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Attention-Deficit/Hyperactivity Disorder

What is adhd.

Attention-deficit/hyperactivity disorder (ADHD) is marked by an ongoing pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. People with ADHD experience an ongoing pattern of the following types of symptoms:

  • Inattention means a person may have difficulty staying on task, sustaining focus, and staying organized, and these problems are not due to defiance or lack of comprehension.
  • Hyperactivity means a person may seem to move about constantly, including in situations when it is not appropriate, or excessively fidgets, taps, or talks. In adults, hyperactivity may mean extreme restlessness or talking too much.
  • Impulsivity means a person may act without thinking or have difficulty with self-control. Impulsivity could also include a desire for immediate rewards or the inability to delay gratification. An impulsive person may interrupt others or make important decisions without considering long-term consequences.

What are the signs and symptoms of ADHD?

Some people with ADHD mainly have symptoms of inattention. Others mostly have symptoms of hyperactivity-impulsivity. Some people have both types of symptoms.

Many people experience some inattention, unfocused motor activity, and impulsivity, but for people with ADHD, these behaviors:

  • Are more severe
  • Occur more often
  • Interfere with or reduce the quality of how they function socially, at school, or in a job

Inattention

People with symptoms of inattention may often:

  • Overlook or miss details and make seemingly careless mistakes in schoolwork, at work, or during other activities
  • Have difficulty sustaining attention during play or tasks, such as conversations, lectures, or lengthy reading
  • Not seem to listen when spoken to directly
  • Find it hard to follow through on instructions or finish schoolwork, chores, or duties in the workplace, or may start tasks but lose focus and get easily sidetracked
  • Have difficulty organizing tasks and activities, doing tasks in sequence, keeping materials and belongings in order, managing time, and meeting deadlines
  • Avoid tasks that require sustained mental effort, such as homework, or for teens and older adults, preparing reports, completing forms, or reviewing lengthy papers
  • Lose things necessary for tasks or activities, such as school supplies, pencils, books, tools, wallets, keys, paperwork, eyeglasses, and cell phones
  • Be easily distracted by unrelated thoughts or stimuli
  • Be forgetful in daily activities, such as chores, errands, returning calls, and keeping appointments

Hyperactivity-impulsivity

People with symptoms of hyperactivity-impulsivity may often:

  • Fidget and squirm while seated
  • Leave their seats in situations when staying seated is expected, such as in the classroom or the office
  • Run, dash around, or climb at inappropriate times or, in teens and adults, often feel restless
  • Be unable to play or engage in hobbies quietly
  • Be constantly in motion or on the go, or act as if driven by a motor
  • Talk excessively
  • Answer questions before they are fully asked, finish other people’s sentences, or speak without waiting for a turn in a conversation
  • Have difficulty waiting one’s turn
  • Interrupt or intrude on others, for example in conversations, games, or activities

Primary care providers sometimes diagnose and treat ADHD. They may also refer individuals to a mental health professional, such as a psychiatrist or clinical psychologist, who can do a thorough evaluation and make an ADHD diagnosis.

For a person to receive a diagnosis of ADHD, the symptoms of inattention and/or hyperactivity-impulsivity must be chronic or long-lasting, impair the person’s functioning, and cause the person to fall behind typical development for their age. Stress, sleep disorders, anxiety, depression, and other physical conditions or illnesses can cause similar symptoms to those of ADHD. Therefore, a thorough evaluation is necessary to determine the cause of the symptoms.

Most children with ADHD receive a diagnosis during the elementary school years. For an adolescent or adult to receive a diagnosis of ADHD, the symptoms need to have been present before age 12.

ADHD symptoms can appear as early as between the ages of 3 and 6 and can continue through adolescence and adulthood. Symptoms of ADHD can be mistaken for emotional or disciplinary problems or missed entirely in children who primarily have symptoms of inattention, leading to a delay in diagnosis. Adults with undiagnosed ADHD may have a history of poor academic performance, problems at work, or difficult or failed relationships.

ADHD symptoms can change over time as a person ages. In young children with ADHD, hyperactivity-impulsivity is the most predominant symptom. As a child reaches elementary school, the symptom of inattention may become more prominent and cause the child to struggle academically. In adolescence, hyperactivity seems to lessen and symptoms may more likely include feelings of restlessness or fidgeting, but inattention and impulsivity may remain. Many adolescents with ADHD also struggle with relationships and antisocial behaviors. Inattention, restlessness, and impulsivity tend to persist into adulthood.

What are the risk factors of ADHD?

Researchers are not sure what causes ADHD, although many studies suggest that genes play a large role. Like many other disorders, ADHD probably results from a combination of factors. In addition to genetics, researchers are looking at possible environmental factors that might raise the risk of developing ADHD and are studying how brain injuries, nutrition, and social environments might play a role in ADHD.

ADHD is more common in males than females, and females with ADHD are more likely to primarily have inattention symptoms. People with ADHD often have other conditions, such as learning disabilities, anxiety disorder, conduct disorder, depression, and substance use disorder.

How is ADHD treated?

While there is no cure for ADHD, currently available treatments may reduce symptoms and improve functioning. Treatments include medication, psychotherapy, education or training, or a combination of treatments.

For many people, ADHD medications reduce hyperactivity and impulsivity and improve their ability to focus, work, and learn. Sometimes several different medications or dosages must be tried before finding the right one that works for a particular person. Anyone taking medications must be monitored closely by their prescribing doctor.

Stimulants. The most common type of medication used for treating ADHD is called a “stimulant.” Although it may seem unusual to treat ADHD with a medication that is considered a stimulant, it works by increasing the brain chemicals dopamine and norepinephrine, which play essential roles in thinking and attention.

Under medical supervision, stimulant medications are considered safe. However, like all medications, they can have side effects, especially when misused or taken in excess of the prescribed dose, and require an individual’s health care provider to monitor how they may be reacting to the medication.

Non-stimulants. A few other ADHD medications are non-stimulants. These medications take longer to start working than stimulants, but can also improve focus, attention, and impulsivity in a person with ADHD. Doctors may prescribe a non-stimulant: when a person has bothersome side effects from stimulants, when a stimulant was not effective, or in combination with a stimulant to increase effectiveness.

Although not approved by the U.S. Food and Drug Administration (FDA) specifically for the treatment of ADHD, some antidepressants are used alone or in combination with a stimulant to treat ADHD. Antidepressants may help all of the symptoms of ADHD and can be prescribed if a patient has bothersome side effects from stimulants. Antidepressants can be helpful in combination with stimulants if a patient also has another condition, such as an anxiety disorder, depression, or another mood disorder. Non-stimulant ADHD medications and antidepressants may also have side effects.

Doctors and patients can work together to find the best medication, dose, or medication combination. To find the latest information about medications, talk to a health care provider and visit the FDA website  .

Psychotherapy and psychosocial interventions

Several specific psychosocial interventions have been shown to help individuals with ADHD and their families manage symptoms and improve everyday functioning.

For school-age children, frustration, blame, and anger may have built up within a family before a child is diagnosed. Parents and children may need specialized help to overcome negative feelings. Mental health professionals can educate parents about ADHD and how it affects a family. They also will help the child and his or her parents develop new skills, attitudes, and ways of relating to each other.

All types of therapy for children and teens with ADHD require parents to play an active role. Psychotherapy that includes only individual treatment sessions with the child (without parent involvement) is not effective for managing ADHD symptoms and behavior. This type of treatment is more likely to be effective for treating symptoms of anxiety or depression that may occur along with ADHD.

Behavioral therapy is a type of psychotherapy that aims to help a person change their behavior. It might involve practical assistance, such as help organizing tasks or completing schoolwork, or working through emotionally difficult events. Behavioral therapy also teaches a person how to:

  • Monitor their own behavior
  • Give oneself praise or rewards for acting in a desired way, such as controlling anger or thinking before acting

Parents, teachers, and family members also can give feedback on certain behaviors and help establish clear rules, chore lists, and structured routines to help a person control their behavior. Therapists may also teach children social skills, such as how to wait their turn, share toys, ask for help, or respond to teasing. Learning to read facial expressions and the tone of voice in others, and how to respond appropriately can also be part of social skills training.

Cognitive behavioral therapy helps a person learn how to be aware and accepting of one’s own thoughts and feelings to improve focus and concentration. The therapist also encourages the person with ADHD to adjust to the life changes that come with treatment, such as thinking before acting, or resisting the urge to take unnecessary risks.

Family and marital therapy can help family members and spouses find productive ways to handle disruptive behaviors, encourage behavior changes, and improve interactions with the person with ADHD.

Parenting skills training (behavioral parent management training) teaches parents skills for encouraging and rewarding positive behaviors in their children. Parents are taught to use a system of rewards and consequences to change a child’s behavior, to give immediate and positive feedback for behaviors they want to encourage, and to ignore or redirect behaviors they want to discourage.

Specific behavioral classroom management interventions and/or academic accommodations for children and teens have been shown to be effective for managing symptoms and improving functioning at school and with peers. Interventions may include behavior management plans or teaching organizational or study skills. Accommodations may include preferential seating in the classroom, reduced classwork load, or extended time on tests and exams. The school may provide accommodations through what is called a 504 Plan or, for children who qualify for special education services, an Individualized Education Plan (IEP). 

To learn more about the Individuals with Disabilities Education Act (IDEA), visit the  U.S. Department of Education’s IDEA website  .

Stress management techniques can benefit parents of children with ADHD by increasing their ability to deal with frustration so that they can respond calmly to their child’s behavior.

Support groups can help parents and families connect with others who have similar problems and concerns. Groups often meet regularly to share frustrations and successes, to exchange information about recommended specialists and strategies, and to talk with experts.

The National Resource Center on ADHD, a program of Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD®) supported by the Centers for Disease Control and Prevention (CDC), has information and many resources. You can reach this center online   or by phone at 1-866-200-8098.

Learn more about psychotherapy .

Tips to help kids and adults with ADHD stay organized

Parents and teachers can help kids with ADHD stay organized and follow directions with tools such as:

  • Keeping a routine and a schedule. Keep the same routine every day, from wake-up time to bedtime. Include times for homework, outdoor play, and indoor activities. Keep the schedule on the refrigerator or a bulletin board. Write changes on the schedule as far in advance as possible.
  • Organizing everyday items. Have a place for everything, (such as clothing, backpacks, and toys), and keep everything in its place.
  • Using homework and notebook organizers. Use organizers for school material and supplies. Stress to your child the importance of writing down assignments and bringing home necessary books.
  • Being clear and consistent. Children with ADHD need consistent rules they can understand and follow.
  • Giving praise or rewards when rules are followed. Children with ADHD often receive and expect criticism. Look for good behavior and praise it.

For adults:

A professional counselor or therapist can help an adult with ADHD learn how to organize their life with tools such as:

  • Keeping routines.
  • Making lists for different tasks and activities.
  • Using a calendar for scheduling events.
  • Using reminder notes.
  • Assigning a special place for keys, bills, and paperwork.
  • Breaking down large tasks into more manageable, smaller steps so that completing each part of the task provides a sense of accomplishment.

How can I find a clinical trial for ADHD?

Clinical trials are research studies that look at new ways to prevent, detect, or treat diseases and conditions. The goal of clinical trials is to determine if a new test or treatment works and is safe. Although individuals may benefit from being part of a clinical trial, participants should be aware that the primary purpose of a clinical trial is to gain new scientific knowledge so that others may be better helped in the future.

Researchers at NIMH and around the country conduct many studies with patients and healthy volunteers. We have new and better treatment options today because of what clinical trials uncovered years ago. Be part of tomorrow’s medical breakthroughs. Talk to your health care provider about clinical trials, their benefits and risks, and whether one is right for you.

To learn more or find a study, visit:

  • NIMH’s Clinical Trials webpage : Information about participating in clinical trials
  • Clinicaltrials.gov: Current Studies on ADHD  : List of clinical trials funded by the National Institutes of Health (NIH) being conducted across the country
  • Join a Study: Children - ADHD : List of studies being conducted on the NIH Campus in Bethesda, MD

Where can I learn more about ADHD?

Free brochures and shareable resources.

