Attention deficit hyperactivity disorder

Inattention, hyperactivity (restlessness in adults), disruptive behaviour, and impulsivity are common in ADHD. Academic difficulties are frequent, as are problems with relationships. A diagnosis can be hard to ascertain, as it is hard to distinguish between normal levels of symptoms and levels that cause significant impairment in major life activities. According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and its text revision (DSM-5-TR), symptoms must be present for six months or more to a degree that is much greater than others of the same age. However, research indicates the age of onset should not be interpreted as a prerequisite for diagnosis given contextual exceptions. This inattention can be interpreted being "spacey" or being forgetful, rather than being correctly identified as symptoms of ADHD. Frequently, ADHD symptoms in girls worsen later in childhood, compared with boys, and may be more obvious during times of transition, such as when starting in a new school or beginning puberty. Symptoms are expressed differently and more subtly as the individual ages. Hyperactivity tends to become less overt with age and turns into inner restlessness, difficulty relaxing or remaining still, talkativeness or constant mental activity in teens and adults with ADHD. One mechanism behind this fluctuation is the rise and fall of ovulation-related hormones, such as progesterone and estrogen, during the menstrual cycle. Many people with ADHD report an increase in symptoms, such as forgetfulness and emotional deregulation, during their pre-menstrual period, when estrogen levels are at their lowest. In a 2025 study, researchers found that 41.1% of women with ADHD also experience premenstrual dysphoric disorder (PMDD), compared with an incidence of 9.8% in a non-ADHD reference group. Characteristics in childhood Difficulties managing anger are more common in children with ADHD, as are delays in speech, language and motor development. Poorer handwriting is more common in children with ADHD. Poor handwriting can be a symptom of ADHD in itself due to decreased attentiveness. When this is a pervasive problem, it may also be attributable to dyslexia or dysgraphia. There is significant overlap in the symptomatologies of ADHD, dyslexia, and dysgraphia, and 3 in 10 people diagnosed with dyslexia experience co-occurring ADHD. Although it causes significant difficulty, many children with ADHD have an attention span equal to or greater than that of other children for tasks and subjects they find interesting. Emotional dysregulation Although not listed as an official symptom, emotional dysregulation or mood lability is generally understood to be a common symptom of ADHD. This is true for all presentations. About half of children and adolescents with ADHD experience social rejection by their peers compared to 10–15% of non-ADHD children and adolescents. People with attention deficits are prone to having difficulty processing verbal and nonverbal language which can negatively affect social interaction. They may also drift off during conversations, miss social cues, and have trouble learning social skills. Hyperfocus An association between ADHD and hyperfocus, a state characterised by intense and narrow concentration on a specific stimulus, object or task for a prolonged period of time, has been widely reported in the popular science press and media. The phenomenon generally occurs when an individual is engaged in activities they find highly interesting, or which provide instant gratification, such as video games or online chatting. and commonly reported in patients with ADHD in clinical practice. or more acutely. A 2020 study did not find a higher frequency of hyperfocus in adults with ADHD, although it reported a positive correlation with self-reported ADHD traits. The discrepancy with other studies may reflect varying definitions and conceptions of hyperfocus. Recent research has linked hyperfocus to the psychological concepts of flow, an enjoyable experience of deep engagement in an activity, and perseveration, difficulty disengaging or switching from an activity. The connection between mind wandering and ADHD has become a focus of growing research interest. The European Consensus Statement on diagnosis and treatment of adult ADHD (Kooij et al., 2019) identified mind wandering as a common characteristic of adults with ADHD and a strong predictor of the condition, noting that it may be even more predictive than the classic symptoms of inattention or hyperactivity. Studies have consistently found that individuals with ADHD symptoms report significantly more mind wandering than those without ADHD symptoms. Research further indicates that background sounds including music can reduce mind wandering in individuals with elevated ADHD symptoms, suggesting environmental sound as a potential non-pharmacological support strategy. Studies also show that the relationship between ADHD symptoms and mind wandering is detectable as early as kindergarten age, where elevated mind wandering predicts weaker academic performance in arithmetic and phonological tasks. IQ test performance Certain studies have found that people with ADHD tend to have lower scores on intelligence quotient (IQ) tests. The significance of this is controversial due to the differences between people with ADHD and the difficulty determining the influence of symptoms, such as distractibility, on lower scores rather than intellectual capacity. In studies of ADHD, higher IQs may be over-represented