Girls and women with ADHD tend to display fewer hyperactivity and impulsivity symptoms but more symptoms of inattention and distractibility.[54]
Symptoms are expressed differently and more subtly as the individual ages.[55]: 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.[55]: 6–7 Impulsivity in adulthood may appear as thoughtless behaviour, impatience, irresponsible spending and sensation-seeking behaviours,[55]: 6 while inattention may appear as becoming easily bored, difficulty with organization, remaining on task and making decisions, and sensitivity to stress.[55]: 6
Although not listed as an official symptom, emotional dysregulation or mood lability is generally understood to be a common symptom of ADHD.[18][55]: 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.[56] 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.[57]
Difficulties managing anger are more common in children with ADHD[58] as are delays in speech, language and motor development.[59][60] Poorer handwriting is more common in children with ADHD.[61] 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[62][63] or dysgraphia. There is significant overlap in the symptomatologies of ADHD, dyslexia, and dysgraphia,[64] and 3 in 10 people diagnosed with dyslexia experience co-occurring ADHD.[65] 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.[66]
IQ test performance
Certain studies have found that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests.[67] 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.[68] 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.[69]
Studies of adults suggest that negative differences in intelligence are not meaningful and may be explained by associated health problems.[70]
Comorbidities
Psychiatric comorbidities
In children, ADHD occurs with other disorders about two-thirds of the time.[66]
Other neurodevelopmental conditions are common comorbidities. Autism spectrum disorder (ASD), co-occurring at a rate of 21% in those with ADHD, affects social skills, ability to communicate, behaviour, and interests.[71][72] Learning disabilities have been found to occur in about 20–30% of children with ADHD. Learning disabilities can include developmental speech and language disorders, and academic skills disorders.[73] ADHD, however, is not considered a learning disability, but it very frequently causes academic difficulties.[73] Intellectual disabilities[4]: 75 and Tourette's syndrome[72] 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.[74] Adolescents with ADHD who also have CD are more likely to develop antisocial personality disorder in adulthood.[75] Brain imaging supports that CD and ADHD are separate conditions: conduct disorder was shown to reduce the size of one's temporal lobe and limbic system, and increase the size of one's orbitofrontal cortex, whereas ADHD was shown to reduce connections in the cerebellum and prefrontal cortex more broadly. Conduct disorder involves more impairment in motivation control than ADHD.[76] 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.[citation needed]
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.[77] Adults and children with ADHD sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions.[78][79]
Sleep disorders and ADHD commonly co-exist. They can also occur as a side effect of medications used to treat ADHD. In children with ADHD, insomnia is the most common sleep disorder with behavioural therapy being the preferred treatment.[80][81] Problems with sleep initiation are common among individuals with ADHD but often they will be deep sleepers and have significant difficulty getting up in the morning.[13] Melatonin is sometimes used in children who have sleep onset insomnia.[82] Restless legs syndrome has been found to be more common in those with ADHD and is often due to iron deficiency anemia.[83][84] However, restless legs can simply be a part of ADHD and requires careful assessment to differentiate between the two disorders.[85] Delayed sleep phase disorder is also a common comorbidity.[86]
Individuals with ADHD are at increased risk of substance use disorders.[87]: 9 This is most commonly seen with alcohol or cannabis.[55]: 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.[88] Other psychiatric conditions include reactive attachment disorder,[89] 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.[90][91] Individuals with ADHD are three times more likely to be diagnosed with an eating disorder compared to those without ADHD; conversely, individuals with eating disorders are two times more likely to have ADHD than those without eating disorders.[92]
Trauma
ADHD, trauma, and adverse childhood experiences are also comorbid,[93][94] 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.[95][96] This could result in trauma-related disorders or ADHD being mis-identified as the other.[97] Additionally, traumatic events in childhood are a risk factor for ADHD;[98][99] they can lead to structural brain changes and the development of ADHD behaviours.[97] 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).[100][101]
Non-psychiatric
See also: Accident-proneness § Hypophobia
Some non-psychiatric conditions are also comorbidities of ADHD. This includes epilepsy,[72] a neurological condition characterised by recurrent seizures.[102][103] There are well established associations between ADHD and obesity, asthma and sleep disorders,[104] and an association with celiac disease.[105] Children with ADHD have a higher risk for migraine headaches,[106] but have no increased risk of tension-type headaches. Children with ADHD may also experience headaches as a result of medication.[107][108]
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.[109]
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.[110] 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.[111][112]
Problematic digital media use
See also: Screen time, Internet addiction disorder, Problematic smartphone use, Problematic social media use, and Video game addiction
