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We curate evidence by systematically reviewing the scientific literature to select studies meeting a very high level of evidence. We limit our curation to two types of evidence: meta-analyses and very large studies. Meta-analyses combine

Stephen Faraone, PhD

Distinguished Professor and Vice Chair of Research of Psychiatry and Behavioral Sciences Professor of Neuroscience and Physiology , Professor of Neuroscience Graduate Program

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This set of slides provides an overview of the diagnosis and treatment of ADHD.   It can be used as a presentation meant to be given by someone with prior knowledge of these topics.  Feel free to add or delete slides to this set to accommodate your audience.

La Declaration de Consensus International sur le Trouble Déficit d’Attention Hyperactivité:​Implications pour le Diagnostic et le Traitement

Ces diapositives constituent une introduction à la Déclaration de consensus internationale sur le TDAH. Elles décrivent les méthodes et les résultats les plus pertinents pour le diagnostic et le traitement de ce trouble. Le texte qui accompagne chaque diapositive est la manière dont les diapositives ont été présentées par le Professeur Faraone lors du "Symposium international sur le TDAH".

International Consensus Statement

This set of 370 slides is not meant to be a single presentation.  Instead, it is meant to provide slides that describe the findings reported in the International Consensus Statement of ADHD.  Educators can use these slides to create presentations crafted for their educational goals.

La Declaration de Consensus International sur le Trouble Deficit d’Attention Hyperactivityé:​ Implications pour le Diagnostic et le Traitement

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This guide provides information to those who would like to know more about ADHD Coaching. Some countries have official guidelines for treating ADHD and can provide suitable treatment for adults; even some coaching. In other countries, recognition of both ADHD and the various treatments may be rare.

ADHD in Children with Dr. Stephen Faraone

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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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• Attention-deficit/hyperactivity disorder (ADHD) in children

Attention-deficit/hyperactivity disorder (ADHD) is a chronic condition that affects millions of children and often continues into adulthood. ADHD includes a combination of persistent problems, such as difficulty sustaining attention, hyperactivity and impulsive behavior.

Children with ADHD may also struggle with low self-esteem, troubled relationships and poor performance in school. Symptoms sometimes lessen with age. However, some people never completely outgrow their ADHD symptoms. But they can learn strategies to be successful.

While treatment won't cure ADHD , it can help a great deal with symptoms. Treatment typically involves medications and behavioral interventions. Early diagnosis and treatment can make a big difference in outcome.

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The primary features of ADHD include inattention and hyperactive-impulsive behavior. ADHD symptoms start before age 12, and in some children, they're noticeable as early as 3 years of age. ADHD symptoms can be mild, moderate or severe, and they may continue into adulthood.

ADHD occurs more often in males than in females, and behaviors can be different in boys and girls. For example, boys may be more hyperactive and girls may tend to be quietly inattentive.

There are three subtypes of ADHD :

• Predominantly inattentive. The majority of symptoms fall under inattention.
• Predominantly hyperactive/impulsive. The majority of symptoms are hyperactive and impulsive.
• Combined. This is a mix of inattentive symptoms and hyperactive/impulsive symptoms.

Inattention

A child who shows a pattern of inattention may often:

• Fail to pay close attention to details or make careless mistakes in schoolwork
• Have trouble staying focused in tasks or play
• Appear not to listen, even when spoken to directly
• Have difficulty following through on instructions and fail to finish schoolwork or chores
• Have trouble organizing tasks and activities
• Avoid or dislike tasks that require focused mental effort, such as homework
• Lose items needed for tasks or activities, for example, toys, school assignments, pencils
• Be easily distracted
• Forget to do some daily activities, such as forgetting to do chores

Hyperactivity and impulsivity

A child who shows a pattern of hyperactive and impulsive symptoms may often:

• Fidget with or tap his or her hands or feet, or squirm in the seat
• Have difficulty staying seated in the classroom or in other situations
• Be on the go, in constant motion
• Run around or climb in situations when it's not appropriate
• Have trouble playing or doing an activity quietly
• Talk too much
• Blurt out answers, interrupting the questioner
• Have difficulty waiting for his or her turn
• Interrupt or intrude on others' conversations, games or activities

Typical developmental behavior vs. ADHD

Most healthy children are inattentive, hyperactive or impulsive at one time or another. It's typical for preschoolers to have short attention spans and be unable to stick with one activity for long. Even in older children and teenagers, attention span often depends on the level of interest.

The same is true of hyperactivity. Young children are naturally energetic — they often are still full of energy long after they've worn their parents out. In addition, some children just naturally have a higher activity level than others do. Children should never be classified as having ADHD just because they're different from their friends or siblings.

Children who have problems in school but get along well at home or with friends are likely struggling with something other than ADHD . The same is true of children who are hyperactive or inattentive at home, but whose schoolwork and friendships remain unaffected.

When to see a doctor

If you're concerned that your child shows signs of ADHD , see your pediatrician or family doctor. Your doctor may refer you to a specialist, such as a developmental-behavioral pediatrician, psychologist, psychiatrist or pediatric neurologist, but it's important to have a medical evaluation first to check for other possible causes of your child's difficulties.

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While the exact cause of ADHD is not clear, research efforts continue. Factors that may be involved in the development of ADHD include genetics, the environment or problems with the central nervous system at key moments in development.

Risk factors

Risk factors for ADHD may include:

• Blood relatives, such as a parent or sibling, with ADHD or another mental health disorder
• Exposure to environmental toxins — such as lead, found mainly in paint and pipes in older buildings
• Maternal drug use, alcohol use or smoking during pregnancy
• Premature birth

Although sugar is a popular suspect in causing hyperactivity, there's no reliable proof of this. Many issues in childhood can lead to difficulty sustaining attention, but that's not the same as ADHD .

Complications

ADHD can make life difficult for children. Children with ADHD :

• Often struggle in the classroom, which can lead to academic failure and judgment by other children and adults
• Tend to have more accidents and injuries of all kinds than do children who don't have ADHD
• Tend to have poor self-esteem
• Are more likely to have trouble interacting with and being accepted by peers and adults
• Are at increased risk of alcohol and drug abuse and other delinquent behavior

Coexisting conditions

ADHD doesn't cause other psychological or developmental problems. However, children with ADHD are more likely than others to also have conditions such as:

• Oppositional defiant disorder (ODD), generally defined as a pattern of negative, defiant and hostile behavior toward authority figures
• Conduct disorder, marked by antisocial behavior such as stealing, fighting, destroying property, and harming people or animals
• Disruptive mood dysregulation disorder, characterized by irritability and problems tolerating frustration
• Learning disabilities, including problems with reading, writing, understanding and communicating
• Substance use disorders, including drugs, alcohol and smoking
• Anxiety disorders, which may cause overwhelming worry and nervousness, and include obsessive compulsive disorder (OCD)
• Mood disorders, including depression and bipolar disorder, which includes depression as well as manic behavior
• Autism spectrum disorder, a condition related to brain development that impacts how a person perceives and socializes with others
• Tic disorder or Tourette syndrome, disorders that involve repetitive movements or unwanted sounds (tics) that can't be easily controlled

To help reduce your child's risk of ADHD :

• During pregnancy, avoid anything that could harm fetal development. For example, don't drink alcohol, use recreational drugs or smoke cigarettes.
• Protect your child from exposure to pollutants and toxins, including cigarette smoke and lead paint.
• Limit screen time. Although still unproved, it may be prudent for children to avoid excessive exposure to TV and video games in the first five years of life.

Attention-deficit/hyperactivity disorder (ADHD) in children care at Mayo Clinic

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• AskMayoExpert. Attention-deficit/hyperactivity disorder. Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2017.
• Voight RG, et al., eds. Attention-deficit/hyperactivity disorder. In: American Academy of Pediatrics Developmental and Behavioral Pediatrics. 2nd ed. Itasca, IL: American Academy of Pediatrics; 2018.
• Attention-deficit/hyperactivity disorder. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd/index.shtml. Accessed Jan 26, 2019.
• My child has been diagnosed with ADHD ― Now what? Centers for Disease Control and Prevention. https://www.cdc.gov/ncbddd/adhd/treatment.html. Accessed Jan. 26, 2019.
• What is ADHD? American Psychiatric Association. https://www.psychiatry.org/patients-families/adhd/what-is-adhd. Accessed Jan. 26, 2019.
• ADHD. National Alliance on Mental Illness. https://www.nami.org/Learn-More/Mental-Health-Conditions/ADHD/Overview. Accessed Jan. 26, 2019.
• Ra CK, et al. Association of digital media use with subsequent symptoms of attention-deficit/hyperactivity disorder among adolescents. JAMA. 2018;320:255.
• For parents and caregivers. National Resource Center on ADHD. https://chadd.org/for-parents/overview/. Accessed Jan. 28, 2019.
• Complementary and integrative approaches for ADHD: What the science says. National Center for Complementary and Integrative Health. https://nccih.nih.gov/health/providers/digest/adhd-science. Accessed Jan. 28, 2019.
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• Partain PI, et al. New stimulant formulations for pediatric attention-deficit/hyperactivity disorder: A case-based approach for the primary care provider. Current Opinion in Pediatrics. 2019;31:166.
• Attention-deficit/hyperactivity disorder: Data and statistics. Centers for Disease Control and Prevention. https://www.cdc.gov/ncbddd/adhd/data.html. Accessed Jan. 30, 2019.
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• Catala-Lopez F, et al. The pharmacological and non-pharmacological treatment of attention deficit hyperactivity disorder in children and adolescents: A systematic review with network meta-analyses of randomised trials. PloSOne. 2017;12:e0180355.
• Mazhar H, et al. Complementary and alternative medicine use in pediatric attention-deficit hyperactivity disorder (ADHD): Reviewing the safety and efficacy of herbal medicines. Current Developmental Disorders Reports. 2016;3:15.
• Ahn J, et al. Natural product-derived treatments for attention-deficit/hyperactivity disorder: Safety, efficacy, and therapeutic potential of combination therapy. Neural Plasticity. 2016;2016:1320423.
• American Academy of Pediatrics. Media and young minds. Pediatrics. 2016;138:e20162591.
• Voight RG, et al., eds. Complementary health approaches in developmental and behavioral pediatrics. In: American Academy of Pediatrics Developmental and Behavioral Pediatrics. 2nd ed. Itasca, IL: American Academy of Pediatrics; 2018.
• Moran LV, et al. Psychosis with methylphenidate or amphetamine in patients with ADHD. New England Journal of Medicine. 2019;380:1128.
• Berger S. Attention deficit hyperactivity disorder medications in children with heart disease. Current Opinion in Pediatrics. 2016;28:607.
• Storebo OJ, et al. Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents ― Assessment of adverse events in non-randomised studies. Cochrane Database of Systematic Reviews. https://www.cochranelibrary.com/. Accessed April 1, 2019.
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ADHD: Current Concepts and Treatments in Children and Adolescents

Renate drechsler.

1 Department of Child and Adolescent Psychiatry and Psychotherapy, University Hospital of Psychiatry, University of Zurich, Zurich, Switzerland

Silvia Brem

2 Neuroscience Center Zurich, Swiss Federal Institute of Technology and University of Zurich, Zurich, Switzerland

Daniel Brandeis

3 Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany

4 Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland

Edna Grünblatt

Gregor berger, susanne walitza.

Attention deficit hyperactivity disorder (ADHD) is among the most frequent disorders within child and adolescent psychiatry, with a prevalence of over 5%. Nosological systems, such as the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) and the International Classification of Diseases, editions 10 and 11 (ICD-10/11) continue to define ADHD according to behavioral criteria, based on observation and on informant reports. Despite an overwhelming body of research on ADHD over the last 10 to 20 years, valid neurobiological markers or other objective criteria that may lead to unequivocal diagnostic classification are still lacking. On the contrary, the concept of ADHD seems to have become broader and more heterogeneous. Thus, the diagnosis and treatment of ADHD are still challenging for clinicians, necessitating increased reliance on their expertise and experience. The first part of this review presents an overview of the current definitions of the disorder (DSM-5, ICD-10/11). Furthermore, it discusses more controversial aspects of the construct of ADHD, including the dimensional versus categorical approach, alternative ADHD constructs, and aspects pertaining to epidemiology and prevalence. The second part focuses on comorbidities, on the difficulty of distinguishing between “primary” and “secondary” ADHD for purposes of differential diagnosis, and on clinical diagnostic procedures. In the third and most prominent part, an overview of current neurobiological concepts of ADHD is given, including neuropsychological and neurophysiological researches and summaries of current neuroimaging and genetic studies. Finally, treatment options are reviewed, including a discussion of multimodal, pharmacological, and nonpharmacological interventions and their evidence base.

Introduction

With a prevalence of over 5%, attention deficit hyperactivity disorder (ADHD) is one of the most frequent disorders within child and adolescent psychiatry. Despite an overwhelming body of research, approximately 20,000 publications have been referenced in PubMed during the past 10 years, assessment and treatment continue to present a challenge for clinicians. ADHD is characterized by the heterogeneity of presentations, which may take opposite forms, by frequent and variable comorbidities and an overlap with other disorders, and by the context-dependency of symptoms, which may or may not become apparent during clinical examination. While the neurobiological and genetic underpinnings of the disorder are beyond dispute, biomarkers or other objective criteria, which could lead to an automatic algorithm for the reliable identification of ADHD in an individual within clinical practice, are still lacking. In contrast to what one might expect after years of intense research, ADHD criteria defined by nosological systems, such as the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) and the International Classification of Diseases, editions 10 and 11 (ICD-10/11) have not become narrower and more specific. Rather, they have become broader, for example, encompassing wider age ranges, thus placing more emphasis on the specialist's expertise and experience. 1 2 3

Definitions and Phenomenology

Adhd according to the dsm-5 and icd-10/11.

ADHD is defined as a neurodevelopmental disorder. Its diagnostic classification is based on the observation of behavioral symptoms. ADHD according to the DSM-5 continues to be a diagnosis of exclusion and should not be diagnosed if the behavioral symptoms can be better explained by other mental disorders (e.g., psychotic disorder, mood or anxiety disorder, personality disorder, substance intoxication, or withdrawal). 1 However, comorbidity with other mental disorders is common.

