Attention deficit hyperactivity disorder

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Attention deficit hyperactivity disorder
CNS stimulants (methylphenidate, amphetamine)
  • non-stimulants (atomoxetine, viloxazine)
  • alpha-2a agonists (guanfacine XR, clonidine XR)
  • Frequency0.8–1.5% (2019, using DSM-IV-TR and ICD-10)[2]

    Attention deficit hyperactivity disorder (ADHD) is a

    inattention, hyperactivity, impulsivity and emotional dysregulation that are excessive and pervasive, impairing in multiple contexts, and otherwise age-inappropriate.[8]

    ADHD symptoms arise from executive dysfunction,[17] and emotional dysregulation is often considered a core symptom.[22] Difficulties with self-regulation such as time management, inhibition and sustained attention may result in poor academic performance, unemployment and numerous health risks,[23] collectively predisposing to a diminished quality of life[24] and a direct average reduction in life expectancy of 13 years.[25][26] ADHD is associated with other neurodevelopmental and mental disorders as well as some non-psychiatric disorders, which can cause additional impairment, especially in modern society.[27]

    Although people with ADHD struggle to persist on tasks with temporally delayed consequences, they may be able to maintain an unusually prolonged level of attention for tasks they do find intrinsically interesting or immediately rewarding;[28][29] this is known as hyperfocus (more colloquially)[30] or perseverative responding.[31] This is a mental state in which a person is completely absorbed in a task to the point of apparently ignoring or "tuning out" everything else, often with difficulty disengaging[32][33] and can be related to risks such as for internet addiction[34] and types of offending behaviour.[35]

    ADHD represents the extreme lower end of the continuous (bell curve) dimensional trait of executive functioning and self-regulation, which is supported by twin, brain imaging and molecular genetic studies.[36][12][37][16]

    The precise causes of ADHD are unknown in the majority of cases.[38][39] For most people with ADHD, many genetic and environmental risk factors accumulate to cause the disorder.[40] The environmental risks for ADHD most often exert their influence in the prenatal period.[41] However, in rare cases a single event might cause ADHD such as traumatic brain injury,[42][43][44] exposure to biohazards during pregnancy,[45] a major genetic mutation[46] or extreme environmental deprivation early in life.[47] There is no biologically distinct adult onset ADHD except for when ADHD occurs after traumatic brain injury.[48][49][50]

    Signs and symptoms

    Inattention, hyperactivity (restlessness in adults), disruptive behaviour, and impulsivity are common in ADHD.[51][52][53] Academic difficulties are frequent, as are problems with relationships.[52][53][54] 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.[55]

    According to the

    same age.[3][4] 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.[3][4] 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.[3] Additionally, several symptoms must have been present before age twelve.[4] According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and its text revision (DSM-5-TR), the required age of onset of symptoms is currently 12 years.[3][4][56]

    Presentations

    ADHD is divided into three primary presentations:[4][55]

    • 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 DSM-5 and DSM-5-TR symptoms[3][4] ICD-11 symptoms[5]
    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 aren't 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 abandoned 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.[57]

    Symptoms are expressed differently and more subtly as the individual ages.[58]: 6 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.[58]: 6–7 Impulsivity in adulthood may appear as thoughtless behaviour, impatience, irresponsible spending and sensation-seeking behaviours,[58]: 6 while inattention may appear as becoming easily bored, difficulty with organization, remaining on task and making decisions, and sensitivity to stress.[58]: 6

    Although not listed as an official symptom for this condition,

    mood lability is generally understood to be a common symptom of ADHD.[18][58]: 6 People with ADHD of all ages are more likely to have problems with social skills, such as social interaction and forming and maintaining friendships.[59] 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.[60]

    Difficulties managing anger are more common in children with ADHD

    dyslexia[65][66] or dysgraphia. There is significant overlap in the symptomatologies of ADHD, dyslexia, and dysgraphia,[67] and 3 in 10 people diagnosed with dyslexia experience co-occurring ADHD.[68] 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.[69]

    Comorbidities

    Psychiatric comorbidities

    In children, ADHD occurs with other disorders about two-thirds of the time.[69]

    Other neurodevelopmental conditions are common comorbidities.