because many studies exclude individuals who have lower IQs despite those with ADHD scoring on average nine points lower on standardised intelligence measures. However, other studies contradict this, saying that in individuals with high intelligence, there is an increased risk of a missed ADHD diagnosis, possibly because of compensatory strategies in said individuals. Studies of adults suggest that negative differences in intelligence are not meaningful and may be explained by associated health problems. tests often use inter-correlation between subtests and the degree of correlation to the "g-constant" and each other as a part of how they measure IQ and test validity. Individuals with ADHD often have disproportionately lower scores in categories relating to working memory and processing speed, which ruins the correlation that those have with IQ and other tasks, necessitating using more resistant sub-tasks like vocabulary tasks in order to get a clear picture on the actual IQ of a patient. When people with ADHD show discrepancies between certain areas of IQ tests compared to others, it is usually irregularities in sub-tests within sections regarding working memory and processing speed. IQ tests rely on what is known as the g-factor as a way to compare different tests to see how predictive they are of the g-constant (general intelligence), as well as the correlation between other sub-tests on a given test and the predictive power of the g-factor. Some with ADHD may have abnormally low scores on sub-tests that invalidate the full-scale IQ score because the correlation between sub-tests is damaged. The WAIS and WISC have attempted to counter this by introducing a substitute scoring system that only counts sub-tests that are robust against executive dysfunction in studies if a discrepancy occurs. On the Stanford-Binet, youth with ADHD take longer to complete the test, and have widespread irregularities within sub-tests in working memory domains. On the WAIS, the Arithmetic and Digit Span task was the most affected in ADHD and other disabilities. As similar deficits and the lack-thereof also exist in individuals with learning disabilities, autism, and other neurodevelopmental disabilities, discrepancies in sub-tests, even if they satisfy the criteria for successful usage for special scales, such as the one on the WAIS and WISC, cannot alone be used as a definitive way to diagnose an individual with ADHD. Many individuals with NDD's will have similar or even more severe deficits. ==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. Genetic factors play an important role; ADHD has a heritability rate of 70–80%. The remaining 20–30% of variance is mediated by de-novo mutations and non-shared environmental factors that provide for or produce brain injuries; there is no significant contribution of the rearing family and social environment. Very rarely, ADHD can also be the result of abnormalities in the chromosomes. Genetics Literature reviews published in Biological Psychiatry and in Molecular Psychiatry have found the average heritability estimate of ADHD to be from 0.74 to 0.8, based on family, twin studies, and adoption studies. Natural selection has been acting against genetic variants for ADHD over at least 45,000 years, complicating the suggestion that ADHD was adaptive in the human evolutionary past. The disorder may remain at a stable rate by the balance of genetic mutations and removal rate (natural selection) across generations; over thousands of years, these genetic variants become more stable, decreasing disorder prevalence. During human evolution, executive functions disrupted in ADHD likely provide the capacity to bind contingencies across time, thereby directing behaviour toward future over immediate events so as to maximise social consequences for humans. 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. The association of maternal smoking observed in large population studies disappears after adjusting for family history of ADHD, which indicates that the association between maternal smoking during pregnancy and ADHD is due to familial or genetic factors that increase the risk for the confluence of smoking and ADHD. ADHD presents with reduced size, functional connectivity and activation in brain regions and networks crucial for executive functioning and self-regulation. Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF. A common variant of a gene called latrophilin 3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication. The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioural phenotypes, including ADHD symptoms reflecting split attention. The DRD4 gene is both linked to novelty seeking and ADHD. The genes GFOD1 and CDH13 show strong genetic associations with ADHD. CDH13's association with autism spectrum disorder (ASD), schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene. 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. Environment In addition to genetics, some environmental factors might play a role in causing ADHD. Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD-like symptoms. Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD. Perinatal exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive. Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD. Nicotine exposure during pregnancy may be an environmental risk. Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71). At least 30% of children with a traumatic brain injury later develop ADHD and about 5% of cases are due to brain damage. but the evidence is weak and may apply to only children with food sensitivities. The European Union has put in place regulatory measures based on these concerns. In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms. Research does not support popular beliefs that ADHD is caused by eating too much refined sugar, watching too much television, bad parenting, poverty or family chaos; however, they might worsen ADHD symptoms in certain people. Children who enter school earlier and are of a younger age than their classmates are more likely to have educational and behavioural problems than their peers, which can make them more likely to be diagnosed with ADHD. Behaviours typical of ADHD occur more commonly in children who have experienced violence and emotional abuse. == Mechanism ==

