Mind-wandering is loosely defined as thoughts that are not
produced from the current task. Mind-wandering consists of thoughts that
are task-unrelated and stimulus-independent.
This can be in the form of three different subtypes: positive
constructive daydreaming, guilty fear of failure, and poor attentional
control.
In general, a folk explanation of mind-wandering could be
described as the experience of thoughts not remaining on a single topic
for a long period of time, particularly when people are engaged in an
attention-demanding task.
One context in which mind-wandering often occurs is driving. This
is because driving under optimal conditions becomes an almost automatic
activity that can require minimal use of the task positive network,
the brain network that is active when one is engaged in an
attention-demanding activity. In situations where vigilance is low,
people do not remember what happened in the surrounding environment
because they are preoccupied with their thoughts. This is known as the
decoupling hypothesis.
Studies using event-related potentials
(ERPs) have quantified the extent that mind-wandering reduces the
cortical processing of the external environment. When thoughts are
unrelated to the task at hand, the brain processes both task-relevant
and unrelated sensory information in a less detailed manner.
Mind-wandering appears to be a stable trait of people and a transient state. Studies have linked performance problems in the laboratory and in daily life. Mind-wandering has been associated with possible car accidents.
Mind-wandering is also intimately linked to states of affect. Studies
indicate that task-unrelated thoughts are common in people with low or
depressed mood. Mind-wandering also occurs when a person is intoxicated via the consumption of alcohol.
Studies have demonstrated a prospective bias to spontaneous
thought because individuals tend to engage in more future than past
related thoughts during mind-wandering. The default mode network is thought to be involved in mind-wandering and internally directed thought, although recent work has challenged this assumption.
History
The
history of mind-wandering research dates back to 18th century England.
British philosophers struggled to determine whether mind-wandering
occurred in the mind or if an outside source caused it. In 1921,
Varendonck published The Psychology of Day-Dreams, in which he traced his "'trains of thoughts' to identify their origins, most often irrelevant external influences".
Wallas (1926) considered mind-wandering as an important aspect of his second stage of creative thought – incubation. It was not until the 1960s that the first documented studies were conducted on mind-wandering. John Antrobus and Jerome L. Singer developed a questionnaire and discussed the experience of mind-wandering.
This questionnaire, known as the Imaginal Processes Inventory
(IPI), provides a trait measure of mind-wandering and it assesses the
experience on three dimensions: how vivid the person's thoughts are, how
many of those thoughts are guilt- or fear-based, and how deep into the
thought a person goes. As technology continues to develop, psychologists
are starting to use functional magnetic resonance imaging to observe mind-wandering in the brain and reduce psychologists' reliance on verbal reports.
Research methods
Jonathan Smallwood and colleagues popularized the study of mind-wandering using thought sampling and questionnaires.
Mind-wandering is studied using experience sampling either online or
retrospectively. One common paradigm within which to study
mind-wandering is the SART (sustained attention to response task).
In a SART task there are two categories of words. One of the
categories are the target words. In each block of the task a word
appears for about 300 ms, there will be a pause and then another word.
When a target word appears the participant hits a designated key. About
60% of the time after a target word a thought probe will appear to
gauge whether thoughts were on task. If participants were not engaged
in the task they were experiencing task-unrelated thoughts (TUTs),
signifying mind-wandering.
Another task to judge TUTs is the experience sampling method (ESM). Participants carry around a personal digital assistant
(PDA) that signals several times a day. At the signal a questionnaire
is provided. The questionnaire questions vary but can include: (a)
whether or not their minds had wandered at the time of the (b) what
state of control they had over their thoughts and (c) about the content
of their thoughts.
Questions about context are also asked to measure the level of attention necessary for the task.
One process used was to give participants something to focus on and
then at different times ask them what they were thinking about. Those
who were not thinking about what was given to them were considered
"wandering". Another process was to have participants keep a diary of
their mind-wandering. Participants are asked to write a brief
description of their mind-wandering and the time in which it happened. These methodologies are improvements on past methods that were inconclusive.
Neuroscience
Mind-wandering is important in understanding how the brain produces what William James called the train of thought and the stream of consciousness.
This aspect of mind-wandering research is focused on understanding how
the brain generates the spontaneous and relatively unconstrained
thoughts that are experienced when the mind wanders.
One candidate neural mechanism for generating this aspect of experience is a network of regions in the medial frontal and medial parietal cortex known as the default network. This network of regions is highly active even when participants are resting with their eyes closed suggesting a role in generating spontaneous internal thoughts.
One relatively controversial result is that periods of mind-wandering
are associated with increased activation in both the default and
executive system a result that implies that mind-wandering may often be goal oriented.
It is commonly assumed that the default mode network
is known to be involved during mind-wandering. The default mode network
is active when a person is not focused on the outside world and the
brain is at wakeful rest because experiences such as mind-wandering and
daydreaming are common in this state.
It is also active when the individual is thinking about others,
thinking about themselves, remembering the past, and planning for the
future. However, recent studies show that signals in the default mode network provide information regarding patterns of detailed experience in active tasks states. This data suggests that the relationship between the default mode network and mind-wandering remains a matter of conjecture.
In addition to neural models, computational models of consciousness based on Bernard Baars' Global Workspace theory
suggest that mind-wandering, or "spontaneous thought" may involve
competition between internally and externally generated activities
attempting to gain access to a limited capacity central network.
Individual differences
There are individual differences in some aspects of mind-wandering between older and younger adults.
Although older adults reported less mind-wandering, these older
participants showed the same amount of mind-wandering as younger adults.
There were also differences in how participants responded to an error.
After an error, older adults took longer to return focus back to
the task when compared with younger adults. It is possible that older
adults reflect more about an error due to conscientiousness. Research has shown that older adults tend to be more conscientious than young adults. Personality can also affect mind-wandering.
People that are more conscientious are less prone to
mind-wandering. Being more conscientious allows people to stay focused
on the task better which causes fewer instances of mind-wandering.