In the DSM-5, the defining symptoms of ADHD are divided into symptoms of inattention (11 symptoms) and hyperactivity/impulsivity (9 symptoms). 1 The former differentiation between subtypes in the DSM-IV proved to be unstable and to depend on the situational context, on informants, or on maturation, and was therefore replaced by “presentations.” 4 Thus, the DSM-5 distinguishes between different presentations of ADHD: predominantly inattentive (6 or more out of 11 symptoms present), predominantly hyperactive/impulsive (6 or more out of 9 symptoms present), and combined presentation (both criteria fulfilled), as well as a partial remission category. Symptoms have to be present in two or more settings before the age of 12 years for at least 6 months and have to reduce or impair social, academic, or occupational functioning. In adolescents over 17 years and in adults, five symptoms per dimension need to be present for diagnosis. 1 In adults, the use of validated instruments like the Wender Utah rating scale is recommended. 5

In contrast, the ICD-10 classification distinguishes between hyperkinetic disorder of childhood (with at least six symptoms of inattention and six symptoms of hyperactivity/impulsivity, present before the age of 6 years) and hyperkinetic conduct disorder, a combination of ADHD symptoms and symptoms of oppositional defiant and conduct disorders (CD). 3 In the ICD-11 (online release from June 2018, printed release expected 2022), the latter category has been dropped, as has the precise age limit (“onset during the developmental period, typically early to mid-childhood”). Moreover, the ICD-11 distinguishes five ADHD subcategories, which match those of the DSM-5: ADHD combined presentation, ADHD predominantly inattentive presentation, ADHD predominantly hyperactive/impulsive presentation and two residual categories, ADHD other specified and ADHD nonspecified presentation. For diagnosis, behavioral symptoms need to be outside the limits of normal variation expected for the individual's age and level of intellectual functioning. 2

Overlapping Constructs: Sluggish Cognitive Tempo and Emotional Dysregulation

Sluggish cognitive tempo (SCT) is a clinical construct characterized by low energy, sleepiness, and absent-mindedness, and is estimated to occur in 39 to 59% of (adult) individuals with ADHD. 6 7 The question of whether SCT might constitute a feature of ADHD or a separate construct that overlaps with ADHD inattention symptoms is unresolved. 8 While current studies indicate that SCT might be distinct and independent from hyperactivity/impulsivity, as well as from inattention dimensions, it remains uncertain whether it should be considered as a separate disorder. 8 9 Twin studies have revealed a certain overlap between SCT and ADHD, especially with regard to inattention symptoms, but SCT seems to be more strongly related to nonshared environmental factors. 10

Emotion dysregulation is another associated feature that has been discussed as a possible core component of childhood ADHD, although it is not included in the DSM-5 criteria. Deficient emotion regulation is more typically part of the symptom definition of other psychopathological disorders, such as oppositional defiant disorder (ODD), CD, or disruptive mood dysregulation disorder (DSM-5; for children up to 8 years). 11 However, an estimated 50 to 75% of children with ADHD also present symptoms of emotion dysregulation, for example, anger, irritability, low tolerance for frustration, and outbursts, or sometimes express inappropriate positive emotions. The presence of these symptoms increases the risk for further comorbidities, such as ODD and also for anxiety disorders. 12 13 For adult ADHD, emotional irritability is a defining symptom according to the Wender Utah criteria, and has been confirmed as a primary ADHD symptom by several studies (e.g., Hirsch et al). 5 14 15

Whether emotion dysregulation is inherent to ADHD, applies to a subgroup with combined symptoms and a singular neurobiological pathway, or is comorbid with but independent of ADHD, is still a matter of debate (for a description of these three models; Shaw et al 13 ). Faraone et al 12 distinguished three ADHD prototypes with regard to deficient emotion regulation: ADHD prototype 1 with high-emotional impulsivity and deficient self-regulation, prototype 2 with low-emotional impulsivity and deficient self-regulation, and prototype 3 with high-emotional impulsivity and effective self-regulation. All three prototypes are characterized by an inappropriate intensity of emotional response. While prototypes 1 and 3 build up their responses very quickly, prototype 2 is slower to respond but experiences higher subjective emotional upheaval than is overtly shown in the behavior. Prototypes 1 and 2 both need more time to calm down compared with prototype 3 in which emotional self-regulation capacities are intact.

Dimensional versus Categorical Nature of ADHD

Recent research on subthreshold ADHD argues in favor of a dimensional rather than categorical understanding of the ADHD construct, as its core symptoms and comorbid features are dimensionally distributed in the population. 16 17 18 Subthreshold ADHD is common in the population, with an estimated prevalence of approximately 10%. 19 According to Biederman and colleagues, clinically referred children with subthreshold ADHD symptoms show a similar amount of functional deficits and comorbid symptoms to those with full ADHD, but tend to come from higher social-class families with fewer family conflicts, to have fewer perinatal complications, and to be older and female (for the latter two, a confound with DSM-IV criteria cannot be excluded). 20

Temperament and Personality Approaches to ADHD

Another approach which is in accordance with a dimensional concept is to analyze ADHD and categorize subtypes according to temperament/personality traits (for a review and the different concepts of temperament see Gomez and Corr 21 ). Temperament/personality traits are usually defined as neurobiologically based constitutional tendencies, which determine how the individual searches for or reacts to external stimulation and regulates emotion and activity. While temperament traits per se are not pathological, extreme variations or specific combinations of traits may lead to pathological behavior. This approach has been investigated in several studies by Martel and colleagues and Nigg, 22 23 24 who employed a temperament model comprising three empirically derived domains 25 26 : (1) negative affect, such as tendencies to react with anger, frustration, or fear; (2) positive affect or surgency which includes overall activity, expression of happiness, and interest in novelty; and (3) effortful control which is related to self-regulation and the control of action. The latter domain shows a strong overlap with the concept of executive function. 27 In a community sample, early temperamental traits, especially effortful control and activity level, were found to potentially predict later ADHD. 28 Karalunas et al 29 30 distinguished three temperament profiles in a sample of children with ADHD: one with normal emotional functioning; one with high surgency, characterized by high levels of positive approach-motivated behaviors and a high–activity level; and one with high negative (“irritable”) affect, with the latter showing the strongest, albeit only moderate stability over 2 years. Irritability was not reducible to comorbidity with ODD or CD and was interpreted as an ADHD subgroup characteristic with predictive validity for an unfavorable outcome. These ADHD temperament types were distinguished by resting-state and peripheral physiological characteristics as measured by functional magnetic resonance imaging (fMRI). 29

Epidemiology and Prevalence

While ADHD seems to be a phenomenon that is encountered worldwide, 31 prevalence rates and reported changes in prevalence are highly variable, depending on country and regions, method, and sample. 32 A meta-analysis by Polanczyk et al 32 yielded a worldwide prevalence rate of 5.8% in children and adolescents. 33 In an update published 6 years later, the authors did not find evidence for an increase in prevalence over a time span of 30 years. Other meta-analyses reported slightly higher (e.g., 7.2%) 34 or lower prevalence rates, which seems to be attributable to the different criteria adopted for defining ADHD. Prevalence rates in children and adolescents represent averaged values across the full age range, but peak prevalence may be much higher in certain age groups, for example, 13% in 9-year-old boys. 35 Universal ADHD prevalence in adults is estimated to lie at 2.8%, with higher rates in high-income (3.6%) than in low-income (1.4%) countries. 36 True prevalence rates (also called community prevalence, e.g., Sayal et al 37 ) should be based on population-based representative health surveys, that is, the actual base rate of ADHD in the population, in contrast to the administrative base rate, which is related to clinical data collection (Taylor 38 ). Recent reports on the increase in ADHD rates usually refer to administrative rates, drawn from health insurance companies, from the number of clinical referrals for ADHD, 39 clinical case identification estimates, or from the percentage of children taking stimulant medication (prescription data). Changes in these rates may be influenced by increased awareness, destigmatization, modifications in the defining criteria of ADHD, or altered medical practice. According to a recent U.S. health survey on children and adolescents (4–17 years), in which parents had to indicate whether their child had ever been diagnosed with ADHD, the percentage of diagnoses increased from 6.1% in 1997 to 10.2% in 2016. 40 A representative Danish survey based on health registry, data collected from 1995 to 2010 reported that ADHD incidence rates increased by a factor of approximately 12 (for individuals aged 4–65 years) during this period. Moreover, the gender ratio decreased from 7.5:1 to 3:1 at early school age and from 8.1:1 to 1.6:1 in adolescents in the same time frame, 41 42 probably indicating an improved awareness of ADHD symptoms in girls. In other countries, it is assumed that girls are still underdiagnosed. 38

Population register data show that the use of stimulants for ADHD has increased considerably worldwide. 43 In most countries, an increase in stimulant medication use has been observed in children since the 1990s (e.g., United Kingdom from 0.15% in 1992 to 5.1% in 2012/2013), 44 45 but in some European countries, stimulant prescription rates for children and adolescents have remained stable or decreased over the last 5 to 10 years (e.g., Germany). 35 In the United States, the prescription of methylphenidate peaked in 2012 and has since been slightly decreasing, while the use of amphetamines continues to rise. 46

Comorbidity, Differential Diagnosis, and Clinical Assessment

Comorbidity.

ADHD is characterized by frequent comorbidity and overlap with other neurodevelopmental and mental disorders of childhood and adolescence. The most frequent comorbidities are learning disorders (reading disorders: 15–50%, 4 dyscalculia: 5–30%, 47 autism spectrum disorder, which since the DSM-5 is no longer viewed as an exclusion criterion for ADHD diagnosis: 70–85%, 48 49 tic/Tourette's disorder and obsessive compulsive disorder: 20%, and 5%, 50 developmental coordination disorder: 30–50%, 51 depression and anxiety disorders: 0–45%, 52 53 and ODD and CD: 27–55% 54 ). ADHD increases the risk of substance misuse disorders 1.5-fold (2.4-fold for smoking) and problematic media use 9.3-fold in adolescence 55 56 and increases the risk of becoming obese 1.23-fold for adolescent girls. 57 58 59 It is also associated with different forms of dysregulated eating in children and adolescents. Enuresis occurs in approximately 17% of children with ADHD, 60 and sleep disorders in 25 to 70%. 61 Frequent neurological comorbidities of ADHD include migraine (about thrice more frequent in ADHD than in typically developing [TD] children) 62 63 64 and epilepsy (2.3 to thrice more frequent in ADHD than in TD children). 65 66 The risk of coexisting ADHD being seen as a comorbid condition and not the primary diagnosis is considerably enhanced in many childhood disorders of different origins. For example, the rate of comorbid ADHD is estimated at 15 to 40% 67 68 in children with reading disorders and at 26 to 41% 69 70 in children with mild intellectual dysfunction. While comorbidity in neurodevelopmental disorders may arise from a certain genetic overlap (see details under genetic associations), ADHD symptoms are also present in several disorders with well-known and circumscribed genetic defects, normally not related to ADHD (e.g., neurofibromatosis, Turner's syndrome, and Noonan's syndrome) 71 or disorders with nongenetic causes, such as traumatic brain injuries, pre-, peri- or postnatal stroke, or syndromes due to toxic agents, such as fetal alcohol syndrome. Comorbid ADHD is estimated in 20 to 50% of children with epilepsy, 72 73 in 43% of children with fetal alcohol syndrome, 74 and in 40% of children with neurofibromatosis I. 75 ADHD is three times more frequent in preterm-born children than in children born at term and four times more frequent in extremely preterm-born children. 76

Differential Diagnosis, Primary and Secondary ADHD

A range of medical and psychiatric conditions show symptoms that are also present in primary ADHD. The most important medical conditions which are known to “mimic” ADHD and need to be excluded during the diagnostic process are epilepsy (especially absence epilepsy and rolandic epilepsy), thyroid disorders, sleep disorder, drug interaction, anemia, and leukodystrophy. 77 78 The most important psychiatric conditions to be excluded are learning disorder, anxiety disorders, and affective disorders, while an adverse home environment also needs to be excluded.

However, the picture is complex, as many differential diagnoses may also occur as comorbidities. For instance, bipolar disorder, which is frequently diagnosed in children and adolescents in the United States but not in Europe, is considered as a differential diagnosis to ADHD, but ADHD has also been found to be a comorbidity of bipolar disorder in 21 to 98% of cases. 79 Similarly, absence epilepsy is a differential diagnosis of ADHD but is also considered to be a frequent comorbidity, occurring in 30 to 60% of children with absence epilepsy. 80 The prevalence of the ADHD phenotype in benign childhood epilepsy with centrotemporal spikes (rolandic epilepsy) lies at 64 to 65%, 81 and is possibly related to the occurrence of febrile convulsions. 82 The literature often does not draw a clear distinction between an ADHD phenotype, which includes all types of etiologies and causes, and a yet to be specified developmental ADHD “genotype.” Some authors use terms, such as “idiopathic” ADHD, 83 “primary,” or “genotypic” ADHD, 84 in contrast to ADHD of circumscribed origin other than developmental, the latter being referred to as ADHD “phenotype,” or “phenocopy,” 85 or “ADHD-like.” 86 “Secondary ADHD” usually refers to newly acquired ADHD symptoms arising after a known event or incident, for example, a head trauma or stroke. After early childhood stroke, the ADHD phenotype occurs in 13 to 20% of cases, and after pediatric traumatic brain injury, ADHD symptoms are observed in 15 to 20% of children. 87 Having ADHD considerably increases the risk of suffering a traumatic brain injury, 88 89 90 and most studies on secondary ADHD after traumatic brain injury control for or compare with premorbid ADHD (e.g., Ornstein et al 91 ). Whether and to what extent “phenotypic” and “genotypic” ADHD need to be distinguished on a phenomenological level is not clear. It is possible that shared neurobiological mechanisms will prevail and that genetic vulnerability and epigenetic factors may play a role in both types. For example, James et al 86 compared neurophysiological markers in two groups of adolescents with ADHD, one born very preterm and the other born at term. While the authors found very similar ADHD-specific markers in the two groups, some additional deficits only emerged in the preterm group, indicating more severe impairment. Other examples are rare genetic diseases with known genetic defects, which are often comorbid with ADHD. One may ask whether, for example, ADHD in Turner's syndrome should be considered as a rare genetic ADHD variant and count as genotypic ADHD, or whether it results from a different genetic etiology, with the status of an ADHD phenotype.

Clinical Diagnostic Procedure

Clinical assessment in children should mainly be based on a clinical interview with parents, including an exploration of the problems, the detailed developmental history of the child including medical or psychiatric antecedents, information on family functioning, peer relationships, and school history. According to the guidelines of the National Institute for Health and Care Excellence (NICE) in the United Kingdom, this may also include information on the mental health of the parents and the family's economic situation. The child's mental state should be assessed, possibly using a standardized semistructured clinical interview containing ADHD assessments (e.g., Kiddie Schedule for Affective Disorders and Schizophrenia Present and Lifetime version, DSM-5) 92 93 and by observer reports. The exploration should cover behavioral difficulties and strengths in several life contexts, for example, school, peer relationships, and leisure time. The use of informant rating scales, such as Conners' Rating Scales, 3rd edition, 94 or the Strengths and Difficulties Questionnaire 95 may be useful, but diagnosis should not be solely based on rating scales (NICE, AWFM ADHD). 96 97 A further interview should be conducted with the child or adolescent to gain a picture of the patient's perspective on current problems, needs, and goals, even though self-reports are considered less reliable for diagnosis. Information should also be obtained from the school, for example, by face-to-face or telephone contact with the teacher and, if possible, by direct school-based observation. A medical examination should be performed to exclude somatic causes for the behavioral symptoms and to gain an impression of the general physical condition of the patient. Current guidelines do not recommend including objective test procedures (intelligence and neuropsychological tests), neuroimaging, or neurophysiological measures in routine ADHD assessment but do suggest their use as additional tools when questions about cognitive functions, academic problems, coexisting abnormalities in electroencephalography (EEG), or unrecognized neurological conditions arise. After completion of the information gathering, the NICE guidelines recommend a period of “watchful waiting” for up to 10 weeks before delivering a formal diagnosis of ADHD. A younger age of the diagnosed child relative to his/her classmates has to be mentioned as one of the many pitfalls in the assessment of ADHD. It has been shown that the youngest children in a class have the highest probability of being diagnosed with ADHD and of being medicated with stimulants. 98

There is consensus that the diagnosis of ADHD requires a specialist, that is, a child psychiatrist, a pediatrician, or other appropriately qualified health care professionals with training and expertise in diagnosing ADHD. 97

Current Neurobiological and Neuropsychological Concepts

Neuropsychology, neuropsychological pathways and subgroups.

