Attention deficit hyperactivity disorder (ADHD) 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. ADHD symptoms arise from executive dysfunction. Impairments resulting from deficits in self-regulation such as time management, cognitive inhibition, task initiation, and sustained attention can include poor professional performance, relationship difficulties, and numerous health risks, collectively predisposing to a diminished quality of life and a reduction in life expectancy. It is associated with other mental disorders as well as non-psychiatric disorders, which can cause additional impairment. While ADHD involves a lack of sustained attention to tasks, inhibitory deficits also can lead to difficulty interrupting an ongoing response pattern, manifesting in the perseveration of actions despite a change in context whereby the individual intends the termination of those actions. This symptom is known colloquially as hyperfocus and is related to risks such as addiction and types of offending behaviour. ADHD can be difficult to tell apart from other conditions. 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. ADHD treatment is most effective when medications (primarily stimulants like methylphenidate or amphetamines, as well as non-stimulants such as atomoxetine or alpha-2 agonists) are used, often in combination with psychotherapy; exercise and dietary modifications have no proven benefit. The precise causes of ADHD are unknown in most individual cases. Meta-analyses have shown that the disorder is primarily genetic with a heritability rate of 70–80%, where risk factors are highly accumulative. The environmental risks are not related to social or familial factors; they exert their effects very early in life, in the prenatal or early postnatal period. However, in rare cases, ADHD can be caused by a single event including traumatic brain injury, exposure to biohazards during pregnancy, or a major genetic mutation. As it is a neurodevelopmental disorder, there is no biologically distinct adult-onset ADHD except for when ADHD occurs after traumatic brain injury.
Signs and symptoms Inattention, hyperactivity (restlessness in adults), disruptive behaviour, and impulsivity are common in ADHD. Academic difficulties are frequent, as are problems with relationships. A diagnosis can be hard to ascertain, as it is hard to distinguish between normal levels of symptoms and levels that cause significant impairment in major life activities. 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. 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. 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. Additionally, several symptoms must have been present before age 12 as per DSM-5 criteria. However, research indicates the age of onset should not be interpreted as a prerequisite for diagnosis given contextual exceptions.
Presentations ADHD is divided into three primary presentations:
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.
Girls and women with ADHD tend to display fewer hyperactivity and impulsivity symptoms but more symptoms of inattention and distractibility. This inattention can be interpreted being "spacey" or being forgetful, rather than being correctly identified as symptoms of ADHD. Frequently, ADHD symptoms in girls worsen later in childhood, compared with boys, and may be more obvious during times of transition, such as when starting in a new school or beginning puberty. Symptoms are expressed differently and more subtly as the individual ages. 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. Impulsivity in adulthood may appear as thoughtless behaviour, impatience, irresponsible spending and sensation-seeking behaviours, while inattention may appear as becoming easily bored, difficulty with organisation, remaining on task and making decisions, and sensitivity to stress. Research suggests that ADHD symptoms may fluctuate with the menstrual cycle. One mechanism behind this fluctuation is the rise and fall of ovulation-related hormones, such as progesterone and estrogen, during the menstrual cycle. Many people with ADHD report an increase in symptoms, such as forgetfulness and emotional deregulation, during their pre-menstrual period, when estrogen levels are at their lowest. In a 2025 study, researchers found that 41.1% of women with ADHD also experience premenstrual dysphoric disorder (PMDD), compared with an incidence of 9.8% in a non-ADHD reference group.
Characteristics in childhood Difficulties managing anger are more common in children with ADHD, as are delays in speech, language and motor development. Poorer handwriting is more common in children with ADHD. 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 or dysgraphia. There is significant overlap in the symptomatologies of ADHD, dyslexia, and dysgraphia, and 3 in 10 people diagnosed with dyslexia experience co-occurring ADHD. 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.
Emotional dysregulation Although not listed as an official symptom, emotional dysregulation or mood lability is generally understood to be a common symptom of ADHD.
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. 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.
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, has been widely reported in the popular science press and media. 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. Hyperfocus is not a recognised symptom of ADHD in diagnostic manuals, but is frequently referred to as a symptom of ADHD in academic literature and commonly reported in patients with ADHD in clinical practice. There is a lack of research into hyperfocus in ADHD. Studies in 2016, 2019 and 2024 found that individuals with ADHD diagnoses or self-reported ADHD symptoms experience hyperfocus more often, or more acutely. 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. A state of hyperfocus has been hypothesised as being beneficial, allowing individuals to focus on tasks for much longer than is typical. Conversely, it can be difficult to disengage from and shift attention to other stimuli or tasks, leading to excessively prolonged attention. This can lead to neglect of other activities or personal needs, such as eating or using the toilet. It is related to risks such as internet addiction (see § Problematic digital media use) and to some types of offending behaviour. 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.