Differences in mind-wandering between young and older adults may be
limited because of this personality difference.
Mental disorders such as ADHD (attention deficit hyperactivity disorder)
are linked to mind-wandering. Seli et al. (2015) found that spontaneous
mind-wandering, the uncontrolled or unwarranted shifting of attention,
is a characteristic of those who have ADHD. However, they note that
deliberate mind-wandering, or the purposeful shifting of one's attention
to different stimuli, is not a consistent characteristic of having
ADHD.
Franklin et al. (2016) arrived at similar conclusions; they had
college students take multiple psychological evaluations that gauge ADHD
symptom strength. Then, they had the students read a portion of a
general science textbook. At various times and at random intervals
throughout their reading, participants were prompted to answer a
question that asked if their attention was either on task, slightly on
task, slightly off task, or off task prior to the interruption.
In addition, they were asked if they were aware, unaware, or
neither aware nor unaware of their thoughts as they read. Lastly, they
were tasked to press the space bar if they ever caught themselves
mind-wandering. For a week after these assessments, the students
answered follow-up questions that also gauged mind-wandering and
awareness.
This study's results revealed that students with higher ADHD
symptomology showed less task-oriented control than those with lower
ADHD symptomology. Additionally, those with lower ADHD symptomology were
more likely to engage in useful or deliberate mind-wandering and were
more aware of their inattention. One of the strengths of this study is
that it was performed in both lab and daily-life situations, giving it
broad application.
Mind-wandering in and of itself is not necessarily indicative of
attention deficiencies. Studies show that humans typically spend 25-50%
of their time thinking about thoughts irrelevant to their current
situations.
In many disorders it is the regulation of the overall amount of
mind-wandering that is disturbed, leading to increased distractibility
when performing tasks.
Additionally, the contents of mind-wandering is changed; thoughts can
be more negative and past-oriented, particularly unstable or
self-centered.
Recent research has studied the relationship between mind-wandering and working memory capacity. Working memory capacity represents personal skill to have a good command of individual's mind. This relationship
requires more research to understand how they influence one another.
It is possible that mind-wandering causes lower performance on working
memory capacity tasks or that lower working memory capacity causes more
instances of mind-wandering.
Only the second of these has actually been proven. Reports of task-unrelated thoughts are less frequent when performing tasks that do not demand continuous use of working memory than tasks which do. Moreover, individual difference studies
demonstrate that when tasks are non-demanding, high levels of working
memory capacity are associated with more frequent reports of
task-unrelated thinkingespecially when it is focused on the future.
By contrast, when performing tasks that demand continuous attention,
high levels of working memory capacity are associated with fewer reports
of task-unrelated thoughts.
Together these data are consistent with the claim that working
memory capacity helps sustain a train of thought whether it is generated
in response to a perceptual event or is self-generated by the
individual. Therefore, under certain circumstances, the experience of
mind-wandering is supported by working memory resources.
Working memory capacity variation in individuals has been proven to be a
good predictor of the natural tendency for mind-wandering to occur
during cognitively demanding tasks and various activities in daily life.
Mind-wandering sometimes occurs as a result of saccades,
which are the movements of one's eyes to different visual stimuli. In
an antisaccade task, for example, subjects with higher working memory
capacity scores resisted looking at the flashing visual cue better than
participants with lower working memory capacity. Higher working memory capacity is associated with fewer saccades toward environmental cues.
Mind-wandering has been shown to be related to goal orientation;
people with higher working memory capacity keep their goals more
accessible than those who have lower working memory capacity, thus
allowing these goals to better guide their behavior and keep them on
task.
Another study compared differences in speed of processing information between people of different ages. The task they used was a go/no go
task where participants responded if a white arrow moved in a specific
direction but did not respond if the arrow moved in the other direction
or was a different color. In this task, children and young adults showed
similar speed of processing but older adults were significantly slower.
Speed of processing information affects how much information can be processed in working memory. People with faster speed of processing can encode information into memory
better than people that have slower speed of processing. This can lead
to memory of more items because more things can be encoded.
Retention
Mind-wandering
affects retention where working memory capacity is directly related to
reading comprehension levels. Participants with lower working memory
capacity perform worse on comprehension-based tests.
When investigating how mind-wandering affects retention of
information, experiments are conducted where participants are asked a
variety of questions about factual information, or deducible information
while reading a detective novel. Participants are also asked about the
state of their mind before the questions are asked.
Throughout the reading itself, the author provides important cues
to identify the villain, known as inference critical episodes (ICEs).
The questions are asked randomly and before critical episodes are
reached. It was found that episodes of mind-wandering, especially early
on in the text led to decreased identification of the villain and worse
results on both factual and deducible questions.
Therefore, when mind-wandering occurs during reading, the text is
not processed well enough to remember key information about the story.
Furthermore, both the timing and the frequency of mind-wandering helps
determine how much information is retained from the narrative.
Reading comprehension
Reading
comprehension must also be investigated in terms of text difficulty. To
assess this, researchers provide an easy and hard version of a reading
task. During this task, participants are interrupted and asked whether
their thoughts at the time of interruption had been related or unrelated
to the task. What is found is that mind-wandering has a negative effect
on text comprehension in more difficult readings.
This supports the executive-resource hypothesis which describes
that both task related and task-unrelated thoughts (TUT) compete for
executive function resources. Therefore, when the primary task is
difficult, little resources are available for mind-wandering, whereas
when the task is simple, the possibility for mind-wandering is abundant
because it takes little executive control to focus on simple tasks.
However, mind-wandering tends to occur more frequently in harder
readings as opposed to easier readings. Therefore, it is possible that
similar to retention, mind-wandering increases when readers have
difficulty constructing a model of the story.
Happiness
As part of his doctoral research at Harvard University, Matthew Killingsworth used an iPhone app that captured a user's feelings in real time. The tool alerts the user at random times and asks: "How are you feeling right now?" and "What are you doing right now?"