    Tourette's syndrome[71]
    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.[4][page needed] It is characterised by angry or irritable mood, argumentative or defiant behaviour and vindictiveness which are age-inappropriate. Conduct disorder (CD) occurs in about 25% of adolescents with ADHD.[4][page needed] It is characterised by aggression, destruction of property, deceitfulness, theft and violations of rules.[73] Adolescents with ADHD who also have CD are more likely to develop antisocial personality disorder in adulthood.[74] Brain imaging supports that CD and ADHD are separate conditions, wherein 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.[75] 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.

    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.[76] Adults and children with ADHD sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions.[77][78]

    iron deficiency anemia.[82][83] However, restless legs can simply be a part of ADHD and requires careful assessment to differentiate between the two disorders.[84] Delayed sleep phase disorder is also a common comorbidity of those with ADHD.[85]

    There are other psychiatric conditions which are often co-morbid with ADHD, such as substance use disorders.[86] Individuals with ADHD are at increased risk of substance abuse.: 9 This is most commonly seen with alcohol or cannabis.[58]: 9 The reason for this may be an altered reward pathway in the brains of ADHD individuals, self-treatment and increased psychosocial risk factors.: 9 This makes the evaluation and treatment of ADHD more difficult, with serious substance misuse problems usually treated first due to their greater risks.[87] Other psychiatric conditions include reactive attachment disorder,[88] 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.[89][90] Individuals with ADHD are three times more likely to develop and 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.[91]

    Trauma

    ADHD, trauma, and Adverse Childhood Experiences are also comorbid,[92][93] 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.[94][95] This could result in trauma-related disorders or ADHD being mis-identified as the other.[96] Additionally, traumatic events in childhood are a risk factor for ADHD[97][98] - it can lead to structural brain changes and the development of ADHD behaviours.[96] 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).[99][non-primary source needed]

    Non-psychiatric

    Some non-psychiatric conditions are also comorbidities of ADHD. This includes epilepsy,[71] a neurological condition characterised by recurrent seizures.[100][101] There are well established associations between ADHD and obesity, asthma and sleep disorders,[102] and an association with celiac disease.[103] Children with ADHD have a higher risk for migraine headaches,[104] but have no increased risk of tension-type headaches. In addition, children with ADHD may also experience headaches as a result of medication.[105][106]

    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.[107]

    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 in ADHD patients over the lifespan.[108] 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 and/or conduct disorder comorbidities.[109][110]

    Problematic digital media use

    In April 2018, the International Journal of Environmental Research and Public Health published a systematic review of 24 studies researching associations between internet gaming disorder (IGD) and various psychopathologies that found an 85% correlation between IGD and ADHD.[111] In October 2018, PNAS USA published a systematic review of four decades of research on the relationship between children and adolescents' screen media use and ADHD-related behaviours and concluded that a statistically small relationship between children's media use and ADHD-related behaviours exists.[112] In November 2018, Cyberpsychology published a systematic review and meta-analysis of 5 studies that found evidence for a relationship between problematic smartphone use and impulsivity traits.[113] In October 2020, the Journal of Behavioral Addictions published a systematic review and meta-analysis of 40 studies with 33,650 post-secondary student subjects that found a weak-to-moderate positive association between mobile phone addiction and impulsivity.[114] In January 2021, the Journal of Psychiatric Research published a systematic review of 29 studies including 56,650 subjects that found that ADHD symptoms were consistently associated with gaming disorder and more frequent associations between inattention and gaming disorder than other ADHD scales.[115]