Current models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems, particularly those involving dopamine and norepinephrine. The dopamine and norepinephrine pathways that originate in the ventral tegmental area and locus coeruleus project to diverse regions of the brain and govern a variety of cognitive processes. Brain structure In children with ADHD, there is a general reduction of volume in certain brain structures, with a proportionally greater decrease in the volume in the left-sided prefrontal cortex. The posterior parietal cortex also shows thinning in individuals with ADHD compared to controls. Other brain structures in the prefrontal-striatal-cerebellar and prefrontal-striatal-thalamic circuits have also been found to differ between people with and without ADHD. Structural MRI studies have also revealed differences in white matter, with marked differences in inter-hemispheric asymmetry between ADHD and typically developing youths. Functional MRI (fMRI) studies have revealed a number of differences between ADHD and control brains. Mirroring what is known from structural findings, fMRI studies have shown evidence for a higher connectivity between subcortical and cortical regions, such as between the caudate and prefrontal cortex. The degree of hyperconnectivity between these regions correlated with the severity of inattention or hyperactivity. Hemispheric lateralisation processes have also been postulated as being implicated in ADHD, but empiric results showed contrasting evidence on the topic. Neurotransmitter pathways Previously, it had been suggested that the elevated number of dopamine transporters in people with ADHD was part of the pathophysiology, but it appears the elevated numbers may be due to adaptation following exposure to stimulant medication. Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system. PET mapping of neocortex receptor distribution indicates that the distribution of μ-opioid receptors is the strongest contributor to cortical abnormalities in ADHD, followed by CB1 cannabinoid receptors. Executive function and motivation ADHD arises from a core deficit in executive functions (e.g., attentional control, inhibitory control, and working memory), which are a set of cognitive processes that are required to successfully select and monitor behaviours that facilitate the attainment of one's chosen goals. 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. 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 ( of patients). These are unexpected reactions in the opposite direction as with a normal effect, or otherwise significant different reactions. These are reactions to neuroactive substances such as local anesthetic at the dentist, sedative, caffeine, antihistamine, weak neuroleptics and central and peripheral painkillers. Since the causes of paradoxical reactions are at least partly genetic, it may be useful in critical situations, for example before operations, to ask whether such abnormalities may also exist in family members. ==Diagnosis==

ADHD is diagnosed by an assessment of a person's behavioural and mental development, including ruling out the effects of drugs, medications, and other medical or psychiatric problems as explanations for the symptoms. Childhood and adolescent ADHD diagnosis often takes into account feedback from parents and teachers with most diagnoses begun after a teacher raises concerns. While many tools exist to aid in the diagnosis of ADHD, their validity varies in different populations, and a reliable and valid diagnosis requires confirmation by a clinician while supplemented by standardised rating scales and input from multiple informants across various settings. Most diagnosis in children is seen in low-income families, and more in Caucasian children in comparison to Black, Hispanic, and Asian children, however, the diagnosis may be influenced by racial and socio-economic biases. The 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). 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. Electroencephalography is not accurate enough to make an ADHD diagnosis. A 2024 systematic review concluded that the use of biomarkers such as blood or urine samples, electroencephalogram (EEG) markers, and neuroimaging such as MRIs, in diagnosis for ADHD remains unclear; studies showed great variability, did not assess test-retest reliability, and were not independently replicable. or a disruptive behaviour disorder along with ODD, CD, and antisocial personality disorder. A diagnosis does not imply a neurological disorder. out of nine long-term (lasting at least six months) symptoms of inattention, hyperactivity–impulsivity, or both. and there must be clear evidence that they are causing impairment in multiple domains of life. The DSM-5 and the DSM-5-TR also provide two diagnoses for individuals who have symptoms of ADHD but do not entirely meet the requirements. Other Specified ADHD allows the clinician to describe why the individual does not meet the criteria, whereas Unspecified ADHD is used where the clinician chooses not to describe the reason. In the tenth revision (ICD-10), the symptoms of hyperkinetic disorder were analogous to ADHD in the ICD-11. When a conduct disorder (as defined by ICD-10) is present, the condition was referred to as hyperkinetic conduct disorder. Otherwise, the disorder was classified as disturbance of activity and attention, other hyperkinetic disorders or hyperkinetic disorders, unspecified. The latter was sometimes referred to as hyperkinetic syndrome. Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and then given a name". Adults Adults with ADHD are diagnosed under the same criteria, including that their signs must have been present by the age of six to twelve. The individual is the best source for information in diagnosis, however others may provide useful information about the individual's symptoms currently and in childhood; a family history of ADHD also adds weight to a diagnosis. 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. In 2020, this was 139.84 million and 366.33 million affected adults respectively. Many adults with ADHD without diagnosis and treatment have a disorganised life, and some use non-prescribed drugs or alcohol as a coping mechanism. Other problems may include relationship and job difficulties, and an increased risk of criminal activities. Differential diagnosis The DSM provides differential diagnoses – potential alternate explanations for specific symptoms. Assessment and investigation of clinical history determines which is the most appropriate diagnosis. The DSM-5 suggests oppositional defiant disorder, intermittent explosive disorder, and other disorders such as stereotypic movement disorder and Tourette syndrome, in addition to specific learning disorder, intellectual disability, autism, reactive attachment disorder, anxiety disorders, depressive disorders, bipolar disorder, disruptive mood dysregulation disorder, substance use disorder, personality disorders, psychotic disorders, medication-induced symptoms, and neurocognitive disorders. Many but not all of these are also common comorbidities of ADHD. It is thus recommended that children with ADHD be regularly assessed for sleep problems. Sleepiness in children may result in symptoms ranging from the classic ones of yawning and rubbing the eyes, to disinhibition and inattention. Obstructive sleep apnea can also cause ADHD-like symptoms. In general, the DSM-5-TR can help distinguish between many conditions associated with ADHD-like symptoms by the context in which the symptoms arise. Tantrums may differ from the outbursts in intermittent explosive disorder if there is no aggression involved. The fidgetiness observed in ADHD may be differentiated from tics or stereotypies common in Tourette syndrome or autism. Also, the social difficulties often experienced by individuals with ADHD due to inattention (e.g., being unfocused during the interaction and therefore missing cues or being unaware of one's behaviour) or impulsivity (blurting things out, asking intrusive questions, interrupting) may be contrasted with the social detachment and deficits in understanding social cues associated with Autism Spectrum Disorder. Individuals with ADHD may also present signs of the social impairment or emotional and cognitive dysregulation seen in personality disorders, but not necessarily such features as a fear of abandonment, an unstable sense of self, narcissistic tendencies, aggressiveness, or other personality features. While it is possible and common for many of these different conditions to be comorbid with ADHD, the symptoms must not be better explained by them, as per diagnostic criterion E in the DSM-5. The symptoms must arise early in life, appear across multiple environments, and cause significant impairment. Moreover, when some of these conditions are in fact comorbid with ADHD, it is still important to distinguish them, as each may need to be treated separately. ==Comorbidities==

Psychiatric comorbidities Nearly 78% of children with ADHD have at least one other co-occurring condition, according to data collected in 2022 by the U.S. Centers for Disease Control and Prevention. 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. ADHD, however, is not considered a learning disability, but it very frequently causes academic difficulties. Adolescents with ADHD who also have CD are more likely to develop antisocial personality disorder in adulthood. 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. 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. Borderline personality disorder has also been noted to co-occur with ADHD, though more recent research suggests this may be due to historical biases leading to misdiagnoses. The current diagnostic assessment of either disorder is often complex, as both have overlapping symptoms, thus these assessments can follow a differential diagnosis to determine whether there is a co-occurrence of both disorders or not. 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). While boys tend to present with comorbidities that involve externalization, girls tend to internalise their symptoms, leading to the possibility of increased misdiagnosis via standards designed to recognise male ADHD. Adults and children with ADHD sometimes also have bipolar disorder, which requires careful assessment to accurately diagnose and treat both conditions. 