Killingsworth and Gilbert's analysis suggested that mind-wandering was
much more typical in daily activities than in laboratory settings.
They also describe that people were less happy when their minds
were wandering than when they were otherwise occupied. This effect was
somewhat counteracted by people's tendency to mind-wander to happy
topics, but unhappy mind-wandering was more likely to be rated as more
unpleasant than other activities.
The authors note that unhappy moods can also cause
mind-wandering, but the time-lags between mind-wandering and mood
suggests that mind-wandering itself can also lead to negative moods.
Furthermore, research suggests that regardless of working memory
capacity, subjects participating in mind-wandering experiments report
more mind-wandering when bored, stressed, or unhappy.
Executive functions
Executive functions (EFs) are cognitive processes that make a person pay attention or concentrate on a task. Three executive functions that relate to memory are inhibiting,
updating and shifting. Inhibiting controls a person's attention and
thoughts when distractions are abundant. Updating reviews old information and replaces it with new information in the working memory. Shifting controls the ability to go between multiple tasks. All three EFs have a relationship to mind-wandering.
Executive functions have roles in attention problems, attention control, thought control, and working memory capacity. Attention problems relate to behavioral problems such as inattention, impulsivity and hyperactivity. These behaviors make staying on task difficult leading to more mind-wandering. Higher inhibiting and updating abilities correlates to lower levels of attention problems in adolescence.
The inhibiting executive function controls attention and thought.
The failure of cognitive inhibition is a direct cause of
mind-wandering. Mind-wandering is also connected to working memory capacity (WMC).
People with higher WMC mind-wander less on high concentration tasks no
matter their boredom levels. People with low WMC are better at staying
on task for low concentration tasks, but once the task increases in
difficulty they had a hard time keeping their thoughts focused on task.
Updating takes place in the working memory, therefore those with low WMC have a lower updating executive function ability. That means a low performing updating executive function can be an indicator of high mind-wandering. Working memory relies on executive functions, with mind-wandering as an indicator of their failure. Task-unrelated thoughts (TUTs) are empirical behavioral manifestations of mind-wandering in a person. The longer a task is performed the more TUTs reported. Mind-wandering is an indication of an executive control failure that is characterized by TUTs.
Metacognition serves to correct the wandering mind, suppressing spontaneous thoughts and bringing attention back to more "worthwhile" tasks.
Fidgeting
Paul Seli and colleagues have shown that spontaneous mind-wandering is associated with increased fidgeting; by contrast, interest, attention and visual engagement lead to Non-Instrumental Movement Inhibition.
One possible application for this phenomenon is that detection of
non-instrumental movements may be an indicator of attention or boredom in computer aided learning.
Traditionally teachers and students have viewed fidgeting as a sign of diminished attention,
which is summarized by the statement, “Concentration of consciousness,
and concentration of movements, diffusion of ideas and diffusion of
movements go together.”
However, James Farley and colleagues have proposed that fidgeting is
not only an indicator of spontaneous mind-wandering, but is also a
subconscious attempt to increase arousal in order to improve attention
and thus reduce mind-wandering.
ADHD symptoms arise from executive dysfunction, and emotional dysregulation is often considered a core symptom.
Difficulties in self-regulation such as time management, inhibition and
sustained attention may cause poor professional performance,
relationship difficulties and numerous health risks, collectively predisposing to a diminished quality of life and a direct average reduction in life expectancy of 13 years. ADHD is associated with other neurodevelopmental and mental disorders as well as non-psychiatric disorders, which can cause additional impairment.
Although people with ADHD struggle to persist on tasks with
temporally delayed consequences, they may be able to do so on tasks they
find intrinsically interesting or immediately rewarding; this is known as hyperfocus (more colloquially) or perseverative responding. This mental state is often hard to disengage from and can be related to risks such as for internet addiction and types of offending behaviour.
ADHD represents the extreme lower end of the continuous
dimensional trait (bell curve) of executive functioning and
self-regulation, which is supported by twin, brain imaging and molecular
genetic studies.
The precise causes of ADHD are unknown in the majority of cases. For most people with ADHD, many genetic and environmental risk factors accumulate to cause the disorder. The environmental risks are biological and most often exert their effects in the prenatal period. However, in rare cases ADHD may be caused by a single event such as traumatic brain injury, exposure to biohazards during pregnancy, a major genetic mutation or extreme environmental deprivation very early in life. There is no biologically distinct adult-onset ADHD except for when ADHD occurs after traumatic brain injury.
Signs and symptoms
Inattention, hyperactivity (restlessness in adults), disruptive behaviour, and impulsivity are common in ADHD. Academic difficulties are frequent, as are problems with relationships.
The signs and symptoms can be difficult to define, as it is hard to
draw a line at where normal levels of inattention, hyperactivity, and
impulsivity end and significant levels requiring interventions begin.
According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and its text revision (DSM-5-TR), symptoms must be present for six months or more to a degree that is much greater than others of the same age.
This requires at least six symptoms of either inattention or
hyperactivity/impulsivity for those under 17 and at least five symptoms
for those 17 years or older. The symptoms must be present in at least two settings (e.g., social,
school, work, or home), and must directly interfere with or reduce
quality of functioning. Additionally, several symptoms must have been present before age twelve. The DSM-5 's required age of onset of symptoms is 12 years.However, research indicates the age of onset should not be interpreted
as a prerequisite for diagnosis given contextual exceptions.
predominantly hyperactive-impulsive (ADHD-PH or ADHD-HI)
combined presentation (ADHD-C).
The table "Symptoms" lists the symptoms for ADHD-I and ADHD-HI from
two major classification systems. Symptoms which can be better explained
by another psychiatric or medical condition which an individual has are
not considered to be a symptom of ADHD for that person. In DSM-5,
subtypes were discarded and reclassified as presentations of the
disorder that change over time.