    In July 2021, Frontiers in Psychiatry published a meta-analysis reviewing 40 voxel-based morphometry studies and 59 functional magnetic resonance imaging studies comparing subjects with IGD or ADHD to control groups that found that IGD and ADHD subjects had disorder-differentiating structural neuroimage alterations in the putamen and orbitofrontal cortex (OFC) respectively, and functional alterations in the precuneus for IGD subjects and in the rewards circuit (including the OFC, the anterior cingulate cortex, and striatum) for both IGD and ADHD subjects.[116] In March 2022, JAMA Psychiatry published a systematic review and meta-analysis of 87 studies with 159,425 subjects 12 years of age or younger that found a small but statistically significant correlation between screen time and ADHD symptoms in children.[117] In April 2022, Developmental Neuropsychology published a systematic review of 11 studies where the data from all but one study suggested that heightened screen time for children is associated with attention problems.[118] In July 2022, the Journal of Behavioral Addictions published a meta-analysis of 14 studies comprising 2,488 subjects aged 6 to 18 years that found significantly more severe problematic internet use in subjects diagnosed with ADHD to control groups.[119]

    In December 2022, European Child & Adolescent Psychiatry published a systematic literature review of 28 longitudinal studies published from 2011 through 2021 of associations between digital media use by children and adolescents and later ADHD symptoms and found reciprocal associations between digital media use and ADHD symptoms (i.e. that subjects with ADHD symptoms were more likely to develop problematic digital media use and that increased digital media use was associated with increased subsequent severity of ADHD symptoms).[120] In May 2023, Reviews on Environmental Health published a meta-analysis of 9 studies with 81,234 child subjects that found a positive correlation between screen time and ADHD risk in children and that higher amounts of screen time in childhood may significantly contribute to the development of ADHD.[121] In December 2023, the Journal of Psychiatric Research published a meta-analysis of 24 studies with 18,859 subjects with a mean age of 18.4 years that found significant associations between ADHD and problematic internet use,[122] while Clinical Psychology Review published a systematic review and meta-analysis of 48 studies examining associations between ADHD and gaming disorder that found a statistically significant association between the disorders.[123]

    Suicide risk

    Systematic reviews conducted 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.[124][125] Potential causes include ADHD's association with functional impairment, negative social, educational and occupational outcomes, and financial distress.[126][127] 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.[126] There is no clear data on whether there is a direct relationship between ADHD and suicidality, or whether ADHD increases suicide risk through comorbidities.[125]

    IQ test performance

    Certain studies have found that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests.[128] 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.[129] 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.[130]

    Studies of adults suggest that negative differences in intelligence are not meaningful and may be explained by associated health problems.[131]

    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.[132][133] 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.[132][134]

    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.[141] Very rarely, ADHD can also be the result of abnormalities in the chromosomes.[142]

    Genetics

    In November 1999,

    sex ratio in the epidemiology of autism as an analogue.[145][146][147]

    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 adaptative trait in ancient times.[148] 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.[149]

    ADHD has a high

    polygenic and arises through the combination of many gene variants which each have a small effect.[150][151] The siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder.[152]

    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.[153][154]

    Arousal is related to

    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.[161] The DRD4 gene is both linked to novelty seeking and ADHD. The genes GFOD1 and CDH13 show strong genetic associations with ADHD. CHD13's association with ASD, schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene.[162] 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.[162]

    For

    SNARE complex of the synapse can reliably predict a person's response to stimulant medication.[162] Rare genetic variants show more relevant clinical significance as their penetrance (the chance of developing the disorder) tends to be much higher.[163] 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.[163]

    Environment

    In addition to genetics, some environmental factors might play a role in causing ADHD.

    polychlorinated biphenyls, may develop problems which resemble ADHD.[38][167] Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.[168] Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.[38][169] Nicotine exposure during pregnancy may be an environmental risk.[170]

    Extreme

    premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk[171][38][172] 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).[173] At least 30% of children with a traumatic brain injury later develop ADHD[174] and about 5% of cases are due to brain damage.[175]

    Some studies suggest that in a small number of children, artificial

    food sensitivities.[164][176][177] The European Union has put in place regulatory measures based on these concerns.[178] In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.[179]

    Individuals with hypokalemic sensory overstimulation are sometimes diagnosed as having attention deficit hyperactivity disorder (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.[51]

    The youngest children in a class have been found to be more likely to be diagnosed as having ADHD, possibly due to them being developmentally behind their older classmates.[180][181] One study showed that the youngest children in fifth and eight grade was nearly twice as likely to use stimulant medication than their older peers.[182]