ADHD is related to multiple underlying neurobiological pathways and heterogeneous neuropsychological (NP) profiles. Twenty-five years ago, ADHD was characterized as a disorder of inhibitory self-control, 54 and an early dual pathway model distinguished between an inhibitory/executive function pathway and a motivational/delay aversion pathway (also called “cool” and “hot” executive function pathways in later publications), which are related to distinct neurobiological networks. 99 100 101 Still, the two systems may also interact. 102

Since then, other pathways have been added, such as time processing, 103 but a definitive number of possible pathways is difficult to define. For example, Coghill and colleagues 104 differentiated six cognitive factors in children with ADHD (working memory, inhibition, delay aversion, decision-making, timing, and response time variability) derived from seven subtests of the Cambridge neuropsychological test automated battery. Attempts to empirically classify patients into subgroups with selective performance profiles departing from comprehensive NP data collection were inconclusive. For example, using delay aversion, working memory, and response-time tasks, Lambek and colleagues 105 expected to differentiate corresponding performance profile subgroups in children with ADHD. However, their analysis resulted in subgroups differentiated by the severity of impairments, and not by selective profiles. Other empirical studies using latent profile or cluster analysis of NP tasks in large ADHD samples have differentiated three 106 107 or four 108 NP profile groups, which all included children with ADHD, as well as TD children, differing in severity but not in the type of profile. This might indicate that the identified NP deficit profiles were not ADHD-specific, but rather reflected characteristic distributions of NP performances, which are also present in the general population, with extreme values in children with ADHD. Some other empirical studies in the search for subgroups, however, identified ADHD-specific performance profiles (“poor cognitive control,” 109 “with attentional lapses and fast processing speed” 110 ), among other profiles being shared with TD controls. Obviously, divergent results regarding subgrouping may also be related to differing compilations of tested domains, consequently leading to a limited comparability of these studies.

Which Neuropsychological Functions are Impaired in ADHD and When?

A meta-analysis conducted in 2005 identified consistent executive function deficits with moderate effect sizes in children with ADHD in terms of response inhibition, vigilance, working memory, and planning. 67 Since then, a vast number of studies on NP deficits in children with ADHD compared with TD controls have been published. A recent meta-analysis included 34 meta-analyses on neurocognitive profiles in ADHD (all ages) published until 2016, referring to 12 neurocognitive domains. 111 The authors found that 96% of all standardized mean differences were positive in favor of the control group. Unweighted effect sizes ranged from 0.35 (set shifting) to 0.66 (reaction time variability). Weighted mean effect sizes above 0.50 were found for working memory (0.54), reaction time variability (0.53), response inhibition (0.52), intelligence/achievement (0.51), and planning/organization (0.51). Effects were larger in children and adolescents than in adults. The other domains comprised vigilance, set shifting, selective attention, reaction time, fluency, decision making, and memory.

Nearly every neuropsychological domain has been found to be significantly impaired in ADHD compared with TD controls, though effect sizes are often small. This includes, for example, altered perception (e.g., increased odor sensitivity 112 ; altered sensory profile 113 ; impaired yellow/blue color perception, e.g., Banaschewski et al, 114 for review, see Fuermaier et al 115 ), emotional tasks (e.g., facial affect discrimination), 116 social tasks (e.g., Marton et al 117 ), communication, 118 and memory. 119 Several of the described impairments may be related to deficient top-down cognitive control and strategic deficits, 120 121 122 but there is also evidence for basic processing deficits. 123

Neuropsychological Deficits as Mediators of Gene-Behavior Relations

A vast amount of research has been devoted to the search for neuropsychological endophenotypes (or intermediate phenotypes) for ADHD, that is, neurobiologically based impairments of NP performance characteristic of the disorder that may also be found in nonaffected close relatives. ADHD neuropsychological endophenotypes are assumed to mediate genetic risk from common genetic variants. 124 So far, deficits in working memory, reaction-time variability, inhibition, time processing, response preparation, arousal regulation, and others have been identified as probable endophenotypes for ADHD. 124 125 126 127 Genetic studies indicate an association of an ADHD-specific polygenetic general risk score (i.e., the total number of genetic variants that may be associated with ADHD, mostly related to dopaminergic transmission) with working memory deficits and arousal/alertness, 124 or with a lower intelligence quotient (IQ) and working memory deficits, 128 respectively. More specifically, a link of ADHD-specific variants of DAT1 genes with inattention and hyperactivity symptoms seems to be mediated by inhibitory control deficits. 129

Individual Cognitive Profiles and the Relevance of Cognitive Testing for the Clinical Assessment

Heterogeneity is found with regard to profiles, as well as with regard to the severity of cognitive impairment in individuals with ADHD, as measured by standardized tests. ADHD does not necessarily come with impaired neuropsychological test performance: about one-third of children with ADHD will not present any clinically relevant impairment, while another one-third shows unstable or partial clinical impairment, and about another one-third performs below average in NP tests. The classic concept of NP impairment, which assumes relative stability over time, possibly does not apply to NP deficits observed in ADHD, or only to a lesser extent. For the larger part, the manifestation of performance deficits may depend on contextual factors, 130 such as reward, or specifically its timing, amount, and nature, or on energetic factors, 131 for example, the rate of stimulus presentation or the activation provided by the task.

Many studies have shown that behavioral ratings of ADHD symptoms or questionnaires on executive function deficits are not, or at best weakly, correlated with NP test performance, even when both target the same NP domain. 132 133 In consequence, questionnaires on executive functioning are not an appropriate replacement for neuropsychological testing. Likewise, ADHD symptom rating scales do not predict results of objective attention or executive function tests and vice versa. Although mild intellectual disability and low IQ are more typically associated with the disorder, ADHD can be encountered across the entire IQ spectrum, including highly gifted children. 134 Therefore, an intelligence test should be part of the diagnostic procedure, but is not mandatory according to ADHD guidelines. In some children, intellectual difficulties and not ADHD may be the underlying cause for ADHD-like behaviors, while in other children with ADHD, academic underachievement despite a high IQ may be present.

It has been argued that symptoms defining ADHD may be understood as dimensional markers of several disorders belonging to an ADHD spectrum and, in consequence, the diagnosis of these behavioral symptoms should be the starting point for a more in-depth diagnosis rather than the endpoint. 135 This should include the cognitive performance profile. The ADHD behavioral phenotype predicts neither NP impairment nor intellectual achievement in the individual case, and objective testing is the only way to obtain an accurate picture of the child's cognitive performance under standardized conditions. Its goal is not ADHD classification, but rather to obtain the best possible understanding of the relation between cognitive functioning and behavioral symptoms for a given patient, to establish an individually tailored treatment plan.

Neurophysiology

Neurophysiological methods like EEG, magnetoencephalography, and event-related potentials (ERPs) as task-locked EEG averages capture brain functions in ADHD at high (ms) temporal resolution. The approach covers both fast and slow neural processes and oscillations, and clarifies the type and timing of brain activity altered in ADHD at rest and in tasks. It reveals neural precursors, as well as correlates, and consequences of ADHD behavior. 136 Neurophysiological and particularly EEG measures also have a long and controversial history as potential biomarkers of ADHD. Current evidence clarifies how multiple pathways and deficits are involved in ADHD at the group level, but recent attempts toward individual clinical translation have also revealed considerable heterogeneity, which does not yet support a clinical application for diagnostic uses or treatment personalization, as explained below.

Resting Electroencephalography

The EEG is dominated by oscillations in frequency bands ranging from slow δ (<4 Hz) and θ (4–7 Hz) via α (8–12 Hz) to faster β (13–30 Hz) and γ (30–100 Hz) band activity. The spectral profile reflects maturation and arousal, with slow frequencies dominating during early childhood and slow-wave sleep. Source models can link scalp topography to brain sources and distributed networks.

Initial studies suggested a robust link between ADHD diagnosis and resting EEG markers of reduced attention, hypoarousal, or immaturity, such as increased θ and an increased θ/β ratio (TBR). However, more recent studies, 137 138 some with large samples, 139 140 failed to replicate a consistent TBR increase in ADHD. Instead, the results indicated heterogeneous θ and β power deviations in ADHD not explained by ADHD subtype and psychiatric comorbidity. 141 A cluster analysis of EEG in children with ADHD also revealed considerable heterogeneity regarding θ excess and β attenuation in ADHD. While several clusters with EEG patterns linked to underarousal and immaturity could be identified, only three of the five EEG clusters (60% of the cases with ADHD) had increased θ. 139 Several recent θ and TBR studies that no longer found TBR association with ADHD diagnosis still replicated the reliable age effects, 137 138 142 confirming the high quality of these studies. Increasing sleepiness in adolescents, 143 or shorter EEG recordings, may have reduced the sensitivity to time effects and state regulation deficits in ADHD, 136 144 potentially contributing to these replication failures. Also, conceptualizing TBR as a marker of inattention or maturational lag may be too simple, since θ activity can also reflect concentration, cognitive effort, and activation. 145 146

During sleep, stage profiles reveal no consistent deviations in ADHD, but the slow-wave sleep topography is altered. In particular, frontal slow waves are reduced, leading to a more posterior topography as observed also in younger children. 147 This delayed frontalization can be interpreted as a maturational delay in ADHD, in line with a cluster of resting EEG, changes in task related ERPs during response inhibition, 148 and structural magnetic resonance imaging (MRI) findings. 149

Task Related Event-Related Potentials

Task-related processing measures, particularly ERPs, have critically advanced our understanding of ADHD through their high-time resolution, which can separate intact and compromised brain functions. ERPs have revealed impairments during preparation, attention, inhibition, action control, as well as error, and reward processing, with partly distinct networks but often present during different phases of the same task. In youth and adults with ADHD, the attentional and inhibitory P3 components and the preparatory contingent negative variation (CNV) component are most consistently affected, but state regulation and error or reward processing are also compromised. 136 150 Activity during preparation, attention, or inhibition is typically weaker and more variable but not delayed. This often occurs in task phases without visible behavior and precedes the compromised performance. Familial and genetic factors also modulate these markers of attention and control. Some impairment is also observed in nonaffected siblings or in parents without ADHD, 151 152 and genetic correlates often implicate the dopamine system. 125 Some ERP changes, like the attenuated CNV during preparation, remain stable throughout maturation, and are also markers of persistent ADHD, while other markers, such as the inhibition related P3, remain attenuated despite clinical remission. 148 153

Overall, the ERP results confirm attentional, cognitive, and motivational, rather than sensory or motor impairments in ADHD, in line with current psychological and neurobiological models. However, different ERP studies hardly used the same tests and measures, so valid statements regarding classification accuracy and effect size are particularly difficult, 154 and there is an urgent need for meta-analyses regarding the different ERPs.

Clinical Translation

Despite published failures to replicate robust TBR based classification of ADHD, a TBR-based EEG test was recently approved by the U.S. Food and Drug Administration to assist ADHD diagnosis. 155 Although not promoted as a stand-alone test, children with suspected ADHD, and increased TBR were claimed to likely meet full diagnostic criteria for ADHD; while children with suspected ADHD but no TBR increase should undergo further testing, as they were likely to have other disorders better explaining ADHD symptoms (see also DSM-5 exclusionary criterion E).

This multistage diagnostic approach could possibly identify a homogeneous neurophysiological subgroup, but it omits critical elements of careful, guideline-based ADHD diagnostics. Reliability and predictive value of the TBR remain untested, and the increasing evidence for poor validity of TBR renders it unsuitable for stand-alone ADHD diagnosis. Accordingly, the use of TBR as a diagnostic aid was broadly criticized. 156 157

In sum, the recent literature suggests that neither TBR nor other single EEG or ERP markers are sufficient to diagnose ADHD and are not recommended for clinical routine use, in line with the increasing evidence for heterogeneity in ADHD.

Combining measures across time, frequency, and tasks or states into multivariate patterns may better characterize ADHD. The potential of such approaches is evident in improved classification using machine-learning algorithms based on combinations of EEG measures 142 or EEG and ERP measures. 138 158 However, claims of high-classification accuracies up to 95% (e.g., Mueller et al 158 ) require further independent replication and validation with larger samples, and plausible mapping to neural systems and mechanisms. Modern pattern classification is particularly sensitive to uncontrolled sample characteristics and needs validation through independent large samples. 159

Focusing on EEG-based prediction rather than diagnosis may hold more promise for clinical translation, and may utilize the EEG heterogeneity in clinical ADHD samples. For example, early studies on predicting stimulant response suggested that children with altered wave activity, in particular increased TBR, θ or α slowing, respond well to stimulant medication. However, in recent prospective work with a large sample, TBR was not predictive, and α slowing allowed only limited prediction in a male adolescent subgroup. 160

Predicting response to intense nonpharmacological treatment is of particular interest given the high costs and time requirements. Promising findings have been reported for one neurofeedback study, where α EEG activity and stronger CNV activity together predicted nearly 30% of the treatment response. 161 Still, the lack of independent validation currently allows no clinical application.

In conclusion, neurophysiological measures have clarified a rich set of distinct impairments but also preserved functions which can also serve as markers of persistence or risk. These markers may also contribute in the classification of psychiatric disorders based on neuromarkers (research domain criteria approach). As potential predictors of treatment outcome they may support precision medicine, and proof-of-concept studies also highlight the potential of multivariate profiling. The findings also demonstrate the challenge with this approach, including notable replication failures, and generalizability of most findings remains to be tested. Neurophysiological markers are not ready to serve as tools or aids to reliably diagnose ADHD, or to personalize ADHD treatment in individual patients.

Neuroimaging

Modern brain imaging techniques have critically contributed to elucidating the etiology of ADHD. While MRI provides detailed insights into the brain microstructure, such as for example gray matter volume, density, cortical thickness, or white matter integrity, fMRI allows insights into brain functions through activation and connectivity measures with high–spatial resolution.