Symptoms
Presentations
DSM-5 and DSM-5-TR symptoms
ICD-11 symptoms
Inattention
Six or more of the following symptoms in children, and five or more
in adults, excluding situations where these symptoms are better
explained by another psychiatric or medical condition:
Frequently overlooks details or makes careless mistakes
Often has difficulty maintaining focus on one task or play activity
Often appears not to be listening when spoken to, including when there is no obvious distraction
Frequently does not finish following instructions, failing to complete tasks
Often struggles to organise tasks and activities, to meet deadlines, and to keep belongings in order
Is frequently reluctant to engage in tasks which require sustained attention
Frequently loses items required for tasks and activities
Is frequently easily distracted by extraneous stimuli, including thoughts in adults and older teenagers
Often forgets daily activities, or is forgetful while completing them.
Multiple symptoms of inattention that directly negatively impact
occupational, academic or social functioning. Symptoms may not be
present when engaged in highly stimulating tasks with frequent rewards.
Symptoms are generally from the following clusters:
Struggles to maintain focus on tasks that aren't highly
stimulating/rewarding or that require continuous effort; details are
often missed, and careless mistakes are frequent in school and work
tasks; tasks are often abandoned before they are completed.
Easily distracted (including by own thoughts); may not listen when spoken to; frequently appears to be lost in thought
Often loses things; is forgetful and disorganised in daily activities.
The individual may also meet the criteria for hyperactivity-impulsivity, but the inattentive symptoms are predominant.
Hyperactivity-Impulsivity
Six or more of the following symptoms in children, and five or more
in adults, excluding situations where these symptoms are better
explained by another psychiatric or medical condition:
Is often fidgeting or squirming in seat
Frequently has trouble sitting still during dinner, class, in meetings, etc.
Frequently runs around or climbs in inappropriate situations. In adults and teenagers, this may be present only as restlessness.
Often cannot quietly engage in leisure activities or play
Frequently seems to be "on the go" or appears uncomfortable when not in motion
Often talks excessively
Often answers a question before it is finished, or finishes people's sentences
Often struggles to wait their turn, including waiting in lines
Frequently interrupts or intrudes, including into others'
conversations or activities, or by using people's things without asking.
Multiple symptoms of hyperactivity/impulsivity that directly
negatively impact occupational, academic or social functioning.
Typically, these tend to be most apparent in environments with structure
or which require self-control. Symptoms are generally from the
following clusters:
Excessive motor activity; struggles to sit still, often leaving
their seat; prefers to run about; in younger children, will fidget when
attempting to sit still; in adolescents and adults, a sense of physical
restlessness or discomfort with being quiet and still.
Talks too much; struggles to quietly engage in activities.
Blurts out answers or comments; struggles to wait their turn in
conversation, games, or activities; will interrupt or intrude on
conversations or games.
A lack of forethought or consideration of consequences when making
decisions or taking action, instead tending to act immediately (e.g.,
physically dangerous behaviours including reckless driving; impulsive
decisions).
The individual may also meet the criteria for inattention, but the hyperactive-impulsive symptoms are predominant.
Combined
Meet the criteria for both inattentive and hyperactive-impulsive ADHD.
Criteria are met for both inattentive and hyperactive-impulsive ADHD, with neither clearly predominating.
Girls and women with ADHD tend to display fewer hyperactivity and
impulsivity symptoms but more symptoms of inattention and
distractibility.
Symptoms are expressed differently and more subtly as the individual ages.
Hyperactivity tends to become less overt with age and turns into inner
restlessness, difficulty relaxing or remaining still, talkativeness or
constant mental activity in teens and adults with ADHD.
Impulsivity in adulthood may appear as thoughtless behaviour,
impatience, irresponsible spending and sensation-seeking behaviours,
while inattention may appear as becoming easily bored, difficulty with
organization, remaining on task and making decisions, and sensitivity to
stress.
Although not listed as an official symptom, emotional dysregulation or mood lability is generally understood to be a common symptom of ADHD. People with ADHD of all ages are more likely to have problems with social skills, such as social interaction and forming and maintaining friendships. This is true for all presentations. About half of children and adolescents with ADHD experience social rejection
by their peers compared to 10–15% of non-ADHD children and adolescents.
People with attention deficits are prone to having difficulty
processing verbal and nonverbal language which can negatively affect
social interaction. They may also drift off during conversations, miss
social cues, and have trouble learning social skills.
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.
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.
Comorbidities
Psychiatric comorbidities
In children, ADHD occurs with other disorders about two-thirds of the time.
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. 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. Intellectual disabilities and Tourette's syndrome 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.
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. It is characterised by aggression, destruction of property, deceitfulness, theft and violations of rules. 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.
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.
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. Melatonin is sometimes used in children who have sleep onset insomnia. Restless legs syndrome has been found to be more common in those with ADHD and is often due to iron deficiency anemia. 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.This is most commonly seen with alcohol or cannabis.
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. Other psychiatric conditions include reactive attachment disorder, 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. 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.
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.
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).
Some non-psychiatric conditions are also comorbidities of ADHD. This includes epilepsy, a neurological condition characterised by recurrent seizures. 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 in ADHD patients over the lifespan. 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 disordercomorbidities.
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. 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. 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. 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. 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.
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. 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. 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. 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.
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). 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. 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, 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.
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.
There is no clear data on whether there is a direct relationship
between ADHD and suicidality, or whether ADHD increases suicide risk
through comorbidities.
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. Their reduced size, functional connectivity, and activation contribute
to the pathophysiology of ADHD, as well as imbalances in the
noradrenergic and dopaminergic systems that mediate these brain regions.
Genetic factors play an important role; ADHD has a heritability
rate of 70-80%. The remaining 20-30% of variance is mediated by de-novo
mutations and non-shared environmental factors that provide for or
produce brain injuries; there is no significant contribution of the
rearing family and social environment. Very rarely, ADHD can also be the result of abnormalities in the chromosomes.
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.
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.
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.
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 siblings of children with ADHD are three to four times more likely
to develop the disorder than siblings of children without the disorder.