    In some cases, an inappropriate diagnosis of ADHD may reflect a

    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 get extra financial and educational support for their child.[175] Behaviours typical of ADHD occur more commonly in children who have experienced violence and emotional abuse.[184]

    Pathophysiology

    Current models of ADHD suggest that it is associated with functional impairments in some of the brain's

    executive function (cognitive control of behaviour), motivation, reward perception, and motor function;[185][14] these pathways are known to play a central role in the pathophysiology of ADHD.[186][14][187][188] Larger models of ADHD with additional pathways have been proposed.[187][188]

    Brain structure

    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.[185][189] 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.[185][187][188]

    The subcortical volumes of the

    accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with controls.[190] Structural MRI studies have also revealed differences in white matter, with marked differences in inter-hemispheric asymmetry between ADHD and typically developing youths.[191]

    Function MRI (fMRI) studies have revealed a number of differences between ADHD and control brains. Mirroring what is known from structural findings, fMRI studies have showed 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 [192] Hemispheric lateralization processes have also been postulated as being implicated in ADHD, but empiric results showed contrasting evidence on the topic.[193][194]

    Neurotransmitter pathways

    Previously, it had been suggested that the elevated number of

    locus coeruleus-noradrenergic system.[186][185][14] ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems.[185][14][196] There may additionally be abnormalities in serotonergic, glutamatergic, or cholinergic pathways.[196][197][198]

    Executive function and motivation

    The symptoms of ADHD arise from a deficiency in certain

    executive functions (e.g., attentional control, inhibitory control, and working memory).[185] Executive functions are a set of cognitive processes that are required to successfully select and monitor behaviours that facilitate the attainment of one's chosen goals.[14][15] The executive function impairments that occur in ADHD individuals result in problems with staying organised, time keeping, excessive procrastination, maintaining concentration, paying attention, ignoring distractions, regulating emotions, and remembering details.[13][185][14] 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.[199] 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.[13] Conversely, brain maturation trajectories, potentially exhibiting diverging longitudinal trends in ADHD, may support a later improvement in executive functions after reaching adulthood.[193]

    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.[200]

    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

    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.[201][202]

    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.[87] ADHD diagnosis often takes into account feedback from parents and teachers[203] with most diagnoses begun after a teacher raises concerns.[175] It may be viewed as the extreme end of one or more continuous human traits found in all people.[204] Imaging studies of the brain do not give consistent results between individuals; thus, they are only used for research purposes and not a diagnosis.[205]

    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 3–4 times more likely to diagnose ADHD than is the ICD-10 criteria.[206] ADHD is alternately classified as neurodevelopmental disorder[207] or a disruptive behaviour disorder along with ODD, CD, and antisocial personality disorder.[208] A diagnosis does not imply a neurological disorder.[184]

    Associated conditions that should be screened for include anxiety, depression, ODD, CD, and learning and language disorders. Other conditions that should be considered are other neurodevelopmental disorders, tics, and sleep apnea.[209]

    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.[210] Electroencephalography is not accurate enough to make an ADHD diagnosis.[211][212][213]

    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, disorganization, 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)[214] out of nine long-term (lasting at least six months) symptoms of inattention, hyperactivity–impulsivity, or both.[3][4] 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[215] and there must be clear evidence that they are causing social, school or work related problems.[216]

    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.[3][4]

    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 (with the code 6A05). The defined subtypes are similar to those of the DSM-5: predominantly inattentive presentation (6A05.0); predominantly hyperactive-impulsive presentation(6A05.1); 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.[5]

    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)[62] 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.[62]

    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.[217] Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and then given a name".[218]

    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.[58]: 7, 9  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.[58]: 6 

    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).[219] In 2020, this was 139.84 million and 366.33 million affected adults respectively.[219] 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.[58]: 2 As of 2010, most adults remain untreated.[220] Many adults with ADHD without diagnosis and treatment have a disorganised life, and some use non-prescribed drugs or alcohol as a coping mechanism.[221] Other problems may include relationship and job difficulties, and an increased risk of criminal activities.[222][58]: 6 Associated mental health problems include depression, anxiety disorders, and learning disabilities.[221]