Delayed Maturation and Persistent Alterations in the Brain Microstructure in ADHD

The brain undergoes pronounced developmental alterations in childhood and adolescence. Gray matter volume and cortical thickness show nonlinear inverted U -shaped trajectories of maturation with a prepubertal increase followed by a subsequent decrease until adulthood while white matter volume progressively increases throughout adolescence and early adulthood in a rather linear way. 162 163 164 165 Large variations of the maturational curves in different brain regions and subregions suggest that phylogenetically older cortical areas mature earlier than the newer cortical regions. Moreover, brain areas associated with more basic motor or sensory functions mature earlier than areas associated with more complex functions including cognitive control or attention. 163 164 Altered maturation of the cortex for ADHD has been reported for multiple areas and cortical dimensions, 166 167 mainly in the form of delayed developmental trajectories in ADHD but recently also as persistent reductions, particularly in the frontal cortex. 168 Such findings speak for delayed maturation in specific areas rather than a global developmental delay of cortical maturation in ADHD. Microstructural alterations in ADHD have been associated with a decreased intracranial volume 169 and total brain size reduction of around 3 to 5%. 100 168 170 In accordance, increasing ADHD symptoms in the general population correlated negatively with the total brain size. 171 A meta-analysis (Frodl et al) and a recent cross-sectional mega- and meta-analysis (Hoogman et al) indicate that such reductions in brain volume may be due to decreased gray matter volumes in several subcortical structures, such as the accumbens, amygdala, caudate, hippocampus, and putamen but also cortical areas (prefrontal, the parietotemporal cortex) and the cerebellum. 170 172 173 174 175 176 177 Effects sizes of subcortical alterations were highest in children with ADHD and the subcortical structures showed a delayed maturation. 169 Moreover, higher levels of hyperactivity/impulsivity in children were associated with a slower rate of cortical thinning in prefrontal and cingulate regions. 167 178 Differences in brain microstructure have also been reported in a meta-analysis for white matter integrity as measured with diffusion tensor imaging in tracts subserving the frontostriatal-cerebellar circuits. 179 To summarize, diverse neuroanatomical alterations in total brain volume and multiple cortical and subcortical dimensions characterize ADHD. These alterations are most pronounced in childhood and suggest a delayed maturation of specific cortical and subcortical areas along with some persistent reductions in frontal areas in a subgroup of ADHD patients with enduring symptoms into adulthood.

Alterations in the Brain Function of Specific Networks in ADHD

Specific functional networks, mainly those involved in inhibition, attention processes, cognitive control, reward processing, working memory, or during rest have been intensively studied in ADHD using fMRI in the past. Alterations have been reported in the corresponding brain networks and the main findings are summarized below.

Atypical Resting State Connectivity in Children with ADHD

Resting state examines spontaneous, low frequency fluctuations in the fMRI signal during rest, that is , in absence of any explicit task. 180 Resting state networks describe multiple brain regions for which the fMRI signal is correlated (functionally connected) at rest, but the same networks may coactivate also during task-based fMRI. 181 One important resting state network, the so-called default mode network (DMN), comprises brain areas that show higher activation during wakeful rest and deactivations with increasing attentional demands. 182 183 While the DMN usually shows decreasing activation with increasing attentional demands, the cognitive control network shows an opposite pattern and increases its activation. This inverse correlation of DMN and the cognitive control networks is diminished or absent in children and adults with ADHD and may explain impaired sustained attention through attentional lapses that are mediated by the DMN. 181 184 185 186 In addition, a more diffuse pattern of resting state networks connectivity and a delayed functional network development in children with ADHD have been reported. 187 Finally, atypical connectivity in cognitive and limbic cortico-striato-thalamo-cortical loops of patients with ADHD suggest that the neural substrates may either reside in impaired cognitive network and/or affective, motivational systems. 181

Altered Processing of Attention and Inhibition in Fronto-basal Ganglia Circuits in ADHD

Meta-analyses summarizing the findings of functional activation studies report most consistent alterations in brain activation patterns as hypoactivation of the frontoparietal network for executive functions and the ventral attention system for attentional processes in children with ADHD. 188 189 190 More specifically, motor or interference inhibition tasks yielded consistent decreases in a (right lateralized) fronto-basal ganglia network comprising supplementary motor area, anterior cingulate gyrus, left putamen, and right caudate in children with ADHD. 189 190 For tasks targeting attentional processes, decreased activation in a mainly right lateralized dorsolateral fronto-basal ganglia-thalamoparietal network characterized children with ADHD. Depending on the task, hyperactivation can cooccur in partly or distinct cerebellar, cortical, and subcortical regions. 188 189 190

Altered Reward Processing and Motivation

Emotion regulation and motivation is mediated by extended orbitomedial and ventromedial frontolimbic networks in the brain. 191 Abnormal sensitivity to reward seems to be an important factor in the etiology of ADHD as suggested by several models of ADHD, 192 193 194 mainly due to a hypofunctioning dopaminergic system. 195 In accordance, impairments in specific signals that indicate violations of expectations, the so called reward prediction errors (RPE), were shown in the medial prefrontal cortex of adolescents with ADHD during a learning task. 196 RPE signals are known to be encoded by the dopaminergic system of the brain, and deficient learning and decision making in ADHD may thus be a consequence of impaired RPE processing. 196 Abnormal activation has also been reported for the ventral striatum during reward anticipation and in other cortical and subcortical structures of the reward circuitry. 197

Normalization of Atypical Activation and Brain Structural Measures after Treatment

Stimulant medication and neurofeedback studies have pointed to a certain normalization of dysfunctional activation patterns in critical dorsolateral frontostriatal and orbitofrontostriatal regions along with improvements in ADHD symptoms. 198 199 200 201 Also, brain microstructure, especially the right caudate, has shown some gradual normalization with long-term stimulant treatment. 176 190

To conclude, a wide range of neuroimaging studies reveal relatively consistent functional deficits in ADHD during executive functions, including inhibitory control, working memory, reward processes, and attention regulation but also during rest. Some of these alterations are more persistent, others are specific to children and may thus represent a developmental delay. Specific treatments showed trends toward a normalization of alterations in brain microstructure and functional networks.

Genetic Associations with ADHD and ADHD Related Traits

From family studies, as well as twin studies, the heritability for ADHD has been estimated to be between 75 upto 90%. 202 Moreover, the heritability was found to be similar in males and females and for inattentive and hyperactive-impulsive components of ADHD. 202 Interestingly, a strong genetic component was also found when the extreme and subthreshold continuous ADHD trait symptoms were assessed in the Swedish twins. 19 Even over the lifespan, adult ADHD was found to demonstrate high heritability that was not affected by shared environmental effects. 203 Recently, structural and functional brain connectivity assessed in families affected by ADHD has been shown to have heritable components associated with ADHD. 204 Similarly, the heritability of ERPs elicited in a Go/No-Go-task measuring response inhibition known to be altered in ADHD, was found to be significantly heritable. 205

In several studies, ADHD-related traits have also shown significant heritability. For example, in two independent, population based studies, significant single nucleotide polymorphism heritability estimates were found for attention-deficit hyperactivity symptoms, externalizing problems, and total problems. 206 In another study, investigating the two opposite ends of ADHD symptoms, low-extreme ADHD traits were significantly associated with shared environmental factors without significant heritability. 207 While on the other hand, high-extreme ADHD traits showed significant heritability without shared environmental influences. 207 A crossdisorder study including 25 brain disorders from genome wide association studies (GWAS) of 265,218 patients and 784,643 controls, including their relationship to 17 phenotypes from 1,191,588 individuals, could demonstrate significant shared heritability. 208 In particular, ADHD shared common risk variants with bipolar disorder, major depressive disorder, schizophrenia, and with migraine. 208 Indeed, in general, population-based twin studies suggest that genetic factors are associated with related-population traits for several psychiatric disorders including ADHD. 209 This suggests that many psychiatric disorders are likely to be a continuous rather than a categorical phenotype.

Though ADHD was found to be highly heritable, the underlying genetic risk factors are still not fully revealed. The current consensus suggests, as in many other psychiatric disorders, a multifactorial polygenic nature of the common disorder. Both common genetic variants studied by hypothesis-driven candidate gene association or by the hypothesis-free GWAS could only reveal the tip of the iceberg. Through the candidate gene approach, only very few findings could show replicable significant association with ADHD, as reported by meta-analysis studies for the dopaminergic, noradrenergic, and serotonergic genes. 210 211 Several GWAS have been conducted followed by meta-analysis, which again failed reaching genome-wide significant results. 212 213 214 215 216 217 218 219 220 221 222 223 224 However, recently, the first genome-wide significance has been reached in a GWAS meta-analysis consisting of over 20,000 ADHD patients and 35,000 controls. 225 Twelve independent loci were found to significantly associate with ADHD, including genes involved in neurodevelopmental processes, such as FOX2 and DUSP6 . 225 But even in these findings the effect sizes are rather small to be used for diagnostic tools. Therefore, polygenic risk score approaches have emerged as a possible tool to predict ADHD. 202 Yet this approach needs further investigation now that genome-wide significance has been reached by Demontis et al. 225 However, at this point, it is not yet possible to exclude that rare SNPs of strong effect may also be responsible (similar to breast cancer) for a small proportion of ADHD cases due to the heterogeneity of symptomatology, illness course, as well as biological marker distribution, as outlined above.

Multimodal Treatment of ADHD

A variety of national and international guidelines on the assessment and management of ADHD have been published over the last 10 years, not only for clinicians but also for patients and caregivers. 96 97 226 227 228 All guidelines recommend a multimodal treatment approach in which psychoeducation forms a cornerstone of the treatment and should be offered to all of those receiving an ADHD diagnosis, as well as to their families and caregivers.

According to the NICE Guidelines, the first step is always a planning process for the multimodal treatment with respect to the psychological, behavioral, and occupational or educational needs of the child and his/her family. 97 This planning phase could be organized as a “round table” with the child, parents, and other caregivers. The following aspects should be taken into account: the severity of ADHD symptoms and impairment, the relative impact of other neurodevelopmental or mental health conditions and how these affect or may affect everyday life (including sleep). In addition, resilience and protective factors, as well as the goals of the child and family, should be considered in the intervention process. The participation of child and parents in the planning and treatment process is more centrally outlined in recent guidelines and is emphasized in detail for the different treatment steps (e.g., NICE and S3 Guidelines). 96 97 The participation process is not just a one-time dialogue but should rather continue throughout all steps of the treatment process. Benefits and harms of nonpharmacological and pharmacological treatments should be discussed carefully and on the basis of the latest evidence. Preferences and concerns, and the importance of adherence to treatment, should be discussed and taken into account within the treatment process. Patients and their families or caregivers should be reassured, as appropriate that they can revisit decisions about treatments.

Multimodal treatment approaches also advocate a systematic adaptive procedure that combines different treatment modules according to the needs and situation of the patient and family. This may, for instance, include a first stage in which parent counseling is initiated, a second-stage encompassing, for example, individual behavioral therapy for the child, while the parents participate in a parent training program in parallel, followed by a third stage in which stimulant medication is started, etc. 229 230 Environment-centered interventions aim at the counseling or training of parents or the instruction of teachers at school or preschool. Parent training programs may be administered individually or in groups and have shown positive effects on parenting skills, ADHD behavior, and comorbid conduct problems. 231 232 233 Family therapy for ADHD focuses on the ADHD family, with the ADHD patient being a part of the family system with dysfunctional interactional patterns. 234 School-based interventions may target (1) the conditions in the classroom, for example, by minimizing distractions; (2) the instruction of the teacher, for example, by suggesting more appropriate teaching methods or by promoting peer tutoring; or (3) the student, for example, by improving self-management and social skills, or by helping to cope with stigma. 235 236 237

Pharmacological Approaches

Starting medication.

All medication for ADHD should only be initiated by a health care professional with training and expertise in diagnosing and managing ADHD. The expert should be familiar with the pharmacokinetic profiles and bioavailability of all the short- and long-acting preparations available for ADHD. The following parameters should be considered before first medication: medical history of the child but possibly also of the parents, current medication, height and weight, baseline pulse and blood pressure, a cardiovascular assessment, and an electrocardiogram if the treatment may affect the QT interval. A cardiology expert opinion should be sought before starting medication for ADHD if there is a history of congenital heart disease, previous cardiac surgery, or a history of sudden death in a first-degree relative under the age of 40 years, or if the blood pressure is consistently above the 95th centile for age and height for children and young people.

Age-Specific Needs

Treatment recommendations are often based on the specific needs of children, youth, or adults. 97 226 According to the NICE guidelines 97 and also pharmacological recommendations (e.g., Walitza and colleagues 238 239 ), a distinction should also be made between children under 5 years of age or preschool children, and school children. For the younger children (under 5 years of age), parent or career training programs and parent group training programs are always first-line treatments. Medication for children under 5 years with ADHD should only be given following a second specialist opinion from an ADHD service with expertise in managing ADHD in young children (ideally from a tertiary service). For children over 5 years of age, education and information about the causes and impact of ADHD and advice on parenting strategies should be offered, as well as liaison with school, college, or university if consent to do so is provided. 97 Children aged 5 years and over and young people should only receive medication if the ADHD symptoms are still causing a persistent significant impairment in at least one life domain after environmental modifications have been implemented and evaluated.

Selection of Pharmacotherapy

In Europe, methylphenidate either as short- or long-acting preparation is the first-line medication for ADHD across the life span. Second-line medications are lisdexamfetamine, atomoxetine, and guanfacine. A switch to lisdexamfetamine is only recommended if children have first undergone at least a 6-week trial of methylphenidate at an adequate dose and have not derived sufficient benefit in terms of reduced ADHD symptoms and associated impairment, or if patients experience adverse side effects. 238 The Canadian Guidelines (2018) recommend an individual treatment approach, which can start with different options, and if medication is to be used, long-acting formulations of psychostimulants or atomoxetine are always the first choice. 226 Comorbid disorders may necessitate adjustments to the treatment plan or alternative treatments.

According to the NICE guidelines, atomoxetine and guanfacine should only be offered if patients cannot tolerate methylphenidate or lisdexamfetamine or if their symptoms have not responded to separate 6-week trials of methylphenidate and lisdexamfetamine, having considered alternative preparations and adequate doses. 97

Evidence for ADHD Medications

In the first “gold standard” study comparing the different treatment approaches for ADHD alone and in combination (National Institute of Mental Health Collaborative Multimodal Treatment Study of Children with ADHD [MTA study]), the effects of both pharmacological therapy (methylphenidate and intensive counseling) and of multimodal therapy (methylphenidate and intensive behavioral therapy) were significantly more effective after 14 months than behavioral therapy alone or than the “standard” therapy (treatment as usual in the community) of the control group. The multimodal therapy was not significantly superior to pharmacological therapy alone, but did result in significant improvements in ADHD symptoms at a lower dosage of methylphenidate. 240 241 242 Since the MTA study, numerous studies have investigated methylphenidate, amphetamine, and nonstimulants like atomoxetine or α 2 -adrenoceptor agonists, such as clonidine and guanfacine, regarding different aspects of effectiveness and tolerability.