The association of maternal smoking observed in large population
studies disappears after adjusting for family history of ADHD, which
indicates that the association between maternal smoking during pregnancy
and ADHD is due to familial or genetic factors that increase the risk
for the confluence of smoking and ADHD.
ADHD presents with reduced size, functional connectivity and activation as well as low noradrenergic and dopaminergic functioning in brain regions and networks crucial for executive functioning and self-regulation. Typically, a number of genes are involved, many of which directly affect brain functioning and neurotransmission. Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH.Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF. A common variant of a gene called latrophilin 3
is estimated to be responsible for about 9% of cases and when this
variant is present, people are particularly responsive to stimulant
medication. The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioural phenotypes, including ADHD symptoms reflecting split attention. The DRD4 gene is both linked to novelty seeking and ADHD. The genes GFOD1 and CDH13 show strong genetic associations with ADHD. CDH13's association with ASD, schizophrenia, bipolar disorder, and depression make it an interesting candidate causative gene. Another candidate causative gene that has been identified is ADGRL3. In zebrafish, knockout of this gene causes a loss of dopaminergic function in the ventral diencephalon and the fish display a hyperactive/impulsive phenotype.
For genetic variation to be used as a tool for diagnosis, more validating studies need to be performed. However, smaller studies have shown that genetic polymorphisms in genes related to catecholaminergic neurotransmission or the SNARE complex of the synapse can reliably predict a person's response to stimulant medication.
Rare genetic variants show more relevant clinical significance as their
penetrance (the chance of developing the disorder) tends to be much
higher.
However their usefulness as tools for diagnosis is limited as no single
gene predicts ADHD. ASD shows genetic overlap with ADHD at both common
and rare levels of genetic variation.
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 or symptoms like it. Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD. 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 zosterencephalitis, rubella, enterovirus 71). At least 30% of children with a traumatic brain injury later develop ADHD and about 5% of cases are due to brain damage.
Some studies suggest that in a small number of children, artificial food dyes or preservatives may be associated with an increased prevalence of ADHD or ADHD-like symptoms, but the evidence is weak and may apply to only children with food sensitivities. The European Union has put in place regulatory measures based on these concerns. In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.
Individuals with hypokalemic sensory overstimulation
are sometimes diagnosed as having ADHD, raising the possibility that a
subtype of ADHD has a cause that can be understood mechanistically and
treated in a novel way. The sensory overload is treatable with oral potassium gluconate.
Research does not support popular beliefs that ADHD is caused by eating
too much refined sugar, watching too much television, bad parenting,
poverty or family chaos; however, they might worsen ADHD symptoms in
certain people.
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.
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. Behaviours typical of ADHD occur more commonly in children who have experienced violence and emotional abuse.
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. The dopamine and norepinephrine pathways that originate in the ventral tegmental area and locus coeruleus project to diverse regions of the brain and govern a variety of cognitive processes. The dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum are directly responsible for modulating executive function (cognitive control of behaviour), motivation, reward perception, and motor function; these pathways are known to play a central role in the pathophysiology of ADHD. Larger models of ADHD with additional pathways have been proposed.
Brain structure
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. The posterior parietal cortex
also shows thinning in individuals with ADHD compared to controls.
Other brain structures in the prefrontal-striatal-cerebellar and
prefrontal-striatal-thalamic circuits have also been found to differ
between people with and without ADHD.
The subcortical volumes of the accumbens, amygdala, caudate, hippocampus, and putamen appears smaller in individuals with ADHD compared with controls.
Structural MRI studies have also revealed differences in white matter,
with marked differences in inter-hemispheric asymmetry between ADHD and
typically developing youths.
Functional MRI
(fMRI) studies have revealed a number of differences between ADHD and
control brains. Mirroring what is known from structural findings, fMRI
studies have 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.
Hemispheric lateralization processes have also been postulated as being
implicated in ADHD, but empiric results showed contrasting evidence on
the topic.
Neurotransmitter pathways
Previously, it had been suggested that the elevated number of dopamine transporters
in people with ADHD was part of the pathophysiology, but it appears the
elevated numbers may be due to adaptation following exposure to
stimulant medication. Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system. ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems. There may additionally be abnormalities in serotonergic, glutamatergic, or cholinergic pathways.
Executive function and motivation
ADHD arises from a core deficit in executive functions (e.g., attentional control, inhibitory control, and working memory), which are a set of cognitive processes that are required to successfully select and monitor behaviours that facilitate the attainment of one's chosen goals.
The executive function impairments that occur in ADHD individuals
result in problems with staying organised, time keeping, excessive procrastination, maintaining concentration, paying attention, ignoring distractions, regulating emotions, and remembering details. People with ADHD appear to have unimpaired long-term memory, and
deficits in long-term recall appear to be attributed to impairments in
working memory.
Due to the rates of brain maturation and the increasing demands for
executive control as a person gets older, ADHD impairments may not fully
manifest themselves until adolescence or even early adulthood.
Conversely, brain maturation trajectories, potentially exhibiting
diverging longitudinal trends in ADHD, may support a later improvement
in executive functions after reaching adulthood.
ADHD has also been associated with motivational deficits in
children. Children with ADHD often find it difficult to focus on
long-term over short-term rewards, and exhibit impulsive behaviour for
short-term rewards.
Paradoxical reaction to neuroactive substances
Another sign of the structurally altered signal processing in the
central nervous system in this group of people is the conspicuously
common paradoxical reaction (c. 10–20%
of patients). These are unexpected reactions in the opposite direction
as with a normal effect, or otherwise significant different reactions.
These are reactions to neuroactive substances such as local anesthetic at the dentist, sedative, caffeine, antihistamine, weak neuroleptics and central and peripheral painkillers. Since the causes of paradoxical reactions
are at least partly genetic, it may be useful in critical situations,
for example before operations, to ask whether such abnormalities may
also exist in family members.