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. 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. Restless legs syndrome has been found to be more common in those with ADHD and is often due to iron-deficiency anaemia. However, restless legs can simply be a part of ADHD and requires careful assessment to differentiate between the two disorders. Delayed sleep phase disorder is also a common comorbidity. Individuals with ADHD are at increased risk of substance use disorders. 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-PI have been found to have CDS instead. 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 twice as likely to have ADHD than those without eating disorders. Trauma ADHD, trauma, and adverse childhood experiences are also comorbid, 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. This could result in trauma-related disorders or ADHD being mis-identified as the other. Additionally, traumatic events in childhood are a risk factor for ADHD; they can lead to structural brain changes and the development of ADHD behaviours. Non-psychiatric Some non-psychiatric conditions are also comorbidities of ADHD. This includes epilepsy, There are well established associations between ADHD and obesity, asthma and sleep disorders, and an association with celiac disease. Children with ADHD have a higher risk for migraine headaches, but have no increased risk of tension-type headaches. Children with ADHD may also experience headaches as a result of medication. 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. In June 2021, Neuroscience & Biobehavioral Reviews published a systematic review of 82 studies that all confirmed or implied elevated accident-proneness in ADHD patients, and whose data suggested that the type of accidents or injuries—and overall risk—changes over the lifespan of ADHD patients. In January 2014, Accident Analysis & Prevention published a meta-analysis of 16 studies examining the relative risk of traffic collisions for drivers with ADHD, finding an overall relative risk estimate of 1.36 without controlling for exposure, a relative risk estimate of 1.29 when controlling for publication bias, a relative risk estimate of 1.23 when controlling for exposure, and a relative risk estimate of 1.86 for ADHD drivers with oppositional defiant disorder or conduct disorder comorbidities. Problematic digital media use 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. Potential causes include ADHD's association with functional impairment, negative social, educational and occupational outcomes, and financial distress. 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. Others posit that rejection sensitivity stems from early attachment relationships and parental rejection; peer rejection is also thought to play a role. Bullying, an extreme form of peer rejection, is likely connected to later rejection sensitivity. She suggested that it is a component of the neurotic personality, and that it is a tendency to feel deep anxiety and humiliation at the slightest rebuff. Simply being made to wait, for example, could be viewed as a rejection and met with extreme anger and hostility. Albert Mehrabian developed an early questionnaire measure of rejection sensitivity. Mehrabian suggested that sensitive individuals are reluctant to express opinions, tend to avoid arguments or controversial discussions, are reluctant to make requests or impose on others, are easily hurt by negative feedback from others, and tend to rely too much on familiar others and situations so as to avoid rejection. A more recent (1996) definition of rejection sensitivity is the tendency to "anxiously expect, readily perceive, and overreact" to social rejection. People differ in their readiness to perceive and react to rejection. The causes of individual differences in rejection sensitivity are not well understood. Because of the association between rejection sensitivity and neuroticism, there is a likely genetic predisposition. ==Management==

The management of ADHD typically involves counselling or medications, either alone or in combination. While there are various options of treatment to improve ADHD symptoms, medication therapies substantially improve long-term outcomes, and while eliminating some elevated risks such as obesity, Medications used include stimulants, atomoxetine, alpha-2 adrenergic receptor agonists, and sometimes antidepressants. In those who have trouble focusing on long-term rewards, a large amount of positive reinforcement improves task performance. and any side effects are typically mild and easy to resolve ADHD stimulants also improve persistence and task performance in children with ADHD. Data also suggest that combining medication with cognitive behavioural therapy (CBT) can have positive effects: although CBT is substantially less effective, it can help address problems that reside after medication has been optimised. In most studies, the efficacy of treatment is determined by reductions in symptoms. However, some studies have included subjective ratings from teachers and parents as part of their assessment of treatment efficacies. Psychological therapies used include: psychoeducational input, behaviour therapy, cognitive behavioural therapy, interpersonal psychotherapy, family therapy, school-based interventions, social skills training, behavioural peer intervention, organisation training, and parent management training. Neurofeedback for ADHD is controversial, and the literature is mixed. It appears to not be clinically significant. 