Attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder (ADHD)<ref name="AD" /> is a neurodevelopmental disorder characterised by symptoms of inattention, hyperactivity, impulsivity, and emotional dysregulation that are excessive and pervasive, impairing in multiple contexts, and developmentally inappropriate.Template:Refn ADHD symptoms arise from executive dysfunction.Template:Refn

Impairments resulting from deficits in self-regulation such as time management, inhibition, task initiation, and sustained attention<ref>Template:Cite journal</ref> can include poor professional performance, relationship difficulties, and numerous health risks,<ref name="Barkley_2011">Template:Cite journal</ref><ref name="fleming_et_al_2017">Template:Cite journal</ref> collectively predisposing to a diminished quality of life<ref name="Coghill_2017" /> and a reduction in life expectancy.<ref name="Barkley & Fischer"/><ref name="Adverse_2022">Template:Cite journal</ref> As a consequence, the disorder costs society hundreds of billions of US dollars each year, worldwide.<ref>Template:Cite journal</ref> It is associated with other mental disorders as well as non-psychiatric disorders, which can cause additional impairment.<ref name="Faraone_2021" />

While ADHD involves a lack of sustained attention to tasks,<ref name="Antshel_2014" /><ref name="Barkley_2011" /> inhibitory deficits also can lead to difficulty interrupting an already ongoing response pattern, manifesting in the perseveration of actions despite a change in context whereby the individual intends the termination of those actions.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> This symptom is known colloquially as hyperfocus<ref name="Groen_et_al_2020"/> and is related to risks such as addiction<ref name="use">Template:Cite journal</ref><ref name="Ishii_et_al_2023">Template:Cite journal</ref> and types of offending behaviour.<ref>Template:Cite journal</ref>

ADHD can be difficult to tell apart from other conditions.<ref name="Executive functions"/><ref name="Coghill_2017" /> ADHD represents the extreme lower end of the continuous dimensional trait (bell curve) of executive functioning and self-regulation, which is supported by twin, brain imaging and molecular genetic studies.Template:Refn

The precise causes of ADHD are unknown in most individual cases.<ref name=nimh/><ref>Template:Cite journal</ref> Meta-analyses have shown that the disorder is primarily genetic with a heritability rate of 70–80%,<ref name="HD" /><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> where risk factors are highly accumulative.<ref>Template:Cite journal</ref> The environmental risks are not related to social or familial factors;<ref>Template:Cite journal</ref><ref name="Intergenerational">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name=hl>Template:Cite journal</ref> they exert their effects very early in life, in the prenatal or early postnatal period.<ref name="Faraone_2021" /> However, in rare cases, ADHD can be caused by a single event including traumatic brain injury,<ref name="HD">Template:Cite journal</ref><ref>Template:Cite journal</ref><ref name="Eme-2012">Template:Cite journal</ref><ref>Template:Cite journal</ref> exposure to biohazards during pregnancy,<ref name = "Faraone_2021" /> or a major genetic mutation.<ref name="Faraone_2019">Template:Cite journal</ref> As it is a neurodevelopmental disorder, there is no biologically distinct adult-onset ADHD except for when ADHD occurs after traumatic brain injury.<ref name="Faraone_2021"/><ref name="Faraone_2016">Template:Cite journal</ref>

Signs and symptoms

Inattention, hyperactivity (restlessness in adults), disruptive behaviour, and impulsivity are common in ADHD.<ref name=cdc2016facts/><ref name="National Institute of Mental Health_2023">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="National Institute of Mental Health">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Academic difficulties are frequent, as are problems with relationships.<ref name="National Institute of Mental Health_2023" /><ref name="National Institute of Mental Health" /><ref name="ICSI2012">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> The signs and symptoms can be difficult to define, as it is hard to draw a line at where normal levels of inattention, hyperactivity, and impulsivity end and significant levels requiring interventions begin.<ref name ="Ramsay_2007">Template:Cite book</ref>

According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and its text revision (DSM-5-TR), symptoms must be present for six months or more to a degree that is much greater than others of the same age.<ref name=DSM5/><ref name=DSM5TR/> This requires at least six symptoms of either inattention or hyperactivity/impulsivity for those under 17 and at least five symptoms for those 17 years or older.<ref name=DSM5/><ref name=DSM5TR/> The symptoms must be present in at least two settings (e.g., social, school, work, or home), and must directly interfere with or reduce quality of functioning.<ref name=DSM5/> Additionally, several symptoms must have been present before age 12 as per DSM-5 criteria.<ref name=DSM5TR/><ref name=DSM5/><ref>Template:Cite journal</ref> However, research indicates the age of onset should not be interpreted as a prerequisite for diagnosis given contextual exceptions.<ref name="Faraone_2016" />

Template:Anchor Presentations

ADHD is divided into three primary presentations:<ref name=DSM5TR/><ref name="Ramsay_2007" />

• predominantly inattentive (ADHD-PI or ADHD-I)
• predominantly hyperactive-impulsive (ADHD-PH or ADHD-HI)
• combined presentation (ADHD-C).

The table "Symptoms" lists the symptoms for ADHD-I and ADHD-HI from two major classification systems. Symptoms which can be better explained by another psychiatric or medical condition which an individual has are not considered to be a symptom of ADHD for that person. In DSM-5, subtypes were discarded and reclassified as presentations of the disorder that change over time.

Symptoms

Presentations	Template:Abbr and Template:Abbr symptoms<ref name=DSM5/><ref name=DSM5TR/>	Template:Abbr symptoms<ref name="ICD-11" />
Inattention	Six or more of the following symptoms in children, and five or more in adults, excluding situations where these symptoms are better explained by another psychiatric or medical condition: Frequently overlooks details or makes careless mistakes Often has difficulty maintaining focus on one task or play activity Often appears not to be listening when spoken to, including when there is no obvious distraction Frequently does not finish following instructions, failing to complete tasks Often struggles to organise tasks and activities, to meet deadlines, and to keep belongings in order Is frequently reluctant to engage in tasks which require sustained attention Frequently loses items required for tasks and activities Is frequently easily distracted by extraneous stimuli, including thoughts in adults and older teenagers Often forgets daily activities, or is forgetful while completing them.	Multiple symptoms of inattention that directly negatively impact occupational, academic or social functioning. Symptoms may not be present when engaged in highly stimulating tasks with frequent rewards. Symptoms are generally from the following clusters: Struggles to maintain focus on tasks that are not highly stimulating/rewarding or that require continuous effort; details are often missed, and careless mistakes are frequent in school and work tasks; tasks are often abruptly abandoned in favour of another before they are completed. Easily distracted (including by own thoughts); may not listen when spoken to; frequently appears to be lost in thought Often loses things; is forgetful and disorganised in daily activities. The individual may also meet the criteria for hyperactivity-impulsivity, but the inattentive symptoms are predominant.
Hyperactivity-Impulsivity	Six or more of the following symptoms in children, and five or more in adults, excluding situations where these symptoms are better explained by another psychiatric or medical condition: Is often fidgeting or squirming in seat Frequently has trouble sitting still during dinner, class, in meetings, etc. Frequently runs around or climbs in inappropriate situations. In adults and teenagers, this may be present only as restlessness. Often cannot quietly engage in leisure activities or play Frequently seems to be "on the go" or appears uncomfortable when not in motion Often talks excessively Often answers a question before it is finished, or finishes people's sentences Often struggles to wait their turn, including waiting in lines Frequently interrupts or intrudes, including into others' conversations or activities, or by using people's things without asking.	Multiple symptoms of hyperactivity/impulsivity that directly negatively impact occupational, academic or social functioning. Typically, these tend to be most apparent in environments with structure or which require self-control. Symptoms are generally from the following clusters: Excessive motor activity; struggles to sit still, often leaving their seat; prefers to run about; in younger children, will fidget when attempting to sit still; in adolescents and adults, a sense of physical restlessness or discomfort with being quiet and still. Talks too much; struggles to quietly engage in activities. Blurts out answers or comments; struggles to wait their turn in conversation, games, or activities; will interrupt or intrude on conversations or games. A lack of forethought or consideration of consequences when making decisions or taking action, instead tending to act immediately (e.g., physically dangerous behaviours including reckless driving; impulsive decisions). The individual may also meet the criteria for inattention, but the hyperactive-impulsive symptoms are predominant.
Combined	Meet the criteria for both inattentive and hyperactive-impulsive ADHD.	Criteria are met for both inattentive and hyperactive-impulsive ADHD, with neither clearly predominating.

Girls and women with ADHD tend to display fewer hyperactivity and impulsivity symptoms but more symptoms of inattention and distractibility.<ref>Template:Cite journal</ref>

Symptoms are expressed differently and more subtly as the individual ages.<ref name="Kooij_2010">Template:Cite journal</ref>Template:Rp Hyperactivity tends to become less overt with age and turns into inner restlessness, difficulty relaxing or remaining still, talkativeness or constant mental activity in teens and adults with ADHD.<ref name="Kooij_2010"/>Template:Rp Impulsivity in adulthood may appear as thoughtless behaviour, impatience, irresponsible spending and sensation-seeking behaviours,<ref name="Kooij_2010"/>Template:Rp while inattention may appear as becoming easily bored, difficulty with organisation, remaining on task and making decisions, and sensitivity to stress.<ref name="Kooij_2010"/>Template:Rp

Characteristics in childhood

Difficulties managing anger are more common in children with ADHD,<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> as are delays in speech, language and motor development.<ref name="ICD10"/><ref name="pmid22201208">Template:Cite journal</ref> Poorer handwriting is more common in children with ADHD.<ref name="Racine_2008">Template:Cite journal</ref> Poor handwriting can be a symptom of ADHD in itself due to decreased attentiveness. When this is a pervasive problem, it may also be attributable to dyslexia<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> or dysgraphia. There is significant overlap in the symptomatologies of ADHD, dyslexia, and dysgraphia,<ref name="Nicolson_2011">Template:Cite journal</ref> and 3 in 10 people diagnosed with dyslexia experience co-occurring ADHD.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Although it causes significant difficulty, many children with ADHD have an attention span equal to or greater than that of other children for tasks and subjects they find interesting.<ref name="Walitza_2012">Template:Cite journal</ref>

Emotional dysregulation

Although not listed as an official symptom, emotional dysregulation or mood lability is generally understood to be a common symptom of ADHD.<ref name="Retz_2012">Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref name="Kooij_2010"/>Template:Rp

Relationship difficulties

People with ADHD of all ages are more likely to have problems with social skills, such as social interaction and forming and maintaining friendships.<ref>Template:Cite journal</ref> This is true for all presentations. About half of children and adolescents with ADHD experience social rejection by their peers compared to 10–15% of non-ADHD children and adolescents. People with attention deficits are prone to having difficulty processing verbal and nonverbal language which can negatively affect social interaction. They may also drift off during conversations, miss social cues, and have trouble learning social skills.<ref>Template:Cite journal</ref>