Diagnosis
ADHD is diagnosed by an assessment of a person's behavioural and
mental development, including ruling out the effects of drugs,
medications, and other medical or psychiatric problems as explanations
for the symptoms. 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 standardized
rating scales and input from multiple informants across various
settings.
The diagnosis of ADHD has been criticised as being subjective because it
is not based on a biological test. The International Consensus
Statement on ADHD concluded that this criticism is unfounded, on the
basis that ADHD meets standard criteria for validity of a mental
disorder established by Robins and Guze. They attest that the disorder
is considered valid because: 1) well-trained professionals in a variety
of settings and cultures agree on its presence or absence using
well-defined criteria and 2) the diagnosis is useful for predicting a)
additional problems the patient may have (e.g., difficulties learning in
school); b) future patient outcomes (e.g., risk for future drug abuse);
c) response to treatment (e.g., medications and psychological
treatments); and d) features that indicate a consistent set of causes
for the disorder (e.g., findings from genetics or brain imaging), and
that professional associations have endorsed and published guidelines
for diagnosing ADHD.
The most commonly used rating scales for diagnosing ADHD are the Achenbach System of Empirically Based Assessment (ASEBA) and include the Child Behavior Checklist (CBCL)
used for parents to rate their child's behaviour, the Youth Self Report
Form (YSR) used for children to rate their own behaviour, and the
Teacher Report Form (TRF) used for teachers to rate their pupil's
behaviour. Additional rating scales that have been used alone or in
combination with other measures to diagnose ADHD include the Behavior
Assessment System for Children (BASC), Behavior Rating Inventory of
Executive Function - Second Edition (BRIEF2), Revised Conners Rating Scale (CRS-R),
Conduct-Hyperactive-Attention Problem-Oppositional Symptom scale
(CHAOS), Developmental Behavior Checklist Hyperactivity Index (DBC-HI), Parent Disruptive Behavior Disorder Ratings Scale (DBDRS),
Diagnostic Infant and Preschool Assessment (DIPA-L), Pediatric Symptom
Checklist (PSC), Social Communication Questionnaire (SCQ), Social
Responsiveness Scale (SRS), Strengths and Weaknesses of ADHD Symptoms
and Normal Behavior Rating Scale (SWAN). and the Vanderbilt ADHD diagnostic rating scale.
The ASEBA, BASC, CHAOS, CRS, and Vanderbilt diagnostic rating
scales allow for both parents and teachers as raters in the diagnosis of
childhood and adolescent ADHD. Adolescents may also self report their
symptoms using self report scales from the ASEBA, SWAN, and the Dominic
Interactive for Adolescents-Revised (DIA-R). Self-rating scales, such as the ADHD rating scale and the Vanderbilt ADHD diagnostic rating scale, are used in the screening and evaluation of ADHD.
Based on a 2024 systematic literature review and meta analysis
commissioned by the Patient-Centered Outcomes Research Institute
(PCORI), rating scales based on parent report, teacher report, or
self-assessment from the adolescent have high internal consistency as a
diagnostic tool meaning that the items within the scale are highly
interrelated. The reliability of the scales between raters (i.e. their
degree of agreement) however is poor to moderate making it important to
include information from multiple raters to best inform a diagnosis.
Imaging studies of the brain do not give consistent results
between individuals; thus, they are only used for research purposes and
not a diagnosis. Electroencephalography is not accurate enough to make an ADHD diagnosis. A 2024 systematic review concluded that the use of biomarkers such as blood or urine samples, electroencephalogram (EEG) markers, and neuroimaging such as MRIs,
in diagnosis for ADHD remains unclear; studies showed great
variability, did not assess test-retest reliability, and were not
independently replicable.
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.
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) out of nine long-term (lasting at least six months) symptoms of inattention, hyperactivity–impulsivity, or both.
To be considered, several symptoms must have appeared by the age of six
to twelve and occur in more than one environment (e.g. at home and at
school or work). The symptoms must be inappropriate for a child of that
age and there must be clear evidence that they are causing impairment in multiple domains of life.
The DSM-5 and the DSM-5-TR also provide two diagnoses for
individuals who have symptoms of ADHD but do not entirely meet the
requirements. Other Specified ADHD allows the clinician to describe why the individual does not meet the criteria, whereas Unspecified ADHD is used where the clinician chooses not to describe the reason.
International Classification of Diseases
In the eleventh revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-11) by the World Health Organization, the disorder is classified as Attention deficit hyperactivity disorder (code 6A05). The defined subtypes are predominantly inattentive presentation (6A05.0); predominantly hyperactive-impulsive presentation(6A05.1); and combined presentation
(6A05.2). However, the ICD-11 includes two residual categories for
individuals who do not entirely match any of the defined subtypes: other specified presentation (6A05.Y) where the clinician includes detail on the individual's presentation; and presentation unspecified (6A05.Z) where the clinician does not provide detail.
In the tenth revision (ICD-10), the symptoms of hyperkinetic disorder were analogous to ADHD in the ICD-11. When a conduct disorder (as defined by ICD-10) is present, the condition was referred to as hyperkinetic conduct disorder. Otherwise, the disorder was classified as disturbance of activity and attention, other hyperkinetic disorders or hyperkinetic disorders, unspecified. The latter was sometimes referred to as hyperkinetic syndrome.
Social construct theory
The social construct theory of ADHD
suggests that, because the boundaries between normal and abnormal
behaviour are socially constructed (i.e. jointly created and validated
by all members of society, and in particular by physicians,
parents, teachers, and others), it then follows that subjective
valuations and judgements determine which diagnostic criteria are used
and thus, the number of people affected. Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and then given a name".
Adults 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.
Worldwide, it is estimated that 2.58% of adults have persistent
ADHD (where the individual currently meets the criteria and there is
evidence of childhood onset), and 6.76% of adults have symptomatic ADHD
(meaning that they currently meet the criteria for ADHD, regardless of
childhood onset). In 2020, this was 139.84 million and 366.33 million affected adults respectively.