  • Attention-Deficit/Hyperactivity Disorder in Children and Teens: What You Need to Know : This brochure provides information about attention-deficit/hyperactivity disorder (ADHD) in children and teens including symptoms, how it is diagnosed, causes, treatment options, and helpful resources. Also available en español .
  • Attention-Deficit/Hyperactivity Disorder in Adults: What You Need to Know : This brochure provides information about attention-deficit/hyperactivity disorder (ADHD) in adults including symptoms, how ADHD is diagnosed, causes, treatment options, and resources to find help for yourself or someone else. Also available en español .
  • Shareable Resources on ADHD : These digital resources, including graphics and messages, can be used to spread the word about ADHD and help promote awareness and education in your community.
  • Mental Health Minute: ADHD : Take a mental health minute to learn about ADHD.
  • NIMH Expert Discusses Managing ADHD : Learn the signs, symptoms, and treatments of ADHD as well as tips for helping children and adolescents manage ADHD during the pandemic.

Federal resources

  • ADHD   : CDC offers fact sheets, infographics, and other resources about the signs, symptoms, and treatment of children with ADHD.
  • ADHD   : (MedlinePlus – also available  en español   .)

Research and statistics

  • Journal Articles   : This webpage provides information on references and abstracts from MEDLINE/PubMed (National Library of Medicine).
  • ADHD Statistics : This web page provides statistics about the prevalence and treatment of ADHD among children, adolescents, and adults.

Last Reviewed: September 2023

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  • v.15(2); 2013

Using Stimulants for Attention-Deficit/Hyperactivity Disorder: Clinical Approaches and Challenges

Clinical points.

  • ▪ Attention-deficit/hyperactivity disorder (ADHD) is a common disorder of children, adolescents, and adults; moreover, it coexists with a bevy of other psychiatric and medical disorders. Pharmacotherapy of ADHD with stimulants is a mainstay of evidence-based treatment for ADHD across the lifespan.
  • ▪ Stimulants have relatively few serious interactions with commonly prescribed medications.
  • ▪ Certain adverse effects of stimulants (eg, decreased appetite, insomnia) can be anticipated by virtue of their known pharmacologic properties, whereas others (eg, tics, mood changes, sudden death) are idiosyncratic.

Have you prescribed a stimulant and been concerned about the risk of substance misuse or diversion, the emergence of tics, or even sudden death? Have you been reluctant to prescribe stimulants for patients with attention-deficit/hyperactivity disorder (ADHD) and comorbid autism, bipolar disorder, or seizures for fear of exacerbating the underlying disorder? Have you felt confused or bewildered as the number of approved stimulant preparations has tripled over the past 15 years? In this article, we explore prescribing practices regarding stimulants for patients with ADHD and examine clinical concerns and challenges to safe and effective prescribing.

WHAT IS ADHD AND HOW IS IT DIAGNOSED?

ADHD is a cognitive and behavioral syndrome characterized by varying levels and expressions of deficits in attention and problem-solving, along with hyperactivity and impulsiveness. ADHD is a common childhood disorder; however, it often persists through adolescence into adulthood. Stimulants, a first-line treatment for this condition, are among the most effective and most studied psychotropic medications. As the diagnosis of ADHD in children and adults has increased over the past decade, the use of stimulants has also increased.

As DSM-IV-TR 1 criteria now stand, at least 6 of 9 symptoms of inattention must be present for the inattentive subtype diagnosis, at least 6 of 9 hyperactive/impulsive symptoms must be present for the hyperactive/impulsive subtype diagnosis, and at least 6 of 9 symptoms for both of the first 2 subtypes must be present for a combined subtype diagnosis. These symptoms must begin in childhood and be present in at least 2 settings (eg, school, work, or home).

Establishing a diagnosis of ADHD requires the synthesis of multiple sources of information. Children with behavior disorders (especially under the age of 12 years) notoriously underreport their disruptiveness compared to the adults around them. While parents and teachers tend to agree when identifying a child with a behavioral disorder, the correlation between their reports is often low. 2 In contrast, adult patients with ADHD (or their significant other) will often describe their symptoms in terms of work-related performance (eg, frequent job changes; poor organizational, prioritization, and time management skills; or excessive absences) and functional impairment (eg, effort required and coping strategies). 3 Establishing a family history of ADHD is important for both children and adults given the high heritability of the condition.

Several rating scales are available to determine the presence of ADHD symptoms; these tests are most useful when combined with other information to provide a fuller picture of a patient, family, and educational/occupational functioning. Rating scales may have advantages to supplement, but not supplant, the clinical interview. Similarly, neuropsychological testing can provide objective measures of sustained attention, impulsivity, and frontal lobe functioning. An individual neuropsychological test cannot confirm symptom criteria for ADHD as much as reflect a person’s cognitive functioning at a given moment in time. 4

Recent advances in genetic, neuroanatomical, and neuroimaging approaches have begun to yield insights into the pathogenetic and pathophysiologic basis of ADHD. This emerging picture suggests dysfunction of the prefrontal cortex and subcortical structures with which it is connected. However, at present, these advanced technologies cannot be used in the diagnosis of ADHD and do not replace clinical judgment on the basis of thorough information gathering. Another common pitfall in ADHD diagnosis involves equating a positive response to ADHD medicine (stimulants or otherwise) with confirmation that ADHD is present.

HOW COMMON IS ADHD AND WHO HAS IT?

ADHD affects an estimated 7% to 8% of school-aged children in the United States. 5 Recent prevalence estimates indicate that boys (aged 8 to 15 years) have a 2.1 times greater prevalence of ADHD than girls (whereas girls have 2-fold higher rates of mood disorders). 6 In clinical samples of children with ADHD, there may be up to a 10:1 overrepresentation of boys to girls, conceivably because disruptive behavior is often a primary reason for an initial referral (thus underrepresenting girls). Girls with predominantly inattentive symptoms are particularly prone to being underrecognized or referred for treatment.

In adult clinical samples, the male:female ratio of patients with ADHD is closer to 3:2. 7 The National Comorbidity Survey Replication screened over 3,000 adults and found an estimated 4.4% prevalence of ADHD in the United States, suggesting that 9 million adults are affected nationwide. 8 This prevalence rate is similar to the 3.4% estimated prevalence of ADHD in adults based on a subsequent survey of more than 11,000 adults in 10 countries in the Americas, Middle East, and Europe. 9

HOW CAN ADHD BE TREATED?

As the understanding of ADHD has grown, so has the appreciation of the need to successfully diagnose and treat ADHD as early as possible in order to avoid risk of complications later in life. A range of successful treatment options exists. Of these, the stimulants are considered first-line treatments for ADHD, supported by decades of research and a history of robust response, good tolerability, and safety across the lifespan. Stimulants are classified by the US Food and Drug Administration (FDA) and the Drug Enforcement Agency as schedule 2 agents. Nonstimulant treatments (eg, atomoxetine and α2 agonists, both schedule 4 agents, respectively) are also available among current medical treatment options. Lastly, nonpharmacologic approaches—including cognitive-behavioral therapies (eg, tutoring, coaching, and traditional behavioral methods)—serve as important adjuncts to medical treatment.

WHY SHOULD ADHD BE TREATED WHEN IT IS DIAGNOSED?

Untreated ADHD has a significant negative impact on society, resulting in stress upon families and relationships, impact on schools, decreased productivity, and increased health costs. Children with ADHD who remain untreated are at elevated risk for new psychiatric disorders later in life (eg, mood disorders, antisocial behaviors, and substance use disorders). 10 Children with ADHD entering adulthood without adequate treatment demonstrate poorer driving abilities and greater traffic-related adverse outcomes, 11 including risk of citations for speeding, suspended driving licenses, crashes, and crashes causing bodily injury in unmedicated patients. 12 Untreated ADHD significantly increases the risk of early initiation into smoking 13 and addictive behaviors overall. 14

The suggestion that ADHD is overdiagnosed and overtreated—an argument often popularized in the media—is not supported by scientific literature. Prevalence rates by the National Institute of Mental Health indicate that less than a third of children with ADHD in the United States were diagnosed; moreover, in the preceding 12 months, only 13% of children diagnosed with ADHD were treated for their symptoms. 15 More recently, data from the National Comorbidity Survey Adolescent Supplement showed that only 14.2% of youth with a DSM-IV disorder received psychotropic medication in the preceding year. Of those adolescents with ADHD, 20.4% reported stimulant use in the past 12 months, whereas only 0.8% of those without a DSM-IV disorder endorsed stimulant use. 16

WHICH STIMULANTS ARE CURRENTLY AVAILABLE AND HOW DO THEY DIFFER FROM ONE ANOTHER?

Two groups of stimulants (methylphenidates [MPH] and amphetamines [AMPH]) have been approved by the FDA for the treatment of ADHD in the pediatric population. These agents are available in both branded and generic formulations. Table 1 lists the names, preparations, strengths, and duration of behavioral effects of the commonly used stimulants.

Stimulants: Names, Formulations, and Strengths

Several different stimulant formulations have been approved by the FDA since April 2000. These formulations include extended-release preparations of oral MPH, transdermal MPH, extended-release dexmethylphenidate ( d -MPH), lisdexamfetamine, and an oral solution of dextroamphetamine sulfate. By and large, these longer-acting forms of MPH and AMPH circumvent the short-acting effects (eg, 3–5 hours of efficacy for ADHD) of the immediate-release stimulants.

Methylphenidate Preparations

Immediate-acting MPH comes in 3 preparations: a tablet, a chewable tablet, and an oral solution. A sustained-release form of MPH (MPH sustained release) and its branded generic (MPH extended release) are essentially identical in that they are both MPH molecules mixed into a wax matrix. A chewable, extended-release MPH preparation is also available as a branded generic, offering MPH in a hydrophilic polymer.

d -MPH is the dextroisomer of MPH. MPH, as a secondary amine, gives rise to 4 optical isomers: d -threo, l -threo, d -erythro, and l -erythro. The standard preparation of racemic MPH comprises d , l -threo-MPH. Data suggest that the d -threo-MPH ( d -MPH) isomer is the active form. A head-to-head study showed d -MPH to be similar in efficacy to immediate-release, racemic MPH when used in children with ADHD, although its duration of action was longer. 17 A longer-acting version of dexmethylphenidate has been approved for pediatric and adult patients with ADHD.

Of the long-acting versions of MPH, osmotic release oral system (OROS) MPH uses an osmotic pump mechanism that creates an ascending profile of MPH in the blood, providing effective treatment for up to 10 to 12 hours. OROS MPH tablets cannot be crushed without losing their prolonged action. Unlike OROS MPH, several extended-release MPH preparations—MPH controlled delivery, MPH long acting, and d -MPH extended release—utilize a beaded technology that contains spheres of active medication containing anywhere from 30% (MPH controlled delivery) to 50% (MPH long acting and d -MPH extended release) of immediate-release MPH (providing a stimulant effect during the morning hours). These beaded preparations are useful for children who cannot take or who dislike taking pills, as parents can open the capsules and sprinkle the medicine on their child’s food. These preparations are also easier-to-ingest versions of immediate-release MPH, including a chewable tablet or liquid form. These latter 2 MPH forms have not yet been subject to large-scale clinical trials.

The MPH transdermal system was approved in 2006, with a recommended “wear time” of 9 hours. 18 This patch can be applied to the skin (eg, on the hip) prior to or upon awakening, 19 and it is removed approximately 3 hours before the effect would be prudent to conclude. 20 The MPH transdermal system is advantageous for patients (or their parents) who desire having an “off switch” for controlling the delivery of active drug. The latest MPH preparation is a once-daily liquid form of racemic MPH. Initially supplied as a powder, after reconstitution with water, it forms an extended-release oral suspension of MPH. The manufacturer recommends shaking the medication bottle vigorously to ensure that the proper dose is administered. 21

Amphetamine Preparations

AMPH is manufactured in the dextro isomer, such as dextroamphetamine ( d -AMPH), or in racemic forms with mixtures of d - and l -amphetamine (mixed amphetamine salts). An extended-release mixed amphetamine salt formulation is a dual-pulse capsule preparation that includes both immediate- and extended-release beads.

Lisdexamfetamine is an inactive prodrug that converts to d -AMPH upon cleavage of the lysine portion of the molecule; it was developed with the intention of creating a longer-lasting and more difficult to misuse version of d -AMPH. Lisdexamfetamine has been approved for use in both pediatric and adult patients with ADHD. Intravenously and intranasally administered lisdexamfetamine produces effects comparable to the orally administered form, thereby reducing the likelihood of abuse by these routes of administration. 22

HOW ARE STIMULANTS ABSORBED AND METABOLIZED?