Hyperfocus

An association between ADHD and hyperfocus, a state characterised by intense and narrow concentration on a specific stimulus, object or task for a prolonged period of time,<ref name="Chutko_et_al_2024">Template:Cite journal</ref> has been widely reported in the popular science press and media.<ref name="Groen_et_al_2020" >Template:Cite journal</ref> The phenomenon generally occurs when an individual is engaged in activities they find highly interesting, or which provide instant gratification, such as video games or online chatting.<ref name="epa_consensus_2019" /> Hyperfocus is not a recognised symptom of ADHD in diagnostic manuals, but is frequently referred to as a symptom of ADHD in academic literature<ref name="Ashinoff_Abu_Akel_2019">Template:Cite journal</ref> and commonly reported in patients with ADHD in clinical practice.<ref name="Groen_et_al_2020" /> There is a lack of research into hyperfocus in ADHD.<ref name="Ashinoff_Abu_Akel_2019" /> Studies in 2016, 2019 and 2024 found that individuals with ADHD diagnoses or self-reported ADHD symptoms experience hyperfocus more often,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> or more acutely.<ref name="Glassey_Smilek_2024">Template:Cite journal</ref> A 2020 study did not find a higher frequency of hyperfocus in adults with ADHD, although it reported a positive correlation with self-reported ADHD traits. The discrepancy with other studies may reflect varying definitions and conceptions of hyperfocus.<ref name="Groen_et_al_2020"/>

A state of hyperfocus has been hypothesised as being beneficial, allowing individuals to focus on tasks for much longer than is typical.<ref name="Ashinoff_Abu_Akel_2019" /> Conversely, it can be difficult to disengage from and shift attention to other stimuli or tasks, leading to excessively prolonged attention.<ref name="Chutko_et_al_2024"/> It is related to risks such as internet addiction (see Template:Section link)<ref name="Ishii_et_al_2023" /> and to some types of offending behaviour.<ref>Template:Cite journal</ref> Recent research has linked hyperfocus to the psychological concepts of flow, an enjoyable experience of deep engagement in an activity, and perseveration, difficulty disengaging or switching from an activity.<ref name="Glassey_Smilek_2024"/>

IQ test performance

Certain studies have found that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests.<ref name="Frazier_2004">Template:Cite journal</ref> The significance of this is controversial due to the differences between people with ADHD and the difficulty determining the influence of symptoms, such as distractibility, on lower scores rather than intellectual capacity. In studies of ADHD, higher IQs may be over-represented because many studies exclude individuals who have lower IQs despite those with ADHD scoring on average nine points lower on standardised intelligence measures.<ref name="Mackenzie_2016">Template:Cite journal</ref> However, other studies contradict this, saying that in individuals with high intelligence, there is an increased risk of a missed ADHD diagnosis, possibly because of compensatory strategies in said individuals.<ref>Template:Cite journal</ref>

Studies of adults suggest that negative differences in intelligence are not meaningful and may be explained by associated health problems.<ref>Template:Cite journal</ref>

Causes

ADHD arises from brain maldevelopment especially in the prefrontal executive networks that can arise either from genetic factors (different gene variants and mutations for building and regulating such networks) or from acquired disruptions to the development of these networks and regions involved in executive functioning and self-regulation.<ref name="Faraone_2021" /><ref name="Antshel_2014" /> Their reduced size, functional connectivity, and activation contribute to the pathophysiology of ADHD, as well as imbalances in the noradrenergic and dopaminergic systems that mediate these brain regions.<ref name="Faraone_2021" /><ref name="Biederman_2005">Template:Cite journal</ref>

Genetic factors play an important role; ADHD has a heritability rate of 70–80%. The remaining 20–30% of variance is mediated by de-novo mutations and non-shared environmental factors that provide for or produce brain injuries; there is no significant contribution of the rearing family and social environment.Template:Refn Very rarely, ADHD can also be the result of abnormalities in the chromosomes.<ref>Template:Cite journal</ref>

Genetics

In November 1999, Biological Psychiatry published a literature review by psychiatrists Joseph Biederman and Thomas Spencer found the average heritability estimate of ADHD from twin studies to be 0.8,<ref>Template:Cite journal</ref> while a subsequent family, twin, and adoption studies literature review published in Molecular Psychiatry in April 2019 by psychologists Stephen Faraone and Henrik Larsson that found an average heritability estimate of 0.74.<ref name="Faraone_2019" /> Additionally, evolutionary psychiatrist Randolph M. Nesse has argued that the 5:1 male-to-female sex ratio in the epidemiology of ADHD suggests that ADHD may be the end of a continuum where males are overrepresented at the tails, citing clinical psychologist Simon Baron-Cohen's suggestion for the sex ratio in the epidemiology of autism as an analogue.<ref name="Baron-Cohen 2002">Template:Cite journal</ref><ref name="Nesse 2005 p. 918">Template:Cite book</ref><ref name="Nesse 2016 p. 1019">Template:Cite book</ref>

Natural selection has been acting against the genetic variants for ADHD over the course of at least 45,000 years, indicating that it was not an adaptive trait in ancient times.<ref>Template:Cite journal</ref> The disorder may remain at a stable rate by the balance of genetic mutations and removal rate (natural selection) across generations; over thousands of years, these genetic variants become more stable, decreasing disorder prevalence.<ref>Template:Cite journal</ref> Throughout human evolution, the executive functions involved in ADHD likely provide the capacity to bind contingencies across time thereby directing behaviour toward future over immediate events so as to maximise future social consequences for humans.<ref>Template:Cite book</ref>

ADHD has a high heritability of 74%, meaning that 74% of the presence of ADHD in the population is due to genetic factors. There are multiple gene variants which each slightly increase the likelihood of a person having ADHD; it is polygenic and thus arises through the accumulation of many genetic risks each having a very small effect.<ref name="Faraone_2021" /><ref name="Faraone_2019" /> The siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder.<ref>Template:Cite book</ref>

The association of maternal smoking observed in large population studies disappears after adjusting for family history of ADHD, which indicates that the association between maternal smoking during pregnancy and ADHD is due to familial or genetic factors that increase the risk for the confluence of smoking and ADHD.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

ADHD presents with reduced size, functional connectivity and activation<ref name="Faraone_2021" /> as well as low noradrenergic and dopaminergic functioning<ref name="Biederman_2005" /><ref>Template:Cite journal</ref> in brain regions and networks crucial for executive functioning and self-regulation.<ref name="Faraone_2021" /><ref name="Barkley_2011a" /><ref name="Antshel_2014" /> Typically, a number of genes are involved, many of which directly affect brain functioning and neurotransmission.<ref name="Faraone_2021" /> Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH.<ref name="Kebir_2011">Template:Cite journal</ref><ref name="Berry_2007" /><ref>Template:Cite journal</ref> Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF.<ref name="Gizer_2009">Template:Cite journal</ref> A common variant of a gene called latrophilin 3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication.<ref>Template:Cite journal</ref> The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioural phenotypes, including ADHD symptoms reflecting split attention.<ref>Template:Cite journal</ref> The DRD4 gene is both linked to novelty seeking and ADHD. The genes GFOD1 and CDH13 show strong genetic associations with ADHD. CDH13's association with ASD, schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene.<ref name="Grimm_2020" /> Another candidate causative gene that has been identified is ADGRL3. In zebrafish, knockout of this gene causes a loss of dopaminergic function in the ventral diencephalon and the fish display a hyperactive/impulsive phenotype.<ref name="Grimm_2020" />

For genetic variation to be used as a tool for diagnosis, more validating studies need to be performed. However, smaller studies have shown that genetic polymorphisms in genes related to catecholaminergic neurotransmission or the SNARE complex of the synapse can reliably predict a person's response to stimulant medication.<ref name="Grimm_2020" /> Rare genetic variants show more relevant clinical significance as their penetrance (the chance of developing the disorder) tends to be much higher.<ref name="Zayats_2020">Template:Cite journal</ref> However their usefulness as tools for diagnosis is limited as no single gene predicts ADHD. ASD shows genetic overlap with ADHD at both common and rare levels of genetic variation.<ref name="Zayats_2020" />

Environment

In addition to genetics, some environmental factors might play a role in causing ADHD.<ref name="Sonu_2013" /><ref name="cdc2016">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it.<ref name="Burger_2011">Template:Cite journal</ref> Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD.<ref name="nimh" /><ref name="Eubig_2010">Template:Cite journal</ref> Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.<ref name="de_Cock_2012">Template:Cite journal</ref> Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.<ref name="nimh">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="Abbott_2012">Template:Cite journal</ref> Nicotine exposure during pregnancy may be an environmental risk.<ref>Template:Cite journal</ref>

Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk<ref>Template:Cite journal</ref><ref name="nimh" /><ref name="Thapar-2012">Template:Cite journal</ref> as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71).<ref name="Millichap_2008">Template:Cite journal</ref> At least 30% of children with a traumatic brain injury later develop ADHD<ref name="Eme-2012" /> and about 5% of cases are due to brain damage.<ref name="Erk_2009" />

Some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of ADHD or ADHD-like symptoms,<ref name="nimh" /><ref name="pmid22232312">Template:Cite journal</ref> but the evidence is weak and may apply to only children with food sensitivities.<ref name="Sonu_2013" /><ref name="pmid22232312" /><ref name="EncycFoodSafety">Template:Cite encyclopedia</ref> The European Union has put in place regulatory measures based on these concerns.<ref name="FDAdyecomm">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.<ref name="Nigg_2014" />

Individuals with hypokalemic sensory overstimulation are sometimes diagnosed as having ADHD, raising the possibility that a subtype of ADHD has a cause that can be understood mechanistically and treated in a novel way. The sensory overload is treatable with oral potassium gluconate.<ref>Template:Cite journal</ref>

Template:Anchor Research does not support popular beliefs that ADHD is caused by eating too much refined sugar, watching too much television, bad parenting, poverty or family chaos; however, they might worsen ADHD symptoms in certain people.<ref name="cdc2016facts">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

In some cases, an inappropriate diagnosis of ADHD may reflect a dysfunctional family or a poor educational system, rather than any true presence of ADHD in the individual.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>Template:Better source needed In other cases, it may be explained by increasing academic expectations, with a diagnosis being a method for parents in some countries to obtain extra financial and educational support for their child.<ref name="Erk_2009" /> Additionally, children who enter school earlier and are of a younger age than their classmates are more likely to have educational and behavioral problems than their peers, which can make them more likely to be diagnosed with ADHD.<ref>Template:Cite journal</ref> Behaviours typical of ADHD occur more commonly in children who have experienced violence and emotional abuse.<ref name="NICE 2009">Template:Cite book</ref>