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. ADHD-specific support groups can provide information and may help families cope with ADHD. 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. Digital interventions Several clinical trials have investigated the efficacy of digital therapeutics, particularly Akili Interactive Labs's video game-based digital therapeutic AKL-T01, marketed as EndeavourRx. The paediatric STARS-ADHD randomised, double-blind, parallel-group, controlled trial demonstrated that AKL-T01 significantly improved performance on the Test of Variables of Attention, an objective measure of attention and inhibitory control, compared to a control group after four weeks of at-home use. A subsequent paediatric open-label study, STARS-Adjunct, published in Nature Portfolio's npj Digital Medicine evaluated AKL-T01 as an adjunctive treatment for children with ADHD who were either on stimulant medication or not on stimulant pharmacotherapy. Results showed improvements in ADHD-related impairment (measured by the Impairment Rating Scale) and ADHD symptoms after 4 weeks of treatment, with effects persisting during a 4-week pause and further improving with an additional treatment period. Notably, the magnitude of the measured improvement was similar for children both on and off stimulants. In addition to paediatric populations, a 2023 study in the Journal of the American Academy of Child & Adolescent Psychiatry investigated the efficacy and safety of AKL-T01 in adults with ADHD. After six weeks of at-home treatment with AKL-T01, participants showed significant improvements in objective measures of attention (TOVA - Attention Comparison Score), reported ADHD symptoms (ADHD-RS-IV inattention subscale and total score), and reported quality of life (AAQoL). The magnitude of improvement in attention was nearly seven times greater than that reported in paediatric trials. According to Effective Health Care Systematic Review, FDA-approved stimulant and non-stimulant medications shows sufficient evidence showing that they greatly improve the core symptoms of ADHD. Stimulants Methylphenidate and amphetamine or its derivatives are often first-line treatments for ADHD. About 70 percent respond to the first stimulant tried and as few as 10 percent respond to neither amphetamines nor methylphenidate. 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. A 2018 review found the greatest short-term benefit with methylphenidate in children, and amphetamines in adults. Studies and meta-analyses show that amphetamine is slightly-to-modestly more effective than methylphenidate at reducing symptoms, and they are more effective pharmacotherapy for ADHD than α2-agonists but methylphenidate has comparable efficacy to non-stimulants such as atomoxetine. In a Cochrane clinical synopsis, Dr Storebø and colleagues summarised their meta-review on methylphenidate for ADHD in children and adolescents. The meta-analysis raised substantial doubts about the drug's efficacy relative to a placebo. This led to a strong critical reaction from the European ADHD Guidelines Group and individuals in the scientific community, who identified a number of flaws in the review. Since at least September 2021, there is a unanimous and global scientific consensus that methylphenidate is safe and highly effective for treating ADHD. The same journal released a subsequent systematic review (2022) of extended-release methylphenidate for adults, concluding similar doubts about the certainty of evidence. Other recent systematic reviews and meta-analyses, however, find certainty in the safety and high efficacy of methylphenidate for reducing ADHD symptoms, for alleviating the underlying executive functioning deficits, and for substantially reducing the adverse consequences of untreated ADHD with continuous treatment. 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. The safety of these medications in pregnancy is unclear. Symptom improvement is not sustained if medication is ceased. The long-term effects of ADHD medication have yet to be fully determined, although stimulants are generally beneficial and safe for up to two years for children and adolescents. 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. Regular monitoring has been recommended in those on long-term treatment. 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. Although potentially addictive at high doses, stimulants used to treat ADHD have low potential for abuse. 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). Pseudoephedrine and ephedrine do not affect ADHD symptoms. Modafinil has shown some efficacy in reducing the severity of ADHD in children and adolescents. The only recorded side effect was increased loss of appetite. Non-stimulants Two non-stimulant medications, atomoxetine and viloxazine, are approved by the FDA and in other countries for the treatment of ADHD. Atomoxetine, due to its lack of addiction liability, may be preferred in those who are at risk of recreational or compulsive stimulant use, although evidence is lacking to support its use over stimulants for this reason. Meta-analyses and systematic reviews have found that atomoxetine has comparable efficacy, equal tolerability and response rate (75%) to methylphenidate in children and adolescents. In adults, efficacy and discontinuation rates are equivalent. Amantadine was shown to induce similar improvements in children treated with methylphenidate, with less frequent side effects. A 2021 retrospective study showed that amantadine may serve as an effective adjunct to stimulants for ADHD–related symptoms and appears to be a safer alternative to second- or third-generation antipsychotics. Bupropion is also used off-label by some clinicians due to research findings. It is effective, but modestly less than atomoxetine and methylphenidate. There is little evidence on the effects of medication on social behaviours. Antipsychotics may also be used to treat aggression in ADHD. 