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. As of 2010, most adults remain untreated. Many adults with ADHD without diagnosis and treatment have a disorganised life, and some use non-prescribed drugs or alcohol as a coping mechanism. Other problems may include relationship and job difficulties, and an increased risk of criminal activities. Associated mental health problems include depression, anxiety disorders, and learning disabilities.
Some ADHD symptoms in adults differ from those seen in children.
While children with ADHD may climb and run about excessively, adults may
experience an inability to relax, or may talk excessively in social
situations. Adults with ADHD may start relationships impulsively, display sensation-seeking behaviour, and be short-tempered. Addictive behaviour such as substance abuse and gambling are common. This led to those who presented differently as they aged having outgrown the DSM-IV criteria.
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.
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.
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 ODD, intermittent explosive
disorder, and other neurodevelopmental disorders (such as stereotypic
movement disorder and Tourette's disorder), in addition to specific
learning disorder, intellectual developmental disorder, ASD, reactive
attachment disorder, anxiety disorders, depressive disorders, bipolar
disorder, disruptive mood dysregulation disorder, substance use
disorder, personality disorders, psychotic disorders, medication-induced
symptoms, and neurocognitive disorders. Many but not all of these are
also common comorbidities of ADHD. The DSM-5-TR also suggests post-traumatic stress disorder.
Primary sleep disorders may affect attention and behaviour and the symptoms of ADHD may affect sleep. 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 hyperactivity and
inattentiveness. Obstructive sleep apnea can also cause ADHD-type symptoms.
The management of ADHD typically involves counseling
or medications, either alone or in combination. While there are various
options of treatment to improve ADHD symptoms, medication therapies
substantially improves long-term outcomes, and while completely
eliminating some elevated risks such as obesity, they do come with some risks of adverse events. 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. Medications are the most effective treatment, and any side effects are typically mild and easy to resolve although any improvements will be reverted if medication is ceased. ADHD stimulants also improve persistence and task performance in children with ADHD.
To quote one systematic review, "recent evidence from observational and
registry studies indicates that pharmacological treatment of ADHD is
associated with increased achievement and decreased absenteeism at
school, a reduced risk of trauma-related emergency hospital visits,
reduced risks of suicide and attempted suicide, and decreased rates of
substance abuse and criminality".
Data also suggest that combining medication with CBT is a good idea:
although CBT is substantially less effective, it can help address
problems that reside after medication has been optimised.
The nature and range of desirable endpoints of ADHD treatment vary among diagnostic standards for ADHD. 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.
Behavioural therapies
There is good evidence for the use of behavioural therapies in ADHD. They are the recommended first-line treatment in those who have mild symptoms or who are preschool-aged. Psychological therapies used include: psychoeducational input, behavior therapy, cognitive behavioral therapy, interpersonal psychotherapy, family therapy, school-based interventions, social skills training, behavioural peer intervention, organization training, and parent management training. Neurofeedback
has greater treatment effects than non-active controls for up to 6
months and possibly a year following treatment, and may have treatment
effects comparable to active controls (controls proven to have a
clinical effect) over that time period.
Despite efficacy in research, there is insufficient regulation of
neurofeedback practice, leading to ineffective applications and false
claims regarding innovations. Parent training may improve a number of behavioural problems including oppositional and non-compliant behaviours.
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 pediatric STARS-ADHD randomized, 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 pediatric open-label study, STARS-Adjunct, published in Nature Portfolio's npj Digital Medicine
evaluated AKL-T01 as an adjunctive treatment for children with ADHD who
were either on stimulant medication or not on stimulant
pharmacotherapy. Results showed improvements in ADHD-related impairment
(measured by the Impairment Rating Scale) and ADHD symptoms after 4
weeks of treatment, with effects persisting during a 4-week pause and
further improving with an additional treatment period. Notably, the magnitude of the measured improvement was similar for children both on and off stimulants. In 2020, AKL-T01 received marketing authorization for pediatric ADHD from the FDA, becoming "the first game-based therapeutic granted marketing authorization by the FDA for any type of condition."
In addition to pediatric populations, a 2023 study in the Journal of the American Academy of Child & Adolescent Psychiatry
investigated the efficacy and safety of AKL-T01 in adults with ADHD.
After six weeks of at-home treatment with AKL-T01, participants showed
significant improvements in objective measures of attention (TOVA - Attention Comparison Score), reported ADHD symptoms (ADHD-RS-IV inattention subscale and total score), and reported quality of life (AAQoL). The magnitude of improvement in attention was nearly seven times greater than that reported in pediatric trials. The treatment was well-tolerated, with high compliance and no serious adverse events.
Medication
The medications for ADHD appear to alleviate symptoms via their
effects on the pre-frontal executive, striatal and related regions and
networks in the brain; usually by increasing neurotransmission of norepinephrine and dopamine.
Stimulants
Methylphenidate and amphetamine or its derivatives are often first-line treatments for ADHD.
About 70 per cent respond to the first stimulant tried and as few as 10
per cent respond to neither amphetamines nor methylphenidate. Stimulants may also reduce the risk of unintentional injuries in children with ADHD. 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.
Clinical guidelines internationally are also consistent in approving
the safety and efficacy of methylphenidate and recommending it as a
first-line treatment for the disorder.
Safety and efficacy data have been reviewed extensively by
medical regulators (e.g., the US Food and Drug Administration and the
European Medicines Agency), the developers of evidence-based
international guidelines (e.g., the UK National Institute for Health and
Care Excellence and the American Academy of Pediatrics), and government
agencies who have endorsed these guidelines (e.g., the Australian
National Health and Medical Research Council). These professional groups
unanimously conclude, based on the scientific evidence, that
methylphenidate is safe and effective and should be considered as a
first-line treatment for ADHD.
The likelihood of developing insomnia for ADHD patients taking stimulants has been measured at between 11 and 45 per cent for different medications, 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. Stimulant psychosis and mania
are rare at therapeutic doses, appearing to occur in approximately 0.1%
of individuals, within the first several weeks after starting
amphetamine therapy. 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. Treatment with stimulants is either protective against substance abuse or has no effect.
