Any drug used for ADHD may have adverse drug reactions such as psychosis and mania,[144] though methylphenidate-induced psychosis is uncommon. Regular monitoring of individuals receiving long-term stimulant therapy for possible treatment emergent psychosis has been recommended.[145] Tolerance to the therapeutic effects of stimulants can occur,[106] and abrupt withdrawal is not recommended.[146] People with ADHD have an increased risk of substance abuse, and stimulant medications reduce this risk.[147][148] Stimulant medications in and of themselves however have the potential for abuse and dependence.[149] 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.[150]
Prognosis
Children diagnosed with ADHD have significant difficulties in adolescence, regardless of treatment.[151][152] 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.[153] 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.[154] Also in the US, less than 5 percent of individuals with ADHD get a college degree[155] compared to 28 percent of the general population.[156] 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.[121][157][158] ADHD persists into adulthood in about 30 to 50 percent of cases.[8] Those affected are likely to develop coping mechanisms as they mature, thus compensating for their previous ADHD.[9]
Epidemiology
Percent of United States youth 4–17 ever diagnosed with ADHD as of 2007
Percent of United States youth 4–17 ever diagnosed with ADHD as of 2003
[159]
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.[160] Published studies have found rates of ADHD as low as 2 percent and as high as 14 percent among school-aged children.[161] The rates of diagnosis and treatment of ADHD are also much higher on the East Coast of the USA than on the West Coast.[162] The frequency of the diagnosis differs between male children (10%) and female children (4%) in the United States.[163] This difference between genders may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.[164]
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.[22]
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.[165]
History
Main article: History of attention-deficit hyperactivity disorder
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.[166][167] 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),[168] "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.[169] The use of stimulants to treat ADHD was first described in 1937.[170]
Society and culture
See also: List of people diagnosed with attention-deficit hyperactivity disorder
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."[171] 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"[172] 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.[173] 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.[174] 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.[175] 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."[176]
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).[177]
Legal status of medications
Stimulants legal status was recently reviewed by several international organizations:
- Internationally, methylphenidate is a Schedule II drug under the Convention on Psychotropic Substances.[178]
- In the United States, methylphenidate is classified as a Schedule II controlled substance, the designation used for substances that have a recognized medical value but present a high likelihood for abuse because of their addictive potential.
- In the United Kingdom, methylphenidate is a controlled 'Class B' substance, and possession without prescription is illegal, with a sentence up to 14 years and/or an unlimited fine.[179]
- In New Zealand, it is a 'class B2 controlled substance'. unlawful possession is punishable by 6-month prison sentence and distribution of it is punishable by a 14-year sentence.
Controversies
Main article: Attention-deficit hyperactivity disorder controversies
ADHD and its diagnosis and treatment have been considered controversial since the 1970s.[16][17][180] The controversies have involved clinicians, teachers, policymakers, parents and the media. Opinions regarding ADHD range from not believing it exists at all[181] to believing there are genetic and physiological bases for the condition as well as disagreement about the use of stimulant medications in treatment.[181][17][18] 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.[19][20][21] 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."[182][183] 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.[184] In its guideline, it states that available evidence indicate that ADHD is a valid diagnosis and that medication should be the first-line treatment for adults, for children with severe ADHD, or for children with mild ADHD who do not respond to non-medication interventions. 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.[181] 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.[185] Possible long-term side-effects of stimulants and their usefulness are largely unknown because of a lack of long-term studies.[186] Some research raises questions about the long-term effectiveness and side-effects of medications used to treat ADHD.[187]
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.[188]
With a "wide variation in diagnosis across states, races, and ethnicities"[189] some investigators[who?] suspect that factors other than neurological conditions play a role when the diagnosis of ADHD is made.[189][190] 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.[189][190] 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).[191]
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Bibliography
- Dr Jennifer Erkulwater; Dr Rick Mayes; Dr Catherine Bagwell (2009). Medicating Children: ADHD and Pediatric Mental Health. Cambridge: Harvard University Press. p. 5. ISBN 0-674-03163-6.
