name | Attention-deficit/hyperactivity disorder |
---|---|
diseasesdb | 6158 |
icd10 | |
icd9 | , |
omim | 143465 |
medlineplus | 001551 |
emedicinesubj | med |
emedicinetopic | 3103 |
emedicine mult | |
meshid | D001289 }} |
Attention deficit hyperactivity disorder (ADHD or AD/HD or ADD) is a developmental disorder. It is primarily characterized by "the co-existence of attentional problems and hyperactivity, with each behavior occurring infrequently alone" and symptoms starting before seven years of age.
ADHD is the most commonly studied and diagnosed psychiatric disorder in children, affecting about 3 to 5 percent of children globally and diagnosed in about 2 to 16 percent of school aged children. It is a chronic disorder with 30 to 50 percent of those individuals diagnosed in childhood continuing to have symptoms into adulthood. Adolescents and adults with ADHD tend to develop coping mechanisms to compensate for some or all of their impairments. It is estimated that 4.7 percent of American adults live with ADHD. Standardized rating scales such as WHO's Adult ADHD Self-Report Scale can be used for ADHD screening and assessment of the disorder’s symptoms severity.
ADHD is diagnosed two to four times more frequently in boys than in girls, though studies suggest this discrepancy may be partially due to subjective bias of referring teachers. ADHD management usually involves some combination of medications, behavior modifications, lifestyle changes, and counseling. Its symptoms can be difficult to differentiate from other disorders, increasing the likelihood that the diagnosis of ADHD will be missed. Additionally, most clinicians have not received formal training in the assessment and treatment of ADHD, particularly in adult patients.
ADHD and its diagnosis and treatment have been considered controversial since the 1970s. The controversies have involved clinicians, teachers, policymakers, parents and the media. Topics include the actuality of the disorder, its causes, and the use of stimulant medications in its treatment. 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. The American Medical Association concluded in 1998 that the diagnostic criteria for ADHD are based on extensive research and, if applied appropriately, lead to the diagnosis with high reliability.
ADHD has three subtypes:
The symptom categories of ADHD in children yield three potential classifications of ADHD—predominantly inattentive type, predominantly hyperactive-impulsive type, or combined type if criteria for both subtypes are met:
Predominantly inattentive type symptoms may include:
Predominantly hyperactive-impulsive type symptoms may include:
and also these manifestations primarily of impulsivity:
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.
Symptoms may persist into adulthood for up to half of children diagnosed with ADHD. Estimating this is difficult as there are no official diagnostic criteria for ADHD in adults. ADHD in adults remains a clinical diagnosis. The signs and symptoms may differ from those during childhood and adolescence due to the adaptive processes and avoidance mechanisms learned during the process of socialisation.
A 2009 study found that children with ADHD move around a lot because it helps them stay alert enough to complete challenging tasks.
Inattention and "hyperactive" behavior are not the only problems in children with ADHD. ADHD exists alone in only about 1/3 of the children diagnosed with it. 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 (35%) and conduct disorder (26%) which both are characterized by antisocial behaviors such as stubbornness, aggression, frequent temper tantrums, deceitfulness, lying, or stealing, inevitably linking these comorbid disorders with antisocial personality disorder (ASPD); about half of those with hyperactivity and ODD or CD develop ASPD in adulthood. 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. 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. Mood disorders. Boys diagnosed with the combined subtype have been shown likely to suffer from a mood disorder. Bipolar disorder. As many as 25 percent of children with ADHD have bipolar disorder. Children with this combination may demonstrate more aggression and behavioral problems than those with ADHD alone. Anxiety disorder, which has been found to be common in girls diagnosed with the inattentive subtype of ADHD. Obsessive-compulsive disorder. OCD is believed to share a genetic component with ADHD and shares many of its characteristics.
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, dopamine beta-hydroxylase monoamine oxidase A, catecholamine-methyl transferase, serotonin transporter promoter (SLC6A4), 5HT2A receptor, 5HT1B receptor, the 10-repeat allele of the DAT1 gene, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI). 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.
The broad selection of targets indicates that ADHD does not follow the traditional model of "a simple genetic disease" and should therefore be viewed as a complex interaction among genetic and environmental factors. Even though all these genes might play a role, to date no single gene has been shown to make a major contribution to ADHD.
The hunter vs. farmer theory is a hypothesis proposed by author Thom Hartmann about the origins of ADHD. The theory proposes that hyperactivity may be an adaptive behavior in pre-modern humans and that those with ADHD retain some of the older "hunter" characteristics associated with early pre-agricultural human society. According to this theory, individuals with ADHD may be more adept at searching and seeking and less adept at staying put and managing complex tasks over time. Further evidence showing hyperactivity may be evolutionarily beneficial was put forth in 2006 in a study which found it may carry specific benefits for certain forms of ancient society. In these societies, those with ADHD are hypothesized to have been more proficient in tasks involving risk or competition (i.e. hunting, mating rituals, etc.). 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. 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.