    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.[58]: 6  Adults with ADHD may start relationships impulsively, display sensation-seeking behaviour, and be short-tempered.[58]: 6  Addictive behaviour such as substance abuse and gambling are common.[58]: 6  This led to those who presented differently as they aged having outgrown the DSM-IV criteria.[58]: 5–6  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.[58]: 5 

    For diagnosis in an adult, having symptoms since childhood is required. Nevertheless, 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.[223]

    Differential diagnosis

    Symptoms related to other disorders[224]
    Depression 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
    • being hyperalert
    • inability to pay attention
    • tire easily
    • low tolerance for
      stress
    • difficulty maintaining attention

    in manic state

    in depressive state

    • same symptoms as in depression section

    The DSM provides potential 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 ODD, intermittent explosive disorder, and other neurodevelopmental disorders (such as stereotypic movement disorder and Tourette's disorder), in addition to specific learning disorder, intellectual developmental disorder, ASD, 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.[3] The DSM-5-TR also suggests post-traumatic stress disorder.[4]

    Symptoms of ADHD, such as low mood and poor self-image, mood swings, and irritability, can be confused with

    better source needed
    ]

    Primary sleep disorders may affect attention and behaviour and the symptoms of ADHD may affect sleep.[226] It is thus recommended that children with ADHD be regularly assessed for sleep problems.[227] Sleepiness in children may result in symptoms ranging from the classic ones of yawning and rubbing the eyes, to hyperactivity and inattentiveness. Obstructive sleep apnea can also cause ADHD-type symptoms.[228]

    Management

    The management of ADHD typically involves

    positive reinforcement improves task performance.[200] Medications are the most effective pharmaceutical treatment,[230] although there may be side effects[233] and any improvements will be reverted if medication is ceased.[234] ADHD stimulants also improve persistence and task performance in children with ADHD.[185][200] 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".[235]

    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.[236][237] Psychological therapies used include: psychoeducational input, behavior therapy, cognitive behavioral therapy,[238] interpersonal psychotherapy, family therapy, school-based interventions, social skills training, behavioural peer intervention, organization training,[239] and parent management training.[184] 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.[240] Despite efficacy in research, there is insufficient regulation of neurofeedback practice, leading to ineffective applications and false claims regarding innovations.[241] Parent training may improve a number of behavioural problems including oppositional and non-compliant behaviours.[242]

    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.[243] ADHD-specific support groups can provide information and may help families cope with ADHD.[244]

    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.[245]

    Medication

    Stimulants

    Methylphenidate and amphetamine or its derivatives are often first-line treatments for ADHD.[246][247] About 70 per cent respond to the first stimulant tried and as few as 10 per cent respond to neither amphetamines nor methylphenidate.[230] Stimulants may also reduce the risk of unintentional injuries in children with ADHD.[248] 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.[249][250][251] A 2018 review found the greatest short-term benefit with methylphenidate in children, and amphetamines in adults.[252] Studies and meta-analyses show that amphetamine is slightly-to-modestly more effective than methylphenidate at reducing symptoms,[253][254] and they are more effective pharmacotherapy for ADHD than α2-agonists[255] but methylphenidate has comparable efficacy to non-stimulants such as atomoxetine.

    The likelihood of developing insomnia for ADHD patients taking stimulants has been measured at between 11 and 45 per cent for different medications,[256] 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.[230] 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.[257][258][259] The safety of these medications in pregnancy is unclear.[260] Symptom improvement is not sustained if medication is ceased.[232][234][261]

    The long-term effects of ADHD medication have yet to be fully determined,[262][263] although stimulants are generally beneficial and safe for up to two years for children and adolescents.[264] 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.[265] Regular monitoring has been recommended in those on long-term treatment.[266] 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.[267][268] Although potentially addictive at high doses,[269][270] stimulants used to treat ADHD have low potential for abuse.[246] Treatment with stimulants is either protective against substance abuse or has no effect.[58]: 12[262][269]

    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.[271] 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).[272] Pseudoephedrine and ephedrine do not affect ADHD symptoms.[246]

    Modafinil has shown some efficacy in reducing the severity of ADHD in children and adolescents.[273] It may be prescribed off-label to treat ADHD.