Both MPH and AMPH are almost completely absorbed after oral administration 23 ; food in the stomach has little impact on absorption. 24 Immediate-release MPH reaches a peak concentration after 1.5 to 2.5 hours, and it has an elimination half-life that is independent of the preparation of MPH (2.5 to 3.5 hours after oral administration). MPH undergoes extensive presystemic metabolism through hydrolysis or de-esterification with limited oxidation. 23 , 25 Carboxylesterase-1A1 ( CES-1 ), located in the stomach and liver, is the primary enzyme involved with first-pass MPH metabolism. Differences in an individual’s hydrolyzing enzyme activity that are linked to variants in the human CES-1 gene 26 can lead to wide variations in MPH metabolism and to corresponding MPH blood concentrations in certain individuals. MTS avoids much of the first-pass metabolism through CES-1 , 27 thereby producing potentially higher plasma MPH levels.

AMPH absorption is typically rapid, with peak plasma levels of AMPH generally observed 3 hours after oral ingestion. 23 The half-life of AMPH is considerably longer than that of MPH (appropriately 7 hours). All types of AMPH are metabolized in the liver by side-chain oxidative deamination and by ring hydroxylation. Because AMPH formulations are basic compounds, urinary excretion is highly dependent on urinary pH. Acidification of the urine increases urinary output of AMPH. 28 Therefore, taking the medicine with ascorbic acid or fruit juice may decrease its absorption, while use of alkalinizing agents (eg, sodium bicarbonate) may increase AMPH absorption 29 (although the clinical correlates of these alterations remain unclear).

Peak plasma concentrations for both MPH and AMPH vary by a factor of 4 or 5 in children and adults, most likely a result of interindividual variability in metabolism and plasma clearance. 25 Interindividual pharmacokinetic differences may be less dramatic when stimulant doses are adjusted for body weight (using mg/kg as a general guide). 30 Interindividual variability may also argue for examining an individual’s pharmacokinetics when a person fails to respond to conventional dosing strategies. 30 Laboratory testing for plasma levels of stimulants (particularly MPH) is increasingly available; however, the levels are uncommonly assessed in clinical practice.

WHEN AND HOW ARE STIMULANTS TYPICALLY DOSED?

When starting a psychostimulant, it is wise to start by choosing a stimulant class (eg, MPH or AMPH) and then the desired duration of action of the preparation chosen (eg, longer-acting versus short-acting). There is no evidence of preferential response to one of the stimulant classes. Contemporary guidelines suggest that long-acting, once-daily preparations are preferred for most patients. 31 The dose for each patient should be individually optimized on the basis of the drug’s therapeutic efficacy and side effect profile. Steady titration of treatment is advisable until an acceptable response is noted, with the addition of a similar (or sculpted) afternoon dose that is dependent on the presence of breakthrough symptoms.

The starting dose for many preparations of MPH, AMPH compounds, and d -AMPH in most children is typically 2.5 to 5 mg, with a suggested target daily dose ranging between 0.3 to 1 mg/kg for AMPH and 0.6 to 2 mg/kg for MPH. Once pharmacotherapy is initiated, frequent contact with the patient and family is necessary during the initial phase of treatment to carefully monitor the response and any adverse effects. Apparent stimulant “ineffectiveness” may stem from excessively deliberate dose titration or medication underdosing. This underdosing may occur early in the course of a stimulant trial or months (or even years) later in treatment when a previously successful stimulant regimen loses its efficacy because the child has grown and requires a higher dosage to compensate for improved stimulant metabolism and/or clearance. For instance, data suggest that over the first 6 months of treatment, MPH treatment is associated with mild tolerance that may necessitate a 20% to 30% increase in the dose to maintain efficacy. 32

Stimulant dosing often varies widely depending on the treatment setting. In the National Institute of Mental Health (NIMH) Multimodal Treatment Study of ADHD, 33 mean daily MPH doses for children were significantly lower for those receiving community care (18.7 mg/d) than for investigator-treated subjects (32.8 mg/d); the latter group had superior outcomes.

HOW HIGH CAN STIMULANT DOSES GO?

Absolute dose limits (in mg) of stimulants do not adequately consider use in refractory cases or adult-sized adolescents or adults. For example, the FDA recommends maximum daily MPH doses of up to 60 mg/d for short-acting forms and 72 mg/d for extended-release preparations. Others have proposed prescribing 1 mg/kg/d 34 to 2 mg/kg/d of racemic MPH. 35

Stevens and associates 36 examined serum levels of MPH in patients receiving relatively higher doses of OROS MPH (mean of 169 mg, 3 mg/kg/d) and found acceptable levels of blood pressure and heart rates; serum levels were also within the accepted levels of therapeutic (MPH levels < 50 ng/mL). In fact, no one in that study developed toxic levels. 36 While MPH levels can be helpful for patients receiving higher than FDA-approved stimulant doses, results from several studies that have examined the association between plasma levels of stimulants and the improvement of ADHD symptoms have generally been equivocal. Monitoring of serum drug levels may be of some value for confirming compliance and in patients receiving higher than FDA-approved doses of stimulants. These recommendations are tentative, and further clinical research in this area is warranted.

CAN STIMULANT THERAPY BE WITHHELD ON WEEKENDS, OVER THE SUMMER, OR ON HOLIDAYS?

The appropriateness or merits of medication holidays remain unresolved. The symptoms of ADHD, although usually more noticeable in the school or work setting, are often disruptive to the patient’s family and social life. In cases in which important adverse effects are present (eg, appetite suppression), it may be necessary to allow for periodic drug holidays (either during weekends or the summer). In patients whose major symptoms occur during school/work and who prefer to be treated during workdays only, weekends or vacations off medication may be appropriate. Conversely, in patients who manifest symptoms predominately in the home, medication-free holidays may be more problematic. In general, children should begin the academic year receiving an appropriate stimulant dose (initiated 1 or 2 weeks before the resumption of classes). Following a sufficient period of clinical stabilization (eg, 6 to 12 months), it is prudent to reevaluate the need for continued pharmacologic intervention. Supervised discontinuation trials in the middle of the school year (as opposed to the summer months) may facilitate close assessment of a child’s behavior and academic performance from multiple viewpoints.

WHAT DRUG-DRUG INTERACTIONS SHOULD BE CONSIDERED WHEN PRESCRIBING STIMULANTS?

Most interactions between stimulants and the vast majority of prescription and nonprescription medications are typically mild. Stimulants create few worrisome interactions when used with commonly prescribed medications (eg, selective serotonin reuptake inhibitors, second-generation antipsychotics, atomoxetine, or α2-adrenergic medications). However, less common interactions with stimulants may involve increased plasma levels of tricyclic antidepressants; increased plasma levels of phenobarbital, primidone, and phenytoin; increased prothrombin times on anticoagulants; attenuation or reversal of the guanethidine antihypertensive effect; and increased pressor responses to vasopressor drugs. 37 The relative lack of drug-drug interactions of MPH and other psychostimulants in the context of more complex medical regimens may be due to the low bioavailability (20% to 30%) of orally administered forms of MPH. 24

HOW EFFICACIOUS AND SAFE ARE STIMULANTS FOR ADHD?

The efficacy and safety of stimulants for the treatment of pediatric patients with ADHD are based on a large number of studies of (primarily) latency-age children wherein the average response rate is 70%. 38 – 40 When clinical response is assessed quantitatively via rating scales, the effect size of stimulant treatment relative to placebo is robust, averaging about 1.0, one of the largest effects for any psychotropic medication. 31 , 41

Treatment data for preschoolers (aged 3 to 5 years) are less robust, although studies suggest that this group may have a lower response rate to stimulants and may be more treatment refractory or be diagnostically heterogenous. 42 Results from the largest preschool stimulant treatment study to date, a NIMH-sponsored multisite study of 165 children who tolerated study medication, showed that 85% of patients were MPH responders (versus 10% of placebo responders). 43 The effect sizes were smaller than in school-aged youth (with improvement noted in both school and home settings). Findings from the NIMH multisite Preschool ADHD Treatment Study study support the results of earlier, smaller, controlled stimulant studies in preschoolers, showing mostly a modest-to-robust response and improvements in mother-child interactions, behavior, and structured tasks. 44

As with preschoolers, there is a smaller body of research of stimulants in adolescents. 45 , 46 The majority of existing studies report at least a moderate response to treatment (without tolerance or evidence of misuse or abuse). For instance, 2 multisite studies demonstrated the efficacy of OROS MPH and mixed amphetamine salts extended release for ADHD. In a controlled study of 177 adolescents with ADHD treated with OROS MPH, over a third (37%) required the highest FDA-approved dose (72 mg) for outcome. 45 In another controlled study of 318 adolescents with ADHD, mixed amphetamine salts extended release resulted in significant improvements in mean ADHD measures of inattentiveness and hyperactivity/impulsivity subscales versus placebo. 46 In the majority of stimulant studies previously cited, the most common study drug was MPH, followed by AMPH. A review of the existing literature provides little evidence of a differential response for various stimulants. 44 Moreover, in many stimulant studies, a crossover design was used and the study lengths were brief (ranging from a few days to a few weeks). 45 Most studies have been conducted on white males; there have been fewer data on the safety and efficacy of stimulants in females and those from various minority groups. 47

WHICH STIMULANT-RELATED ADVERSE EFFECTS ARE COMMON AND EXPECTED?

Common adverse effects during stimulant treatment include the delay of sleep onset, headache, appetite suppression, transient headache, transient stomachache, and behavioral rebound (ie, the sudden or pronounced recurrence of ADHD symptoms). Less frequently observed outcomes include mood dysregulation or tics.

Charach et al 48 collected side effect data during a 5-year period in children with ADHD who were initially randomized to use of a stimulant or to no medication. The most common sustained side effect reported was loss of appetite. At least 1 physiologic adverse effect (eg, headache, appetite loss, abdominal pain) was reported by half of the children by the end of the fifth year of monitoring. Importantly, children continued to use the medication, suggesting that the adverse events were mild and of minor health concern. 48 Although AMPH or MPH were equally likely to produce an improvement in ADHD symptoms, 49 the occurrence of stimulant-related side effects may be greater with the use of AMPH (or d -AMPH) compared with MPH (10% versus 6%, P < .05), although idiosyncratic patterns were noted for individual children. 50

Table 2 delineates suggested strategies for managing common stimulant-related adverse effects. Attempts should be made to manage adverse effects that occur in the context of a satisfactory clinical response to stimulants. In cases of stimulant-induced medical (headaches) or psychiatric symptoms (eg, dysphoria, anxiety), it is necessary to assess whether these symptoms develop 1 to 2 hours postadministration (acute phase) or during the postadministration (wear-off phase). Acute effects generally indicate the need to reduce the maximum concentration in the blood by reducing the dose or altering the release mechanism of the stimulant (eg, changing from immediate-release to extended-release forms), whereas wear-off symptoms necessitate slowing of the stimulant decay curve by adding a stimulant just before symptom onset or changing to a more extended-release agent.

Possible Strategies for Stimulant Side Effects

WHAT ARE THE LONG-TERM OR UNEXPECTED EFFECTS OF STIMULANTS?

Height and weight changes.

Numerous studies have investigated abnormalities in the growth process related to ADHD, but controversies remain concerning both the direction of the deviation from the norm and the cause of that deviation. Even with the plethora of studies conducted in this area, myriad methodological difficulties interfere with drawing a simple conclusion (eg, the absence of a comparable control group [untreated children with ADHD] or an ADHD group receiving medication treatment with psychotropics other than stimulants).

In the past 10 years, several investigations have confirmed that reduction of growth is stimulant related, 50 – 53 whereas others have failed to show any statistically significant growth delay during treatment. Growth slowdown for height and weight was reported in children aged 7 to 10 years with ADHD who were treated with MPH at a mean dosage of 30 mg/kg/d in the NIMH Multimodal Treatment Study of ADHD. 52 School-aged children grew 1.0 cm less and gained 2.5 kg less than predicted by the Centers for Disease Control and Prevention growth charts. 52 Similar effects were observed for preschool children who grew 1.5 cm less in height and gained 2.5 kg less weight than predicted while being treated with MPH at a mean dosage of 14 mg/kg/d. 54

Spencer and associates 55 hypothesized that the disorder-related delay suggested that the observed growth deficit may be connected with ADHD, rather than with stimulant medication. Children with ADHD could develop more slowly than the norm, and the consequence of this would be lower rates of growth in succeeding years than expected and the later achievement of biological maturity than in their healthy peers. Others have reported dissimilar findings 50 and have shown that unmedicated children with ADHD were taller than were medicated children.