Further reading
- Faraone Stephen V (2005). "The scientific foundation for understanding attention-deficit/hyperactivity disorder as a valid psychiatric disorder". Eur Child Adolesc Psychiatry 14 (1): 1–10. doi:10.1007/s00787-005-0429-z. PMID 15756510.
- Faraone, Stephen, V.Straight Talk about Your Child's Mental Health: What to Do When Something Seems Wrong (2003) New York:Guilford Press
- Hartmann, Thom (2003). The Edison gene: ADHD and the gift of the hunter child. Rochester, Vt: Park Street Press. ISBN 0-89281-128-5.
- Matlen, Terry. (2005) "Survival Tips for Women with AD/HD". ISBN 1-886941-59-9
- Millichap, J. Gordon, MD, FRCP Attention Deficit Hyperactivity Disorder Handbook: A Physician’s Guide to ADHD. New York: Springer, 2010 ISBN 978-1-4419-1396-8
- Southall, Angela (2007). The Other Side of ADHD:Attention Deficit Hyperactivity Disorder Exposed and Explained. Radcliffe Publishing Ltd. ISBN 1-84619-068-1. http://books.google.com/?id=AKXhThWgvyYC&pg=PA41&lpg=PA41&dq=barkley+drug+company+funding. Retrieved 2009-05-02.
External links
- National Institute of Mental Health on ADHD
- "CG72 Attention deficit hyperactivity disorder (ADHD): full guideline" (PDF). NHS. 9 March 2009. http://www.nice.org.uk/nicemedia/pdf/ADHDFullGuideline.pdf. Retrieved 2009-01-08.
- New Zealand MOH Guidelines for the Assessment and Treatment of Attention-Deficit/Hyperactivity Disorder
- Functional Disconnection Identified Between Key Brain Areas in Children With ADHD
- Hellenic Society for the Study of ADHD
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Attention deficit hyperactivity disorder (F90, 314)
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| Main articles |
- History of ADHD
- ADHD in adults
- ADHD controversies
- ADHD management
- List of ADHD organizations
- Social construct theory of ADHD
- ADHD coaching
- Major characteristics: Attention
- Hyperactivity
- Impulsivity
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| Sub-types |
- ADHD predominantly inattentive (ADHD-I, formerly ADD)
- ADHD predominantly hyperactive (ADHD-H, formerly ADHD)
- ADHD combined type (ADHD-C)
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| Notable publications |
- Driven to Distraction (1994)
- Delivered from Distraction (2005)
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| Notable experts |
- Russell Barkley
- Stephen Faraone
- Edward Hallowell
- John Ratey
- Joseph Biederman
- 19th century: Alexander Crichton
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| Relevant drugs |
- methylphenidate (Ritalin, Concerta, and others)
- dextroamphetamine (Dexedrine)
- mixed amphetamine salts (Adderall)
- Non-stimulant: Atomoxetine (Strattera)
- More...
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| Other |
- Low arousal theory
- Sluggish cognitive tempo
- Sensory integration dysfunction
- Hypokalemic sensory overstimulation
- Deficits in Attention, Motor control and Perception
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dsrd (o, p, m, p, a, d, s), sysi/epon, spvo
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proc(eval/thrp), drug(N5A/5B/5C/6A/6B/6D)
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Mental and behavioral disorders (F 290–319)
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Neurological/symptomatic
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Dementia
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- Mild cognitive impairment
- Alzheimer's disease
- Multi-infarct dementia
- Pick's disease
- Creutzfeldt–Jakob disease
- Huntington's disease
- Parkinson's disease
- AIDS dementia complex
- Frontotemporal dementia
- Sundowning
- Wandering
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Autism spectrum
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- Autism
- Asperger syndrome
- Savant syndrome
- PDD-NOS
- High-functioning autism
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Other
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- Delirium
- Post-concussion syndrome
- Organic brain syndrome
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Psychoactive substances, substance abuse, drug abuse and substance-related disorders
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- Intoxication/Drug overdose
- Physical dependence
- Substance dependence
- Rebound effect
- Double rebound
- Withdrawal
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Schizophrenia, schizotypal and delusional
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| Psychosis |
- Schizoaffective disorder
- Schizophreniform disorder
- Brief reactive psychosis
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| Schizophrenia |
- Disorganized schizophrenia
- Delusional disorder
- Folie à deux
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Mood (affective)
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- Mania
- Bipolar disorder
- (Bipolar I
- Bipolar II
- Cyclothymia
- Bipolar NOS)
- Depression
- (Major depressive disorder
- Dysthymia