    Non-stimulants

    Two non-stimulant medications, atomoxetine and viloxazine, are approved by the FDA and in other countries for the treatment of ADHD. They produce comparable efficacy and tolerability to methylphenidate, but all three tend to be modestly more tolerable and less effective than amphetamines.

    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.[58]: 13  Atomoxetine has been shown to significantly improve academic performance.[274][275] Meta-analyses and systematic reviews have found that atomoxetine has comparable efficacy and equal tolerability to methylphenidate in children and adolescents. In adults, efficacy and tolerability are equivalent.[276][277][278][279]

    Analyses of clinical trial data suggests that viloxazine is about as effective as atomoxetine and methylphenidate but with fewer side effects.[280]

    Amantadine was shown to induce similar improvements in children treated with methylphenidate, with less frequent side effects.[281] A 2021 retrospective study showed 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.[282]

    Bupropion is also used off-label by some clinicians due to research findings. It is effective, but modestly less than atomoxetine and methylphenidate.[283]

    There is little evidence on the effects of medication on social behaviours.[284] Antipsychotics may also be used to treat aggression in ADHD.[285]

    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).[286][287] They appear to be modestly less effective than the stimulants (amphetamine and methylphenidate) and non-stimulants (atomoxetine and viloxazine) at reducing symptoms,[288][289] but can be useful alternatives or used in conjunction with a stimulant.[230]

    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.[290] Conversely, most United States guidelines recommend medications in most age groups.[291] Medications are especially not recommended for preschool children.[290][184] Underdosing of stimulants can occur, and can result in a lack of response or later loss of effectiveness.[292] 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.[293][294][295]

    Exercise

    Regular

    add-on treatment for ADHD in children and adults, particularly when combined with stimulant medication (although the best intensity and type of aerobic exercise for improving symptoms are not currently known).[296] The long-term effects of regular aerobic exercise in ADHD individuals include better behaviour and motor abilities, improved executive functions (including attention, inhibitory control, and planning, among other cognitive domains), faster information processing speed, and better memory.[297] Parent-teacher ratings of behavioural and socio-emotional outcomes in response to regular aerobic exercise include: better overall function, reduced ADHD symptoms, better self-esteem, reduced levels of anxiety and depression, fewer somatic complaints, better academic and classroom behaviour, and improved social behaviour. Exercising while on stimulant medication augments the effect of stimulant medication on executive function.[298] It is believed that these short-term effects of exercise are mediated by an increased abundance of synaptic dopamine and norepinephrine in the brain.[298]

    Diet

    Dietary modifications are not recommended as of 2019[update] 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.[299][290] 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 eating of artificial food colouring.[164] These benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications.[164] This review also found that evidence does not support removing other foods from the diet to treat ADHD.[164] A 2014 review found that an elimination diet results in a small overall benefit in a minority of children, such as those with allergies.[179] A 2016 review stated that the use of a gluten-free diet as standard ADHD treatment is not advised.[225] 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.[300] Chronic deficiencies of iron, magnesium and iodine may have a negative impact on ADHD symptoms.[301] There is a small amount of evidence that lower tissue zinc levels may be associated with ADHD.[302] In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as treatment for ADHD.[303] However, zinc supplementation may reduce the minimum effective dose of amphetamine when it is used with amphetamine for the treatment of ADHD.[304]

    Prognosis

    ADHD persists into adulthood in about 30–50% of cases.[305] Those affected are likely to develop coping mechanisms as they mature, thus compensating to some extent for their previous symptoms.[221] Children with ADHD have a higher risk of unintentional injuries.[248] Effects of medication on functional impairment and quality of life (e.g. reduced risk of accidents) have been found across multiple domains.[306] Rates of smoking among those with ADHD are higher than in the general population at about 40%.[307]

    It affects about 5–7% of children when diagnosed via the

    text–source integrity?] In adults, hyperactivity is usually replaced by inner restlessness, and adults often develop coping skills to compensate for their impairments. The condition can be difficult to tell apart from other conditions, as well as from high levels of activity within the range of normal behaviour. ADHD has a negative impact on patient 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.[235]