The aggregate literature seems to suggest small but clinically insignificant reductions in weight over time. Height may be negatively influenced over the first 1 to 2 years of treatment; however, catch-up or rebound in height to expected values emerges with chronic treatment. 56 Monitoring of growth (in height and weight) should be part of the management of ADHD-affected youth receiving stimulants.

Stimulant use in patients with mild-to-moderate tics remains of concern. Most studies have failed to confirm the hypothesis that stimulants exacerbate tic severity in youth with ADHD. 57 , 58 For example, Palumbo and colleagues 59 pooled data from 3 placebo-controlled trials (total N = 416) and 2 open-label studies involving patients receiving OROS MPH, MPH, or placebo. Although approximately 13% of patients in each of the 3 groups had a history of tics, there was no significant difference between the 3 groups in the number of children who experienced tics. 59 Double-blind clinical trials of both immediate-release and long-acting stimulants have not found that stimulants increase the rate of tics relative to placebo. 60 , 61 Children with comorbid ADHD and tic disorders, on average, show a decline in tics that persists even after a year of treatment when treated with a stimulant. 62

If a patient has treatment-emergent tics during a trial of a given stimulant, an alternative stimulant or a nonstimulant should be tried. If the patient’s ADHD symptoms respond adequately only to a stimulant that induces tics, then combined pharmacotherapy of the stimulant and an α-agonist (eg, clonidine or guanfacine) is recommended. 63 Withdrawal of stimulants in a placebo-controlled double-blind fashion did not change the frequency or severity of tics in a series of 19 children with ADHD, and the frequency and severity of vocal or motor tics did not change when stimulants were used for an extended time. 64

Sudden Death and Cardiac Complications

A disputed cardiovascular effect of stimulants is sudden death; this has been a source of great concern and publicity in recent years. Wilens and coworkers 65 summarized the literature, and a commentary was provided by the FDA in 2009. 66 Wilens and colleagues 65 cited more than 300 controlled trials of stimulant medication involving more than 5,000 subjects; no cases of sudden death were observed. Moreover, the autopsy-assessed anatomic characteristics of subjects who had sudden death during stimulant treatment were found to be similar to those of individuals who had sudden death in the general population. However, Gould and associates 67 found an association between stimulant use and sudden death in a matched case-control study of 564 cases of sudden unexplained death in youth and a comparison group (who died as passengers in motor vehicle traffic accidents). Ten of the subjects (1.8%) in the unexplained sudden death group were taking MPH, whereas only 2 (0.4%) in the comparison group of young people who died in road traffic accidents were taking stimulants (odds ratio of 7.4, 95% CI, 1.4–74.9). As a case-controlled study, this analysis could not determine causality. 67 Referring to this study, in 2009 the FDA commented that it was unable to “conclude that the data in the study affect the overall risk-benefit profile of stimulant medications used to treat ADHD in children.” 66

More recently, Hammerness and colleagues 68 reviewed relevant clinical literature through 2011 and found that stimulants were associated with small elevations of blood pressure (≤ 5 mm Hg) and heart rate (≤ 10 beats/min) without electrocardiographic changes (eg, QTc prolongation). However, it was extremely rare for a child or adolescent receiving stimulants to have a serious cardiovascular event during treatment; in fact, the overall cardiovascular risk was the same as that of groups of youth not receiving stimulant medication. 68 This last finding was further supported by a large retrospective cohort study 69 involving greater than 1 million children and young adults analyzed for potential serious cardiovascular events (eg, sudden death, acute myocardial infarction, or stroke). Users of ADHD medicine were not at an increased risk for serious cardiovascular events compared to nonusers or former users of stimulants. 69

At this stage, it appears that sudden death is a rare event in youth with ADHD, and there are insufficient data to establish a causal link with stimulant medication used to treat this condition. 70 Nevertheless, it would be prudent to follow the guidelines of the use of stimulants in youth (monitoring risk factors and measuring blood pressure and pulse), although obtaining an electrocardiogram is not mandatory. 71 , 72 Pertinent questions that should be asked with regard to family history of premature sudden death and a personal history of cardiovascular symptoms are summarized in Table 3 . Patients answering any of these questions affirmatively should be examined and investigated more carefully.

Massachusetts General Hospital Cardiovascular Screen a , b

Psychosis or Mania

Psychosis or mania may be a rare adverse effect of stimulant (and nonstimulant) therapy for ADHD. A recent pooled analysis 73 of 49 randomized trials in children and > 800 reports in adults and children treated for ADHD (some with nonstimulants, including atomoxetine) found events in 1.48 per 100 person-years in the pooled drug group compared to none in the placebo group. In approximately 90% of the cases, there was no history of a similar psychiatric condition prior to ADHD treatment. 73 Hallucinations (involving visual and/or tactile sensations of insects, snakes, or worms) were common in cases involving children. 73 In reviewing several trials, the FDA found that stimulant-associated psychotic-like and manic-like symptoms occurred rarely (ie, in approximately 0.25% of children treated with stimulants). In 55 of 60 reported cases of psychotic-like or manic-like symptoms in response to stimulants, the symptoms resolved when the stimulant was discontinued. 73 In the 5 cases in which symptoms persisted, the patients were rediagnosed with schizophrenia or bipolar disorder. The occurrence of psychosis and other pronounced mood dysregulation with stimulant treatment generally warrants consideration of an alternative agent. In some cases, children may tolerate a carefully monitored rechallenge of a stimulant used at a lower dose. 73

Carcinogenic Effects

In 2005, El-Zein and colleagues 74 reported “chromosomal breaks” in the peripheral lymphocytes of children taking therapeutic doses of MPH. This study added to a sparse body of animal literature that showed increased hepatic tumors in rodents treated with very high (4 to 47 mg/kg) oral doses of MPH. 75 However, the preponderance of data seems to suggest a lack of association between the use of stimulants and the development of cancer. For instance, an older study of pharmacy records suggested that the number of cancers in patients receiving stimulants was actually less than expected. 76 Moreover, a large systematic review found either negative or weakly positive results for chromosomal changes in rodent assay systems. 77 In what is likely to be one of many follow-up studies addressing this pressing issue, Ponsa and associates 78 followed a similar strategy as El-Zein and coworkers 74 and found no evidence of an increased frequency of micronuclei (indicative of genomic damage). In the 3 endpoints studied (ie, a cytokinesis-block micronucleus assay, a sister chromatid exchange analysis, and a determination of chromosome aberrations), the results did not support a potential increased risk of cancer after exposure.

WHAT IS THE RISK OF SUBSEQUENT SUBSTANCE ABUSE AFTER TREATMENT WITH A STIMULANT?

Wilens and colleagues 79 performed a meta-analysis and reported that the use of stimulants did not increase the risk for later substance use disorders in either adolescents or adults. Subsequently, Katusic and colleagues 80 and Wilens and associates 81 reported a protective effect of stimulants into young adulthood, whereas Biederman et al 82 and Mannuzza et al 83 simultaneously reported that early stimulant treatment neither increased nor decreased the risk for subsequent substance use disorders in young adulthood. The waning of the protective effect in adults may be a reflection of findings in adolescents not spanning the full age of risk of substance use disorders or that most adolescents have stopped their ADHD treatment, thus losing the protective effect of stimulants.

HOW ARE STIMULANTS MISUSED AND DIVERTED?

There has been substantial interest in the misuse and diversion of stimulants prescribed for ADHD (for review see Wilens et al 84 ). While the majority of individuals treated for their ADHD use their medications appropriately, 85 some appear to misuse the stimulants. Survey studies have indicated that approximately 5% of college students have misused stimulants 86 , 87 and that it is more common in competitive colleges and that the drugs are more often misused for their procognitive effects than for euphoria 87 Data regarding those to whom the stimulants were diverted show that these individuals misused the stimulants in context with other substances of abuse 88 and other psychopathology (such as depression 89 and conduct disorder 87 ).

CAN STIMULANTS BE USED EFFECTIVELY IN THOSE WITH COMORBID CONDITIONS?

The use of stimulants in the treatment of ADHD and common comorbid conditions is an important topic. The lifetime prevalence of comorbid psychiatric or learning disorders is estimated to be as high as 80%. 35 , 90 Common comorbid diagnoses with ADHD include mood disorders (eg, major depressive disorder, bipolar disorder, dysthymia), anxiety disorders, and substance use disorders. Some medical conditions (eg, epilepsy) are more likely to be comorbid with ADHD. The presence of comorbidities often worsens the prognosis of these patients and complicates their treatment, thereby warranting special mention.

Bipolar Disorder

The majority of youth with bipolar disorder have co-occurring psychiatric illnesses. Among these, ADHD is the most common comorbidity with pediatric bipolar disorder. 91 Clinical studies generally demonstrate high rates of ADHD, ranging from 60% to 90%, in patients who have bipolar disorder. 92 Likewise, cross-sectional studies have found rates of bipolar disorder ranging from 11% to 23% in youth who have ADHD. 93

Two controlled trials suggest that stimulants are effective in treating comorbid ADHD without precipitating hypomania or mania in mood-stabilized youth with bipolar disorder. Scheffer and colleagues 94 performed a double-blind, placebo-controlled trial of pediatric patients diagnosed with bipolar disorder and ADHD. In this study of 31 children, treatment with divalproex sodium (mean dose: 750 mg/d) reduced manic symptoms in 80% of participants, but reduced ADHD symptoms in only 7.5% of participants. With the addition of AMPH, the subsequent improvement in ADHD was significantly greater than with placebo. 94 Findling and colleagues 95 reported that in youth stabilized with a dose of at least 1 mood stabilizer, concomitant treatment with MPH improved ADHD in a dose-dependent manner (without destabilization of mood). Therefore, for bipolar youth with co-occurring ADHD, mood stabilization with a traditional mood stabilizer or an atypical antipsychotic medication is recommended before starting stimulant therapy. 96 Clinicians must take into account the risk of adverse effects or potential mood destabilization from stimulants and discuss this risk with families; however, they should not overvalue potential risks when making a recommendation.

Developmental Disorders

The recent rise in the diagnosis of autistic disorder and other pervasive developmental disorders has refocused attention on stimulants as a possible therapeutic option for patients with functionally impairing hyperactivity, distractibility, and impulsiveness.

Several randomized, controlled studies have supported the appropriateness of stimulant use in pervasive developmental disorders in children. 97 – 100 These studies contradict the results of a retrospective review of stimulant use in 195 patients with pervasive developmental disorders, 101 which suggested a low rate of treatment success and frequent side effects (eg, irritability and increased stereotypic movements). A preponderance of the evidence suggests that symptoms of ADHD are common in pervasive developmental disorders and that MPH is an empirically supported treatment to target ADHD symptoms in pervasive developmental disorders. However, tolerability remains a problem, and caregivers should be cautioned to be watchful for potential adverse effects. With the increasing recognition of autism spectrum disorders in young children, further studies are needed to clarify the roles of AMPH and nonstimulant medications in the treatment of ADHD symptoms in children with pervasive developmental disorders.

Seizure Disorders

Studies in pediatric epilepsy have found a 2.5-fold to 5.5-fold increased risk of ADHD compared with healthy controls. 102 , 103 Although not a contraindication, the Physicians’ Desk Reference 104 discourages the use of stimulants in children with seizure disorders because stimulants lower the seizure threshold. Baptista-Neto and colleagues 105 have reviewed this topic, citing retrospective chart reviews, open-label trials, and controlled trials of MPH in patients with epilepsy and ADHD showing significant improvements in ADHD symptoms without an exacerbation of seizures or an adverse effect on antiepileptic drug serum levels. Moreover, a large retrospective cohort study of > 30,000 pediatric patients found no statistically significant association between the use of stimulants and seizure risk in children with ADHD and without a prior seizure disorder. 106 Recently, a pilot randomized controlled trial of OROS MPH to treat ADHD plus epilepsy (N = 31) found that stimulant treatment reduced ADHD symptoms more than placebo treatment. 107 However, there were too few seizures during the active (5 seizures) and placebo (3 seizures) arms to assess seizure risk. 107 These recent works suggest that stimulants may be a safe and effective treatment in certain children with seizure disorders.