Pathophysiology

Current models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems, particularly those involving dopamine and norepinephrine.<ref name="Malenka ADHD neurosci">Template:Cite book</ref> The dopamine and norepinephrine pathways that originate in the ventral tegmental area and locus coeruleus project to diverse regions of the brain and govern a variety of cognitive processes.<ref name="VTA+LC projection systems">Template:Cite journal</ref><ref name="Malenka pathways" /> The dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum are directly responsible for modulating executive function (cognitive control of behaviour), motivation, reward perception, and motor function;<ref name="Malenka ADHD neurosci" /><ref name="Malenka pathways" /> these pathways are known to play a central role in the pathophysiology of ADHD.<ref name="VTA+LC projection systems" /><ref name="Malenka pathways" /><ref name="pmid22169776" /><ref name="pmid22983386" /> Larger models of ADHD with additional pathways have been proposed.<ref name="pmid22169776">Template:Cite journal</ref><ref name="pmid22983386">Template:Cite journal</ref>

Brain structure

File:Attention deficit hyperactivity disorder - Attention deficit hyperactivity disorder - Reduced brain volume on the left side from ADHD.jpg

The left prefrontal cortex, shown here in blue, is often affected in ADHD

In children with ADHD, there is a general reduction of volume in certain brain structures, with a proportionally greater decrease in the volume in the left-sided prefrontal cortex.<ref name="Malenka ADHD neurosci" /><ref name="Krain2006">Template:Cite journal</ref> The posterior parietal cortex also shows thinning in individuals with ADHD compared to controls. Other brain structures in the prefrontal-striatal-cerebellar and prefrontal-striatal-thalamic circuits have also been found to differ between people with and without ADHD.<ref name="Malenka ADHD neurosci" /><ref name="pmid22169776" /><ref name="pmid22983386" />

The subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with controls.<ref>Template:Cite journal</ref> Structural MRI studies have also revealed differences in white matter, with marked differences in inter-hemispheric asymmetry between ADHD and typically developing youths.<ref>Template:Cite journal</ref>

Functional MRI (fMRI) studies have revealed a number of differences between ADHD and control brains. Mirroring what is known from structural findings, fMRI studies have shown evidence for a higher connectivity between subcortical and cortical regions, such as between the caudate and prefrontal cortex. The degree of hyperconnectivity between these regions correlated with the severity of inattention or hyperactivity<ref name="Damiani_2021">Template:Cite journal</ref> Hemispheric lateralisation processes have also been postulated as being implicated in ADHD, but empiric results showed contrasting evidence on the topic.<ref name="Tarchi_2022">Template:Cite journal</ref><ref>Template:Cite journal</ref>

Neurotransmitter pathways

Previously, it had been suggested that the elevated number of dopamine transporters in people with ADHD was part of the pathophysiology, but it appears the elevated numbers may be due to adaptation following exposure to stimulant medication.<ref name="pmid22294258">Template:Cite journal</ref> Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system.<ref name="VTA+LC projection systems" /><ref name="Malenka ADHD neurosci" /><ref name="Malenka pathways" /> ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems.<ref name="Malenka ADHD neurosci" /><ref name="Malenka pathways">Template:Cite book</ref><ref name="cognition enhancers" /> There may additionally be abnormalities in serotonergic, glutamatergic, or cholinergic pathways.<ref name="cognition enhancers" /><ref name="Cortese-2012">Template:Cite journal</ref><ref name="pmid22939004">Template:Cite journal</ref>

PET mapping of neocortex receptor distribution indicates that the distribution of μ-opioid receptors is the strongest contributor to cortical abnormalities in ADHD, followed by CB₁ cannabinoid receptors.<ref>Template:Cite journal</ref>

Executive function and motivation

ADHD arises from a core deficit in executive functions (e.g., attentional control, inhibitory control, and working memory), which are a set of cognitive processes that are required to successfully select and monitor behaviours that facilitate the attainment of one's chosen goals.<ref name="Malenka pathways" /><ref name="Executive functions" /> The executive function impairments that occur in ADHD individuals result in problems with staying organised, time keeping, procrastination control, maintaining concentration, paying attention, ignoring distractions, regulating emotions, and remembering details.<ref name="Brown_2008" /><ref name="Malenka ADHD neurosci" /><ref name="Malenka pathways" /> People with ADHD appear to have unimpaired long-term memory, and deficits in long-term recall appear to be attributed to impairments in working memory.<ref name="pmid24232170">Template:Cite journal</ref> Due to the rates of brain maturation and the increasing demands for executive control as a person gets older, ADHD impairments may not fully manifest themselves until adolescence or even early adulthood.<ref name="Brown_2008" /> Conversely, brain maturation trajectories, potentially exhibiting diverging longitudinal trends in ADHD, may support a later improvement in executive functions after reaching adulthood.<ref name="Tarchi_2022" />

ADHD has also been associated with motivational deficits in children. Children with ADHD often find it difficult to focus on long-term over short-term rewards, and exhibit impulsive behaviour for short-term rewards.<ref name="Motivation">Template:Cite journal</ref>

Paradoxical reaction to neuroactive substances

Another sign of the structurally altered signal processing in the central nervous system in this group of people is the conspicuously common paradoxical reaction (Template:Circa of patients). These are unexpected reactions in the opposite direction as with a normal effect, or otherwise significant different reactions. These are reactions to neuroactive substances such as local anesthetic at the dentist, sedative, caffeine, antihistamine, weak neuroleptics and central and peripheral painkillers. Since the causes of paradoxical reactions are at least partly genetic, it may be useful in critical situations, for example before operations, to ask whether such abnormalities may also exist in family members.<ref name="PMID21886668">Template:Cite journal</ref><ref>Template:Cite journal</ref>

Diagnosis

ADHD is diagnosed by an assessment of a person's behavioural and mental development, including ruling out the effects of drugs, medications, and other medical or psychiatric problems as explanations for the symptoms.<ref name="NICE2009-part2">Template:Cite book</ref> ADHD diagnosis often takes into account feedback from parents and teachers<ref name="Lake2011">Template:Cite book</ref> with most diagnoses begun after a teacher raises concerns.<ref name="Erk_2009">Template:Cite book</ref> While many tools exist to aid in the diagnosis of ADHD, their validity varies in different populations, and a reliable and valid diagnosis requires confirmation by a clinician while supplemented by standardised rating scales and input from multiple informants across various settings.<ref name="Peterson_2024">Template:Cite journal</ref> The diagnosis of ADHD has been criticised as being subjective because it is not based on a biological test. The International Consensus Statement on ADHD concluded that this criticism is unfounded, on the basis that ADHD meets standard criteria for validity of a mental disorder established by Robins and Guze. They attest that the disorder is considered valid because: 1) well-trained professionals in a variety of settings and cultures agree on its presence or absence using well-defined criteria and 2) the diagnosis is useful for predicting a) additional problems the patient may have (e.g., difficulties learning in school); b) future patient outcomes (e.g., risk for future drug abuse); c) response to treatment (e.g., medications and psychological treatments); and d) features that indicate a consistent set of causes for the disorder (e.g., findings from genetics or brain imaging), and that professional associations have endorsed and published guidelines for diagnosing ADHD.<ref name="Faraone_2021" />

The most commonly used rating scales for diagnosing ADHD are the Achenbach System of Empirically Based Assessment (ASEBA) and include the Child Behavior Checklist (CBCL) used for parents to rate their child's behaviour, the Youth Self Report Form (YSR) used for children to rate their own behaviour, and the Teacher Report Form (TRF) used for teachers to rate their pupil's behaviour. Additional rating scales that have been used alone or in combination with other measures to diagnose ADHD include the Behavior Assessment System for Children (BASC), Behavior Rating Inventory of Executive Function - Second Edition (BRIEF2), Revised Conners Rating Scale (CRS-R), Conduct-Hyperactive-Attention Problem-Oppositional Symptom scale (CHAOS), Developmental Behavior Checklist Hyperactivity Index (DBC-HI), Parent Disruptive Behavior Disorder Ratings Scale (DBDRS), Diagnostic Infant and Preschool Assessment (DIPA-L), Pediatric Symptom Checklist (PSC), Social Communication Questionnaire (SCQ), Social Responsiveness Scale (SRS), Strengths and Weaknesses of ADHD Symptoms and Normal Behavior Rating Scale (SWAN) and the Vanderbilt ADHD diagnostic rating scale.<ref name="Peterson_2024a">Template:Cite journal</ref>

The ASEBA, BASC, CHAOS, CRS, and Vanderbilt diagnostic rating scales allow for both parents and teachers as raters in the diagnosis of childhood and adolescent ADHD. Adolescents may also self report their symptoms using self report scales from the ASEBA, SWAN, and the Dominic Interactive for Adolescents-Revised (DIA-R).<ref name="Peterson_2024a" /> Self-rating scales, such as the ADHD rating scale and the Vanderbilt ADHD diagnostic rating scale, are used in the screening and evaluation of ADHD.<ref name="Smith(2007) in Mash & Barkley EBA">Template:Cite book</ref>

Based on a 2024 systematic literature review and meta analysis commissioned by the Patient-Centered Outcomes Research Institute (PCORI), rating scales based on parent report, teacher report, or self-assessment from the adolescent have high internal consistency as a diagnostic tool meaning that the items within the scale are highly interrelated. The reliability of the scales between raters (i.e. their degree of agreement) however is poor to moderate making it important to include information from multiple raters to best inform a diagnosis.<ref name="Peterson_2024a" />

Imaging studies of the brain do not give consistent results between individuals; thus, they are only used for research purposes and not a diagnosis.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Electroencephalography is not accurate enough to make an ADHD diagnosis.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> A 2024 systematic review concluded that the use of biomarkers such as blood or urine samples, electroencephalogram (EEG) markers, and neuroimaging such as MRIs, in diagnosis for ADHD remains unclear; studies showed great variability, did not assess test-retest reliability, and were not independently replicable.<ref name="Peterson_2024" />

In North America and Australia, DSM-5 criteria are used for diagnosis, while European countries usually use the ICD-10. The DSM-IV criteria for diagnosis of ADHD is Template:Nowrap more likely to diagnose ADHD than is the ICD-10 criteria.<ref name="Singh_2008" /> ADHD is alternately classified as neurodevelopmental disorder<ref name="Caroline2010">Template:Cite book</ref> or a disruptive behaviour disorder along with ODD, CD, and antisocial personality disorder.<ref name="google-book-ref">Template:Cite book</ref> A diagnosis does not imply a neurological disorder.<ref name="NICE 2009" />