This section is an excerpt from Digital media use and mental health § ADHD.[edit]
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.[113] 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.[114] 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.[115] 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.[116] 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.[117]
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.[118] 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.[119] 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.[120] 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.[121]
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).[122] 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.[123] 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,[124] 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.[125]
Suicide risk
Systematic reviews in 2017 and 2020 found strong evidence that ADHD is associated with increased suicide risk across all age groups, as well as growing evidence that an ADHD diagnosis in childhood or adolescence represents a significant future suicidal risk factor.[126][127] Potential causes include ADHD's association with functional impairment, negative social, educational and occupational outcomes, and financial distress.[128][129] 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.[128] There is no clear data on whether there is a direct relationship between ADHD and suicidality, or whether ADHD increases suicide risk through comorbidities.[127]
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.[7][16] 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.[7][130]
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.[137] Very rarely, ADHD can also be the result of abnormalities in the chromosomes.[138]
Genetics
See also: Missing heritability problem
In November 1999, Biological Psychiatry published a literature review by psychiatrists Joseph Biederman and Thomas Spencer found the average heritability estimate of ADHD from twin studies to be 0.8,[139] while a subsequent family, twin, and adoption studies literature review published in Molecular Psychiatry in April 2019 by psychologists Stephen Faraone and Henrik Larsson that found an average heritability estimate of 0.74.[140] 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.[141][142][143]
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.[144] 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.[145] Throughout human evolution, the EFs involved in ADHD likely provide the capacity to bind contingencies across time thereby directing behaviour toward future over immediate events so as to maximise future social consequences for humans.[146]
ADHD has a high heritability of 74%, meaning that 74% of the presence of ADHD in the population is due to genetic factors. There are multiple gene variants which each slightly increase the likelihood of a person having ADHD; it is polygenic and thus arises through the accumulation of many genetic risks each having a very small effect.[7][147] The siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder.[148]
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.[149][150]
ADHD presents with reduced size, functional connectivity and activation[7] as well as low noradrenergic and dopaminergic functioning[151][152] in brain regions and networks crucial for executive functioning and self-regulation.[7][38][16] Typically, a number of genes are involved, many of which directly affect brain functioning and neurotransmission.[7] Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH.[153][154][155] Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF.[156] 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.[157] 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.[158] The DRD4 gene is both linked to novelty seeking and ADHD. The genes GFOD1 and CDH13 show strong genetic associations with ADHD. CDH13's association with ASD, schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene.[135] 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.[135]
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.[135] Rare genetic variants show more relevant clinical significance as their penetrance (the chance of developing the disorder) tends to be much higher.[159] 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.[159]
Environment
In addition to genetics, some environmental factors might play a role in causing ADHD.[160][161] Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it.[162] Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD.[40][163] Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.[164] Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.[40][165] Nicotine exposure during pregnancy may be an environmental risk.[166]
Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk[167][40][168] 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).[169] At least 30% of children with a traumatic brain injury later develop ADHD[170] and about 5% of cases are due to brain damage.[171]
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,[40][172] but the evidence is weak and may apply to only children with food sensitivities.[160][172][173] The European Union has put in place regulatory measures based on these concerns.[174] In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.[175]
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.[citation needed]
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.[48]
In some cases, an inappropriate diagnosis of ADHD may reflect a dysfunctional family or a poor educational system, rather than any true presence of ADHD in the individual.[176][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.[171] Behaviours typical of ADHD occur more commonly in children who have experienced violence and emotional abuse.[177]
Pathophysiology