CAN STIMULANTS PROTECT AGAINST THE DEVELOPMENT OF PSYCHIATRIC DISORDERS?

One of the newest areas of interest discussed in the stimulant literature concerns whether treatment with stimulants modifies long-term outcomes. Daviss and colleagues 108 examined the association between stimulant treatment for ADHD and the risk for subsequent major depressive disorder by comparing the rates of pharmacotherapy in teenagers with ADHD and major depressive disorder (history of major depressive disorder: n = 36) to those without a lifetime history of major depressive disorder (never depressed: n = 39). The investigators found that stimulants protected youth against subsequent development of major depressive disorder. More recently, a case-control, 10-year prospective follow-up study of white males with (n = 140) and without (n = 120) ADHD was conducted. 109 At the 10-year follow-up, participants with ADHD who were treated with stimulants were significantly less likely to develop depressive and anxiety disorders and disruptive behavior and were less likely to repeat a grade compared with participants with ADHD who were not treated. This study highlights additional protective effects of stimulants (eg, lower risk for the subsequent development of psychopathology and grade retention). 109

WHEN TO REFER TO A SPECIALIST?

Primary care physicians may consider referring a difficult or unclear case to a psychiatrist, psychologist, or developmental pediatrician, especially if the physician suspects comorbid conditions (eg, depression, anxiety disorders, or bipolar disorder). If the symptom presentation cannot be differentiated from neurologic disorders such as seizures, referral to a neurologist is appropriate. Patients who are refractory to treatment (ie, fail 2 classes of stimulants) or who experience an atypical response are also ideal candidates for referral. 2 , 4 Ultimately, a clinician’s referral offers the opportunity to confirm or refine a diagnosis, optimize treatment, and achieve greater adherence with treatment regimens such as pharmacotherapy.

Pharmacotherapy with stimulants is a mainstay of evidence-based treatment for pediatric and adult populations with ADHD and comorbid conditions. The use of stimulants should follow a careful evaluation of the child and his or her family, including psychiatric, social, cognitive, and educational evaluations. Early therapeutic intervention is important before complications, chronicity, and social incapacitation occur. Otherwise, the challenge of treatment and restabilization of functional life habits becomes more difficult. The patient and family of the patient need to be made familiar with the risks and benefits of such intervention, the availability of alternative treatments, and the likely short-term and long-term adverse effects. Certain adverse effects can be anticipated on the basis of known pharmacologic properties of the drug (eg, decreased appetite, insomnia), whereas others are idiosyncratic and are difficult to anticipate on the basis of the drug properties. Short-term adverse effects can be minimized by introducing the medication at low initial doses and titrating upward steadily. Long-term side effects require monitoring of potential adverse effects (such as growth impairment). Idiosyncratic adverse effects generally require drug discontinuation and selection of alternative treatment modalities. Special attention must be given to issues of comorbidity with other psychiatric and medical disorders.

LESSONS LEARNED AT THE INTERFACE OF MEDICINE AND PSYCHIATRY

The Psychiatric Consultation Service at Massachusetts General Hospital (MGH) sees medical and surgical inpatients with comorbid psychiatric symptoms and conditions. Such consultations require the integration of medical and psychiatric knowledge. During their twice-weekly rounds, Dr Stern and other members of the Consultation Service discuss the diagnosis and management of conditions confronted. These discussions have given rise to rounds reports that will prove useful for clinicians practicing at the interface of medicine and psychiatry.

Dr Stevens is an attending psychiatrist in Behavioral Health Services at Henry Ford Health Systems, Dearborn, and clinical assistant professor at Wayne State University, Detroit, Michigan; Dr Wilens is an attending psychiatrist in the Pediatric Psychopharmacology Clinic and codirector of the Center of Addiction Medicine at Massachusetts General Hospital, Boston, and associate professor of psychiatry at Harvard Medical School, Boston, Massachusetts; Dr Stern is chief of the Psychiatric Consultation Service at Massachusetts General Hospital, Boston, and a professor of psychiatry at Harvard Medical School, Boston, Massachusetts.

Dr Wilens has served as a consultant to Abbott, Eli Lilly, Euthymics, McNeil, Merck, National Institutes of Health, Novartis, and Shire; has received grant/research support from Abbott, Eli Lilly, McNeil, Merck, National Institutes of Health, National Institute on Drug Abuse, and Shire; has served as a speaker for Eli Lilly, McNeil, Novartis, and Shire; and has published a book ( Straight Talk About Psychiatric Medications for Kids ) with Guilford Press. Dr Stern is an employee of the Academy of Psychosomatic Medicine, has served on the speaker’s board of Reed Elsevier, is a stock shareholder in WiFiMD (Tablet PC), and has received royalties from Mosby/Elsevier and McGraw Hill. Dr Stevens reports no conflicts of interest related to the subject of this article.

Attention deficit/hyperactivity disorder in adults: A case study

Affiliations.

  • 1 University of North Dakota, United States of America. Electronic address: [email protected].
  • 2 University of North Dakota, United States of America.
  • 3 Dana Wiley, MD PA.
  • PMID: 35461644
  • DOI: 10.1016/j.apnu.2021.12.003

Attention-Deficit/Hyperactivity Disorder (ADHD) is often misdiagnosed or mistreated in adults because it is often thought of as a childhood problem. If a child is diagnosed and treated for the disorder, it often persists into adulthood. In adult ADHD, the symptoms may be comorbid or mimic other conditions making diagnosis and treatment difficult. Adults with ADHD require an in-depth assessment for proper diagnosis and treatment. The presentation and treatment of adults with ADHD can be complex and often requires interdisciplinary care. Mental health and non-mental health providers often overlook the disorder or feel uncomfortable treating adults with ADHD. The purpose of this manuscript is to discuss the diagnosis and management of adults with ADHD.

Keywords: Adult; Attention Deficit/Hyperactivity Disorder; Misuse; Psychoeducation; Stimulant.

Copyright © 2022 Elsevier Inc. All rights reserved.

  • Attention Deficit Disorder with Hyperactivity* / diagnosis
  • Attention Deficit Disorder with Hyperactivity* / epidemiology
  • Attention Deficit Disorder with Hyperactivity* / therapy
  • Comorbidity
  • Mental Health*
  • Conclusions
  • Article Information

eTable 1 . Association Between ADHD and Serious Transport Accidents in Swedish Adults

eTable 2 . Rate of Serious Transport Accident During Medication Periods Compared With Nonmedication Periods Among Swedish Adults With ADHD

eTable 3 . Differences in Risk of Serious Transport Accidents Between 2 Consecutive Periods (Without ADHD Medication vs With ADHD Medication) for Patients Who Changed Their Medication Status

eTable 4 . Rate of Serious Transport Accident During Medication Periods Compared With Nonmedication Periods Among Swedish Adults With ADHD

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Chang Z , Lichtenstein P , D’Onofrio BM , Sjölander A , Larsson H. Serious Transport Accidents in Adults With Attention-Deficit/Hyperactivity Disorder and the Effect of Medication : A Population-Based Study . JAMA Psychiatry. 2014;71(3):319–325. doi:10.1001/jamapsychiatry.2013.4174

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Serious Transport Accidents in Adults With Attention-Deficit/Hyperactivity Disorder and the Effect of Medication : A Population-Based Study

  • 1 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
  • 2 Department of Psychological and Brain Sciences, Indiana University, Bloomington

Importance   Studies have shown that attention-deficit/hyperactivity disorder (ADHD) is associated with transport accidents, but the magnitude of the association remains unclear. Most important, it is also unclear whether ADHD medication reduces this risk.

Objectives   To estimate the association between ADHD and the risk of serious transport accidents and to explore the extent to which ADHD medication influences this risk among patients with ADHD.

Design, Setting, and Participants   In total, 17 408 patients with a diagnosis of ADHD were observed from January 1, 2006, through December 31, 2009, for serious transport accidents documented in Swedish national registers. The association between ADHD and accidents was estimated with Cox proportional hazards regression. To study the effect of ADHD medication, we used stratified Cox regression to compare the risk of accidents during the medication period with the risk during the nonmedication period within the same patients.

Main Outcomes and Measures   Serious transport accident, identified as an emergency hospital visit or death due to transport accident.

Results   Compared with individuals without ADHD, male patients with ADHD (adjusted hazard ratio, 1.47; 95% CI, 1.32-1.63) and female patients with ADHD (1.45; 1.24-1.71) had an increased risk of serious transport accidents. In male patients with ADHD, medication was associated with a 58% risk reduction (hazard ratio, 0.42; 95% CI, 0.23-0.75), but there was no statistically significant association in female patients. Estimates of the population-attributable fractions suggested that 41% to 49% of the accidents in male patients with ADHD could have been avoided if they had been receiving treatment during the entire follow-up.

Conclusions and Relevance   Attention-deficit/hyperactivity disorder is associated with an increased risk of serious transport accidents, and this risk seems to be possibly reduced by ADHD medication, at least among male patients. This should lead to increased awareness among clinicians and patients of the association between serious transport accidents and ADHD medication.

Quiz Ref ID Transport accidents are a major public health problem. According to the World Health Organization, approximately 1.3 million individuals are killed each year in traffic accidents, and 50 million are injured or disabled. 1 Transport accidents are also associated with a substantial economic burden, accounting for about 2% of the gross national product of the entire global economy. 1

Inattention and distractibility are the most common reasons for transport accidents. 2 An emerging literature has documented an association between attention-deficit/hyperactivity disorder (ADHD) and transport accidents (eg, collision and trauma). 3 - 7 The association is driven by the core symptoms of ADHD (inattention, hyperactivity, and impulsivity), as well as by problems that frequently co-occur with ADHD, such as excessive risk taking, poor control of aggression, and substance use. 3 , 8 However, small sample sizes, lack of female participants in the studies, absence of objective measures, inadequate controls, and referral bias 3 , 6 raise uncertainty about the magnitude of the association.

Randomized clinical trials suggest that ADHD medication has beneficial short-term effects on the core symptoms of ADHD, 9 - 12 but to our knowledge, there are no population-based studies on the association between ADHD medication and transport accidents. A few studies have explored whether ADHD medication improves driving ability in virtual reality driving simulators. 3 , 5 , 6 , 13 The extent to which these effects generalize to real-world situations remains uncertain, however, and most available studies have been industry sponsored. 6 Because decisions regarding the prescription of ADHD medication need to consider the effect sizes of the benefits and risks of medication at the population level, 14 , 15 a population-based prospective study with measures of transport accidents in real life (such as injuries and deaths) is needed.

In this longitudinal study, we used data from population-based registers in Sweden to assess 2 research questions. First, we estimated the magnitude of the association between ADHD and serious transport accidents (injuries and deaths). Second, we explored the extent to which ADHD medication influences this risk among patients with ADHD.

We used data from several longitudinal population-based registers in Sweden, which were linked using unique personal identification numbers. 16 We identified all individuals born from 1960 through 1988 with at least 1 diagnosis of ADHD (code F90 in the International Classification of Diseases, Tenth Revision ) in the Patient Register since 2001 (N = 17 408). These patients were observed from January 1, 2006, through December 31, 2009 (48 months), for any serious transport accident via the Patient Register and Cause of Death Register. The Prescribed Drug Register was used to obtain information on all prescribed medications since July 2005. 17 Information regarding sociodemographic variables, crime records, and migrations was obtained from the Integrated Database for Labour Market Research, the Crime Register, and the Migration Register, respectively. A non-ADHD general population sample, matched 1 to 10 on age, sex, and residential area at the time of the diagnosis, was extracted from the Total Population Register. The study was approved by the ethics committee at Karolinska Institutet.

The exposure (or risk factor) for the first research question was ADHD. The exposure for the second research question was ADHD medication, which was identified according to the Anatomical Therapeutic Chemical codes in the Prescribed Drug Register. Both stimulant (codes N06BA04, N06BA01, and N06BA02) and nonstimulant (code N06BA09) medications are used in Sweden for ADHD treatment. 18 In accordance with previous studies, 18 - 20 an individual was defined as on medication during the interval between 2 dispensed prescriptions (picked up by the individuals themselves, family members, or health care staff) of ADHD medication, unless the prescription occurred more than 6 months apart. An individual was defined as off medication during intervals of 6 months or more without any prescription.