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.
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.
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.
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. The risk may be related to the length of time the children spent in an orphanage, especially if they were neglected or abused. Many of these families who adopted the affected children feel overwhelmed and frustrated, since managing their children may entail more responsibilities than originally anticipated. The adoption agencies may be aware of the child's behavioral history, but decide to withhold the information prior to the adoption. This in turn has resulted in some parents suing adoption agencies, in the abuse of children, and even in the relinquishment of the child.
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. 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.
Without enough stimulation coming from the environment, an ADHD child will create it him or herself by walking around, fidgeting, talking, etc. This theory also explains why stimulant medications have high success rates and can induce a calming effect at therapeutic dosages among children with ADHD. It establishes a strong link with scientific data that ADHD is connected to abnormalities with the neurochemical dopamine and a powerful link with low-stimulation PET scan results in ADHD subjects.
The pathophysiology of ADHD is unclear and there are a number of competing theories. 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 particularly the cerebellum have also been implicated. Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are only used for research not diagnostic purposes. 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.
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. It should be noted that stimulant medication itself may affect growth factors of the central nervous system.
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.
Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity), 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 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. 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 which is otherwise boring. Neuroimaging studies also found that neurotransmitters level (e.g. dopamine and serotonin) in the synaptic cleft goes down during depression.
A 1990 PET scan study by Alan J. Zametkin et al. found that global cerebral glucose metabolism was 8 percent lower in medication-naive adults who had been hyperactive since childhood. Further studies found that chronic stimulant treatment had little effect on global glucose metabolism, a 1993 study in girls failed to find a decreased global glucose metabolism, but found significant differences in glucose metabolism in 6 specific regions of the brains of ADHD girls as compared to control subjects. The study also found that differences in one specific region of the frontal lobe were statistically correlated with symptom severity. A further study in 1997 also failed to find global differences in glucose metabolism, but similarly found differences in glucose normalization in specific regions of the brain. The 1997 study also noted that their findings were somewhat different than those in the 1993 study, and concluded that sexual maturation may have played a role in this discrepancy. The significance of the research by Zametkin has not been determined and neither his group nor any other has been able to replicate the 1990 results.
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 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. They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology.
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.
Many of the symptoms of ADHD occur from time to time in everyone; in patients with ADHD, the frequency of these symptoms is greater and patients' lives are significantly impaired. Impairment must occur in multiple settings to be classified as ADHD. 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:
# ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months # ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months # ADHD, Predominantly Hyperactive-Impulsive Type: if criterion 1B is met but criterion 1A is not met for the past six months.
The previously used term ADD expired with the most recent revision 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).
IB. Six or more of the following signs of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level: :* Hyperactivity: :# Often fidgets with hands or feet or squirms in seat. :# Often gets up from seat when remaining in seat is expected. :# Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless). :# Often has trouble playing or enjoying leisure activities quietly. :# Is often "on the go" or often acts as if "driven by a motor". :# Often talks excessively.
:* Impulsiveness: :# Often blurts out answers before questions have been finished. :# Often has trouble waiting one's turn. :# Often interrupts or intrudes on others (example: butts into conversations or games).
II. Some signs that cause impairment were present before age 7 years.
III. Some impairment from the signs is present in two or more settings (such as at school/work and at home).
IV. There must be clear evidence of significant impairment in social, school, or work functioning.
V. The signs do not happen only during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder. The signs are not better accounted for by another mental disorder (such as Mood Disorder, Anxiety Disorder, Dissociative Identity Disorder, or a Personality Disorder).
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. 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.
The American Academy of Child Adolescent Psychiatry (AACAP) considers it necessary that the following be present before attaching the label of ADHD to a child:
If a child seems too active on the playground but not elsewhere, the problem might not be ADHD. It might also not be ADHD if the behaviors occur in the classroom but nowhere else. A child who shows some symptoms would not be diagnosed with ADHD if his or her schoolwork or friendships are not impaired by the behaviors.
Medical conditions
Medical conditions that must be excluded include: hypothyroidism, anemia, lead poisoning, chronic illness, hearing or vision impairment, substance abuse, medication side effects, sleep impairment and child abuse, 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. 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.
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. Many sleep disorders are important causes of symptoms which may overlap with the cardinal symptoms of ADHD; children with ADHD should be regularly and systematically assessed for sleep problems.
From a clinical standpoint, mechanisms that account for the phenomenon of excessive daytime sleepiness include:
Methods of treatment often involve some combination of behavior modification, life-style changes, counseling, and medication. A 2005 study found that medical management and behavioral treatment is the most effective ADHD management strategy, followed by medication alone, and then behavioral treatment. While medication has been shown to improve behavior when taken over the short term, they have not been shown to alter long term outcomes. Medications have at least some effect in about 80% of people.