Very few studies have been conducted on diagnosis of ADHD on children younger than 7 years of age, and those that have were found in a 2024 systematic review to be of low or insufficient strength of evidence.<ref name="Peterson_2024a" /> A 2024 systematic review commissioned by the Patient-Centered Outcomes Research Institute (PCORI) highlighted that although a variety of diagnostic approaches show potential, there is substantial variability in their performance across studies. The CBCL and Disruptive Behavior Diagnostic Observation Schedule (DB-DOS) showed good performance, while BRIEF worked very well. However, there is not enough studies on children younger than 7 years of age to determine which diagnosis method is the most effective.<ref>Template:Cite report</ref> The review emphasised that diagnostic accuracy often depends on the comparison group—whether children with ADHD are being distinguished from typically developing peers or from other clinically referred youth—and that multiple informants (such as parents, teachers, and the youth themselves) may be necessary to improve diagnostic accuracy due to poor-to-moderate agreement between raters.<ref name="Peterson_2024a" />

Classification

Diagnostic and Statistical Manual

As with many other psychiatric disorders, a formal diagnosis should be made by a qualified professional based on a set number of criteria. In the United States, these criteria are defined by the American Psychiatric Association in the DSM. Based on the DSM-5 criteria published in 2013 and the DSM-5-TR criteria published in 2022, there are three presentations of ADHD:

1. ADHD, predominantly inattentive presentation, presents with symptoms including being easily distracted, forgetful, daydreaming, disorganisation, poor sustained attention, and difficulty completing tasks.
2. ADHD, predominantly hyperactive-impulsive presentation, presents with excessive fidgeting and restlessness, hyperactivity, and difficulty waiting and remaining seated.
3. ADHD, combined presentation, is a combination of the first two presentations.

This subdivision is based on presence of at least six (in children) or five (in older teenagers and adults)<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> out of nine long-term (lasting at least six months) symptoms of inattention, hyperactivity–impulsivity, or both.<ref name="DSM5" /><ref name="DSM5TR" /> To be considered, several symptoms must have appeared by the age of six to twelve and occur in more than one environment (e.g. at home and at school or work). The symptoms must be inappropriate for a child of that age<ref name="pmid21991721">Template:Cite journal</ref> and there must be clear evidence that they are causing impairment in multiple domains of life.<ref name="pmid23755024">Template:Cite journal</ref>

The DSM-5 and the DSM-5-TR also provide two diagnoses for individuals who have symptoms of ADHD but do not entirely meet the requirements. Other Specified ADHD allows the clinician to describe why the individual does not meet the criteria, whereas Unspecified ADHD is used where the clinician chooses not to describe the reason.<ref name="DSM5" /><ref name="DSM5TR" />

International Classification of Diseases

In the eleventh revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-11) by the World Health Organization, the disorder is classified as Attention deficit hyperactivity disorder (code 6A05). The defined subtypes are predominantly inattentive presentation (6A05.0); predominantly hyperactive-impulsive presentation (6A05.1); and combined presentation (6A05.2). However, the ICD-11 includes two residual categories for individuals who do not entirely match any of the defined subtypes: other specified presentation (6A05.Y) where the clinician includes detail on the individual's presentation; and presentation unspecified (6A05.Z) where the clinician does not provide detail.<ref name="ICD-11">Template:Cite encyclopedia</ref>

In the tenth revision (ICD-10), the symptoms of hyperkinetic disorder were analogous to ADHD in the ICD-11. When a conduct disorder (as defined by ICD-10)<ref name="ICD10">Template:Cite book</ref> is present, the condition was referred to as hyperkinetic conduct disorder. Otherwise, the disorder was classified as disturbance of activity and attention, other hyperkinetic disorders or hyperkinetic disorders, unspecified. The latter was sometimes referred to as hyperkinetic syndrome.<ref name="ICD10" />

Social construct theory

The social construct theory of ADHD suggests that, because the boundaries between normal and abnormal behaviour are socially constructed (i.e. jointly created and validated by all members of society, and in particular by physicians, parents, teachers, and others), it then follows that subjective valuations and judgements determine which diagnostic criteria are used and thus, the number of people affected.<ref>Template:Cite journal</ref> Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and then given a name".<ref>Template:Cite book</ref>

Adults

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Adults with ADHD are diagnosed under the same criteria, including that their signs must have been present by the age of six to twelve. The individual is the best source for information in diagnosis, however others may provide useful information about the individual's symptoms currently and in childhood; a family history of ADHD also adds weight to a diagnosis.<ref name="Kooij_2010" />Template:Rp Certain assessments, such as the Wender Utah Rating Scale (WURS), attempt to assess these childhood ADHD symptoms by having adults retrospectively recall their experiences as children.<ref name="pmid38369740">Template:Cite journal</ref> While the core symptoms of ADHD are similar in children and adults, they often present differently in adults than in children: for example, excessive physical activity seen in children may present as feelings of restlessness and constant mental activity in adults.<ref name="Kooij_2010" />Template:Rp

Worldwide, it is estimated that 2.58% of adults have persistent ADHD (where the individual currently meets the criteria and there is evidence of childhood onset), and 6.76% of adults have symptomatic ADHD (meaning that they currently meet the criteria for ADHD, regardless of childhood onset).<ref name="Song_2021">Template:Cite journal</ref> In 2020, this was 139.84 million and 366.33 million affected adults respectively.<ref name="Song_2021" /> Around 15% of children with ADHD continue to meet full DSM-IV-TR criteria at 25 years of age, and 50% still experience some symptoms.<ref name="Kooij_2010" />Template:Rp Template:As of, most adults remain untreated.<ref name="pmid21494335">Template:Cite journal</ref> Many adults with ADHD without diagnosis and treatment have a disorganised life, and some use non-prescribed drugs or alcohol as a coping mechanism.<ref name="Art.218">Template:Cite journal</ref> Other problems may include relationship and job difficulties, and an increased risk of criminal activities.<ref>Template:Cite journal</ref><ref name="Kooij_2010" />Template:Rp Associated mental health problems include depression, anxiety disorders, and learning disabilities.<ref name="Art.218" />

Some ADHD symptoms in adults differ from those seen in children. While children with ADHD may climb and run about excessively, adults may experience an inability to relax, or may talk excessively in social situations.<ref name="Kooij_2010" />Template:Rp Adults with ADHD may start relationships impulsively, display sensation-seeking behaviour, and be short-tempered.<ref name="Kooij_2010" />Template:Rp Addictive behaviour such as substance abuse and gambling are common.<ref name="Kooij_2010" />Template:Rp This led to those who presented differently as they aged having outgrown the DSM-IV criteria.<ref name="Kooij_2010" />Template:Rp The DSM-5 criteria does specifically deal with adults unlike that of DSM-IV, which does not fully take into account the differences in impairments seen in adulthood compared to childhood.<ref name="Kooij_2010" />Template:Rp

For diagnosis in an adult, the presence of symptoms since childhood is generally required. However, a proportion of adults who meet the criteria for ADHD in adulthood would not have been diagnosed with ADHD as children. Most cases of late-onset ADHD develop the disorder between the ages of 12–16 and may therefore be considered early adult or adolescent-onset ADHD.<ref>Template:Cite journal</ref>

Differential diagnosis

Symptoms related to other disorders<ref name="BBDADHD">Template:Cite journal</ref>

Depressive disorder	Anxiety disorder	Bipolar disorder
feelings of hopelessness, low self-esteem, or unhappiness loss of interest in hobbies or regular activities fatigue sleep problems difficulty maintaining attention change in appetite irritability or hostility low tolerance for stress thoughts of death unexplained pain	persistent feeling of anxiety irritability occasional feelings of panic or fear hypervigilance inability to pay attention tire easily low tolerance for stress difficulty maintaining attention	in manic state excessive happiness hyperactivity racing thoughts aggression excessive talking grandiose delusions decreased need for sleep inappropriate social behaviour difficulty maintaining attention in depressive state same symptoms as in depression section

The DSM provides differential diagnoses – potential alternate explanations for specific symptoms. Assessment and investigation of clinical history determines which is the most appropriate diagnosis. The DSM-5 suggests oppositional defiant disorder, intermittent explosive disorder, and other disorders such as stereotypic movement disorder and Tourette syndrome, in addition to specific learning disorder, intellectual disability, autism, reactive attachment disorder, anxiety disorders, depressive disorders, bipolar disorder, disruptive mood dysregulation disorder, substance use disorder, personality disorders, psychotic disorders, medication-induced symptoms, and neurocognitive disorders. Many but not all of these are also common comorbidities of ADHD.<ref name="DSM5" /> The DSM-5-TR also suggests post-traumatic stress disorder.<ref name="DSM5TR" />

Symptoms of ADHD that particularly relate to disinhibition and irritability in addition to low-mood and self-esteem as a result of symptom expression might be confusable with dysthymia and bipolar disorder as well as with borderline personality disorder, however they are comorbid at a significantly increased rate relative to the general population.<ref name="Kooij_2010" />Template:Rp Some symptoms that are viewed superficially due to anxiety disorders, intellectual disability or the effects of substance abuse such as intoxication and withdrawal can overlap to some extent with ADHD. These disorders can also sometimes occur along with ADHD.

Primary sleep disorders may affect attention and behaviour and the symptoms of ADHD may affect sleep.<ref name="Owens2008">Template:Cite journal</ref> It is thus recommended that children with ADHD be regularly assessed for sleep problems.<ref>Template:Cite journal</ref> Sleepiness in children may result in symptoms ranging from the classic ones of yawning and rubbing the eyes, to disinhibition and inattention. Obstructive sleep apnea can also cause ADHD-like symptoms.<ref name="pmid22670023">Template:Cite journal</ref>

In general, the DSM-5-TR can help distinguish between many conditions associated with ADHD-like symptoms by the context in which the symptoms arise.<ref name="DSM5TR" /> For example, children with learning disabilities may feel distractable and agitated when asked to engage in tasks that require the impaired skill (e.g., reading, math), but not in other situations. A person with an intellectual disability may develop symptoms that overlap with ADHD when placed in a school environment that is inappropriate for their needs. The type of inattention implicated in ADHD, of poor persistence and sustained attention, differs substantially from selective or oriented inattention seen in cognitive disengagement syndrome (CDS), as well as from rumination, reexperiencing or mind blanking seen in anxiety disorders or PTSD.

In mood disorders, ADHD-like symptoms may be limited to manic or depressive states of an episodic nature. Symptoms overlapping with ADHD in psychotic disorders may be limited to psychotic states. Substance use disorder, some medications, and certain medical conditions may cause symptoms to appear later in life, while ADHD, as a neurodevelopmental disorder, requires for them to have been present since childhood.