Current models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems, particularly those involving dopamine and norepinephrine.[178] 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.[179][14] 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;[178][14] these pathways are known to play a central role in the pathophysiology of ADHD.[179][14][180][181] Larger models of ADHD with additional pathways have been proposed.[180][181]
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.[178][182] 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.[178][180][181]
The subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with controls.[183] Structural MRI studies have also revealed differences in white matter, with marked differences in inter-hemispheric asymmetry between ADHD and typically developing youths.[184]
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 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 [185] Hemispheric lateralization processes have also been postulated as being implicated in ADHD, but empiric results showed contrasting evidence on the topic.[186][187]
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.[188] Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system.[179][178][14] ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems.[178][14][189] There may additionally be abnormalities in serotonergic, glutamatergic, or cholinergic pathways.[189][190][191]
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.[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][178][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.[192] 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.[186]
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.[193]
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.[194][195]
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.[88] ADHD diagnosis often takes into account feedback from parents and teachers[196] with most diagnoses begun after a teacher raises concerns.[171] While many tools exist to aide 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 standardized rating scales and input from multiple informants across various settings.[197] 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.[7]
The most commonly used rating scales for diagnosing ADHD are the Achenbach System of Empirically Based Assessment (ASEBA) and include the Child Behavior Checklist (CBCL) used for parents to rate their child's behaviour, the Youth Self Report Form (YSR) used for children to rate their own behaviour, and the Teacher Report Form (TRF) used for teachers to rate their pupil's behaviour. Additional rating scales that have been used alone or in combination with other measures to diagnose ADHD include the Behavior Assessment System for Children (BASC), Behavior Rating Inventory of Executive Function - Second Edition (BRIEF2), Revised Conners Rating Scale (CRS-R), Conduct-Hyperactive-Attention Problem-Oppositional Symptom scale (CHAOS), Developmental Behavior Checklist Hyperactivity Index (DBC-HI), Parent Disruptive Behavior Disorder Ratings Scale (DBDRS), Diagnostic Infant and Preschool Assessment (DIPA-L), Pediatric Symptom Checklist (PSC), Social Communication Questionnaire (SCQ), Social Responsiveness Scale (SRS), Strengths and Weaknesses of ADHD Symptoms and Normal Behavior Rating Scale (SWAN). and the Vanderbilt ADHD diagnostic rating scale.[198]
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).[198] 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.[199]
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.[198]
Imaging studies of the brain do not give consistent results between individuals; thus, they are only used for research purposes and not a diagnosis.[200] Electroencephalography is not accurate enough to make an ADHD diagnosis.[201][202][203] 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.[197]
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.[204] ADHD is alternately classified as neurodevelopmental disorder[205] or a disruptive behaviour disorder along with ODD, CD, and antisocial personality disorder.[206] A diagnosis does not imply a neurological disorder.[177]
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.[198]
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, disorganization, 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)[207] 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[208] and there must be clear evidence that they are causing impairment in multiple domains of life.[209]
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 (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.[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)[59] 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.[59]
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.[210] Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and then given a name".[211]
Adults
Main article: Adult attention deficit hyperactivity disorder
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.[55]: 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.[55]: 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).[212] In 2020, this was 139.84 million and 366.33 million affected adults respectively.[212] 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.[55]: 2 As of 2010, most adults remain untreated.[213] Many adults with ADHD without diagnosis and treatment have a disorganised life, and some use non-prescribed drugs or alcohol as a coping mechanism.[214] Other problems may include relationship and job difficulties, and an increased risk of criminal activities.[215][55]: 6 Associated mental health problems include depression, anxiety disorders, and learning disabilities.[214]
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.[55]: 6 Adults with ADHD may start relationships impulsively, display sensation-seeking behaviour, and be short-tempered.[55]: 6 Addictive behaviour such as substance abuse and gambling are common.[55]: 6 This led to those who presented differently as they aged having outgrown the DSM-IV criteria.[55]: 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.[55]: 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.[216]