The main outcome for both research questions was serious transport accident, which was identified as an emergency hospital visit or death due to transport-related trauma (codes V01-V99 in the International Classification of Diseases, Tenth Revision ) 7 through the Patient Register and Cause of Death Register.

Several potential confounding factors were measured. Five sociodemographic factors (civil, employment, and education status; living in 1 of 3 large cities in Sweden; and disposable family income in 2006) were retrieved from the Integrated Database for Labour Market Research. Information on previous psychiatric diagnoses (other than ADHD), other common psychotropic medications, and criminal convictions was obtained from the Patient Register, Prescribed Drug Register, and Crime Register, respectively.

To explore the association between ADHD and serious transport accidents, we first compared the rate of accidents between individuals with and without ADHD using Cox proportional hazards regression. Second, we included measured covariates into the model to control for confounding.

To investigate the association between ADHD medication and accidents among patients with ADHD, we first used ordinary between-individual Cox proportional hazards regression, with robust standard errors accounting for the correlations between periods within the same individual. Next, within-individual analyses were performed using stratified Cox proportional hazards regression with each individual entering as a separate stratum. 21 That is, each patient served as his or her own control, and the rate of accidents during ADHD medication use was compared with the same individual while untreated. Current ADHD medication, age, history of ADHD medication, and transport accidents were included as time-varying covariates. As such, the within-individual hazard ratio is adjusted for confounding by all unmeasured covariates that are constant within each individual during the follow-up (eg, genetic predisposition and early environments) and by all measured time-varying covariates. A more detailed description of this method can be found in a recent study of ADHD medication and criminality. 20

To assess the public health effect of ADHD medication on serious transport accidents, we used the population-attributable fraction (PAF). The PAF was originally proposed for cross-sectional data, 22 but extensions are available for cohort studies. 23 In the absence of unmeasured confounding, this PAF measures the proportion of accidents that would be eliminated if the entire cohort of patients with ADHD would be medicated during the follow-up. Details regarding the estimation and interpretation of PAF can be found in the eMethods section in the Supplement .

Because of the sex difference of patients with ADHD 24 and those involved in transport accidents, 25 all analyses were conducted for men and women separately. Since young males are the single most risky demographic group, 26 separate analyses were also conducted in young and middle-aged adults.

To examine the robustness of our findings, we analyzed the association between ADHD medication and serious transport accidents with different definitions of the cohort, exposure, and outcome. First, we analyzed a cohort of individuals who received at least 1 prescription for ADHD medication during the follow-up (identified from the Prescribed Drug Register) but did not necessarily have a registered ADHD diagnosis, which avoids potential bias because some counties have historically been less consistent in reporting outpatient data to the Patient Register (the Prescribed Drug Register has complete coverage). 17 Second, to explore if the association between ADHD medication and accidents was explained by drug abuse or criminality, we excluded from the analysis individuals with any drug abuse diagnosis or crime conviction during the follow-up. Third, we performed sensitivity analysis with selective serotonin reuptake inhibitor treatment as exposure (instead of ADHD medication). This analysis enabled us to compare the general effects of being prescribed medication with the specific effects of ADHD medication. Fourth, to explore whether the association depends on the type of ADHD medication (stimulants vs nonstimulants), we performed sensitivity analysis on individuals who received only stimulant medications. Fifth, because the health registers lack information about whether the patient was a driver or passenger in an accident, we performed a sensitivity analysis restricted to motorcycle rider injuries (assuming that most patients were drivers). Finally, it is possible that the association between medication and transport accidents was due to life changes accompanied with medication status changes. We addressed this potential confounding by comparing the differences in risk of accidents between 2 consecutive periods (without ADHD medication vs with ADHD medication) for patients with different patterns of medication changes. 20

Quiz Ref ID The study included 10 528 men and 6880 women with ADHD aged 18 to 46 years in 2006 (see Table 1 for descriptive data at baseline and during follow-up). Among men diagnosed with ADHD, 57.5% had been prescribed ADHD medication and 6.5% had at least 1 serious transport accident during follow-up. The corresponding numbers in the matched general population controls were 0.3% and 2.6%, respectively. Among women with ADHD, 65.3% had been prescribed ADHD medication and 3.9% had at least 1 serious transport accident during follow-up compared with 0.2% and 1.8%, respectively, among controls.

Men with ADHD showed significantly higher rates of accidents than those without ADHD ( Table 2 ); the unadjusted hazard ratio (HR) was 2.45 (95% CI, 2.27-2.65). The association was attenuated but remained significant when controlling for sociodemographic factors, previous psychiatric diagnosis, other psychotropic medications, and criminal convictions (HR, 1.47; 95% CI, 1.32-1.63). Similar results were observed in young and middle-aged men (eTable 1 in the Supplement ). We found similar results for women (adjusted HR, 1.45; 95% CI, 1.24-1.71).

To explore the association between ADHD medication and serious transport accidents, we based all subsequent analyses on patients with ADHD. Comparing the accident rate during medication and nonmedication periods in men showed that ADHD medication decreased the accident rate by 29% (HR, 0.71; 95% CI, 0.57-0.89) ( Table 3 ). The association was not statistically significant in women (HR, 0.92; 95% CI, 0.78-1.23).

Quiz Ref ID Since patients receiving medication might be different from the nonmedicated patients, a within-individual analysis comparing the risk between medication and nonmedication periods is a more informative test of the association. For men, the stratified Cox proportional hazards regression, a within-individual comparison, showed that medication decreased the accident rate by 58% (HR, 0.42; 95% CI, 0.23-0.75) ( Table 3 ), illustrating that even within an individual (ie, after controlling for all confounders that are constant during follow-up and measured time-varying covariates), ADHD medication was associated with a significant reduction of accidents. The associations were similar in young and middle-aged men with ADHD (eTable 2 in the Supplement ). Again, we did not observe a significant association among women.

Because of the absence of significant associations in women, all sensitivity analyses of the association between ADHD medication and serious transport accidents were performed in men only. We observed a similar within-individual result when the cohort was identified from the Prescribed Drug Register (HR, 0.38) ( Table 5 ), suggesting our result was robust to selection criteria. We also observed similar results when excluding individuals with drug abuse or criminal convictions during the follow-up, although the estimate did not reach statistical significance because of the smaller sample size. In contrast to the reductions in risks when analyzing ADHD medication, there was no statistically significant association when we investigated the association between selective serotonin reuptake inhibitor medication and accidents (HR, 1.39; 95% CI, 0.62-3.14), suggesting the associations with ADHD medication were not due to the proclivity to take or discontinue medications in general. When analyzing stimulant medication only, we found a similar reduction in the rate of accidents (HR, 0.31). When restricting the outcome to motorcycle rider injuries, a strong rate reduction was observed (HR, 0.10). Finally, the risk of accidents increased when patients with ADHD moved from medication periods to nonmedication periods and decreased when moving from nonmedication periods to medication periods (eTable 3 in the Supplement ).

The present study found that patients with ADHD were at increased risk for serious transport accidents and that in male patients, ADHD medication was associated with reduced rates of accidents, even when using within-individual analyses.

Quiz Ref ID We found that individuals with ADHD had a 45% to 47% increased rate of serious transport accidents compared with individuals without ADHD, in both men and women. The magnitude of the association is similar to results from a population-based case-control study in North America. 7 Studies have suggested that visual inattentiveness and impulsiveness are the largest contributions to the risk of transport accidents in patients with ADHD. 6 Although the stability of ADHD from childhood to adulthood is increasingly recognized, 24 ADHD is still commonly underdiagnosed in adults. 11 , 29 Our results provide further evidence that the adverse effects of ADHD extend beyond the early years of driving.

Medications that alleviate ADHD symptoms might be expected to translate into safer driving behavior and subsequently reduce the risk of accidents. 30 Similar to a study on criminality 20 and experimental and clinical studies on stimulant medication effects on driving, 3 , 5 , 13 , 31 the results presented here clearly suggest that ADHD medication was associated with reduced rates of serious transport accidents. Compared with nonmedication periods, the transport accident rate during medication periods significantly decreased by 58% in men; a similar effect was found in young and middle-aged men. Our estimates of the PAF suggest that, under certain assumptions, 41% to 49% of the accidents in male patients with ADHD could have been avoided if they had been medicated the entire follow-up. It is important to note, however, that PAF estimates will be lower in countries with higher prescription rates than in Sweden 26 , 27 and that the beneficial effects of ADHD medication need to be weighed against potential adverse effects, including potential overprescription.

To our knowledge, this is the first population-based study of ADHD medication and serious transport accidents. Population-based register data have several strengths compared with clinical studies. The sample size is substantial and representative for the population, therefore avoiding referral bias, selective participation, and other threats to validity and generalizability. Diagnoses of ADHD are made by specialized psychiatrists in Sweden 32 and masked to outcomes. Medication for ADHD is recorded when a prescription is filled and free from recall bias. Nevertheless, observational studies are always liable to selection effects. 33 The biggest threat is that some patients might receive medication because they are different (usually more symptoms or with comorbid conditions). Unlike randomized clinical trials, observational studies such as ours cannot account for all possible confounders that select individuals to treatment. Our main attempt to control for this was within-individual analyses, which adjust for all potential confounders that are constant during the follow-up (genetic predisposition and early environment). However, unmeasured confounders and mediators that varied during follow-up (engagement with services that provide prescriptions, cyclic nature of the disorder itself, substance use, or crime records) can never be fully ruled out in this research design. To address this issue, we first analyzed accident rates among patients who had discontinued selective serotonin reuptake inhibitors instead of ADHD medication, where no association was found. Second, we analyzed the association in a subgroup of patients without any substance abuse or crime records during follow-up, and the within-individual estimate did not change substantially. Third, we compared the differences in risk of accidents between 2 consecutive periods when patients changed their medication status, and the association remained regardless of the order of change in medication status. Although these analyses are consistent with a causal hypothesis, they are only suggestive. Thus, future randomized clinical trials or observational studies with medication dosage information are obviously needed.

The findings should also be considered in the context of other limitations. First, we measured ADHD medication using dispensed prescriptions, and our study might be affected by poor medication adherence. This is similar to randomized clinical trials, and our effect estimate can be compared with an intent-to-treat analysis. We used a 6-month cutoff between prescriptions to define “off medication,” which is an empirical cutoff based on previous research. 18 - 20 To explore the potential influence of exposure misclassification, we reanalyzed the data with a 3-month cutoff and found a similar result (eTable 4 in the Supplement ). If some individuals did not take medication as prescribed, this would reduce the effect estimates; hence, our findings are probably conservative estimates of the actual effects of medication on accidents. Second, because of small numbers, we were not able to explore the specific effect of nonstimulant medication or compare different types of medication. However, the magnitude of the associations was similar when considering all medication and stimulant medication only. Third, we used emergency hospital visits or deaths due to transport accidents as our primary outcome, which is a serious outcome. In addition, we have no information on who was responsible for an accident, so an alternative interpretation might be that ADHD may impair one’s ability to avoid accidents initiated by others. Regardless of the culpability of the accident, injuries and deaths due to transport accidents are important public health concerns. Future research will need to explore whether the findings generalize to less severe outcomes of transport accidents. Fourth, we found no statistically significant evidence that medication was associated with serious transport accidents in female patients with ADHD. The between-individual estimate showed a small protective effect of medication. In contrast, the within-individual estimate suggested that medication increased the risk of accidents. However, these results were most likely chance findings as indicated by the wide confidence intervals. Finally, the findings are based on Swedish population data, and generalizations across cultures and countries should be made with caution. Although the ADHD prevalence and the overall rates of traffic fatality and disability are lower in Sweden compared with other developed counties, 1 , 24 the magnitude of risk among patients with ADHD was similar to other studies. 7

Quiz Ref ID We found that ADHD was associated with an increased risk of serious transport accidents and that ADHD medication use was associated with a reduced rate of accidents among male adult patients with ADHD. The World Health Organization predicts that traffic injuries will become the fifth leading cause of death by 2030. 1 The findings call attention to a prevalent, preventable, and costly cause of mortality and morbidity. The association between ADHD and serious transport accidents does not by itself justify withholding a driver’s license; nevertheless, our findings suggest that a large number of injuries and deaths due to traffic accidents associated with ADHD were conferred to periods when patients were off medication. Clinicians should consider informing patients about the increased risk for transport accidents associated with ADHD, 34 as well as possible benefits of ADHD medication. This would not only provide opportunities to reduce morbidity and mortality for patients with ADHD but also contribute to the public’s safety in transport.