Furthermore, a careful understanding of the nature of the symptoms may help establish the difference between ADHD and other disorders.<ref name="DSM5TR" /> For example, the forgetfulness and impulsivity typical of ADHD (e.g., in completing school assignments or following directions) may be distinguished from opposition when there is no hostility or defiance, although ADHD and ODD are highly comorbid.Template:Cn Tantrums may differ from the outbursts in intermittent explosive disorder if there is no aggression involved. The fidgetiness observed in ADHD may be differentiated from tics or stereotypies common in Tourette syndrome or autism.Template:Cn

Also, the social difficulties often experienced by individuals with ADHD due to inattention (e.g., being unfocused during the interaction and therefore missing cues or being unaware of one's behavior)<ref>Template:Cite book</ref> or impulsivity (blurting things out, asking intrusive questions, interrupting) may be contrasted with the social detachment and deficits in understanding social cues associated with autism. Individuals with ADHD may also present signs of the social impairment or emotional and cognitive dysregulation seen in personality disorders, but not necessarily such features as a fear of abandonment, an unstable sense of self, narcissistic tendencies, aggressiveness, or other personality features.<ref name="DSM5TR" />

While it is possible and common for many of these different conditions to be comorbid with ADHD, the symptoms must not be better explained by them, as per diagnostic criterion E in the DSM-5.<ref name="DSM5" /><ref name="DSM5TR" /> The symptoms must arise early in life, appear across multiple environments, and cause significant impairment. Moreover, when some of these conditions are in fact comorbid with ADHD, it is still important to distinguish them, as each may need to be treated separately.<ref>Template:Cite book</ref>

Comorbidities

Psychiatric comorbidities

In children, ADHD occurs with other disorders about two-thirds of the time.<ref name="Walitza_2012" />

Other neurodevelopmental conditions are common comorbidities. Autism spectrum disorder (ASD), co-occurring at a rate of 21% in those with ADHD, affects social skills, ability to communicate, behaviour, and interests.<ref name="Young_2020">Template:Cite journal</ref><ref name="NHS2018">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Learning disabilities have been found to occur in about 20–30% of children with ADHD. Learning disabilities can include developmental speech and language disorders, and academic skills disorders.<ref name="BaileyHC">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> ADHD, however, is not considered a learning disability, but it very frequently causes academic difficulties.<ref name="BaileyHC" /> Intellectual disabilities<ref name="DSM5TR" />Template:Rp and Tourette syndrome<ref name="NHS2018" /> are also common.

ADHD is often comorbid with disruptive, impulse control, and conduct disorders. Oppositional defiant disorder (ODD) occurs in about 25% of children with an inattentive presentation and 50% of those with a combined presentation.<ref name="DSM5TR" />Template:Rp It is characterised by angry or irritable mood, argumentative or defiant behaviour and vindictiveness which are age-inappropriate. Conduct disorder (CD) is another common comorbid disorder of adolescents with ADHD, and occurs in 25% of individuals with combined presentation.<ref name="DSM5TR" />Template:Rp It is characterised by aggression, destruction of property, deceitfulness, theft and violations of rules.<ref name="UTP2008">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Adolescents with ADHD who also have CD are more likely to develop antisocial personality disorder in adulthood.<ref name="pmid19428109">Template:Cite journal</ref> Brain imaging supports that CD and ADHD are separate conditions: conduct disorder was shown to reduce the size of one's temporal lobe and limbic system, and increase the size of one's orbitofrontal cortex, whereas ADHD was shown to reduce connections in the cerebellum and prefrontal cortex more broadly. Conduct disorder involves more impairment in motivation control than ADHD.<ref name="pmid21094938">Template:Cite journal</ref> Intermittent explosive disorder is characterised by sudden and disproportionate outbursts of anger and co-occurs in individuals with ADHD more frequently than in the general population.<ref>Template:Cite journal</ref>

Borderline personality disorder has also been noted to co-occur with ADHD,<ref name="PM">Template:Cite journalTemplate:Primary source inline</ref> though more recent research suggests this may be due to historical biases leading to misdiagnoses.<ref>Template:Bulleted list</ref> The current diagnostic assessment of either disorder is often complex, as both of them have overlapping symptoms, thus these assessments often follow a differential diagnosis (following the American Psychiatric Association Guidelines for diagnosis) to determine whether there's a co-occurrence of both disorders or not.Template:Cn

Anxiety and mood disorders are frequent comorbidities. Anxiety disorders have been found to occur more commonly in the ADHD population, as have mood disorders (especially bipolar disorder and major depressive disorder). Boys diagnosed with the combined ADHD subtype are more likely to have a mood disorder.<ref name="Wilens_2010">Template:Cite journal</ref> Adults and children with ADHD sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions.<ref name="pmid21717696">Template:Cite journal</ref><ref name="Wilens_2011">Template:Cite journal</ref>

Sleep disorders and ADHD commonly co-exist. They can also occur as a side effect of medications used to treat ADHD. In children with ADHD, insomnia is the most common sleep disorder with behavioural therapy being the preferred treatment.<ref name="pmid21600348">Template:Cite journal</ref><ref name="pmid20451036">Template:Cite journal</ref> Problems with sleep initiation are common among individuals with ADHD but often they will be deep sleepers and have significant difficulty getting up in the morning.<ref name="Brown_2008" /> Melatonin is sometimes used in children who have sleep onset insomnia.<ref name="pmid20028959">Template:Cite journal</ref> Restless legs syndrome has been found to be more common in those with ADHD and is often due to iron deficiency anemia.<ref name="pmid21365608">Template:Cite journal</ref><ref name="pmid20620105">Template:Cite journal</ref> However, restless legs can simply be a part of ADHD and requires careful assessment to differentiate between the two disorders.<ref name="pmid18656214">Template:Cite journal</ref> Delayed sleep phase disorder is also a common comorbidity.<ref>Template:Cite journal</ref>

Individuals with ADHD are at increased risk of substance use disorders.<ref name="use" />Template:Rp This is most commonly seen with alcohol or cannabis.<ref name="Kooij_2010" />Template:Rp The reason for this may be an altered reward pathway in the brains of ADHD individuals, self-treatment and increased psychosocial risk factors.Template:Rp This makes the evaluation and treatment of ADHD more difficult, with serious substance misuse problems usually treated first due to their greater risks.<ref name="NICE2009-part2" /> Other psychiatric conditions include reactive attachment disorder,<ref>Template:Cite journal</ref> characterised by a severe inability to appropriately relate socially, and cognitive disengagement syndrome, a distinct attention disorder occurring in 30–50% of ADHD cases as a comorbidity, regardless of the presentation; a subset of cases diagnosed with ADHD-PIP have been found to have CDS instead.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> Individuals with ADHD are three times more likely to be diagnosed with an eating disorder compared to those without ADHD; conversely, individuals with eating disorders are two times more likely to have ADHD than those without eating disorders.<ref name="Nazar_2016">Template:Cite journal</ref>

Trauma

ADHD, trauma, and adverse childhood experiences are also comorbid,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> which could in part be potentially explained by the similarity in presentation between different diagnoses. The symptoms of ADHD and PTSD can have significant behavioural overlap—in particular, motor restlessness, difficulty concentrating, distractibility, irritability/anger, emotional constriction or dysregulation, poor impulse control, and forgetfulness are common in both.<ref name="Ford_2009">Template:Cite journal</ref><ref>Template:Cite journal</ref> This could result in trauma-related disorders or ADHD being mis-identified as the other.<ref name="Szymanski_2011">Template:Cite journal</ref> Additionally, traumatic events in childhood are a risk factor for ADHD;<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> they can lead to structural brain changes and the development of ADHD behaviours.<ref name="Szymanski_2011" /> Finally, the behavioural consequences of ADHD symptoms cause a higher chance of the individual experiencing trauma (and therefore ADHD leads to a concrete diagnosis of a trauma-related disorder).<ref>Template:Cite journal</ref><ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Non-psychiatric

Some non-psychiatric conditions are also comorbidities of ADHD. This includes epilepsy,<ref name="NHS2018" /> a neurological condition characterised by recurrent seizures.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> There are well established associations between ADHD and obesity, asthma and sleep disorders,<ref name="pmid27664125">Template:Cite journal</ref> and an association with celiac disease.<ref>Template:Cite journal</ref> Children with ADHD have a higher risk for migraine headaches,<ref>Template:Cite journal</ref> but have no increased risk of tension-type headaches. Children with ADHD may also experience headaches as a result of medication.<ref name="Salem_2017">Template:Cite journal</ref><ref name="Pan_2021">Template:Cite journal</ref>

A 2021 review reported that several neurometabolic disorders caused by inborn errors of metabolism converge on common neurochemical mechanisms that interfere with biological mechanisms also considered central in ADHD pathophysiology and treatment. This highlights the importance of close collaboration between health services to avoid clinical overshadowing.<ref>Template:Cite journal</ref>

In June 2021, Neuroscience & Biobehavioral Reviews published a systematic review of 82 studies that all confirmed or implied elevated accident-proneness in ADHD patients, and whose data suggested that the type of accidents or injuries -- and overall risk -- changes over the lifespan of ADHD patients.<ref>Template:Cite journal</ref> In January 2014, Accident Analysis & Prevention published a meta-analysis of 16 studies examining the relative risk of traffic collisions for drivers with ADHD, finding an overall relative risk estimate of 1.36 without controlling for exposure, a relative risk estimate of 1.29 when controlling for publication bias, a relative risk estimate of 1.23 when controlling for exposure, and a relative risk estimate of 1.86 for ADHD drivers with oppositional defiant disorder or conduct disorder comorbidities.<ref>Template:Cite journal</ref><ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Suicide risk

Systematic reviews in 2017 and 2020 found strong evidence that ADHD is associated with increased suicide risk across all age groups, as well as growing evidence that an ADHD diagnosis in childhood or adolescence represents a significant future suicidal risk factor.<ref>Template:Cite journal</ref><ref name="Garas_2020">Template:Cite journal</ref> Potential causes include ADHD's association with functional impairment, negative social, educational and occupational outcomes, and financial distress.<ref name="Septier_2019">Template:Cite journal</ref><ref>Template:Cite journal</ref> A 2019 meta-analysis indicated a significant association between ADHD and suicidal spectrum behaviours (suicidal attempts, ideations, plans, and completed suicides); across the studies examined, the prevalence of suicide attempts in individuals with ADHD was 18.9%, compared to 9.3% in individuals without ADHD, and the findings were substantially replicated among studies which adjusted for other variables. However, the relationship between ADHD and suicidal spectrum behaviours remains unclear due to mixed findings across individual studies and the complicating impact of comorbid psychiatric disorders.<ref name="Septier_2019" /> There is no clear data on whether there is a direct relationship between ADHD and suicidality, or whether ADHD increases suicide risk through comorbidities.<ref name="Garas_2020" />