Mind wandering
Mind wandering is a situation in which attention drifts from the main task to personal inner thoughts. The connection between mind wandering and ADHD has become a focus of growing research interest. The European Consensus Statement on diagnosis and treatment of adult ADHD (Kooij et al., 2019) identified mind wandering as a common characteristic of adults with ADHD and a strong predictor of the condition, noting that it may be even more predictive than the classic symptoms of inattention or hyperactivity. Studies have consistently found that individuals with ADHD symptoms report significantly more mind wandering than those without ADHD symptoms. Research further indicates that background sounds including music can reduce mind wandering in individuals with elevated ADHD symptoms, suggesting environmental sound as a potential non-pharmacological support strategy. Studies also show that the relationship between ADHD symptoms and mind wandering is detectable as early as kindergarten age, where elevated mind wandering predicts weaker academic performance in arithmetic and phonological tasks.
IQ test performance Certain studies have found that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests. 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. 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. Studies of adults suggest that negative differences in intelligence are not meaningful and may be explained by associated health problems.
When people with ADHD show discrepancies between certain areas of IQ tests compared to others, it is usually irregularities in sub-tests within sections regarding working memory and processing speed. IQ tests rely on what is known as the g-factor as a way to compare different tests to see how predictive they are of the g-constant (general intelligence), as well as the correlation between other sub-tests on a given test and the predictive power of the g-factor. Some with ADHD may have abnormally low scores on sub-tests that invalidate the full-scale IQ score because the correlation between sub-tests is damaged. The WAIS and WISC have attempted to counter this by introducing a substitute scoring system that only counts sub-tests that are robust against executive dysfunction in studies if a discrepancy occurs. On the Stanford-Binet, youth with ADHD take longer to complete the test, and have widespread irregularities within sub-tests in working memory domains. On the WAIS, the Arithmetic and Digit Span task was the most affected in ADHD and other disabilities. As similar deficits and the lack-thereof also exist in individuals with learning disabilities, autism, and other neurodevelopmental disabilities, discrepancies in sub-tests, even if they satisfy the criteria for successful usage for special scales, such as the one on the WAIS and WISC, cannot alone be used as a definitive way to diagnose an individual with ADHD. Many individuals with NDD's will have similar or even more severe deficits. ADHD patients with a naturally high IQ will likely not have visible deficits in working memory on standardised tests that are normed on average individuals, and that cognitive heterogeneity in the ADHD population signals that many with ADHD will not have any visible working memory or processing speed deficits visible.
Causes ADHD arises from atypical brain development 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. 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. 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. Very rarely, ADHD can also be the result of abnormalities in the chromosomes.
Genetics
Literature reviews published in Biological Psychiatry and in Molecular Psychiatry have found the average heritability estimate of ADHD to be from 0.74 to 0.8, based on family, twin studies, and adoption studies. 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. Natural selection has been acting against genetic variants for ADHD over at least 45,000 years, complicating the suggestion that ADHD was adaptive in the human evolutionary past. 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. During human evolution, executive functions disrupted in ADHD likely provide the capacity to bind contingencies across time, thereby directing behaviour toward future over immediate events so as to maximise social consequences for humans. 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. The siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder. 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. ADHD presents with reduced size, functional connectivity and activation as well as low noradrenergic and dopaminergic functioning in brain regions and networks crucial for executive functioning and self-regulation. Typically, a number of genes are involved, many of which directly affect brain functioning and neurotransmission. Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH. Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF. 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. 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. 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 autism spectrum disorder (ASD), schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene. 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. 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. Rare genetic variants show more relevant clinical significance as their penetrance (the chance of developing the disorder) tends to be much higher. 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. Evolutionary theorists view ADHD traits (such as novelty-seeking, rapid task-switching, and high exploratory drive) as possible cognitive specialisations that were advantageous in ancestral forager-gatherer environments. In modern structured settings these traits may become mismatched, leading to functional impairment. A recent evolutionary-mismatch hypothesis proposes that high trait curiosity associated with ADHD prepared ancestors to discover new opportunities in unpredictable environments, but in information-saturated, stable modern settings this drive may manifest as distractibility or impulsivity.
Environment In addition to genetics, some environmental factors might play a role in causing ADHD. Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD-like symptoms. Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD. Perinatal exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive. Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD. Nicotine exposure during pregnancy may be an environmental risk. Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk 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). At least 30% of children with a traumatic brain injury later develop ADHD and about 5% of cases are due to brain damage. 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, but the evidence is weak and may apply to only children with food sensitivities. The European Union has put in place regulatory measures based on these concerns. In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms. 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.