The psychostimulants methylphenidate and amphetamine are the most effective agents for the treatment of core ADHD symptoms, with a favorable efficacy and adverse event profile. 243 244 245 Compared with methylphenidate and amphetamine, which both show immediate symptom reduction, the full effects of atomoxetine and guanfacine on reducing ADHD symptoms usually only unfold after some weeks of administration. Atomoxetine and guanfacine are not controlled substances, and are licensed in various European countries and in the United States for treatment of ADHD in children above the age of 6 years. Both have been shown to be effective in decreasing ADHD core symptoms with an effect size of around 0.7, which is somewhat lower than the effect size for methylphenidate, depending on the underlying studies (e.g., Sallee et al 246 ).

Management Strategies and Duration of Pharmacological Treatment

Following an adequate dosage of medication ( Table 1 ) and treatment response, medication for ADHD should be titrated to an optimized dosage with regard to the clinical efficacy, safety, and side effects, which should be continued for as long as it remains clinically necessary and effective. This should be reviewed at least annually, also with a planned “medication break” to decide whether there is a continuing need for care. 238 239 However, there is little available empirical evidence to guide clinicians on questions, such as the optimum duration of treatment and when it is appropriate to consider drug discontinuation. As ADHD can persist into adulthood, decisions on treatment discontinuation need to be taken on a case-by-case basis. 226

Abbreviations: ADHD, attention deficit hyperactivity disorder; max. maximum.

Adapted from (1) Walitza S, Romanos M, Greenhill LL, Banaschewski T. Attention-Deficit/Hyperactivity Disorders. In: Gerlach M, Warnke A, Greenhill LL, eds. Psychiatric Drugs in Children and Adolescents. Wien: Springer; 2014:369–381 238 and (2) Walitza S, Gerlach M, Romanos M, Renner T. Psychostimulanzien und andere Arzneistoffe, die zur Behandlung der Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS) angewendet werden. In: Gerlach M, Mehler-Wex C, Walitza S, Warnke A, Wewetzer C, eds. Neuro-/Psychopharmaka im Kindes- und Jugendalter: Grundlagen und Therapie. Berlin, Heidelberg: Springer Berlin Heidelberg; 2016:289–331. 239

Among the most frequent side effects of psychostimulant therapy ( Table 2 ) are reduced appetite and sleep disturbances. 247 Appetite reduction following treatment initiation with an ADHD drug often attenuates with time. Reduced appetite at mealtimes can be avoided by taking the medication after meals rather than before. Should a clinically significant lack of appetite persist, dosage reduction (by one-fourth or half tablet of methylphenidate), discontinuation (rarely necessary), or switching to a different formulation or medication should be considered.

Adapted from (1) Walitza S, Romanos M, Greenhill LL, Banaschewski T. Attention-Deficit/Hyperactivity Disorders. In: Gerlach M, Warnke A, Greenhill LL, eds. Psychiatric Drugs in Children and Adolescents. Wien: Springer; 2014:369–381 238 ; (2) Walitza S, Gerlach M, Romanos M, Renner T. Psychostimulanzien und andere Arzneistoffe, die zur Behandlung der Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS) angewendet werden. In: Gerlach M, Mehler-Wex C, Walitza S, Warnke A, Wewetzer C, eds. Neuro-/Psychopharmaka im Kindes- und Jugendalter: Grundlagen und Therapie. Berlin, Heidelberg: Springer Berlin Heidelberg; 2016:289–331 239 ; (3) Huang YS, Tsai MH. Long-term outcomes with medications for attention-deficit hyperactivity disorder: current status of knowledge. CNS Drugs 2011;25:539–554; (4) Storebo OJ, Pedersen N, Ramstad E et al. Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents - assessment of adverse events in non-randomized studies. Cochrane Database Syst Rev 2018;5:CD012069284; and (5) Wigal T, Greenhill L, Chuang S et al. Safety and tolerability of methylphenidate in preschool children with ADHD. J Am Acad Child Adolesc Psychiatry 2006;45:1294–1303.

Nonpharmacological Treatments

Cognitive behavioral therapy.

Cognitive behavioral therapy (CBT) is a form of behavioral intervention which aims at reducing ADHD behaviors or associated problems by enhancing positive behaviors and creating situations in which desired behaviors may occur. In the case of preschool and young school children, CBT focuses on parents and educators, who are instructed and trained to act according to CBT principles, while older children and adolescents may be trained directly to use more appropriate behavioral strategies. 248 CBT and its more specific forms (e.g., social skills training, training of planning and organizational skills, and self-management techniques) have positive effects on behavior, parenting skills, child–parent relationships, and certain daily living skills, 232 249 although effects on ADHD core symptoms are inconsistent and relatively low when only blinded assessments are considered. 250 A recent meta-analysis suggested that the combined treatment of medication with CBT is more efficacious than stimulant medication alone (with an estimated standardized mean difference of 0.5). 251

Neuropsychological Treatments

In cognitive training interventions, either PC-supported or in a manualized format, cognitive exercises that tap into cognitive domains, such as working memory or inhibitory control, are performed in a repetitive manner and with increasing difficulty. The evidence base for this type of intervention is poor according to recent studies (e.g., Bikic et al 252 ) and metastudies (e.g., Cortese et al 253 ). While some “near-transfer” improvements in neuropsychological tests tapping into the trained domain are probable, the evidence for “far transfer” to academic achievements or to the ADHD symptom level is weak. Most studies, however, used the same kind of cognitive training with all participants, irrespective of their actual individual cognitive difficulties. Moreover, they did not adhere to theoretically based training principles, which recommend domain-specific training for the functional improvement of a selective neuropsychological deficit. Possibly, future approaches that combine repetitive exercise and top-down strategy application may provide larger benefits for children with ADHD.

In neurofeedback training (NF), EEG activity measured by one or more electrodes applied to the head is transformed into a visual or acoustic signal and fed back online, for example, by a stimulus moving up and down. By steering the stimulus on the screen, the participant may gain control over his/her EEG activity. Many different training protocols have been applied to ADHD. Those which have received the best evaluation are the NF training of the θ/β frequency bands ratio (the goal is generally to decrease θ and to increase β frequencies) and the training of slow cortical potentials (learning to intentionally increase and decrease cortical excitability over short periods of time). However, “normalizing” an ADHD-specific deviant EEG pattern can no longer qualify as a meaningful goal, as no characteristic ADHD pattern seems to exist (Loo et al, 254 see neurophysiology section), although gaining control over one's brain activity and over attentional states continues to be a valid treatment goal. According to parent ratings, clinical improvements after NF are stronger and longer-lasting compared with other behavioral treatment methods, but teacher ratings usually fail to yield significant effects. 255 Recent research has focused on the specificity of treatment effects, defined as the association between the learned regulation of EEG activity and the behavioral outcome. 256 To date, there is no convincing evidence that the learned control over brain activity is responsible for the observed behavioral improvements. Instead, nonspecific treatment effects, such as improved self-efficacy, positive reinforcement, and learning to sit still, seem to contribute in large part to the positive clinical outcome.

Methodologically more sophisticated NF approaches, such as tomographic NF, 257 fMRI-NF, 258 or near-infrared spectroscopy feedback (feedback of hemoglobin oxygenation) 259 are still in the experimental stage.

Noninvasive Brain Stimulation

Repetitive transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) represent other potential means to modulate cortical activity. Therefore, these approaches may also be promising in terms of improving clinical and cognitive ADHD symptoms such as inattention and impulsiveness. 258 260 261 262 Based on a meta-analysis, Westwood et al 263 suggested that left and/or right prefrontal stimulation may improve performance in attention, inhibition and/or working memory tasks. However, these approaches are not yet recommended by therapy guidelines.

Alternative Nonpharmacological Treatment Methods

Mindfulness training, physical activity, and yoga seem to have positive effects on ADHD behavior, but for the time being, the scientific evidence is weak and these treatments are seen at best as complementary to other interventions. 264 265 266 267 268 Digital home treatment programs or support apps are currently being developed for ADHD patients or their parents 269 270 ; their usefulness or clinical validity still needs to be tested. Children and adolescents with ADHD often show a great affinity with digital media, which may improve compliance, but one has to take into account that the rate of problematic internet use and gaming is enhanced in youth with ADHD (estimated at 37% in ADHD vs. 12% in TD). 271 Free fatty acid supplementation has been described to bring about small but significant reductions in ADHD symptoms even with probably blinded assessments (standardized mean difference = 0.16). 250

Long-Term Outcome

Follow-up studies have reported divergent results, with some reporting high rates of persistence until adulthood (up to 79%), 153 and others showing much higher rates of remission from childhood to adolescence (e.g., 45–55% of syndromal remissions). 272 273 274 Recent population-based studies from Brazil, the United Kingdom, and New Zealand have claimed that a large portion of de novo ADHD cases emerge at adult age, 275 276 277 but these results can probably be explained by methodological artifacts and missed subthreshold cases. 76 278 279 However, meta-analytic findings by Bonvicini et al 280 indicate that in part, different genes and polymorphisms seem to contribute to childhood ADHD and adulthood ADHD, lending some genetic plausibility to findings of a late manifestation of the disorder. According to the MTA study, the contribution of interventions administered during childhood to outcome in adulthood is negligible, but controlled intervention was limited to a relatively short period of time (14 months). 281 Neurobiologically, the course of ADHD may be explained by different models. 274 According to the first model, remission at adult age may be reduced to the normalization of brain functions through maturation. A second model explains remission through the recruitment of compensatory brain functions. The third model claims that brain function anomalies show life-long persistence, even though behavioral dysfunction may have remitted. 274 Possibly, all of these models, and probably additional ones too (see e.g., Doehnert et al 148 ), apply to different subgroups of patients or functions and may account for the divergent results in the literature.

Conflict of Interest D.B. reports having served as an unpaid scientific advisor for an EU-funded neurofeedback trial unrelated to the present work.

S.W. reports grants from Gertrud Thalmann Fonds of the UPK Basel, Collaborative Project, grants from Ebnet Foundation, grants from Mensia Technologies SA & EU H2020 SME Instrument, grants from University Medical Center Utrecht & Stanley Medical Research Institute, Collaborative Project, grants from Swiss National Foundation, Investigator Initiated Clinical Trial, other from Thieme Neuropychopharmakologie des Kindes und Jugendalters, outside the submitted work; and S.W. has received in the last 5 years royalities from Thieme Hogrefe, Kohlhammer, Springer, Beltz. S.W. has received lecture honoraria from Opopharma in the last 5 years. Her work was supported in the last 5 years by the Swiss National Science Foundation (SNF), diff. EU FP7s, HSM Hochspezialisierte Medizin of the Kanton Zurich, Switzerland, Bfarm Germany, ZInEP, Hartmann Müller Stiftung, Olga Mayenfisch, Gertrud Thalmann Fonds. Outside professional activities and interests are declared under the link of the University of Zurich www.uzh.ch/prof/ssl-dir/interessenbindungen/client/web/ .

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• Data and Statistics on ADHD
• Free Materials on ADHD
• Attention-Deficit / Hyperactivity Disorder Articles
• Clinical Care and Treatment

Symptoms of ADHD

• ADHD symptoms can present as mostly inattentive, mostly hyperactive-impulsive, or a combination of both types of symptoms.
• If you think you or someone you know might have ADHD, the first step is to talk with a healthcare provider.

Signs and symptoms

It is normal for children to have trouble focusing and behaving at one time or another. However, children with ADHD do not just grow out of these behaviors. The symptoms continue, can be severe, and can cause difficulty at school, at home, or with friends.

A child with ADHD might

• daydream a lot
• forget or lose things a lot
• squirm or fidget
• talk too much
• make careless mistakes or take unnecessary risks
• have a hard time resisting temptation
• have trouble taking turns
• have difficulty getting along with others

Based on the types of symptoms, three kinds (presentations) of ADHD can occur:

• Predominantly Inattentive Presentation
• Predominantly Hyperactive-Impulsive Presentation
• Combined Presentation (a combination of inattentive and hyper-impulsive symptoms)

Because symptoms can change over time, the presentation may change over time as well.

When to talk to your doctor

If you are concerned about whether a child might have ADHD, the first step is to talk with a healthcare provider to find out if the symptoms fit an ADHD diagnosis. The diagnosis can be made by a mental health professional, such as a psychologist or psychiatrist, or by a primary care provider, like a pediatrician.

Is there a test for ADHD? ‎

Deciding if a person has ADHD is a process with several steps. There is no single test to diagnose ADHD, and many other problems, such as sleep disorders, anxiety, depression, and certain types of learning disabilities, can also have symptoms similar to ADHD.

Read more about diagnosing ADHD.

• About ADHD | CDC
• Treatment of ADHD | CDC
• Other Concerns and Conditions with ADHD | CDC

Attention-Deficit / Hyperactivity Disorder (ADHD)

CDC's Attention-Deficit / Hyperactivity Disorder (ADHD) site includes information on symptoms, diagnosis, treatment, data, research, and free resources.

For Everyone

Health care providers.

Adult ADHD: A Review of the Clinical Presentation, Challenges, and Treatment Options

The clinical presentation and functional impacts of ADHD in adults vary greatly from their child and adolescent counterparts. Here: latest information on this complex topic.

Table 1 – Stimulant drug therapy options

Table 2 – Nonstimulant drug therapy options

Premiere Date: October 20, 2015 Expiration Date: April 20, 2017

This activity offers CE credits for:

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ACTIVITY GOAL

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The inattentive and the hyperactive-impulsive subtypes of ADHD are particularly evident in adults. This inherent heterogeneity complicates the diagnosis and contributes to the lack of uniformly recognized criteria in the adult population. Historically, the diagnostic criteria that were developed based on the traditional childhood presentation have been applied to adult patients. Practitioners have attempted to adapt these criteria to adults in practice, and DSM-5 has also modified some of the qualifiers in order to facilitate the utilization of the criteria in adults. However, the clinical presentation and functional impacts of ADHD in adults vary greatly from their child and adolescent counterparts.

As patients mature and their roles and responsibilities evolve, the functional impairments and symptom presentation evolve in response, thereby presenting a barrier to fulfilling diagnostic criteria. Adults are exposed to a variety of social and professional situations that can provide an opportunity for previously unnoticed symptoms to manifest. Inattentive symptoms may present as difficulty in completing tasks, poor time management, difficulty in sustaining attention in work-related activities, distractibility and forgetfulness, and poor concentration. Occupational performance and professional interpersonal relationships can suffer, and ultimately result in frequent job changes, unemployment, failure to live up to one’s occupational potential, and lower salaries. Moreover, deficits in global performance in the adult patient’s life role, follow-through, and memory can have pervasive effects that extend to those who depend on him or her (eg, children, spouses, employers, friends).

Perhaps the most significant evolution of symptoms occurs in the hyperactivity-impulsivity domain. It is often assumed that these symptoms fade or resolve entirely in adults as they grow older. However, maturation results in a shift in this symptom cluster, and it evolves from behavioral to cognitive-adult patients feel restless as opposed to running around and being disruptive in school. Approximately 90% of adult patients have symptoms of inattention. 1

Challenges in assessing ADHD in adult patients

There are many challenges associated with a diagnosis of ADHD in adults. Objective assessment is difficult because of many factors, including the extensive degree of symptom overlap with other psychiatric diagnoses (eg, psychiatric comorbidities, adaptive compensatory mechanisms, difficulty in assessing functional impact).