Rejection sensitive dysphoria

Rejection sensitive dysphoria, while not a formal diagnosis, is also a common symptom of ADHD, estimated to affect a majority of people with ADHD.<ref>Template:Cite journal</ref><ref>Template:Cite magazine</ref><ref>Template:Cite journal</ref> Others posit that rejection sensitivity stems from early attachment relationships and parental rejection;<ref name="Butler">Template:Cite journal</ref> peer rejection is also thought to play a role.<ref name="Butler" /><ref>Template:Cite journal</ref> Bullying, an extreme form of peer rejection, is likely connected to later rejection sensitivity.<ref name="Butler" /> However, there is no conclusive evidence for any of these theories.<ref name="Butler" />

Management

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The management of ADHD typically involves counseling or medications, either alone or in combination. While there are various options of treatment to improve ADHD symptoms, medication therapies substantially improve long-term outcomes, and while eliminating some elevated risks such as obesity,<ref name="Faraone_2021" /> they do come with some risks of adverse events.<ref>Template:Cite journal</ref> Medications used include stimulants, atomoxetine, alpha-2 adrenergic receptor agonists, and sometimes antidepressants.<ref name="Wilens_2010" /><ref name="cognition enhancers">Template:Cite journal</ref> In those who have trouble focusing on long-term rewards, a large amount of positive reinforcement improves task performance.<ref name="Motivation" /> Medications are the most effective treatment,<ref name="Faraone_2021" /><ref name="CNS09">Template:Cite journal</ref> and any side effects are typically mild and easy to resolve<ref name="Faraone_2021" /> although any improvements will be reverted if medication is ceased.<ref name="May_2008">Template:Cite journal</ref> ADHD stimulants also improve persistence and task performance in children with ADHD.<ref name="Malenka ADHD neurosci" /><ref name="Motivation" /> To quote one systematic review, "recent evidence from observational and registry studies indicates that pharmacological treatment of ADHD is associated with increased achievement and decreased absenteeism at school, a reduced risk of trauma-related emergency hospital visits, reduced risks of suicide and attempted suicide, and decreased rates of substance abuse and criminality".<ref name="Coghill_2017">Template:Cite journal File:CC-BY icon.svg Text was copied from this source, which is available under a Creative Commons Attribution 4.0 International License {{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Data also suggest that combining medication with cognitive behavioral therapy (CBT) can have positive effects: although CBT is substantially less effective, it can help address problems that reside after medication has been optimised.<ref name="Faraone_2021" /> The nature and range of desirable endpoints of ADHD treatment vary among diagnostic standards for ADHD.<ref>Template:Cite journal</ref> In most studies, the efficacy of treatment is determined by reductions in symptoms.<ref>Template:Cite journal</ref> However, some studies have included subjective ratings from teachers and parents as part of their assessment of treatment efficacies.<ref name="Comparative efficacy and tolerabili"/>

Behavioural therapies

There is good evidence for the use of behavioural therapies in ADHD. They are the recommended first-line treatment in those who have mild symptoms or who are preschool-aged.<ref>Template:Cite journal</ref><ref name="Clinics09">Template:Cite journal</ref> Psychological therapies used include: psychoeducational input, behavior therapy, cognitive behavioral therapy,<ref>Template:Cite journal</ref> interpersonal psychotherapy, family therapy, school-based interventions, social skills training, behavioural peer intervention, organisation training,<ref name="Evans2014">Template:Cite journal</ref> and parent management training.<ref name="NICE 2009" /> Neurofeedback has greater treatment effects than non-active controls for up to 6 months and possibly a year following treatment, and may have treatment effects comparable to active controls (controls proven to have a clinical effect) over that time period.<ref>Template:Cite journal</ref> Despite efficacy in research, there is insufficient regulation of neurofeedback practice, leading to ineffective applications and false claims regarding innovations.<ref>Template:Cite journal</ref> Parent training may improve a number of behavioural problems including oppositional and non-compliant behaviours.<ref name="Dal2017">Template:Cite journal</ref>

There is little high-quality research on the effectiveness of family therapy for ADHD—but the existing evidence shows that it is similar to community care, and better than placebo.<ref>Template:Cite journal</ref> ADHD-specific support groups can provide information and may help families cope with ADHD.<ref name="Brain encyclopedia">Template:Cite encyclopedia</ref>

Social skills training, behavioural modification, and medication may have some limited beneficial effects in peer relationships. Stable, high-quality friendships with non-deviant peers protect against later psychological problems.<ref name="pmid20490677">Template:Cite journal</ref>

Digital interventions

Several clinical trials have investigated the efficacy of digital therapeutics, particularly Akili Interactive Labs's video game-based digital therapeutic AKL-T01, marketed as EndeavourRx. The pediatric STARS-ADHD randomised, double-blind, parallel-group, controlled trial demonstrated that AKL-T01 significantly improved performance on the Test of Variables of Attention, an objective measure of attention and inhibitory control, compared to a control group after four weeks of at-home use.<ref name="STARS-ADHD">Template:Cite journal</ref> A subsequent pediatric open-label study, STARS-Adjunct, published in Nature Portfolio's npj Digital Medicine evaluated AKL-T01 as an adjunctive treatment for children with ADHD who were either on stimulant medication or not on stimulant pharmacotherapy. Results showed improvements in ADHD-related impairment (measured by the Impairment Rating Scale) and ADHD symptoms after 4 weeks of treatment, with effects persisting during a 4-week pause and further improving with an additional treatment period.<ref name="STARS-ADHD-Adjunct">Template:Cite journal</ref> Notably, the magnitude of the measured improvement was similar for children both on and off stimulants.<ref name="STARS-ADHD-Adjunct" /> In 2020, AKL-T01 received marketing authorisation for pediatric ADHD from the FDA, becoming "the first game-based therapeutic granted marketing authorisation by the FDA for any type of condition."<ref name="FDA AKL-T01">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

In addition to pediatric populations, a 2023 study in the Journal of the American Academy of Child & Adolescent Psychiatry investigated the efficacy and safety of AKL-T01 in adults with ADHD. After six weeks of at-home treatment with AKL-T01, participants showed significant improvements in objective measures of attention (TOVA - Attention Comparison Score), reported ADHD symptoms (ADHD-RS-IV inattention subscale and total score), and reported quality of life (AAQoL).<ref name="STARS-ADHD-Adults">Template:Cite journal</ref> The magnitude of improvement in attention was nearly seven times greater than that reported in pediatric trials.<ref name="STARS-ADHD-Adults" /> The treatment was well-tolerated, with high compliance and no serious adverse events.<ref name="STARS-ADHD-Adults" />

Medication

The medications for ADHD appear to alleviate symptoms via their effects on the pre-frontal executive, striatal and related regions and networks in the brain; usually by increasing neurotransmission of norepinephrine and dopamine.<ref>Template:Cite journal</ref><ref name="Schulz_2012">Template:Cite journal</ref><ref name="Koda_2010">Template:Cite journal</ref>

Stimulants

Methylphenidate and amphetamine or its derivatives are often first-line treatments for ADHD.<ref name="Dodson_2005" /><ref>Template:Cite journal</ref> About 70 per cent respond to the first stimulant tried and as few as 10 per cent respond to neither amphetamines nor methylphenidate.<ref name="CNS09" /> Stimulants may also reduce the risk of unintentional injuries in children with ADHD.<ref name="Ruiz-Goikoetxea_2017">Template:Cite journal</ref> Magnetic resonance imaging studies suggest that long-term treatment with amphetamine or methylphenidate decreases abnormalities in brain structure and function found in subjects with ADHD.<ref name="Neuroplasticity 1">Template:Cite journal</ref><ref name="Neuroplasticity 2">Template:Cite journal</ref><ref name="Neuroplasticity 3">Template:Cite journal</ref> A 2018 review found the greatest short-term benefit with methylphenidate in children, and amphetamines in adults.<ref name="Comparative efficacy and tolerabili">Template:Cite journal</ref> Studies and meta-analyses show that amphetamine is slightly-to-modestly more effective than methylphenidate at reducing symptoms,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> and they are more effective pharmacotherapy for ADHD than α2-agonists<ref>Template:Cite journal</ref> but methylphenidate has comparable efficacy to non-stimulants such as atomoxetine. In a Cochrane clinical synopsis, Dr Storebø and colleagues summarised their meta-review<ref>Template:Cite journal</ref> on methylphenidate for ADHD in children and adolescents. The meta-analysis raised substantial doubts about the drug's efficacy relative to a placebo. This led to a strong critical reaction from the European ADHD Guidelines Group and individuals in the scientific community, who identified a number of flaws in the review.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> Since at least September 2021, there is a unanimous and global scientific consensus that methylphenidate is safe and highly effective for treating ADHD.<ref name="Faraone_2021" /><ref name="epa_consensus_2019" >Template:Cite journal</ref> The same journal released a subsequent systematic review (2022) of extended-release methylphenidate for adults, concluding similar doubts about the certainty of evidence.<ref name="y943">Template:Cite journal</ref> Other recent systematic reviews and meta-analyses, however, find certainty in the safety and high efficacy of methylphenidate for reducing ADHD symptoms,<ref name="Comparative efficacy and tolerabili"/><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> for alleviating the underlying executive functioning deficits,<ref>Template:Cite journal</ref> and for substantially reducing the adverse consequences of untreated ADHD with continuous treatment.<ref name="Faraone_2021" /> Clinical guidelines internationally are also consistent in approving the safety and efficacy of methylphenidate and recommending it as a first-line treatment for the disorder.<ref name="Faraone_2021" />

Safety and efficacy data have been reviewed extensively by medical regulators (e.g., the US Food and Drug Administration and the European Medicines Agency), the developers of evidence-based international guidelines (e.g., the UK National Institute for Health and Care Excellence and the American Academy of Pediatrics), and government agencies who have endorsed these guidelines (e.g., the Australian National Health and Medical Research Council). These professional groups unanimously conclude, based on the scientific evidence, that methylphenidate is safe and effective and should be considered as a first-line treatment for ADHD.<ref name="Faraone_2021" /> The likelihood of developing insomnia for ADHD patients taking stimulants has been measured at between 11 and 45 per cent for different medications,<ref name="Wynchank_2017">Template:Cite journal</ref> and may be a main reason for discontinuation. Other side effects, such as tics, decreased appetite and weight loss, or emotional lability, may also lead to discontinuation.<ref name="CNS09" /> Stimulant psychosis and mania are rare at therapeutic doses, appearing to occur in approximately 0.1% of individuals, within the first several weeks after starting amphetamine therapy.<ref name="Cochrane recreational amph psychosis">Template:Cite journal</ref><ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name="pmid19171629">Template:Cite journal</ref> The safety of these medications in pregnancy is unclear.<ref>Template:Cite journal</ref> Symptom improvement is not sustained if medication is ceased.<ref name="PRBM.S49114">Template:Cite journal</ref><ref name="May_2008"/><ref name="Castells_2018">Template:Cite journal</ref>