Submitted for Publication: June 26, 2013; final revision received August 31, 2013; accepted October 4, 3013.

Corresponding Author: Zheng Chang, PhD, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, PO Box 281, 17177 Stockholm, Sweden ( [email protected] ).

Published Online: January 29, 2014. doi:10.1001/jamapsychiatry.2013.4174.

Author Contributions: Drs Chang and Lichtenstein contributed equally to this work. They had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Chang, Lichtenstein, D’Onofrio, Larsson.

Acquisition of data: Lichtenstein, Larsson.

Analysis and interpretation of data: Chang, Lichtenstein, Sjölander.

Drafting of the manuscript: Chang.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Chang, Lichtenstein, Sjölander.

Obtained funding: Lichtenstein, D’Onofrio.

Administrative, technical, or material support: Chang, Lichtenstein, D’Onofrio.

Study supervision: Lichtenstein, Larsson.

Conflict of Interest Disclosures: None reported.

Funding/Support: This study was supported in part by grants 2010-3184 and 2011-2492 from the Swedish Research Council, grant 2006-1625 from the Swedish Council for Working Life and Social Research, and grant HD061817 from the National Institute of Child Health and Human Development.

Role of the Sponsor: The funding sources had no role in the design and conduct of the study; collection, management, analysis, or interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

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  • Open access
  • Published: 26 February 2024

Polygenic risk for major depression, attention deficit hyperactivity disorder, neuroticism, and schizophrenia are correlated with experience of intimate partner violence

  • Andrew Ratanatharathorn   ORCID: orcid.org/0000-0001-9855-0438 1 , 2 ,
  • Luwei Quan 3 ,
  • Karestan C. Koenen   ORCID: orcid.org/0000-0003-2978-7655 2 , 4 , 5 , 6 ,
  • Lori B. Chibnik   ORCID: orcid.org/0000-0001-6293-806X 2 , 7 ,
  • Marc G. Weisskopf 2 , 3 ,
  • Natalie Slopen 4 &
  • Andrea L. Roberts   ORCID: orcid.org/0000-0001-5023-4399 3  

Translational Psychiatry volume  14 , Article number:  119 ( 2024 ) Cite this article

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Research has suggested that mental illness may be a risk factor for, as well as a sequela of, experiencing intimate partner violence (IPV). The association between IPV and mental illness may also be due in part to gene-environment correlations. Using polygenic risk scores for six psychiatric disorders - attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BPD), major depressive disorder (MDD), neuroticism, and schizophrenia—and a combined measure of overall genetic risk for mental illness, we tested whether women’s genetic risk for mental illness was associated with the experience of three types of intimate partner violence. In this cohort of women of European ancestry ( N  = 11,095), participants in the highest quintile of genetic risk for ADHD (OR range: 1.38–1.49), MDD (OR range: 1.28–1.43), neuroticism (OR range: (1.18–1.25), schizophrenia (OR range: 1.30–1.34), and overall genetic risk (OR range: 1.30–1.41) were at higher risk for experiencing more severe emotional and physical abuse, and, except schizophrenia, more severe sexual abuse, as well as more types of abuse and chronic abuse. In addition, participants in the highest quintile of genetic risk for neuroticism (OR = 1.43 95% CI: 1.18, 1.72), schizophrenia (OR = 1.33 95% CI: 1.10, 1.62), and the overall genetic risk (OR = 1.40 95% CI: 1.15, 1.71) were at higher risk for experiencing intimate partner intimidation and control. Participants in the highest quintile of genetic risk for ADHD, ASD, MDD, schizophrenia, and overall genetic risk, compared to the lowest quintile, were at increased risk for experiencing harassment from a partner (OR range: 1.22–1.92). No associations were found between genetic risk for BPD with IPV. A better understanding of the salience of the multiple possible pathways linking genetic risk for mental illness with risk for IPV may aid in preventing IPV victimization or re-victimization.

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In the United States, an estimated 37% of women will experience sexual violence, physical violence, or stalking by an intimate partner in their lifetimes [ 1 ]. Following an experience of intimate partner violence (IPV), women are more likely to also experience physical injury [ 2 ], job loss [ 3 ], and poorer mental health [ 1 ]. Poorer mental health includes mental illness, which has been found to precede [ 4 , 5 , 6 , 7 ] as well as follow [ 6 , 7 ] experiences of IPV, indicating that mental illness may be both a risk factor for and sequela of IPV. It is also possible that IPV and mental illness co-occur in part due to heritable genetic risk for mental illness [ 8 ]. Better understanding of the salience of the multiple possible pathways linking mental illness with risk for IPV may aid in treating IPV victimization or preventing re-victimization [ 8 ].

Co-occurrence between the environmental experience of IPV and genetic risk for mental illness is an example of gene-environment correlation (rGE), which could arise through at least two pathways (Fig. 1 ) [ 8 ]. In the passive rGE pathway, parental genetic risk for mental illness increases the likelihood of an adverse childhood environment for offspring, such as experiencing childhood abuse [ 9 , 10 , 11 ], low socioeconomic status (SES) [ 12 ], and parental divorce [ 9 , 13 , 14 , 15 ], which could then increase risk of offspring experiencing IPV. As offspring also inherit genetic risk for mental illness [ 16 ], a correlation is induced between offspring’s experience of IPV and mental illness. In the evocative rGE pathway, offspring genetic risk for mental illness may increase the likelihood of experiencing risk factors for IPV victimization, such as social isolation [ 7 , 17 , 18 ] or insecure attachment [ 19 , 20 ], or traits, such as low self-esteem [ 21 , 22 ], deficits in emotional dysregulation [ 23 , 24 ], or reduced ability to interpret facial expressions [ 25 , 26 , 27 ], that are associated with increased risk of IPV.

figure 1

Potential pathways by which genetic risk for mental illness may be associated with intimate partner violence.

Whether rGE exists between genetic risk for mental illness and experience of IPV may be informative to clinicians treating people with experience of IPV. For example, the experience of IPV may indicate a genetic liability for depression. Over time, the clinical utility of genotyping in determining the best pharmacological and psychotherapy treatment may improve, along with our understanding of the role of gene-by-environment interactions. If so, genotyping patients with depression and history of IPV may result in more personalized treatment [ 28 , 29 ]. However, to date, only a single twin study has examined rGE between depression and IPV finding modest evidence for rGE [ 30 ], but no study has tested whether genetic risk for a range of mental illnesses and genetic traits are correlated with the experience of IPV using genetic data. To address this, we estimated individual-level genetic risk for mental illness using polygenic risk scores (PRS) from publicly available summary statistics of genome-wide association studies of attention deficit hyperactivity disorder (ADHD) [ 31 ], autism spectrum disorders (ASD) [ 32 ], bipolar disorder (BPD) [ 33 ], major depressive disorder (MDD) [ 34 ], neuroticism [ 35 ], and schizophrenia (SCZ) [ 36 ] in a large cohort of US women, the Nurses’ Health Study II (NHS2), to examine whether genetic risk for mental illness was associated with experience of IPV. We additionally examined whether PRS was associated with experiencing multiple types of victimization (e.g., emotional, physical, sexual), chronic victimization, and harassment or stalking.

Materials and methods

The NHS2 is an ongoing cohort of 116,430 female nurses recruited in 1989 and assessed every two years. Participants were ages 24–44 years at baseline. Blood samples were collected from 29,611 participants between 1996 and 1999, as previously described [ 37 ]. Genome-wide data was available for 13,313 women based on three genotyping platforms: (1) Illumina Human Hap Array ( N  = 781), (2) Illumina OncoArray ( N  = 2722), and 3) Illumina HumanCore Exome Chip (Batch 1  N  = 3276; Batch 2  N  = 4568). Of these 13,313 participants, 11 701 (87.9%) completed questions assessing intimate partner violence. Following a standard quality control pipeline (call rate >0.90), participant genotype data were imputed using 1000 Genomes phase 3 reference data [ 38 ]. We included only participants of European ancestry ( N  = 11,344) as <2% of participants reported non-European ancestries and previous findings that PRS for mental illness developed from GWAS of European ancestry participants do not perform well for non-European ancestries due to differences in linkage disequilibrium patterns and frequency of alleles [ 39 ]. Informed consent was received from all participants. The study protocol was approved by the Institutional Review Boards of the Brigham and Women’s Hospital and the Harvard T.H. Chan School of Public Health (protocol number: 2012P002031).

Polygenic risk scores

PRS for ADHD [ 31 ], ASD [ 32 ], BPD [ 33 ], MDD [ 34 ], neuroticism [ 35 ], and schizophrenia [ 36 ] were calculated using the summary statistics from the largest published GWAS, with p value thresholds, clumping parameters, minor allele frequencies, and imputation score cutoffs based on those found to explain maximum variance based on Nagelkerke’s R 2 from each analysis (see Supplementary Table 1 ) [ 40 , 41 ]. Participant’s PRS for each mental illness was calculated by taking the weighted sum of risk alleles, with each allele weighted by the log odds ratio reported in published GWAS summary statistics using PRSice-2 [ 31 , 32 , 33 , 34 , 35 , 36 , 42 , 43 ]. PRS were then standardized using z score transformations. An overall PRS for mental illness for each participant was created by summing the six standardized PRS and then standardizing the result. Quintiles of genetic risk for each mental illness and the overall PRS were then calculated for each participant.

Intimate partner violence

In 2001, three sets of questions were used to assess experiences of IPV. First, participants were asked about lifetime occurrence of three types of abuse by their spouse or significant other: emotional (“ever been emotionally abused”); physical (“ever been hit, slapped, kicked, or otherwise physically hurt); and sexual (“ever forced to have sexual activities”). For each type, participants could respond “no, this never happened”, “yes, this happened once”, or “yes this happened more than once.” They were then asked to indicate the calendar years in which they experienced any of these types of abuse (1962–2001). To estimate severity of IPV, we calculated number of types of abuse as a count of types a respondent reported experiencing more than once (range: 0–3). We calculated abuse chronicity as the number of years in which they experienced abuse (0, 1, 2–3, or 4+ years).

Second, the experience of intimate partner intimidation and control was assessed with the 10-item Relationship Assessment Tool (RAT), which queried the degree to which women felt fearful, ashamed, disempowered, and controlled by their significant other [ 44 , 45 , 46 ] (e.g., “my partner can scare me without laying a hand on me”; “my partner makes me feel I have no control over my life…”), with responses ranging from 1: “strongly agree” to 6: “strongly disagree”. Scores on the RAT range from 10 to 60, with 10 indicating no feelings of intimidation and control and 60 indicating severe intimidation and control. Based on prior research, the scale was dichotomized at ≥20 to indicate the experience of intimate partner intimidation and control [ 46 ].

Third, eight questions based on the National Violence Against Women Survey assessed experience of harassment or stalking, including having someone spying or standing outside their home, school, or workplace; receiving unwanted letters, phone calls, or items; having property vandalized; or having to file a restraining order [ 47 ]. Participants were asked whether the perpetrator was a spouse or significant other, ex-spouse or ex-significant other, or other person. We defined harassment as having experienced any of these circumstances and created separate variables for history of harassment perpetrated by: 1) partners (spouses/significant others); 2) ex-partners (ex-spouses/ex-significant others); and 3) other persons, each coded any/none.

To account for residual population stratification—systematic differences in allele frequencies across ancestries that can lead to spurious results—we included 10 principal components derived from the genetic data as covariates [ 48 ].

Statistical analyses

Pearson correlations between each pair of PRS were calculated to examine the relationships between PRS. To ascertain whether genetic risk for mental illness was associated with emotional, physical, or sexual IPV, we fit separate ordinal logistic regressions with each type of IPV (emotional, physical, sexual) as the dependent variable coded as none, once, or more than once, and quintile of genetic risk as the independent variable. To estimate the association of PRS with number of types and chronicity of abuse, we fit separate ordinal logistic models to estimate odds ratios (ORs) of experiencing more severe abuse or more chronic abuse in association with a quintile of polygenic risk for each mental illness. The validity of the proportional odds assumption was assessed using Brant tests [ 49 ] and a likelihood test comparing an ordinal logistic model and multinomial (unconstrained) logistic model. Next, we fit a logistic regression to estimate the association between polygenic risk and lifetime experience of intimate partner intimidation and control, coded any/none. Finally, we estimated odds of lifetime experience of harassment perpetrated by: (1) partners; (2) ex-partners; and (3) others, with separate logistic regressions for each. To test whether linear increases in PRS for each trait were associated with an outcome, we refit models coding PRS as a continuous variable rather than in quintiles. All models adjusted for genomic assay and top 10 principal components of genetic ancestry. To assess the independent effect of each PRS, models were refit including the PRS of ADHD, ASD, BPD, MDD, neuroticism, and schizophrenia. Analyses were performed using R version 4.02 [ 50 ].