The majority of studies on nicotine and other nicotinic agonists as treatments for ADHD have shown favorable results; however, no nicotinic drug has been approved for ADHD treatment. 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. It may be prescribed off-label to treat ADHD.
Non-stimulants
Two non-stimulant medications, atomoxetine and viloxazine, are approved by the FDA and in other countries for the treatment of ADHD.
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.
Atomoxetine alleviates ADHD symptoms through norepinephrine reuptake
and by indirectly increasing dopamine in the pre-frontal cortex, sharing 70-80% of the brain regions with stimulants in their produced effects. Atomoxetine has been shown to significantly improve academic performance. 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.
Analyses of clinical trial data suggests that viloxazine is about as effective as atomoxetine and methylphenidate but with fewer side effects.
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.Underdosing of stimulants can occur, and can result in a lack of response or later loss of effectiveness.
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.
The conclusion by the International Consensus Statement is based on two
meta-analyses: one of 10 studies with 300 children and the other of 15
studies and 668 participants, which showed that exercise yields no
statistically significant reductions on ADHD symptoms. A 2024 systematic
review and meta analysis commissioned by the Patient-Centered Outcomes
Research Institute (PCORI) identified seven studies on the effectiveness
of physical exercise for treating ADHD symptoms.
The type and amount of exercise varied widely across studies from
martial arts interventions to treadmill training, to table tennis or
aerobic exercise. Effects reported were not replicated, causing the
authors to conclude that there is insufficient evidence that exercise
intervention is an effective form of treatment for ADHD symptoms.
Diet
Dietary modifications are not recommended as of 2019 by the American Academy of Pediatrics, the National Institute for Health and Care Excellence, or the Agency for Healthcare Research and Quality due to insufficient evidence.
A 2013 meta-analysis found less than a third of children with ADHD see some improvement in symptoms with free fatty acid supplementation or decreased consumption of artificial food colouring.
These benefits may be limited to children with food sensitivities or
those who are simultaneously being treated with ADHD medications. This review also found that evidence does not support removing other foods from the diet to treat ADHD. A 2014 review found that an elimination diet results in a small overall benefit in a minority of children, such as those with allergies. 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
ADHD persists into adulthood in about 30–50% of cases.
Those affected are likely to develop coping mechanisms as they mature,
thus compensating to some extent for their previous symptoms. Children with ADHD have a higher risk of unintentional injuries. Effects of medication on functional impairment and quality of life (e.g. reduced risk of accidents) have been found across multiple domains. Rates of smoking among those with ADHD are higher than in the general population at about 40%.
About 30–50% of people diagnosed in childhood continue to have ADHD in adulthood, with 2.58% of adults estimated to have ADHD which began in childhood. In adults, hyperactivity is usually replaced by inner restlessness, and adults often develop coping
skills to compensate for their impairments. The condition can be
difficult to tell apart from other conditions, as well as from high
levels of activity within the range of normal behaviour. ADHD has a
negative impact on patient health-related quality of life that may be
further exacerbated by, or may increase the risk of, other psychiatric
conditions such as anxiety and depression. Individuals with ADHD may also face misconceptions and stigma.
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%.
Percentage of people 4–17 ever diagnosed in the US as of 2011
ADHD is estimated to affect about 6–7% of people aged 18 and under when diagnosed via the DSM-IV criteria. When diagnosed via the ICD-10 criteria, rates in this age group are estimated around 1–2%. 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.) As of 2019, 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,
although the disorder is overlooked in girls or diagnosed in later life
because their symptoms sometimes differ from diagnostic criteria. 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.
Studies from multiple countries have reported that children born
closer to the start of the school year are more frequently diagnosed
with and medicated for ADHD than their older classmates.
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.
Rates of diagnosis and treatment have increased in both the
United Kingdom and the United States since the 1970s. Prior to 1970, it
was rare for children to be diagnosed with ADHD, while in the 1970s
rates were about 1%. This is believed to be primarily due to changes in how the condition is diagnosed and how readily people are willing to treat it with medications rather than a true change in incidence.
With widely differing rates of diagnosis across countries, states
within countries, races, and ethnicities, some suspect factors other
than symptoms of ADHD are playing a role in diagnosis, such as cultural
norms.
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
color. Due to ADHD's subjectively determined symptoms, medical
professionals may diagnose individuals based on stereotyped behaviour or
misdiagnose due to cultural differences in symptom presentation.
History
Timeline of ADHD diagnostic criteria, prevalence, and treatment
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: minimal brain dysfunction in the DSM-I (1952), hyperkinetic reaction of childhood in the DSM-II (1968), and attention-deficit disorder with or without hyperactivity in the DSM-III (1980).
In 1987, this was changed to ADHD in the DSM-III-R, and in 1994 the
DSM-IV in split the diagnosis into three subtypes: ADHD inattentive
type, ADHD hyperactive-impulsive type, and ADHD combined type. These terms were kept in the DSM-5 in 2013 and in the DSM-5-TR in 2022. Prior to the DSM, terms included minimal brain damage in the 1930s.
ADHD, its diagnosis, and its treatment have been controversial since the 1970s. Positions range from the view that ADHD is within the normal range of behaviour to the hypothesis that ADHD is a genetic condition. Other areas of controversy include the use of stimulant medications in children, the method of diagnosis, and the possibility of overdiagnosis.
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.
In 1934, Benzedrine became the first amphetamine medication approved for use in the United States. Methylphenidate was introduced in the 1950s, and enantiopure dextroamphetamine in the 1970s. The use of stimulants to treat ADHD was first described in 1937.
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. These measurements could serve as diagnostic biomarkers for
ADHD, but more research is needed to establish their diagnostic utility.
Urinary and blood plasma
phenethylamine concentrations are lower in ADHD individuals relative to
controls. 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.