The long-term effects of ADHD medication have yet to be fully determined,<ref name="ADHD 2015 review">Template:Cite journal</ref><ref name="pmid21519262">Template:Cite journal</ref> although stimulants are generally beneficial and safe for up to two years for children and adolescents.<ref>Template:Cite journal</ref> A 2022 meta-analysis found no statistically significant association between ADHD medications and the risk of cardiovascular disease (CVD) across age groups, although the study suggests further investigation is warranted for patients with preexisting CVD as well as long-term medication use.<ref>Template:Cite journal</ref> Regular monitoring has been recommended in those on long-term treatment.<ref name="pmid20571380">Template:Cite journal</ref> There are indications suggesting that stimulant therapy for children and adolescents should be stopped periodically to assess continuing need for medication, decrease possible growth delay, and reduce tolerance.<ref name="pmid21530185">Template:Cite journal</ref><ref>Template:Cite journal</ref> Although potentially addictive at high doses,<ref name="NHM therapeutic stim addiction liability">Template:Cite book</ref><ref>Template:Cite book</ref> stimulants used to treat ADHD have low potential for abuse.<ref name="Dodson_2005"/> Treatment with stimulants is either protective against substance abuse or has no effect.<ref name="Kooij_2010" />Template:Rp<ref name="ADHD 2015 review" /><ref name="NHM therapeutic stim addiction liability" />

The majority of studies on nicotine and other nicotinic agonists as treatments for ADHD have shown favorable results; however, no nicotinic drug has been approved for ADHD treatment.<ref>Template:Cite journal</ref> Caffeine was formerly used as a second-line treatment for ADHD but research indicates it has no significant effects in reducing ADHD symptoms. Caffeine appears to help with alertness, arousal and reaction time but not the type of inattention implicated in ADHD (sustained attention/persistence).<ref>Template:Cite journal</ref> Pseudoephedrine and ephedrine do not affect ADHD symptoms.<ref name="Dodson_2005">Template:Cite journal</ref>

Modafinil has shown some efficacy in reducing the severity of ADHD in children and adolescents.<ref>Template:Cite journal</ref> It may be prescribed off-label to treat ADHD.<ref>Template:Cite journal</ref>

Non-stimulants

Two non-stimulant medications, atomoxetine and viloxazine, are approved by the FDA and in other countries for the treatment of ADHD.

Atomoxetine, due to its lack of addiction liability, may be preferred in those who are at risk of recreational or compulsive stimulant use, although evidence is lacking to support its use over stimulants for this reason.<ref name="Kooij_2010"/>Template:Rp Atomoxetine alleviates ADHD symptoms through norepinephrine reuptake and by indirectly increasing dopamine in the pre-frontal cortex,<ref name="Koda_2010"/> sharing 70–80% of the brain regions with stimulants in their produced effects.<ref name="Schulz_2012"/> Atomoxetine has been shown to significantly improve academic performance.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> Meta-analyses and systematic reviews have found that atomoxetine has comparable efficacy, equal tolerability and response rate (75%) to methylphenidate in children and adolescents. In adults, efficacy and discontinuation rates are equivalent.<ref name="Bushe_2016">Template:Cite journal</ref><ref name="Hazell_2011">Template:Cite journal</ref><ref name="Hanwella_2011">Template:Cite journal</ref><ref name="Rezaei_2016">Template:Cite journal</ref><ref>Template:Cite report</ref>

Analyses of clinical trial data suggests that viloxazine is about as effective as atomoxetine and methylphenidate but with fewer side effects.<ref>Template:Cite journal</ref>

Amantadine was shown to induce similar improvements in children treated with methylphenidate, with less frequent side effects.<ref>Template:Cite journal</ref> A 2021 retrospective study showed that amantadine may serve as an effective adjunct to stimulants for ADHD–related symptoms and appears to be a safer alternative to second- or third-generation antipsychotics.<ref>Template:Cite journal</ref>

Bupropion is also used off-label by some clinicians due to research findings. It is effective, but modestly less than atomoxetine and methylphenidate.<ref>Template:Cite journal</ref>

There is little evidence on the effects of medication on social behaviours.<ref name="McDonagh_20112">Template:Cite report</ref> Antipsychotics may also be used to treat aggression in ADHD.<ref>Template:Cite journal</ref>

Alpha-2a agonists

Two alpha-2a agonists, extended-release formulations of guanfacine and clonidine, are approved by the FDA and in other countries for the treatment of ADHD (effective in children and adolescents but effectiveness has still not been shown for adults).<ref>Template:Cite journal</ref><ref name="Huss Chen Ludolph 2016 pp. 1–252">Template:Cite journal</ref> They appear to be modestly less effective than the stimulants (amphetamine and methylphenidate) and non-stimulants (atomoxetine and viloxazine) at reducing symptoms,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> but can be useful alternatives or used in conjunction with a stimulant. These medications act by adjusting the alpha-2a ports on the outside of noradrenergic nerve cells in the pre-frontal executive networks, so the information (electrical signal) is less confounded by noise.<ref>Template:Cite journal</ref>

Guidelines

Guidelines on when to use medications vary by country. The United Kingdom's National Institute for Health and Care Excellence recommends use for children only in severe cases, though for adults medication is a first-line treatment.<ref name="NICE_2019">Template:Cite book</ref> Conversely, most United States guidelines recommend medications in most age groups.<ref name="CADDRA">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Medications are especially not recommended for preschool children.<ref name="NICE_2019" /><ref name="NICE 2009" /> Underdosing of stimulants can occur, and can result in a lack of response or later loss of effectiveness.<ref>Template:Cite journal</ref> This is particularly common in adolescents and adults as approved dosing is based on school-aged children, causing some practitioners to use weight-based or benefit-based off-label dosing instead.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref>Template:Cite journal</ref>

Exercise

Exercise does not reduce the symptoms of ADHD.<ref name="Faraone_2021" /> The conclusion by the International Consensus Statement is based on two meta-analyses: one of 10 studies with 300 children and the other of 15 studies and 668 participants, which showed that exercise yields no statistically significant reductions on ADHD symptoms. A 2024 systematic review and meta analysis commissioned by the Patient-Centered Outcomes Research Institute (PCORI) identified seven studies on the effectiveness of physical exercise for treating ADHD symptoms.<ref name="Peterson_2024a" /> The type and amount of exercise varied widely across studies from martial arts interventions to treadmill training, to table tennis or aerobic exercise. Effects reported were not replicated, causing the authors to conclude that there is insufficient evidence that exercise intervention is an effective form of treatment for ADHD symptoms.<ref name="Peterson_2024a" />

Diet

Dietary modifications are not recommended Template:As of by the American Academy of Pediatrics, the National Institute for Health and Care Excellence, or the Agency for Healthcare Research and Quality due to insufficient evidence.<ref name="APP2019">Template:Cite journal</ref><ref name="NICE_2019" /> A 2013 meta-analysis found less than a third of children with ADHD see some improvement in symptoms with free fatty acid supplementation or decreased consumption of artificial food colouring.<ref name="Sonu_2013">Template:Cite journal</ref> These benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications.<ref name="Sonu_2013" /> This review also found that evidence does not support removing other foods from the diet to treat ADHD.<ref name="Sonu_2013" /> A 2014 review found that an elimination diet results in a small overall benefit in a minority of children, such as those with allergies.<ref name="Nigg_2014">Template:Cite journal</ref> A 2016 review stated that the use of a gluten-free diet as standard ADHD treatment is not advised.<ref name="pmid26825336">Template:Cite journal</ref> A 2017 review showed that a few-foods elimination diet may help children too young to be medicated or not responding to medication, while free fatty acid supplementation or decreased eating of artificial food colouring as standard ADHD treatment is not advised.<ref name="Pelsser_2017">Template:Cite journal</ref> Chronic deficiencies of iron, magnesium and iodine may have a negative impact on ADHD symptoms.<ref name="pmid22928358">Template:Cite journal</ref> There is a small amount of evidence that lower tissue zinc levels may be associated with ADHD.<ref name="pmid16190793">Template:Cite journal</ref> In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as treatment for ADHD.<ref name="pmid25220092">Template:Cite journal</ref> However, zinc supplementation may reduce the minimum effective dose of amphetamine when it is used with amphetamine for the treatment of ADHD.<ref name="Kraus_2008">Template:Cite journal</ref>

Prognosis

About 30–50% of people diagnosed in childhood continue to have ADHD in adulthood, with 2.58% of adults estimated to have ADHD which began in childhood.<ref name="Song_2021" /><ref name="Ginsberg_2014">Template:Cite journal</ref>Template:Text-source inline Children with ADHD have worse educational outcomes<ref name="fleming_et_al_2017" /> and a higher risk of unintentional injuries.<ref name="Ruiz-Goikoetxea_2017" /> In adults, hyperactivity is often replaced by inner restlessness, and adults affected are likely to develop coping mechanisms as they mature, thus compensating to some extent for their previous symptoms.<ref name="Coghill_2017" /><ref name="Art.218" />

The negative impacts of ADHD symptoms contribute to poor health-related quality of life that may be further exacerbated by, or may increase the risk of, other psychiatric conditions such as anxiety and depression.<ref name="Coghill_2017" /><ref>Template:Cite journal</ref> Individuals with ADHD may also face misconceptions and stigma.<ref name="Faraone_2021" /> A number of recent studies have found that ADHD is associated with a significant reduction in average life expectancy.<ref name="Barkley & Fischer">Template:Cite journal</ref><ref name="Adverse_2022" /><ref>Template:Cite journal</ref> A US study found rates of smoking among those with ADHD are higher than in the general population.<ref>Template:Cite journal</ref> Positive effects of medication on functional impairment and quality of life (e.g. reduced risk of accidents) have been found across multiple domains.<ref>Template:Cite journal</ref>

Individuals with ADHD are significantly overrepresented in prison populations. Although there is no generally accepted estimate of ADHD prevalence among inmates, a 2015 meta-analysis estimated a prevalence of 25.5%, and a larger 2018 meta-analysis estimated the frequency to be 26.2%.<ref>Template:Cite journal</ref>