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). They appear to be modestly less effective than the stimulants (amphetamine and methylphenidate) and non-stimulants (atomoxetine and viloxazine) at reducing symptoms, but can be useful alternatives or used in conjunction with a stimulant. These medications act by adjusting the alpha-2a ports on the outside of noradrenergic nerve cells in the pre-frontal executive networks, so the information (electrical signal) is less confounded by noise. 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. Conversely, most United States guidelines recommend medications in most age groups. Medications are especially not recommended for preschool children. 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. Exercise Exercise does not reduce the symptoms of ADHD according to the International Consensus Statement. These benefits may be limited to children with food sensitivities or those who are simultaneously being treated with ADHD medications. A 2016 review stated that the use of a gluten-free diet as standard ADHD treatment is not advised. 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. Chronic deficiencies of iron, magnesium and iodine may have a negative impact on ADHD symptoms. There is a small amount of evidence that lower tissue zinc levels may be associated with ADHD. In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as treatment for ADHD. However, zinc supplementation may reduce the minimum effective dose of amphetamine when it is used with amphetamine for the treatment of ADHD. ==Prognosis==

About one to two thirds of people diagnosed in childhood continue to have ADHD in adulthood, with 2.58% of adults estimated to have ADHD which began in childhood. Individuals with ADHD may also face misconceptions and stigma. A US study found rates of smoking among those with ADHD are higher than in the general population. Positive effects of medication on functional impairment and quality of life (e.g. reduced risk of accidents) have been found across multiple domains. 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%. New research in 2025 indicates that adults diagnosed with ADHD may have a shorter lifespan compared to those without the condition. The study revealed that, on average, men with ADHD lived seven years less than men without ADHD, while women with ADHD had a lifespan nine years shorter than their peers. Although the study did not pinpoint exact causes of death, it highlighted that individuals with ADHD were more likely to engage in smoking, alcohol misuse, and face other health challenges such as depression, self-harm, or personality disorders. ==Epidemiology==

ADHD is estimated to affect about 6–7% of people aged 18 and under when diagnosed via the DSM-IV criteria. Rates are similar between countries and differences in rates depend mostly on how it is diagnosed. Children in North America appear to have a higher rate of ADHD than children in Africa and the Middle East; this is believed to be due to differing methods of diagnosis rather than a difference in underlying frequency. (The same publication which describes this difference also notes that the difference may be rooted in the available studies from these respective regions, as far more studies were from North America than from Africa and the Middle East.) it was estimated to affect 84.7 million people globally. ADHD is diagnosed approximately twice as often in boys as in girls, and 1.6 times more often in men than in women, In 2014, Keith Conners, one of the early advocates for recognition of the disorder, spoke out against overdiagnosis in a New York Times article. In contrast, a 2014 peer-reviewed medical literature review indicated that ADHD is underdiagnosed in adults. Boys who were born in December where the school age cut-off was 31 December were shown to be 30% more likely to be diagnosed and 41% more likely to be treated than those born in January. Girls born in December had a diagnosis and treatment percentage increase of 70% and 77% respectively compared to those born in January. Children who were born at the last three days of a calendar year were reported to have significantly higher levels of diagnosis and treatment for ADHD than children born at the first three days of a calendar year. The studies suggest that ADHD diagnosis is prone to subjective analysis. This is believed to be primarily due to changes in how the condition is diagnosed Despite showing a higher frequency of symptoms associated with ADHD, non-White children in the US are less likely than White children to be diagnosed or treated for ADHD, a finding that is often explained by bias among health professionals, as well as parents who may be reluctant to acknowledge that their child has ADHD. Crosscultural differences in diagnosis of ADHD can also be attributed to the long-lasting effects of harmful, racially targeted medical practices. Medical pseudosciences, particularly those that targeted Black populations during the period of slavery in the US, lead to a distrust of medical practices