    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%.[317] ADHD is more common among longer-term inmates; a 2010 study at Norrtälje Prison, a high-security prison in Sweden, found an estimated ADHD prevalence of 40%.[318]

    Epidemiology

    Percentage of people 4–17 ever diagnosed in the US as of 2011[319]

    ADHD is estimated to affect about 6–7% of people aged 18 and under when diagnosed via the DSM-IV criteria.[308] When diagnosed via the ICD-10 criteria, rates in this age group are estimated around 1–2%.[309] 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.[320][verification needed] As of 2019, it was estimated to affect 84.7 million people globally.[2] If the same diagnostic methods are used, the rates are similar between countries.[310] ADHD is diagnosed approximately three times more often in boys than in girls.[314][206] This may reflect either a true difference in underlying rate, or that women and girls with ADHD are less likely to be diagnosed.[321] 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.[322]

    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%.[323] This is believed to be primarily due to changes in how the condition is diagnosed[324] and how readily people are willing to treat it with medications rather than a true change in how common the condition is.[309] It was believed changes to the diagnostic criteria in 2013 with the release of the DSM-5 would increase the percentage of people diagnosed with ADHD, especially among adults.[325]

    Due to disparities in the treatment and understanding of ADHD between caucasian and non-caucasian populations, many non-caucasian children go undiagnosed and unmedicated.[326] It was found that within the US that there was often a disparity between caucasian and non-caucasian understandings of ADHD. This led to a difference in the classification of the symptoms of ADHD, and therefore, its misdiagnosis. It was also found that it was common in non-caucasian families and teachers to understand the symptoms of ADHD as behavioural issues, rather than mental illness.

    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 African American 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 non-caucasian individuals. Due to ADHD's subjectively determined symptoms, medical professionals may diagnose individuals based on stereotyped behaviour or misdiagnose due to differences in symptom presentation between caucasian and non-caucasian individuals.[327]

    History

    Timeline of ADHD diagnostic criteria, prevalence, and treatment

    Hyperactivity has long been part of the human condition. Sir

    George Still in 1902 during a series of lectures he gave to the Royal College of Physicians of London.[330][324]
    He noted both nature and nurture could be influencing this disorder.

    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.

    Alfred Tredgold proposed an association between brain damage and behavioural or learning problems which was able to be validated by the encephalitis lethargica epidemic from 1917 through 1928.[331][332][333]

    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).[324] In 1987, this was changed to ADHD in the DSM-III-R, and in 1994 the DSM-IV in split the diagnosis into three subtypes: ADHD inattentive type, ADHD hyperactive-impulsive type, and ADHD combined type.[334] These terms were kept in the DSM-5 in 2013 and in the DSM-5-TR in 2022.[3][4] Prior to the DSM, terms included minimal brain damage in the 1930s.[335]

    In 1934, Benzedrine became the first amphetamine medication approved for use in the United States.

    enantiopure dextroamphetamine in the 1970s.[324] The use of stimulants to treat ADHD was first described in 1937.[337] Charles Bradley gave the children with behavioural disorders Benzedrine and found it improved academic performance and behaviour.[338][339]

    Once neuroimaging studies were possible, studies conducted in the 1990s provided support for the pre-existing theory that neurological differences - particularly in the frontal lobes - were involved in ADHD. During this same period, a genetic component was identified and ADHD was acknowledged to be a persistent, long-term disorder which lasted from childhood into adulthood.[340][341]

    ADHD was split into the current three sub-types because of a field trial completed by Lahey and colleagues.[342]

    Controversy

    ADHD, its diagnosis, and its treatment have been controversial since the 1970s.