New research in 2025 indicates that adults diagnosed with ADHD may have a shorter lifespan compared to those without the condition.<ref>Template:Cite news</ref> The study revealed that, on average, men with ADHD lived seven years less than men without ADHD, while women with ADHD had a lifespan nine years shorter than their peers.<ref>Template:Cite journal</ref> Although the study did not pinpoint exact causes of death, it highlighted that individuals with ADHD were more likely to engage in smoking, alcohol misuse, and face other health challenges such as depression, self-harm, or personality disorders.<ref>Template:Cite news</ref>

Epidemiology

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ADHD is estimated to affect about 6–7% of people aged 18 and under when diagnosed via the DSM-IV criteria.<ref name="pmid22976615"/> When diagnosed via the ICD-10 criteria, rates in this age group are estimated around 1–2%.<ref name="Cowen_2012">Template:Cite book</ref> Rates are similar between countries and differences in rates depend mostly on how it is diagnosed.<ref name="Jones_2011">Template:Cite book</ref> Children in North America appear to have a higher rate of ADHD than children in Africa and the Middle East; this is believed to be due to differing methods of diagnosis rather than a difference in underlying frequency. (The same publication which describes this difference also notes that the difference may be rooted in the available studies from these respective regions, as far more studies were from North America than from Africa and the Middle East.)<ref name="Polanczyk_2007">Template:Cite journal</ref> Template:As of it was estimated to affect 84.7 million people globally.<ref name=GBD2019>Template:Cite journal. Both DSM-IV-TR and ICD-10 criteria were used.</ref>

ADHD is diagnosed approximately twice as often in boys as in girls,<ref name="DSM5TR" /><ref name="pmid22976615">Template:Cite journal</ref> and 1.6 times more often in men than in women,<ref name="DSM5TR" /> although the disorder is overlooked in girls or diagnosed in later life because their symptoms sometimes differ from diagnostic criteria.Template:Refn<ref>Template:Cite journal</ref> In 2014, Keith Conners, one of the early advocates for recognition of the disorder, spoke out against overdiagnosis in a New York Times article.<ref name="NYT2013">Template:Cite news</ref> In contrast, a 2014 peer-reviewed medical literature review indicated that ADHD is underdiagnosed in adults.<ref name="Ginsberg_2014" />

Studies from multiple countries have reported that children born closer to the start of the school year are more frequently diagnosed with and medicated for ADHD than their older classmates.<ref>Template:Cite journal</ref> Boys who were born in December where the school age cut-off was 31 December were shown to be 30% more likely to be diagnosed and 41% more likely to be treated than those born in January. Girls born in December had a diagnosis and treatment percentage increase of 70% and 77% respectively compared to those born in January. Children who were born at the last three days of a calendar year were reported to have significantly higher levels of diagnosis and treatment for ADHD than children born at the first three days of a calendar year. The studies suggest that ADHD diagnosis is prone to subjective analysis.<ref name="Ford-Jones_2015" />

Rates of diagnosis and treatment have increased in both the United Kingdom and the United States since the 1970s. Prior to 1970, it was rare for children to be diagnosed with ADHD, while in the 1970s rates were about 1%.<ref>Template:Cite periodical</ref> This is believed to be primarily due to changes in how the condition is diagnosed<ref name="CDCTime2013" /> and how readily people are willing to treat it with medications rather than a true change in incidence.<ref name="Cowen_2012" /> With widely differing rates of diagnosis across countries, states within countries, races, and ethnicities, some suspect factors other than symptoms of ADHD are playing a role in diagnosis, such as cultural norms.<ref name="Elder-2010">Template:Cite journal</ref><ref name="Ford-Jones_2015">Template:Cite journal</ref>

Despite showing a higher frequency of symptoms associated with ADHD, non-White children in the US are less likely than White children to be diagnosed or treated for ADHD, a finding that is often explained by bias among health professionals, as well as parents who may be reluctant to acknowledge that their child has ADHD.<ref>Template:Cite journal</ref> Crosscultural differences in diagnosis of ADHD can also be attributed to the long-lasting effects of harmful, racially targeted medical practices. Medical pseudosciences, particularly those that targeted Black populations during the period of slavery in the US, lead to a distrust of medical practices within certain communities. The combination of ADHD symptoms often being regarded as misbehaviour rather than as a psychiatric condition, and the use of drugs to regulate ADHD, result in a hesitancy to trust a diagnosis of ADHD. Cases of misdiagnosis in ADHD can also occur due to stereotyping of people of color. Due to ADHD's subjectively determined symptoms, medical professionals may diagnose individuals based on stereotyped behaviour or misdiagnose due to cultural differences in symptom presentation.<ref name="Slobodin_2020">Template:Cite journal</ref>

A 2024 study in CDC's Morbidity and Mortality Weekly Report reports around 15.5 million U.S. adults have attention-deficit hyperactivity disorder, with many facing challenges in accessing treatment.<ref>Template:Cite journal</ref> One-third of diagnosed individuals had received a prescription for a stimulant drug in the past year but nearly three-quarters of them reported difficulties filling the prescription due to medication shortages.<ref>Template:Cite news</ref>

History

File:CDCHisGraph.png

Timeline of ADHD diagnostic criteria, prevalence, and treatment

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ADHD was officially known as attention deficit disorder (ADD) from 1980 to 1987; prior to the 1980s, it was known as hyperkinetic reaction of childhood. Symptoms similar to those of ADHD have been described in medical literature dating back to the 18th century. Sir Alexander Crichton describes "mental restlessness" in his book An inquiry into the nature and origin of mental derangement written in 1798.<ref>Template:Cite journal</ref><ref>Template:Cite book</ref> He made observations about children showing signs of being inattentive and having the "fidgets". The first clear description of ADHD is credited to George Still in 1902 during a series of lectures he gave to the Royal College of Physicians of London.<ref>Template:Cite journal</ref><ref name="CDCTime2013">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

The terminology used to describe the condition has changed over time and has included: minimal brain dysfunction in the DSM-I (1952), hyperkinetic reaction of childhood in the DSM-II (1968), and attention-deficit disorder with or without hyperactivity in the DSM-III (1980).<ref name="CDCTime2013" /> In 1987, the symptoms of inattention, impulsivity, and hyperactivity were collectively combined to define the new diagnosis of ADHD,<ref>Template:Cite journal</ref> and in 1994 the DSM-IV in split the diagnosis into three subtypes: ADHD inattentive type, ADHD hyperactive-impulsive type, and ADHD combined type.<ref name="Millichap_2010_chap1">Template:Cite book</ref> These terms were kept in the DSM-5 in 2013 and in the DSM-5-TR in 2022.<ref name=DSM5/><ref name=DSM5TR/> Prior to the DSM, terms included minimal brain damage in the 1930s.<ref>Template:Cite book</ref>

ADHD, its diagnosis, and its treatment have been controversial since the 1970s.<ref name="May_2008" /><ref name="Foreman_2006">Template:Cite journal</ref> For example, positions differ on whether ADHD is within the normal range of behaviour,<ref name="NICE2009-part2" /><ref name="Faraone_2005">Template:Cite journal</ref> and to degree to which ADHD is a genetic condition.<ref>Template:Cite news</ref> Other areas of controversy include the use of stimulant medications in children,<ref name="May_2008" /> the method of diagnosis, and the possibility of overdiagnosis.<ref name="Cormier_2008">Template:Cite journal</ref> In 2009, the National Institute for Health and Care Excellence states that the current treatments and methods of diagnosis are based on the dominant view of the academic literature.<ref name="NICE2009-Diagnosis">Template:Cite book</ref>

Once neuroimaging studies were possible, studies in the 1990s provided support for the pre-existing theory that neurological differences (particularly in the frontal lobes) were involved in ADHD. A genetic component was identified and ADHD was acknowledged to be a persistent, long-term disorder which lasted from childhood into adulthood.<ref>Template:Cite journal</ref><ref name="Barkley_2006">Template:Cite book</ref> ADHD was split into the current three sub-types because of a field trial completed by Lahey and colleagues and published in 1994.<ref>Template:Cite journal</ref> In 2021, global teams of scientists curated the International Consensus Statement compiling evidence-based findings about the disorder.<ref name="Faraone_2021" />

In 1934, Benzedrine became the first amphetamine medication approved for use in the United States.<ref name="Rasmussen_2006">Template:Cite journal</ref> Methylphenidate was introduced in the 1950s, and enantiopure dextroamphetamine in the 1970s.<ref name="CDCTime2013" /> The use of stimulants to treat ADHD was first described in 1937.<ref>Template:Cite journal</ref> Charles Bradley gave the children with behavioural disorders Benzedrine and found it improved academic performance and behaviour.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

Research directions

Possible positive traits

Possible positive traits of ADHD are a new avenue of research, and therefore limited.

A 2020 review found that creativity may be associated with ADHD symptoms, particularly divergent thinking and quantity of creative achievements, but not with the disorder of ADHD itself – i.e. it has not been found to be increased in people diagnosed with the disorder, only in people with subclinical symptoms or those that possess traits associated with the disorder. Divergent thinking is the ability to produce creative solutions which differ significantly from each other and consider the issue from multiple perspectives. Those with ADHD symptoms could be advantaged in this form of creativity as they tend to have diffuse attention, allowing rapid switching between aspects of the task under consideration; flexible associative memory, allowing them to remember and use more distantly related ideas which is associated with creativity; and impulsivity, allowing them to consider ideas which others may not have.<ref name="Hoogman_2020">Template:Cite journal</ref>

Possible biomarkers for diagnosis

Reviews of ADHD biomarkers have noted that platelet monoamine oxidase expression, urinary norepinephrine, urinary MHPG, and urinary phenethylamine levels consistently differ between ADHD individuals and non-ADHD controls. These parameters could serve as prognostic biomarkers for ADHD, but more research is needed to establish their prognostic utility. Urinary and blood plasma phenethylamine concentrations are lower in ADHD individuals relative to controls.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> The two most commonly prescribed drugs for ADHD, amphetamine and methylphenidate, increase phenethylamine biosynthesis in treatment-responsive individuals with ADHD.<ref name="Berry_2007">Template:Cite journal</ref> Lower urinary phenethylamine concentrations are associated with symptoms of inattentiveness in ADHD individuals.<ref name="Scassellati_2012">Template:Cite journal</ref>

See also

• Attention deficit hyperactivity disorder controversies
• Directed attention fatigue – a temporary state sharing many of the symptoms of ADHD
• Self-medication

Further reading

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External links

• National Institute of Mental Health. NIMH Pages About Attention-Deficit/Hyperactivity Disorder (ADHD). National Institutes of Health (NIH), U.S. Department of Health and Human Services.