One-quarter of participants reported experiencing physical IPV (once: 13.2%, more than once: 11.1%), 41.5% reported emotional IPV (once: 8.4%, more than once: 33.1%) and 12.3% reported sexual IPV (once: 5.7%, more than once 6.6%, Table 1 ). Overall, 21.4% of participants reported experiencing at least one type of abuse more than once, and 3.4% reported experiencing all three types of abuse more than once. 13.5% of participants reported experiencing intimate partner intimidation and control. Regarding experiences of harassment, women experienced these perpetrated by a partner least often (9.2%), followed by an ex-partner (13.3%), and then by someone else (15.7%). In our analysis of correlations among PRS, we found, first, that ADHD and BPD ( r  = 0.63), BPD and schizophrenia ( r  = 0.48), and ADHD and schizophrenia ( r  = 0.38) were positively correlated with each other and negatively correlated with neuroticism ( r range: −0.17 to −0.29) and MDD (r range: −0.04 to −0.15). Second, we found that neuroticism and MDD were correlated with each other ( r  = 0.26). ASD was not correlated with any other PRS (see Supplementary Fig. S1 ).

Participants in the highest quintile of PRS for ADHD were at increased risk for experiencing intimate partner emotional (OR = 1.44, 95% CI: 1.18, 1.77, Fig. 2 ; Supplementary Table 2 ), physical (OR = 1.38, 95% CI: 1.09, 1.74), and sexual IPV (OR = 1.42, 95% CI: 1.04, 1.94) as well as more types of IPV (OR = 1.49, 95% CI: 1.21, 1.84) and chronic IPV (OR = 1.39, 95% CI: 1.15, 1.69) as compared to the lowest quintile. In tests of trend, increasing ADHD PRS was associated with experience of emotional (OR = 1.12, 95% CI: 1.05, 1.20) and physical IPV (OR = 1.14, 95% CI: 1.05, 1.23), but not sexual IPV (OR = 1.08, 95% CI: 0.98, 1.20; Supplementary Table 2 ). Participants with PRS in the top quintile for MDD (OR range: 1.28–1.43), neuroticism (OR range: (1.18–1.25), and schizophrenia (OR range: 1.13–1.36) were also at increased risk of experiencing emotional, physical, and sexual IPV (MDD only), as well as more types of IPV and more chronic IPV (Fig. 2 ; Supplementary Table 2 ) as compared to the bottom quintile. Tests of trend were significant for polygenic risk for each of these outcome-trait pairs, except for the experience of sexual IPV and the neuroticism and schizophrenia PRS (Supplementary Table 2 ). The highest quintile of combined PRS for mental illness was associated with experiencing emotional (OR = 1.37, 95% CI: 1.20, 1.57), physical (OR = 1.39, 95% CI: 1.19, 1.63), and sexual IPV (OR = 1.30, 95% CI: 1.06, 1.59), as well as more types of IPV (OR = 1.41, 95% CI: 1.23, 1.62) and more chronic IPV (OR = 1.37, 95% CI: 1.21, 1.56) as compared to those in the lowest quintile. Models including PRS for all six traits, excluding the combined PRS, yielded similar results (see Supplementary Fig. 2 ).

figure 2

Odds ratios and 95% confidence intervals (CI) associated with quintiles of mental disorder polygenic risk score (PRS) for experiencing emotional, physical, or sexual abuse, greater number of types of IPV, and more chronic IPV, adjusted for genomic assay, and the top 10 principal components of genetic ancestry.

Participants in the highest quintile of PRS for neuroticism (OR = 1.43 95% CI: 1.18, 1.72), schizophrenia (OR = 1.33 95% CI: 1.10, 1.62), and the combined PRS (OR = 1.40 95% CI: 1.15, 1.71) were at higher risk (Fig. 3 ; Supplementary Table 3 ) for experiencing intimate partner violence and control compared to those in the lowest quintile. Participants in the second quintile of genetic risk for BPD were less likely to experience intimate partner violence and control. However, increasing quintiles of genetic risk were not associated, nor was a test of trend. Tests of the trend for neuroticism, schizophrenia, and the combined PRS were statistically significant (Supplementary Table 3 ). Associations between each PRS and experience of intimate partner violence and control were consistent when all PRS were included in a single model (see Supplementary Fig. 3 ).

figure 3

Odds ratios and 95% confidence intervals (CI) associated with quintiles of each mental disorder polygenic risk score (PRS) for experiencing intimate partner intimidation and control as measured by a score ≥20 on the RAT, adjusted for parental education, parental occupation, genomic assay, and the top 10 principal components of genetic ancestry.

Participants in the highest quintile of PRS for ADHD (OR = 1.92, 95% CI: 1.35, 2.74), ASD (OR = 1.30, 95% CI: 1.06, 1.59), schizophrenia (OR = 1.38, 95% CI: 1.10, 1.72), and overall genetic risk (OR = 1.45, 95% CI: 1.16, 1.81) were likely to experience harassment by a partner (Fig. 4 ; Supplementary Table 4 ). Participants in the highest quintile of PRS for ADHD, MDD, schizophrenia, and overall genetic risk were at increased risk of experiencing harassment by an ex-partner (OR range: 1.28–1.49), while participants in the highest quintile of PRS for MDD (OR = 1.33, 95% CI: 1.13, 1.57) and overall PRS (OR = 1.38, 95% CI:1.15, 1.65) were at increased risk for experiencing harassment from another person. Results were consistent when all six PRS were included in a single model for each type of harassment (see Supplementary Fig. 4 ).

figure 4

The association between the ADHD PRS and experiencing harassment by a partner was (OR = 1.91; 95% CI: 1.34, 2.72).

In this study of 11,344 women, PRS for ADHD, MDD, neuroticism, schizophrenia, and combined mental illness were consistently associated with experience of physical, emotional, and sexual IPV, number of types of IPV experienced, and chronicity of IPV. Beyond the experience of IPV, we found that PRS for neuroticism, schizophrenia, and overall genetic risk were also associated with intimate partner intimidation and control. PRS for ADHD, ASD, MDD, schizophrenia, and combined mental illness were significantly associated with harassment from a current or former partner.

Although previous work in this cohort and another have found that genetic risk for BPD was associated with the experience of childhood abuse [ 51 , 52 ], the BPD PRS was not associated with increased risk for any type of IPV and was mildly protective for the experience of intimate partner intimidation and control. One possible reason for the lack of associations with BPD is that genetic risk for BDP has been shown to be genetically correlated with higher educational attainment [ 33 ], which has been shown to be a protective factor for IPV [ 53 , 54 , 55 ]. Any increased risk for experiencing IPV stemming from genetic risk for BPD may be reduced by increased educational attainment or other protective factors associated with genetic risk for BPD.

These results build upon prior studies, which have found that depression [ 17 ] and ADHD [ 6 ] are associated with a higher likelihood of subsequently experiencing IPV. Studies examining neuroticism [ 56 , 57 ] and ASD [ 58 , 59 ] as predictors of experiencing interpersonal and intimate partner violence have yielded mixed results. However, these studies did not uniformly adjust for identified predictors of IPV that may have confounded the findings, such as childhood abuse [ 9 , 15 ], low parental educational attainment [ 60 ], and low adulthood SES [ 12 , 61 ], while our study utilized genetic data unaffected by environmental stressors [ 62 , 63 ] and not subjected to confounding by these factors or to reverse causation as PRS are set at birth and are not influenced by later experiences of IPV.

Our results expand upon previous findings that genetic risk for mental illness is positively associated with the likelihood of experiencing stressful life events such as childhood abuse [ 52 , 64 ] and trauma [ 65 , 66 ]. Multiple pathways potentially link genetic risk for mental illness with risk of IPV victimization, through selection of romantic partners, dynamics within relationships, and ability to leave abusive relationships. First, childhood factors that were not measured in the present study, such as parents modeling healthy interpersonal relationships [ 67 , 68 ], teaching communication skills [ 69 ], and positive parenting [ 70 , 71 ], may account for some of the associations we found. These factors are positively associated with parents’ mental well-being and, therefore likely to be negatively associated with parents’ PRS for mental illness. The absence of these childhood factors is associated with increased IPV risk in offspring. Second, a higher genetic risk for mental illnesses may be linked to cognitive and behavioral factors that increase the risk of experiencing IPV. For example, higher PRS for ASD [ 72 ] and schizophrenia [ 73 ] have been associated with greater inability to recognize facial emotions in others, which is a risk factor for experiencing IPV[ 25 , 26 , 27 ]. Third, genetic risk for mental illness may be associated with reduced emotional, instrumental, and informational social support from friends and family in adulthood, which may affect women’s risk of IPV and impair their ability to exit an abusive relationship [ 74 , 75 , 76 ].

Our study is subject to several limitations. First, the PRS for mental illness typically explains a low proportion of variability when predicting out-of-sample outcomes (Nagelkerke R 2  = 0.01, see Supplementary Table 1 .). This may have led to attenuated estimates of true associations between genetic risk and IPV. Second, our study was conducted in a sample of female European ancestry nurses. Our analyses should be replicated in a sample with greater demographic diversity. Moreover, the manner in which high PRS for mental illnesses manifests within this sample of high-functioning individuals may vary from that of the general public.

In providing evidence that genetic risk for mental illness is associated with experience of IPV, our study has potential implications for future treatment and prevention efforts. First, screening for and interventions to reduce the risk of IPV should be considered among women seeking treatment for mental illness, where prevalence rates of IPV are higher [ 77 ]. Currently, the broad incorporation of IPV screening tools in mental health services is still largely absent [ 77 ], and 60% of mental health providers feel unprepared to properly support survivors of IPV [ 78 ]. Second, a better understanding of the salience of the multiple possible pathways linking genetic risk for mental illness with risk for IPV may aid in preventing IPV victimization or re-victimization (e.g., difficulties with peer relations, lower academic attainment, and lower self-esteem have been identified as sequelae of ADHD that may lead to other difficulties) [ 79 , 80 ]. Without blaming victims, if specific traits, behaviors, or circumstances in persons with genetic loading for various mental illnesses were found, for example, to adversely affect the selection of romantic partners, then addressing these factors might reduce the risk of victimization. Third, although our findings do not have immediate clinical implications, a better understanding of the co-occurrence of IPV and genetic risk for mental illness may lead to more personalized treatments for patients with experiences of IPV. For example, it is hypothesized that depression is a heterogeneous disorder in part due to co-occurrence of, and interaction between, adverse environments and genetic risk factors [ 28 ]. Future studies may benefit from examining the extent to which risk for IPV results from interactions of familial, relationship, community, and cultural drivers of IPV with genetic loading for mental illness.

Data availability

All data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials . Data from the Nurses Health Study are available through the study’s website: https://nurseshealthstudy.org/researchers .

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Acknowledgements

This research was funded in part by R01HD094725 (to ALR). The Nurses’ Health Study II is funded by U01 CA176726. We would like to thank the participants and staff of the NHS2 for their valuable contributions and acknowledge the Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital for its management of the NHS2. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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Conceptualization: ALR methodology: AR, LBC, ALR writing—original draft: AR, ALR, LQ. Writing—review & editing: ALR, AR, LQ, KCK, LBC, MW, NS.

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Ratanatharathorn, A., Quan, L., Koenen, K.C. et al. Polygenic risk for major depression, attention deficit hyperactivity disorder, neuroticism, and schizophrenia are correlated with experience of intimate partner violence. Transl Psychiatry 14 , 119 (2024). https://doi.org/10.1038/s41398-024-02814-1

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Received : 16 January 2023

Revised : 15 December 2023

Accepted : 01 February 2024

Published : 26 February 2024

DOI : https://doi.org/10.1038/s41398-024-02814-1

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