within certain communities. The combination of ADHD symptoms often being regarded as misbehaviour rather than as a psychiatric condition, and the use of drugs to regulate ADHD, result in a hesitancy to trust a diagnosis of ADHD. Cases of misdiagnosis in ADHD can also occur due to stereotyping of people of colour. Due to ADHD's subjectively determined symptoms, medical professionals may diagnose individuals based on stereotyped behaviour or misdiagnose due to cultural differences in symptom presentation. A 2024 study in CDC's Morbidity and Mortality Weekly Report reports about 15.5 million U.S. adults have attention-deficit hyperactivity disorder, with many facing challenges in accessing treatment. One-third of diagnosed individuals had received a prescription for a stimulant drug in the past year but nearly three-quarters of them reported difficulties filling the prescription due to medication shortages. ==History==

ADHD was officially known as attention deficit disorder (ADD) from 1980 to 1987; prior to the 1980s, it was known as hyperkinetic reaction of childhood. Symptoms similar to those of ADHD have been described in medical literature dating back to the 18th century. Sir Alexander Crichton describes "mental restlessness" in his book An inquiry into the nature and origin of mental derangement written in 1798. He made observations about children showing signs of being inattentive and having the "fidgets". The first clear description of ADHD is credited to George Still in 1902 during a series of lectures he gave to the Royal College of Physicians of London. The terminology used to describe the condition has changed over time and has included: , hyperkinetic reaction of childhood in the DSM-II (1968), and attention-deficit disorder with or without hyperactivity in the DSM-III (1980). and in 1994 the DSM-IV in split the diagnosis into three subtypes: ADHD inattentive type, ADHD hyperactive-impulsive type, and ADHD combined type. These terms were kept in the DSM-5 in 2013 and in the DSM-5-TR in 2022. ADHD, its diagnosis, and its treatment have been controversial since the 1970s. For example, positions differ on whether ADHD is within the normal range of behaviour, and the degree to which ADHD is a genetic condition. Other areas of controversy include the use of stimulant medications in children, In 2009, the National Institute for Health and Care Excellence states that the current treatments and methods of diagnosis are based on the dominant view of the academic literature. Once neuroimaging studies were possible, studies in the 1990s provided support for the pre-existing theory that neurological differences (particularly in the frontal lobes) were involved in ADHD. A genetic component was identified and ADHD was acknowledged to be a persistent, long-term disorder which lasted from childhood into adulthood. ADHD was split into the current three sub-types because of a field trial completed by Lahey and colleagues and published in 1994. In 2021, global teams of scientists curated the International Consensus Statement compiling evidence-based findings about the disorder. Methylphenidate was introduced in the 1950s, and enantiopure dextroamphetamine in the 1970s. Psychiatrist Charles Bradley gave the children with behavioural disorders Benzedrine and found it improved academic performance and behaviour. == Research directions ==

Possible positive traits Possible positive traits of ADHD are a new avenue of research, and therefore limited. A 2020 review found that creativity may be associated with ADHD symptoms, particularly divergent thinking and quantity of creative achievements, but not with the disorder of ADHD itself – i.e. it has not been found to be increased in people diagnosed with the disorder, only in people with subclinical symptoms or those that possess traits associated with the disorder. Divergent thinking is the ability to produce creative solutions which differ significantly from each other and consider the issue from multiple perspectives. Those with ADHD symptoms could be advantaged in this form of creativity as they tend to have diffuse attention, allowing rapid switching between aspects of the task under consideration; flexible associative memory, allowing them to remember and use more distantly related ideas which is associated with creativity; and impulsivity, allowing them to consider ideas which others may not have. 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 in aggregate. These parameters could serve as prognostic biomarkers for ADHD, but more research is needed to establish their prognostic utility. Urinary and blood plasma phenethylamine concentrations are lower in ADHD individuals relative to controls. The two most commonly prescribed drugs for ADHD, amphetamine and methylphenidate, increase phenethylamine biosynthesis in treatment-responsive individuals with ADHD. Lower urinary phenethylamine concentrations are associated with symptoms of inattentiveness in ADHD individuals. Possible biomarkers for selecting treatment There exists evidence to suggest that certain biomarkers, particularly those derived from non-invasive EEG assessment, may have potential utility in predicting response to pharmacological treatments for ADHD, with evidence relating non-pharmacological treatments being more limited. Repeated biomarker assessments indicate that different treatments are associated with distinct changes in specific neurophysiological profiles over time, which parallel treatment-related clinical improvements in some studies. == See also ==