    New York Times article.[346] In contrast, a 2014 peer-reviewed medical literature review indicated that ADHD is underdiagnosed in adults.[316]

    With widely differing rates of diagnosis across countries, states within countries, races, and ethnicities, some suspect factors other than the presence of the symptoms of ADHD are playing a role in diagnosis, such as cultural norms.[347][348] Some sociologists consider ADHD to be an example of the medicalization of deviant behaviour, that is, the turning of the previously non-medical issue of school performance into a medical one.[349] Most healthcare providers accept ADHD as a genuine disorder, at least in the small number of people with severe symptoms. Among healthcare providers the debate mainly centers on diagnosis and treatment in the much greater number of people with mild symptoms.[175][350][351]

    The nature and range of desirable endpoints of ADHD treatment vary among diagnostic standards for ADHD.[352] In most studies, the efficacy of treatment is determined by reductions in ADHD symptoms.[353] However, some studies have included subjective ratings from teachers and parents as part of their assessment of ADHD treatment efficacies.[354] By contrast, the subjective ratings of children undergoing ADHD treatment are seldom included in studies evaluating the efficacy of ADHD treatments.

    There have been notable differences in the diagnosis patterns of birthdays in school-age children. Those born relatively younger to the school starting age than others in a classroom environment are shown to be more likely diagnosed with ADHD. Boys who were born in December in which the school age cut-off was 31 December were shown to be 30% more likely to be diagnosed and 41% to be treated than others born in January. Girls born in December had a diagnosis percentage of 70% and 77% treatment more than ones born the following month. Children who were born at the last 3 days of a calendar year were reported to have significantly higher levels of diagnosis and treatment for ADHD than children born at the first 3 days of a calendar year. The studies suggest that ADHD diagnosis is prone to subjective analysis.[348]

    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, which causes people with ADHD symptoms to consider ideas which others may not have. However, people with ADHD may struggle with convergent thinking, which is a cognitive process through which a set of obviously relevant knowledge is utilised in a focused effort to arrive at a single perceived best solution to a problem.[355]

    A 2020 article suggested that historical documentation supported Leonardo da Vinci's difficulties with procrastination and time management as characteristic of ADHD and that he was constantly on the go, but often jumping from task to task.[356]

    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 measurements could potentially serve as diagnostic biomarkers for ADHD, but more research is needed to establish their diagnostic utility. Urinary and blood plasma phenethylamine concentrations are lower in ADHD individuals relative to controls and the two most commonly prescribed drugs for ADHD, amphetamine and methylphenidate, increase phenethylamine biosynthesis in treatment-responsive individuals with ADHD.[157] Lower urinary phenethylamine concentrations are also associated with symptoms of inattentiveness in ADHD individuals.[357]

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    157. ^ . Although there is little direct evidence, changes in trace amines, in particular PE, have been identified as a possible factor for the onset of attention deficit/hyperactivity disorder (ADHD). ... Further, amphetamines, which have clinical utility in ADHD, are good ligands at trace amine receptors. Of possible relevance in this aspect is modafanil, which has shown beneficial effects in ADHD patients and has been reported to enhance the activity of PE at TAAR1. Conversely, methylphenidate, ...showed poor efficacy at the TAAR1 receptor. In this respect it is worth noting that the enhancement of functioning at TAAR1 seen with modafanil was not a result of a direct interaction with TAAR1.
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    164. ^ . Free fatty acid supplementation and artificial food color exclusions appear to have beneficial effects on ADHD symptoms, although the effect of the former are small and those of the latter may be limited to ADHD patients with food sensitivities...
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    232. ^ . Results suggest there is moderate-to-high-level evidence that combined pharmacological and behavioral interventions, and pharmacological interventions alone can be effective in managing the core ADHD symptoms and academic performance at 14 months. However, the effect size may decrease beyond this period. ... Only one paper examining outcomes beyond 36 months met the review criteria. ... There is high level evidence suggesting that pharmacological treatment can have a major beneficial effect on the core symptoms of ADHD (hyperactivity, inattention, and impulsivity) in approximately 80% of cases compared with placebo controls, in the short term.
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    256. . In varying percentages of trial participants, insomnia is a treatment-emergent adverse effect in triple-bead mixed amphetamine salts (40–45%), dasotraline (35–45%), lisdexamfetamine (10–19%), and extended-release methylphenidate (11%).
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    262. ^ . In addition, a consensus has not been reached on the optimal diagnostic criteria for ADHD. Moreover, the benefits and long-term effects of medical and complementary therapies for this disorder continue to be debated. These gaps in knowledge hinder the ability of clinicians to effectively recognise and treat ADHD.
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