Lack of validated diagnostic criteria

The most contemporary multidimensional approach to a relatively objective diagnosis in children and adolescents are DSM-5 criteria, which assess symptoms in all 3 domains. Until the release of DSM-5, there was very little consideration for the assessment of adult patients because DSM criteria had not been validated in the adult population. DSM-5 adapted the previous set of diagnostic criteria to be more accurately applicable to adult symptom presentation. The nomenclature has evolved to reflect more adult-specific situations, such as having difficulty focusing during lectures, avoidance of reviewing lengthy papers, and forgetfulness related to paying bills or keeping appointments.

Revisions that facilitate the application of the criteria to adults are the decrease in the number of required symptoms for adults to fulfill criteria as well as an increase in the age of initial presentation. Previously, adult patients needed to satisfy at least 6 of the 9 inattentive criteria, which is consistent with diagnosis in the pediatric and adolescent population. In DSM-5, adults need to satisfy only 5 of the 9 criteria and children and adolescents still need to satisfy 6 of the 9 inattentive criteria. DSM-IV required that symptoms present before age 7-a challenging retrospective for adult patients who had not previously sought an intervention.

Even with the new criteria, practitioners need to make a retrospective evaluation of the presence of ADHD in childhood in order to establish a diagnosis in adulthood. This was cited as one of the most problematic components of the criteria because many patients could not recall childhood symptoms or they could not produce documentation substantiating a childhood diagnosis. Because ADHD is considered a developmental disorder, the presence of current symptoms as well as a history of previous symptoms (in childhood) needs to be established. Patients with ADHD, however, have impaired short- and long-term memory; therefore, recall bias can affect the accuracy of assessments. The practitioner is faced with the challenge of determining whether this was an established childhood diagnosis, a missed diagnosis in childhood, or a late-onset adult ADHD.

There are a host of validated rating scales for assessing adult patients with suspected ADHD, although each has inherent limitations. The Adult Self-Report Scale (ASRS) is an 18-item screening tool that is based on DSM-IV criteria. Patients rate the items based on the frequency and degree to which they occur. A 6-item version of the ASRS captures abnormalities in the domains related to follow-through, memory, organization, procrastination, restlessness, and hyperactivity.

The Conners Self-Report Scale is a multidimensional assessment scale that both the patient and an observer complete. The long version of this scale has 66 items that assess symptoms consistent with inattention and memory deficits, impulsivity and emotional lability, hyperactivity and restlessness, and problems with self-conceptualization. 2 Having multiple perspectives is ideal in that the observer can contribute critical data that the patient may be either unaware of or not willing to disclose. One of the most significant limitations of self-report scales is that they are generally not sufficient independently to establish a diagnosis in the absence of more objective data or documentation. A 30-item version of the Conners Adult ADHD Self-Report Scale can also be used.

Psychiatric comorbidity and symptom overlap

Another challenge in the evaluation of adult ADHD is the symptom overlap between ADHD and mood and anxiety disorders. Patients with ADHD tend to have high rates of comorbidity with anxiety, depression, and substance abuse disorders, with prevalence rates that are more than double those observed in patients without ADHD. 3-5 In a 2006 study, 87% of adult patients had at least one psychiatric comorbidity and 56% had two. 4 Determining whether ADHD is present alone or whether it is comorbid with another psychiatric disorder is critical-a mood or anxiety disorder may be responsible for the ADHD-like symptoms.

Compared with patients who have a depressive disorder, those with ADHD tend to have more occupational or functional impairment, organizational deficits, and impulsivity issues. The distinction between ADHD and bipolar disorder can be especially challenging, since the manic and hypomanic features of bipolar disorder are similar to the hyperactive and impulsive symptoms associated with ADHD. In patients with ADHD, these symptoms tend to be constant, but in bipolar disorder there is a waxing and waning of manic symptoms interrupted with periods of depression. Patients with bipolar disorder tend to be goal-directed and are usually productive, while patients with ADHD are less able to complete tasks.

Substance use disorders are more common in patients with ADHD, and the clinical course of ADHD tends to be more challenging in this patient population. In patients with an opiate or cocaine addiction, the prevalence of ADHD is as high as 35%; and for alcohol-addicted patients, the ADHD prevalence exceeds 70%. 4,6 Alcohol and certain prescription and illicit drugs can produce symptoms that mirror those of ADHD, which may artificially inflate the prevalence of ADHD in patients with an addiction problem and may not be reflective of the true prevalence.

Compensatory mechanisms

Adult patients may develop and depend on compensatory mechanisms in order to overcome some of the functional impairments associated with ADHD. 4,7 Patients who are highly functioning with higher than average IQs tend to develop useful coping mechanisms to overcome symptoms or to hide them from others. Some patients become compulsive list makers or develop a highly structured daily routine in order to complete tasks and to minimize forgetting details or losing belongings.

6 Challenges in Assessing ADHD in Adult Patients

They may unknowingly rely on coworkers or family members to an inappropriate extent for reminders or assistance in completing tasks or fulfilling responsibilities. Although compensatory mechanisms are generally therapeutic for the patient, they may cloud the clinical picture particularly in cases where the patient does not self-suspect ADHD but rather a family member or the practitioner suspects ADHD.

Engaging in compensatory mechanisms such as relying significantly on others or forgoing sleep to finish tasks may mask the symptoms of ADHD or suggest that a patient is adequately coping when he or she is not. In any case, the use of appropriate compensatory mechanisms should also be taken into consideration when determining whether drug therapy is indicated. Some patients can manage without a clinically significant functional impact by relying on compensatory mechanisms and are able to avoid drug therapy.

Evidence of significant clinical impact

Among the DSM criteria is an item that evaluates the degree of clinical impact of ADHD symptoms on life domains. For a diagnosis of ADHD, there must be clear evidence of significant clinical impact, which can be especially difficult to objectively assess. Failure to demonstrate significant clinical impact precludes a diagnosis of ADHD even if all other criteria are satisfied. Examples of true clinical impact include disciplinary action at work, risk of job loss, relationship discord, or frequent automobile accidents or accidents in the home.

Underdiagnosis vs overdiagnosis

Given the high degree of psychiatric symptom overlap, the realistic possibility of feigning ADHD symptoms, and a general fear of enabling drug addiction or diversion, the underdiagnosis versus overdiagnosis of ADHD in practice has been called into question. There are no available data to quantify this concern, and therefore no support can be lent to the argument of failure to recognize ADHD or misdiagnosis of ADHD. A psychiatric comorbidity and the point of entry into the health care system (primary care versus a psychiatrist) may influence whether ADHD is overdiagnosed or underdiagnosed. The most frequent point of entry into the health care system and the most common place for ADHD to be evaluated and diagnosed is in the primary care setting, where it may be overdiagnosed. However, when patients are seen by a psychiatrist, it usually is the comorbid psychiatric diagnosis that is treated and not ADHD. Thus, ADHD may be underdiagnosed when patients present to a psychiatrist. Given the assertion that ADHD is overdiagnosed in primary care and underdiagnosed by specialists, the true prevalence of ADHD theoretically lies somewhere in between. 8,9

Prescription drug abuse and drug-seeking behavior

According to the most recent survey by the National Institute on Drug Abuse, adults between the ages of 18 and 25 are statistically the most likely to abuse prescription drugs. 10 Adults between the ages of 18 and 22 are the most likely to abuse stimulant medications, with rates in college students double those in non-college students. 11 The majority of adult patients who present with self-suspected ADHD are between the ages of 18 and 24; therefore, the unfortunate but realistic risk of drug seeking must be considered.

A definitive statistic that quantifies the risk and rates of stimulant medication abuse is elusive owing to patient unwillingness to admit abuse or diversion. However, multiple studies have attempted to capture this rate through anonymous surveys and emergency-department visits. Generally stimulants with a rapid onset of effect and shorter half-life are more likely to be abused, since there is a more narrow window between ingesting the drug and realizing the perceived reward. Variability exists within the therapeutic class in terms of abuse potential: rates of abuse of amphetamine salts exceed those of methylphenidate. 12

Establishing a meaningful comparison of the rates of abuse of stimulant medications compared with prescription drugs for other indications is also challenging. Considering the physiologic consequences of abusing stimulants, opioids, or sedative-hypnotics, it may not be surprising that accidental death due to abuse of a prescription drug is by far the highest for the opioids. Prescription opioid-related accidental deaths were more frequent than cocaine, heroin, and stimulant overdoses combined. 13

Treatment modalities

Psychostimulants remain the drug class of choice in treating adults and children with ADHD. Most product formulations available are derived from one of two parent molecules: methylphenidate or amphetamine ( Table 1 ). Pharmacologically, the stimulants inhibit the reuptake of dopamine and norepinephrine, thereby increasing concentrations in the presynaptic cleft. Amphetamines also directly stimulate the release of dopamine and norepinephrine. About 14 products are currently available in the US: some of them are immediate-release and others are extended-release formulations. It is generally recommended that drug therapy, particularly in adults, should consist of an extended-release product in order to maximize compliance and minimize the risk of abuse. Stimulant medications mitigate traditional ADHD symptoms and have demonstrated utility in improving interpersonal relationships, self-esteem, and cognition, as well as alleviating symptoms of comorbid anxiety disorders. 14,15 Stimulants are arguably the most effective in resolving ADHD symptoms and comorbid psychopathology; however, because of the risk of adverse effects and abuse potential, these agents may be underprescribed for adult ADHD. 16

Common, transient adverse effects include sleep disturbance, appetite suppression and associated weight loss, agitation, and nervousness. These are typically minimized by taking the drugs with food and using an extended-release formulation. Serious concerns exist regarding cardiotoxicity. Patients can experience palpitations, tachycardia, and elevations in blood pressure. Serious cardiovascular effects include rhythm disturbances and cardiomyopathy, which precludes use in patients who have an existing cardiovascular abnormality.

Nonstimulants

Owing to their less impressive effectiveness compared with stimulants, the nonstimulant medications tend to be prescribed less frequently among all age groups. Generally, practitioners do not initiate drug therapy with a nonstimulant unless the patient has a contraindication to stimulants (cardiac abnormalities, previous or current substance abuse) or is intolerant to or has failed a trial of a stimulant. Currently, the nonstimulant therapeutic class includes atomoxetine, immediate- and extended-release guanfacine, clonidine, and bupropion (Table 2 ).

Atomoxetine’s efficacy and safety have been demonstrated in adults and children; however, its associated rates of response are less impressive than those of the stimulants. It remains an appropriate option in patients who have contraindications to stimulants or who have a comorbid anxiety disorder, as anecdotal evidence suggests some level of anxiolytic activity.

Bupropion has been evaluated in a small number of studies involving children, adolescents, and adults, in whom its efficacy compared with placebo or with an active stimulant comparator has been established. This is not an approved indication for bupropion in any age group, however. Bupropion may be a therapeutic alternative in adults who have contraindications or are intolerant to stimulant medications, or in patients who have a comorbid depressive illness.

Guanfacine and clonidine are typically reserved for children who also have a hyperactive component. Of the newer extended-release formulations, only extended-release clonidine has an indication for the treatment of adult ADHD.

CASE VIGNETTE

A 42-year-old woman presents to a primary care clinic for an evaluation of her attention issues. Alice’s symptoms became apparent in early grade school, but with extra effort she managed to get good grades throughout elementary school, high school, and college. Lately she has had increasing difficulty in remembering appointments and completing her projects; she has also been losing her belongings, avoiding tasks, getting distracted at meetings, and failing to listen to people when they speak to her. Her direct superior has brought this to her attention and has mentioned possible disciplinary action. Symptoms occur all day, regardless of setting. Her past medical history includes dyslipidemia, anxiety, and gastroesophageal reflux disease. Prescription medications include 20-mg atorvastatin daily, 10-mg escitalopram daily, and 20-mg omeprazole daily. Evaluations for mood and anxiety disorders reveal no additional diagnoses. There is no documented history of or current issues with substance abuse.

Does this patient fulfill DSM-5 diagnostic criteria for ADHD?   Yes . She reports at least 5 symptoms of inattention (remembering appointments, finishing projects, losing belongings, task avoidance, easy distraction, failing to listen to others in conversation). The symptoms (per patient report) began before age 12, occur both at work and at home, and have resulted in functional impairment (evidenced by her supervisor’s threat of disciplinary action). Given her age, it would be difficult to collect collateral supporting information from a teacher or parent, and so the patient report alone will need to be the only account of symptoms. The clinician’s judgment about the validity of these claims will also need to be taken into consideration. If possible, an attempt could be made to discuss these issues with the patient’s husband or work supervisor in order to acquire different perspectives and additional supporting information. Other psychiatric diagnoses and substance abuse issues are ruled out; therefore, the ADHD symptoms are not better explained by another psychiatric disorder.

Is this patient a candidate for a pharmacotherapeutic intervention?   Yes. Current treatment guidelines recommend initiating drug therapy in adults as a first-line treatment.

Is this patient a candidate for non-drug therapy?   Yes, if necessary. There is no treatment guideline that specifically recommends non-drug therapy for adult patients because there is a lack of efficacy data to support it. However, if the patient complains of specific symptoms that may be behavior-mediated (such as time management or procrastination-related symptoms), counseling or other workshop-based interventions may help her to manage these symptoms more effectively and may eventually reduce her dependence on drug therapy for the monotherapy of ADHD.

What pharmacotherapeutic intervention(s) would be most appropriate? Consistent with the domestic guidelines for the management of ADHD in children, the National Institute for Health and Care Excellence guidelines in Europe recommend initiating a stimulant medication as first-line therapy. None of the stimulants are considered superior with regard to safety or efficacy in adults or children. However, a long-acting formulation is generally preferred because of the reduced likelihood of abuse. This patient has no history of substance abuse, but use of longer-acting formulations will minimize any risk.

Longer-acting products tend to have a smoother onset and offset of action compared with immediate-release agents, which produce a noticeable onset in most patients. A longer-acting product will reduce the pill burden and will require less frequent dosing-an advantage for someone who needs coverage throughout the day.

If this patient has a contraindication to stimulants, what is the next most appropriate intervention? Contraindications to stimulants generally include cardiovascular issues such as arrhythmias, uncontrolled hypertension, or concomitant administration of other drugs that can be arrhythmogenic. In the setting of a contraindication, the nonstimulants could be considered. Atomoxetine is generally used first because its efficacy data are more robust than that of clonidine, guanfacine, and bupropion.

If this patient had a comorbid diagnosis of depression or anxiety, how might the treatment plan for ADHD be different? Depending on the severity of symptoms, the practitioner may choose to treat the mood or anxiety disorder first. This depends on which symptoms are most distressing and which are causing the most functional impairment. Improvement in a comorbid mood and/or anxiety disorder may also indirectly improve ADHD symptoms because patients who are euthymic and not anxious may be better equipped to deal with the ADHD symptoms. Assuming that the comorbid diagnosis is depression, a stimulant and an antidepressant could be initiated, but not at the same time in order to gauge which drug resulted in the resolution of which symptoms.