Stimulant medication are the medical treatment of choice. There are a number of non-stimulant medications, such as atomoxetine, that may be used as alternatives. 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. While stimulants and atomoxetine are generally safe, there are side effects and contraindications to their use. Medications are not recommended for preschool children, as their long-term effects in such young people are unknown. There is very little data on the long-term adverse effects or benefits of stimulants for ADHD. Guidelines on when to use medications vary internationally, with the UK's National Institute of Clinical Excellence, for example, only recommending use in severe cases, while most United States guidelines recommend medications in nearly all cases.
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.
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.
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 this interview he spoke about postpartum depression and also referred to Ritalin and Adderall as being "street drugs" rather than as ADHD medication. In England Baroness Susan Greenfield, a leading neuroscientist, spoke out publicly about the need for a wide-ranging inquiry in the House of Lords into the dramatic increase in the diagnosis of ADHD in the UK and possible causes following a 2007 BBC Panorama programme which highlighted US research (The Multimodal Treatment Study of Children with ADHD by the University of Buffalo showing treatment results of 600) suggesting drugs are no better than other forms of therapy for ADHD in the long term.
Neil Bush (brother of former President George W. Bush) is credited in the cast of a 2005 ADHD documentary called The Drugging of Our Children directed by Gary Null. In the film's trailer Bush says: "Just because it is easy to drug a kid and get them to be compliant doesn't make it right to do it".
, 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).
Others have included that it may stem from a misunderstanding of the diagnostic criteria and how they are utilized by clinicians, teachers, policymakers, parents and the media. 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. Long term possible side effects of stimulants and their usefulness are largely unknown because of a lack of long term studies. Some research raises questions about the long term effectiveness and side effects of medications used to treat ADHD.
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.
With a "wide variation in diagnosis across states, races, and ethnicities" some investigators suspect that factors other than neurological conditions play a role when the diagnosis of ADHD is made. 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.
Researchers found that 60 percent of the children diagnosed with ADHD continue having symptoms well into adulthood. Many adults, however, remain untreated. 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. They often have such associated psychiatric comorbidities as depression, anxiety disorder, bipolar disorder, substance abuse, or a learning disability. A diagnosis of ADHD may offer adults insight into their behaviors and allow patients to become more aware and seek help with coping and treatment strategies. There is controversy amongst some experts on whether ADHD persists into adulthood. Recognized as occurring in adults in 1978, it is currently not addressed separately from ADHD in childhood. Obstacles that clinicians face when assessing adults who may have ADHD include developmentally inappropriate diagnostic criteria, age-related changes, comorbidities and the possibility that high intelligence or situational factors can mask ADHD.
Category:Attention Category:Attention disorders Category:Childhood psychiatric disorders Category:Educational psychology Category:Emotional and behavioral disorders in childhood and adolescence Category:Learning disabilities
af:Aandagsgebreksindroom ar:قصور الانتباه وفرط الحركة bg:Синдром на дефицит на вниманието и хиперактивност ca:Trastorn per dèficit d'atenció amb hiperactivitat cs:ADHD da:ADHD de:Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung el:Διαταραχή Ελλειμματικής Προσοχής – Υπερκινητικότητα et:Hüperaktiivsus tähelepanu puudulikkusega es:Trastorno por déficit de atención con hiperactividad eo:Atentomanka-hiperaktiva perturbo eu:Arreta Galdu - Hiperaktibitate Asaldura fa:اختلال کمتوجهی - بیشفعالی fr:Trouble du déficit de l'attention gl:Trastorno por déficit de atención con hiperactividade ko:주의력결핍 과다행동장애 hi:ध्यानाभाव एवं अतिसक्रियता विकार hr:Poremećaj hiperaktivnosti i deficita pažnje is:Athyglisbrestur it:Sindrome da deficit di attenzione e iperattività he:הפרעת קשב, ריכוז והיפראקטיביות lt:Aktyvumo ir dėmesio sutrikimas hu:Figyelemhiányos hiperaktivitás-zavar nl:ADHD ja:注意欠陥・多動性障害 no:Attention Deficit Hyperactivity Disorder nn:ADHD pl:ADHD pt:Transtorno do déficit de atenção com hiperatividade ro:ADHD ru:Синдром дефицита внимания и гиперактивности simple:Attention-deficit hyperactivity disorder sr:Хиперкинетички поремећај fi:Tarkkaavaisuus- ja ylivilkkaushäiriö sv:ADHD th:สมาธิสั้น tr:Dikkat eksikliği ve hiperaktivite bozukluğu uk:СДУГ vi:Rối loạn tăng động giảm chú ý wuu:注意力弗足过动症 zh:注意力不足過動症This text is licensed under the Creative Commons CC-BY-SA License. This text was originally published on Wikipedia and was developed by the Wikipedia community.
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