- Seasonal affective disorder
- Atypical depression
- Melancholic depression)
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Neurotic, stress-related and somatoform
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Anxiety disorder
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Phobia
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- Agoraphobia
- Social anxiety
- Social phobia
- (Anthropophobia)
- Specific phobia
- (Claustrophobia)
- Specific social phobia
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Other
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- Panic disorder
- Panic attack
- Generalized anxiety disorder
- OCD
- stress
- (Acute stress reaction
- PTSD)
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Adjustment disorder
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- Adjustment disorder with depressed mood
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Somatoform disorder
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- Somatization disorder
- Body dysmorphic disorder
- Hypochondriasis
- Nosophobia
- Da Costa's syndrome
- Psychalgia
- Conversion disorder
- (Ganser syndrome
- Globus pharyngis)
- Neurasthenia
- Mass Psychogenic Illness
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Dissociative disorder
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- Dissociative identity disorder
- Psychogenic amnesia
- Fugue state
- Depersonalization disorder
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Physiological/physical behavioral
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Eating disorder
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- Anorexia nervosa
- Bulimia nervosa
- Rumination syndrome
- NOS
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Nonorganic
sleep disorders
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- (Nonorganic hypersomnia
- Nonorganic insomnia)
- Parasomnia
- (REM behavior disorder
- Night terror
- Nightmare)
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Sexual
dysfunction
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- sexual desire
- (Hypoactive sexual desire disorder
- Hypersexuality)
- sexual arousal
- (Female sexual arousal disorder)
- Erectile dysfunction
- orgasm
- (Anorgasmia
- Delayed ejaculation
- Premature ejaculation
- Sexual anhedonia)
- pain
- (Vaginismus
- Dyspareunia)
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Postnatal
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- Postpartum depression
- Postnatal psychosis
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Adult personality and behavior
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Sexual and
gender identity
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- Sexual maturation disorder
- Ego-dystonic sexual orientation
- Sexual relationship disorder
- Paraphilia
- (Voyeurism
- Fetishism)
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Other
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- Personality disorder
- Impulse control disorder
- (Kleptomania
- Trichotillomania
- Pyromania
- Dermatillomania)
- Body-focused repetitive behavior
- Factitious disorder
- (Münchausen syndrome)
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Mental disorders diagnosed in childhood
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Mental retardation
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- X-Linked mental retardation
- (Lujan-Fryns syndrome)
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Psychological development
(developmental disorder)
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Emotional and behavioral
|
- ADHD
- Conduct disorder
- (ODD)
- emotional disorder
- (Separation anxiety disorder)
- social functioning
- (Selective mutism
- RAD
- DAD)
- Tic disorder
- (Tourette syndrome)
- Speech
- (Stuttering
- Cluttering)
- Movement disorder
- (Stereotypic)
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Symptoms and uncategorized
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- Catatonia
- False pregnancy
- Intermittent explosive disorder
- Psychomotor agitation
- Sexual addiction
- Stereotypy
- Psychogenic non-epileptic seizures
- Klüver-Bucy syndrome
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dsrd (o, p, m, p, a, d, s), sysi/epon, spvo
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proc(eval/thrp), drug(N5A/5B/5C/6A/6B/6D)
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Emotional and behavioral disorders (F90–F98, 312–314)
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| Emotional and behavioral |
- ADHD
- Conduct disorder
- emotional disorder
- Separation anxiety disorder
- social functioning
- Tic disorder
- Speech
- Movement disorder
- Nose-picking
- Nail biting
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dsrd (o, p, m, p, a, d, s), sysi/epon, spvo
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proc(eval/thrp), drug(N5A/5B/5C/6A/6B/6D)
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