Bupropion might be a possible intervention if a reduction in pill burden is important. Bupropion is not indicated for ADHD, but there is some evidence to support its use. Assuming that the comorbidity is anxiety, the initiation of a stimulant may or may not worsen symptoms. This is highly patient-specific and will depend on whether the anxiety is worsening the ADHD or vice versa. It may be advisable to initiate medication therapy for the anxiety first and once improved or resolved, initiate drug therapy carefully for the ADHD and monitor for worsening of anxious symptoms.

Historically considered a diagnosis of childhood, ADHD persists into adulthood for a vast majority of patients. Secondary to the absence of validated screening tools for adults, the pervasive symptom overlap with other psychiatric illnesses, frequent comorbidity with other psychiatric diagnoses, feigned ADHD, and the risk of drug diversion or abuse, diagnosis in adults has proven to be challenging. However, utilizing the available diagnostic criteria, gathering as much data as possible from as many sources as possible, considering the possible influence of other psychiatric comorbidities, and being diligent in assessing risk of abuse, the diagnosis of ADHD in an adult can be achieved responsibly and with minimal risk.

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Disclosures:

Dr Reinhold is Associate Professor of Clinical Pharmacy in the department of pharmacy practice/pharmacy administration at The Philadelphia College of Pharmacy at the University of the Sciences in Philadelphia.

References:

1. Davidson MA. ADHD in adults: a review of the literature. J Atten Disord . 2008;11:628-641.

2. Taylor A, Deb S, Unwin G. Scales for the identification of adults with attention deficit hyperactivity disorder (ADHD): a systematic review. Res Dev Disabil . 2011;32:924-938.

3. Haavik J, Halmøy A, Lundervold AJ, Fasmer OB. Clinical assessment and diagnosis of adults with attention-deficit/hyperactivity disorder. Expert Rev Neurother . 2010;10:1569-1580.

4. Kessler RC, Adler L, Barkley R, et al. The prevalence and correlates of adult ADHD in the United States: results from the National Comorbidity Survey Replication. Am J Psychiatry . 2006;163:716-723.

5. McGough JJ, Smalley SL, McCracken JT, et al. Psychiatric comorbidity in adult attention deficit hyperactivity disorder: findings from multiplex families. Am J Psychiatry . 2005;162:1621-1627.

6. Levin FR. Diagnosing attention-deficit/hyperactivity disorder in patients with substance use disorders. J Clin Psychiatry . 2007;68(suppl 11):9-14.

7. Santosh PJ, Sattar S, Canagaratnam M. Efficacy and tolerability of pharmacotherapies for attention-deficit hyperactivity disorder in adults. CNS Drugs . 2011;25:737-763.

8. Fayyad J, De Graaf R, Kessler R. Cross-national prevalence and correlates of adult attention-deficit hyperactivity disorder. Br J Psychiatry . 2007;190:402-409.

9. Ginsberg Y, Quintero J, Anand E, et al. Underdiagnosis of attention-deficit/hyperactivity disorder in adult patients: a review of the literature. Prim Care Companion CNS Disord . 2014;16.

10. US Department of Health and Human Services. National Institute on Drug Abuse. Stimulants . October 2011. http://www.drugabuse.gov/publications/research-reports/prescription-drugs/stimulants . Accessed September 1, 2015.

11. Substance Abuse and Mental Health Services Administration. Results from the 2013 National Survey on Drug Use and Health: Summary of National Findings. 2013.

. Accessed August 31, 2015.

12. Romach MK, Schoedel KA, Sellers EM. Human abuse liability evaluation of CNS stimulant drugs. Neuropharmacol . 2014;87:81-90.

13. Calcaterra S, Glanz J, Binswanger IA. National trends in pharmaceutical opioid related overdose deaths compared to other substance related overdose deaths: 1999-2009. Drug Alcohol Depend . 2013;131:263-270.

14. Upadhyaya HP. Managing attention-deficit/hyperactivity disorder in the presence of substance use disorder. J Clin Psychiatry . 2007;68(suppl 11):23-30.

15. Primich C, Iennaco J. Diagnosing adult attention-deficit hyperactivity disorder: the importance of establishing daily life contexts for symptoms and impairments. J Psychiatr Ment Health Nurs . 2012;19:362-373.

16. Greenhill LL, Pliszka S, Dulcan MK, et al. Practice parameter for the use of stimulant medications in the treatment of children, adolescents, and adults. J Am Acad Child Adolesc Psychiatry . 2002;41(suppl 2):26S-49S.

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7 Sneaky Signs Of ADHD In Women

Wellness Reporter, HuffPost

Earlier this spring, actress Busy Philipps announced that she was diagnosed with attention-deficit/hyperactivity disorder (ADHD) alongside her 15-year-old daughter. Philipps’ diagnosis is part of a recent trend of more and more women and girls being diagnosed with ADHD .

From 2020 to 2022, the rate of ADHD diagnoses in women has doubled, said Suwilanji Kuezi-Nke , a clinical psychologist at Transcend Counseling Chicago. This steep rise “may be due to the ways in which the pre-COVID-19 pace and structure of life masked symptoms,” she said, but also speaks to something larger.

“ADHD was once a diagnostic category that was dominated by boys with too much energy,” said Madison Perry, a psychologist and owner of Austin Holistic Psychology in Texas. In fact, boys are roughly three times more likely to receive an ADHD diagnosis than girls, according to Medical News Today .

“More women are being diagnosed with ADHD because information is spreading. With more awareness of the varied presentations of ADHD, more women are likely to be referred for an evaluation,” Perry said.

When thinking about ADHD, you likely imagine someone who is rambunctious and can’t sit still. While that isn’t wrong, that is not the way ADHD tends to show up in women and girls. A number of factors play into the differences in ADHD presentation, but one major one is the societal pressures and norms expected for women.

“There is a theory that this is more of a product of how women are socialized in the Western societies rather than a biological difference between men and women,” Perry said.

So when it comes to how ADHD presents in women, it looks a little different. Here are the signs of ADHD in women and girls:

Difficulty focusing on singular tasks.

Rather than the hyperactivity and impulse control issues seen in boys, “ADHD tends to present in women as more inattention [and] difficulty focusing and completing tasks,” Perry explained.

Your mind may feel like it can’t focus on one task — especially one that you don’t find interesting. For example, you might start cleaning the bathroom but get distracted halfway through. Or you may set out to try a new creative project ― like knitting ― but it doesn’t hold your interest long enough to finish the blanket.

Hyper-focusing on certain topics or situations.

It’s also not unheard of for people with ADHD to hyper-focus on certain topics while struggling to focus on others, noted Marcy Caldwell, a psychologist and the owner of the Center for ADHD in Philadelphia.

When you’re hyper-focused, it feels impossible to stop doing the task at hand, or you get totally lost in whatever project you’re working on. Your brain is only interested in the one thing you’re doing.

“A lot of the things that can create that hyper-focus are things that people are really interested in ... that’s one of the motivating factors for an ADHD brain,” Caldwell said. “So, they’ll judge themselves for like, ‘If I can hyper focus on this thing, which is really compelling, why can’t I focus on the assignments that my boss gave me?’”

Racing thoughts.

While women are less likely to visually show hyperactivity and impulsivity, it does still show up in a different way. “There’s still a lot of cognitive hyperactivity that can happen, so thoughts can be going a mile a minute, but it’s often less physically presented,” Caldwell said.

According to the non-profit Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD) , this may also feel like trouble focusing on one topic.

Trouble keeping friendships.

According to Kuezi-Nke, women with ADHD may have difficulty sustaining friendships, too. “A lot of hyperactive symptomatology presents relationally for women, which is very different — it’s not as easy to see,” Kuezi-Nke said.

This does not mean difficulty making friends , but instead keeping those friendships alive. You may feel too emotionally drained to text a friend after a big meeting or may be too focused on other things to return their call; the emotional labor it takes to maintain friends can be tough for women with ADHD, according to ADDitude magazine .

Emotional outbursts and dysregulation.

According to Caldwell, it’s common for folks with ADHD to deal with emotional dysregulation; it’s even more common in women.

“ADHD brains are very prone to having very big emotions very frequently, and so they’re more likely to experience their emotions in a way that feels to the outside world disproportionate to the event,” Caldwell said.

For example, if a friend cancels plans you may find that you’re overcome with sadness and think that friend no longer cares about you. Or you may lose your temper over a small inconvenience at work.

Talking a lot.

Talking excessively can be another sign of ADHD in women, Kuezi-Nke noted. “Or kind of not thinking before you speak — reacting impulsively in conversation.” Similarly, interrupting other people while they’re talking can also be a symptom of ADHD.

Overall, women are more likely to internalize their ADHD symptoms.

“Women are also more likely to mask their symptoms, they’re more likely to internalize their symptoms,” Caldwell said. “So, they’re more likely to end up with symptoms like depression and anxiety and low self-esteem.” (In fact, in many women, ADHD can be misdiagnosed as anxiety, Kuezi-Nke said.)

Men, oppositely, are more likely to externalize their symptoms — which is also one of the big reasons why boys are more diagnosed than girls, she noted.

For girls and women, the distress they feel is kept inside and doesn’t present until much later in life, Caldwell added.

If you have these symptoms ― or think you have ADHD ― it’s important to seek professional help.

“If you or a loved one suspect that you may meet criteria for ADHD, I would recommend searching for an appropriate evaluator near you,” Perry said.

Caldwell stressed that when looking for a provider, it’s perfectly OK to interview them to ensure they have ample experience treating people, specifically women, with ADHD. Caldwell said you can ask about their ADHD training, how they work with people with ADHD and how many clients of theirs have ADHD. “You just really want to be careful that people have a lot of experience,” Caldwell added, noting that CHADD has a provider directory you can reference, too.

Perry noted that for a comprehensive approach, which she recommends, you should seek out an assessment by a neurologist, primary care physician and a psychologist. This way, they can determine if you have ADHD or another diagnosis.

“You want to be sure that your team understands how to create a differential diagnosis so that you will leave the evaluation process with an appropriate treatment plan,” Perry said.

Additionally, “I really encourage all people, but specifically women ... to not let [mental health stigma] deter them from seeking the information that they need,” said Kuezi-Nke. “If anyone is noticing impairment, it is human. Right? We all struggle.”

ADHD runs on a spectrum, Kuezi-Nke added, so “even if you aren’t specifically diagnosed with ADHD, it doesn’t mean that those symptoms aren’t relevant and worth taking care of yourself for.” Never hold yourself back when it comes to getting proper support.

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Before You Go

Therapists Recommend These Back-To-School Items For Kids With ADHD

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ORIGINAL RESEARCH article

The implementation of a zero-suicide framework in a child and youth mental health service in australia: processes and learnings.

• 1 Mental Health and Specialist Services, Gold Coast Hospital and Health Service, Southport, QLD, Australia
• 2 Faculty of Health Sciences and Medicine, Bond University, Robina, QLD, Australia
• 3 Departments of Psychiatry and Pediatrics, Center for the Study and Prevention of Suicide, University of Rochester, New York, NY, United States
• 4 Mental Health and Specialist Services, Metro North Hospital and Health Service, Herston, QLD, Australia

Suicide in children is a significant and growing problem. The “zero suicide” framework (ZSF) is one approach to suicide prevention used in health services for adults and children. This paper reports on the introduction of the first suicide prevention pathway (SPP) based on ZSF at a Child and Youth Mental Health Service (CYMHS) in Australia. It begins by describing the adaptations made to elements of the SPP originally designed for adults to meet the needs of children. Lessons learned in applying the SPP in the service are then discussed. The aim is to inform and improve practice in the use of zero suicide approaches in child and youth mental health settings in Australia and worldwide.

1 Introduction

1.1 suicide in children.

Suicide attempts and suicidal ideation among children (people aged ≤17 years) are significant and growing problems. In large American and European school samples, up to 39.4% of children reported experiencing suicidal thoughts, and up to 9.0% had made at least one suicide attempt ( 1 , 2 ). Preventing and addressing suicidal ideation and attempts in children is, therefore, a priority. Systematic reviews consistently show that school-based interventions (e.g., suicide education, counselling) are moderately effective in reducing suicidal ideation and suicide attempts ( 3 , 4 ). Other community-based interventions (e.g., support for young people bereaved by a suicide) and many therapeutic clinical interventions do not have consistent and/or sustained effects ( 3 – 5 ).

1.2 The zero suicide framework and suicide prevention pathway in Australia

One strategy for suicide prevention in health care settings, for adults and children, is the zero suicide framework (ZSF), developed by the National Action Alliance for Suicide Prevention ( 6 ). The framework involves suicide-specific practices which are delivered through whole systems of care and aim to continuously improve service access, quality, and safety ( 7 , 8 ). It is a systems approach to suicide prevention that focuses on understanding the suicide event, formulating individualised risk, delivering first line interventions and follow-up, and drawing on the child’s strengths and resources. It also endorses support for staff through training and ongoing learning within services, and via evaluation of care and incidents within a Restorative Just Culture framework ( 9 ). The approach is rooted in a service culture that does not accept suicide as an outcome.

The ZSF and its clinical approach, the suicide prevention pathway (SPP), are new to the Australian setting and were first implemented at Gold Coast Mental Health and Specialist Services (GCMHSS) in Queensland, Australia in 2016 alongside the introduction of Australia-wide suicide prevention strategies ( 10 ). Implementation occurred in response to a review of increases in suicides in the service, and broader challenges around the delivery of suicide prevention interventions ( 11 ).

The GCMHSS sees >5,400 suicidal presentations each year via its two hospital emergency departments (EDs) ( 12 ). Young people aged 15-24 years account for 37.4% of suicidal presentations by females and 28.1% of presentations by males to GCMHSS ( 12 ). Children aged ≤17 years of age who engage in a suicide attempt or are deemed at risk of suicide by family or professionals are directed to the Child and Youth Mental Health Service (CYMHS) within GCMHSS. This service provides 24-hour multidisciplinary care to children who are experiencing severe and/or complex psychological, emotional, or behavioural problems, including (but not limited to) suicidality ( 13 , 14 ).

The aim of this paper is to describe the adaptations made to the elements of the SPP originally designed for adults to meet the needs of children aged ≤17 years of age. Key lessons learned in applying the SPP in a children’s mental health setting are then presented. The intention is to inform and improve the use of zero suicide approaches in child and youth mental health settings globally.

2 The GCMHSS suicide prevention pathway for children

In this section we describe how the components of the SPP originally designed for adults have been adapted to meet the needs of children. We describe our experience and observations in using the SPP’s tools and highlight specific aspects to consider when providing care to suicidal children and their caregivers. Figure 1 lists the key components of the SPP for children at the GCMHSS:

Figure 1 Key components of the SPP for children at the GCMHSS.