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. Children who enter school earlier and are of a younger age than their classmates are more likely to have educational and behavioural problems than their peers, which can make them more likely to be diagnosed with ADHD. Behaviours typical of ADHD occur more commonly in children who have experienced violence and emotional abuse.
Mechanism 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. 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. 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; these pathways are known to play a central role in the pathophysiology of ADHD. Larger models of ADHD with additional pathways have been proposed.
Brain structure
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. 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. The subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with controls. Structural MRI studies have also revealed differences in white matter, with marked differences in inter-hemispheric asymmetry between ADHD and typically developing youths. 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. Hemispheric lateralisation processes have also been postulated as being implicated in ADHD, but empiric results showed contrasting evidence on the topic.
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. Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system. ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems. There may additionally be abnormalities in serotonergic, glutamatergic, or cholinergic pathways. 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.
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. 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. 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. 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. Conversely, brain maturation trajectories, potentially exhibiting diverging longitudinal trends in ADHD, may support a later improvement in executive functions after reaching adulthood. 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.
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 (c. 10–20% 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.
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. Childhood and adolescent ADHD diagnosis often takes into account feedback from parents and teachers with most diagnoses begun after a teacher raises concerns. 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. Most diagnosis in children is seen in low-income families, and more in Caucasian children in comparison to Black, Hispanic, and Asian children, however, the diagnosis may be influenced by racial and socio-economic biases. 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. The most commonly used rating scales for diagnosing ADHD in children 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. 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). 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. 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. Imaging studies of the brain do not give consistent results between individuals; thus, they are only used for research purposes and not a diagnosis. Electroencephalography is not accurate enough to make an ADHD diagnosis. 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. In North America and Australia, DSM-5 criteria are used for diagnosis, while European countries usually use the ICD-11 criteria. ADHD is alternately classified as neurodevelopmental disorder or a disruptive behaviour disorder along with ODD, CD, and antisocial personality disorder. A diagnosis does not imply a neurological disorder. 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. 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 same review found that many studies did not include information on the impact associated with a misdiagnosis or the downsides of administering diagnostic assessments. The CBCL and Disruptive Behavior Diagnostic Observation Schedule (DB-DOS) showed good performance, while BRIEF worked very well. However, there are not enough studies on children younger than 7 years of age to determine which diagnosis method is the most effective. The review emphasized that diagnostic accuracy often depends on the comparison group—specifically, whether children with ADHD are being distinguished from typically developing peers or from other clinically referred youth. About half of the diagnostic studies in the review evaluated clinical samples, defined as children undergoing diagnostic workup for a potential diagnosis of ADHD, conduct disorders, autism, or depression, rather than typically developing children. 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.
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:
ADHD, predominantly inattentive presentation, presents with symptoms including being easily distracted, forgetful, daydreaming, disorganisation, poor sustained attention, and difficulty completing tasks. ADHD, predominantly hyperactive-impulsive presentation, presents with excessive fidgeting and restlessness, hyperactivity, and difficulty waiting and remaining seated. 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) out of nine long-term (lasting at least six months) symptoms of inattention, hyperactivity–impulsivity, or both. 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 and there must be clear evidence that they are causing impairment in multiple domains of life. 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.
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. 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) 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.
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. Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and then given a name".
Adults
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. 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. 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. 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). In 2020, this was 139.84 million and 366.33 million affected adults respectively. About 15% of children with ADHD continue to meet full DSM-IV-TR criteria at 25 years of age, and 50% still experience some symptoms. As of 2010, most adults remain untreated. Many adults with ADHD without diagnosis and treatment have a disorganised life, and some use non-prescribed drugs or alcohol as a coping mechanism. Other problems may include relationship and job difficulties, and an increased risk of criminal activities. Associated mental health problems include depression, anxiety disorders, and learning disabilities. 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. Adults with ADHD may start relationships impulsively, display sensation-seeking behaviour, and be short-tempered. Addictive behaviour such as substance abuse and gambling are common. Previously, changes in ADHD presentation over time led to those diagnosed as children appearing to have outgrown the DSM-IV criteria. The DSM-5 addresses this issue by differentiating childhood and adult diagnostic criteria, a marked departure from the DSM-IV, which did not fully take into account the differences in impairments seen in adulthood compared to childhood. 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.
Differential diagnosis
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. The DSM-5-TR also suggests post-traumatic stress disorder. 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 w