The components of the SPP are similar for children and for adults. However, the way the SPP is implemented differs between children and adults. For example: a child’s participation in components such as safety planning increases as their age and capacity does. Where a child does not have the capacity to participate or is too distressed to engage fully in components such as safety planning, parents/carers are more involved. We also acknowledge here that many components of the SPP, and the underlying philosophy, are fundamentally similar to other approaches to youth suicide prevention, such as SAFETY-Acute ( 15 ).

2.1 Screening

Screening to identify children at risk of suicide is an essential first component of the Zero Suicide framework. However, a standardised screening tool is not used to determine access to interventions or to predict an individual’s risk. At the GCMHSS CYMHS, screening and assessment for suicidality is undertaken using the Chronological Assessment of Suicidal Events (CASE) approach.

The CASE approach assists a clinician to explore suicidal ideation, planning, behaviours, and intent with a child, while maximising engagement with them ( 16 ). A strong therapeutic alliance and collaborative, non-judgmental stance is key. The CASE approach complements the broader comprehensive psychiatric assessment that considers risk/protective factors and warning signs ( 16 ).

With children, the CASE approach time interval format is applied more fluidly to enhance engagement. The child is supported to take control and to guide the process of disclosure, while the clinician gently navigates the conversation to ensure all timeframes are covered. Some of the questioning techniques in the CASE approach can be implemented with children with good effect. For example, the subtle shift of a closed questioning style (e.g., “Have you thought of ways to end your life?” ) to a gentle assumption (e.g., “What ways have you thought of to end your life?” ) may help a child to feel more comfortable discussing their methods. Open-ended questioning encourages clinically rich data, which is vital to informing safety planning. It also assumes that the young person is thinking of means of suicide, which gives them permission to share this with the clinician. The use of the behavioural incident techniques (e.g., fact finding, sequencing) is often well-received by children, who feel as though the clinician is comfortable with discussing their suicidality.

Consideration should be given to the power differences between the clinician and the child, along with the potential suggestibility of some children (e.g., the technique of denial of the specific and symptom amplification). Specific consideration should be given to younger children and those with developmental difficulties due to their potential suggestibility. The relevant CASE question has been altered to either include visual scales or by adding context (e.g., by asking the young person, “On your worst day, do you think about suicide when you wake up? When you are at school? When you are with your friends? When you are at home with mum and dad?” ). A more narrative approach and interview style is helpful for younger children and for children with Aboriginal and/or Torres Strait Islander heritage, ensuring the timeframes are still woven into the assessment.

When working with children, the involvement of parents/carers in the CASE assessment is essential to ensuring comprehensive information-gathering. Parent/carer involvement is a strong protective factor for children who have attempted suicide ( 17 ). Parents/carers can provide valuable information about the observed amount of thinking, planning, or actions taken in relation to suicidal ideation that may reflect the intensity of the actual suicidal intent. Our clinicians identified that suicide attempts in children are frequently impulsive and reactive to feeling overwhelmed by shame, loss of control, hopelessness, and sadness, and interpersonal difficulties, especially with family/peers. We find that the time spent by a child on suicidal planning is, often, a more reliable reflection of the seriousness of their intent and of the proximity of their desire to proceed on that intent, than is the stated intent.

Where possible, and providing the clinician has consent, interviews should be conducted with the child without their parent/carer present. Our clinicians have observed that children often feel more comfortable to disclose risk without their parent/carer present. Interviews need to be conducted with the parent/carer separately to obtain information that may not be appropriate to discuss with the child. Subsequently, collaborative discussion with the child and their parent/carer are essential. This encourages understanding of the child’s suicidal thoughts and behaviours, equips the parent/carer with the necessary insight to provide adequate support, and is essential in informing safety planning. Equipping the parent/carer might involve, for example, providing psychoeducation on suicide, engaging them in safely planning, recognizing when their child is distressed and at risk of harming themselves, and supporting them to proactively restrict lethal means.

In our experience, in comparison to working with adults, using the CASE approach with a child is a more time-intensive process. As a service we learned to take younger children’s (<12 years) behavioural and verbal statements of hopelessness and wishing to die seriously when utilising this approach, whereas before these reactions were all too often deemed to be the child “acting out”.

Figure 2 lists the criteria for commencing a child on the SPP at CYMHS:

Figure 2 Criteria used at CYMHS to commence a child on the SPP and for admitting a child as an inpatient for suicidality.

2.2 Risk formulation

Categorical suicide risk stratification based on yes/no questions is widely accepted as inadequate in predicting future risk of suicide, and unreliable in determining who should and should not receive care ( 18 – 21 ). However, alternative approaches are limited and lack an evidence base. It has been argued that engagement, building a strong therapeutic relationship, understanding the context such as precipitating and perpetuating factors of a suicide attempt, and developing a management plan in collaboration with the consumer – in this case, the child – to mitigate and manage risks is of more value and importance than risk categorisation ( 18 , 20 , 22 ).

When implementing the SPP with children, we extended on this idea, recognising the importance of parents/carers as the key support system. Parents/carers are vital in understanding the child’s suicide attempt, developing a management plan collaboratively with the child, and engaging in a therapeutic alliance. Equally, including a child’s wider identified support network in safety planning is helpful.

The prevention oriented risk formulation ( 23 ) synthesises information gathered through an assessment of the child and their support network. Risk status and risk state are two ways of contextualising risk. ‘Risk status’ describes a judgment of the child’s risk relative to others in a specific population (e.g., the local general population of the same age and/or same developmental age) or setting (e.g. population attending local community or inpatient mental health settings). ‘Risk state’ describes a judgment about risk in relation to the child’s own baseline or other selected time points. Clinicians arrive at judgments about risk status and state through reports from the child, reports from their parent/carer, and information from clinical observations.

More important than the determination of risk status/state is communicating the factors and thinking behind the determination. Prevention-oriented risk formulation then directs attention to identifying available internal resources (individual) and external resources (parents’/carers’ and others’), and foreseeable changes which might lead to a rapid increase or decrease in risk ( 23 ). One of the foreseeable changes should always be the driver/s of the suicide attempt, as addressing driver/s is an important part in planning for effective treatment ( 24 ). Importantly, the risk formulation is not used for predictive purposes or to determine acceptability for treatment, but rather for communication within the team, with the parent/carer, and with the child. It enables broader understanding of the issues for the child so that an individual, forward-looking, and collaborative plan can be developed.

2.3 Universal interventions

After assessment, safety planning with the child and their parent/carer, and risk formulation, a child will be offered care through the SPP. This will include universal interventions, which aim to enhance safety as part of an individualised care plan. ED settings are focus areas for brief interventions ( 25 ). Universal interventions identified as deliverable in busy ED settings include safety planning intervention (SPI), counselling on restricting access to lethal means (embedded in SPI), crisis numbers (delivered as part of SPI), brief patient and carer information, and arranging rapid follow up ( 26 ).

Children who present with acute suicidality and a risk profile above baseline can be challenging to engage in assessment, treatment, and follow up care. In our experience, when in crisis, children frequently struggle to talk about their feelings and thoughts. Parent/carers can also be significantly overwhelmed, distressed, anxious, and unable to meet the needs of their child. To manage the stress, both the child and the parent/carer might minimise the suicidal event, or they might be unable to reflect and develop insight into what triggered and maintained or what might resolve it. Hence, support through a structured and brief process to problem-solve safety issues is beneficial. Issues identified through this process are revisited and further explored during the follow-up appointments.

Suicidal thoughts often fluctuate over time ( 27 ). Children who are given skills and strategies for future use may be able to resist or delay acting on suicidal thoughts until they subside or care can be accessed. The SPI is a prioritised set of coping skills and supports, developed in collaboration with the child and a parent/carer or other support person, used for this purpose ( 28 ).

The SPI includes processes to identify warning signs, internal coping strategies, social contacts to distract from suicidal thoughts, social and professional supports, and strategies to restrict access to lethal means of suicide. There is growing evidence that the SPI improves consumer engagement, helps in resolving suicidal crises ( 25 , 29 ), and reduces repeated self-harm and suicide risk ( 29 , 30 ).

The SPI was modified for the SPP to include two additional questions about the drivers of suicide and solutions to these, contact details of the consumer and an alternative contact, and information on local and national 24-hours crisis numbers. A child-friendly version was developed to help children in crisis to overcome barriers to reflect, communicate, and problem-solve. The redesign involved input from children, CYMHS multidisciplinary clinicians, and other stakeholders. It includes pictures, colours, prompts to stimulate reflection and problem-solving and more child-friendly language throughout (e.g., a shift from ‘Internal coping strategies’ to ‘Things I can do to help me get through this’ ). It also includes child-specific crisis numbers, webchat options, and apps to support safety planning. When delivering the SPI, clinicians employ features of motivational interviewing, which has been used with success in youth suicide prevention ( 31 , 32 ), to encourage engagement.

Clinicians also developed an approach to engaging parents/carers as part of the SPI. This is collaborative, with emphasis on the child feeling heard, understood, and supported in a way that they perceive to be helpful. It provides an opportunity to bring the child and their support system closer, and to safety plan with the support system in times when the child themselves might struggle.

2.4 Preventing access to lethal means

Lethal means counselling is an essential component of safety planning, and it has been shown to reduce the risk of a suicide attempt and death ( 33 ). It is conducted with both the child and the parent/carer and based on the information obtained through earlier interviews. It is imperative that counselling is followed up with a phone call to the parent/carer to ensure the agreed actions were, or are being, implemented. A child in crisis often places the whole family system in crisis, and this can impact a family’s ability to retain information and take the appropriate steps to meet the needs of the child. Hence, it is paramount to extend ongoing support to the family and broader networks.

One of the complexities of safety planning occurs when access to a method of high lethality has been identified by the clinician but is not recognised by the child (for example, when a child lives on a rural property and has access to firearms but the child has not identified this as a method of suicide). Often children are not as advanced as adults with identifying methods, yet these must be included in safety planning. In such instances, separate conversations need to be held with the parent/carer to ensure safety planning has occurred. A parent/carer version of a safety plan might be drafted.

2.5 Structured follow-up and transition of care

Effective transitions of care are of central importance in the ZSF, considering the elevated risk of suicide in the post-discharge period ( 34 ), however engaging with consumers following a suicide attempt can be very challenging. In children specifically, only 76% may attend follow-up outpatient treatment appointments ( 35 ). In adults, strategies such as scheduling the first appointment within two to three days, and intensive outreach in the post discharge period, may improve follow-up ( 36 ).

Community follow-up requires a consistent, structured approach. It include clinical activities such as Mental State Examination with a focus on mood and reassessment of suicidality, the child’s risk state and status and foreseeable changes, available resources, collaborative review and revision of the safety plan, collaborative development of a care plan, identification of barriers to implementing the care plan, and agreement on further follow-up care. A care plan should be completed collaboratively with the parent/carer and should involve the driver for the suicide attempt and the strategies to mitigate risk. The clinician explores whether ongoing care is necessary and which services are best suited, and provides a seamless handover where the child has their first appointment with the next provider prior to closure of care under the SPP. Closure of the SPP is not a process-driven decision (e.g. as the child has their first appointment with the next provider); sometimes, there is no onward referral.

3 Discussion

3.1 learnings from spp implementation.

Sustained change in large health systems is challenging to bring about, and change initiatives have high failure rates ( 37 ). We have outlined the steps taken to implement and embed a significant change in clinical approach to suicide prevention in a large child and youth mental health service in Australia. Implementing and maintaining fidelity to such a change in the absence of a significant increase in clinical resources can be achieved but has not been without challenges. Figure 3 shows the learning highlights from implementing the SPP at the GCMHSS CYMHS:

Figure 3 Learning highlights from implementing the SPP at the GCMHSS CYMHS.

3.2 Conclusions

Globally, suicide in children is a significant and growing problem. The Zero Suicide Framework (ZSF) is one approach to suicide prevention adopted in health services for adults and children. This paper reports on the introduction of the first Suicide Prevention Pathway (SPP) based on ZSF at a Child and Youth Mental Health Service in Australia. It describes the adaptations made to elements of the SPP originally designed for adults to meet the needs of children, and presents the lessons learned. It shows that a standardised approach to suicide prevention improves consistency in the delivery of first line interventions and, hence, has the potential for significant positive clinical outcomes.

Data availability statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

Ethics statement

The studies involving humans were approved by Gold Coast Health Human Research Ethics Committee (HREC) Reference LNR/2018/QGC/47473, 11 October 2018. The studies were conducted in accordance with the local legislation and institutional requirements. The ethics committee/institutional review board waived the requirement of written informed consent for participation from the participants or the participants’ legal guardians/next of kin because This study is exempt from ethical review as it involves routine data collection undertaken for clinical quality assurance.

Author contributions

GB: Formal analysis, Investigation, Methodology, Project administration, Visualization, Writing – original draft, Writing – review & editing. LM: Formal analysis, Investigation, Methodology, Project administration, Visualization, Writing – original draft, Writing – review & editing, Validation. DJ: Data curation, Writing – original draft, Writing – review & editing. SM: Data curation, Methodology, Writing – original draft, Writing – review & editing. PW: Resources, Software, Writing – original draft, Writing – review & editing. SC: Resources, Software, Writing – original draft, Writing – review & editing. HJ: Resources, Software, Writing – original draft, Writing – review & editing. AP: Conceptualization, Validation, Writing – original draft, Writing – review & editing. CS: Conceptualization, Methodology, Validation, Writing – original draft, Writing – review & editing. MW: Conceptualization, Writing – original draft, Writing – review & editing. KT: Conceptualization, Methodology, Writing – original draft, Writing – review & editing. SW-M: Conceptualization, Investigation, Methodology, Supervision, Validation, Writing – original draft, Writing – review & editing.

The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.

Acknowledgments

We would like to acknowledge the staff, children, and families we work with.

Conflict of interest

AP is the equity owner of SafeSide Prevention / SafeSide Australia which licensed educational materials from University of Rochester. SafeSide receives fees for education, consultation, and leadership services for healthcare organisations and government. The University of Rochester receives royalties from SafeSide and declares this financial interest. A conflict of interest management plan is in place at the University of Rochester and routinely communicated and monitored per University guidelines. AP receives book royalties from Cambridge University Press.

The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Keywords: zero suicide framework, suicide, prevention, pathway, youth, child, mental health

Citation: Branjerdporn G, McCosker LK, Jackson D, McDowell S, Williams P, Chand S, Joshi H, Pisani AR, Stapelberg C, Welch M, Turner K and Woerwag-Mehta S (2024) The implementation of a zero-suicide framework in a child and youth mental health service in Australia: processes and learnings. Front. Psychiatry 15:1370256. doi: 10.3389/fpsyt.2024.1370256

Received: 14 January 2024; Accepted: 16 April 2024; Published: 16 May 2024.

Reviewed by:

Copyright © 2024 Branjerdporn, McCosker, Jackson, McDowell, Williams, Chand, Joshi, Pisani, Stapelberg, Welch, Turner and Woerwag-Mehta. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Sabine Woerwag-Mehta, [email protected]

†These authors share first authorship

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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